Foundations of Periodontics for the Dental Hygienist [4 ed.] 1451194153, 9781451194159

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Q ck F d G de 1

Pe rio d o n t iu m

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Be st Pra ct ice s

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Micro sco p ic An a t o m y

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No n su rg ica l Th e ra p y

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Ove rvie w o Dise a se s

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Pa t ie n t ’s Ro le

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Dise a se Cla ssi ica t io n

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Irrig a t io n

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Clin ica l Fe a t u re s

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Ch e m ica l Ag e n t s

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Gin g iva l Dise a se s

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Ho st Mo d u la t io n

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Ch o n ic Pe rio d o n t it is

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Su rg ica l Co n ce p t s

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Ag g re ssive Pe rio d o n t it is

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Em e rg e n cie s

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Ot h e r Co n d it io n s

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Mo t iva t io n

10

De cisio n -Ma kin g

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Ma in t e n a n ce

11

Et io lo g ic Fa ct o rs

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De n t a l Im p la n t s

12

Ora l Bio ilm s

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Pe rio -Syst e m ic

13

Im m u n it y/In la m m a t io n

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Ma lo d o r/Xe ro st o m ia

14

Ho st Re sp o n se

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Do cu m e n t a t io n

15

Syst e m ic Fa ct o rs

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Fu t u re Dire ct io n s

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Lo ca l Fa ct o rs

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Pa t ie n t Ca se s

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Nu t rit io n

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Ra d io g ra p h ic a n a lysis (o n lin e re so u rce )

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To b a cco & Sm o kin g

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Pe rio d o n t a l Asse ssm e n t

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Ra d io g ra p h ic An a lysis

In st ru ct o r/St u d e n t Re so u rce s (o n lin e )

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da

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Pe d he De Hyg e s

cs al

Fo u r t H EDit io n

J ll S. Ge h g , r DH, MA Dean Emeritus, Division o Allied H ealth & Public Service Education Asheville-Buncombe Technical Community College Asheville, N orth Carolina

D

ald E. W llma

, DDS, MS

Pro essor Emeritus, Department o Periodontics University o Texas H ealth Science Center at San Antonio San Antonio, Texas

Senior A cquisitions Editor: Jonathan Joyce Product D evelopm ent Editor: John Larkin Production Project M anager: David Saltzberg D esign Coordinator: Steve Druding M ark eting M anager: Leah Thompson M anufacturing Coordinator: M argie O rzech Prepress Vendor: Aptara, Inc. 4th Edition Copyright © 2016 Wolters Kluwer. All rights reserved. This book is protected by copyright. N o part o this book may be reproduced or transmitted in any orm or by any means, including as photocopies or scanned-in or other electronic copies, or utilized by any in ormation storage and retrieval system without written permission rom the copyright owner, except or brie quotations embodied in critical articles and reviews. M aterials appearing in this book prepared by individuals as part o their o cial duties as U.S. government employees are not covered by the above-mentioned copyright. To request permission, please contact Wolters Kluwer at Two Commerce Square, 2001 M arket Street, Philadelphia, PA 19103, via email at [email protected], or via our website at lww.com (products and services). 9 8 7 6 5 4 3 2 1 Printed in China Library of Congress Cataloging-in-Publication Data Gehrig, Jill S. (Jill Shi er), author. Foundations o periodontics or the dental hygienist/Jill S. Gehrig, Donald E. Willmann. – Fourth edition. p. ; cm. Includes bibliographical re erences and index. ISBN 978-1-4511-9415-9 I. Willmann, Donald E., author. II. Title. [DN LM : 1. Periodontics. 2. Dental H ygienists. 3. Periodontal Diseases–therapy. WU 240] RK361 617.6’32–dc23 2015006097 This work is provided “ as is,” and the publisher disclaims any and all warranties, express or implied, including any warranties as to accuracy, comprehensiveness, or currency o the content o this work. This work is no substitute or individual patient assessment based upon health care pro essionals’ examination o each patient and consideration o , among other things, age, weight, gender, current or prior medical conditions, medication history, laboratory data and other actors unique to the patient. The publisher does not provide medical advice or guidance and this work is merely a re erence tool. H ealth care pro essionals, and not the publisher, are solely responsible or the use o this work including all medical judgments and or any resulting diagnosis and treatments. Given continuous, rapid advances in medical science and health in ormation, independent pro essional veri cation o medical diagnoses, indications, appropriate pharmaceutical selections and dosages, and treatment options should be made and health care pro essionals should consult a variety o sources. When prescribing medication, health care pro essionals are advised to consult the product in ormation sheet (the manu acturer’s package insert) accompanying each drug to veri y, among other things, conditions o use, warnings and side e ects and identi y any changes in dosage schedule or contraindications, particularly i the medication to be administered is new, in requently used or has a narrow therapeutic range. To the maximum extent permitted under applicable law, no responsibility is assumed by the publisher or any injury and/or damage to persons or property, as a matter o products liability, negligence law or otherwise, or rom any re erence to or use by any person o this work. LWW.com

L ab l y S a e me

This textbook endeavors to present an evidence-based discussion o periodontology based on in ormation rom recent research. Periodontology, however, is a rapidly changing science. The authors, editors, and publisher have made every e ort to con rm the accuracy o the in ormation presented and to describe generally accepted practices at the time o publication. H owever, as new in ormation becomes available, changes in treatment may become necessary. The reader is encouraged to keep up with dental and medical research through the many peer-reviewed journals available to veri y in ormation ound here and to determine the best treatment or each individual patient. The authors, contributors, editors, and publisher are not responsible or errors or omissions or or any consequences rom application o the in ormation in this book and make no warranty, express or implied, with respect to the contents o this publication.

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r alph M. A ld, DDS Associate Pro essor, Retired Department o Periodontics University o Texas H ealth Science Center at San Antonio San Antonio, Texas

P a Eme ce -H ja, DDS, MS Assistant Pro essor Department o Periodontics University o Kentucky College o Dentistry Lexington, Kentucky

r b Bla Ma l , r DH, BSDH, JD Pro essor M ount Ida College Dental H ygiene Program N ewton, M assachusetts

A M. B h , BSDH, MS Assistant Pro essor and Continuing Education Coordinator School o Dental H ygiene O ld Dominion University N or olk, Virginia

r cha d F s e , DMD Department Chair, Dental Science Guil ord Technical Community College Jamestown, N orth Carolina

De b ah P. M ll ke , BS, DMD Pro essor and Chair, Dental Education South Florida Community College Avon Park, Florida

Ca l A. Jah , r DH, MS Senior Pro essional Relations M anager Water Pik, Inc. Fort Collins, Colorado

C a g S. M lle , DMD, MS Pro essor o O ral M edicine Division o O ral Diagnosis, O ral M edicine and O ral Radiology Department o O ral H ealth Practice College o Dentistry Lexington, Kentucky

El zabe h Ca , r DH, MDH Assistant Pro essor o Dental Hygiene University o M ississippi M edical Center Jackson, M ississippi De lw y Ca le y, PhD Pro essor o Psychology and Dentistry Director o H ealth Behavior Change Laboratory Department o Psychology University o Missouri – Kansas City Kansas City, M issouri Cha le s C bb, DDS, MS, PhD Pro essor Emeritus Department o Periodontics School o Dentistry University o Missouri – Kansas City Kansas City, M issouri t e e sa B le D ca , r DH, MDH Assistant Pro essor Department o Dental H ygiene School o Health Related Pro essions University o M ississippi M edical Center Jackson, M ississippi

A ch e A. J e s, DDS, MBA Pro essor Department o Periodontics University o Texas H ealth Science Center at San Antonio San Antonio, Texas Ma g a e Le mas e , BSDH, MS Assistant Pro essor School o Dental H ygiene O ld Dominion University N or olk, Virginia Sha L g e , r DH, MPH Virginia Department o H ealth Richmond, Virginia Dental H ealth Program

W ll am S. M e , DDS, MS Assistant Pro essor and Radiology Clinic Director Department o Comprehensive Dentistry School o Dentistry University o Texas H ealth Science Center at San Antonio San Antonio, Texas J h P e e ce , DDS, MS Pro essor, Retired Division o O ral & M axillo acial Radiology Department o Dental Diagnostic Science University o Texas H ealth Science Center at San Antonio San Antonio, Texas

Contributors Ch s ph A. r amse e , MAS D . Me d. De . Assistant Pro essor Department o Periodontology University o Berne, School o Dental M edicine Bern, Switzerland

Ca l S ha d, r n , MSn Tobacco Treatment Specialist O sher Center or Integrative M edicine N orthwestern M edical Group N orthwestern M edicine Chicago, Illinois

Ke e ha a Sa he e sh, DDS, MS Associate Pro essor and Director o Advanced Education Department o Periodontics School o Dentistry University o Missouri – Kansas City Kansas City, M issouri

r e be cca S da, r DH, MS Dean, H ealth Sciences South Florida State College Avon Park, Florida

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D a e Glassc e Wa e s , r DH, MBA Chie Executive O cer Pro essional Dental Management, Inc. Frederick, M aryland Ka e W ll ams, r DH, MS, PhD Pro essor and Chair Department o Biomedical and H ealth In ormatics School o M edicine University o Missouri – Kansas City Kansas City, M issouri

r ev ew e s

Ge e v e ve Be , r DH, MEd Pro essor Dental H ygiene LSUH SC School o Dentistry N ew O rleans, Louisiana

D a e Es e s, BS, MEd Instructor/Clinical Coordinator Dental H ygiene Athens Technical College Athens, Georgia

L sa H e , CDA, MA Dental Assisting Program Director O zarks Technical Community College Spring eld, M issouri

B e Bla k, MA Instructor – Dental H ygiene Camosun College Victoria, British Columbia, Canada

L sa Fle ck, r DH, MS Chairperson, Advisor College o Allied H ealth & N ursing – Dental H ygiene Minnesota State University – Mankato M ankato, M innesota

De b a Jame s, MSDS Dental Programs Director Fortis College – Phoenix Phoenix, Arizona

Me g a B g h b lk, r DH, MEd Instructor, Dental H ygiene H arrisburg Area Community College H arrisburg, Pennsylvania Ly a B. B ya , BSDH, MEd Associate Clinical Pro essor M arquette University School o Dentistry M ilwaukee, Wisconsin Ap l Ca le , MDH Program Chair Dental H ygiene Central Georgia Technical College M acon, Georgia Ch s e Ch e Vancouver College o Dental Hygiene Vancouver, British Columbia, Canada t ammy Cl sse , r DH, PhD Associate Pro essor, Dental H ygiene Pennsylvania College o Technology Williamsport, Pennsylvania L De F e , r DH, BS, Bt h Dental H ygiene Instructor Southeastern Technical College Vidalia, Georgia

L da He cke , CDA, r DH, BS, MA Director o Dental H ygiene Burlington County College Pemberton, N ew Jersey r se ma y He ma , r DH, MEd First Year Dental H ygiene Coordinator Montgomery County Community College Blue Bell, Pennsylvania Je e K.L. He w , r DH, MSHCM, FADPo Assistant Pro essor LSUH SC School o Dentistry N ew O rleans, Louisiana Sa d a H e , MHSA, r DH Associate Pro essor o Dental H ygiene University o M ississippi M edical Center Jackson, M ississippi

L Kacz , r DH, MS Associate Pro essor Dental H ygiene Erie Community College Williamsville, N ew York C e K ache , PhD, MSD Director o Dental Assisting Program Department o Dental Education Indiana University – Purdue University Fort Wayne Fort Wayne, Indiana n a cy Ma , r DH, MSEd Clinical Pro essor Indiana University – Purdue University Fort Wayne Fort Wayne, Indiana J y o sb , r DH, BS, MA Associate Pro essor School o Dentistry University o M innesota M inneapolis, M innesota Ma y A Sch e de ma , r DH, MS Clinical Assistant Pro essor and Senior Clinic Coordinator University o M aryland School o Dentistry Baltimore, M aryland

Reviewers S ac e Sc v e , r DH, MEd Ahead o Dental H ygiene Department M issouri Southern State University Joplin, M issouri

Me la e t ave a, MS, r DH Assistant Pro essor/Clinical Faculty University o Texas H ealth Care Center at San Antonio San Antonio, Texas

Phyll s Sp ag g e , r DH, MA Dental H ygiene Director Foothill College Los Altos H ill, Cali ornia

Ma a t g e , DDS Pro essor o Dental Programs H ealth, Sa ety and Community Service Algonquin College O ttawa, O ntario, Canada

Ma be h S , BSDH, r DH, MEd Pro essor and Director o Dental H ygiene Program Lone Star College – Kingwood Kingwood, Texas

K s y u e b k, BSDH, MEd Allied H ealth and N ursing Lorain County Community College Elyria, O hio

La a We bb, r DH, MS, CDA LJW Education Services Fallon, N evada

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Foundations of Periodontics for the D ental H ygienist, 4th edition, is written with two primary goals in mind. First and oremost, this textbook ocuses on the dental hygienist’s role in periodontics. O ur second goal was to develop a book with an instructional design that acilitates the teaching and learning o the complex subject o periodontics—as it relates to dental hygiene practice—without omitting salient concepts or “ watering down” the material. Written primarily or dental hygiene students, Foundations of Periodontics for the D ental H ygienist also would be a valuable resource on current concepts in periodontics or the practicing dental hygienist or general dentist.

ONLINE INSTRUCTOR AND STUDENT RESOURCES Follow the steps in Box 1 to access the online instructor resources.

B x 1. Acce ss g o l e i s

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1. Op e n a n in t e rn e t b ro w se r a n d se le ct : h p:/ / he p 2. Exist in g u se rs: Click o n “ r e

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3. Ne w u se rs: Se le ct “ n e w u se .” Co m p le t e a ll re q u ire d f e ld o n t h e o n lin e a cce ss re q u e st o rm . • Ed u ca t o rs: In st ru ct o r a cce ss co d e s co m e d ire ct ly ro m yo u r sa le s re p re se n t a t ive . Acce ss co d e s in t h e p ro d u ct p a cka g in g a re in t e n d e d o n ly o r a cce ss t o st u d e n t re so u rce s. I yo u n e e d a d d it io n a l h e lp e n t e rin g a co d e , p le a se co n t a ct yo u r sa le s re p re se n t a t ive . • St u d e n t s: Acce ss co d e s a re lo ca t e d in sid e t h e ro n t o r b a ck co ve r o t h e b o o k. 4. Lo ca t e F da s Pe d cs he De al Hyg e s . Se le ct e it h e r “ St u d e n t Re so u rce s” o r “ In st ru ct o r Re so u rce s.”

Preface for Course Instructors

TEXTBOOK FEATURES The ourth edition o Foundations of Periodontics for the D ental H ygienist has many eatures designed to acilitate learning and teaching. 1. M d le o ve v e w a d o l e . Each module begins with a concise overview o the module content. The module outline makes it easier to locate material within the module. The outline provides the reader with an organizational ramework with which to approach new material. 2. Le a g o bje c ve s a d Ke y t e ms. Learning objectives assist students in recognizing and studying important concepts in each chapter. Key terms are listed at the beginning o each chapter. O ne o the most challenging tasks or any student is learning a whole new dental vocabulary and gaining the con dence to use new terms with accuracy and ease. The key terms list assists students in this task by identi ying important terminology and acilitating the study and review o terminology in each chapter. Terms are highlighted in bold type and clearly de ned within the chapter. 3. i s c al De s g • Each chapter is subdivided into sections to help the reader recognize major content areas. • Chapters are written in an expanded outline ormat that makes it easy or students to identi y, learn, and review key concepts. • M aterial is presented in a manner that recognizes that students have di erent learning styles. H undreds o illustrations and clinical photographs visually rein orce chapter content. • Chapter content is supplemented in a visual ormat with boxes, tables, and f ow charts. 4. F c s Pa e s. The “ Focus on Patients” items allow the reader to apply chapter content in the context o clinical practice. The cases provide opportunities or students to integrate knowledge into their clinical work. Three types o scenarios help students to apply content to the real world setting. • Clinical Patient Care scenarios • Evidence in Action scenarios • Ethical Dilemma scenarios 5. Pa e Case S d e s Chapter 36 presents ve ctitious patient cases. Patient assessment data pertinent to the periodontium challenges the student to interpret and use the in ormation in periodontal care planning or the patient. Chapter 38 provides radiographs or several cases. These cases give students the opportunity to develop skills in radiographic analysis as it pertains to the hard tissues o the periodontium in health and disease. 6. Gl ssa y. An online audio glossary provides quick access to common periodontal terminology and pronunciation. 7. o • • •

l e r es ce s Chapter 37: Patient Cases Radiographic Analysis Instructor Resources Student Resources

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Preface for Course Instructors

NEW CONTENT SEQUENCING FOR THE FOURTH EDITION The book is divided into nine major content areas: Part 1: The Periodontium in H ealth Part 2: Diseases A ecting the Periodontium Part 3: Risk Factors or Periodontal Diseases Part 4: Assessment and Planning or Patients with Periodontal Disease Part 5: Implementation o Therapy or Patients with Periodontal Disease Part 6: H ealth M aintenance in Treated Periodontal Patients Part 7: O ther Aspects o the M anagement o Patients with Periodontal Diseases Part 8: Comprehensive Patient Cases Part 9: O nline Resources Foundations of Periodontics for the D ental H ygienist, 4th edition, strives to present the complex subject o periodontics in a reader- riendly manner. The authors greatly appreciate the comments and suggestions rom educators and students about previous editions o this book. It is our sincere hope that this textbook will help students and practitioners alike to acquire knowledge that will serve as a oundation or the prevention and management o periodontal diseases. Jill S. G ehrig, R D H , M A D onald E. W illm ann, D D S, M S

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It is a great pleasure to acknowledge the ollowing individuals whose assistance was indispensable to this third edition: • Charles D. Whitehead and Holly R. Fischer, M FA the highly skilled medical illustrators, who created all the wonder ul illustrations or the book. • Kevin Dietz, a colleague and riend or his vision and guidance or all our editions o this book. • And with great thanks to our wonder ul team at Wolters Kluwer without whose expertise and support this book would not have been possible: Jonathan Joyce, John Larkin, and Jennifer Clements. Jill S. G ehrig, R D H , M A D onald E. W illm ann, D D S, M S

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Contributors vi R eviewers viii Preface for Course Instructors A ck now ledgem ents x iii

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PART 1 : THE PERIODONTIUm IN HEALTH

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Pe d m: t he t S c es 1

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Jill G ehrig and D onald W illm ann Tissues o the Periodontium 3 N erve Supply, Blood Supply, and Lymphatic System Focus on Patients 19

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Jill G ehrig and D onald W illm ann H istology o the Body’s Tissues 23 H istology o the Gingiva 28 H istology o the Root Cementum and Alveolar Bone 40 Focus on Patients 43

PART 2 : DISEASES AFFECTING THE PERIODONTIUm

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Jill G ehrig and Sharon L ogue The Periodontium in H ealth and Disease 47 Pathogenesis o Bone Destruction 55 Periodontal Pockets 60 Theories o Disease Progression 63 Epidemiology o the Diseases o the Periodontium Focus on Patients 71

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Jill G ehrig and D onald W illm ann M ajor Diagnostic Categories o Periodontal Disease 74 Disease Classi cation Systems 76 The 1999 AAP Classi cation System or Periodontal Diseases and Conditions Focus on Patients 82

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R ebecca Sroda Clinical Features o H ealthy Gingiva 84 Clinical Features o Gingival Inf ammation 87 Extent and Distribution o Inf ammation 92 Focus on Patients 94

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R ebecca Sroda; Ethical D ilem m a by R obin M atloff Classi cation o Gingival Diseases 96 Dental Plaque–Induced Gingival Diseases 97 N on–Plaque-Induced Gingival Lesions 104 Focus on Patients 109

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Jill G ehrig and D onald W illm ann; Ethical D ilem m a by R obin M atloff Chronic Periodontitis—The M ost Common Form Focus on Patients 125

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Jill G ehrig and D onald W illm ann; Ethical D ilem m a by R obin M atloff Aggressive Periodontitis—H ighly Destructive Form Focus on Patients 135

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Jill G ehrig and D onald W illm ann; Ethical D ilem m a by R obin M atloff Periodontitis as a M ani estation o Systemic Diseases 138 N ecrotizing Periodontal Diseases 144 Developmental or Acquired De ormities and Conditions 148 Focus on Patients 153

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D onald W illm ann and Jill G ehrig Guidelines Related to Arriving at a Periodontal Diagnosis 158 Guidelines Related to Periodontal Treatment Sequencing 163

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Guidelines Related to Consent or Periodontal Treatment 166 Guidelines Related to the N eed or O ngoing Decision M aking 170 Focus on Patients 171

PART 3 : RISK FACTORS FOR PERIODONTAL DISEASES

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Jill G ehrig and D onald W illm ann; Ethical D ilem m a by R obin M atloff Risk Factors or Periodontal Disease 175 Balance Between Periodontal H ealth and Disease 177 Focus on Patients 185

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Jill G ehrig and D onald W illm ann Bacterial Bio lms 191 Structure and Colonization o Dental Plaque Bio lms Control o Plaque Bio lms 203 The Role o Bacteria in Periodontitis 204 Focus on Patients 208

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Jill G ehrig and D onald W illm ann The Body’s De ense System 212 Leukocyte M igration, Chemotaxis, and Phagocytosis 219 The Inf ammatory Process 221 Focus on Patients 227

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Jill G ehrig and D onald W illm ann; Ethical D ilem m a by R obin M atloff The H ost Response in Periodontal Disease 230 The Immune Response and Periodontitis 234 Focus on Patients 243

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Sys e m c C d s ha Ampl y S sce p b l y Pe d al D se ase 246 Jill G ehrig and D onald W illm ann; Ethical D ilem m a by R obin M atloff Systemic Risk Factors or Periodontitis 248 Genetic Risk Factors or Periodontitis 261 Systemic M edications with Periodontal Side E ects 265 Focus on Patients 269

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D onald W illm ann and Jill G ehrig Introduction to Local Contributing Factors 275 Local Factors That Can Increase Bio lm Retention

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Local Factors That Can Increase Bio lm Pathogenicity Local Factors That Cause Direct Damage 282 Focus on Patients 289

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R ebecca Sroda and Jill G ehrig; Ethical D ilem m a by R obin M atloff Association Between O besity and Periodontal Disease 291 M icronutrients, Antioxidants, and Periodontal Disease 294 M acronutrients and Periodontal Disease 297 Focus on Patients 299

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Keerthana Satheesh, Charles Cobb, Carol Southard Tobacco as a Risk Factor or Periodontal Disease 305 M echanisms o Smoking-M ediated Periodontal Disease 306 Smoking and Peri-Implant Disease 309 Tobacco Cessation or the Periodontal Patient 310 Focus on Patients 316

PART 4 : ASSESSm ENT AND PLANNING FOR PATIENTS WITH PERIODONTAL DISEASE

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D onald W illm ann and Jill G ehrig; Ethical D ilem m a by R obin M atloff Introduction to Periodontal Assessment 320 Periodontal Screening Examination 321 Comprehensive Periodontal Assessment 323 Clinical Features that Require Calculations 333 Focus on Patients 337

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W illiam M oore; Ethical D ilem m a by R obin M atloff Radiographic Appearance o the Periodontium 340 Use o Radiographic Images or Periodontal Evaluation Focus on Patients 350

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Carol Jahn: Ethical D ilem m a by R obin M atloff What is Best Practice? 353 Role o Evidence-Based Decision M aking in Best Practice 355 Finding Clinically Relevant In ormation 359 Li elong Learning Skills or Best Practice 365 Focus on Patients 367

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PART 5 : Im PLEm ENTATION OF THERAPy FOR PATIENTS WITH PERIODONTAL DISEASE

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D onald W illm ann and Jill G ehrig; Ethical D ilem m a by R obin M atloff O verview o N onsurgical Periodontal Therapy 371 Instrumentation During N onsurgical Therapy 376 Decisions Following N onsurgical Periodontal Therapy Focus on Patients 389

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Carol Jahn and Jill G ehrig; Ethical D ilem m a by R obin M atloff Patient Sel -Care in N onsurgical Therapy 393 Sel -Care Challenges or Patients with Periodontitis Tongue Cleaning as an Adjunct 403 Focus on Patients 404

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Carol Jahn; Ethical D ilem m a by R obin M atloff Patient-Applied H ome Irrigation 408 Pro essional Subgingival Irrigation 415 Focus on Patients 417

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A nn Bruhn and D onald W illm ann; Ethical D ilem m a by R obin M atloff Introduction to Chemical Agents in Bio lm Control 421 Use o Systemic Antibiotics to Control Bio lm 424 Use o Topically Delivered Chemical Agents 427 Focus on Patients 437

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D onald W illm ann and Jill G ehrig; Ethical D ilem m a by R obin M atloff Introduction to the H ost M odulation Therapy 441 Potential H ost M odulating Therapies in Periodontal Patients 443 H ost M odulation Therapy as a Part o Comprehensive Periodontal Patient M anagement 447 Focus on Patients 449

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Pe d al S g cal C Hyg e s 451

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D onald W illm ann and Jill G ehrig Introduction to Periodontal Surgery 453 Understanding the Periodontal Flap 461

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Descriptions o Common Types o Periodontal Surgery 466 Biological Enhancement o Surgical O utcomes 495 Patient M anagement Following Periodontal Surgery 497 Focus on Patients 508

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D onald W illm ann and Jill G ehrig; Ethical D ilem m a by R obin M atloff Introduction to Acute Periodontal Conditions Abscesses o the Periodontium 512 N ecrotizing Periodontal Diseases 521 Primary H erpetic Gingivostomatitis 525 Focus on Patients 528

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PART 6 : HEALTH m AINTENANCE IN TREATED PERIODONTAL PATIENTS

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u s g M va al i e v e w Be hav Cha g e 531

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D elw yn Catley, Karen W illiam s, Christoph R am seier; Ethical D ilem m a by R obin M atloff Introduction to H uman Behavior Change 533 Components o M otivational Interviewing 537 Implications or Dental H ygiene Practice 543 Focus on Patients 548

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D onald W illm ann and Teresa Butler D uncan Introduction to Periodontal M aintenance 553 Planning Periodontal M aintenance 556 Periodontal Disease Recurrence 562 Patient Compliance with Periodontal M aintenance 564 Root Caries as a Complication During M aintenance 566 Focus on Patients 572

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A rchie Jones Anatomy o the Dental Implant 577 Failing Implants: Peri-implant Disease 581 Clinical M onitoring o Peri-implant Disease 585 M aintenance Therapy or Dental Implants 587 Focus on Patients 595

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PART 7 : OTHER ASPECTS OF THE m ANAGEm ENT OF PATIENTS WITH PERIODONTAL DISEASES

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M argaret L em aster and Jill G ehrig Associations o Periodontitis with Systemic Disease 599 Plausible M echanisms Linking Periodontitis to Systemic Disease 601 Focus on Patients 610

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ma

613

D onald W illm ann and Jill G ehrig; Ethical D ilem m a by R obin M atloff O ral M alodor 614 Xerostomia 622 Focus on Patients 630

34

D c me a a d i s a ce r e p Pe d al Ca e 633

g

D ianne G lasscoe W atterson; Ethical D ilem m a by R obin M atloff Legal Issues in the Provision and Documentation o Care 634 Documentation o Periodontal Care 636 Computer-Based Patient Records 643 Insurance Codes or Periodontal Treatment 644 Focus on Patients 647

35

F Pe

e D ec s d al Pa e

Ma ag e me s 650

D onald W illm ann and Jill G ehrig Diagnostic Technology or Periodontal Diseases 651 Periodontal Disease/Systemic Disease Connections 652 Protocols or M aintaining Dental Implants 653 Treatment M odalities in Periodontal Care 654

PART 8 : COm PREHENSIv E PATIENT CASES

36

C mp e he s ve Pa e

Case s

659

D onald W illm ann, R ichard Foster, Jill G ehrig, M argaret L em aster, A nn Bruhn Fictitious Fictitious Fictitious Fictitious Fictitious

Patient Patient Patient Patient Patient

Case Case Case Case Case

1: 2: 3: 4: 5:

M r. Karn 660 M r. Wilton 667 M rs. Sandsky 675 M r. Verosky 681 M r. Tomlinson 686

Contents

PART 9 : ONLINE RESOURCES

37

Pa e

Case s: r ad g aph c A alys s

John Preece Case Case Case Case Case Case

1 2 3 4 5 6

4 5 6 8 10 12

t he P :o l e i s c (h p:/ / he P .lw w .c m)

&S

de

r es

ce s

Sharon L ogue, M argaret L em aster, R ebecca Sroda, D onald W illm ann, and Jill G ehrig

Index

691

xx

r e t p a h C

1 S ct o n 1

P o o nt : Th To o th-S ppo t ng St ct s T ss

s o f th P

o o nt

3

The Gingiva Periodontal Ligament Root Cementum Alveolar Bone

S ct o n 2

N v S ppl , Blo o

S ppl , an L

phat c S st

14

Nerve Supply to the Periodontium Blood Supply to the Periodontium Lymphatic System and the Periodontium

S ct o n 3

Fo c s o n Pat nts

19

Clinical Patient Care

Cl n cal Appl cat o n.

The dental hygienist is involved in a continuous process of interacting with patients, making clinical decisions, performing clinical procedures, evaluating new techniques, and adapting to evolving technologies. Nearly every action taken by a hygienist throughout a successful career requires a detailed knowledge of the anatomy of the tooth-supporting structures—the periodontium. Chapters 1 and 2 outline current knowledge of the anatomy of the periodontium. Chapter 1 deals with what is known about the fundamental structure of the complex system of tissues that support the teeth and can serve as a basis for organizing thoughts about additional anatomical information as it becomes available through additional research. Chapter 2 deals with the microscopic anatomy of these same structures.

L a n ng Obj ct v s • Identify the tissues of the periodontium on an unlabeled drawing depicting the periodontium in cross section. • Describe the function that each tissue serves in the periodontium, including the gingiva, periodontal ligament, cementum, and alveolar bone. • In a clinical setting or on a color photograph, identify the following anatomical areas of the gingiva: free gingiva, gingival sulcus, interdental gingiva, and attached gingiva. • In a clinical setting or on a color photograph, identify the following boundaries of the gingiva: gingival margin, free gingival groove, and mucogingival junction. • In a clinical setting, identify the free gingiva on an anterior tooth by inserting a periodontal probe to the base of the sulcus.

2

Pa t 1

The Periodontium in Health

• In a clinical setting, contrast the coral pink tissue of the attached gingiva with the darker, shiny tissue of the alveolar mucosa. • In the clinical setting, use compressed air to detect the presence or absence of stippling of the attached gingiva. • Identify the alveolar process (alveolar bone) on a human skull. • Describe the position and contours of the alveolar crest of the bone in health. • Describe the nerve and blood supply to the periodontium. • Explain the role of the lymphatic system in the health of the periodontium.

K

T

s

Periodontium Gingiva Periodontal ligament Cementum Alveolar bone Gingival margin Alveolar mucosa Free gingival groove Mucogingival junction Free gingiva

Attached gingiva Stippling Interdental gingiva Papillae Gingival col Gingival sulcus Gingival crevicular fluid Alveolar process Alveolar bone proper Alveolus

Cortical bone Alveolar crest Cancellous bone Periosteum Innervation Trigeminal nerve Anastomose Lymphatic system Lymph nodes

Chapt

S ct o n 1

T ss

s o f th P

1

3

Periodontium: The Tooth-Supporting Structures

o o nt

The periodontium (peri = around and odontos = tooth) is the unctional system o tissues that surrounds the teeth and attaches them to the jawbone (Figs. 1-1 and 1-2). An excellent overview o the periodontium is located on the M adison Area Technical College website at http://learningobjects.madisoncollege.edu/window_holder.asp? =16654_Periodontium_ Gingiva.sw . The periodontium is also called the “supporting tissues o the teeth” and “the attachment apparatus.” The tissues o the periodontium include the ollowing: 1. Gingiva—the tissue that covers the cervical portions o the teeth and the alveolar processes o the jaws. 2. Periodontal ligament (PDL)—the bers that surround the root o the tooth. These bers attach to the bone o the socket on one side and to the cementum o the root on the other side. 3. Cementum—the thin layer o mineralized tissue that covers the root o the tooth. 4. Alveolar bone—the bone that surrounds the roots o the teeth. It orms the bony sockets that support and protect the roots o the teeth.

Gin g iva

Tis s u e s o f the p e rio d o n t iu m

Ce m e n tu m P e rio d o n t a l lig a m e n t

Fg 1-1. T ss s Co p s ng th P o o nt . A graphic representation of the periodontium in cross section.

Alve o la r b one

Sulc us Gingiva Cre s t of a lve ola r b one P e riod onta l liga me nt Ce me ntum Alve ola r b one

Fg 1-2. H alth P o o nt Clinical photograph and drawing depicting the structures of the periodontium.

.

4

Pa t 1

The Periodontium in Health

TABLe 1 -1 . THe Pe r iOd ONTiu m St

ct

B

G ng va

f d sc pt o n o f its F nct o n

• p o vid s

issu s

• Co v s • h o ld s P C

o o ntal l g a nt

nt

• Su s

issu

Alv o la bo n

g in s in s

nds of oo

c vic l o io n (n ck) o f

o c ss s o f

n d s n d m in

cs

ound

lv o l

• a nc o s • p o

l

j ws

oo

d u in g m s ic io n

oo

in i s so ck

io d o n

l lig m n fib

s o

s ys in i s so ck d n in o f

• Su o u n d s n d su

o s

oo

oo oo s of

oo

Each o the tissues o the periodontium plays a vital role in maintaining the health and unction o the periodontium (Table 1-1). Knowledge o the periodontal tissues in health is a necessary oundation or understanding the concepts o (1) normal unction o the periodontium, (2) disease prevention, and (3) the periodontal disease process. Dental hygiene students usually are introduced to the tissues o the periodontium during the rst semester or quarter o the dental hygiene curriculum. In the preclinical stages o the curriculum, mastering dental terminology and anatomy can sometimes be overwhelming and con using. This chapter provides an opportunity to review this complex system o tissues known as the periodontium.

Th e Gin Giv a 1. Overview o the Gingiva A. Description. The gingiva is the part o the mucosa that surrounds the cervical portions o the teeth and covers the alveolar processes o the jaws (Fig. 1-3). 1. The gingiva ends coronal to the cementoenamel junction (CEJ) o each tooth and attaches to the tooth by means o a specialized type o epithelial tissue (junctional epithelium). 2. It is composed o a thin outer layer o epithelium and an underlying core o connective tissue. 3. The gingiva is divided into our anatomical areas (Fig. 1-4). a. Free gingiva b. Gingival sulcus c. Interdental gingiva d. Attached gingiva B. Function. The gingiva protects the underlying tooth-supporting structures o the periodontium rom the oral environment. The oral environment is exposed to a wide range o temperatures in ood and drink, mechanical orces, and a large number o oral bacteria. To accomplish these unctions, the gingiva has several de ense mechanisms, including the saliva and immune system de ense mechanisms.

oo

, so

Chapt

1

Periodontium: The Tooth-Supporting Structures

Alve ola r mucos a Mucogingiva l junction Atta che d gingiva Fre e gingiva Inte rde nta l gingiva

Fg 1-3. Th G ng val T ss interdental gingiva.

s. Photograph of healthy gingival tissues showing the free, attached, and

Fg 1-4. G ng val T ss o f th Palat . On the palate, the lingual gingiva is directly continuous with the keratinized masticatory mucosa.

C. Boundaries o the Gingiva 1. The coronal boundary, or upper edge, o the gingiva is the gingival margin (Fig. 1-5). 2. The apical boundary, or lower edge, o the gingiva is the alveolar mucosa. The alveolar mucosa can be distinguished easily rom the gingiva by its dark red color and smooth, shiny sur ace. D. Demarcations o the Gingiva 1. The ree gingival groove is a shallow linear depression that separates the ree and attached gingiva (this line may be visible clinically but is not obvious in many instances). 2. The mucogingival junction is the clinically visible boundary where the pink attached gingiva meets the red, shiny alveolar mucosa. (Clinically visible means that this landmark can be seen in the oral cavity.)

5

6

Pa t 1

The Periodontium in Health

Gingiva l ma rgin Fre e gingiva l line

Fre e gingiva Atta c he d gingiva

Muc ogingiva l junc tion

Fg

1-5. Bo n a

Alve ola r muc os a

s of th G ng va. Illustration showing the boundaries and anatomical areas of the gingiva.

2. Free Gingiva. The ree gingiva is the unattached portion o the gingiva that surrounds the tooth in the region o the CEJ. The ree gingiva is also known as the unattached gingiva or the marginal gingiva. A. Location o the Free Gingiva 1. The ree gingiva is located coronal to (above) the CEJ. 2. It surrounds the tooth in a turtleneck or cu -like manner. 3. The ree gingiva attaches to the tooth by means o a specialized epithelium— the junctional epithelium. B. Characteristics o the Free Gingiva 1. The tissue o the ree gingiva ts closely around the tooth but is not directly attached to it. 2. This tissue, because it is unattached, may be gently stretched away rom the tooth sur ace with a periodontal probe. 3. The ree gingiva also orms the so t tissue wall o the gingival sulcus. C. Contour o the Free Gingival Margin 1. The tissue o the ree gingiva meets the tooth in a thin rounded edge called the gingival margin. 2. The gingival margin ollows the contours o the teeth, creating a scalloped (wavy) outline around them. 3. Attached Gingiva. The attached gingiva is the part o the gingiva that is tightly connected to the cementum on the cervical-third o the root and to the periosteum (connective tissue cover) o the alveolar bone. A. Location o the Attached Gingiva. The attached gingiva lies between the ree gingiva and the alveolar mucosa (Fig. 1-6). B. Width o the Attached Gingiva 1. The attached gingiva is widest in the incisor and molar regions, ranging rom 3.3 to 3.9 mm on the mandible and 3.5 to 4.5 mm on the maxilla (Fig. 1-7). 2. The attached gingiva is narrowest in premolar regions (1.8 mm on mandible and 1.9 mm on maxilla). 3. The width o the attached gingiva is not measured on the palate since clinically it is not possible to determine where the attached gingiva ends and the palatal mucosa begins (Fig. 1-4). 4. It was once believed that a minimum 2-mm width o attached gingiva is necessary to maintain the health o the periodontium; this concept is not accepted today (1).

Chapt

1

Periodontium: The Tooth-Supporting Structures

7

C. Color o the Attached Gingiva 1. In health, the attached gingiva is pale or coral pink. 2. The attached gingiva may be pigmented (Fig. 1-8). a. Pigmentation occurs more requently in dark-skinned individuals (2). b. The pigmented areas o the attached gingiva may range rom light brown to black.

Atta c he d gingiva

Muc ogingiva l junc tion

Alve ola r muc os a

Fg 1-6. Lo cat o n o f th Attach G ng va. The attached gingiva extends from the free gingival groove to the mucogingival junction.

Atta c he d gingiva

G ng va. The Fg 1-7. m an W th o f th Attach attached gingiva is widest in the incisor and molar regions and narrowest in premolar regions.

A

B

Fg 1-8. Colo Va at ons of No al G ng va. The color of the normal gingiva varies among different persons. A: The color is a lighter, coral pink in individuals with fair complexions. B: In individuals with dark skin and hair, the gingiva may be pigmented. (Courtesy of Elizabeth Carr, University of Mississippi Medical Center, Jackson, MS)

8

Pa t 1

The Periodontium in Health

D. Texture o the Attached Gingiva. In health, the sur ace o the attached gingiva may have a dimpled appearance similar to the skin o an orange peel. This dimpled appearance is known as stippling (Fig. 1-9). H ealthy tissue may or may not exhibit a stippled appearance as the presence o stippling varies greatly rom individual to individual. Stippling is present in 40% o adults. E. Function o the Attached Gingiva 1. The attached gingiva allows the gingival tissue to withstand the mechanical orces created during activities such as mastication, speaking, and toothbrushing. 2. The attached gingiva prevents the ree gingiva rom being pulled away rom the tooth when tension is applied to the alveolar mucosa. 4. Interdental Gingiva. The interdental gingiva is the portion o the gingiva that lls the interdental embrasure between two adjacent teeth apical to the contact area (Fig. 1-10). A. Parts o Interdental Gingiva 1. The interdental gingiva consists o two interdental papillae—one acial papilla and one lingual papilla (papilla = singular noun; papillae = plural noun). a. The lateral borders and tip o an interdental papilla are ormed by the ree gingiva rom the adjacent teeth. b. The center portion o the interdental papilla is ormed by the attached gingiva. 2. The gingival col is a valley-like depression in the portion o the interdental gingiva that lies directly apical to the contact area o two adjacent (touching) teeth and connects the acial and lingual papillae. The col is not present if the adjacent teeth are not in contact (i.e., there is a space between two adjacent teeth), there is no adjacent tooth (i.e., the lingual sur ace o the posterior most tooth in the arch), or i the interdental gingiva has receded (Fig. 1-11). B. Function o Interdental Gingiva. The interdental gingiva prevents ood rom becoming packed between the teeth during mastication.

S tippling

Fg 1-9. G ng val St ppl ng . In health, the surface of the attached gingiva may have a dimpled appearance known as gingival stippling.

Fg 1-10. Th int ntal G ng va. The interdental tissue fills the area between two adjacent teeth.

Chapt

1

Periodontium: The Tooth-Supporting Structures

5. Gingival Sulcus. The gingival sulcus is the space between the ree gingiva and the tooth sur ace (Fig. 1-12). A. Description. The sulcus is a V-shaped, shallow space around the tooth (3). 1. The depth o a clinically normal gingival sulcus is rom 1 to 3 mm, as measured using a periodontal probe. 2. Base o Sulcus. The base o the sulcus is ormed by the junctional epithelium (a specialized type o epithelium that attaches to the tooth sur ace). B. Gingival Crevicular Fluid. The gingival crevicular f uid, also called the gingival sulcular f uid, is a f uid that seeps rom the underlying connective tissue into the sulcular space. 1. Little or no f uid is ound in the healthy gingival sulcus but the f uid f ow increases in the presence o dental plaque bio lm and the resulting gingival inf ammation (4). 2. Fluid f ow increases in response to toothbrushing, mastication, or other stimulation o the gingivae. The f ow is greatly increased when the gingivae are inf amed. 3. I a lter strip is inserted into the sulcus, it aborbs the f uid in the sulcus. Using the lter strip the amount o gingival crevicular f uid can be measured and used as an index o gingival inf ammation.

Conta c t a re a Fa c ia l p a p illa

Conta c t a re a Fa c ia l p a p illa Col

Col

Lingua l p a p illa

Lingua l p a p illa

P ro xim a l vie w

Fg 1-11. int ntal Co l. Apical to the contact area between two teeth, the interdental gingiva has a concave (depressed) form. The concavity, the “ col” is located between the facial and lingual papillae and extends beneath the contact area of two adjacent teeth.

Fg 1-12. G ng val S lc s. This photograph shows a periodontal probe inserted into the gingival sulcus, the space between the free gingiva and the tooth.

9

10

Pa t 1

The Periodontium in Health

De n t in B

Fg Lga

o

C

n e

e

o o ntal

o

e

f

• On to o th s

m

P e rio d o n t a l lig a m e n t

1-13. P nt.

n

o

t u

t o

m

t h s o c k e t

, the ends of the periodontal ligament fibers are anchored in the cementum of the root. • On th bo n s , the ends of the periodontal ligament fibers are anchored in the alveolar bone of the tooth socket.

Pe r io d o n Ta l l iGa m e n T 1. Description A. The PDL is a layer o so t connective tissue that covers the root o the tooth and attaches it to the bone o the tooth socket (Fig. 1-13). 1. The PDL is composed mainly o dense brous connective tissue (3). 2. The bers o the PDL attach on one side to the root cementum and on the other side to the alveolar bone o the tooth socket (5). B. The PDL not only connects the tooth to the alveolar process, but also supports the tooth in the socket and absorbs mechanical loads placed on the tooth, thus protecting the tooth in its socket. 2. Functions. The PDL has ve unctions in the periodontium: A. Supportive unction—suspends and maintains the tooth in its socket. B. Sensory unction—provides sensory eeling to the tooth, such as pressure and pain sensations. C. N utritive unction—provides nutrients to the cementum and bone. D. Formative unction—builds and maintains cementum and the alveolar bone o the tooth socket. The tissues o the PDL contain specialized cells such as broblasts, cementoblasts, and osteoblasts. E. Resorptive unction—can remodel the alveolar bone in response to pressure, such as that applied during orthodontic treatment (braces).

r o o T Ce m e n Tu m 1. Description. Cementum is a thin layer o hard, mineralized connective tissue that covers the sur ace o the tooth root (Fig. 1-14). 2. Characteristics o Cementum A. Cementum overlies and is attached to the dentin o the root. It is light yellow in color and so ter than dentin or enamel. B. Cementum is a bone-like tissue that is more resistant to resorption than bone (6). 1. Resistance to resorption (loss o substance) is an important characteristic o cementum that makes it possible or the teeth to be moved during orthodontic treatment (7).

Chapt

1

Periodontium: The Tooth-Supporting Structures

Fg 1-14. C nt . Cementum is mineralized connective tissue that covers the root of the tooth; it is light yellow in color.

2. The high resistance o cementum to resorption allows the pressure applied during orthodontics to cause resorption o the alveolar bone, or tooth movement, without resulting in root resorption. C. Cementum is ormed slowly throughout li e. There are two main types o cementum: cellular and acellular. D. Cementum does not have its own blood or nutrient supply; it receives its nutrients rom the PDL. 3. Functions o Cementum in the Periodontium. Cementum per orms several important roles in the periodontium, and, there ore, conservation o cementum should be a goal o periodontal instrumentation. A. The primary unction o cementum is to give attachment to the collagen bers o the PDL. Cementum anchors the ends o the PDL bers to the tooth; without cementum, the tooth would all out o its socket. B. The outer layer o cementum protects the underlying dentin and seals the ends o the open dentinal tubules. C. Cementum ormation compensates or tooth wear at the occlusal or incisal sur ace due to attrition. Cementum is ormed at the apical area o the root to compensate or occlusal attrition.

a l v e o l a r Bo n e 1. Description A. The alveolar process or alveolar bone is the bone o the upper or lower jaw that surrounds and supports the roots o the teeth (Fig. 1-15). B. Bone is mineralized connective tissue and consists by weight o about 60% inorganic material, 25% organic material and about 15% water. C. The existence o the alveolar bone is dependent on the presence o teeth; when teeth are extracted, in time, the alveolar bone resorbs. I teeth do not erupt, the alveolar bone does not develop. 2. Function o the Alveolar Bone in the Periodontium. The alveolar bone orms the bony sockets that provide support and protection or the roots o the teeth.

11

12

Pa t 1

The Periodontium in Health

Alve ola r p roc e s s Ra mus

Bod y Sc a llop e d b one c ontour

Fg 1-15. Alv o la P o c ss. The alveolar process is the bone that surrounds and supports the roots of the teeth.

Alve o la r b o n e p ro p e r

C o rt ic a l b o n e

C a n c e llo u s bone

Fg 1-16. La s o f th Alv o la P o c ss. A lateral section of the mandible reveals the three bony layers: the alveolar bone proper, cancellous bone, and cortical bone.

Cortic a l b one

Ca nc e llous b one Ma nd ib ula r c a na l

Alve ola r p roc e s s

Bod y of ma nd ib le

Fg 1-17. C o ss S ct o n o f th m an bl . The dotted line indicates the boundary of the alveolar process with the body of the mandible.

Chapt

1

Periodontium: The Tooth-Supporting Structures

13

3. Layers that compose the Alveolar Process. When viewed in cross section, the alveolar process is composed o three layers o hard tissue and covered by a thin layer o connective tissue (Figs. 1-16 and 1-17). A. The alveolar bone proper (or cribri orm plate) is the thin layer o bone that lines the socket to surround the root o the tooth. 1. The alveolus is the bony socket, a cavity in the alveolar bone that houses the root o a tooth (alveolus = singular; alveoli = plural) (Fig. 1-18). 2. The alveolar bone proper has numerous holes that allow blood vessels rom the cancellous bone to connect with the vessels o the PDL space. 3. The ends o the PDL bers are embedded in the alveolar bone proper. B. The cortical bone is a layer o compact bone that orms the hard, outside wall o the mandible and maxilla on the acial and lingual aspects. This cortical bone surrounds the alveolar bone proper and gives support to the socket. 1. The buccal cortical bone is thin in the incisor, canine, and premolar regions; cortical bone is thicker in molar regions. 2. Since the cortical plate is only on the acial and lingual sides o the jaw, it will not show up in a radiograph; only the cancellous bone and the alveolar bone proper can be seen on a radiograph. 3. The alveolar crest is the coronal most portion o the alveolar process. a. In health, the alveolar crest is located 1 to 2 mm apical to (below) the CEJs o the teeth (Fig. 1-19). b. When viewed rom the acial or lingual aspect, the alveolar crest meets the teeth in a scalloped (wavy) line that ollows the countours o the CEJs. C. The cancellous bone (or spongy bone) is the lattice-like bone that lls the interior portion o the alveolar process (between the cortical bone and the alveolar bone proper). The cancellous bone is oriented around the tooth to orm support or the alveolar bone proper. D. The periosteum is a layer o connective so t tissue covering the outer sur ace o bone; it consists o an outer layer o collagenous tissue and an inner layer o ne elastic bers.

Fg 1-18. Alv o l o f th m an bl . The alveoli are the sockets in the alveolar bone that house the roots of the teeth. (Courtesy of Dr. Don Rolfs, Periodontal Foundations, Wenatchee, WA)

Fg 1-19. Bo n Co nto s. The alveolar crest meets the teeth in a scalloped line that follows the contours of the cementoenamel junctions. (Courtesy of Dr. Don Rolfs, Periodontal Foundations, Wenatchee, WA)

14

Pa t 1

The Periodontium in Health

S ct o n 2

N v S ppl , Blo o

S ppl , an L

phat c S st

n e r v e Su PPl y To Th e Pe r io d o n Tiu m 1. Description. The innervation o the periodontium—nerve supply to the periodontium—occurs via the branches o the trigeminal nerve (Fig. 1-20). Innervation to the maxilla (Fig. 1-21) is by the second branch o the trigeminal nerve (the maxillary nerve) and the mandible by the third branch (the mandibular nerve). A. The trigeminal nerves have sensory, motor, and intermediate roots that attach directly to the brain. B. The trigeminal nerve is responsible or the sensory sensibility o most o the skin on the ront part o the ace and head, the teeth, oral cavity, maxillary sinus, and nasal cavity. C. The motor unction o the trigeminal nerve is essential or the act o chewing. 2. Functions o the N erve Supply to the Periodontium A. N erve receptors in the gingiva, alveolar bone, and PDL register pain, touch, and pressure. B. Nerves in the PDL provide in ormation about movement and tooth position. These nerves provide the sensations o light touch or pressure against the teeth and play an important role in the regulation o chewing orces and movements. When biting down on something hard, it is the nerves o the PDL that are stimulated, allowing the individual to experience a sense o pressure with the teeth against the hard object. 3. Innervation o the Periodontium A. Innervation o the Gingiva 1. Innervation o the gingiva o the maxillary arch is rom the superior alveolar nerves (anterior, middle, and posterior branches), in raorbital nerve, and the greater palatine and nasopalatine nerves. 2. Innervation o the gingiva o the mandibular arch is rom the mental nerve, buccal nerve, and the sublingual branch o the lingual nerve (Fig. 1-22). B. Innervation o the Teeth and PDL 1. Innervation o the teeth and PDL o the maxillary arch is rom the superior alveolar nerves (anterior, middle, and posterior branches). 2. Innervation o the teeth and PDL o the mandibular arch is rom the in erior alveolar nerve.

Trig e m in a l n e rve (V)

In fra o rb it a l n e rve

S u p e rio r a lve o la r n e rve s : P o s t e rio r Mid d le An t e rio r

Bu c c a l n e rve Lin g u a l n e rve In fe rio r a lve o la r n e rve La t e ra l vie w

Me n t a l n e rve

Fg 1-20. N v S ppl to th P o o nt (Lat al V w ). The nerve supply to the periodontium is derived from the branches of the trigeminal nerve.

Chapt

1

Periodontium: The Tooth-Supporting Structures

15

Na s a l b ra n c h o f s u p e rio r a lve o la r n e rve

Gre a t e r p a la t in e n e rve

In t e rn a l b ra n c h o f in fra o rb it a l n e rve Na s o p a la t in e n e rve

Fg 1-21. N v inn Palat .

vat o n to th

CNS A

C A Mes encephalic s ens ory neurons of the trigeminal nerve

B TG

B Motor nucleus of the trigeminal C Sens ory nucleus of the trigeminal D Spinal s ens ory trigeminal nucleus E Fibers of the mas ticatory mus culature

D

E CNS

TG Trigeminal ganglion (Gas s erian ganglion) with its three branches : ophthalmic, maxillary, and mandibular CNS Ce ntra l ne rvous s ys te m

Fg 1-22. inn vat o n o f m an b la T th. Innervation of the gingiva and periodontium is via the mandibular nerve.

Bl o o d Su PPl y To Th e Pe r io d o n Tiu m 1. Description. The vessels o the periodontium anastomose (join together) to create a complex system of blood vessels that supply blood to the periodontal tissues. A. This network o blood vessels acts as a unit, supplying blood to the so t and hard tissues o the maxilla and mandible. B. It is the proli eration o this rich blood supply to the gingiva that accounts or the dramatic color changes that are seen in gingivitis.

16

Pa t 1

The Periodontium in Health

2. Function. The major unction o the complex network o blood vessels o the periodontium is to transport oxygen and nutrients to the tissue cells o the periodontium and to remove carbon dioxide and other waste products rom the cells or elimination. 3. Vascular Supply to the Periodontium (Fig. 1-23) A. M axillary gingiva, PDL, and alveolar bone 1. Anterior and posterior-superior alveolar arteries 2. In raorbital artery 3. Greater palatine artery B. M andibular gingiva, PDL, and alveolar bone 1. In erior alveolar artery 2. Branches o the in erior alveolar artery: the buccal, acial, mental, and sublingual arteries 4. Vascular Supply to the Teeth and Periodontal Tissues A. The major arteries 1. Superior alveolar arteries—maxillary periodontal tissues 2. In erior alveolar artery—mandibular periodontal tissues B. Branch arteries (Figs. 1-24 and 1-25) 1. The dental artery: a branch o the superior or in erior alveolar artery 2. Intraseptal artery: enters the tooth socket 3. Rami per orantes: terminal branches o the intraseptal artery; they penetrate the tooth socket and enter the PDL space where they anastomose (join) with the blood vessels rom the alveolar bone and PDL 4. Supraperiosteal blood vessels: located in the ree gingiva and are the main supply o blood to the ree gingiva; these vessels anastomose with blood vessels rom the alveolar bone and PDL 5. Subepithelial plexus: branches o the supraperiosteal blood vessels located in the connective tissue beneath the ree and attached gingiva 6. PDL vessels: supply the PDL and orm a complex network o vessels that surrounds the root 7. Dentogingival plexus: a ne-meshed network o blood vessels located in the connective tissue beneath the gingival sulcus

Gre a t e r p a la t in e a rt e ry Bu c c a l a rt e ry

In fra o rb it a l a rt e ry

Ma xilla ry a rt e ry

In fe rio r a lve o la r a rt e ry

P o s t e rio r s u p e rio r a lve o la r a rt e ry Me n t a l a rt e ry

Fa c ia l a rt e ry Lin g u a l a rt e ry Ext e rn a l c a ro t id a rt e ry

S u b lin g u a l a rt e ry S u b m e n t a l a rte ry

Fg 1-23. Vasc la S ppl to th P o o nt . A complex network of blood vessels supplies blood to the periodontium.

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Periodontium: The Tooth-Supporting Structures

17

G in g iva l a n a s t o m o s is o f ve s s e ls P e rio d o n t a l lig a m e n t a rt e rie s Ra m i p e rfo ra n t e s In t e rs e p t a l a rt e ry De n t a l a rt e ry In fe rio r a lve o la r a rt e ry

s. The branch arteries Fg 1-24. B anch A t supply blood to the teeth and periodontium.

De ntogingiva l p le xus

Sub e p ithe lia l p le xus with c a p illa ry loop s

Sup ra p e rios tia l a rte ry Intra s e p ta l a rte ry

Comp le x ne twork of p e riod onta l liga me nt ve s s e ls

Fg 1-25. N tw o k o f V ss ls. A fine network of vessels supplies blood to gingiva, gingival connective tissue, and periodontal ligament.

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l y m Ph a TiC Sy STe m a n d Th e Pe r io d o n Tiu m 1. Description. The lymphatic system is a network o lymph nodes connected by lymphatic vessels that plays an important role in the body’s de ense against in ection. 2. Function. Lymph nodes (pronounced: lim nodes) are small bean shaped structures located on either side o the head, neck, armpits, and groin. These nodes lter out and trap bacteria, ungi, viruses, and other unwanted substances to sa ely eliminate them rom the body. 3. Lymph Drainage o the Periodontium. The lymph rom the periodontal tissues is drained to the lymph nodes o the head and neck (Fig. 1-26). A. Submandibular lymph nodes—drain most o the periodontal tissues B. Deep cervical lymph nodes—drain the palatal gingiva o the maxilla C. Submental lymph nodes—drain the gingiva in the region o the mandibular incisors D. Jugulodigastric lymph nodes—drain the gingiva in the third molar region

De e p c e rvic a l nod e s J u g u lo d ig a s t ric node De e p c e rvic a l nod e s

S ub m e nta l no d e s S u b m a n d ib u la r n o d e s

Fg 1-26. L phat c S st o f th P o o nt . The lymph from the periodontium is drained to the lymph nodes of the head and neck.

Chapt

Chapt

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a

Stat

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Periodontium: The Tooth-Supporting Structures

19

nt

The gingiva, PDL, cementum, and alveolar bone make up a system o tissues that surround the teeth and attach them to the alveolar bone. Each tissue o the periodontium plays a vital role in the unctioning and retention o the teeth. • The gingiva provides a tissue seal around the cervical portion o the teeth and covers the alveolar process. • The PDL supports the tooth in its socket, provides nutrients and sensory eeling to the tooth, and maintains cementum and the alveolar bone o the tooth socket. • The cementum anchors the PDL to the tooth and seals the ends o the open dentinal tubules. Cementum ormation compensates or tooth wear due to occlusal attrition. • The alveolar bone orms the bony sockets that provide support and protection or the roots o the teeth.

S ct o n 3

Fo c s o n Pat nts Cl n cal Pat nt Ca CA S e

1

A patient involved in an automobile accident receives a penetrating wound involving the oral cavity. The wound enters the alveolar mucosa near the apex o a lower premolar tooth and extends rom the sur ace mucosa all the way through the tissues to the premolar tooth root. List periodontal tissues most likely injured by this penetrating wound.

CA S e

2

A patient who has lost a maxillary lateral incisor tooth is scheduled to have a dental implant placed. The dental implant placement will require the clinician to prepare a hole with a drill in the bone ormerly occupied by the lateral incisor tooth. N ame the types o bone that will most probably be penetrated by the drill.

CA S e

3

A dentist injects a local anesthetic be ore working on a maxillary molar tooth. The injection results in complete loss o sensation in the molar tooth and in most o the gingiva surrounding the molar tooth. N ame the nerves that most likely have been a ected by the injection o the local anesthetic.

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nc s

1. Lang N P, Loe H . The relationship between the width o keratinized gingiva and gingival health. J Periodontol. 1972;43(10):623–627. 2. Ainamo J, Loe H . Anatomical characteristics o gingiva. A clinical and microscopic study o the ree and attached gingiva. J Periodontol. 1966;37(1):5–13. 3. Cho M I, Garant PR. Development and general structure o the periodontium. Periodontol 2000. 2000;24:9–27. 4. Cimasoni G. Crevicular f uid updated. M onogr O ral Sci. 1983;12:III-VII, 1–152. 5. Saygin N E, Giannobile WV, Somerman M J. M olecular and cell biology o cementum. Periodontol 2000. 2000;24:73–98. 6. Diekwisch TG. The developmental biology o cementum. Int J D ev Biol. 2001;45(5–6):695–706. 7. Sodek J, M cKee M D. M olecular and cellular biology o alveolar bone. Periodontol 2000. 2000;24:99–126.

STu d e NT ANCiLLAr y r e SOu r Ce S A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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Micro sco pic A ato m o f the Pe rio do ti m 1

Histo lo g o f the Bo d ’s Tiss e s

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Microscopic Anatomy o a Tissue Microscopic Anatomy o Epithelial Tissue Microscopic Anatomy o Connective Tissue Epithelial–Connective Tissue Inter ace Epithelial Cell Junctions

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Histo lo g o f the Gi g iva

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Microscopic Anatomy o Gingival Epithelium Why the Teeth Need a Junctional Epithelium? Attachment o the Cells o the Junctional Epithelium Microscopic Anatomy o Gingival Connective Tissue

Se ctio

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Histo lo g o f the Ro o t Ce me t m a d Alve o lar Bo e

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Microscopic Anatomy o Cementum Microscopic Anatomy o Alveolar Bone

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Fo c s o

Patie ts

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Clinical Patient Care

Cli ical Applicatio .

The dental hygienist is involved in a continuous process o interacting with patients, making clinical decisions, per orming clinical procedures, evaluating new techniques, and adapting to evolving technologies. Nearly every action taken by a hygienist throughout a success ul career requires a detailed knowledge o the anatomy o the tooth-supporting structures—the periodontium. Chapter 1 dealt with what is known about the undamental structure o the complex system o tissues that support the teeth. Chapter 2 deals with the microscopic anatomy o these same structures. The in ormation presented in these two chapters can serve as a basis or organizing thoughts about additional anatomical in ormation as it becomes available through additional research.

Le ar i g Obje ctive s • Describe the histology o the tissues and the unction that each serves in the human body. • List and def ne the layers that comprise the stratif ed squamous epithelium o the skin. • Def ne keratin and describe its unction in the epithelium. • Describe the composition and unction o the connective tissue. • Describe the epithelium–connective tissue inter ace ound in most tissues o the body, such as the inter ace between the epithelium and connective tissues o the skin.

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• Def ne the term cell junction and describe its unction in the epithelial tissues. • Compare and contrast the terms desmosome and hemidesmosome. • Identi y the three anatomical areas o the gingival epithelium on an unlabeled drawing depicting the microscopic anatomy o the gingival epithelium. • Describe the location and unction o the ollowing regions o the gingival epithelium: oral epithelium, sulcular epithelium, and junctional epithelium. • State the level o keratinization present in each o the three anatomical areas o the gingival epithelium (keratinized, nonkeratinized, or parakeratinized). • State which o the anatomical areas o the gingival epithelium have an uneven, wavy epithelium–connective tissue inter ace i he alth and which have a smooth junction in he alth. • Identi y the enamel, gingival connective tissue, junctional epithelium, internal basal lamina, external basal lamina, epithelial cells, desmosomes, and hemidesmosomes on an unlabeled drawing depicting the microscopic anatomy o the junctional epithelium and surrounding tissues. • Def ne and describe the unction o the supragingival f ber bundles and the periodontal ligament in the periodontium. • Identi y the principal f ber groups o the periodontal ligament on an unlabeled drawing. • Def ne the terms cementum and Sharpey f bers and describe their unction in the periodontium. • State the three relationships that the cementum may have in relation to the enamel at the cementoenamel junction. • Def ne the term alveolar bone and describe its unction in the periodontium.

Ke Te rms Histology Tissue Cells Extracellular matrix Epithelial tissue Strati ied squamous epithelium Basal lamina Keratinization Keratinized epithelial cells Nonkeratinized epithelial cells Connective tissue Epithelial–connective tissue inter ace

Basement membrane Epithelial ridges Connective tissue papillae Cell junctions Desmosome Hemidesmosome Gingival epithelium Oral epithelium (OE) Sulcular epithelium (SE) Junctional epithelium (JE) Keratinized Parakeratinized Keratin Gingival crevicular luid

Internal basal lamina External basal lamina Collagen ibers Supragingival iber bundles Dentogingival unit Periosteum Periodontal ligament (PDL) Fiber bundles o the PDL Sharpey ibers Cementum OMG (overlap, meet, gap) Alveolar process

Chapte r 2

Se ct io

Microscopic Anatomy o the Periodontium

23

1

Histo lo g o f the Bo d ’s Tiss e s Histology is a branch o anatomy concerned with the study o microscopic structures o tissues. Knowledge o the microscopic characteristics o tissues is a prerequisite or understanding the microscopic anatomy o the periodontium. Section 1 reviews the microscopic anatomy o the epithelial and connective tissues o the body.

M ic r o s c o p ic An At o M y o f A t is s u e A tissue is a group o interconnected cells that per orm a similar unction within an organism. For example, muscle cells group together to orm muscle tissue that unctions to move parts o the body. The tissues and organs o the body are composed o several di erent types o cells and extracellular elements outside o the cells. 1. Cells A. Cells are the smallest structural unit o living matter capable o unctioning independently. B. Cells group together to orm a tissue. C. The our basic types o tissues are epithelial, connective, nerve, and muscle tissues. 2. Extracellular Matrix. Tissues are not made up solely o cells. A gel-like substance containing interwoven protein bers surrounds most cells. A. The extracellular matrix is a mesh-like material that surrounds the cells (Fig. 2-1). It is like sca olding or the cells. This material helps hold cells together and provides a ramework within which cells can migrate and interact with one another. B. The extracellular matrix consists o ground substance and bers. 1. The ground substance is a gel-like material that lls the space between the cells. 2. The bers consist o collagen, elastin, and reticular bers. Collagens are the major proteins o the extracellular matrix. C. Amount o Extracellular M atrix 1. In epithelial tissue, the extracellular matrix is scanty, consisting mainly o a thin mat called the basal lamina, which underlies the epithelium. 2. In connective tissue, the extracellular matrix is more plenti ul than the cells that it surrounds.

Fib rob la s t Extra c e llula r ma trix Ma s t c e ll Colla ge n fib e r b und le Ma c rop ha ge P la s ma c e ll Ela s tic fib e r B-lymp hoc yte

Fig re 2-1. Extrace ll lar Matrix. The extracellular matrix surrounds the cells o a tissue and comprises ibers and a gel-like substance.

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M ic r o s c o p ic An At o M y o f e p it h e l iAl t is s u e 1. Description. The epithelial tissue is the tissue that makes up the outer sur ace o the body (skin) and lines the body cavities such as the mouth, stomach, and intestines (mucosa). The skin and mucosa o the oral cavity are made up o strati ed squamous epithelium—a type o epithelium that comprises f at cells arranged in several layers. 2. Composition o Epithelial Tissue A. Plenti ul Cells. M ost o the volume o epithelial tissue consists o many closely packed epithelial cells (Fig. 2-2). Epithelial cells are bound together into sheets. B. Sparse Extracellular Matrix 1. The extracellular matrix is a minor component o the epithelial tissue consisting mainly the basal lamina. 2. The basal lamina is a thin mat o extracellular matrix secreted by the epithelial cells. This basal lamina mat supports the epithelium (somewhat like the sca olding o a building). 3. Keratinization. Keratinization—the process by which epithelial cells on the sur ace o the skin become stronger and waterproo . A. Keratinized Epithelial Cells 1. Keratinized epithelial cells have no nuclei and orm a tough, resistant layer on the sur ace o the skin. 2. The most heavily keratinized epithelium o the body is ound on the palms o the hands and soles o the eet. B. N onkeratinized Epithelial Cells 1. Nonkeratinized epithelial cells have nuclei and act as a cushion against mechanical stress and wear. Nonkeratinized epithelial cells are so ter and more f exible. 2. N onkeratinized epithelium is ound in areas such as the mucosal lining o the cheeks—permitting the mobility needed to speak, chew, and make acial expressions. 4. Blood Supply. Epithelial tissues do not contain blood vessels; nourishment is received rom blood vessels contained in the underlying connective tissue (Fig. 2-2).

Ep it h e liu m

C o n n e c t ive t is s u e

Fig re 2-2. Stratifie d Sq amo s Epithe li m a d Co e ctive Tiss e o f the Ski . The epithelium o the skin consists o many closely packed epithelial cells and a thin basal lamina. The epithelium o the skin rests on a supporting bed o connective tissue. The epithelium does not contain blood vessels; nourishment is received rom blood vessels in the underlying connective tissue.

Chapte r 2

Microscopic Anatomy o the Periodontium

M ic r o s c o p ic An At o M y o f c o n n e c t iv e t is s u e 1. Description. Connective tissue lls the spaces between the tissues and organs in the body. It supports and binds other tissues. Connective tissue consists o cells separated by abundant extracellular substance. 2. Composition o Connective Tissue A. Sparse Cells. Connective tissue cells are sparsely distributed in the extracellular matrix. 1. Fibroblasts (“ ber-builders” )—cells that orm the extracellular matrix ( bers and ground substance) and secrete it into the intercellular spaces 2. M acrophages and neutrophils—phagocytes (“ cell-eaters” ) that devour dying cells and microorganisms that invade the body 3. Lymphocytes—cells that play a major role in the immune response B. Plenti ul Extracellular Matrix. The extracellular matrix—a rich gel-like substance containing a network o strong bers—is the major component o connective tissue. The network o bers matrix, rather than the cells, gives connective tissue the strength to withstand mechanical orces. 3. Dental Connective Tissue. All dental tissues o the tooth—cementum, dentin, alveolar bone, and the pulp—are specialized orms o connective tissue ex cept enam el. Enamel is an epithelial tissue.

e p it h e l iAl –c o n n e c t iv e t is s u e in t e r f Ac e 1. Description. The epithelial–connective tissue inter ace is the boundary where the epithelial and connective tissues meet. 2. The Basement Membrane and Basal Lamina A. As discussed previously, the basal lamina is a thin layer secreted by the epithelial cells on which the epithelium sits. The term basal lam ina o ten is con used with the term basem ent m em brane and is sometimes used inconsistently in the literature. B. The basal lamina is not visible under the light microscope but can be distinguished under the higher magni cation o an electron microscope. The basal lamina assists the attachment o the epithelial cells to adjacent structures, such as the tooth sur ace. C. The term basement membrane speci es a thin layer o tissue visible with a light microscope beneath the epithelium. The basement membrane is ormed by the combination o a basal lamina and a reticular lamina. 3. Characteristics o the Epithelial–Connective Tissue Boundary A. Wavy Boundary. In most places in the body, the epithelium meets the connective in a wavy, uneven manner (Fig. 2-3). 1. Epithelial ridges—deep extensions o epithelium that reach down into the connective tissue. The epithelial ridges are also known as rete pegs. 2. Connective tissue papillae— nger-like extensions o connective tissue that extend up into the epithelium. B. Smooth Boundary 1. Some specialized epithelial tissues in the body meet the connective tissue in a smooth inter ace that has no epithelial ridges or connective tissue papillae. 2. Some anatomical areas o the gingiva have an epithelial–connective tissue inter ace that is smooth.

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Ep it h e liu m Ep it h e lia l rid g e Wa vy t is s u e b o u n d a ry

C o n n e c t ive t is s u e p a p illa

C o n n e c t ive t is s u e

Fig re 2-3. Wav Epithe lial– Co e ctive Tiss e I te rface . In most cases, the epithelium meets the connective tissue at an uneven, wavy border. Epithelial ridges extend down into the connective tissue. Connective tissue papillae extend upward into the epithelium.

4. Function o the Wavy Tissue Boundary A. Enhances Adhesion. The wavy tissue inter ace enhances the adhesion o the epithelium to the connective tissue by increasing the sur ace area o the junction between the two tissues. This strong adhesion o the epithelium allows the skin to resist mechanical orces. B. Provides N ourishment. The wavy junction between the epithelium and connective tissue also increases the area rom which the epithelium can receive nourishment rom the underlying connective tissue. The epithelium does not have its own blood supply; blood vessels are carried close to the epithelium in the connective tissue papillae.

e p it h e l iAl c e l l Ju n c t io n s N eighboring epithelial cells attach to one another by specialized cell junctions that give the tissue strength to withstand mechanical orces and to orm a protective barrier. 1. De nition. Cell junctions are cellular structures that mechanically attach a cell and its cytoskeleton to its neighboring cells or to the basal lamina. 2. Purpose. Cell junctions bind cells together, so that they can unction as a strong structural unit. Tissues such as the epithelium o the skin that must withstand severe mechanical stresses have the most abundant number o cell junctions. 3. Forms o Epithelial Cell Junctions A. Desmosome—a specialized cell junction that connects two neighboring epithelial cells and their cytoskeletons together. You might think o desmosomes as being like the snaps used to close a denim jacket. Instead o astening the ront o a jacket together, desmosomes asten epithelial cells together (Fig. 2-4A,B). 1. A cell-to-cell connection 2. An important orm o cell junction ound in the gingival epithelium B. Hemidesmosome—a specialized cell junction that connects the epithelial cells to the basal lamina (Fig. 2-4B). 1. A cell-to-basal lamina connection 2. An important orm o cell junction ound in the gingival epithelium

Chapte r 2

Microscopic Anatomy o the Periodontium

27

Ep ithe lia l c e lls

Nuc le us

De s mos ome s

He mid e s mos ome s

Conne c tive tis s ue

He mid e s mos ome Ba s e me nt me mb ra ne zone Ba s a l la mina

Re tic ula r la mina

A

Fig re 2-4. A: The Epithe li m–Co e ctive Tiss e I te rface . The epithelium–connective tissue inter ace is the site o the basement membrane zone, a complex structure mostly synthesized by the epithelial cells. I se t: A representation o an electron micrograph showing the hemidesmosomal attachment to the basal lamina. (Adapted with permission rom Rubin R, Strayer DS. Rubin’s Pathology: Clinicopathologic Foundations o Medicine. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008.)

De s m o s o m e Ep it h e lia l c e lls

Ba s a l la m in a

C o n n e c t ive t is s u e

He m id e s m o s o m e

B

Fig re 2-4. B: Epithe lial Ce ll J ctio s. Epithelial cells attach to each other with specialized cell junctions called desmosomes. Hemidesmosomes attach the epithelial cells to the basal lamina.

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2

Histo lo g o f the Gi g iva Knowledge o the microscopic anatomy o the gingiva is a prerequisite or understanding the periodontium in health and in disease. At rst glance, the microscopic anatomy o the periodontium may seem to be impossibly complicated (1). The anatomy o the periodontium, however, is much like that o tissues elsewhere in the body. The gingiva consists o an epithelial layer and an underlying connective tissue layer. This section reviews the microscopic anatomy o the gingival epithelium, junctional epithelium (JE), and gingival connective tissues.

M ic r o s c o p ic An At o M y o f Gin Giv Al e p it h e l iu M

a n E

D

e

n

t

m

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The gingival epithelium is a specialized strati ed squamous epithelium that unctions well in the wet environment o the oral cavity (2). The microscopic anatomy o the gingival epithelium is similar to the epithelium o the skin. The gingival epithelium may be di erentiated into three anatomical areas (Fig. 2-5): 1. Oral Epithelium (OE): epithelium that aces the oral cavity 2. Sulcular Epithelium (SE): epithelium that aces the tooth sur ace w ithout being in contact w ith the tooth surface 3. Junctional Epithelium (JE): epithelium that attaches the gingiva to the tooth

SE CEJ JE

OE

Ce m e ntum C o n n e c t ive t is s u e

Bo n e

Fig re 2-5. Thre e Are as o f the Gi g ival Epithe li m. The gingival epithelium has three distinct areas:

• JE—junctional epithelium at the base o the sulcus • SE—sulcular epithelium that lines the sulcus • OE—oral epithelium covering the ree and attached gingiva

1. Oral epithelium (OE). The oral epithelium covers the outer sur ace o the ree gingiva and attached gingiva; it extends rom the crest o the gingival margin to the mucogingival junction. The O E is the only part o the periodontium that is visible to the unaided eye. A. Cellular Structure o the Oral Epithelium 1. The O E may be keratinized or parakeratinized (partially keratinized). Keratin is a tough, brous structural protein that occurs in the outer layer o the skin and the O E (Fig. 2-6).

Chapte r 2

Microscopic Anatomy o the Periodontium

2. The O E is strati ed squamous epithelium that can be divided into the ollowing cell layers (Fig. 2-6): a. Basal cell layer: cube-shaped cells b. Prickle cell layer: spine-like cells with large intercellular spaces. The cells o both the basal and prickle cell layers attach to each other with desmosomes c. Granular cell layer: f attened cells and increased intracellular keratin d. Keratinized cell layer: f attened cells with extensive intracellular keratin B. Inter ace with Gingival Connective Tissue. In health, O E joins w ith the connective tissue in a wavy interface w ith epithelial ridges (Figs. 2-7 and 2-8). 2. Sulcular Epithelium. Sulcular epithelium (SE) is the epithelial lining o the gingival sulcus. It extends rom the crest o the gingival margin to the coronal edge o the JE. A. Cellular Structure o the Sulcular Epithelium 1. The SE is a thin, nonkeratinized epithelium (3). 2. The SE has three cellular layers (Fig. 2-6): a. Basal cell layer b. Prickle cell layer c. Super cial cell layer: f attened cells without keratin 3. The SE is permeable allowing f uid to f ow rom the gingival connective tissue into the sulcus. This f uid is known as the gingival crevicular f uid. The f ow o gingival crevicular f uid is slight in health and increases in disease. B. Inter ace with Gingival Connective Tissue. In health, the SE joins the connective tissue at a smooth interface with no epithelial ridges (no wavy junction). 3. Junctional Epithelium. Junctional epithelium (JE) is the specialized epithelium that orms the base o the sulcus and joins the gingiva to the tooth sur ace. The gingiva surrounds the cervix of the tooth and attaches to the tooth by means of the JE. The base of the sulcus is made up of the coronal-most cells of the JE. In health, the JE attaches to the tooth at a level that is slightly coronal to the cementoenamel junction (CEJ). A. Cellular Structure o the Junctional Epithelium 1. Keratinization o JE a. The JE is a thin, nonkeratinized epithelium. b. N onkeratinized epithelial cells o both the sulcular and junctional areas o the gingival epithelium make them a less e ective protective covering. Thus, the sulcular and junctional areas provide the easiest point o entry or bacteria or bacterial products to invade the connective tissue o the gingiva. 2. The JE has only two cell layers (Figs. 2-6 and 2-7): a. Basal cell layer b. Prickle cell layer 3. Length and Width o the JE a. The JE ranges rom 0.71 to 1.35 mm in length (4). b. The JE is about 15 to 30 cells thick at the coronal zone—the zone that attaches highest on the crown o the tooth. c. The JE tapers to 4 to 5 cells thick at the apical zone. B. JE Inter ace with Gingival Connective Tissue. In health, the JE has a smooth tissue interface with the connective tissue (no wavy junctions).

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The Periodontium in Health Oral Epi. KL GL PL BL

Sulc ular Epi. SL PL BL

SE

Junc tio nal Epi. Tooth PL BL

OE

JE

Fig re 2-6. Ce ll La e rs o f the Gi g ival Epithe li m. The cell layers o the oral, sulcular, and junctional epithelium. Illustration key: KL, keratinized cell layer; GL, granular cell layer; SL, super icial cell layer; PL, prickle cell layer; BL, basal cell layer.

Sulcular epithelium Gingival s ulcus Oral epithelium

Enamel s pace

J unctional epithelium Epithelial ridge

Fig re 2-7. H ma Gi g iva. This photograph shows a decalci ied longitudinal section o an incisor tooth as seen through an ordinary light microscope. All o the calcium hydroxyapatite crystals have been extracted rom the tooth and rom its bony alveolus. Since enamel is composed almost completely o calcium hydroxyapatite crystals, only the space where enamel used to be—the enamel space—is represented in this photograph. The sulcular epithelium o the ree gingiva borders a space known as the gingival sulcus. Observe the well-developed epithelial ridges (identi ied by label and arrows) o the oral epithelium. (Adapted with permission rom Gartner LP, Hiatt JL. Color Atlas and Text o Histology. Philadelphia, PA: Lippincott Williams & Wilkins; 2013.)

Chapte r 2

Microscopic Anatomy o the Periodontium

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Epithelium

Epithelial ridge

Connective tis s ue

Collagen ber bundles

Fig re 2-8. Epithe lial Ridg e s. This photograph shows the epithelial–connective junction as seen through an ordinary light microscope. The tall epithelial ridges o the epithelium (in dark red) extend down into the underlying connective tissue. Collagen iber bundles are visible in the connective tissue. (Adapted with permission rom Gartner LP, Hiatt JL. Color Atlas and Text o Histology. Philadelphia, PA: Lippincott Williams & Wilkins; 2013.)

Wh y t h e t e e t h n e e d A Ju n c t io n Al e p it h e l iu M ? 1. The Teeth Create a Break in the Epithelial Protective Covering A. Protective Epithelial Sheet Covers the Body 1. A continuous sheet o epithelium protects the body by covering its outer sur aces and lining the body’s cavities, including the oral cavity. 2. The teeth penetrate this protective covering by erupting through the epithelium, thus creating an opening through which microorganisms can enter the body. B. The Teeth Puncture the Protective Epithelial Sheet 1. The body attempts to seal the opening created when a tooth penetrates the epithelium by attaching the epithelium to the tooth. 2. The word “ junction” means “ connection” ; thus, the epithelium that is connected to the tooth is termed the “ junctional epithelium.” 2. Functions o Junctional Epithelium A. Epithelial Attachment. The JE provides an attachment between the gingiva and the tooth sur ace, thus providing a seal at the base o the gingival sulcus or periodontal pocket (Fig. 2-9). B. Barrier. The JE provides a protective barrier between the plaque bio lm and the connective tissue o the periodontium.

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C. Host De ense. The epithelial cells play a role in de ending the periodontium rom bacterial in ection by signaling the immune response (5).

OE

En a m e l

Ke ra t in iz e d

SE

D

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No n ke ra t in iz e d

Ba s a l c e ll la ye r o f e p it h e liu m

Fig re 2-9. Micro sco pic A ato m o f the Thre e Are as o f the Gi g ival Epithe li m. I te rface w ith Co e ctive Tiss e .

• OE (oral epithelium)—these epithelial cells orm the outer layer o the ree and attached gingiva.

• SE (sulcular epithelium)—these epithelial cells

JE No n ke ra t in iz e d C o n n e c t ive t is s u e

extend rom the edge o the JE coronally to the crest o the gingival margin.

• JE (junctional epithelium)—these epithelial cells join the gingiva to the tooth sur ace at the base o the sulcus.

At t Ac h M e n t o f t h e c e l l s o f t h e Ju n c t io n Al e p it h e l iu M 1. Microscopic Anatomy o Junctional Epithelium A. Components o the Junctional Epithelium (JE). The JE consists o the ollowing: 1. Plenti ul Cells a. Layers o closely packed epithelial cells b. Desmosomes and hemidesmosomes—specialized cell junctions 2. A Sparse Extracellular M atrix a. Internal basal lamina—a thin basal lamina between the JE and the tooth sur ace. b. External basal lamina—a thin basal lamina between the JE and the gingival connective tissue. 2. Attachment o Junctional Epithelium to the Tooth Sur ace A. Attachment to the Tooth Sur ace 1. The JE cells next to the tooth sur ace orm hemidesmosomes that enable these cells to attach to the internal basal lamina and the sur ace o the tooth (6–9). 2. The internal basal lamina is a thin sheet o extracellular matrix adjacent to the tooth sur ace.

Chapte r 2

Microscopic Anatomy o the Periodontium

3. The epithelial cells physically attach to the tooth sur ace by our to eight hemidesmosomes per micron at the coronal zone and two hemidesmosomes per micron in the apical zone o the JE (10,11). The apical zone is the area o the JE with the least adhesiveness. 4. The attachment o the hemidesmosomes and internal basal lamina to the tooth sur ace is not static; rather, the cells o the JE appear to be capable o moving along the tooth sur ace. B. Attachment to the Underlying Gingival Connective Tissue 1. The epithelial cells o the JE attach to the underlying gingival connective tissue via hemidesmosomes and the external basal lamina (Fig. 2-10) (8,12,13). 2. In health, the JE has a sm ooth tissue interface with the connective tissue (no wavy junctions).

D

e

n

t

i

n

En a m e l

De s mos ome s

Ena me l Ce me ntum

He mid e s mos ome s Inte rna l b a s a l la mina Exte rna l b a s a l la mina Gingiva l fib e rs

Fig re 2-10. Micro sco pic A ato m o f the J ctio al Epithe li m (JE). Microscopic structures o the junctional epithelium include the epithelial cells, desmosomes, external and internal basal laminae, and hemidesmosomes.

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M ic r o s c o p ic An At o M y o f Gin Giv Al c o n n e c t iv e t is s u e 1. Function o Gingival Connective Tissue. The gingival connective tissue o the ree and attached gingiva provides solidity to the gingiva and attaches the gingiva to the cementum o the root and the alveolar bone (14–16). The gingival connective tissue is also known as the lamina propria. 2. Components o the Gingival Connective Tissue A. Cells 1. In contrast to the gingival epithelium (which has an abundance o cells and sparse extracellular matrix), the gingival connective tissue has an abundance o extracellular matrix and ew cells (Fig. 2-11). 2. Cells comprise about 5% o the gingival connective tissue. 3. The di erent types o cells present in the gingival connective tissue are the ollowing a. Fibroblasts b. M ast cells c. Immune cells, such as macrophages, neutrophils, and lymphocytes 4. The bers o the connective tissue are produced by the broblasts. B. Extracellular Matrix 1. The major components o the connective tissue are protein bers, broblasts, vessels, and nerves that are embedded in the extracellular matrix. The matrix o the connective tissue is produced mainly by the broblasts. 2. The matrix is the medium in which the connective tissue cells are embedded and it is essential or the maintenance o the normal unction o the connective tissue. The transportation o water, nutrients, metabolites, oxygen, and so on to and rom the individual connective tissue cells occurs within the matrix. 3. Protein bers account or about 55% to 65% o the gingival connective tissue. M ost o these are collagen bers that orm a dense network o strong, rope-like cables that secure and hold the gingival connective tissues together. 4. The collagen bers enable the gingiva to orm a rigid cu around the tooth. 5. Gel-like material between the cells makes up about 30% to 35% o the gingival connective tissue. This gel-like material helps hold the tissue together.

Ep it h e lia l c e ll s h e e t

Ba s a l la m in a Ma c ro p h a g e

C a p illa ry

Ge l- like g ro u n d s u b s t a n c e

C

F ib r o b l a s t

Ela s t in fib e rs

gen o ll a

f ib e r s

Lym p h o c yt e

Fig re 2-11. Micro sco pic A ato m o f Gi g ival Co e ctive Tiss e . The gingival connective tissue comprises a gel-like substance, protein ibers, and cells.

Chapte r 2

Microscopic Anatomy o the Periodontium

35

Ena me l

Sulc us

Sulc ula r e p ithe lium

J unc tiona l e p ithe lium Sup ra gingiva l fib e rs

Bone Ce me ntum

Soft tis s ue a tta c hme nt

Fig re 2-12. S prag i g ival Fibe rs o f Gi g ival Co e ctive Tiss e . The gingival ibers are rope-like collagen iber bundles in the gingival connective tissue. These ibers orm a so t tissue attachment coronal to the alveolar bone.

3. The Supragingival Fiber Bundles o the Gingival Connective Tissue. The supragingival ber bundles (gingival bers) are a network o rope-like collagen ber bundles in the gingival connective tissue (Fig. 2-12). These bers are located coronal to (above) the crest o the alveolar bone. A. Characteristics o the Fiber Bundles 1. The ber bundles are embedded in the gel-like extracellular matrix o the gingival connective tissue. 2. The subgingival ber bundles strengthen the attachment o the JE to the tooth by bracing the gingival margin against the tooth sur ace. 3. Together the JE and the gingival bers are re erred to as the dentogingival unit. The dentogingival unit acts to provide structural support to the gingival tissue. B. Functions o the Gingival Fiber Bundles 1. Brace the ree gingiva rmly against the tooth and rein orce the attachment o the JE to the tooth. 2. Provide the ree gingiva with the rigidity needed to withstand the rictional orces that result during mastication. 3. Unite the ree gingiva with the cementum o the root and alveolar bone. 4. Connect adjacent teeth to one another to control tooth positioning within the dental arch. C. Classi cation o Gingival Fiber Groups. The supragingival ber bundles are classi ed based on their orientation, sites o insertion, and the structures that they connect (Figs. 2-13 and 2-14). 1. Alveologingival bers—extend rom the periosteum o the alveolar crest into the gingival connective tissue. These ber bundles attach the gingiva to the bone. (The periosteum is a dense membrane composed o brous connective tissue that closely wraps the outer sur ace o the alveolar bone.)

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2. Circular bers—encircle the tooth in a ring-like manner coronal to the alveolar crest and are not attached to the cementum o the tooth. These ber bundles connect adjacent teeth to one another. 3. Dentogingival bers—embedded in the cementum near the CEJ and an out into the gingival connective tissue. These bers act to attach the gingiva to the teeth. 4. Periostogingival bers—extend laterally rom the periosteum o the alveolar bone. These bers attach the gingiva to the bone. 5. Intergingival bers—extend in a mesiodistal direction along the entire dental arch and around the last molars in the arch. These ber bundles link adjacent teeth into a dental arch unit. 6. Intercircular bers—encircle several teeth. These ber groups link adjacent teeth into a dental arch unit. 7. Interpapillary bers-–are located in the papillae coronal to (above) the transseptal ber bundles. These ber groups connect the oral and vestibular interdental papillae o posterior teeth. 8. Transgingival bers—extend rom the cementum near the CEJ and run horizontally between adjacent teeth. These ber bundles link adjacent teeth into a dental arch unit. 9. Transseptal—pass rom the cementum o one tooth, over the crest o alveolar bone, to the cementum o the adjacent tooth. These ber bundles connect adjacent teeth to one another and secure alignment o teeth in the arch.

IG C

TG IC C TS

D G DG IP AG PG

Fig re 2-13. S prag i g ival Fibe r Gro ps.

• • • •

C—circular AG—alveologingival DG—dentogingival PG—periostogingival

Fig re 2-14. S prag i g ival Fibe r Gro ps o f the Ma dib lar Arch (Occl sal Vie w , Lo o ki g Do w Ma dib lar Arch).

• • • • • • •

C—circular IG—intergingival IC—intercircular IP—interpapillary DG—dentogingival TG—transgingival TS—transseptal

o

the

Chapte r 2

Microscopic Anatomy o the Periodontium

4. The Periodontal Ligament Fibers o the Gingival Connective Tissue A. De nition. The periodontal ligament (PDL) is a thin sheet o brous connective tissue that surrounds the roots o the teeth and joins the root cementum with the socket wall. The thickness o the PDL ranges rom 0.05 to 0.25 mm depending on the age o the patient and the unction o the tooth (17,18).

Alve o la r c re s t fib e rs Ho riz o n t a l fib e rs In t e rra d ic u la r fib e rs Ob liq u e fib e rs Ap ic a l fib e rs

Fig re 2-15. Pri cipal Fibe r Gro ps o f the Pe rio do tal Lig ame t. The ibers o the PDL are classi ied as the alveolar crest, horizontal, interradicular, oblique, and apical.

B. Components o the Periodontal Ligament. The PDL consists o connective tissue bers, cells, and extracellular matrix. 1. Cells. The cells o the PDL are mainly broblasts with some cementoblasts and osteoblasts. 2. Extracellular M atrix. a. The extracellular matrix o the PDL is similar to the extracellular matrix o other connective tissue. This rich gel-like substance contains specialized connective bers. 3. Fiber Bundles. The ber bundles o the PDL are a specialized connective tissue that surrounds the root o the tooth and connects it with the alveolar bone. These bers are the largest component o the PDL. a. The rope-like collagen ber bundles o the PDL stretch across the space between the cementum and the alveolar bone o the tooth socket (Fig. 2-15). b. The collagen ber bundles are anchored on one side in the cementum covering the tooth root; on the other side, they are embedded in the bone o the tooth socket. 4. Blood Vessels and N erve Supply. The PDL has a rich supply o nerves and blood vessels. C. Functions o the Periodontal Ligament 1. Supportive unction—the major unction o the PDL is to anchor the tooth to its bony socket and to separate the tooth rom the socket wall, so that the root does not collide with the bone during mastication. 2. Sensory unction—the PDL is supplied with nerve bers that transmit tactile pressure (such as a tap with dental instrument against tooth) and pain sensations.

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3. N utritive unction—the PDL is supplied with blood vessels that provide nutrients to the cementum and bone. 4. Formative unction—the PDL contains cementoblasts (“ cementum builders” ) that produce cementum throughout the li e o the tooth while the osteoblasts (“ bone builders” ) maintain the bone o the tooth socket. 5. Resorptive unction—in response to severe pressure, cells o the PDL (osteoclasts) can produce rapid bone resorption and, sometimes, resorption o cementum. D. Principal Fiber Groups o the PDL. The tooth is joined to the bone by bundles o collagen bers that can be divided into the ve groups based on their location and orientation (Fig. 2-15). 1. Alveolar crest ber group—extend rom the cervical cementum, running downward in a diagonal direction, to the alveolar crest. This ber group resists horizontal movements o the tooth. 2. Horizontal ber group—located apical to the alveolar crest bers. They extend rom the cementum to the bone at right angles to the long axis to the root. This ber group resists horizontal pressure against the crown o the tooth. 3. Oblique ber group—located apical to the horizontal group. They extend rom the cementum to the bone, running in a diagonal direction. This ber group resists vertical pressures that threaten to drive the root into its socket. 4. Apical ber group—extend rom the apex o the tooth to the bone. This ber group secures the tooth in its socket and resists orces that might li t the tooth out o the socket. 5. Interradicular ber group (present only in multirooted teeth)—extend rom the cementum in the urcation area o the tooth to the interradicular septum o the alveolar bone. These ber groups help to stabilize the tooth in its socket. E. Sharpey Fibers o the Periodontal Ligament 1. The ends o the PDL bers that are embedded in the cementum and alveolar bone are known as Sharpey bers (Figs. 2-16 and 2-17). 2. The attachment o the ber bundles occurs when the cementum and bone are orming. As cementum orms, the tissue hardens around the ends o the periodontal bers (Sharpey bers) surrounding them with cementum. The same process occurs during bone ormation. As the bony wall o the tooth socket hardens, it surrounds the ends o the periodontal bers with bone. The ends o the ber bundles become trapped in the bone that orms around them.

De n t in

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lv A

P e rio d o n t a l lig a m e n t

e

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t u

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o n e

S h a rp e y fib e rs

Fig re 2-16. Sharpe Fibe rs. The ends o the periodontal ligament ibers that are embedded in the alveolar bone and the cementum are known as Sharpey Fibers.

Chapte r 2

P e riod onta l liga me nt

P e riod onta l liga me nt

Alve ola r b one

Ce me ntum

Alve ola r b one

Alve ola r b one

C

Fig re 2-17. De ve lo pme t o f the Pe rio do tal Lig ame t Fibe rs.

P e riod onta l liga me nt Ce me ntum

B: The ibers grow into the midportion o periodontal ligament space.

B

P e riod onta l liga me nt

39

A: Fine collagen ibers arise rom the root cementum. Similarly, collagen ibers arise rom the alveolar bone proper.

A

P e riod onta l liga me nt

Microscopic Anatomy o the Periodontium

P e riod onta l liga me nt Ce me ntum

C: The ibers rom the root cementum use with ibers rom the alveolar bone proper.

40

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3

Histo lo g o f the Ro o t Ce me t m a d Alve o lar Bo e Section 3 reviews the microscopic anatomy o the cementum and alveolar bone. Knowledge o the microscopic anatomy o these structures is a prerequisite to understanding the unction o these structures in health and the alterations in disease.

M ic r o s c o p ic An At o M y o f c e M e n t u M 1. De nition. Cementum is a mineralized layer o connective tissue that covers the root o the tooth. Anatomically, cementum is part o the tooth; however, it is also a part o the periodontium. A. Functions o Cementum 1. Seals and covers the open dentinal tubules and acts to protect the underlying dentin (Fig. 2-18). 2. Attaches the periodontal bers to the tooth. 3. Compensates or attrition o teeth at their occlusal or incisal sur aces. O ver time, teeth experience wear at their occlusal or incisal sur aces. Cementum is ormed at the apical areas o the roots to compensate or loss o tooth tissues due to attrition. B. Conservation o Cementum During Periodontal Instrumentation 1. Conservation o cementum is ideal since loss o cementum is accompanied by exposure o the dentinal tubules and by a loss o attachment o PDL bers to the root sur ace. 2. Until recently, intentional aggressive removal o cementum was the standard o care or treatment during instrumentation o root sur aces exposed by the apical migration o the JE. a. Intentional removal cementum on the coronal hal o the root should be avoided as the cementum is important to the health o the periodontium. b. O ver the course o many years, overzealous instrumentation can result in removal o all cementum and exposure o the underlying dentin.

Fig re 2-18. Ce me t m a d To o th-S ppo rti g Str ct re s.

• A thin layer o cementum (appearing as a bl e ba d) covers the dentin o the root. • The periodontal ligament (L) holds the tooth in the bony socket o the alveolar bone (B). (Used with permission rom Mills SE. Histology or Pathologists. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006:423, Figure 15-39.)

Chapte r 2

Microscopic Anatomy o the Periodontium

41

2. Components o Mature Cementum. Cementum contains collagen bers embedded in an organic matrix (19). A. Collagen Fibers. The organic matrix o cementum is composed o a ramework o densely packed collagen bers held together by the gel-like extracellular ground substance. These bers are oriented more or less parallel to the long axis o the tooth. B. Mineralized Portion. The mineralized portion o cementum is made up o hydroxyapatite crystals (calcium and phosphate). C. Vessels and Innervation. Cementum contains no blood vessels or nerves. (H ypersensitivity o the root sur ace occurs when the cementum is removed exposing the dentin. It is the dentin that is sensitive to brushing or the touch o a dental instrument.) 3. Types o Cementum A. Acellular Cementum. Acellular cementum is primarily responsible or attaching the tooth to the alveolar bone (Fig. 2-19). 1. Contains no living cells within its mineralized tissue 2. First to be ormed and covers approximately the cervical-third or hal o the root 3. N o new acellular cementum is produced during the li e o the tooth 4. Thickness ranges rom 30 to 60 microns 5. Sharpey bers make up most o the structure o acellular cementum B. Cellular Cementum 1. Contains cementoblasts and broblasts within its mineralized tissue (Fig. 2-19) 2. Formed a ter the tooth has erupted and is less calci ed than acellular cementum 3. Deposited in intervals throughout the li e o the tooth (thickness increases with age) 4. Thickness ranges rom 150 to 200 microns 5. Sharpey bers make up a smaller portion o cellular cementum

Ac e llula r c e me ntum

Ce llula r c e me ntum

Fig re 2-19. T pe s o f Ce me t m. Acellular cementum covers approximately the cervical third or hal o the root. New acellular cementum normally is not produced during the li e o the tooth. Cellular cementum covers the apical hal o the root. It is deposited throughout the li e o the tooth and increases in thickness with age.

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4. Relationship o Cementum to Enamel at the CEJ. The cementum covering the root may have any one o three relationships with the enamel o the tooth crown. In order o requency, the cementum may overlap the enamel, meet the enamel, or there is a gap between the cementum and enamel. This order o requency is known as the OMG (overlap, meet, gap) (Fig. 2-20). A. Overlap—in 60% o all cases, the cementum overlaps the enamel or a short distance. B. Meet—in 30% o all cases, the cementum meets the enamel. C. Gap—in 10% o all cases, there is a small gap between the cementum and enamel (exposing the dentin in this area). The patient may experience discom ort (dentinal sensitivity) during instrumentation. The use o local anesthesia may be help ul during instrumentation, and desensitization o sensitive areas should be per ormed ollowing instrumentation.

En a m e l

Ce m e ntum De n t in

Fig re 2-20. Re latio ship o f Ce me t m to E ame l at the Ce me to e ame l J ctio . In order o requency, the cementum may (1) overlap the enamel, (2) meet the enamel, or (3) not meet, leaving a gap between the cementum and enamel.

M ic r o s c o p ic An At o M y o f Al v e o l Ar Bo n e 1. De nition. The alveolar process or alveolar bone is the part o the maxilla and mandible that orm and support the sockets o the teeth (Fig. 2-21). 2. Function o Alveolar Bone in the Periodontium A. Protects Roots o Teeth. The alveolar bone orms the bony sockets that provide support and protection or the roots o the teeth. B. Remodels in Response to Mechanical Forces and Inf ammation. Alveolar bone constantly undergoes periods o bone ormation and resorption (loss) in response to mechanical orces on the tooth and inf ammation o the periodontium. 3. Characteristics o Alveolar Bone A. Components. Alveolar bone is mineralized connective tissue made by cells called osteoblasts (“ bone builders” ) (20). 1. M ajor Cell Types a. O steoblasts—bone- orming cells—produce the bone matrix consisting o collagen bers and other protein bers. b. O steoclasts—bone consumers—cells that remove the mineral materials and organic matrix o alveolar bone. 2. Extracellular M atrix a. Collagen bers and gel-like substance orm the major component o the alveolar bone. b. The bone matrix is rigid because it undergoes mineralization by the deposition o minerals such as calcium and phosphate, which are subsequently trans ormed into hydroxyapatite (Fig. 2-22). B. Vessels and Innervation. The alveolar bone has blood vessels and nerve innervation.

Chapte r 2

1

2

Microscopic Anatomy o the Periodontium

3

Fig re 2-21. A ato m o f Alve o lar Bo e . (1) Alveolar bone proper, (2) trabecular bone, and (3) compact bone.

Fig re 2-22. Histo lo g o f Alve o lar Bo e . A histologic section through a mandibular irst molar and its alveolar process. (Used with permission rom Mel i RC. Permar’s Oral Embryology and Microscopic Anatomy. 10th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000:215, Figure 9-20.)

Chapte r S mmar State me t Knowledge o the microscopic anatomy o the periodontium is undamental in understanding the (1) unction o the periodontium in health and (2) changes that occur during the periodontal disease process. The JE plays an important role in the health o the periodontium by attaching the gingival epithelium to the tooth via hemidesmosomes and an internal basal lamina. In health, the PDL, cementum, and alveolar bone act as a unctional unit to support and maintain the teeth in the oral cavity.

Se ct io

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Patie ts

Cli ical Patie t Care CA S E 1 A clinician penetrates the oral mucosa with a needle be ore injecting a local anesthetic. The needle tip stops in the loose connective tissue underlying the sur ace structures. N ame the layers o epithelium that have been penetrated by the needle.

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CA S E 2 A clinician nds it necessary to use a unique type o injection to achieve total anesthesia o a tooth being treated. The injection involves sliding a small-diameter needle into the PDL space to a point hal way down the tooth root. N ame the PDL bers most likely encountered by the needle tip during insertion.

CA S E 3 Recession o the gingival margin exposes a portion o tooth root on a maxillary canine tooth. M icroscopic examination o the cementum in the area o the crown margin on the canine will reveal what possible relationships between the level o cementum and the level o the tooth crown?

Re fe re ce s 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

Cho M I, Garant PR. Development and general structure o the periodontium. Periodontol 2000. 2000;24:9–27. Bartold PM , Walsh LJ, N arayanan AS. M olecular and cell biology o the gingiva. Periodontol 2000. 2000;24:28–55. Weinmann JP, M eyer J. Types o keratinization in the human gingiva. J Invest D erm atol. 1959;32(2, Part 1):87–94. Listgarten M A. Electron microscopic study o the gingivo-dental junction o man. A m J A nat. 1966;119(1):147–177. Dale BA. Periodontal epithelium: a newly recognized role in health and disease. Periodontol 2000. 2002;30:70–78. Schroeder H E. Ultrastructure o the junctional epithelium o the human gingiva. H elv O dontol A cta. 1969;13(2):65–83. Listgarten M A. The ultrastructure o human gingival epithelium. A m J A nat. 1964;114:49–69. Schroeder H E, Listgarten M A. The gingival tissues: the architecture o periodontal protection. Periodontol 2000. 1997; 13:91–120. Thilander H , Bloom GD. Cell contacts in oral epithelia. J Periodontal R es. 1968;3(2):96–110. Sabag N , Saglie R, M ery C. Ultrastructure o the normal human epithelial attachment to the cementum root sur ace. J Periodontol. 1981;52(2):94–95. Pollanen M T, Salonen JI, Uitto VJ. Structure and unction o the tooth-epithelial inter ace in health and disease. Periodontol 2000. 2003;31:12–31. Schroeder H E, Listgarten M A. The junctional epithelium: rom strength to de ense. J D ent R es. 2003;82(3):158–161. Schroeder H E, Theilade J. Electron microscopy o normal human gingival epithelium. J Periodontal R es. 1966;1(2):95–119. Bartold PM . Connective tissues o the periodontium. Research and clinical implications. A ust D ent J. 1991;36(4):255–268. Bartold PM . Connective tissues o the periodontium–pre ace. Periodontol 2000. 2000;24:7–8. Wang Y, Wang Q, D Arora P, et al. Cell adhesion proteins: roles in periodontal physiology and discovery by proteomics. Periodontol 2000. 2013;63(1):48–58. H o SP, M arshall SJ, Ryder M I, et al. The tooth attachment mechanism de ned by structure, chemical composition and mechanical properties o collagen bers in the periodontium. Biom aterials. 2007;28(35):5238–5245. Beertsen W, M cCulloch CA, Sodek J. The periodontal ligament: a unique, multi unctional connective tissue. Periodontol 2000. 1997;13:20–40. Saygin N E, Giannobile WV, Somerman M J. M olecular and cell biology o cementum. Periodontol 2000. 2000;24:73–98. Sodek J, M cKee M D. M olecular and cellular biology o alveolar bone. Periodontol 2000. 2000;24:99–126.

STu DEn T An CILLARy RESOu RCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

r e t p a h C

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Three Basic States o the Periodontium Periodontium in Health Gingivitis—Reversible Tissue Damage Periodontitis—Permanent Tissue Destruction

Se ct o

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Changes in Alveolar Bone Height in Disease Patterns o Bone Loss in Periodontitis

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Characteristics o Periodontal Pockets Pocket Formation

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The o e s o D se ase P o

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Clinical Patient Care

Cl

cal Appl cat o .

Each o the various types o diseases that a ect the periodontium will be discussed in detail in subsequent chapters o this book. To understand these upcoming detailed discussions, clinicians need to be aware o a ew important ideas that relate to most o these disease conditions, and these topics are discussed in Chapter 3. This overview gives the student an understanding o the undamental changes seen in the diseased periodontium and discusses concepts related to the epidemiology, occurrence, and progression o periodontal diseases.

Le a

Obje ct e s

• De ne the term disease progression. • De ne the term periodontal disease and contrast it with the term periodontitis. • Describe and contrast the (1) position o the junctional epithelium, (2) characteristics o the epithelial–connective tissue junction, and (3) position o the crest o the alveolar bone in health, gingivitis, and periodontitis. • Explain why there is a band o intact transseptal bers even in the presence o severe bone loss. • Describe the progressive destruction o alveolar bone loss that occurs in periodontitis.

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Diseases A ecting the Periodontium

• Describe the pathway o inf ammation that occurs in horizontal bone loss and contrast it with the pathway o inf ammation that occurs in vertical bone loss. • Contrast the characteristics o gingival and periodontal pockets. • For patients in the clinical setting, identi y visible clinical signs o health and periodontal disease or your clinic instructor. • For a patient with periodontal disease, measure the probing depth o the sulci or pockets on the acial aspect o one sextant o the mouth. Using the in ormation gathered visually and with the periodontal probe, explain whether this patient’s disease is gingivitis or periodontitis. • Given a drawing o a periodontal pocket, determine whether the pocket illustrated is a suprabony or in rabony pocket. • Describe variables associated with periodontal disease that an epidemiologist might include in a research study. • De ne prevalence and incidence as measurements o disease within a population. • Describe how clinical dental hygiene practice can be a ected by epidemiological research.

Ke Te ms Disease progression Gingivitis Acute gingivitis Chronic gingivitis Reversible (tissue damage) Periodontitis Apical migration o the junctional epithelium In lammation Alveolar bone loss

Horizontal bone loss Vertical bone loss Osseous de ect In rabony de ect Osseous crater Furcation involvement Attachment loss Disease site Inactive disease site Active disease site

Gingival pocket Periodontal pocket Suprabony pocket In rabony pocket Intermittent disease progression theory Epidemiology Incidence Prevalence

Chapte 3

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47

Overview o Diseases o the Periodontium

He alth a d D se ase

Th r e e Ba s ic s Ta Te s o f Th e Pe r io d o n Tiu m Disease progression (pathogenesis) is the sequence o events that occur during the development o a disease or abnormal condition. The periodontium exists in three basic states: health, gingivitis, and periodontitis (Fig. 3-1). It is important to recognize the di erences among health, gingivitis, and periodontitis (Figs. 3-2 to 3-4). This section provides an overview o these three basic states at the clinical and microscopic levels. The term periodontal disease should not be con used with the term periodontitis. Gingivitis and periodontitis are the two basic categories o periodontal disease (1–4). • Gingivitis is a bacterial in ection that is con ned to the gingiva. The tissue damage that occurs in gingivitis results in reversible destruction to the tissues o the periodontium (Fig. 3-3). • Periodontitis is a bacterial in ection o all parts o the periodontium including the gingiva, periodontal ligament, bone, and cementum. The tissue damage that occurs in periodontitis results in irreversible destruction to the tissues o the periodontium (Fig. 3-4). He a lth

Bas ic s tate s o f the pe rio do ntium

Ging ivitis

P e rio d o ntitis

F e 3-1. Th e e Bas c State s o the Pe o do t m. In the absence o disease, the periodontium is healthy. The two basic categories o periodontal disease are gingivitis and periodontitis.

TABLE 3 -1 . HiSTOLOg iC CHAn g ES in g in g iv iTiS An D PEr iODOn TiTiS State

J ct o al Ep the l m

Co e ct e T ss e Attachme t

Pe o do tal L ame t F be s

Al e o la Bo e

He alth

Je co o n l o Ce J

In

In

In

t ig

fib

bundl s

su

o

in

c llu l

ju n c io n s

c ; su

g in g iv l o vid

o g in g iv

c:

c

o

bon of

oo

so ck

oo

su

Je

ts

Ce J

Co n n c iv

Wid n d in ju n c io n s;

c llu l i

o s nd o

c s oo

of oo

n d Je g

c;

issu

In

c

In

c

d m g

li l

x n sio n s in o co n n c iv Pe o do t t s

Je

issu D s u c io n o f

ic l o Ce J

Wid n d in ju n c io n s;

c llu l i

li l

su

Je , ju n c io n l

i

io d o n

g in g iv l fib

bundl s

x n sio n s in o co n n c iv

D s u c io n o f

issu

liu m ; Ce J, c m n o n m l ju n c io n .

fib

D s u c io n

l lig m n

s; x o su

of

c m n um o

o ck

n vi o n m n

of bon ev n u l oo

lo ss

48

Pa t 2

Diseases A ecting the Periodontium

He a lth C lin ic a l

H is t o lo g ic a l

Clin ic a l p ic tu re o f h e a lth

He a lth y s u lc u s

P in k Firm No b le e d in g

J E c orona l to C E J Sup ra gingiva l fib e rs inta c t Alve ola r b one inta c t P e riod onta l liga me nt inta c t

F e 3-2. Cha acte st cs o He alth Pe o do t m. The clinical and histologic characteristics o the tissues o the periodontium in health.

Ging ivitis (Re ve rs ib le d a m a g e )

C lin ic a l

H is t o lo g ic a l

Clinic a l p ic ture o f g ing ivitis

Gin g iva l p o c ke t

Re d S wo lle n Ble e d in g like ly

J E at C E J Sup ra gingiva l fib e r d e s truc tion Alve ola r b one inta c t P e riod onta l liga me nt inta c t

F e 3-3. Cha acte st cs o g t s. The clinical and histologic characteristics o gingivitis. Some reversible tissue damage occurs in gingivitis.

P e rio d o n t it is

(Pe rma nent de s truc tion)

C lin ic a l

H is t o lo g ic a l

Clinic a l pic ture of p e riodontitis

P e rio d o nta l p o c ke t

P in k o r p urp lis h S wo lle n o r fib ro tic Ble e d ing

J E on c e me ntum Sup ra gingiva l fib e r d e s truc tion Alve ola r b one d e s truc tion Pe riod onta l liga me nt de s truc tion

F e 3-4. Cha acte st cs o Pe o do t t s. The clinical and histologic characteristics o periodontitis. Permanent tissue damage occurs in periodontitis.

Chapte 3

Overview o Diseases o the Periodontium

49

Pe r io d o n Tiu m in h e a l Th 1. Clinical Picture o Healthy Gingiva A. Color: Pink, may be pigmented, and is resilient in consistency. B. Gingival Margin 1. Scalloped outline. 2. Located coronal to (above) the cementoenamel junction (CEJ). C. Interdental Papillae: Firm and occupy the embrasure spaces apical to the contact areas. D. Absence o Bleeding: N o bleeding upon probing. E. Sulcus: Probing depths range rom 1 to 3 mm. 2. The Microscopic Picture o Healthy Gingiva (Fig. 3-5) A. Junctional Epithelium: The JE is rmly attached by hemidesmosomes to the enamel slightly coronal to (above) the CEJ. B. Epithelial–Connective Tissue Junction: In health, the junctional epithelium has no epithelial ridges. C. Gingival Fibers: Intact supragingival ber bundles support the junctional epithelium. D. Alveolar Bone: The crest o the alveolar bone is intact and located 2 to 3 mm apical to (below) the base o the junctional epithelium. E. Periodontal Ligament Fibers: Intact periodontal ligament ber bundles stretch between the bony walls o the tooth socket to the cementum o the root. F. Cementum: Cementum is normal.

Gingival s ulcus Oral epithelium J unctional epithelium

Gingival connective tis s ue Alveolar bone Cementum Periodontal ligament

CEJ Probing depth J unctional epithelium

F

e 3-5. The He alth Pe o do t m.

• Plaq e B o lm: light accumulation • J ct o al e p the l m: slightly coronal to the CEJ, no epithelial ridge ormation al be s: intact • S p a • Pe o do tal l ame t be s: intact • Al e o la bo e : intact ill st at o Ke : The white wedge indicates the location o the CEJ; the depth o the sulcus is shown by the blue vertical rectangle; the length o junctional epithelium is indicated by the pink vertical rectangle.

50

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Diseases A ecting the Periodontium

Gin Giv iTis —r e v e r s iBl e Tis s u e d a m a Ge 1. Characteristics o Gingivitis. Gingivitis is a type o periodontal disease characterized by changes in the color, contour, and consistency o the gingival tissues (Fig. 3-6). A. Onset o Gingivitis. Gingivitis is observed clinically rom 4 to 14 days a ter plaque bio lm accumulates in the gingival sulcus (5). 1. Acute gingivitis is a gingivitis that lasts or a short period o time. Acute gingivitis o ten is characterized by f uid in the gingival connective tissues that results in swollen gingiva. 2. Chronic gingivitis is a gingivitis that lasts or months or years. a. When gingivitis is chronic, the body may attempt to repair the tissue damage by orming new collagen bers in the gingival connective tissue. b. Excess collagen bers lead to gingival tissues that are enlarged and brotic (leathery) in consistency. c. The excess collagen bers conceal the redness caused by the increased blood f ow, making the tissue appear less red. B. Tissue Enlargement. Gingival enlargement may be caused by swelling (acute gingivitis) or brosis (chronic gingivitis). 1. Tissue enlargement causes the gingival margin to cover more o the crown o the tooth and results in deeper probing depths. 2. This enlargement o the gingival tissue is said to produce a alse or gingival pocket. 3. A gingival pocket has a sulcus depth over 3 mm. This increased probing depth is caused solely by enlarged gingival tissue. M icroscopically, the junctional epithelium remains in its normal position coronal to CEJ on the tooth in a gingival pocket. C. Reversible Tissue Damage. The tissue damage in gingivitis is reversible—that is, with good patient sel -care the body can repair the damage. D. Duration o Gingivitis. In many cases, gingivitis may persist or years without ever progressing to the next stage, periodontitis. In some cases, a combination o risk actors may result in gingivitis progressing to periodontitis. 2. Clinical Picture o Gingivitis A. Color: In gingivitis, the gingival tissue usually is red or reddish blue in color (Table 3-1). 1. The blood f ow increases in the gingival connective tissue and the gingival blood vessels become engorged with blood, causing the gingiva to appear red. 2. I the gingivitis persists, the gingival blood vessels may become congested. This slow-moving blood f ow causes the gingiva to have a bluish color. B. Gingival Margin 1. The gingival margin is swollen and loses its kni e-edge adaptation to the tooth. 2. Gingival tissue may cover more o the crown o the tooth due to tissue swelling or brosis. C. Interdental Papillae. The interdental papillae o ten are bulbous and swollen. D. Bleeding. There is bleeding upon gentle probing. E. Sulcus. Probing depths may be greater than 3 mm due to swelling o the tissues. It is important to note that there is NO apical migration o the junctional epithelium in gingivitis. 3. The Microscopic Picture o Gingivitis A. Junctional Epithelium: The hemidesmosomes still attach to the enamel coronal to the CEJ (Fig. 3-6 and Table 3-2). B. Epithelial–Connective Tissue Junction 1. The junctional epithelium extends epithelial ridges down into the connective tissue.

Chapte 3

C. D. E. F.

Overview o Diseases o the Periodontium

51

2. Such extension o the epithelial ridges only can occur because destruction o the gingival bers creates space or the growing epithelium. Gingival Fibers. Damage has occurred to the supragingival ber bundles. This damage is reversible i the bacterial in ection is brought under control. Alveolar Bone. The bacterial in ection has not progressed into the alveolar bone. There is no destruction o alveolar bone. Periodontal Ligament Fibers. The bacterial in ection has not progressed into the periodontal ligament bers. Cementum. The cementum covering the root o the tooth is normal.

Gingival pocket Epithelial ridges Swo lle n tis s ue J unctional epithelium Gingival ber des truction

Alveolar bone intact Cementum intact Periodontal ligament intact

CEJ Probing depth J unctional epithelium

F

e 3-6. g

t s.

• Plaq e B o lm: increased numbers o •

• • •

bacteria J ct o al e p the l m: slightly coronal to the CEJ; the coronal portion o the JE detaches rom the tooth; probing depth increases; epithelial ridges extend down into gingival connective tissue S p a al be s: some iber destruction Pe o do tal l ame t be s: intact Al e o la bo e : intact

ill st at o Ke : Note in this illustration that the JE, as indicated by the pink rectangle, is still coronal to the CEJ (white wedge). The blue rectangle has increased in depth due to the swelling o the gingival margin, so that the gingival tissue covers more o the crown o the tooth.

Pe r io d o n TiTis —Pe r m a n e n T Tis s u e d e s Tr u c Tio n 1. Characteristics o Periodontitis A. Extent o Tissue Destruction 1. Periodontitis is a type o periodontal disease that is characterized by the (1) apical migration o the junctional epithelium, (2) loss o connective tissue attachment, and (3) loss o alveolar bone (6). 2. The tissue damage o periodontitis is permanent. B. Process o Tissue Destruction 1. The tissue destruction o periodontitis is not a continuous process. Rather, the disease process occurs in an intermittent manner with extended periods o disease inactivity ollowed by short periods o destruction (3).

52

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2. Tissue destruction progresses at di erent rates throughout the mouth. Destruction does not occur in all parts o the mouth at the same time, but instead, destruction usually occurs in only a ew speci c sites (tooth sur aces) at a time. 2. Clinical Picture o Periodontitis A. Color: The gingival tissue shows visible alternations in color, contour, and consistency. 1. Edematous tissue (spongy tissue)—bluish red or purplish red with a smooth, shiny appearance. 2. Fibrotic tissue ( rm, nodular tissue)—light pink with a leathery consistency. Beginning clinicians o ten mistakenly interpret this light pink color as a sign o tissue health. B. Gingival Margin 1. The gingival margin may be swollen or brotic and does not have a close kni eedged adaptation to the tooth. 2. The position o the gingival margin varies greatly in periodontitis. The margin may be apical to the CEJ (recession) resulting in a portion o the root being visible in the mouth. C. Interdental Papillae. The interdental papillae may not ll the interdental embrasure spaces. D. Bleeding. There o ten is bleeding upon probing, and suppuration (a discharge o pus) may be visible. E. Pocket. Probing depths are 4 mm or greater in depth because the junctional epithelium is attached to the root sur ace. 1. Pus may be evident upon probing. 2. Pain is usually absent; however, probing may cause some pain due to ulceration o the pocket epithelium. 3. The Microscopic Picture o Periodontitis A. Junctional Epithelium 1. The junctional epithelium is located on the cementum, apical to—below—its normal location. M ovement o the junctional epithelium apical to its normal location is termed the apical migration o the junctional epithelium. 2. The coronal-most portion o the junctional epithelium detaches rom the tooth sur ace. As the bacterial in ection progresses, the apical portion o the junctional epithelium moves urther in an apical direction along the root sur ace creating a periodontal pocket (Fig. 3-7 and Table 3-2). 3. The extracellular matrix o the gingiva and the attached collagen bers at the apical edge o the junctional epithelium are destroyed. B. Epithelial–Connective Tissue Junction 1. The junctional epithelium proli erates and extends epithelial ridges into the connective tissue. 2. The sulcular epithelium o the pocket wall thickens and extends epithelial ridges deep into the connective tissue. Small ulcerations o the pocket epithelium expose the underlying inf amed connective tissue. C. Gingival Connective Tissue 1. Changes in the gingival connective tissue are severe. Collagen destruction in the area o inf ammation is almost complete. 2. There is widespread destruction o the supragingival ber bundles, reducing them to ber ragments. The destruction o the periodontal ligament ber bundles makes it easier or the junctional epithelium to migrate apically along the root sur ace.

Chapte 3

D. E. F. G.

Overview o Diseases o the Periodontium

53

3. The transseptal ber bundles, however, are regenerated continuously across the crest o bone. A band o intact transseptal bers separates the site o inf ammation rom the remaining alveolar bone even in cases o extensive bone loss (Fig. 3-8). 4. Epithelium grows over the root sur ace in areas where the ber bundles have been destroyed. T he loss o f ber attachm ent is perm anent because the epithelium grow ing over the root sur ace prevents the reinsertion o the periodontal ligam ent f bers in the cem entum . Alveolar Bone. There is permanent destruction o the alveolar bone that supports the teeth. Tooth mobility may be present. Periodontal Ligament Fibers. There is permanent destruction o some or all o the periodontal ligament ber bundles. Cementum. Cementum within the periodontal pocket is exposed to dental plaque bio lm. Pulp. H istologic studies o the dental pulp o patients with severe periodontitis show inf amed, edematous pulps, pulpal necrosis, vascular congestion, and dentin demineralization (7,8).

Epithelial ridges Swo lle n tis s ue Periodontal pocket Gingiva l ber des truction, collagen des truction in conne ctive tis s ue Bone a nd periodontal liga ment des truction

CEJ Probing depth J unctional epithelium

F

e 3-7. Pe o do t t s.

• Plaq e B o lm: vast numbers o bacteria • J ct o al e p the l m: apical to the CEJ with attachment on cementum; a remnant o the JE persists at the base o the periodontal pocket: epithelial ridges extend down into gingival connective tissue • S p a al be s: iber destruction • Pe o do tal l ame t be s: iber destruction • Al e o la bo e : portions o alveolar bone destroyed ill st at o Ke : Note the blue rectangle shows that the pocket in this illustration is increased by (1) the swollen gingiva margin and (2) the location o the JE apical to (below) the CEJ. The level o the CEJ is indicated by the white wedge.

54

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In t a c t tra n s s e p ta l fib e rs

F e 3-8. Ba d o i tact T a sse ptal F be s. Even in the presence o severe horizontal bone loss, there is an intact band o transseptal ibers above the remaining alveolar bone.

TABLE 3 -2 . HiSTOLOg iC CHAn g ES in DiSEASE D se ase State

H sto lo

g

e i li l id g s x n d d o w n in o co n n c iv D s u c io n o f su g in g iv l fib b u n d l s

ts

Pe o do t t s

Ch an g e s in Ep it h e lial Tissu e s: liu m lo c d • Ju n c io n l i • Ju n c io n l • Su lcu l co n n c iv

i i

ic l o

Ce J

liu m g o w s lo n g liu m

issu

o o su f c

ick n s n d x n d s

i

li l id g s d o w n in o

issu

Ch an g e s in Co n n e ct ive Tissu e s an d A lve o lar Bo n e : • Co ll g n d s u c io n • D s u c io n o f su • D s u c io n o f m in in • Ju n c io n l io d o n

g in g iv l fib io d o n

bundl s

l lig m n fib

s;

n ss

l fib

s

c i

liu m g o w s o v

l lig m n fib

s

• r o o c m n u m is x o s d o • D s u c io n o f lv o l

bon

o o su f c in d s oy d l q u b io film

sw

g n

nd

Chapte 3

Se ct o

2

Patho e e s s o Bo e De st

Overview o Diseases o the Periodontium

55

ct o

In ammation is the body’s reaction to injury or invasion by disease-producing organisms. The inf ammatory process that occurs in periodontitis results in permanent destruction to the tissues o the periodontium, including the destruction o gingival connective tissue, periodontal ligament, and alveolar bone. Alveolar bone loss is the resorption o alveolar bone as a result o periodontitis. This section discusses the patterns o bone destruction that occur in periodontitis. The pattern o bone destruction that occurs depends on the pathway o inf ammation as it spreads rom the gingiva into the alveolar bone. It is important to understand the changes that occur in the alveolar bone because it is the reduction in bone height that eventually results in tooth loss.

c h a n Ge s in a l v e o l a r Bo n e h e iGh T in d is e a s e 1. Reduction in Bone Height A. Bone Height in Health and Gingivitis. In health and gingivitis, the crest o the alveolar bone is located approximately 2 mm apical to (below) the CEJs o the teeth (Fig. 3-9). B. Bone Height in Periodontitis. In periodontitis, the bone destruction may be severe (Fig. 3-10). As periodontal disease progresses (worsens) tooth loss may occur rom lack o alveolar bone support (Fig. 3-11).

Gin g iva l m a rg in

C re s t o f b one

F e 3-9. Le e l o Al e o la C e st He alth a d g t s. In health, crest o the alveolar bone is located approximately 2 mm apical to the cementoenamel junction.

Gin g iva l m a rg in

C re s t o f bone

F e 3-10. Le e l o Al e o la C e st D se ase . In periodontitis, the crest o the alveolar bone is located more than 2 mm apical to the cementoenamel junction.

Gin g iva l m a rg in

C re s t o f bone

F e 3-11. Le e l o Al e o la C e st as D se ase P o e sse s. There is a progressive alveolar bone loss in periodontitis. Bone destruction may eventually lead to tooth mobility or loss due to insu icient bone support or the teeth.

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Pa TTe r n s o f Bo n e l o s s in Pe r io d o n TiTis 1. Patterns o Bone Loss. The two types o bone loss are (1) horizontal and (2) vertical bone loss. A. Horizontal Bone Loss 1. Horizontal bone loss is the most common pattern o bone loss (Fig. 3-12). 2. This type o bone loss results in a airly even, overall reduction in the height o the alveolar bone. 3. The alveolar bone is reduced in height, but the margin o the alveolar crest remains more or less perpendicular to the long axis o the tooth. B. Vertical Bone Loss 1. Vertical bone loss is a less common pattern o bone loss (Fig. 3-13). Vertical bone loss is also known as angular bone loss. 2. This type o bone loss results in an uneven reduction in the height o the alveolar bone. 3. In vertical bone loss, the resorption progresses m ore rapidly in the bone next to the root sur ace. This uneven pattern o bone loss leaves a trench-like area o missing bone alongside the root. Tooth #1

Tooth #2

A

B

F e 3-12. Ho zo tal Patte o Bo e Lo ss. A: Horizontal bone loss results in bone levels that are approximately at the same height on adjacent tooth roots. B: On a radiograph, i an imaginary line drawn between the CEJs o adjacent teeth is approximately parallel, then the bone loss is described as horizontal bone loss.

Tooth #1

A

Tooth #2

B

F e 3-13. v e t cal Patte o Bo e Lo ss. A: Vertical bone loss results in an uneven reduction in bone height on adjacent tooth roots, resulting in a trench-like area o missing bone alongside the root o one tooth. B: On a radiograph, i an imaginary line drawn between the CEJs o adjacent teeth is not parallel, then the bone loss is described as vertical bone loss.

Chapte 3

Overview o Diseases o the Periodontium

2. Pathways o In ammation into the Alveolar Bone A. Pathway o In ammation in Horizontal Bone Loss 1. In horizontal bone loss, inf ammation spreads into the tissues in this order: (1) within the gingival connective tissue along the connective tissue sheaths surrounding the blood vessels, (2) into the alveolar bone, and (3) nally, into the periodontal ligament space (Fig. 3-14A). 2. Inf ammation usually spreads in this manner because it is the path o least resistance. The periodontal ligament ber bundles act as an e ective barrier to the spread o inf ammation. Thus, the inf ammation spreads into the alveolar bone and then into the periodontal ligament space. B. Pathway o In ammation in Vertical Bone Loss 1. In vertical bone loss, inf ammation spreads into the tissues in this order (1) within the gingival connective tissue, (2) directly into the periodontal ligament space, and (3) nally, into the alveolar bone (Fig. 3-14B). 2. Inf ammation spreads in this manner whenever the crestal periodontal ligament ber bundles are weakened and no longer present an e ective barrier. Prior events such as occlusal trauma can be responsible or the weakened condition o the ber bundles.

1

1

From gingiva l c onne c tive tis s ue

Into c onne c tive tis s ue s he a ths of b lood ve s s e ls

2 Into p e riod onta l liga me nt s p a c e

3

2 Into the a lve ola r b one

3 Into a lve ola r b one

Into the p e riod onta l liga me nt s p a c e

A

B

F e 3-14. Pathw a o i lammat o to Al e o la Bo e . A: In horizontal bone loss, in lammation spreads through the tissues in this order: 1—Into the gingival connective tissue; 2—Into the alveolar bone; 3—Finally, into the periodontal ligament; B: In vertical bone loss, in lammation spreads through the tissues in this order: 1—Into the gingival connective tissue; 2—Into the periodontal ligament; 3—Finally, into the alveolar bone.

57

58

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Diseases A ecting the Periodontium

3. Bone De ects in Periodontal Disease. Periodontitis results in di erent types o de ects in the alveolar bone. These bony de ects are called osseous de ects. A. In rabony De ects. 1. In rabony de ects result when bone resorption occurs in an uneven, oblique direction. In in rabony de ects, the bone resorption primarily a ects one tooth. 2. Classi cation o In rabony De ects. In rabony de ects are classi ed on the basis o the number o osseous walls. In rabony de ects may have one, two, or three walls (Fig. 3-15). B. Osseous Craters. An osseous crater is a bowl-shaped de ect in the interdental alveolar bone with bone loss nearly equal on the roots o two adjacent teeth (Fig. 3-16A,B). 1. Whereas in rabony de ects primarily a ect one tooth, in craters the de ect a ects two adjacent root sur aces to a similar extent. 2. The presence o an osseous crater causes dental plaque bio lm to collect and makes it di cult to clean the interdental area.

A

B

F e 3-15. Osse o s De e cts. A: One-wall in rabony de ect, looking rom the canine tooth root distally toward the premolar, there is only “ one” wall o bone remaining, and that is on the mesial sur ace o the premolar. The acial plate and lingual plate o bone are missing. B: Two-wall in rabony de ect with acial plate o bone missing. The “ two walls” o the bone surrounding this de ect are the remaining lingual plate and bone on the mesial sur ace o the premolar tooth root.

C

D

F e 3-15. C: Three-wall in rabony de ect, the “three walls” o remaining bone that surround this de ect are the lingual plate, acial plate, and the bone on the mesial sur ace o the adjacent premolar root. D: Interproximal osseous crater with the lingual plate and acial plate o bone remaining. The bone between these plates is missing resulting in bone being lost on the mesial sur ace o the premolar and the distal sur ace o the adjacent canine. The term crater re ers to the dip in the contour o the interproximal bone between the acial and lingual plates.

Chapte 3

A

Overview o Diseases o the Periodontium

59

B

F e 3-16. Co to o i te de tal Bo e . A: Normal contour o the alveolar bone on the proximal (mesial or distal) sur ace o a posterior tooth. Note that the bone contour rom the acial to lingual is a relatively lat interproximal contour. B: Osseous crater on the proximal sur ace o a posterior tooth. Note that the contour o the bone rom the acial to the lingual dips apically and orms what is described as a “ crater” between the acial and lingual bone margins.

C. Bone Loss in Furcation Areas 1. Furcation involvement occurs on a multirooted tooth when periodontal in ection invades the area between and around the roots, resulting in a loss o alveolar bone between the roots o the teeth. 2. Bone loss in the urcation area may be hidden by the gingival tissue or may be clinically visible in the mouth (Fig. 3-17).

A

B

C

F e 3-17. F cat o i o l e me t. A: Due to recession, the urcation involvement on this molar is clinically evident. B: A periodontal probe easily can be inserted between the two roots o this mandibular molar. C: A radiograph shows the extensive bone loss around this molar. (Images courtesy o Dr. Richard J. Foster, Guil ord Technical Community College, Jamestown, N.C.)

60

Pa t 2

Se ct o

Diseases A ecting the Periodontium

3

Pe o do tal Po cke ts c h a r a c Te r is Tic s o f Pe r io d o n Ta l Po c k e Ts 1. Attachment Loss in Periodontal Pockets A. Attachment loss is the destruction o the bers and bone that support the teeth. B. Tissue destruction does not spread only in an apical (vertical) direction but also in a lateral (side-to-side) direction. C. A pocket on di erent root sur aces o the same tooth can have di erent depths. The loss o attachment may vary rom sur ace to sur ace o the tooth, with the base o the pocket exhibiting very irregular patterns o tissue destruction (Fig. 3-18). 2. Disease Sites. A disease site is an area o tissue destruction. A disease site may involve only a single sur ace o a tooth, or example, the distal sur ace o a tooth. The disease site may involve several sur aces o the tooth or all our sur aces (mesial, distal, acial, and lingual). A. Inactive disease site—a disease site that is stable, with the attachment level o the junctional epithelium remaining the same over time. B. Active disease site—a disease site that shows continued apical migration o the junctional epithelium over time. C. Assessment o Disease Activity. The disease activity o each site in the mouth should be assessed using a periodontal probe and recorded in the patient chart at regular intervals (scheduled check-up appointments). D. Periodontal Pockets. A periodontal pocket is an area o tissue destruction le t by the disease process. The pocket is much like a demolished home that is le t a ter a hurricane. 1. The presence o a periodontal pocket does not indicate necessarily that there is active disease at that site. Likewise, a demolished house does not necessarily indicate that a hurricane still is pounding the shoreline. A demolished house may indicate that the hurricane is still active or that a hurricane passed through a day, a week, or a year ago. 2. The majority o pockets in most adult patients with periodontitis are inactive disease sites. P o c ke t base

F a c ia l

P o c ke t base

Me s ia l

Lin g u a l

Dis t a l

F e 3-18. i e la Patte o Attachme t Lo ss. The amount o attachment loss can vary greatly on di erent sur aces o the same tooth. The base o a pocket may exhibit very irregular patterns o destruction.

Chapte 3

Overview o Diseases o the Periodontium

61

Po c k e T f o r m a Tio n 1. Gingival Sulcus. In health, the sulcus is 0.5 to 3 mm in depth. The junctional epithelium is coronal to the CEJ and attaches along its entire length to the tooth (Fig. 3-19). 2. Gingival Pockets. A gingival pocket is a deepening o the gingival sulcus as a result o swelling or enlargement o the gingival tissue (Fig. 3-20A,B). A. Why are gingival pockets “ alse” pockets? 1. Gingival pockets sometimes are re erred to “ pseudopockets,” meaning “ alse pockets,” because there is no apical migration o the junctional epithelium. 2. In gingivitis, however, the coronal portion o the junctional epithelium detaches rom the tooth resulting in a slight increase in probing depth. B. What causes the increased probing depth o a gingival pocket? The increased probing depth seen in a gingival pocket is due to (1) detachment o the coronal portion o the JE rom the tooth and/or (2) increased tissue size due to swelling o the tissue.

F e 3-19. g al S lc s. In health, the gingival sulcus has a shallow probing depth ranging rom 0.5 to 2 mm (indicated by the blue rectangle). Th e ju n ct io n al e p it h e liu m (JE) at t ach e s alo n g it s e n t ire le n g t h t o t h e e n am e l o f t h e t o o t h (as represented by the pink rectangle).

CEJ Probing depth J unctional epithelium

A

CEJ

CEJ

Probing depth J unctional epithelium

Probing depth J unctional epithelium

B

F e 3-20. g al Po cke ts. A: There is no apical migration o the JE; however the coronal portion o the JE detaches rom the tooth resulting in increased probing depth. B: In some cases the gingival tissue swells, resulting in a pseudo-pocket.

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3. Periodontal Pockets A. A periodontal pocket is a pathologic deepening o the gingival sulcus. 1. Pocket ormation occurs as the result o the (1) apical migration o the junctional epithelium, (2) destruction o the periodontal ligament bers, and (3) destruction o alveolar bone. 2. Apical migration is the movement o the cells o the junctional epithelium rom their normal position—coronal to the CEJ—to a position apical to the CEJ. In health, the junctional epithelial cells attach to the enamel o the tooth crown. In periodontitis, the junctional epithelial cells attach to the cementum o the tooth root. B. Two Types o Periodontal Pockets. The type o periodontal pocket is determined based on the relationship o the junctional epithelium to the crest o the alveolar bone. 1. Suprabony Pocket a. Suprabony pockets occur when there is horizontal bone loss (Fig. 3-21). b. The junctional epithelium, orming the base o the pocket, is located coronal to (above) the crest o the alveolar bone. 2. In rabony Pocket a. In rabony pockets occur when there is vertical bone loss (Fig. 3-22). b. The junctional epithelium, orming the base o the pocket, is located apical to (below) the crest o the alveolar bone. The base o the pocket is located within the cratered out area o the bone alongside o the root sur ace.

CEJ

CEJ

P robing depth

P robing de pth

J unctional epithelium

J unc tional e pithe lium

F e 3-21. S p abo Po cke t. Characteristics o a suprabony pocket are (1) horizontal bone loss and (2) a pocket base located coronal to (above) the crest o the alveolar bone. Note the position o the JE (indicated by the pink rectangle) in relation to the level o the alveolar bone).

F e 3-22. i abo Po cke t. Characteristics o an in rabony pocket are (1) vertical bone loss and (2) a pocket base located below the crest o the alveolar bone within a trench-like area o the bone. Note the position o the JE (indicated by the pink rectangle) indicated below the uppermost level o the alveolar bone.

Chapte 3

Se ct o

4

The o e s o D se ase P o

Overview o Diseases o the Periodontium

63

e ss o

For years, clinical researchers have been trying to nd an answer to the question, “ H ow does untreated periodontal disease progress?” In this context, disease progression means that the disease gets worse. Data rom ongoing studies suggest that the pattern o disease progression may vary rom (1) one individual to another, (2) one site to another in a person’s mouth, and (3) one type o periodontal disease to another. 1. Historical Perspective on Disease Progression A. Continuous Progression Theory (Historical View o Disease Progression: Prior to 1980). The continuous disease progression theory states that periodontal disease progresses throughout the entire mouth in a slow and constant rate over the adult li e o the patient (Fig. 3-23). 1. This theory suggests that: a. All cases o untreated gingivitis lead to periodontitis. b. All cases o periodontitis progress at a slow and steady rate o tissue destruction. 2. Research studies conducted in the early 1980s indicated that periodontal disease does not progress at a constant rate nor a ect all areas o the mouth simultaneously. The continuous progression theory does not accurately ref ect the complex nature o periodontal disease. 2. Current Theory o Disease Progression A. Intermittent Progression Theory (Current View). Intermittent disease progression theory states that periodontal disease is characterized by periods o disease activity and inactivity (remission) (Fig. 3-24). 1. Tissue destruction is sporadic, with short periods o tissue destruction alternating with periods o disease inactivity (no tissue destruction). The period o inactivity with no disease progression may last or months or or a much longer period o time. 2. Tissue destruction progresses at di erent rates throughout the mouth. Destruction does not occur in all parts o the mouth at the same time. Instead, tissue destruction occurs in only a ew speci c sites (tooth sur aces) at a time. 3. In the majority o cases, untreated gingivitis does not progress to periodontitis. 4. Di erent orms o periodontitis progress at widely di erent rates. 5. Susceptibility to periodontitis varies greatly rom individual to individual and appears to be determined by the host response to periodontal pathogens.

D

i

s

e

a

s

e

p

r

o

g

r

e

s

s

i

o

n

Wo rs e

Be tte r T i m e

F e 3-23. The Co t o s D se ase Mo de l o D se ase P o e ss o (P o to 1980). In the past, clinicians believed that periodontal disease progresses (worsens) throughout the entire mouth in a slow and constant rate over the li e o the patient. It was believed that all cases o untreated gingivitis led to periodontitis.

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D

i

s

e

a

s

e

p

r

o

g

r

e

s

s

i

o

n

Wo rs e

Be tte r T i m e

F e 3-24. i te m tte t D se ase P o e ss o The o . Current research suggests that periodontal disease is characterized by periods o disease activity and inactivity. Furthermore, destruction does not occur in all parts o the mouth at the same time.

Chapte 3

Se ct o

5

Ep de m o lo

Overview o Diseases o the Periodontium

o the D se ase s o the Pe o do t m

M any generations o researchers have asked the question, “ What causes periodontal disease?” while clinicians have asked, “ What is the best care or my patients with periodontal disease?” This section discusses the study o disease in the population (epidemiology) and reviews historical and current perspectives on the causes and progression o periodontal disease. 1. What is Epidemiology? A. Epidemiology is the study o the health and disease within the total population (rather than an individual) and the behavioral, environmental, and genetic risk actors that inf uence health and disease. An epidemiologist assesses how much disease, investigates possible causes and applies results to treatment recommendations. 1. Epidemiological research has three objectives: (1) to determine the amount and distribution o a disease in the total population and in subgroups, (2) to investigate the causes o a disease, and (3) to apply this knowledge to the control and prevention o disease. 2. Through research o population groups, epidemiologists strive to identi y the risk actors associated with disease such as race/ethnicity, heredity, gender, physical environment, systemic actors, socioeconomic status, and personal behavior. 3. An understanding o the risk actors associated with a certain disease can lead to theories o the cause o that disease and then to treatment standards or patient care. B. Epidemiology o Periodontal Disease 1. A large percentage o the adult population has periodontal disease. Epidemiologists study periodontal disease to determine its occurrence in the population and to identi y risk actors or periodontal disease. Some o the questions epidemiologists ask when researching periodontal disease are illustrated in Figure 3-25. 2. Epidemiological research also provides current in ormation to the clinical dental hygienist about methods and behaviors that are success ul in the treatment and prevention o periodontal disease. Current research also may de ne the level o risk a patient may have or periodontal disease.

Why do e s o ne pa rt o f the po pulatio n have le s s pe rio do ntal dis e as e than ano the r?

Ho w pre va le nt is pe rio do ntal dis e as e in the po pulatio n?

What Wha t g e ne tic c ha ra c te ris tic s do e s pula tio n have ha ve to inc re as as e the po pulatio the ir ris k fo r pe rio do ntal dis e as e ?

Que s tio ns a n e p id e m io lo g is t m ig ht a s k a b o ut p e rio d o nta l d is e a s e ...

Wha t is the c a us e o f pe rio do ntal dis e as e ?

Wha t life -s tyle be ha vio rs do e s What the po pulatio pula tio n ha ve to inc re a s e the ir ris k o f pe rio do ntal dis e as e ?

F e 3-25. r e se a ch Pe o do tal D se ase . This diagram illustrates the types o questions asked by epidemiologists when studying periodontal disease.

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3. Studies can be designed to look at the disparities or inequities o disease patterns. For instance a study may explore why more periodontal disease is ound in a speci c segment o the population than in another group o people. O ral diseases occur disproportionately more among individuals with low socioeconomic status and with poor general health (9). 2. Prevalence and Incidence o Disease A. Incidence and Prevalence 1. Incidence is the number o new disease cases in a population that occur over a given period o time. For example, a 2011 clinical study evaluated 250 white adult males with the Gingival Index (GI) to assess gingivitis. The results o this study indicated that 125 o the men had gingivitis. In 2012 a ollow-up study evaluated the same population and the results were that 150 o the men exhibited clinical signs o gingivitis. There ore, the incidence o new cases o gingivitis in this study population was 25 cases. 2. Prevalence re ers to the number o all cases (both old and new) o a disease that can be identi ed within a speci ed population at a given point in time. For example, given the above example, the prevalence o gingivitis within the total 2011 study population was 50% (125/250). O n the date o examination using the GI, the clinician does not know the length o time the men have had gingivitis, and cannot classi y them as new cases o disease (or incidence). B. Variables Associated with the Prevalence o Disease. Research ndings show that variables associated with the prevalence o periodontal disease include a person’s gender, race, socioeconomic status, and age. 1. Gender a. M ales have a greater prevalence and severity o periodontal disease than emales. (10) 2009–2010 N ational H ealth and N utrition Examination Survey (N H AN ES) reports periodontal disease in about 56% men versus 38% women (11). b. There has been some speculation that emales have a tendency to practice better and more requent sel -care than males. These di erences in sel -care behaviors may lead to the greater prevalence o disease in males. 2. Race/ethnicity. Black and H ispanic males living in the United States have poorer periodontal health and a greater incidence o periodontal disease than White males. Results rom the 2009–2010 N H AN ES indicate a disparity with the highest prevalence o periodontal disease in M exican Americans when compared to other races. 3. Education and Socioeconomic Status a. There is a greater incidence o periodontal disease in individuals with less than a high school education and living below the ederal poverty level. b. Underdeveloped countries have a higher incidence o chronic periodontitis, possibly due to a lack o adequate in ormation about disease prevention. 4. Age a. Research studies have shown that the severity o periodontal disease increases with age; however, the exact role that age plays in periodontal disease is di cult to assess. 1) As an individual lives longer, the chances increase that he will be exposed to additional risk actors or periodontal disease. Systemic illness, medications, and stress may contribute to disease risk in this population. With less edentulism, the elderly population has a greater

Chapte 3

Overview o Diseases o the Periodontium

risk o developing periodontal disease. Results rom the 2009–2010 N H AN ES indicate that 64% o adults over 65 years o age were ound to have moderate to severe periodontitis. 2) The higher incidence o periodontal disease in the elderly, there ore, may not be due to age, but rather other risk actors to which an individual has been exposed during his or her long li e. b. Diminished dexterity is sometimes a problem in elderly individuals and can impact the individual’s ability to per orm sel -care. Limited dexterity may also shorten the length o time that sel -care is per ormed on a daily basis. 5. Behavior a. Tobacco use has been identi ed as a behavioral risk actor or the development o periodontal disease. Both smoking tobacco and the use o smokeless tobacco products negatively impacts the periodontium (12,13). The 2009–2010 N H AN ES ound over 64% o current smokers examined had periodontal disease. b. With tobacco use as a risk actor, dental o ces may consider stronger e orts toward including tobacco cessation programs with patient education. 6. Access to Dental Care. Individuals who desire care or need care may not have access to dental care. Barriers to obtaining dental care include transportation, geographic distances to a dental o ce, nancial expense o dental care, and time available to seek care. C. Measuring the Disease Prevalence 1. The prevalence o periodontal disease in the U.S. adult population is determined by per orming clinical examinations on cross sections o groups using indices. Indices measure the amount and severity o disease. Indices used to measure both gingivitis and periodontitis vary across epidemiological studies, as does the extent o disease present when a study begins. Re er to Table 3-3 or a list o indices commonly used to assess periodontal disease. 2. Prevalence is a ected by: new cases o disease (incidence), cures or deaths within a population, and the longer lives o subjects. 3. H istorically gingival indices have used criteria to measure variables o inf ammation such as color changes, presence o edema, and bleeding upon probing. Clinical indices or measuring periodontitis include variable o probing depth, clinical attachment level (CAL), and interpretation o radiographic bone levels (BL). M any studies use sample groups numbering in the thousands. Several groups are then compared and statistically analyzed. Epidemiologists will have di erent approaches to research and will include di erent variables in studies. The selected population can be studied over time. D. Di f culties in Measurement o Periodontal Disease 1. It is ar easier to evaluate a population or prevalence and incidence o dental caries than or periodontal disease because caries lends itsel or more objective measurement. The development and process o caries is well known and involves only tooth structure. The Centers or Disease Control and Prevention (CDC) has provided guidance and standardized methods or public health surveillance o dental caries or many years. 2. Periodontal disease, on the other hand, involves both hard and so t tissues and has multiple variables that must be considered. Determining the presence o gingivitis with or without the presence o periodontitis urther complicates the assessment o disease. Assessment can include: a. So t tissue color changes (redness) b. Tissue swelling (edema)

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Diseases A ecting the Periodontium

c. Loss o periodontal ligament bers that support the teeth d. Loss o alveolar bone/ urcation involvement e. Bleeding upon probing/spontaneous bleeding . Probing depths 3. The multiple variables used to de ne periodontal disease make the numbers or prevalence and incidence o periodontal disease less speci c, more o a range, and more subject to change. N H AN ES most recently used the de nition/classi cation o periodontal disease, as determined by the collaboration o CDC and the American Academy o Periodontology (AAP) to assess the population. 4. H istorically national periodontal health surveys (N H AN ES) have used partial mouth examination protocols that may not accurately represent disease as periodontal disease is not evenly distributed in the entire mouth. For example, attachment loss can vary on tooth sur aces being examined. The 2009–2010 N H AN ES did use a ull-mouth examination and is being described as the most comprehensive survey o periodontal health in the United States (14).

TABLE 3 -3 . COMMOn Ly u SED PEr iODOn TAL in DiCES i de x

Me as

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a ss ss s

(F d

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; ds

l.)

Eastma i te de tal Ble e d (a b

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i de x (EiBi)

a ss ss s in

m s, C o n , n d po lso n )

s n c o f in fl m m

d n

l

u on oo

io n n d b l ick in s

d in g in

io n

(C o n n d po lso n ) g

al Ble e d

(C

i de x (g Bi)

n d B n s)

a ss ss s

s n c o f g in g iv l in fl m m

f o m in

o xim l su lcu s w i

io n b y b l

in 10 s o f flo ssin g

g

al i de x (g i)

a ss ss s s v i y o f g in g ivi is b s d o n co lo ,

(Lo

n d Siln ss)

co n sis n cy, n d b l

Mo d f e d g

al i de x (Mg i)

Sim il

o GI b u

o b in g ; Pe o do tal i de x (Pi)

a ss ss s

(r u ss ll)

a ss ss s

(r m fjo d )

d

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s v i y o f g in g iv l in fl m m

io n w i

ou

s v i y o f g in g iv l in fl m m

io n , o ck

o b in g

Pe o do tal D se ase i de x (PDi)

(a m

d in g o n

d in g

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(PSr )

a ss ss s

io d o n o lo g y n d

l a sso ci io n )

, nd

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o si s

l v l o f g in g iv l io d o n s, b l

l

l

in

d in g , n d

c m n id m n n s nc of

in clu d in g d

Chapte 3

Overview o Diseases o the Periodontium

E. What the Research Shows. Research on periodontal disease indicates it is one o the most widespread diseases in adult Americans, with most individuals who have periodontal disease being unaware o its presence. The ndings are based on data collected as part o CDC’s 2009–2010 N H AN ES, designed to assess the health and nutritional status o adults and children in the United States. The 2009–2010 N H AN ES included or the rst time a ull-mouth periodontal examination to assess or mild, moderate, or severe periodontitis, making it the most comprehensive survey o periodontal health ever conducted in the United States. Researchers measured periodontitis because it is the most destructive orm o periodontal disease. Gingivitis, the earliest stage o periodontal disease, was not assessed. 1. Prevalence or Periodontitis a. A study titled Prevalence o Periodontitis in A dults in the United States: 2009 and 2010 estimates that 47.2% , or 64.7 million American adults, have mild, moderate, or severe periodontitis. In adults 65 and older, prevalence rates increase to 70.1% (14). The ndings also indicate disparities among certain segments o the U.S. population. Periodontal disease is higher in men than women (56.4% vs. 38.4% ) and is highest in M exican Americans (66.7% ) compared to other races. O ther segments with high prevalence rates include current smokers (64.2% ); those living below the ederal poverty level (65.4% ); and those with less than a high school education (66.9% ). b. According to data rom 2009–2012 N H AN ES over 47% o the population had periodontitis: 1) 8.7% had mild periodontitis 2) 30.0% had moderate periodontitis 3) 8.5% had severe periodontitis c. According to data rom 2009–2012 N H AN ES, adults over 65 years o age, 64% had moderate/severe periodontitis. 2. Prevalence o Chronic Periodontitis a. The presence o periodontal disease is measured clinically in several ways. N H AN ES 2009–2010 used attachment loss and probing depths to assess periodontal disease. Loss o attachment is the term used to describe the destruction o periodontal ligament bers and alveolar bone that support the teeth. Figure 5-3 shows that attachment loss o 4 mm or more a ects approximately hal o adults aged 50 to 59 (11). b. By age 60 to 69 less than hal o all adults in the United States have retained 21 teeth or more (11). F. Public Health Surveillance o Periodontal Disease. The most recent N H AN ES data suggests that the amount o periodontal disease may have been underestimated in the general population (14). Both AAP and CDC describe periodontal disease as a public health concern and are working toward improved disease surveillance. CDC’s Division o O ral H ealth and the Association o State and Territorial Dental Directors collaborate to monitor the burden o oral disease and track state data sources.

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Chapte S mma

State me t

Periodontal pathogenesis is the sequence o events that occurs during the development o periodontal disease. The two types o periodontal disease are gingivitis and periodontitis. • Gingivitis is a reversible condition that is characterized by changes in the color, contour, and consistency o the gingiva. There is no apical migration o the junctional epithelium or bone loss in gingivitis. • Periodontitis results in some extent o perm anent tissue destruction characterized by pocket ormation, destruction o the periodontal ligament bers, and resorption o alveolar bone. The pattern o alveolar bone loss and periodontal ligament destruction depends on the pathway that the inf ammatory process takes as it spreads rom the gingiva into the alveolar bone. It is the destruction o periodontal ligament bers and resorption o alveolar bone that leads to tooth mobility and the possibility o tooth loss. Epidemiological research o periodontal disease has three objectives: (1) to determine the amount and distribution o periodontal disease in a population, (2) to investigate the causes o periodontal disease, and (3) to apply this knowledge to the control o periodontal disease. Advances in research have led to many changes in the understanding, prevention, and treatment o periodontal disease. In the uture, ideas about causes and treatment will continue to be re ned and changed as researchers delve urther into the mysteries o periodontal disease.

Chapte 3

Se ct o

6

Fo c s o Cl

Overview o Diseases o the Periodontium

Pat e ts

cal Pat e t Ca e CA S E 1 Your patient has 6 to 7 mm attachment loss on all sur aces o the maxillary rst molar. Which o the tissues o the periodontium have experienced tissue destruction surrounding this tooth?

CA S E 2 Your dental team provides appropriate therapy or a patient with periodontitis. When you began treatment, your initial ndings were redness and edema (swelling) o the gingiva, bleeding on probing, periodontal pockets, and attachment loss. Success ul control o the periodontal disease in the patient should not be expected to result in elimination o which o these initial clinical ndings?

CA S E 3 You nd a newspaper article that estimates that in your home state 73% o state residents have some orm o periodontal disease. You would like to use this statistic in a homework assignment. When you include this in ormation in your homework assignment should you describe this statistic as incidence or prevalence o periodontitis?

CA S E 4 Your dental team has a new patient who has gingivitis. The patient has poor daily sel care, generalized calculus deposits, poorly controlled diabetes mellitus, a history o smoking cigarettes, and inadequate dietary intake o calcium. In your patient counseling how would you characterize the likelihood that the patient will develop periodontitis in the uture and what might you tell the patient about this?

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r e e e ce s 1. Armitage GC. Development o a classi cation system or periodontal diseases and conditions. A nn Periodontol. 1999; 4(1):1–6. 2. Armitage GC. Periodontal diagnoses and classi cation o periodontal diseases. Periodontol 2000. 2004;34:9–21. 3. Armitage GC. Learned and unlearned concepts in periodontal diagnostics: a 50-year perspective. Periodontol 2000. 2013;62(1):20–36. 4. Armitage GC. Classi ying periodontal diseases–a long-standing dilemma. Periodontol 2000. 2002;30:9–23. 5. The pathogenesis o periodontal diseases. J Periodontol. 1999;70(4):457–470. 6. Armitage GC, Cullinan M P. Comparison o the clinical eatures o chronic and aggressive periodontitis. Periodontol 2000. 2010;53:12–27. 7. Caraivan O, M anolea H , Corlan Puscu D, et al. M icroscopic aspects o pulpal changes in patients with chronic marginal periodontitis. R om J M orphol Em bryol. 2012;53(3 suppl):725–729. 8. Fatemi K, Dis ani R, Z are R, et al. Inf uence o moderate to severe chronic periodontitis on dental pulp. J Indian Soc Periodontol. 2012;16(4):558–561. 9. United States. Public H ealth Service, O ce o the Surgeon General, N ational Institute o Dental and Cranio acial Research (U.S.). O ral H ealth in A m erica: A R eport o the Surgeon G eneral. Rockville, M D: Department o H ealth and H uman Services, U.S. Public H ealth Service; 2000. 10. Shiau H J, Reynolds M A. Sex di erences in destructive periodontal disease: a systematic review. J Periodontol. 2010;81(10):1379–1389. 11. www.cdc.gov/nchs/nhanes/nhanes2009-2010/current_nhanes_09_10.htm. Accessed on January 19, 2015 12. Kibayashi M , Tanaka M , N ishida N , et al. Longitudinal study o the association between smoking as a periodontitis risk and salivary biomarkers related to periodontitis. J Periodontol. 2007;78(5):859–867. 13. Laxman VK, Annaji S. Tobacco use and its e ects on the periodontium and periodontal therapy. J Contem p D ent Pract. 2008;9(7):97–107. 14. Eke PI, Dye BA, Wei L, et al; CDC Periodontal Disease Surveillance workgroup: James Beck GDRP. Prevalence o periodontitis in adults in the United States: 2009 and 2010. J D ent R es. 2012;91(10):914–920.

STu DEn T An CiLLAr y r ESOu r CES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

r e t p a h C

4

Class f cat o n o Pe r o do ntal D se ase s and Co nd t o ns

Se ct o n 1

Majo r D ag no st c Cate g o r e s o Pe r o do ntal D se ase

74

Se ct o n 2

D se ase Class f cat o n S ste ms

76

The 1989 Classi cation o Inf ammatory Periodontal Diseases The 1999 AAP Classi cation o Periodontal Diseases and Conditions Comparing the 1989 and 1999 Classi cation Systems

Se ct o n 3

T e 1999 AAP Class f cat o n S ste m o r Pe r o do ntal D se ase s and Co nd t o ns

78

Gingival Diseases Periodontitis and Other Periodontal Conditions

Se ct o n 4

Fo cus o n Pat e nts

82

Clinical Patient Care

Cl n cal Appl cat o n.

A periodontal disease classi cation system assists the dental hygienist in communicating clinical ndings accurately to other dental healthcare providers, patients, and dental insurance providers and provides a starting point or ormulating an individualized treatment plan.

Le arn ng O je ct e s • Name the two major categories o periodontal disease. • De ne and contrast the terms gingival disease, periodontal disease, and periodontitis. • Explain the historical background o the periodontal classi cation systems. • Explain the importance o a classi cation system or periodontal disease. • List, describe, and di erentiate the various periodontal diseases according to the current classi cation system established by the American Academy o Periodontology.

Ke Te rms Gingivitis Periodontitis

Periodontal disease Classi ication system

American Academy o Periodontology

The reader should be aware that at the time o publication o this edition, the American Academy o Periodontology task orce is reviewing the 1999 Classif cation o Periodontal Diseases and Conditions. The work o the task orce will take some time, but i an updated classi cation is made available, it will be posted on the LWW instructor/student website, The Point (http://thepoint.lww.com).

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Se ct o n 1

Majo r D ag no st c Cate g o r e s o Pe r o do ntal D se ase “ Periodontal disease” is a broad term used to re er to a bacterial in ection o the periodontium, just as “ heart disease” is a general term. There are many di erent diseases o the heart, such as coronary artery disease, congestive heart ailure, valvular disease, rheumatic heart disease, and in ectious endocarditis. As with heart disease, there are many speci c periodontal diseases that a ect the gingival tissues, periodontal connective tissues, and/or the supporting alveolar bone. The two major diagnostic categories o periodontal disease are (1) gingivitis and (2) periodontitis (Fig. 4-1). Within each o these major categories speci c types o diseases are identi ed. 1. Gingivitis is inf ammation o the periodontium that is con ned to the gingiva. It results in damage to the gingival tissue that is reversible. 2. Periodontitis is an inf ammatory disease o the supporting structures o the periodontium including the gingiva, periodontal ligament, bone, and cementum. It results in irreversible destruction to the tissues o the periodontium. 3. It is important to recognize the di erences among health, gingivitis, and periodontitis (Fig. 4-2). A. In health, no clinical signs o inf ammation are present. B. In gingivitis, there are clinical signs o inf ammation such as bleeding, redness, and swelling. 1. There is no attachment loss in gingivitis. Attachment loss re ers to the apical migration o the junctional epithelium and the destruction o connective tissue, periodontal ligament bers, and alveolar bone. 2. The tissue destruction in gingivitis can be reversed with pro essional treatment and good sel -care by the patient. C. Periodontitis is characterized by inf ammation, apical migration o the junctional epithelium, and attachment loss. In periodontitis there is irreversible tissue destruction including destruction o connective tissue, periodontal ligament bers, and alveolar bone.

P e r io d o n t a l d is e a s e

1

Gin g iv it is Re ve rs ib le tis s u e d a m a g e

2

Pe rio do ntitis Irre ve rs ib le tis s u e d a m a g e

F g ure 4-1. Pe r o do ntal D se ase . There are two major categories o periodontal disease: (1) gingivitis and (2) periodontitis.

C apte r 4

Classi cation o Periodontal Diseases and Conditions

1

No

Is the re infla m m a tio n?

Ye s 2

He a lt h

No

Is the re lo s s o f a tta c h m e n t?

Gin g iv it is

Ye s P e rio d o n t it is

F g ure 4-2. De c s o n Tre e . Is it health, gingivitis, or periodontitis?

4. Terminology: Periodontal Disease Versus Periodontitis A. M any beginning clinicians con use the meaning o the terms “ periodontal disease” and “ periodontitis.” O ten these terms are used interchangeably as i they mean the same thing. They do not. B. Periodontal disease re ers to inf ammation o the periodontium. 1. Periodontal disease that is limited to an inf ammation o the gingival tissues is called gingivitis. 2. Periodontal disease that involves all the structures o the periodontium is called periodontitis. C. Correct Terminology. It is important to understand that the terms “ periodontal disease” and “ periodontitis” are not identical in their meaning and not interchangeable in their use. 1. When a dental hygienist says to the dentist, “ M y patient has periodontal disease,” the hygienist is conveying the general in ormation that the patient has an inf ammation o the periodontium that could be gingivitis or periodontitis. 2. When the hygienist says, “ M y patient has periodontitis,” the hygienist is conveying the speci c in ormation that the patient has a bacterial in ection that involves all tissues o the periodontium including the periodontal ligament, cementum, and alveolar bone.

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Diseases A ecting the Periodontium

Se ct o n 2

D se ase Class cat o n S ste ms A classif cation system is a grouping o similar entities on the basis o certain di ering characteristics. An everyday example o a classi cation system is grouping vehicles into categories such as passenger cars, crossover vehicles, sport utility vehicles, and trucks. Classi cation systems provide a tool to study the etiology, pathogenesis, and treatment o periodontal diseases in an orderly manner. Clinicians and researchers have struggled to develop a classi cation o the various orms o periodontal disease. O ver the years, classi cation systems have changed in response to new scienti c knowledge about the etiology and pathogenesis o periodontal diseases and conditions. In recent years, there have been several attempts to classi y periodontal diseases. A disease classif cation system, however, should not be regarded as a permanent structure. Rather it must evolve with the development o new knowledge. It is expected that systems o classif cation will change over time. There has never been a per ect disease classi cation o periodontal diseases; as more is learned about the nature o periodontal diseases urther revisions in the current classi cation system will be necessary. A periodontal classi ication system provides in ormation necessary in (1) communicating clinical ndings accurately to other dental healthcare providers and to dental insurance providers, (2) presenting in ormation to the patient about his or her disease, (3) ormulating a diagnosis and individualized treatment plan, and (4) predicting treatment outcomes (prognosis).

Th e 1 9 8 9 Cl a s s if iCa Tio n o f in f l a m m a To r y Pe r io d o n Ta l d is e a s e s The 1989 classi cation system (Table 4-1) included ve types o periodontitis (Table 4-1) (1). The 1989 classi cation system emphasized the age o onset o disease and rates o disease progression. The main problems with the 1989 classi cation system were (1) unclear and overlapping disease categories, (2) inappropriate emphasis on age o onset o disease and rates o progression, and (3) absence o a gingival disease classi cation (2).

TAb LE 4 -1 . 1 9 8 9 CLASSiFiCATiON OF iNFLAMMATORy PERiODONTAL DiSEASES Adult Pe r o do nt t s (AP) Earl Onse t Pe r o do nt t s (EOP) a. p ub l io d o n i is (ppp) B. Ju v n il io d o n i is (Jp) C. r id ly o g ssiv io d o n i is (r pp) Pe r o do nt t s Asso c ate d w t S ste m c D se ase Ne cro t z ng Ulce rat e Pe r o do nt t s (NUG) Re racto r Pe r o do nt t s (RP)

Th e 1 9 9 9 a a P Cl a s s if iCa Tio n o f Pe r io d o n Ta l d is e a s e s a n d Co n d iTio n s The American Academy o Periodontology (AAP) initiated the currently accepted classi cation system by organizing the International W ork shop or a Classif cation o Periodontal D iseases and Conditions in 1999 (3). The AAP Classi cation o Periodontal Diseases and Conditions attempts to correct some o the de ciencies o the 1989

C apte r 4

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classi cation system. The 1999 AAP classi cation system was established to identi y types o periodontal disease by taking into consideration actors such as clinical mani estations, pathogenic microbial f ora and the host response to these bacteria, rate o disease progression, and systemic inf uences. The 1999 classi cation includes eight main categories (Table 4-2). At the time o publication o this textbook, the 1999 AAP Classi cation o Periodontal Diseases and Conditions represents the most recent, internationally accepted classi cation system.

TAb LE 4 -2 . MAiN CATEGORiES: AAP CLASSiFiCATiON OF PERiODONTAL DiSEASES AND CONDiTiONS, 1 9 9 9 G ng al D se ase s pl q u -in d u c d g in g iv l d is

s s

No n – l q u -in d u c d g in g iv l l sio n s C ro n c Pe r o do nt t s Lo c liz d G n

liz d

Ag g re ss e Pe r o do nt t s Lo c liz d G n

liz d

Pe r o do nt t s as a Man e stat o n o S ste m c D se ase Ne cro t z ng Pe r o do ntal D se ase s A sce sse s o t e Pe r o do nt um Pe r o do nt t s Asso c ate d w t Endo do nt c Le s o ns De e lo pme ntal o r Acqu re d De o rm t e s and Co nd t o ns

Co m Pa r in g Th e 1 9 8 9 a n d 1 9 9 9 Cl a s s if iCa Tio n s y s Te m s M uch o the periodontal literature ound in periodontal journals and textbooks is based on the earlier 1989 classi cation. For this reason, readers need to be somewhat amiliar with both the 1989 and 1999 classi cation systems (Table 4-3).

TAb LE 4 -3 . Ch ANGES FROM 1 9 8 9 TO 1 9 9 9 CLASSiFiCATiON Ne w Te rm no lo g

• Ch ro n ic p e rio d o n t it is l c s m id m io lo g ic l vid n c su g g s s so m d o l sc n s. • A g g re ssive p e rio d o n t it is l c s is d ifficu l o d m in g of ons • Ne cro t iz in g p e rio d o n t al d ise ase l c

ad u lt p e rio d o n t it is sin c c o n ic io d o n i is is lso s

n in

m e arly o n se t p e rio d o n t it is b c u s i of io d o n i is in m n y c s s. s n e cro t iz in g u lce rat ive p e rio d o n t it is.

Add t o ns

• • • • •

Gin g iv l d iso d s p io d o n i is s m n if s io n o f sys m ic d is s p io d o n l b sc ss p io d o n i is in co n ju n c io n w i n d o d o n ic l sio n s D v lo m n l o g n ic co n d i io n s

De le t o n

c g o y o f re f ract o ry p e rio d o n t it is is lim in d . In 1999 • t cl ssific io n , d sig n io n re f ract o ry c n b li d o all t yp e s o f io d o n l d is s do no s ond o m n .

78

Part 2

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Se ct o n 3

T e 1999 AAP Class cat o n S ste m o r Pe r o do ntal D se ase s and Co nd t o ns g in g iv a l d is e a s e s The 1999 AAP Classi cation o Periodontal Diseases and Conditions (Table 4-4A,B) subdivides the major diagnostic category o gingivitis into speci c types o diseases: (1) dental plaque-induced gingival diseases and (2) non–plaque-induced gingival lesions. Each gingivitis disease type has two or more subcategories (Fig. 4-3).

Gin g iv a l d is e a s e s

Pla que - induc e d g ing ival dis e as e s

No n–pla que - induc e d g ing iva l le s io ns

F gure 4-3. Tw o Major D agnost c Categor es o G ng al D seases. The 1999 AAP Classi ication o Periodontal Diseases and Conditions subdivides into two major categories. Each o the two major categories has several subcategories.

TAb LE 4 -4 A. AAP CLASSiFiCATiON OF GiNGiv AL DiSEASES G ng al D se ase s • Plaque -induce d G ng al D se ase s C u s d so l ly b y l q u

Mo d ifi d b y sys m ic f c o s

Mo d ifi d b y m d ic io n s

Mo d ifi d b y m ln u i io n

i. G ng al D se ase s A. De ntal plaque - nduce d g ng al d se ase s a 1. Gin g ivi is sso ci d w i d n l l q u b io film o n ly . Wi o u o lo c l co n ib u in g f c o s b . Wi lo c l co n ib u in g f c o s 2. Gin g iv l d is s s m o d ifi d b y sys m ic f c o s . a sso ci d wi n d o c in sys m 1) pu b y- sso ci d g in g ivi is 2) M n s u l cycl - sso ci d g in g ivi is 3) p g n n cy- sso ci d ) Gin g ivi is b ) pyo g n ic g n u lo m 4) Di b s m lli u s- sso ci d g in g ivi is b . a sso ci d w i b lo o d d ysc si s 1) L u k m i - sso ci d g in g ivi is 2) O 3. Gin g iv l d is s s m o d ifi d b y m d ic io n s . D u g -in flu n c d g in g iv l d is s s 1) D u g -in flu n c d g in g iv l n l g m n s 2) D u g -in flu n c d g in g ivi is ) O l co n c iv - sso ci d g in g ivi is b) O 4. Gin g iv l d is s s m o d ifi d b y m ln u i io n . a sco b ic cid d fici n cy g in g ivi is b. O

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TAbLE 4 -4 A. AAP CLASSiFiCATiON OF GiNGiv AL DiSEASES (Co n t in u e d ) • Non–Plaque-induced G ng al Les ons B c i l in f c io n s

Vi l in f c io n s

Fu n g l in f c io n s

G n

ic o ig in

Sys m ic lly

t

r O a

l

d

um

c io n s o fo

ig n b o d i s

b. No n–plaque - nduce d g ng al le s o ns 1. Gin g iv l d is s s o f s cific b c i l o ig in . Ne isse ria g o n o rrh o e ae - sso ci d l sio n s b . Tre p o n e m a p allid u m - sso ci d l sio n s c. S o co cc l s ci s- sso ci d l sio n s d. O 2. Gin g iv l d is s s o f vi l o ig in . h s vi u s in f c io n s 1) p im y ic g in g ivo s o m i is 2) r cu n o l s 3) V ic ll zo s in f c io n s b. O 3. Gin g iv l d is s s o f fu n g l o ig in . Can d id a s ci s in f c io n s 1) G n liz d g in g iv l c n d id i sis b . Lin g in g iv l y m c. h is o l sm o sis d. O 4. Gin g iv l l sio n s o f g n ic o ig in d i y g in g iv l fib o m o sis . h b. O 5. Gin g iv l m n if s io n s o f sys m ic co n d i io n s • Mu co cu n o u s d iso d s Lic n l n u s p m ig o id p m ig u s vu lg is e y m m u l ifo m Lu u s y m o su s D u g in d u c d O c io n s • a ll g ic D n l s o iv m i ls • M cu y • Nick l • a c ylic • O r c io n s ib u b l o s s/d n if ic s • t oo • Mo u in s s/m o u w s s • C w in g g u m d d i iv s • Fo o d s n d d d i iv s O 6. t u m ic l sio n s (f c i io u s, i o g n ic, ccid n . C m ic l in ju y b . p ysic l in ju y c. t m l in ju y 7. Fo ig n b o d y c io n s 8. No o w is s cifi d (NOS)

C n o ccu o n io d o n iu m w i n o c m n lo ss o o n io d o n iu m w i D f o m a m i g GC. D v lo m n o f cl ssific io n sys m fo io d o n l d is m issio n f o m A n n Pe rio d o n t o l. 1999;(4):1–6.)

l)

c m n lo ss is n o og s n d co n d i io n s. (Us d w i

ssin g .

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Pe r io d o n TiTis a n d o Th e r Pe r io d o n Ta l Co n d iTio n s The 1999 AAP Classi cation o Periodontal Diseases and Conditions subdivides the major diagnostic category o periodontitis into speci c types o diseases: (1) chronic periodontitis, (2) aggressive periodontitis, and (3) less common types o periodontitis. Each periodontitis disease type has two or more subcategories (Fig. 4-4).

P e rio d o n t it is

Chro nic pe rio do ntitis

Ag g re s s ive pe rio do ntitis

Le s s c o mm o n type s o f pe rio do ntitis

F g ure 4-4. T re e Majo r Cate g o r e s o Pe r o do nt t s. The 1999 AAP Classi ication o Periodontal Diseases and Conditions subdivides periodontitis into three major categories o periodontitis. Each o the three major categories has two or more subcategories.

TAb LE 4 -4 b . AAP CLASSiFiCATiON OF PERiODONTiTiS AND OTh ER PERiODONTAL CONDiTiONS C ro n c Pe r o do nt t s (CP)

II. C o n ic p io d o n i isa a . Lo c liz d B. G n liz d

Ag g re ss e Pe r o do nt t s (AP)

III.

a g g ssiv p io d o n i isa a . Lo c liz d B. G n liz d

Pe r o do nt t s as Man e stat o n o S ste m c D se ase • Blo o d d iso d s

IV.

p

• G n

M n if s

io n o f Sys m ic Dis

a . a sso ci d wi m o lo g ic l d iso d s 1. a cq u i d n u o n i 2. L u k m i s 3. O B. a sso ci d w i g n ic d iso d s 1. F m ili l n d cyclic n u o n i 2. Do w n syn d o m 3. L u ko cy d sio n d fici n cy syn d o m s 4. p illo n –L fè v syn d o m 5. C é d i k–h ig s i syn d o m 6. h is io cy o sis syn d o m s 7. Glyco g n s o g d is s 8. In f n il g n ic g n u lo cy o sis 9. Co n syn d o m 10. e l s–D n lo s syn d o m (t y s IV n d VIII) 11. h y o o s si 12. O C. No o w is s cifi d (NOS)

ic f c o s

Ne cro t z ng Pe r o do ntal D se ase s

io d o n i is s

V. N c o izin g p io d o n l Dis s s a . N c o izin g u lc iv g in g ivi is (NUG) B. N c o izin g u lc iv io d o n i is (NUp)

A sce sse s o t e Pe r o do nt um

VI.

a b sc ss s o f p io d o n iu m a . Gin g iv l b sc ss B. p io d o n l b sc ss C. p ico o n l b sc ss

Pe r o do nt t s Asso c ate d w t Endo do nt c Le s o ns

VII. p io d o n i is a sso ci d w i e n d o d o n ic L sio n s a . Co m b in d io d o n ic– n d o d o n ic l sio n s

s

C apte r 4

Classi cation o Periodontal Diseases and Conditions

TAb LE 4 -4 b . AAP CLASSiFiCATiON OF PERiODONTiTiS AND OTh ER PERiODONTAL CONDiTiONS (Co n t in u e d ) De o rm t e s and Co nd t o ns d • t oo - l

• Mu co g in g iv l co n d i io n s

• Mu co g in g iv l d fo m i i s

• Occlu s l

um

VIII. D v lo m n l o a cq u i d D fo m i i s n d Co n d i io n s a . Lo c liz d o o - l df co s m o d ify o d is o s o l q u -in d u c d g in g iv l d is s s o io d o n i is 1. t o o n o m ic f c o s 2. D n l s o io n s/ li n c s 3. r o o f c u s 4. C vic l o o so io n n d c m n l s B. Mu co g in g iv l d fo m i i s n d co n d i io n s o u n d 1. Gin g iv l/so f issu c ssio n . F ci l o lin g u l su f c s b . In o xim l ( ill y) 2. L ck o f k in iz d g in g iv 3. D c s d v s ib u l d 4. a b n f n u m /m u scl o si io n 5. Gin g iv l xc ss . ps u d o o ck b . In co n sis n g in g iv l m g in c. e xc ssiv g in g iv l d is l y d . Gin g iv l n l g m n 6. a b n o m l co lo C. Mu co g in g iv l d fo m i i s n d co n d i io n s o n d n u lo u s id g s 1. V ic l n d /o o izo n l id g d fici n cy 2. L ck o f g in g iv /k in iz d issu 3. Gin g iv l/so f issu nl g m n 4. a b n f n u m /m u scl o si io n 5. D c s d v s ib u l d 6. a b n o m l co lo D. Occlu s l um 1. p im y o cclu s l um 2. S co n d y o cclu s l um

a

C n b fu cl ssifi d o n b sis o f x n n d s v i y. D f o m a m i g GC. D v lo m n o f cl ssific io n sys m fo m issio n f o m A n n Pe rio d o n t o l. 1999; (4):1–6.)

io d o n

l d is

s

n d co n d i io n s. (Us d w i

C apte r Summar State me nt The two basic diagnostic categories o periodontal disease are (1) gingivitis and (2) periodontitis. It is important to be thoroughly amiliar with the terms periodontal disease, gingivitis, and periodontitis and the precise de nition o each term. Classi cation systems, like the one or periodontal diseases and conditions, group similar diseases and conditions into general categories. Classi cation systems provide a tool to study the etiology, pathogenesis, and treatment o periodontal diseases in an orderly manner. From the clinician' s point o view, the classi cation system provides a starting point or ormulating a diagnosis and individualized treatment plan. In addition, periodontal disease classi cations assist the dental hygienist in communicating with other dental healthcare providers, patients, and dental insurance providers.

81

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Diseases A ecting the Periodontium

Se ct o n 4

Fo cus o n Pat e nts Cl n cal Pat e nt Care CA S E1 During the assessment o the periodontium, you note the ollowing: apical migration o the junctional epithelium and attachment loss. The patient's medical history is normal; he takes no medications. According to the 1999 AAP Classi cation o Periodontal Diseases and Conditions, would this patient be classi ed as having plaque-induced gingivitis, non–plaque-induced gingivitis, plaque-induced gingival disease modi ed by systemic actors or periodontitis?

CA S E 2 During the assessment o the periodontium, you note the ollowing: bleeding, redness, and swelling o the tissue; abundant plaque bio lm, no apical migration o the junctional epithelium, and no attachment loss. The patient's medical history is normal; he takes no medications. According to the 1999 AAP Classi cation o Periodontal Diseases and Conditions, would this patient be classi ed as having plaque-induced gingivitis, non–plaque-induced gingivitis, plaqueinduced gingival disease modi ed by systemic actors or periodontitis?

CA S E 3 During the assessment o the periodontium, you note the ollowing: bleeding, redness, and swelling o the tissue; abundant plaque bio lm, no apical migration o the junctional epithelium, and no attachment loss. The patient has a history o diabetes mellitus or which he takes daily insulin injections. According to the 1999 AAP Classi cation o Periodontal Diseases and Conditions, would this patient be classi ed as having plaque-induced gingivitis, non–plaqueinduced gingivitis, plaque-induced gingival disease modi ed by systemic actors or periodontitis?

Re e re nce s 1. N evins M , Becker W, Kornman KS. A m erican A cademy o Periodontology. Proceedings o the World Workshop in Clinical Periodontics, Princeton, N ew Jersey, July 23–27, 1989. Chicago, IL: American Academy o Periodontology; 1989. 2. Armitage GC. Development o a classi cation system or periodontal diseases and conditions. A nn Periodontol. 1999;4(1):1–6. 3. Armitage GC. Classi ying periodontal diseases—a long-standing dilemma. Periodontol 2000. 2002;30:9–23.

STUDENT ANCiLLARy RESOURCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

r e t p a h C

5 Se ctio

Cli ical Fe at the Gi g iva 1

Cli ical Fe at

es o

e s o He alth Gi g iva

84

Tissue Color and Contour in Health Tissue Consistency and Texture in Health Position o Gingival Margin in Health Absence o Bleeding in Health

Se ctio

2

Cli ical Fe at

e s o Gi g ival I f ammatio

87

Characteristics o Gingivitis Tissue Consistency and Texture in Gingivitis Position o Margin in Gingivitis Presence o Bleeding in Gingivitis

Se ctio

3

Exte t a d Dist ib tio

o I f ammatio

92

Gingival In ammation

Se ctio

4

Fo c s o

Patie ts

94

Clinical Patient Care

Cli ical Applicatio .

A dental hygienist’s ability to recognize the clinical eatures o both healthy and diseased gingiva plays a part in nearly every patient care visit. Knowledge o these clinical eatures continuously will be expanded throughout the hygienist’s career. The outline o these eatures presented in this chapter provides a undamental ramework or recognition o clinical eatures and will allow a new clinician to enter a clinical setting with conf dence.

Le a

i g Obje ctive s

• Describe characteristics o the gingiva in health. • List clinical signs o gingival in ammation. • Compare and contrast clinical eatures o healthy and in amed gingival tissue. • Explain the di erence in color between acute and chronic in ammation. • Di erentiate between bulbous, blunted, and cratered papilla. • Write a description o gingival in ammation that includes descriptors o duration, extent, and distribution o in ammation.

Ke Te ms Stippling In lammation Gingivitis

Bulbous papilla Blunted papilla Cratered papilla

Extent o in lammation

84

Pa t 2

Se ct io

1

Diseases A ecting the Periodontium

Cli ical Fe at

e s o He alth Gi g iva

It is important or clinicians to recognize the appearance o healthy gingiva and to recognize all o its variations in health. In addition, clinicians must be able to describe gingiva accurately when documenting the ndings rom a periodontal assessment. Care ul choice o verbal descriptors documents the state o gingival health, or lack o it, and allows the clinician to ocus on areas that may need additional treatment. 1. Tissue Color and Contour in Health A. Tissue Color 1. H ealthy gingival tissue has a uni orm, pink color. The precise color depends on the number and size o blood vessels in the connective tissue and the thickness o the gingival epithelium. 2. The shade o pink usually is lighter in blondes with air complexions and darker in brunettes with dark complexions (Fig. 5-1). 3. The coral pink o the gingiva is easily distinguished rom the darker alveolar mucosa. 4. H ealthy tissue also can be pigmented. The pigmented areas o the attached gingiva may range rom light brown to black. B. Tissue Contour (Size and Shape) 1. In health, the gingival tissue lies snugly around the tooth and rmly against the alveolar bone (Fig. 5-2). 2. The gingival margin is smoothly scalloped in an arched orm as the gingiva margin f ows across the tooth sur ace rom papilla to papilla. 3. The gingival margin meets the tooth with a tapered (kni e-edge), f at, or slightly rounded edge. 4. Papillae come to a point and ll the space between teeth (Fig. 5-2). 5. Teeth with a diastema—no contact between adjacent teeth—or large spaces between teeth will have f at papillae. 2. Tissue Consistency and Texture in Health A. Tissue Consistency 1. The attached gingiva is rmly connected to the underlying cementum and bone. 2. The tissue is resilient (elastic). I gentle pressure is applied to the gingiva with the side o a probe, the tissue resists compression and springs back almost immediately. 3. The attached gingiva will not pull away rom the tooth when air is blown into the sulcus.

A

B

Fig e 5-1. Tiss e Co lo i He alth. A: Periodontal health showing coral pink gingiva. Note the distinct di erence in appearance between the keratinized gingiva and the nonkeratinized alveolar mucosa. B: Pigmentation o the gingiva showing how the gingiva can vary in color in some patients.

Chapte 5

Clinical Features o the Gingiva

85

B. Sur ace Texture o the Tissue 1. In health, the sur ace o the attached gingiva is rm and may have a dimpled appearance similar to the skin o an orange peel (Fig. 5-3). 2. This dimpled appearance is known as stippling, appearing as minute elevations and depressions o the sur ace o the gingiva due to connective tissue projections within the epithelial tissue (connective tissue papillae). Stippling varies greatly rom individual to individual and in some patients healthy tissue may not exhibit a stippled appearance. The presence o stippling is best viewed by drying the tissue with compressed air. 3. H ealthy tissue may or may not exhibit a stippled appearance as the presence o stippling varies greatly rom individual to individual. 3. Position o Gingival Margin in Health. Ideally, the gingival margin is slightly coronal to the cementoenamel junction (CEJ) (Figs. 5-4 and 5-5). Patients with a previous history o bone loss, but healthy gingival tissue, may have a gingival margin that is apical to the CEJ (Fig. 5-6). 4. Absence o Bleeding in Health. H ealthy tissue does not bleed when disturbed by clinical procedures such as gentle probing o the sulcus.

Fig e 5-2. Co to s o He alth Gi g iva. This tissue on the acial aspect o the maxillary anteriors exhibits all the characteristics o health, including a smoothly scalloped gingival margin, a tapered margin slightly coronal to the CEJ, and pointed papillae that completely ill the space between the teeth. (Courtesy o Dr. Don Rol s, Wenachee, WA.)

Fig e 5-3. Stippli g o Gi g ival Tiss e . Healthy gingival tissue showing a stippled appearance. Stippling varies greatly rom individual to individual and in some patients healthy tissue may not exhibit a stippled appearance.

86

Pa t 2

Diseases A ecting the Periodontium

Fig e 5-4. Po sitio o the Ma g i i He alth. In health, the gingival margin is slightly coronal to the cementoenamel junction. In anterior sextants, the margin is characterized by pronounced scalloping o the margin and pointed interdental papillae.

Fig e 5-5. Gi g iva i Po ste io Se xta ts i He alth. In posterior sextants, the tissue is characterized by a gently scalloped margin and papillae that ill the interdental embrasure spaces. (Used with permission rom Langlais RP. Color Atlas of Common Oral Diseases. Philadelphia, PA: Wolters Kluwer; 2003.)

Fig e 5-6. He alth o Dise ase ? This i divid al e ce ive d pe io do tal t e atme t o ch o ic pe io do titis se ve al e a s ag o . The assessment at today’s appointment reveals no in lammation and no additional attachment loss since the beginning o periodontal maintenance several years ago. There ore, this tissue is considered healthy. The attachment loss is simply an indicator o previous disease activity. (Courtesy o Dr. Ralph Arnold.)

Chapte 5

Se ct io

2

Cli ical Fe at

87

Clinical Features o the Gingiva

e s o Gi g ival I lammatio

Gingival inf ammation is the body’s reaction to the bacterial in ection o the gingival tissues by periodontal pathogens. The inf ammatory response to this bacterial in ection results in clinical changes in the gingival tissue involving the ree and attached gingiva as well as the papillae. Inf ammation that is con ned to gingival tissue with no e ect on attachment level is called gingivitis, and is the mildest orm o periodontal disease. M ost patients are unaware they have a gingival in ection because there usually is no discom ort. A clinician with a trained eye can discern subtle di erences in color, contour, and consistency even in gingival tissues that appear relatively healthy at rst glance. The phrase “ tissue talks” is a good phrase to remember when assessing the gingival tissue. Indications that the tissue is not healthy include such clinical observations as red, swollen tissue or papillae that do not ll the interdental space. Table 5-1 contrasts the characteristics o healthy versus inf amed gingival tissue.

TABLE 5 -1 . CHAr ACTEr ISTICS OF HEALTHy VEr Su S In FLAMED GIn GIVAL TISSu E He alth Tiss e Co lo

Un ifo m pig m n

Co to

Gi g ivitis

in k co lo io n m y b

M g in l g in g iv M s oo

s n

in

d o slig

ound d dg In d n l ill po in d ill fills

Co siste c

Te xt

e

Fi m r sili n u n d Sm o o

Ma g i

Slig

Ble e di g

No b l

co m

n d /o s i

a cu : b ig C o n ic: b lu is

s

ssio n l d

ly co o n l o

Ce J

d in g u o n

o b in g

c b

w

d d o

ly

M g in l g in g iv M s oo

n

dg In d n l ill Bu lb o u s, b lu n d , c

u

in

lis

o ll d ,

d ick n d

d

S o n g y, fl ccid In d n s sily w n ss d lig ly Co m ss d i d fl c s issu t issu s in y in S c d Co o n l o Bl

d in g u o n

nc nc Ce J o b in g

88

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Diseases A ecting the Periodontium

1. Characteristics o Gingivitis A. Tissue Color in Gingivitis 1. Gingivitis is an inf ammation o the gingiva o ten causing the tissue to become red and swollen, to bleed easily, and sometimes to become slightly tender. There is also an increased f ow o crevicular f uid (sulcular f uid) rom the sulcus, corresponding to the severity o inf ammation (1). 2. Inf ammation results in increased blood f ow to the gingiva causing the tissue to appear bright red. Figures 5-7 and 5-8 show examples o common clinical presentations o gingivitis.

A

B

Fig e 5-7. Co lo Cha g e s i Gi g ivitis. A: Slight marginal redness is a clinical sign o early gingivitis. B: This gingival tissue shows more in lammation than seen in photograph A. The marginal and papillary gingival tissues are bright red in color. Note, also, the swelling o the marginal gingiva and papillae in this example. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

A

B

Fig e 5-8. Co lo Cha g e s i Gi g ivitis. A: This example shows subtle color changes in the marginal and papillary gingival tissues. B: In this example, the color changes are pronounced with iery red marginal gingiva and papillae. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

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Clinical Features o the Gingiva

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B. Tissue Contour (Size and Shape) in Gingivitis 1. An increase o f uid within the tissue spaces—edema—causes enlargement o the gingival tissues. The normal scalloped appearance o the gingiva is lost i the gingival papillae are swollen. 2. Examples o types o changes in the appearance o the papillae are listed below. a. Bulbous papilla—a papilla that is enlarged and appears to bulge out o the interproximal space (Fig. 5-9). b. Blunted papilla—a papilla that is f at and does not ll the interproximal space (Fig. 5-10). c. Cratered papillae—a papilla that appears to have been “ scooped out” leaving a concave depression in the midproximal area. Cratered papillae are associated with necrotizing ulcerative gingivitis (Fig. 5-11).

Fig e 5-9. B lbo s Papillae . In gingivitis, the papillae may be enlarged and appear to bulge out o the interproximal space as seen in the papilla between the central and lateral incisors in this clinical photograph. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

Fig e 5-10. Bl te d Papillae . In gingivitis, the papillae may be blunted and missing as seen in the papillae between the central and lateral incisors. (Courtesy o Dr. Don Rol s, Wenachee, WA.)

Fig e 5-11. C ate e d Papillae . The papillae may have a concave appearance in the midproximal area as seen in the papillae between second premolar and molar in this clinical photo. (Courtesy o Dr. Don Rol s, Wenachee, WA.)

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Fig e 5-12. So t, Spo g Tiss e . In lamed gingival tissue may be so t and spongy. The in lammatory luids can cause the gingival tissues to eel somewhat like a moist sponge. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

Fig e 5-13. Smo o th, Shi Tiss e . In gingivitis, luid in the tissue can cause the tissue to appear smooth and shiny with a stretched appearance. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

2. Tissue Consistency and Texture in Gingivitis A. Tissue Consistency in Gingivitis 1. Increased f uid in the inf amed tissue also causes the gingiva to be so t, spongy, and nonelastic (Fig. 5-12). 2. When pressure is applied to the inf amed gingiva with the side o a probe, the tissue is easily compressed and can retain an imprint o the probe or several seconds. 3. Inf amed gingival tissue loses its rm consistency becoming f accid (so t, movable). When compressed air is directed into the sulcus, it readily def ects the gingival margin and papillae away rom the neck o the tooth. B. Sur ace Texture in Gingivitis 1. The increase in f uid due to the inf ammatory response can cause the gingival tissues to appear smooth and very shiny (Fig. 5-13). 2. The tissue almost has a “ stretched” appearance that resembles plastic wrap that has been pulled tightly. 3. Position o Margin in Gingivitis A. In gingivitis, the position o the gingival margin may move more coronally ( urther above the CEJ). B. This change in the position o the gingival margin is due to tissue swelling and enlargement (Fig. 5-14). 4. Presence o Bleeding in Gingivitis A. Bleeding upon gentle probing is seen clinically be ore changes in color are clinically detectable (Fig. 5-15). B. In gingivitis, the sulcus lining becomes ulcerated and the blood vessels become engorged. The tissues bleed easily during probing or instrumentation. C. There is a direct relationship between inf ammation and bleeding: The more severe the inf ammation, the heavier the bleeding.

Chapte 5

Clinical Features o the Gingiva

91

Gingivitis

Fig e 5-14. Tiss e Ma g i i Gi g ivitis. The tissue swelling in gingivitis may cause the position o the gingival margin to move coronally— urther above the CEJ—than in health. There is no destruction o periodontal ligament ibers or alveolar bone in gingivitis.

Fig e 5-15. Ble e di g o P o bi g . Bleeding is an important clinical indicator o in lammation. In lammation results in ulceration o the sulcus/pocket wall causing the gingival tissues to bleed easily during gentle probing.

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3

Exte t a d Dist ib tio

o I lammatio

In documenting inf ammation o the gingival tissues it is use ul to note both the extent and distribution o the inf ammation. Just documenting the presence o gingival inf ammation is too vague, and does not identi y severity o inf ammation accurately enough to help establish a treatment plan. 1. Gingival Inf ammation A. Extent o Inf ammation. The extent o inf ammation is the area o tissue that is a ected by inf ammation. The extent o inf ammation is described as localized or generalized in the mouth. 1. Localized inf ammation is con ned to the gingival tissue o a single tooth— such as the maxillary right rst molar—or to a group o teeth—such as the mandibular anterior sextant. 2. Generalized inf ammation involves all or most o the tissue in the mouth. B. Distribution o Inf ammation. The distribution o inf ammation describes the area where the gingival tissue is inf amed. 1. The inf ammation may a ect only the interdental papilla, the gingival margin and the papilla, or the gingival margin, papilla, and the attached gingiva. 2. Table 5-2 summarizes how to describe the extent and distribution o inf ammation o the gingival tissue. Figures 5-16 to 5-20 illustrate the use o this descriptive terminology.

TABLE 5 -2 . GIn GIVAL In FLAMMATIOn Exte t

• Lo calize d –-in fl m m

io n co n fin d o

• Ge e alize d –-in fl m m Dist ib tio

De sc iptio s

• Papilla

io n o f

issu o f

io n o f

in

• Ma g i al—in fl m m

io n o f

g in g iv l m

se —in fl m m io n o f

D sc i

iv

su c

s

oo

o

g ou

g in g iv l issu o f ll o m o s o f

—in fl m m

• Di

sin g l

d n

g in g iv l m

m s m y b co m b in d o c

l

mou

ill o n ly g in n d

g in ,

ill

ill , n d

v b l ic u

of

c

d g in g iv in fl m m

fo llo w in g :

• “ Lo c liz d m

g in l in fl m m

io n in

m n d ib u l

• “ Lo c liz d

ill y in fl m m

io n o n

m xill y ig

• “G n

liz d m

g in l in fl m m

• “G n

liz d d iffu s in fl m m

io n ” io n ”

of

n

io s x n ” c n in ”

io n ,

Chapte 5

Clinical Features o the Gingiva

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Fig e 5-16. Lo calize d Ma g i al I lammatio . Note the redness and swelling o the marginal and papillary gingival tissues that is localized to the mandibular anterior sextant. (Courtesy o Dr. Ralph Arnold.)

Fig e 5-17. Lo calize d Di se I lammatio . Redness and edema o the gingival margin, papillae, and attached gingiva in the mandibular anterior sextant. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

Fig e 5-18. Ge e alize d Di se I lammatio . Di use in lammation o the gingival margin, papillae, and attached gingiva throughout the entire mouth. (Courtesy o Dr. Ralph Arnold.)

Fig e 5-19. Lo calize d Ma g i al I lammatio . Note the reddened tissue color along the gingival margin, extending down into the papillae on these maxillary anterior teeth. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

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Fig e 5-20. Lo calize d Di se I lammatio . In lammation involving the gingival margin, papillae, and attached gingiva o the mandibular anterior sextant. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

Chapte S mma

State me t

Clinicians must have a clear mental image o gingival health to recognize the signs o gingival inf ammation when it occurs. Inf ammation in the gingiva causes changes in the color, contour, and consistency o the gingiva that can be recognized even in the earliest stages by the trained clinician.

Se ct io

4

Fo c s o

Patie ts

Cli ical Patie t Ca e CA S E 1 A patient new to your dental team has been appointed with you or a dental prophylaxis. The patient has just relocated to your town. The patient tells you that he saw a dentist just be ore moving who told him that he has gingivitis. During your discussion with the patient, he asks i there is some way he can tell at home i he has gingivitis. How might you reply to this patient’s question?

CA S E 2 Reading through your patient’s treatment notes rom the previous visit, you notice the clinician documented “ presence o gingival inf ammation.” Explain why this statement is not adequate in order to provide quality patient treatment. What would you add to the description to provide another clinician with a clear verbal description o the clinical eatures o the patient’s gingival tissues?

r e e e ce 1. H imani GS, Prabhuji M L, Karthikeyan BV. Gingival crevicular f uid and interleukin-23 concentration in systemically healthy subjects: their relationship in periodontal health and disease. J Periodontal R es. 2014;49(2):237–245.

STu DEn T An CILLAr y r ESOu r CES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

r e t p a h C

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Dis as s o t

Ging i a

S ctio n 1

Classif catio n o Ging i al Dis as s

96

S ctio n 2

D ntal Plaq

97

S ctio n 3

No n–Plaq

S ctio n 4

Fo c s o n Pati nts

–Ind c d Ging i al Dis as s -Ind c d Ging i al L sio ns

104 109

Clinical Patient Care Ethical Dilemma

Clinical Applicatio n.

Examination o the gingiva is part o every patient visit. The dynamic nature o the gingival tissue allows these tissues to show signs o disease in early stages. The dental hygienist o ten is the rst member o the dental team to be able to note these early signs o periodontal disease. This chapter outlines the numerous conditions that can a ect the gingiva and can serve as a oundation re erence or organizing knowledge about these conditions.

L a ning Obj cti

s

• De ne the two major subdivisions o gingival disease as established by the American Academy o Periodontology. • Compare and contrast dental plaque–induced gingival diseases and non–plaque-induced gingival lesions. • Describe the clinical signs o inf ammation you would expect to nd in a patient with moderate plaque-induced gingivitis. • List systemic actors that may modi y gingival disease. • Name three types o medications that may cause gingival enlargement. • Explain how the use o certain medications and malnutrition can modi y gingival disease. • Develop a list o suggestions or managing patients with primary herpetic gingivostomatitis.

K

T ms

Gingival diseases Dental plaque–induced gingival diseases Acute gingivitis Chronic gingivitis

Gingival diseases associated with modi ying actors Pregnancy-associated pyogenic granuloma Non–plaque-induced gingival lesions

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S ct io n 1

Classi icatio n o Ging i al Dis as s Gingival diseases usually involve in ammation o the gingival tissues, most o ten in response to bacterial plaque biof lm. Certain characteristics must be present or a periodontal disease to be classif ed as a gingival disease (Box 6-1). The 1999 AAP Classif cation o Periodontal Diseases and Conditions subdivides the major diagnostic category o gingivitis into specif c types o diseases: (1) dental plaque–induced gingival diseases and (2) non–plaque-induced gingival lesions. Each gingivitis disease type has two or more subcategories (Fig. 6-1).

Bo x 6-1. C a act istics Co mmo n to Ging i al Dis as s 1. Sig n s o sym o m s o in m m io n co n f n d o g in g iv . 2. No lo ss o c m n (n o d s u c io n o io d o n l lig m n f b s o lv o l b o n ) is sso ci d wi in m m io n o g in g iv l issu s. 3. t s n c o d n l l q u b io f lm in i i s n d /o g g v s in m m io n . 4. Clin ic l sig n s o in m m io n in clu d c n g s su c s n l g d g in g iv l co n o u s, co lo n si io n o d n d /o b lu is - d u , b l d in g u o n s im u l io n , in c s d c vicu l u id o w.

Gin g iv a l d is e a s e s

Plaque -induc e d g ing iva l dis e a s e s P la q u e -in d u c e d g in g ivitis

No n–plaque -induc e d g ing ival le s io ns Gin g iva l d is e a s e s o f s p e c ific b a c te ria l o rig in

On a p e riod ontium with no a tta c hme nt los s

Gin g iva l d is e a s e s o f vira l o rig in

On a re d u c e d b u t s ta b le p e rio d o n tiu m

Gin g iva l d is e a s e s o f fu n g a l o rig in

Gingiva l d is e a s e s mod ifie d b y s ys te mic fa c tors

Gin g iva l d is e a s e s o f g e n e tic o rig in

Gin g iva l d is e a s e s m o d ifie d b y m e d ic a tio ns

Gingiva l ma nife s ta tions of s ys te mic c ond itions

Gin g iva l d is e a s e s m o d ifie d b y m a ln utritio n

Tra um a tic le s io n s Fo re ig n b o d y re a c tio n s

Fig 6-1. T o Majo S bdi isio ns o Ging i al Dis as s. The two major subdivisions o gingival diseases are (1) dental plaque–induced gingival diseases and (2) non–plaque-induced gingival lesions. These two major subdivisions are urther subdivided into types.

C apt

S ct io n 2

D ntal Plaq

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Diseases o the Gingiva

97

–Ind c d Ging i al Dis as s

Dental plaque–induced gingival diseases are periodontal diseases involving in ammation o the gingiva in response to plaque biof lm. Ine ective plaque biof lm control triggers the body’s immune response. As long as bacteria remain in contact with the gingival tissue, in ammation continues. Certain species o bacteria that are elevated during times o gingival in ammation are listed in Table 6-1.

TABLe 6 -1 . BACTe r IA ASSOCIATe D w ITh h e ALTh AND GINGIv ITIS Bact ial Sp ci s Asso ciat d it h alt

Bact ial Sp ci s e l at d in Ging i itis

G am-Po siti

r o ds

A ct in o m yce s israe lii A ct in o m yce s n ae slu n d ii A ct in o m yce s o d o n t o lyt icu s Ro t h ia d e n t o cario sa A ct in o m yce s g e re n cse riae

A ct in o m yce s n ae slu n d ii III

G am-Po siti

Co cci

St re p t o co ccu s m it is St re p t o co ccu s o ralis Pe p t o st re p t o co ccu s m icro s St re p t o co ccu s san g u is St re p t o co ccu s g o rd o n ii

St re p t o co ccu s an g in o su s St re p t o co ccu s san g u is

Se le n o m o n as sp u t ig e n a Cap n o cyt o p h ag a g in g ivalis Pre vo t e lla in t e rm e d ia Fu so b act e riu m n u cle at u m

Cam p ylo b act e r co n cisu s Po rp h yro m o n as g in g ivalis

G am-N g ati

r o ds

G am-N g ati

Diplo co cci

Spi o c

t

Ne isse ria g o n o rrh o e ae Tre p o n e m a p allid u m

1. Gingivitis Associated with Dental Plaque Biof lm Only A. Characteristics 1. G ingivitis associated w ith plaque bio lm is by ar the most common type o periodontal disease. 2. The clinical signs o gingivitis may vary between individuals and also within the dentition o an individual. 3. Three separate stages o gingivitis mark the progression o disease: a. Initial lesion—develops within 4 days o plaque biof lm accumulation; sulcus heavily populated with gram-positive cocci. b. Early lesion—in ammation can be detected clinically a ter 7 days; gramnegative bacteria begin to ourish. c. Established lesion—bleeding upon probing; spirochetes and gram-negative rods are detected microscopically. 4. Incidence o gingivitis di ers between children and adults. a. In ammation is not as intense in children versus young adults with the same quantity o plaque biof lm (1–3). b. Adolescents may have elevated levels o certain bacteria: Actinomyces, Capnocytophaga, Leptotrichia, and Selenomonas species (4).

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c. Children may have ewer pathogenic bacteria in their plaque biof lm, a thicker junctional epithelium, and a less developed immune response (5,6). d. Gingival in ammation in senior adults is more pronounced even when similar amounts o plaque biof lms are present, perhaps attributed to agerelated di erences in cellular in ammatory response to plaque biof lm (7,8). 5. Local actors—such as dental restorations, appliances, root ractures, and tooth anatomy—act as a site or plaque biof lm retention and may contribute to the disease. B. Clinical Signs o Gingivitis Associated with Dental Plaque Only 1. Clinical signs o gingival in ammation include changes in gingival color, contour, and consistency. Common clinical signs include redness (erythema), swelling (edema), bleeding, and tenderness (Box 6-2, Figs. 6-2A, 2B). 2. The disease process begins at the gingival margin—the site o plaque biof lm accumulation—and is characterized clinically by red, swollen, tender gums that bleed easily. C. Duration o Gingivitis 1. Acute gingivitis—gingivitis o a short duration, a ter which pro essional care and patient sel -care returns the gingiva to a healthy state. 2. Chronic gingivitis—long-lasting gingivitis; gingivitis may exist or years without ever progressing to periodontitis.

Bo x 6-2. Ging i itis Asso ciat d

it D ntal Plaq

• Mo s co m m o n o m o io d o n l d is s s n g in g iv l • pl q u b io f lm m g in • Gin g iv l d n ss; n d n ss • In c s in su lcu l m u • Bl d in g u o n o b in g • S bl c m n l v ls • Co n d i io n v sib l w i l qu b io f lm m o v l

Onl

A

Fig 6-2A. Plaq -Ind c d Ging i itis. Plaque-induced gingivitis in this patient has resulted in rolled gingival margins and enlarged papillae.

Fig 6-2B. r adio g ap r als No Bo n Lo ss. The dental radiographs o an individual with plaque-induced gingivitis do not reveal any changes in either the alveolar bone height or the character o the alveolar bone.

B

C apt

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Diseases o the Gingiva

99

2. Plaque-Associated Gingival Diseases with Modi ying Factors. The category gingival diseases associated with modi ying actors includes the less common types o plaqueinduced gingivitis. There are three main subcategories o gingival diseases with modi ying actors: (1) gingival diseases modif ed by systemic actors, (2) gingival diseases modif ed by medications, and (3) gingival diseases modif ed by malnutrition. A. Gingival Diseases Modif ed by Systemic Factors. In this orm o gingival disease, plaque biof lm initiates the disease; then, specif c systemic actors ound in the host will modi y the disease process (9). 1. G ingival diseases associated w ith the endocrine system and f uctuations in sex horm ones. In this subcategory, changes in the endocrine system or levels o sex hormones result in an exaggerated response to the presence o plaque biof lm. Gingival tissues may appear bright red, so t, riable (easily damaged; thinly stretched), smooth, and exhibit bleeding rom slight provocation. a. Puberty-associated gingivitis is an exaggerated in ammatory response o the gingiva to a relatively small amount o plaque biof lm and hormones during puberty. 1. Although severity is directly related to the amount o plaque biof lm, gingivitis will mani est with a very small amount o plaque biof lm. 2. Puberty-associated gingivitis is ound in both male and emale adolescents. 3. Clinical eatures are in amed gingiva with prominent bulbous papillae on the acial aspect (Fig. 6-3). Bulbous papillae are rarely seen on the lingual gingival tissue. b. M enstrual cycle–associated gingivitis is an exaggerated in ammatory response o the gingiva to plaque biof lm and hormones estrogen and progesterone be ore ovulation. c. O ral contraceptive–associated gingivitis is an exaggerated in ammatory response o the gingiva to plaque biof lm and in patients taking oral contraceptives. 1. A recent study by Taichman and Eklund (10) ound no association between the use o oral contraceptives and increased gingival in ammation in young women. 2. Long-term use o oral contraceptives may a ect periodontal attachment levels. A study o 50 women aged 20 to 35 years, ound that current pill users had deeper mean probing depths compared to nonusers (3.3 vs. 2.7 mm) and more severe attachment loss (2.6 vs. 1.7 mm). Pill users had more sites with bleeding on probing (44.0% vs. 31.1% ) (11).

Fig 6-3. P b t -Asso ciat d Ging i itis. Pubertyassociated gingivitis is an exaggerated in lammatory response o the gingiva to a relatively small amount o plaque bio ilm. The exaggerated response is modulated by hormones released during puberty. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

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Fig 6-4. P g nanc -Asso ciat d Ging i itis. Note the red gingiva and bulbous interdental papilla on this patient with pregnancy-associated gingivitis. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

Fig 6-5. P g nanc -Asso ciat d P o g nic G an lo ma. This mushroom-like mass o the gingiva bleeds easily i disturbed.

d. Pregnancy-associated gingivitis is an exaggerated in ammatory response o the gingiva to plaque biof lm and hormone changes usually occurring during the second and third trimesters o pregnancy (12–15). During pregnancy, the levels o estrogen and progesterone continue to rise and reach their peak in the eighth month o gestation. H igh levels in both blood and saliva cause an exaggerated tissue response to plaque biof lm. Increased quantities o hormones also trigger gingival crevicular uid ow, which may precipitate gingival in ammation. 1. Pregnancy-associated gingivitis can mani est in response to even small amounts o plaque biof lm. 2. The gingival tissue may be edematous and dark red, with bulbous interdental papillae (Fig. 6-4). 3. Pregnancy-associated gingivitis can spontaneously resolve postpartum. 4. In some cases, a gingival papilla can react so strongly to plaque biof lm that a large, localized overgrowth o gingival tissue called a pregnancyassociated pyogenic granuloma (pregnancy tumor), may orm on the interdental gingiva or on the gingival margin.

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e. Pregnancy-associated pyogenic granulom a (“pregnancy tum or”) is a localized, mushroom-shaped gingival mass projecting rom the gingival margin or more commonly rom a gingival papilla during pregnancy. 1. This condition is the result o an exaggerated tissue response to plaque biof lm or other irritants that usually occurs a ter the f rst trimester o pregnancy. 2. The gingival mass is characterized by a mushroom-like tissue mass that most commonly occurs in the maxilla and interproximally (Fig. 6-5). 3. A pregnancy-associated pyogenic granuloma is painless and noncancerous. 4. The tissue mass bleeds easily i disturbed and may appear to be covered with dark red pinpoint markings. 5. The growth usually resolves a ter childbirth. . D iabetes-associated gingivitis is an in ammatory response o the gingiva to plaque biof lm that is aggravated by poorly controlled blood glucose levels (16–19). 1. This condition is o ten seen in children with poorly controlled type I diabetes mellitus. 2. Reduction in gingival in ammation in adults with diabetes may reduce the amount o insulin needed to control blood glucose levels. Diabetes mellitus is discussed in more detail in Chapter 15. 2. G ingival diseases associated w ith blood dyscrasias a. L eukem ia-associated gingivitis is an exaggerated in ammatory response o the gingiva to plaque biof lm resulting in increased bleeding and tissue enlargement. O ral lesions may be the f rst clinical signs o leukemia; there ore, dental healthcare providers can be the f rst to suspect that a patient may have leukemia. 1. Gingival tissues appear swollen, spongy, shiny, and red to deep purple in appearance (Fig. 6-6). 2. Tissues are very riable (tear easily) and have a tendency to hemorrhage with slight provocation. 3. The presence o plaque biof lm is N OT a prerequisite or gingivitis in patients with leukemia. 4. Typically, leukemia-associated gingivitis begins in the papillae and spreads to the marginal and then, the attached gingiva. b. Blood dyscrasias–associated gingivitis is gingivitis associated with abnormal unction or number o blood cells.

Fig 6-6. L k mia-Asso ciat d Ging i itis. Note the red, swollen appearance o the gingiva in this patient with leukemia. (Courtesy o Dr. Ralph Arnold.)

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3. Plaque-Associated Gingival Diseases Modif ed by Medications A. D rug-inf uenced gingivitis is an exaggerated in ammatory response o the gingiva to plaque biof lm and a systemic medication. B. D rug-inf uenced gingival enlargem ent is an increase in size o the gingiva resulting rom systemic medications, most commonly anticonvulsants, calcium channel blockers, and immunosuppressants. Plaque biof lm accumulation is not necessary or the initiation o gingival enlargement, but it will exacerbate the gingival disease. M eticulous plaque biof lm control can reduce but will not eliminate gingival overgrowth. 1. M edications Associated with Gingival Enlargement a. Anticonvulsants (e.g., phenytoin, Celontin, zerontin, Paganone, sodium valproate). Anticonvulsants are a diverse group o pharmaceuticals used in the treatment o epileptic seizures. In addition, anticonvulsants are now used in the treatment o bipolar disorder. b. Immunosuppressants (e.g., cyclosporine). Immunosuppressant drugs suppress the natural immune responses. Immunosuppressants are given to transplant patients to prevent organ rejection or to patients with autoimmune diseases. The immunosuppressant stimulates f broblast proli eration with excessive extracellular matrix accumulation in gingival tissues (20). c. Calcium Channel Blocking Agents (e.g., amlodipine, ni edipine, verapamil). Calcium channel blocking agents relax the blood vessels and increase the supply o blood and oxygen to the heart while reducing its workload. Some o the calcium channel blocking agents are used to relieve and control angina pectoris (chest pain). Some are also used to treat high blood pressure (hypertension). These drugs a ect gingival connective tissues by stimulating an increase o f broblasts and increasing the production o connective tissue matrix. 2. Clinical Appearance o Gingival Enlargement a. Tissue enlargement is an exaggerated in ammatory response in relation to the amount o plaque biof lm present. b. The onset o tissue enlargement usually occurs within 3 months o taking medication. c. The pattern o tissue enlargement is irregular, f rst observed in papillae. Begins as a painless area o enlargement on the papilla and then proceeds to the marginal gingiva. d. Gingiva in anterior sextants is most commonly a ected, however, can occur in posterior sextants (Figs. 6-7 and 6-8). e. The severity o overgrowth is directly a ected by level o sel -care; scrupulous homecare can reduce the severity o the overgrowth. . Gingival overgrowth appears more requently in the maxillary and mandibular anterior sextants. g. Gingival enlargement is characterized by an increased ow o crevicular uid rom the sulcus and bleeding upon probing with no attachment loss. h. Drug-in uenced gingival enlargement is more commonly seen in children. 4. Plaque-Associated Gingival Diseases Modif ed by Malnutrition. Even with our adequate ood supply in N orth America, in ants, institutionalized elderly, and alcoholics are all at risk or vitamin def ciencies. A. A scorbic acid–de ciency gingivitis is an in ammatory response o the gingiva to plaque biof lm aggravated by chronically low ascorbic acid (vitamin C) levels. Ascorbic acid–def ciency gingivitis mani ests as bright red, swollen, ulcerated gingival tissue that bleeds with the slightest provocation (Fig. 6-9) (21,22).

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B. Other. Specif c nutrient def ciencies can decrease the e f ciency o the immune system and exacerbate the response o the gingival tissues to plaque biof lm. In animal studies, a def ciency in vitamin A and B-complex vitamins has had an e ect on the gingival tissues. Vitamin A helps maintain healthy sulcular epithelium. B-complex vitamins help maintain healthy mucosal tissues.

Fig 6-7. P n to in-Ind c d Ging i al e nla g m nt. Massive tissue overgrowth may be seen in phenytoin-induced gingival enlargement.

Fig 6-8. C clo spo in -Ind c d Ging i al e nla g m nt. Gingival changes seen in cyclosporine-induced gingival enlargement.

Fig 6-9. Asco bic Acid–D ici nc Gingi itis. A photograph o a patient with scurvy. Scurvy is the clinical state arising rom dietary de iciency o vitamin C (ascorbic acid). Note the bright red, swollen, and ulcerated gingival tissue. (Courtesy o Mediscan Company.)

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A small percentage o gingival diseases—non–plaque-induced gingival lesions—are not caused by plaque biof lm and do not disappear a ter plaque biof lm removal. It should be emphasized, however, that the presence o plaque bio lm could increase the severity o the gingival inf ammation in noninduced lesions. N on–plaque-induced gingivitis can result rom such varied causes as bacterial, viral, or ungal in ections; genetic origin; dermatological (skin) diseases; allergic reactions; and mechanical trauma. • Specif c bacteria can in ect the gingival tissues and cause a orm o gingivitis (23). • Some types o gingivitis can be caused by an in ection with a specif c virus (24–27). Although rare in otherwise healthy individuals, gingival lesions can be caused by ungal in ections (24,28,29). • There are some gingival lesions that are not in ections at all, but rather have a genetic etiology (30). • There are a wide variety o gingival lesions that occur as mani estations o systemic conditions such as mucocutaneous disorders or allergic reactions (24,31). This section presents some examples o this small percentage o gingival disease in which plaque biof lm does not have an etiologic role. O the non–plaque-induced gingival lesions, the two most commonly seen in the dental o f ce are primary herpetic gingivostomatitis and allergic reactions. 1. Gingival Diseases o Specif c Bacterial Origin A. Def nition. Gingival diseases in this category are characterized by a bacterial in ection o the gingiva by a specif c bacterium that is not a common component o the bacterial plaque biof lm. B. Characteristics o Gingival Diseases o Specif c Bacterial Origin 1. Gingival diseases o specif c bacterial origin occur on rare occasions when a bacterial in ection overwhelms the host resistance. In these cases, the gingivitis is due to an in ection by a specif c bacterium that is usually not considered a periodontal pathogen. Examples include in ections with N eisseria gonorrhea, Treponem a pallidum , and streptococcal species (32–34). 2. The gingival lesions mani est as pain ul ulcerations, chancres or mucous patches, or atypical highly in amed gingivitis (Fig. 6-10). 3. Lesions may not be present elsewhere on the body.

Fig 6-10. At pical M co bact ial In ctio n. This patient has an atypical bacterial in ection o the gingiva. The ingers shown in this photograph are the patient’s own. (Courtesy o Mediscan Company.)

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2. Primary Herpetic Gingivostomatitis (PHG) is a severe reaction to the initial in ection with—f rst exposure o an individual to—the herpes simplex type-I virus (H SV-1). A. Disease Characteristics 1. By the time individuals reach middle age about 70% have been in ected with H SV-1. a. In most cases, the virus never causes symptoms during this primary H SV-1 in ection. This is known as a subclinical—symptom ree—in ection. b. In some individuals, however, this initial in ection presents with intensely pain ul gingivitis and multiple vesicles that easily rupture to orm pain ul ulcers. This severe reaction to the initial H SV-1 in ection is known as primary herpetic gingivostomatitis (Fig. 6-11). c. Once in ected, most individuals develop immunity to the virus. In certain individuals, the herpes simplex virus type-1 can remain latent in the trigeminal ganglion and is responsible or recurrent oral herpetic lesions (cold sores). 2. The initial in ection with the H SV-1 usually a ects young children—with heightened incidence rom 1 to 3 years o age—but may a ect adolescents and adults. a. O children with primary in ections, 99% are symptom ree or the symptoms are attributed to teething. b. The remaining 1% develops signif cant gingival in ammation and ulceration o the lips and mucous membranes (35). 3. The in ection is contagious during the vesicular stage as the virus is contained in the clear uid in the vesicles. The virus may be easily spread through close personal contact. 4. PH G is associated with severe pain that makes eating and drinking di f cult. 5. Associated symptoms o PH G are headache, swollen lymph nodes, and sore throat. Because this condition is a viral in ection, there may be a low-grade ever usually not above 101°F. 6. Regresses spontaneously within 10 to 20 days without scarring. B. Clinical Mani estations o PHG. PH G may occur anywhere on the ree or the attached gingiva or in the alveolar mucosa. 1. PH G is characterized by widespread in ammation o the marginal and attached gingiva. 2. The gingiva will demonstrate intense gingivitis and pain. 3. Small clusters o vesicles rapidly erupt throughout the mouth. 4. Later, these vesicles burst, orming yellowish ulcers that are surrounded by a red halo. Ulcers may occur on the lips, tongue, palate, and buccal mucosa (Fig. 6-12). 5. H eadache, ever, swollen lymph nodes, and sore throat usually are present.

Fig 6-11. P ima h p tic Ging i o sto matitis. This photograph shows an initial HSV-1 in ection in a young child. (Courtesy o Mediscan Company.)

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Fig 6-12. P ima h p tic Ging i o sto matitis. Primary herpetic gingivostomatitis is seen on the palate o this patient. Note the iery red gingival margins and ulcers surrounded by red halos.

C. Treatment or Primary Herpetic Gingivostomatitis 1. Encourage the intake o uids to prevent dehydration that can result rom ever. Athletic drinks, such as Gatorade , can be consumed to replenish electrolytes lost due to dehydration. 2. A dietary replacement drink, such as PediaSure or Ensure, can be a good source o nutrition since eating will be di f cult. The patient may be able to eat oods processed in a blender. 3. Counsel the patient that adequate intake o uids is important. Since eating and drinking are pain ul, dehydration is a major concern with these individuals. 4. An antimicrobial mouthwash like Listerine or Peridex should be recommended to prevent a secondary in ection. 5. Precautions should be taken to prevent the spread o the virus to the patient’s eyes or rom the in ected individual to other persons. The in ected patient should wash with soap and water requently. Wash toys that an in ected child puts in his or her mouth be ore and a ter play time. Do not let an in ected child share contaminated items, such as eating utensils with another person. 3. Linear Gingival Erythema (LGE) A. Disease Characteristics 1. LGE is a gingival mani estation o immunosuppression (36–38). 2. It is characterized by in ammation that is exaggerated or the amount o plaque biof lm present. 3. LGE does not respond well to improved oral sel -care or pro essional therapy. 4. For a diagnosis o LGE, the condition must persist a ter removal o plaque biof lms (39). B. Clinical Mani estations o LGE 1. LGE is characterized by a distinct red band that is limited to the ree gingiva (Fig. 6-13). 2. There is no evidence o attachment loss in LGE. 3. A key eature o LGE is a lack o bleeding on probing (40). 4. LGE is o ten associated with H IV in ection. 5. LGE usually does not respond well to therapy.

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Fig 6-13. Lin a Ging i al e t ma. This patient has linear gingival erythema associated with HIV in ection. Note the distinct red band along the ree gingiva.

Fig 6-14. O al Lic n Plan s. Oral lichen planus o the maxillary gingiva. The gingival tissues are erythematous, ulcerated, and pain ul. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

4. Lichen Planus A. Disease Characteristics 1. Lichen planus is a disease o the skin and mucous membranes in which there is an itchy, swollen rash on the skin or in the mouth. Both the skin and mucous membranes may be a ected; however, oral involvement or skin involvement alone is common. The exact cause o lichen planus is unknown. H owever, it is likely to be related to an allergic or immune reaction. 2. Lichen planus is the most common mucocutaneous disease a ecting the gingiva (41). 3. O ral lichen planus may a ect persons o any age although it is rarely seen in children (26). 4. An initial episode o oral lichen planus may last or weeks or months. Un ortunately, oral lichen planus is usually a chronic condition and can last or many years. 5. Good patient sel -care can relieve the pain ul symptoms o the gingival lesions (42). B. Clinical Mani estations 1. O ral mani estations include intense erythema o the gingiva (Fig. 6-14). 2. Ulcerations o the gingiva may be present and are associated with pain. 3. Interlacing white lines (Wickham striae) may be present on the buccal mucosa and gingiva. 4. Raised white lesions may be present as individual papules or in plaque-like conf gurations.

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Fig 6-15. e t ma M lti o m . Erythema multi orme with ulcerations o the gingiva and crust ormation o the lower lip. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

Fig 6-16. All g ic r actio n. Clinical signs o allergic reactions in the gingival tissues include redness extending rom the gingival margin to the mucogingival junction.

5. Erythema Multi orme A. Disease Characteristics 1. Erythema multi orme is a disorder o the skin and mucous membranes due to an allergic reaction or in ection. Large, symmetrical red blotches, resembling a target, appear all over the skin in a circular pattern. 2. O n mucous membranes, it begins as blisters and progresses to ulcers. O ral involvement occurs in as many as 25% to 60% o cases and is sometimes the only involved site (43,44). 3. The exact cause is unknown, though may involve a hypersensitivity reaction. B. Clinical Mani estations 1. O ral mani estations include swollen lips o ten with extensive crust ormation. 2. Lesions on the gingiva involve bullae that rupture and leave ulcers (Fig. 6-15). 6. Allergic Reactions. Allergic reactions can occur to ingredients in toothpastes, mouthwashes, or chewing gum (45). These reactions are usually the result o a avor additive or preservatives in the product. Flavor additives known to cause gingival reactions are cinnamon and carvone (45–47). A. Occurrence o Allergic Reactions 1. Allergic reactions occur most commonly in patients who have a history o allergic conditions such as hay ever, allergic skin rashes, or asthma. 2. Allergic patients seem to be particularly sensitive to the avoring agent. The most secret part o the ormulation o toothpastes and mouthwashes is the avoring agent, and this is usually the most allergenic component.

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B. Clinical Mani estations. The clinical mani estations o allergy are a di use f ery red gingivitis sometimes with ulcerations (Fig. 6-16). C. Recognition and Treatment o Allergic Reaction 1. The hygienist might suspect this problem in a patient with good sel -care who previously has had healthy gingiva (especially i the patient has a history o allergies). Inquire i the patient is using a new toothpaste or mouthwash or chewing gum. 2. Advise the patient to change brands or avors o gum, toothpaste, or mouthwash. Cessation o the allergen-containing product should result in a resolution o the gingivitis. 3. I necessary, the diagnosis o allergic response can be conf rmed by a biopsy with a diagnosis o plasma cell gingivitis. 4. When the manu acturer becomes aware o allergic reactions, the avoring agent or additive causing the problem is usually altered. For this reason, the patient sometimes can switch back to the original product (a ter 6 to 12 months) and use it without problem.

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Gingival diseases are the mildest orm o periodontal disease. Plaque-induced gingivitis is the most common o the periodontal diseases. Clinically, plaque-induced gingivitis is characterized by gingiva that is red, swollen, bleeds easily, and is slightly tender. Plaqueinduced gingivitis may be modif ed by systemic actors, medications, or malnutrition. N on–plaque-induced gingival lesions are a group o uncommon gingival lesions that are not caused by plaque biof lm. N on–plaque-induced gingivitis can result rom such diverse causes as in ection, skin diseases, allergic reactions, or trauma.

S ct io n 4

Fo c s o n Pati nts Clinical Pati nt Ca CA S e

1

You are scheduled to do a dental prophylaxis on a patient with a diagnosis o localized severe plaque-induced gingivitis. At the time o the appointment the patient in orms you that she has just received notice that lab results indicate that she is pregnant. H ow might this pregnancy alter the periodontal diagnosis?

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2

A patient who has been cared or by your dental team suddenly exhibits poor sel -care with quite a bit o plaque biof lm accumulation. This is unusual or this patient. Discussions reveal that the patient is having di f culty with brushing and ossing due to soreness o the mouth. Examination reveals numerous small mucosal ulcers. Further discussions reveal that the patient has been experiencing this soreness since she began using tartar control toothpaste. H ow might your dental team manage this patient’s diminished e ectiveness o sel -care?

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Your patient is a 12-year-old male, who in spite o good oral hygiene practices, presents with generalized marginal redness and bleeding upon probing. H is demonstration o tooth brushing and ossing indicates high dexterity and ability to remove plaque biof lm and in talking with his mother, she conf rms that he practices daily oral hygiene. H ow would you explain the presence o gingival disease to this patient and what would you recommend to improve his gingival health?

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Your patient reports a change in his medical history rom last visit; he is now taking Depakote as a mood stabilizer. The PDR states it is an anticonvulsant and may cause gingival enlargement. H ow will this new in ormation alter your plan or dental hygiene care and patient education?

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During the oral exam, you see a localized area o marginal redness and edema on the disto acial o the mandibular right f rst molar. While exploring in that area, there is a restoration with an overhanging margin. H ow does the overhang contribute to the presence o gingival in ammation, how can it be treated, and what will happen i the overhang remains?

e t ical Dil mma Lily E, a 17-year-old high school senior, who is a routine 6-month recall patient, is your f rst patient o the a ternoon. She received her driver’s license 3 months ago, and has driven hersel to today’s appointment. You review her medical history, and she states there are “ no changes,” and she has no “ chie complaint.” As you are per orming your intraoral examination, you notice that the tissue between the maxillary central incisors does not appear to be normal. You observe a mushroom-shaped gingival mass, projecting rom the gingival papilla. It appears red, and bleeds easily upon digital palpation. You ask Lily i it bothers her, and she denies any discom ort. She also states that she was not aware o any problem. You are concerned that the lesion may be a pyogenic granuloma associated with pregnancy. You would like to discuss the possible implication o this lesion with Lily, but you are not sure how to proceed. 1. What is the best way or you to handle this ethical dilemma? 2. What is the best way to address/discuss Lily’s treatment plan with her? 3. Under the ethical principle o conf dentiality, can you discuss this with your employer dentist, without violating Lily’s conf dentiality? 4. Do you have the right to divulge your f ndings and concerns to her parents? 5. Can a 17-year-old consent to treatment, or must you receive parental consent?

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1. American Academy o Periodontology-Research, Science and therapy Committee. Periodontal diseases o children and adolescents. Pediatr D ent. 2008;30(7 suppl):240–247. 2. H amadneh N , Khan WA, Sathasivam S, et al. Design optimization o pin f n geometry using particle swarm optimization algorithm. PloS O ne. 2013;8(5):e66080. 3. M atsson L, Goldberg P. Gingival in ammatory reaction in children at di erent ages. J Clin Periodontol. 1985;12(2):98–103. 4. Yang N Y, Z hang Q, Li JL, et al. Progression o periodontal in ammation in adolescents is associated with increased number o Porphyromonas gingivalis, Prevotella intermedia, Tannerella or sythensis, and Fusobacterium nucleatum. Int J Paediatr D ent. 2014;24(3):226–233. 5. Bimstein E, M atsson L. Growth and development considerations in the diagnosis o gingivitis and periodontitis in children. Pediatr D ent. 1999;21(3):186–191. 6. Ga an GP, Lucas VS, Roberts GJ, et al. Prevalence o periodontal pathogens in dental plaque o children. J Clin M icrobiol. 2004;42(9):4141–4146. 7. Fransson C, Berglundh T, Lindhe J. The e ect o age on the development o gingivitis. Clinical, microbiological and histological f ndings. J Clin Periodontol. 1996;23(4):379–385. 8. Fransson C, M ooney J, Kinane DF, et al. Di erences in the in ammatory response in young and old human subjects during the course o experimental gingivitis. J Clin Periodontol. 1999;26(7):453–460. 9. Trombelli L, Farina R. A review o actors in uencing the incidence and severity o plaque-induced gingivitis. M inerva Stom atol. 2013;62(6):207–234. 10. Taichman LS, Eklund SA. O ral contraceptives and periodontal diseases: rethinking the association based upon analysis o N ational H ealth and N utrition Examination Survey data. J Periodontol. 2005;76(8):1374–1385. 11. M ullally BH , Coulter WA, H utchinson JD, et al. Current oral contraceptive status and periodontitis in young adults. J Periodontol. 2007;78(6):1031–1036. 12. Armitage GC. Bi-directional relationship between pregnancy and periodontal disease. Periodontol 2000. 2013;61(1): 160–176. 13. Gursoy M , Gursoy UK, Sorsa T, et al. H igh salivary estrogen and risk o developing pregnancy gingivitis. J Periodontol. 2013;84(9):1281–1289. 14. M arkou E, Eleana B, Lazaros T, et al. The in uence o sex steroid hormones on gingiva o women. O pen D ent J. 2009;3: 114–119. 15. Xie Y, Xiong X, Elkind-H irsch KE, et al. Change o periodontal disease status during and a ter pregnancy. J Periodontol. 2013;84(6):725–731. 16. Botero JE, Yepes FL, Roldan N , et al. Tooth and periodontal clinical attachment loss are associated with hyperglycemia in patients with diabetes. J Periodontol. 2012;83(10):1245–1250. 17. Chang PC, Chien LY, Yeo JF, et al. Progression o periodontal destruction and the roles o advanced glycation end products in experimental diabetes. J Periodontol. 2013;84(3):379–388. 18. Chapple IL, Genco R, working group 2 o the joint EFP/AAP workshop. Diabetes and periodontal diseases: consensus report o the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Periodontol. 2013;84(4 suppl): S106–S112. 19. M ealey BL, O ates TW. Diabetes mellitus and periodontal diseases. J Periodontol. 2006;77(8):1289–1303. 20. Lin YT, Yang FT. Gingival enlargement in children administered cyclosporine a ter liver transplantation. J Periodontol. 2010;81(9):1250–1255. 21. Bacci C, Sivolella S, Pellegrini J, et al. A rare case o scurvy in an otherwise healthy child: diagnosis through oral signs. Pediatr D ent. 2010;32(7):536–538. 22. Chapman JM , M arley JJ. Scurvy and the ageing population. Br D ent J. 2011;211(12):583–584. 23. Siegel M A. Syphilis and gonorrhea. D ent Clin N orth A m . 1996;40(2):369–383. 24. H olmstrup P. N on-plaque-induced gingival lesions. A nn Periodontol. 1999;4(1):20–31. 25. M iller CS, Redding SW. Diagnosis and management o oro acial herpes simplex virus in ections. D ent Clin N orth A m . 1992;36(4):879–895. 26. Scully C, de Almeida O P, Welbury R. O ral lichen planus in childhood. Br J D erm atol. 1994;130(1):131–133. 27. Scully C, Epstein J, Porter S, et al. Viruses and chronic disorders involving the human oral mucosa. O ral Surg O ral M ed O ral Pathol. 1991;72(5):537–544. 28. Loh FC, Yeo JF, Tan WC, et al. H istoplasmosis presenting as hyperplastic gingival lesion. J O ral Pathol M ed. 1989;18(9): 533–536. 29. M achado FC, de Souza IP, Portela M B, et al. Use o chlorhexidine gel (0.2% ) to control gingivitis and candida species colonization in human immunodef ciency virus-in ected children: a pilot study. Pediatr D ent. 2011;33(2):153–157. 30. H art TC, Z hang Y, Gorry M C, et al. A mutation in the SO S1 gene causes hereditary gingival f bromatosis type 1. A m J H um G enet. 2002;70(4):943–954. 31. Cohen DM , Bhattacharyya I. Cinnamon-induced oral erythema multi ormelike sensitivity reaction. J A m D ent A ssoc. 2000;131(7):929–934. 32. Littner M M , Dayan D, Ka e I, et al. Acute streptococcal gingivostomatitis. Report o f ve cases and review o the literature. O ral Surg O ral M ed O ral Pathol. 1982;53(2):144–147. 33. Ramirez-Amador V, M adero JG, Pedraza LE, et al. O ral secondary syphilis in a patient with human immunodef ciency virus in ection. O ral Surg O ral M ed O ral Pathol O ral R adiol Endod. 1996;81(6):652–654. 34. Rivera-H idalgo F, Stan ord TW. O ral mucosal lesions caused by in ective microorganisms. I. Viruses and bacteria. Periodontol 2000. 1999;21:106–124. 35. King DL, Steinhauer W, Garcia-Godoy F, et al. H erpetic gingivostomatitis and teething di f culty in in ants. Pediatr D ent. 1992;14(2):82–85. 36. Lugo RI, Fornatora M L, Reich RF, et al. Linear gingival erythema in an H IV-seropositive man. A ID S R ead. 1999;9(2):97–99. 37. Thaler R, O jha J, Bhola M . O ral pathology quiz #19. Linear gingival erythema. J M ich D ent A ssoc. 2009;91(4):44, 46–47. 38. Velegraki A, N icolatou O, Theodoridou M , et al. Paediatric AIDS–related linear gingival erythema: a orm o erythematous candidiasis? J O ral Pathol M ed. 1999;28(4):178–182.

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39. Umadevi M , Adeyemi O, Patel M , et al. (B2) Periodontal diseases and other bacterial in ections. A dv D ent R es. 2006;19(1):139–145. 40. Robinson PG, Winkler JR, Palmer G, et al. The diagnosis o periodontal conditions associated with H IV in ection. J Periodontol. 1994;65(3):236–243. 41. Camacho-Alonso F, Lopez-Jornet P, Bermejo-Fenoll A. Gingival involvement o oral lichen planus. J Periodontol. 2007;78(4):640–644. 42. Salgado DS, Jeremias F, Capela M V, et al. Plaque control improves the pain ul symptoms o oral lichen planus gingival lesions. A short-term study. J O ral Pathol M ed. 2013;42(10):728–732. 43. Barrett AW, Scully CM , Eveson JW. Erythema multi orme involving gingiva. J Periodontol. 1993;64(9):910–913. 44. H u JC, Weston WL, Tonnesen M G. Erythema multi orme: a critical review o characteristics, diagnostic criteria, and causes. J A m A cad D erm atol. 1983;8(6):763–775. 45. Skaare A, Kjaerheim V, Barkvoll P, et al. Skin reactions and irritation potential o our commercial toothpastes. A cta O dontol Scand. 1997;55(2):133–136. 46. Calapai G, M iroddi M , M annucci C, et al. O ral adverse reactions due to cinnamon- avoured chewing gums consumption. O ral D is. 2013;20(7):637–643. 47. Drake TE, M aibach H I. Allergic contact dermatitis and stomatitis caused by a cinnamic aldehyde- avored toothpaste. A rch D erm atol. 1976;112(2):202–203.

STu De NT ANCILLAr y r e SOu r Ce S A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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General Characteristics o Chronic Periodontitis Severity, Extent, and Progression o Chronic Periodontitis Recurrent and Re ractory Forms o Chronic Periodontitis

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cal Appl cat o .

Chronic periodontitis is the most requently encountered orm o periodontitis. All dental hygienists will participate in helping to diagnose this disease and in providing care designed to bring this rather common disease under control. An understanding o the eatures o behavior o chronic periodontitis is absolutely essential or every member o the dental team.

Le ar

g Obje ct ve s

• In a clinical setting or a patient with chronic periodontitis, describe to your clinical instructor the clinical signs o disease present in the patient’s mouth. • Def ne the term clinical attachment loss and explain its signif cance in the periodontal disease process. • In the clinical setting, explain to your patient the warning signs o chronic periodontal disease. • Recognize and describe clinical and radiographic eatures o chronic periodontitis. • Contrast the extent o periodontal destruction typically seen in localized chronic periodontitis with that o generalized chronic periodontitis. • Describe the change or advancement—disease progression—typically seen in chronic periodontitis. • According to the AAP 1999 classif cation system, def ne the meaning o the descriptors recurrent chronic periodontitis and refractory chronic periodontitis.

Ke Te rms Periodontitis Chronic periodontitis Clinical attachment loss Peri-implantitis Extent Localized chronic periodontitis

Generalized chronic periodontitis Disease progression Site-speci ic Severity Slight (mild) periodontitis

Moderate periodontitis Severe periodontitis Recurrent disease Re ractory disease Re ractory chronic periodontitis

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Periodontitis is b cteri l in ection th t ects ll p rts o the periodontiu including the gingiv , periodont l lig ent, bone, nd ce entu . It is the result o co plex inter ction between the pl que bio l th t ccu ul tes on tooth sur ces nd the body’s e orts to ght this in ection. Periodontitis is the nu ber one c use o tooth loss in dults. There re lso so e individu ls who re genetic lly predisposed to developing periodontitis. Chronic periodontitis is co plex in ection resulting in inf tion within the supporting tissues o the teeth, progressive destruction o the periodont l lig ent, nd loss o supporting lveol r bone (1,2). Chronic periodontitis begins s pl que-induced gingivitis. Pl que-induced gingivitis is reversible condition th t i le t untre ted y develop into chronic periodontitis (3–10). Chronic periodontitis involves irreversible loss o attachment and bone and is the most requently occurring orm o periodontitis.

Ge n e r a l Ch a r a Ct e r is t iCs o f Ch r o n iC Pe r io d o n t it is 1. Alternative Terminology. Chronic periodontitis w s previously known s dult periodontitis. The n e dult periodontitis, however, is isle ding s this type o periodontitis c n occur in individu ls o ny ge: children, dolescents, nd dults. 2. Signs and Symptoms o Chronic Periodontitis. Signs nd sy pto s o chronic periodontitis include swelling, redness, gingiv l bleeding, periodont l pockets, bone loss, tooth obility, suppur tion (pus), oder te or he vy deposits o pl que bio l s, nd dent l c lculus (2). A. Alterations in Color, Texture, and Size o the Marginal Gingiva 1. Red or Purplish Tissue. In chronic periodontitis, the gingiv l tissue y ppe r bright red or purplish. a. In such c ses, the clinic l signs o chronic periodontitis re very evident t the initi l ex in tion o the or l c vity. The gingiv ppe rs swollen with the color r nging ro p le red to gent . Alter tions in contour nd or re evident such s rolled gingiv l rgins, blunted or f ttened p pill e. b. An ex ple o chronic periodontitis exhibiting this type o ppe r nce is shown in Box 7-1, Figure 7-1A,B,C. 2. P le Pink Tissue. In chronic periodontitis, the gingiv l tissue y be p le pink nd h ve n l ost nor l-looking ppe r nce. a. The clinical appearance o the tissues is not a reliable indicator o the presence or severity o chronic periodontitis (Figs. 7-2–7-4). b. In ny p tients, the ch nges in color, contour, nd consistency y not be visible on inspection. At rst gl nce, n inexperienced clinici n y ist ke the clinic l ppe r nce o chronic periodontitis or one o he lth. Closer ex in tion will reve l r , rigid ( brotic) tissue, the presence o pocketing, nd bleeding upon probing. Chronic periodontitis exhibiting this type o ppe r nce is shown in Figure 7-2. B. Bleeding, Crevicular Fluid, and Exudate 1. Gingiv l bleeding is co on, either spont neous bleeding or bleeding in response to probing. 2. Incre sed f ow o gingiv l crevicul r f uid or suppur tion (pus) ro periodont l pockets is co on.

Chapte r 7

Chronic Periodontitis

C. Plaque Bio lm and Calculus Deposits 1. Chronic periodontitis is ch r cterized by ture supr - nd subgingiv l pl que bio l s nd c lculus deposits. Teeth with chronic periodontitis usu lly h ve very co plex nd thick deposits o pl que bio l on ected root sur ces (11). 2. Although chronic periodontitis is initi ted nd sust ined by pl que bio l s, host ctors deter ine the p thogenesis nd r te o progression o the dise se (12–17). D. Loss o Attachment 1. Clinical attachment loss is n esti te o the extent th t the tooth-supporting structures h ve been destroyed round tooth. Loss o tt ch ent occurs in periodontitis nd is ch r cterized by (1) reloc tion o the junction l epitheliu to the tooth root (2), destruction o the bers o the gingiv (3), destruction o the periodont l lig ent bers (4), nd loss o lveol r bone support round the tooth (Figs. 7-5 nd 7-6). The ch nges th t occur in the lveol r bone in periodont l dise se re signi c nt bec use loss o bone height eventu lly c n result in tooth loss. 2. Clinic l tt ch ent loss o 1 to 2 t one or sever l sites c n be ound in ne rly ll e bers o the dult popul tion. 3. Clinic l ch r cteristics o tt ch ent loss y include the ollowing: a. Loss o lveol r bone support to the teeth b. Periodont l pockets or recession o the gingiv l rgin c. Furc tion involve ent in ultirooted teeth (Fig. 7-6) d. Tooth obility nd/or dri ting 4. It h s been est blished th t the extent o probe penetr tion is inf uenced by the inf tory st tus o the periodont l tissues (Fig. 7-7) (18–32). E. Localized or Generalized Inf ammation. In chronic periodontitis, there is no consistent p ttern to the nu ber nd types o teeth involved (2,33). 1. Loc lized inf tion y involve one site on single tooth, sever l sites on tooth, or sever l teeth. Gener lized inf tion y involve the entire dentition. 2. A p tient y si ult neously h ve re s o he lth nd re s with chronic periodontitis with tissue destruction. 3. Chronic periodontitis is cl ssi ed s loc lized when less th n 30% o sites re ected nd gener lized when gre ter th n 30% o sites re ected. F. Contributing Factors 1. Chronic periodontitis y be odi ed by nd/or ssoci ted with loc l ctors. It c n be odi ed by other ctors, especi lly cig rette s oking. 2. Individu ls ected by chronic periodontitis h ve no known edic l or gener l he lth consider tions th t ight contribute to the develop ent o their periodontitis (2). According to the 1999 cl ssi c tion syste , i n individu l h s syste ic dise se th t c n pro oundly odi y the initi tion nd clinic l course o periodont l in ections, the resulting periodontitis is cl ssi ed s “ periodontitis s ni est tion o syste ic dise se” (34). G. Symptoms 1. Chronic periodontitis usu lly is p inless. There ore, n individu l with chronic periodontitis y be tot lly un w re o the dise se, not seek tre t ent, nd be unlikely to ccept tre t ent reco end tions. 2. Individu ls y rst beco e w re th t so ething is wrong when they notice th t their gu s bleed when brushing; th t sp ces occur between the teeth; or th t teeth h ve beco e loose. 3. P tients y co pl in o ood i p ction, sensitivity to hot or cold due to exposed roots, or dull p in r di ting into the j w.

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H. Chronic Periodontitis in Dental Implant Tissues. Peri-implantitis is the ter or chronic periodontitis in the tissues surrounding dent l i pl nt. Peri-i pl ntitis is discussed in ore det il in Ch pter 31. 3. Onset and Progression o Chronic Periodontitis A. Gingivitis as a Risk Factor or Chronic Periodontitis 1. Pl que-induced gingivitis precedes the onset o chronic periodontitis. Pl queinduced gingivitis y re in st ble or ny ye rs nd never progress to beco e periodontitis. 2. B cteri l pl que bio l s will induce gingivitis, but the host susceptibility nd other contributing ctors deter ine whether or not chronic periodontitis will develop. 3. Gingivitis ni ests ter only d ys or weeks o pl que bio l ccu ul tion. In ost c ses, chronic periodontitis requires longer periods (ye rs) o pl que bio l nd c lculus exposure to develop (2,20,35). 4. Findings ro epide iologic studies nd clinic l tri ls indic te th t the presence o gingivitis y be reg rded s risk ctor or chronic periodontitis (36,37). B. Age o Onset. The onset o chronic periodontitis y be t ny ge (2). It is ost co only detected in dults older th n ge 35 but c n occur in children nd dolescents. The prev lence nd severity o chronic periodontitis incre ses with ge. C. Rate o Disease Progression. The r te o dise se progression is considered n i port nt ch r cteristic by which chronic nd ggressive or s o periodontitis c n be clinic lly distinguished (2). In ost c ses, chronic periodontitis progresses in slow to oder te p ce (2,33). D. Patient Education: The Warning Signs o Chronic Periodontitis 1. The w rning signs o periodontitis re red or swollen gingiv , bleeding during brushing, b d t ste in the outh, persistent b d bre th, sensitive teeth, loose teeth, nd pus round teeth nd gingiv (Figs. 7-8 to 7-13). 2. P in usu lly is not sy pto o periodontitis. This bsence o p in y expl in why periodontitis is o ten dv nced be ore the p tient seeks tre t ent nd why p tient y void tre t ent even ter receiving di gnosis o periodontitis. 3. Tools such s or l he lth sel -ev lu tions distributed t he lth irs or other events c n be help ul in incre sing the public’s w reness o the signs nd sy pto s o periodont l dise se.

Chapte r 7

Bo x 7-1. Chro

Chronic Periodontitis

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c Pe r o do t t s

A

B

F g re 7-1A. H g hl V s ble Cha g e s the G g va. Chronic periodontitis may exhibit many clinically visible signs, such as changes in the contour o the tissue.

F g re 7-1B. M mal V s ble Cha g e s G g va. In this example o chronic periodontitis, there are minimal visible tissue changes. Since periodontitis is a disease a ecting the deeper tissues o the periodontium, the appearance o the sur ace tissue o ten is not a reliable indicator o disease severity.

Characte r st cs o f Chro c Pe r o do t t s • Mo st co m m o n ly se e n in a d u lt s o ve r 35 ye a rs o f a g e b u t ca n o ccu r in ch ild re n a n d a d o le sce n t s • In it ia t e d a n d co n t in u e d b y p la q u e b io lm s b u t h o st re sp o n se p la ys a n e sse n t ia l ro le in d ise a se p ro g re ssio n • Occu rs in in d ivid u a ls w it h n o kn o w n m e d ica l o r g e n e ra l h e a lt h co n sid e ra t io n s t h a t m ig h t co n t rib u t e t o t h e d e ve lo p m e n t o f p e rio d o n t it is • Sig n s a n d sym p t o m s o f in a m m a t io n in clu d e sw e llin g , re d n e ss, g in g iva l b le e d in g , p e rio d o n t a l p o cke t s, b o n e lo ss, t o o t h m o b ilit y, su p p u ra t io n (p u s), m o d e ra t e o r h e a vy d e p o sit s o f p la q u e b io lm s, a n d d e n t a l ca lcu lu s • Bo n e lo ss m a y b e e vid e n t o n ra d io g ra p h s • Un t re a t e d ch ro n ic p e rio d o n t it is p ro g re sse s slo w ly o ve r t im e • At t a ch m e n t lo ss m a y o ccu r in o n e a re a o f a t o o t h ’s a t t a ch m e n t , o n se ve ra l t e e t h , o r t h e e n t ire d e n t it io n • It ca n b e m o d i e d b y o t h e r fa ct o rs, e sp e cia lly cig a re t t e sm o kin g

C

F g re 7-1C. Rad o g raph c Ev de ce o f Chro c Pe r o do t t s. Dental radiographs o patients with chronic periodontitis usually reveal horizontal patterns o alveolar bone loss.

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B

F g re 7-2. He alth o r D se ase ? A: The clinical appearance o the tissue in this photograph suggests health. B: When assessed with a probe, however, a deep 7-mm pocket reveals bone loss on the mesio acial o the canine. This example underscores the importance o a thorough periodontal assessment. (Courtesy o Dr. Don Rol s, Wenachee, WA.)

F g re 7-3. He alth o r D se ase ? This individual received periodontal treatment or chronic periodontitis several years ago. The assessment at today’s appointment reveals meticulous patient sel -care and no additional attachment loss since beginning periodontal maintenance several years ago. There ore, this tissue is considered healthy. The attachment loss is simply an indicator o previous disease. (Courtesy o Dr. Ralph Arnold.)

A

B

F g re 7-4. Chro c Pe r o do t t s. Two examples, A and B, o chronic periodontitis showing irm, nodular ( ibrotic) tissue changes.

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P e riod onta l p oc ke t Conne c tive tis s ue d e s truc tion J unc tiona l e p ithe lium Bone los s

P e riod ontitis

F g re 7-5. Cl cal Cha g e s Chro c Pe r o do t t s. Chronic periodontitis is characterized by in lammation within the supporting tissues o the teeth, progressive destruction o the periodontal ligament, and loss o supporting alveolar bone.

A

B

F g re 7-6. Attachme t Lo ss. A: Assessment with a periodontal probe indicates severe loss o attachment on this molar tooth. B: The gingival tissue is li ted away rom the molar during periodontal surgery to reveal the severe loss o alveolar bone and connective tissue attachment. (Courtesy o Dr. Ralph Arnold.)

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P rob e

A

P rob e

P rob e

B

C

F g re 7-7. D ag rammat c Re pre se tat o o f Pro be T p Pe e trat o Re lat ve to the Pe r o do tal T ss e s. It has been established that the extent o probe penetration is in luenced by the in lammatory status o the periodontal tissues (18–32). A: In a normal sulcus, the probe penetrates about one-third o the length o the junctional epithelium. B: With moderate in lammation within the tissues, the probe tip penetrates approximately hal the length o the junctional epithelium. C: Severe in lammation within the tissues, the probe tip penetrates through the length o the junctional epithelium, and only stops when it encounters the collagen ibers o the gingival connective tissue.

F g re 7-8. Chro c Pe r o do t t s. Chronic periodontitis showing pronounced changes in the appearance o the gingiva.

F g re 7-9. Chro c Pe r o do t t s. Palatal gingiva in a patient with chronic periodontitis. Note the calculus deposits on the tooth sur aces and the rolled gingival margins. Clinical signs on the lingual aspect usually are not as evident as those seen on the acial aspect o the gingiva.

Chapte r 7

Chronic Periodontitis

F g re 7-10. Chro c Pe r o do t t s. Chronic periodontitis showing blunting o the interdental papillae and recession o the gingival margin.

F g re 7-11. Chro c Pe r o do t t s. Heavy accumulation o bacterial plaque bio ilms in an individual with chronic periodontitis. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

F g re 7-12. Chro c Pe r o do t t s. Chronic periodontitis case with periodontal probe inserted in a pocket showing attachment loss.

F g re 7-13. Chro c Pe r o do t t s. Chronic periodontitis showing pronounced changes in the appearance o the gingiva. (Courtesy o Dr. Ralph Arnold.)

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s e v e r it y , e x t e n t , a n d Pr o Gr e s s io n o f Ch r o n iC Pe r io d o n t it is 1. Extent o Destruction in Chronic Periodontitis A. Overview. Extent is the degree or ount o periodont l destruction nd c n be ch r cterized b sed on the nu ber o sites th t h ve experienced tissue destruction. 1. Loc lized inf tion y involve one site on single tooth, sever l sites on tooth, or sever l teeth. A p tient y si ult neously h ve re s o he lth nd re s with chronic periodontitis with tissue destruction. 2. Gener lized inf tion y involve the entire dentition. B. Localized or Generalized Extent 1. Localized chronic periodontitis is chronic periodontitis in which 30% or less o the sites in the outh h ve experienced tt ch ent loss nd bone loss. 2. Generalized chronic periodontitis is chronic periodontitis in which ore th n 30% o the sites in the outh h ve experienced tt ch ent loss nd bone loss. 2. Disease Progression A. Overview. Disease progression re ers to the ch nge or dv nce ent o periodont l destruction. For ex ple, how does the ount o tt ch ent loss nd bone destruction seen tod y co p re with th t seen sever l onths go? Is it the s e, so ewh t worse, or uch worse? B. Progression o Chronic Periodontitis. In ost c ses, untre ted chronic periodontitis progresses in slow to oder te p ce. 1. The current view is th t the progression o untre ted chronic periodontitis in ost individu ls nd t ost dise se sites is continuous slow process but th t periods o ex cerb tion occ sion lly y occur. 2. Tissue destruction in untre ted chronic periodontitis does not ect ll teeth evenly but r ther is site-speci c dise se. Th t is, in the s e dentition so e teeth y h ve severe tissue destruction while other teeth re l ost ree o signs o tt ch ent nd bone loss. a. So e dise se sites y re in unch nged or long periods o ti e (35,38,39). b. O ther dise se sites y progress ore r pidly. M ore r pidly progressing dise se sites occur ost requently in interproxi l re s, nd y be ssoci ted with re s o gre ter pl que bio l ccu ul tion nd in ccessibility to pl que bio l control e sures (e.g., sites o lposed teeth, restor tions with overh nging rgins, re s o ood i p ction, deep periodont l pockets, urc tion re s) (40). 3. The desired outco e o periodont l ther py or chronic periodontitis is to stop the progression o the dise se to prevent urther tt ch ent loss. Figures 7-14 to 7-16 show the clinic l e tures be ore nd ter tre t ent or three di erent p tients. 4. The nu ber o sites o tt ch ent loss, bone loss, nd/or deep pockets is good predictor o uture dise se occurrence in n individu l p tient. The best predictor o dise se progression is n individu l’s previous dise se experience. 3. Disease Severity A. Overview. The severity, or seriousness, o the tissue destruction is deter ined by the r te o dise se progression over ti e nd the response o the tissues to tre t ent. B. Tissue Destruction. Dise se severity y be described s slight ( ild), oder te, or severe. These ter s y be used to describe the dise se severity o the entire dentition, p rt o the outh (sext nt or qu dr nt), or the dise se st tus o single tooth. 1. Slight (mild) periodontitis—no ore th n 1 to 2 o clinic l tt ch ent loss. 2. Moderate periodontitis—3 to 4 o clinic l tt ch ent loss h s occurred. 3. Severe periodontitis—5 or ore o clinic l tt ch ent loss h s occurred.

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A

Chronic Periodontitis

123

B

F g re 7-14. Chro c Pe r o do t t s: Be fo re a d Afte r Pe r o do tal The rap . A: Note the tissue changes be ore periodontal therapy. Clinical changes are particularly pronounced on the lower anterior sextant. B: The same individual a ter treatment. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

A

B

F g re 7-15. Chro c Pe r o do t t s: Be fo re a d Afte r Pe r o do tal The rap . A: Very pronounced tissue changes are evident prior to therapy. B: Much improved clinical picture at 3-month ollow-up appointment. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

A

B

F g re 7-16. Chro c Pe r o do t t s: Be fo re a d Afte r Pe r o do tal The rap . A: Very swollen gingival tissues pretreatment. B: The same individual a ter treatment. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

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r e Cu r r e n t a n d r e f r a Ct o r y f o r m s o f Ch r o n iC Pe r io d o n t it is 1. Recurrent disease—new signs nd sy pto s o destructive periodontitis th t re ppe r ter periodont l ther py bec use the dise se w s not dequ tely tre ted nd/or the p tient did not pr ctice dequ te sel -c re. 2. Re ractory disease—periodontitis in p tient who h s been onitored over ti e nd who continues to exhibit ddition l tt ch ent loss in spite o the ollowing conditions: ( ) The p tient h s received ppropri te nd continuous pro ession l periodont l ther py, (b) the p tient pr ctices s tis ctory sel -c re, nd (c) the p tient ollows the reco ended progr o periodont l inten nce visits (Box 7-2, Fig. 7-17 A,B,C). A. Under the 1989 cl ssi c tion syste , “ re r ctory periodontitis” w s sep r te dise se c tegory. It is now believed th t re r ctory periodontitis is not single dise se entity, but r ther th t s ll percent ge o ll or s o periodontitis y not respond to tre t ent. B. In the new 1999 classif cation system, the designation “re ractory” can be applied to all types o periodontal diseases that do not respond to treatment. C ses o chronic periodontitis th t do not respond to periodont l ther py re design ted s re ractory chronic periodontitis.

Bo x 7-2. Re fracto r Chro

c Pe r o do t t s

Ad d it io n a l a t t a ch m e n t lo ss in a p a t ie n t d e sp it e a ll o f t h e fo llo w in g : • Ap p ro p ria t e p e rio d o n t a l t h e ra p y • A p a t ie n t w h o p ra ct ice s sa t isfa ct o ry se lf-ca re • An a p p ro p ria t e p ro g ra m o f p e rio d o n t a l m a in t e n a n ce visit s

A

B

C

F g re 7-17. A–C: Re fracto r Chro c Pe r o do t t s. Chronic periodontitis is considered re ractory when the disease is not controlled by the conventional periodontal therapy normally recommended or patients with chronic periodontitis. In a re ractory case, the patient experiences additional attachment loss despite appropriate periodontal therapy and satis actory sel -care. The dental radiographs o a patient with re ractory periodontitis reveal co n t in u in g e vid e n ce o f b o n e lo ss o ve r t im e d e sp it e ap p ro p riat e t h e rap y.

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Chapte r S mmar State me t Chronic periodontitis is b cteri l in ection resulting in inf tion within the supporting tissues o the teeth, progressive destruction o the periodont l lig ent, nd loss o supporting lveol r bone. • Chronic periodontitis involves irreversible loss o tt ch ent nd bone nd is the ost requently occurring or o periodontitis. • Chronic periodontitis y involve one re o tooth’s tt ch ent, sever l teeth, or the entire dentition. A p tient c n si ult neously h ve re s o he lth nd re s with periodontitis. • Untre ted chronic periodontitis usu lly is ch r cterized by slow to oder te r tes o dise se progression nd vor ble response to periodont l ther py. • The desired outco e o periodont l ther py or chronic periodontitis is to stop the progression o the dise se to prevent urther tt ch ent loss.

Se ct o

2

Fo c s o Cl

Pat e ts

cal Pat e t Care CA S E 1 A new p tient h s di gnosis o severe gener lized chronic periodontitis. The p tient tells you th t it is h rd or hi to believe he h s serious periodont l proble s since he h s never h d ny disco ort nd h s never even noticed ny dent l proble s. H ow could you respond to this p tient’s co ents?

CA S E 2 A p tient who h s recently oved to your city h s n ppoint ent with you reg rding sel -c re instructions. The periodont l di gnosis is severe chronic periodontitis. In your discussion with the p tient you le rn th t the p tient is upset bec use she h s been tre ted or periodontitis twice during the p st dec de in other dent l o ces. She is upset bec use now pp rently she needs periodont l tre t ent g in, nd she st tes she is con used bout how this ight be possible. H ow could you respond to this p tient’s concerns?

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Eth cal D le mma Your next p tient, Josi h S, h s recently reloc ted to your town, pproxi tely 6 onths go, nd is new p tient in your pr ctice. H e is 45-ye r-old divorced le, who d its to s oking pproxi tely 15 cig rettes per d y, nd drinks nightly lcoholic cockt il. H e works in s les, nd due to his hectic tr vel schedule, tells you th t he h s h d to c ncel his l st ew dent l hygiene ppoint ents. Your intr or l ex reve ls th t Josi h presents with oder te c lculus nd pl que bio l . H is gingiv l tissues ppe r red nd swollen, h ve blunted p pill e, nd bleed re dily upon p lp tion. You t ke ull outh series o r diogr phs th t show gener lized horizont l bone loss throughout his outh. You begin to probe his outh, to deter ine his pocket re dings when he sits up in the dent l ch ir nd de nds th t you stop. H e st tes th t he h s lw ys re used periodont l probing, s he just “ c n’t st nd the p in” nd the l st dent l o ce bided by his wishes. H e re uses to let you continue “ poking round his gu s” nd sks th t you just proceed to cle ning his teeth, so he c n be on ti e or his 11:00 a m business ppoint ent. 1. 2. 3. 4. 5.

H ow would you cl ssi y Josi h’s periodont l condition? Wh t ethic l principles re in conf ict in this dile ? Do you h ve n ethic l oblig tion to tre t this p tient? Wh t is the best w y to ddress/discuss Josi h’s tre t ent pl n with hi ? Wh t, i ny ltern tives, c n you o er Josi h in ter s o his tre t ent pl n?

Re fe re ce s 1. Ar it ge GC. Cl ssi ying periodont l dise ses– long-st nding dile . Periodontol 2000. 2002;30:9–23. 2. Ar it ge GC. Co p rison o the icrobiologic l e tures o chronic nd ggressive periodontitis. Periodontol 2000. 2010;53:70–88. 3. Loe H , Theil de E, Jensen SB. Experi ent l gingivitis in n. J Periodontol. 1965;36:177–187. 4. Loesche WJ, Syed SA. B cteriology o hu n experi ent l gingivitis: e ect o pl que nd gingivitis score. Infect Im m un. 1978;21(3):830–839. 5. M oore LV, M oore WE, C to EP, et l. B cteriology o hu n gingivitis. J D ent R es. 1987;66(5):989–995. 6. M oore WE, H olde n LV, S ibert RM , et l. B cteriology o experi ent l gingivitis in young dult hu ns. Infect Im m un. 1982;38(2):651–667. 7. Sey our GJ, Powell RN , Aitken JF. Experi ent l gingivitis in hu ns. A clinic l nd histologic investig tion. J Periodontol. 1983;54(9):522–528. 8. Sey our GJ, Powell RN , Cole KL, et l. Experi ent l gingivitis in hu ns. A histoche ic l nd i unologic l ch r cteriz tion o the ly phoid cell subpopul tions. J Periodontal R es. 1983;18(4):375–385. 9. Theil de E, Wright WH , Jensen SB, et l. Experi ent l gingivitis in n. II. A longitudin l clinic l nd b cteriologic l investig tion. J Periodontal R es. 1966;1:1–13. 10. v n der Velden U, Abb s F, H rt AA. Experi ent l gingivitis in rel tion to susceptibility to periodont l dise se. (I.) Clinic l observ tions. J Clin Periodontol. 1985;12(1):61–68. 11. Listg rten M A. Structure o the icrobi l f or ssoci ted with periodont l he lth nd dise se in n. A light nd electron icroscopic study. J Periodontol. 1976;47(1):1–18. 12. H jee AD, Teles RP, Socr nsky SS. The e ect o periodont l ther py on the co position o the subgingiv l icrobiot . Periodontol 2000. 2006;42:219–258. 13. Ledder RG, Gilbert P, H uws SA, et l. M olecul r n lysis o the subgingiv l icrobiot in he lth nd dise se. A ppl Environ M icrobiol. 2007;73(2):516–523. 14. P ster BJ, Boches SK, G lvin JL, et l. B cteri l diversity in hu n subgingiv l pl que. J Bacteriol. 2001;183(12):3770–3783. 15. Socr nsky SS, H jee AD. Dent l bio l s: di cult ther peutic t rgets. Periodontol 2000. 2002;28:12–55. 16. Socr nsky SS, H jee AD, Teles R, et l. E ect o periodont l ther py on the subgingiv l icrobiot over 2-ye r onitoring period. I. O ver ll e ect nd kinetics o ch nge. J Clin Periodontol. 2013;40(8):771–780. 17. W erh ug J. Subgingiv l pl que nd loss o tt ch ent in periodontosis s ev lu ted on extr cted teeth. J Periodontol. 1977;48(3):125–130. 18. Anderson GB, C esse RG, N sjleti CE, et l. Correl tion o periodont l probe penetr tion nd degree o inf tion. A m J D ent. 1991;4(4):177–183. 19. Ar it ge GC. Periodont l dise ses: di gnosis. A nn Periodontol. 1996;1(1):37–215.

Chapte r 7

Chronic Periodontitis

20. C rr nz FA, N ew n M G, T kei H H , et l. Carranza’s Clinical Periodontology. 10th ed. St. Louis, M O : S unders Elsevier; 2006; xxxvi:1286. 21. C ton J, Greenstein G, Polson AM . Depth o periodont l probe penetr tion rel ted to clinic l nd histologic signs o gingiv l inf tion. J Periodontol. 1981;52(10):626–629. 22. Fowler C, G rrett S, Crigger M , et l. H istologic probe position in tre ted nd untre ted hu n periodont l tissues. J Clin Periodontol. 1982;9(5):373–385. 23. H ncock EB, Wirthlin M R. The loc tion o the periodont l probe tip in he lth nd dise se. J Periodontol. 1981;52(3): 124–129. 24. H e ti AF. Periodont l probing. Crit R ev O ral Biol M ed. 1997;8(3):336–356. 25. Kh n S, C b nill LL. Periodont l probing depth e sure ent: review. Com pend Contin Educ D ent. 2009;30(1):12–14, 16, 18–21; quiz 22, 36. 26. Lindhe J, L ng N P, K rring T. Clinical Periodontology and Im plant D entistry. 5th ed. O x ord; A es, Iow : Bl ckwell M unksg rd; 2008. 27. Listg rten M A, M o R, Robinson PJ. Periodont l probing nd the rel tionship o the probe tip to periodont l tissues. J Periodontol. 1976;47(9):511–513. 28. M gnusson I, Listg rten M A. H istologic l ev lu tion o probing depth ollowing periodont l tre t ent. J Clin Periodontol. 1980;7(1):26–31. 29. M ori rty JD, H utchens LH Jr, Scheitler LE. H istologic l ev lu tion o periodont l probe penetr tion in untre ted ci l ol r urc tions. J Clin Periodontol. 1989;16(1):21–26. 30. Robinson PJ, Vitek RM . The rel tionship between gingiv l inf tion nd resist nce to probe penetr tion. J Periodontal R es. 1979;14(3):239–243. 31. Spr y JR, G rnick JJ, Doles LR, et l. M icroscopic de onstr tion o the position o periodont l probes. J Periodontol. 1978;49(3):148–152. 32. Tessier JF, Ellen RP, Birek P, et l. Rel tionship between periodont l probing velocity nd gingiv l inf tion in hu n subjects. J Clin Periodontol. 1993;20(1):41–48. 33. Lindhe J, H jee AD, Socr nsky SS. Progression o periodont l dise se in dult subjects in the bsence o periodont l ther py. J Clin Periodontol. 1983;10(4):433–442. 34. Ar it ge GC. Develop ent o cl ssi c tion syste or periodont l dise ses nd conditions. A nn Periodontol. 1999;4(1):1–6. 35. Ar it ge GC. Le rned nd unle rned concepts in periodont l di gnostics: 50-ye r perspective. Periodontol 2000. 2013;62(1):20–36. 36. Sch tzle M , Loe H , L ng N P, et l. The clinic l course o chronic periodontitis. J Clin Periodontol. 2004;31(12):1122–1127. 37. Sud R, C o C, H seg w K, et l. 2-ye r observ tion o tt ch ent loss in rur l Chinese popul tion. J Periodontol. 2000;71(7):1067–1072. 38. Ar it ge GC, Cullin n M P. Co p rison o the clinic l e tures o chronic nd ggressive periodontitis. Periodontol 2000. 2010;53:12–27. 39. Lindhe J, O k oto H , Yoney T, et l. Longitudin l ch nges in periodont l dise se in untre ted subjects. J Clin Periodontol. 1989;16(10):662–670. 40. Lindhe J, O k oto H , Yoney T, et l. Periodont l loser sites in untre ted dult subjects. J Clin Periodontol. 1989;16(10):671–678.

STu DEn T An CiLLARy RESOu RCES A wide v riety o resources to enh nce your le rning nd underst nding o this ch pter re v il ble on . • Visit thePoint to ccess: • Audio Gloss ry • Ani tions • Suggested Re dings • Answers to Review Q uestions • C se Studies

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General Characteristics of Aggressive Periodontitis Localized and Generalized Aggressive Periodontitis Screening for Aggressive Periodontitis

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Clinical Patient Care Ethical Dilemma

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Aggressive periodontitis can destroy a dentition in a relatively short time frame. All members of the dental team must remain on continuous alert for this highly destructive condition since delay in its diagnosis can prove disastrous for a patient. Familiarity with the characteristics of both localized and generalized aggressive periodontitis is a valuable tool to help insure that members of the dental team make a timely diagnosis of this condition.

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• Compare and contrast the clinical and radiographic features of chronic periodontitis and aggressive periodontitis. • In the clinical setting, explain to your patient the signs and symptoms of aggressive periodontal disease. • In a clinical setting for a patient with aggressive periodontitis, describe to your clinical instructor the primary clinical signs of disease present in the patient’s mouth. • Compare and contrast the clinical and radiographic features of localized aggressive periodontitis and generalized periodontitis. • Given the clinical and radiographic features for a patient with a history of aggressive periodontitis, determine if the disease is localized or generalized aggressive periodontitis.

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Aggressive periodontitis (AgP) Episodic disease progression

Localized aggressive periodontitis (LAP) Generalized aggressive periodontitis (GAP)

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Aggressive Periodontitis

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Periodontitis is a bacterial in ection that may have many di erent clinical presentations. This chapter discusses aggressive periodontitis. Aggressive periodontitis (AgP) is a complex bacterial in ection characterized by a rapid destruction o the periodontal ligament, rapid loss o supporting bone, high risk or tooth loss, and a poor response to periodontal therapy in an otherwise healthy individual. Fortunately, aggressive periodontitis is less common than chronic periodontitis. Drs. Armitage and Cullinan (1) identi ed a number o signi cant clinical di erences between chronic periodontitis and aggressive periodontitis including (a) age o onset o disease, (b) clinical signs o inf ammation, (c) amount o plaque bio lm and calculus present, and (d) rates o progression (Table 8-1).

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Ge n e r a l Ch a r a Ct e r is t iCs o f a GGr e s s iv e Pe r io d o n t it is 1. Alternative Terminology. Until recently, aggressive periodontitis was de ned as occurring in individuals under the age o 30 years and was known as early-onset periodontitis (EO P). Features o aggressive periodontitis can present at any age and is not con ned to individuals under the arbitrarily chosen age o 30 years. 2. Characteristics A. Primary Features. The primary eatures o aggressive periodontitis are the ollowing (1–5): 1. Rapid destruction o the attachment and rapid loss o supporting bone. Baer estimated that the loss o attachment in aggressive periodontitis patients progressed three or our times aster than in cases o chronic periodontitis (1,6–10). 2. N o obvious signs or symptoms o systemic disease

ssio n

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3. O ther amily members (parents, siblings) with aggressive periodontitis B. Secondary Features. Secondary eatures that are generally but not always present are 1. Relatively small amounts o bacterial plaque bio lm; the disease severity seems to be exaggerated given the light amount o plaque bio lm 2. Elevated proportions o A ggregatibacter actinomycetem com itans (A a) 3. Phagocyte abnormalities 4. Elevated production o prostaglandin E2 (PGE2) and interleukin-1β (IL-1β) in response to bacterial endotoxins 5. A lack o clinical signs o disease a. A ected tissue may have a normal clinical appearance b. Probing reveals deep periodontal pockets on a ected teeth 6. A poor response to periodontal therapy 7. Episodic disease progression (Fig. 8-1) a. Chronic periodontitis is a very slowly progressing disease. b. In aggressive periodontitis, attachment loss is episodic, occurring in a succession o acute destructive phases with intermittent inactive phases.

F u 8-1. e p so d c D s as P o ss o U t at d A ss P o do t t s. Aggressive periodontitis progresses in a series of acute phases of tissue destruction followed by periods of disease inactivity.

l o Ca l iz e d a n d Ge n e r a l iz e d a GGr e s s iv e Pe r io d o n t it is 1. Localized Aggressive Periodontitis (LAP) A. Features of Localized Aggressive Periodontitis (Box 8-1, Figs. 8-2A, 2B, 2C) 1. O nset o localized aggressive periodontitis is around the time o puberty. 2. Localized attachment loss a ecting the rst molars and/or incisors and involving no more than two teeth other than rst molars and incisors (1,6–10) 3. There is a lack o tissue inf ammation and minimal amounts o plaque bio lm that seem inconsistent with the amount o periodontal destruction (1,11). Most patients with LAP exhibit some clinical inf ammation at a ected sites, such as slight redness and swelling o the gingival margin and bleeding upon gentle probing (1). 4. Frequently associated with A a (A . actinomycetem com itans) 5. Vertical bone loss around the rst molars and incisors, beginning around puberty is a classic radiographic sign o LAP. B. Alternative Terminology. LAP was previously known as localized juvenile periodontitis (LJP).

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o do t t s (LAP)

• On s ound im o u b y • Min im l sig n s o in m m io n c m n lo ss in vo lvin g • Lo c liz d f s m o l s n d in ciso s • t in , u n im ssiv b io f lm o n c d d wi Aa • F q u n ly sso ci • p vio u sly c ll d lo c liz d ju v n il io d o n i is

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ss P o do t t s. F u 8-2A. Lo cal z d A The photograph shows a patient with LAP. Note that there are not any supragingival calculus deposits evident.

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F u 8-2b-C. r ad o aph c Cha act st cs o Lo cal z d A ss P o do t t s. Patients with LAP have bone loss on the f irst m o lar an d in ciso r t e e t h . The radiographs shown here reveal a pattern of bone loss on the first molars that is similar on both sides of the mandibular arch.

2. Generalized Aggressive Periodontitis (GAP) A. Features of Generalized Aggressive Periodontitis (Box 8-2, Figs. 8-2A, 2B, 2C) 1. Generalized aggressive periodontitis usually occurs in persons younger than 30 years o age, but patients may be older (1,12). 2. Generalized interproximal attachment loss a ecting at least three permanent teeth other than the rst molars and incisors. In most cases o generalized aggressive periodontitis, most permanent teeth are a ected (1,9,13). 3. Destruction o attachment and alveolar bone is very episodic, occurring in a succession o acute phases rather than in a gradual progression.

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4. Small amounts o bacterial plaque bio lm that seem inconsistent with the amount o periodontal destruction. 5. The appearance o the gingival tissues varies in GAP. a. The gingival tissues may be acutely inf amed, ulcerated, and ery red (1). This tissue response is believed to occur in the destructive phase o disease progression. b. The gingival tissues may appear pink and ree o inf ammation. Deep pockets can be detected, however, with periodontal probing. This tissue response may coincide with periods o disease inactivity (14). B. Alternative Terminology. GAP was previously known as generalized juvenile periodontitis (GJP) or early-onset periodontitis (G-EO P). 3. Clinical Appearance of Aggressive Periodontitis. Figures 8-4 to 8-7 illustrate the clinical appearance o patients with a diagnosis o aggressive periodontitis.

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• Dis s o n s u su lly o ccu s in so n s u n d 30 y s o g , bu i n sm y b o ld • G n liz d in o xim l c m n lo ss c in g l s m n n o n f s mol s nd in ciso s • a sso ci d w i A a • F m ily is o y o Ga p (1,15) • p vio u sly kn o w n s g n liz d ju v n il io d o n i is A

F u 8-3A. g al z d A ss P o do t t s. The rate of attachment loss and bone loss is rapid in GAP compared to chronic periodontitis.

B

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F u 8-3b-C. r ad o aph c Cha act st cs o g al z d A ss patients with GAP reveal severe alveolar bone loss aro u n d m o st t e e t h .

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Aggressive Periodontitis

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F u 8-4. Ch ld th A ss P o do t t s. Aggressive periodontitis in a 5-year-old child with attachment loss on all teeth.

F u 8-5. A ss P o do t t s. Aggressive periodontitis in a patient with good self-care (plaque biofilm control). In aggressive periodontitis, the disease severity typically seems exaggerated given the amount of bacterial plaque biofilm.

F u 8-6. A ss P o do t t s. An example of aggressive periodontitis with continued disease progression despite good daily self-care by the patient. (Courtesy of Dr. John S. Dozier)

F u 8-7. A ss P o do t t s. Aggressive periodontitis in a 30-year-old male with good daily self-care.

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s Cr e e n in G f o r a GGr e s s iv e Pe r io d o n t it is A small but signi cant proportion o children and young adults are thought to be a ected by aggressive periodontitis. A survey o U.S. adolescents aged 14 to 17 reports that 0.13% had aggressive periodontitis (1,12). Early detection is important given the severity and progression o aggressive periodontitis. 1. Screening of Adolescents and Adults A. Periodontal probing is the most accurate screening method or detecting attachment loss currently available. The measurement o attachment by probing is the screening method o choice or adolescents and adults. B. I aggressive periodontitis is suspected, the patient’s medical history should be updated and reviewed to rule out possible systemic contributing actors. Periodontitis as a mani estation o systemic disease is the disease category used when the systemic condition is the major predisposing actor or periodontitis. 2. Screening of Primary and Mixed Dentitions A. The measurement o attachment loss on primary teeth or partially erupted teeth may be di cult. B. M easurement o the distance between the CEJ and the alveolar bone crest on bitewing radiographs is a use ul screening approach with children (Fig. 8-8). Bitewing radiographs routinely are taken on children or caries screening and these radiographs also should be screened or the presence o marginal alveolar bone loss. C. The “ normal” distance between the CEJ and the alveolar bone crest has been evaluated by recent investigations (11,16). 1. The median distances between the CEJ and the alveolar crest o primary molars in 7- to 9-year-old children is 0.8 to 1.4 mm. The CEJ o permanent molars is 0 to 0.5 mm coronal to the alveolar crest in 7- to 9-year-olds. 2. Greater distances between the CEJ and the alveolar crest are seen at sites with caries, restorations, or open contacts. These local conditions may contribute to localized bone loss in children in a similar manner to that seen in adults and are not indicative o aggressive periodontitis. 3. A distance o 2 mm between the CEJ and the alveolar crest, in the absence o local contributing actors, should cause the clinician to suspect periodontitis. I the measurement exceeds this value, periodontitis should be suspected and a comprehensive periodontal examination should be per ormed.

CEJ to alveolar cres t

F u 8-8. Us o b t r ad o aphs Sc o LAP Ch ld . The distance from the CEJ and the alveolar bone crest is measured from a line connecting the CEJs of the two adjacent teeth. Measurements are taken for each mesial and distal surface. Normal CEJ to alveolar bone crest distances for 7- to 9-year-olds are less than 2 mm.

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Aggressive Periodontitis

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Periodontitis is a bacterial in ection o all parts o the periodontium that results in irreversible destruction o the periodontal ligament bers and alveolar bone. Periodontitis is a bacterial in ection that may have many di erent clinical presentations. The 1999 AAP Classi cation o Periodontal Diseases and Conditions reclassi ed the orms o periodontitis into chronic periodontitis, aggressive periodontitis, and less common types o periodontal diseases. Aggressive periodontitis is a bacterial in ection characterized by a rapid destruction o the periodontal ligament, rapid loss o supporting bone, high risk or tooth loss, and a poor response to periodontal therapy. Features o aggressive periodontitis can present at any age. The primary eatures o aggressive periodontitis are (1) rapid destruction o the attachment and rapid loss o supporting bone, (2) no obvious signs or symptoms o systemic disease, and (3) other amily members (parents, siblings) with aggressive periodontitis.

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While reading a journal article you nd a re erence to a periodontal disease called localized juvenile periodontitis (LJP). Since this is not a disease category in the currently accepted disease classi cation system, how does this terminology relate to modern periodontal diagnoses?

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Your small private dental practice, which is within an urban city, has many long-standing patients. A number o patients within the practice are on public assistance and struggle with money issues. Dr. Gordon is very generous and understanding about her patients’ limitations and o ten provides ree dental services. Your next patient o the morning is Jason S, a 14-year-old junior high school soccer player. H is mother has made an emergency appointment, as he was hit in the mouth during a soccer game yesterday. H is mother is concerned that Jason’s ront teeth may be loose as a result. H is mother reports that Jason had a thorough “ cleaning” in another dental o ce 4 months ago. Clinical examination reveals no trauma but some mobility, so you take radiographs. Clinically, Jason presents with no obvious signs or symptoms o disease, with lack o tissue inf ammation and minimal amounts o plaque bio lm. Jason’s radiographs, however, show moderate vertical bone loss around the maxillary central incisors and mandibular central incisors. Bitewing radiographs also indicate moderate bone loss around the maxillary and mandibular rst molars. Probe readings on his incisors and molars are in the 4 to 6 mm range. continued on nex t page

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You present your ndings to Dr. Gordon, who asks you to per orm thorough periodontal instrumentation on Jason. You remind Dr. Gordon, that Jason had a dental hygiene appointment in another o ce 4 months ago and that his insurance only allows or periodontal instrumentation every 6 months. Dr. Gordon states that Jason is in dire need o this treatment and asks you to instruct the o ce manager to hold o on submitting Jason’s insurance claim until it is within the 6-month time rame. 1. 2. 3. 4.

r

H ow would you classi y Jason’s periodontal condition? What ethical principles are in conf ict in this dilemma? What is the best way or you to handle this ethical dilemma? What should you do when treating uture patients?

c s

1. Armitage GC, Cullinan M P. Comparison o the clinical eatures o chronic and aggressive periodontitis. Periodontol 2000. 2010;53:12–27. 2. American Academy o Periodontology. A nnals of Periodontology. Chicago, IL: American Academy o Periodontology; 1996:v. 3. Armitage GC. Periodontal diseases: diagnosis. A nn Periodontol. 1996;1(1):37–215. 4. Lang N P, Bartold PM , Cullinam M , et al. International classi cation workshop. Consensus report: Aggressive periodontitis. In: Lang N P, Bartold PM , Cullinam M , eds. A nnals of periodontology. Chicago, IL: American Academy o Periodontology; 1999;4:53. 5. Armitage GC, Cullinan M P, Seymour GJ. Comparative biology o chronic and aggressive periodontitis: introduction. Periodontol 2000. 2010;53:7–11. 6. Baer PN . The case or periodontosis as a clinical entity. J Periodontol. 1971;42(8):516–520. 7. M anson JD, Lehner T. Clinical eatures o juvenile periodontitis (periodontosis). J Periodontol. 1974;45(8):636–640. 8. Liljenberg B, Lindhe J. Juvenile periodontitis. Some microbiological, histopathological and clinical characteristics. J Clin Periodontol. 1980;7(1):48–61. 9. Burmeister JA, Best AM , Palcanis KG, et al. Localized juvenile periodontitis and generalized severe periodontitis: clinical ndings. J Clin Periodontol. 1984;11(3):181–192. 10. Saxen L, M urtomaa H . Age-related expression o juvenile periodontitis. J Clin Periodontol. 1985;12(1):21–26. 11. N eedleman H L, Ku TC, N elson L, et al. Alveolar bone height o primary and rst permanent molars in healthy seven- to nine-year-old children. A SD C J D ent Child. 1997;64(3):188–196, 65. 12. Loe H , Brown LJ. Early onset periodontitis in the United States o America. J Periodontol. 1991;62(10):608–616. 13. Armitage GC. Development o a classi cation system or periodontal diseases and conditions. A nn Periodontol. 1999; 4(1):1–6. 14. Page RC, Baab DA. A new look at the etiology and pathogenesis o early-onset periodontitis. Cementopathia revisited. J Periodontol. 1985;56(12):748–751. 15. Gri ths GS, Ayob R, Guerrero A, et al. Amoxicillin and metronidazole as an adjunctive treatment in generalized aggressive periodontitis at initial therapy or re-treatment: a randomized controlled clinical trial. J Clin Periodontol. 2011;38(1):43–49. 16. Sjodin B, M atsson L. M arginal bone level in the normal primary dentition. J Clin Periodontol. 1992;19(9 Pt 1):672–678.

STUDe n T An CiLLAr y r e SOUr Ce S A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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Othe Pe io do ntal Co nditio ns Pe io do ntitis as a Mani e statio n o S ste mic Dise ase

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Ne c o tizing Pe io do ntal Dise ase s

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De ve lo pme ntal o Ac ui e d De o mitie s and Co nditio ns

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Tooth-Related Factors Mucogingival De ormities and Conditions Around Teeth Occlusal Trauma in Patients with Periodontitis

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Clinical Applicatio n.

This chapter outlines the interesting array o conditions that can a ect the periodontium in addition to the common varieties o periodontal diseases. Familiarity with these other conditions is critical or all clinicians, since ailure to recognize them may have a pro ound impact on the well-being o some patients. The importance o study o these conditions by the student and experienced clinician cannot be overrated.

Le a ning Obje ctive s • Name and explain systemic or genetic actors that may contribute to the initiation and progression o periodontitis. • Describe the impact o PMN (neutrophil) dys unction and hematologic disorders on the periodontium. • Describe clinical signs o periodontitis that may be associated with HIV in ection. • Describe the tissue destruction that occurs in necrotizing periodontal diseases. • Compare and contrast the clinical f ndings o necrotizing ulcerative gingivitis and necrotizing ulcerative periodontitis. • Compare and contrast the tissue destruction in chronic periodontitis with that seen in necrotizing ulcerative periodontitis. • Name several local actors, such as tooth-related or mucogingival de ormities, that may contribute to the initiation and progression o periodontitis. • Def ne secondary occlusal trauma and explain how it can lead to rapid bone loss.

Ke Te ms Periodontitis as a mani estation o systemic disease Neutropenia Linear gingival erythema (LGE)

Necrotizing periodontal disease (NPD) Tissue necrosis Necrotizing ulcerative gingivitis

Necrotizing ulcerative periodontitis Pseudomembrane Secondary occlusal trauma

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Le s s Co m m o n Fo r m s o F Pe r io d o n t it is This group is composed o uncommon types o periodontitis including (1) periodontitis as a mani estation o systemic diseases (2), necrotizing periodontal diseases (N PDs) (3), abscesses o the periodontium (4), periodontitis associated with endodontic lesions (5), developmental or acquired de ormities and conditions, and (6) occlusal trauma. A bscesses of the periodontium are discussed in the chapter on periodontal em ergencies.

Se ct io n 1

Pe io do ntitis as a Mani e statio n o S ste mic Dise ase s A number o systemic diseases and conditions are a contributing actor in the development o periodontitis. Several hematologic (blood disorders) and genetic disorders are associated with the development o periodontitis (Box 9-1) (1,2). Refer to Chapter 15 for a detailed discussion of system ic disease as a contributing factor to periodontitis. Periodontitis as a mani estation o systemic disease is the diagnosis used when the systemic condition is the major contributing actor or periodontitis and local actors such as heavy accumulations o dental plaque bio lm and calculus deposits are not evident.

Bo x 9-1. Pe io do ntitis as a Mani e statio n o S ste mic Dise ase s 1. Asso ciate d w ith He mato lo g ical Diso de s A. Acq u ire d n e u t ro p e n ia B. Le u ke m ia s C. Ot h e r 2. Asso ciate d w ith Ge ne tic Diso de s A. Fa m ilia l a n d cyclic n e u t ro p e n ia B. Do w n syn d ro m e C. Le u ko cyt e a d h e sio n d e cie n cy syn d ro m e s D. Pa p illo n –Le è vre syn d ro m e E. Ch é d ia k–Hig a sh i syn d ro m e F. Hist io cyt o sis syn d ro m e s G. Glyco g e n st o ra g e d ise a se H. In a n t ile g e n e t ic a g ra n u lo cyt o sis I. Co h e n syn d ro m e J. Eh le rs–Da n lo s syn d ro m e (Typ e s IV a n d VIII) K. Hyp o p h o sp h a t a sia L. Ot h e r 3. No t Othe w ise Spe cif e d (NOS)

Chapte 9

Other Periodontal Conditions

1. Hematologic Disorders. H ematologic disorders are abnormalities in the structure or unction o the blood and blood- orming tissues such as: red cells, white cells, platelets, or clotting actors. There are numerous rare hematologic disorders that may a ect the periodontium (Box 9-3, Fig. 9-2). A. Acquired N eutropenia 1. N eutropenia is a blood disorder characterized by abnormally low levels o neutrophils (polymorphonuclear leukocytes [PM N s]) in the blood. 2. N eutropenia has numerous causes. It may be genetic or may be seen with viral in ections and a ter radiotherapy and chemotherapy. It a ects as many as one in three patients receiving chemotherapy or cancer. 3. N eutropenia lowers the immunologic barrier to bacterial and ungal in ection. 4. N eutrophil disorders that a ect the production or unction o PM N s may result in severe periodontal destruction (Box 9-2, Fig. 9-1). 5. Reported periodontal mani estations include either a localized or generalized pattern o periodontitis (3–5). Pro essional dental hygiene care and meticulous daily sel -care, in combination with systemic antibiotics to supplement therapy or the underlying disease, have been success ul in many cases (4). B. Leukemia 1. Leukemia is cancer that begins in blood cells. In people with leukemia, the bone marrow produces a large number o abnormal white blood cells, that don’t unction properly. 2. At rst, leukemia cells unction almost normally. In time, they may crowd out normal white blood cells, red blood cells, and platelets. 3. Periodontal mani estations o leukemia requently include gingival enlargement, mucosal bleeding and ulceration, petechiae, and opportunistic in ections o the gingiva (6–9).

Bo x 9-2. Pe io do ntitis Asso ciate d w ith PMN D s unctio n • Occu rs in p a t ie n t s o a n y a g e • Se e n in yo u n g ch ild re n b e g in n in g w it h t h e e ru p t io n o p rim a ry t e e t h • Ch a ra ct e rize d w it h se ve re b o n e lo ss a n d t o o t h lo ss • Asso cia t e d w it h syst e m ic co n d it io n s t h a t in t e r e re w it h t h e b o d y’s re sist a n ce t o b a ct e ria l in e ct io n

Fig u e 9-1. Pe io do ntitis Asso ciate d w ith Immune D s unctio n. This photo shows the dentition o a young patient with PMN de iciency. Note the primary dentition is being lost and the permanent dentition is being ex oliated as soon as the permanent teeth erupt.

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Bo x 9-3. He mo hag ic Pe io do ntitis–Asso ciate d Blo o d Diso de • Ch a ra ct e rize d b y so t , sw o lle n g in g iva l t issu e . Ble e d in g o ccu rs sp o n t a n e o u sly o r o n t h e slig h t e st p ro vo ca t io n .

Fig u e 9-2. Pe io do ntitis Asso ciate d w ith a Blo o d Diso de . This male patient has a rare blood disorder. His so t, swollen gingiva bleeds easily. (Courtesy o Dr. Ralph Arnold, San Antonio, TX)

C. AIDS/ HIV In ection 1. Since the early 1990s, the death rate rom AIDS among adults has declined in most developed countries, largely because o newer antiretroviral therapies and improved access to these therapies. In addition, rom 2006 to 2011, the total number o new cases o human immunode ciency virus (H IV) in ection worldwide has declined somewhat and has remained relatively constant (10). 2. The periodontal conditions most closely associated with H IV in ection are linear gingival erythema (LGE) and necrotizing periodontal diseases (N PD) are the most common H IV-associated periodontal conditions reported in the literature (Box 9-4, Fig. 9-3A,B,C) (10). a. Linear gingival erythema (LGE) is a gingival mani estation o immunosuppression. b. A distinct linear erythematous (red) band that is limited to the ree gingiva characterizes the clinical appearance o LGE (Box 9-4). c. LGE does not respond well to improved sel -care or periodontal instrumentation. 3. With the advent o newer pharmacological approaches to the treatment o H IV in ection, the incidence and progression o both atypical and conventional periodontal diseases are changing. The incidence o necrotizing periodontitis and gingival diseases o ungal origin appears to be on the decline as a result o these therapies that have led to increased li e spans or H IV patients. H owever, in cases where these therapies lose their e ectiveness and H IV patients relapse into an immunosuppressed state, these conditions may recur. Recent evidence has shown that H IV patients with more conventional periodontal diseases such as chronic periodontitis may have increased attachment loss and gingival recession when compared to their H IV-negative counterparts (11,12).

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Bo x 9-4. Pe io do ntitis Asso ciate d w ith HIV In e ctio n

A

B

Fig u e 9-3A. Pe io do ntitis Asso ciate d w ith HIV In e ctio n. This HIV-positive individual exhibits a severe orm o necrotizing ulcerative periodontitis with tissue necrosis o the gingival tissues combined with loss o attachment. Clinical signs are visible on the mandibular anterior sextant.

Fig u e 9-3B. Pe io do ntitis Asso ciate d w ith HIV In e ctio n. Palatal candidiasis on the palatal mucosa o an HIV-positive individual. (Courtesy o Dr. Ralph Arnold).

C

Fig u e 9-3C. Line a Ging ival E the ma. Linear gingival erythema in an HIV-in ected patient.

• Th e p e rio d o n t a l co n d it io n s m o st clo se ly a sso cia t e d w it h HIV in e ct io n a re lin e a r g in g iva l e ryt h e m a (LGE) a n d n e cro t izin g p e rio d o n t a l d ise a se s (NPDs). • HIV-in e ct e d p a t ie n t s w it h m o re co n ve n t io n a l p e rio d o n t a l d ise a se s su ch a s ch ro n ic p e rio d o n t it is m a y h a ve in cre a se d a t t a ch m e n t lo ss a n d g in g iva l re ce ssio n w h e n co m p a re d t o t h e ir HIV-n e g a t ive co u n t e rp a rt s. • Ora l m a n i e st a t io n s o HIV in e ct io n in clu d e o ra l ca n d id ia sis, o ra l h a iry Le u ko p la kia , o ra l h yp e rp ig m e n t a t io n , o ra l u lce rs; re d , p u rp le , o r b lu e e d e m a t o u s so t t issu e le sio n s; a n d Ka p o si sa rco m a a n d o t h e r o ra l m a lig n a n cie s.

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2. Genetic Disorders. A genetic disorder is a disease caused by the absence o a gene or by-products o a de ective gene. Genetic diseases are passed rom one generation to the next but do not necessarily appear in each generation. A. Familial and Cyclic N eutropenia 1. H ereditary and congenital disorders that a ect the bone marrow, resulting in abnormally low level o neutrophils (PM N s) in the blood. 2. Individuals with cyclic neutropenia may experience severe periodontal destruction. Periodontal mani estations o this disease appear at a young age (13). B. Down Syndrome 1. A common birth de ect caused by an error in cell division results in the presence o an additional third chromosome. O ne in every 691 babies in the United States is born with Down syndrome, making Down syndrome the most common genetic condition. 2. M ost people with Down syndrome have cognitive delays that are mild to moderate. A ew o the common physical traits o Down syndrome are low muscle tone, small stature, an upward slant to the eyes, and a single deep crease across the center o the palm. People with Down syndrome have an increased risk or certain medical conditions such as congenital heart de ects, respiratory and hearing problems, Alzheimer disease, childhood leukemia, and thyroid conditions. 3. Individuals with Down syndrome o ten develop severe early-onset periodontal diseases (14). Substantial plaque bio lm ormation, deep periodontal pockets, and extensive gingival inf ammation characterize periodontal disease in Down syndrome (Box 9-5, Fig. 9-4). C. Leukocyte Adhesion Def ciency Syndromes 1. An inherited disorder in which there is de ective leukocyte chemotaxis. A ected individuals are susceptible to recurrent bacterial and ungal in ections, impaired pus ormation, delayed wound healing, and periodontitis (15). 2. Cases o periodontal disease attributed to leukocyte adhesion de ciency syndromes are rare. Periodontitis begins upon eruption o the primary teeth with rapid attachment loss and early tooth loss (16). D. Papillon–Le èvre Syndrome 1. An inherited disorder characterized by hyperkeratosis o the palms o the hands and soles o the eet and severe periodontitis a ecting both primary and secondary dentitions (17). 2. Periodontitis causes bone loss and ex oliation o the teeth. Primary teeth may be lost by 5 or 6 years o age. The permanent teeth erupt but are lost due to bone destruction. By age 15 some individuals are edentulous. E. Chédiak–Higashi Syndrome 1. A rare, inherited disorder o the immune and nervous systems characterized by pale-colored hair, eyes, and skin. Impairment o neutrophil chemotaxis is a characteristic o this disease (18). 2. Patients with Chédiak–H igashi Syndrome are prone to severe periodontitis (19). F. Glycogen Storage Disease 1. O ne o the 14 recognized diseases that inter ere with the storage o carbohydrates as glycogen in the body; characterized by neutropenia. 2. Periodontal mani estations o this disease appear at a young age with the potential or early tooth loss (20).

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Bo x 9-5. Pe io do ntitis-Asso ciate d Do w n S nd o me • Ch a ra ct e rize d b y su b st a n t ia l b io lm o rm a t io n , d e e p p e rio d o n t a l p o cke t s, a n d e xt e n sive g in g iva l in f a m m a t io n

Fig u e 9-4. Pe io do ntitis Asso ciate d w ith Do w n S nd o me . (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC)

G. In antile Genetic Agranulocytosis (Kostmann syndrome) 1. A rare inherited orm o severe chronic neutropenia usually detected soon a ter birth (21). 2. Individuals with in antile genetic agranulocytosis experience severe periodontal disease (22). H. Cohen Syndrome 1. An inherited disorder that a ects many parts o the body and is characterized by neutropenia, developmental delay, mental retardation, small head size, and weak muscle tone (23). 2. Individuals with Cohen syndrome have increased susceptibility to early periodontal breakdown, which is likely to be associated with neutropenia. I. Ehlers–Danlos Syndrome (Types IV and VIII) 1. A heritable disorder o connective tissue with easy bruising, joint hypermobility (loose joints), skin laxity, and weakness o tissues (24). 2. Early-onset generalized periodontitis is one o the most signi cant oral mani estations o the syndrome. This can lead to the premature loss o deciduous and permanent teeth (25–27). J. Hypophosphatasia 1. A genetic metabolic disorder o bone mineralization caused by a de ciency in alkaline phosphatase in serum and tissues; characterized by skeletal de ects resembling those o rickets (28). 2. Periodontal mani estations include severe loss o alveolar bone and premature loss o primary and permanent teeth in the absence o an inf ammatory response (29). Early ex oliation particularly a ects the anterior teeth. Children with hypophosphatasia are at risk o developing oral complications during adolescent and adult li e (30).

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Se ct io n 2

Ne c o tizing Pe io do ntal Dise ase s N ecrotizing periodontal diseases include necrotizing ulcerative gingivitis (N UG) and necrotizing ulcerative periodontitis (N UP). To date, there is insu cient evidence to establish i N UG and N UP are two unique diseases or di erent stages o the same disease that progresses rom N UG to N UP. Until a distinction between N UG and N UP can be clari ed, N UG and N UP are classi ed together under the category o necrotizing periodontal diseases. Both N UG and N UP appear to be related to diminished systemic resistance to bacterial in ection. Treatment o necrotizing periodontal diseases is discussed in Chapter 28, Periodontal Emergencies. 1. N ecrotizing periodontal disease (N PD) is an inf ammatory destructive in ection o periodontal tissues that involve tissue necrosis (localized tissue death). Both N UG and N UP are pain ul in ections with ulceration, swelling, and sloughing o o dead epithelial tissue rom the gingiva. A. N ecrotizing ulcerative gingivitis (N UG)—tissue necrosis that is limited to the gingival tissues (Box 9-6, Fig. 9-5). B. N ecrotizing ulcerative periodontitis (N UP)—tissue necrosis o the gingival tissues combined with loss o attachment and alveolar bone loss (Box 9-7, Fig. 9-6). 1. N UP is a pain ul in ection characterized by necrosis o gingival tissues, periodontal ligament, and alveolar bone. 2. N UP is an extremely rapid and destructive orm o periodontitis that can produce loss o periodontal attachment within days. 2. Alternative Terminology. These conditions previously have been known as trench mouth, Vincent in ection, acute ulcerative necrotizing gingivitis (AN UG), and necrotizing ulcerative gingivostomatitis. 3. Signs and Symptoms o N ecrotizing Periodontal Disease A. Oral Signs and Symptoms. The clinical appearance o N PD is noticeably di erent than that o any other periodontal disease (31,32). 1. N PD is a pain ul in ection, primarily involving the interdental and marginal gingiva. 2. NPD is characterized by ulcerated and necrotic papillae and gingival margins, giving the appearance that the papillae and gingival margins have been “punchedout” or “cratered” (Fig. 9-7). The ulcerated margin is bounded by a red halo.

Bo x 9-6. Ne c o tizing Ulce ative Ging ivitis (NUG) • Su d d e n o n se t • Pa in • Ne cro sis o in t e rd e n t a l p a p illa e (cra t e re d , p u n ch e d -o u t p a p illa e ) • Ye llo w ish w h it e o r g ra yish t issu e slo u g h • Fie ry re d g in g iva w it h sp o n t a n e o u s b le e d in g

Fig u e 9-5. Ne c o tizing Ulce ative Ging ivitis.

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Bo x 9-7. Ne c o tizing Ulce ative Pe io do ntitis (NUP) • Th e sa m e sig n s a n d sym p t o m s o NUG • At t a ch m e n t lo ss

Fig u e 9-6. Ne c o tizing Ulce ative Pe io do ntitis.

3. The necrotic areas o the gingiva are covered by a yellowish white or grayish tissue slough, which is termed a pseudomembrane. a. The pseudomembrane consists primarily o brin and necrotic tissue with leukocytes, erythrocytes, and masses o bacteria. (Fibrin is stringy protein ormed during the process o blood clot ormation.) b. The term, pseudomembrane, however, is misleading since the slough has no coherence and is not similar to a true membrane. It is easily wiped o with gauze, exposing an area o ery red, shiny gingiva. c. The pseudomembrane may involve the gingiva o several teeth or it may cover the entire gingiva. d. The sloughing o o dead gingival epithelial tissue exposes the underlying connective tissue. 4. Fiery red gingiva with spontaneous gingival bleeding or bleeding to gentle touch. 5. T he necrotizing lesions develop rapidly and are painful. Intense oral pain that causes a ected patients to seek dental treatment. This symptom is unusual since gingivitis and periodontitis normally are not pain ul. 6. The rst lesions o ten are seen interproximally in the mandibular anterior sextant but may occur in any interproximal papilla. Usually, the papillae swell rapidly and develop a rounded contour (Fig. 9-8). 7. A pronounced, etid oral odor (bad breath) may be present but can vary in intensity and in some cases is not very noticeable. a. The pain associated with N PDs usually causes the individual to stop brushing. b. M ateria alba, plaque bio lm, sloughed tissue, blood, and stagnant saliva collect in the oral cavity causing the oral odor. 8. N PDs may be associated with excessive salivation.

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Fig u e 9-7. Ne c o tic Papillae and Ging ival Ma g ins. This patient with NPD exhibits the characteristic ulcerated, necrotic papillae and gingival margins. (Courtesy o Dr. Ralph Arnold)

Fig u e 9-8. Sw o lle n Papillae . Swollen papillae in the anterior regions o the mouth are characteristic o NPD. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC)

A

B

Fig u e 9-9. Ne c o tizing Ulce ative Pe io do ntitis. NUP is characterized by loss o attachment. (A: Courtesy o Dr. Ralph Arnold; B: Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC)

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9. As tissue necrosis progresses, interproximal craters are ormed. a. Within a ew days the involved papillae are o ten separated into one acial and one lingual portion with a necrotic depression between them. b. This central tissue destruction between the acial and lingual portions o a papilla results in a crater. c. O nce interproximal craters are ormed, the disease process usually involves the periodontal ligament and alveolar bone, resulting in loss o attachment. d. Deep craters in the interdental alveolar bone characterize N UP. e. The deep periodontal pockets seen in other orms o periodontitis are not common in N UP because the tissue necrosis destroys the marginal epithelium and connective tissue, resulting in gingival recession (Fig. 9-9). Progression o the interproximal disease process o ten results in destruction o most o the interdental bone. 10. As the result o pain it is o ten di cult or patients to eat. B. Systemic Signs and Symptoms 1. Swelling o the lymph nodes, especially the submandibular and cervical lymph nodes, may occur in N PDs. 2. Fever and malaise is not a consistent characteristic o N PDs. Investigations indicate that ever is not common (33,34). 4. Etiology o N ecrotizing Periodontal Diseases A. Microorganisms. N PDs are associated with Treponem a species, Selenom onas species, Fusobacterium species, and Bacteroides m elaninogenicus ss. interm edius (Provotella interm edia). B. Predisposing Factors or N ecrotizing Periodontal Diseases 1. Systemic diseases, which impair immunity, including H IV in ection, leukemia, measles, chicken pox, tuberculosis, herpetic gingivostomatitis, and malaria 2. Poor sel -care (plaque control) 3. Emotional stress (35,36) 4. Inadequate sleep, atigue 5. Alcohol use 6. Caucasian background 7. Cigarette smoking—most patients who experience N PDs are smokers (34,37) 8. Increased levels o personal stress 9. Poor nutrition a. In N orth America, N UG is associated with poor eating habits o young adults, such as college students. b. In developing countries, N UG occurs in very young children and appears to be related to poor nutritional status, especially a low protein intake. 10. Pre-existing gingivitis or tissue trauma 11. Young age—this disease can occur at any age, however, the reported mean age or N PDs in industrialized countries is between 22 and 24 years (38).

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Se ct io n 3

De ve lo pme ntal o Ac ui e d De o mitie s and Co nditio ns In general, this classi cation comprises local actors that contribute to the initiation and progression o periodontal disease. These actors all into our subgroups (Table 9-1).

TABLE 9 -1 . DEVELOPMENTAL Or ACq UIr ED DEFOr MITIES AND CONDITIONS 1. Lo ca lize d t o o t h -re la t e d a ct o rs t h a t m o d i y o r p re d isp o se t o p la q u e -in d u ce d g in g iva l d ise a se s o r p e rio d o n t it is A. To o t h a n a t o m ic a ct o rs B. De n t a l re st o ra t io n s/a p p lia n ce s C. Ro o t ra ct u re s D. Ce rvica l ro o t re so rp t io n a n d ce m e n t a l t e a rs 2. Mu co g in g iva l d e o rm it ie s a n d co n d it io n s a ro u n d t e e t h A. Re ce ssio n o t h e g in g iva l m a rg in 1. Fa cia l o r lin g u a l su r a ce s 2. In t e rp ro xim a l (p a p illa ry) B. La ck o ke ra t in ize d g in g iva C. De cre a se d ve st ib u la r d e p t h D. Ab e rra n t re n u m /m u scle p o sit io n E. Gin g iva l e xce ss 1. Pse u d o p o cke t 2. In co n sist e n t g in g iva l m a rg in 3. Exce ssive g in g iva l d isp la y 4. Gin g iva l e n la rg e m e n t F. Ab n o rm a l co lo r 3. Mu co g in g iva l d e o rm it ie s a n d co n d it io n s o n e d e n t u lo u s rid g e s A. Ve rt ica l a n d /o r h o rizo n t a l rid g e d e icie n cy B. La ck o g in g iva /ke ra t in ize d t issu e C. Gin g iva l/so t t issu e e n la rg e m e n t D. Ab e rra n t re n u m /m u scle p o sit io n E. De cre a se d ve st ib u la r d e p t h F. Ab n o rm a l co lo r 4. Occlu sa l t ra u m a A. Prim a ry o cclu sa l t ra u m a B. Se co n d a ry o cclu sa l t ra u m a

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t o o t h -r e La t e d Fa Ct o r s Tooth anatomic actors that predispose to plaque-related gingival diseases or periodontitis include tooth anatomic actors, such as cervical enamel projections and enamel pearls, palatolingual grooves, or tooth malalignment (Figs. 9-10 and 9-11). Local actors such as orthodontic appliances (braces) or aulty dental restorations can lead to plaque bio lm retention (Figs. 9-12 and 9-13) and may impinge on the biologic width.

Fig u e 9-10. Ename l Pe a l as P e dispo sing Facto . This maxillary second molar exhibits enamel pearl. Although not clear on the radiograph, this tooth experienced alveolar bone loss on the acial aspect. (Courtesy o Dr. Ralph Arnold)

A

B

Fig u e 9-11. Palato ling ual G o o ve . A: This patient has a deep periodontal pocket on the lingual o the maxillary lateral incisor. B: Periodontal surgery reveals a palatolingual groove as the predisposing actor or bone loss at this site. (Courtesy o Dr. Ralph Arnold)

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Fig u e 9-12. O tho do ntic Appliance s as a P e dispo sing Facto . In requent sel -care and plaque bio ilm accumulation results in periodontitis in this individual with orthodontic appliances. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC)

Fig u e 9-13. De ntist as P e dispo sing Facto . The photo to the le t shows anterior teeth with a rubber dam in place. The splinting o these mandibular anterior teeth leads to plaque bio ilm accumulation and is a predisposing actor or periodontitis. (Courtesy o Dr. Ralph Arnold)

m u Co g in g iv a L d e Fo r m it ie s a n d Co n d it io n s a r o u n d t e e t h A mucogingival de ormity is a signi cant alteration o the morphology, size, and interrelationships between the gingiva and the alveolar mucosa that may involve the underlying bone. Recession o the gingival margin is the most common mucogingival de ormity and it is characterized by the displacement o the gingival margin apically rom the cementoenamel junction (Figs. 9-14 to 9-17).

Fig u e 9-14. r e ce ssio n o the Ging ival Ma g in. Recession on the mandibular central incisor extending to the mucogingival junction. (Courtesy o Dr. Ralph Arnold)

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Fig u e 9-15. r e ce ssio n o the Ging ival Ma g in. Recession on the mandibular central incisors extending to the mucogingival junction. (Courtesy o Dr. Ralph Arnold)

Fig u e 9-16. F e num Attachme nts. Tension o the renum may pull the gingiva away rom the tooth and may be conducive to plaque bio ilm accumulation and recession o the gingival margin. (Fig. 9-16 courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC)

Fig u e 9-17. F e num Attachme nts. Tension o a renum may pull the gingiva away rom the tooth and may be conducive to plaque bio ilm accumulation and recession o the gingival margin. (Fig. 9-17 courtesy o Dr. Ralph Arnold)

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o CCLu s a L t r a u m a in Pa t ie n t s Wit h Pe r io d o n t it is 1. Secondary occlusal trauma is injury as the result o occlusal orces applied to a tooth or teeth that have previously experienced attachment loss and/or bone loss. 2. In this type of occlusal trauma, the periodontium was unhealthy before experiencing excessive occlusal forces (Box 9-8, Figs. 9-18A, 18B). 3. Rapid bone loss and pocket ormation may result when excessive occlusal orces are applied to a tooth that has previously experienced attachment loss and/or bone loss.

Bo x 9-8. Se co nda

A

Occlusal T auma

B

Fig u e 9-18. Se co nda Occlusal T auma. A: The woman pictured above puts repeated heavy pressure against her central incisor tooth. B: A dental radiograph o her central incisor shows severe bone loss around the central incisor that is subjected to the heavy pressure.

Clin ica l in d ica t o rs o o cclu sa l t ra u m a m a y in clu d e o n e o r m o re o t h e o llo w in g : • To o t h m o b ilit y (p ro g re ssive ) • Fre m it u s (vib ra t io n e lt w h e n p a lp a t in g a t o o t h , a s t h e p a t ie n t t a p s t h e t e e t h t o g e t h e r) • To o t h m ig ra t io n • Fra ct u re d t o o t h • Th e rm a l se n sit ivit y o n ch e w in g o r p e rcu ssio n Ra d io g ra p h ic in d ica t o rs m a y in clu d e o n e o r m o re o t h e o llo w in g : • Wid e n e d p e rio d o n t a l lig a m e n t sp a ce • Bo n e lo ss • Ro o t re so rp t io n

Chapte 9

Chapte Summa

Other Periodontal Conditions

153

State me nt

The 1999 AAP Classi cation o Periodontal Diseases and Conditions includes several less common types o periodontitis as well as other periodontal conditions. These are divided into the ollowing subcategories: • • • • •

Periodontitis as mani estation o systemic disease N ecrotizing periodontal diseases Abscesses o the periodontium Periodontitis associated with endodontic lesions Developmental or acquired de ormities and conditions.

Se ct io n 4

Fo cus o n Patie nts Clinical Patie nt Ca e CA S E 1 A new patient comes to the dental o ce on an emergency basis. The patient complains o severe pain in his gums and reports that he was unable to eat over the weekend due to the pain. A clinical examination reveals necrotic papillae and gingival margins, cratered papillae, a yellowish tissue slough, spontaneous bleeding, and no loss attachment or bone loss. Which type o periodontal disease does this patient exhibit?

Ethical Dile mma Your last patient o the day is Luana G., a 16-year-old girl, who has Down Syndrome. She presents with moderate mental retardation. This is the rst dental appointment in her li e, as she has a ear o clinical settings, and her parents have not wanted to righten or upset her. Your clinical exam reveals substantial plaque, bio lm and calculus ormation, deep periodontal pockets, and extensive gingival inf ammation. Radiographs show severe alveolar bone loss around most o her teeth. There is urcation involvement and some mobility present. There is also extensive cervical decay present on all o her mandibular anterior teeth. Due to Luana’s mental de cits, it is di cult to determine i she is experiencing oral discom ort. H al way through your appointment, however, Luana re uses to open her mouth, starts to cry, and rocks back and orth. H er parents say this is her typical behavior when she is upset. 1. H ow would you classi y Luana’s periodontal condition? 2. What ethical principles are in conf ict in this dilemma? 3. What is the best way or you to handle this ethical dilemma?

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r e e e nce s 1. Kinane D. Blood and lymphoreticular disorders. Periodontol 2000. 1999;1:84–93. 2. Kinane DF. Periodontitis modi ed by systemic actors. A nn Periodontol. 1999;4(1):54–64. 3. O kada M , Kobayashi M , H ino T, et al. Clinical periodontal ndings and microf ora pro les in children with chronic neutropenia under supervised oral hygiene. J Periodontol. 2001;72(7):945–952. 4. Schmidt JC, Walter C, Rischewski JR, et al. Treatment o periodontitis as a mani estation o neutropenia with or without systemic antibiotics: a systematic review. Pediatr D ent. 2013;35(2):E54–E63. 5. Z aromb A, Chamberlain D, Schoor R, et al. Periodontitis as a mani estation o chronic benign neutropenia. J Periodontol. 2006;77(11):1921–1926. 6. Gillette WB. Re: oral mani estations o acute myelomonocytic leukemia: a case report and review o the classi cation o leukemias. Wu J, Fantasia Je, Kaplan R. (2002;73:664–668). J Periodontol. 2002;73(10):1228. 7. H aytac M C, Antmen B, Dogan M C, et al. Severe alveolar bone loss and gingival hyperplasia as initial mani estation o Burkitt cell type acute lymphoblastic leukemia. J Periodontol. 2003;74(4):547–551. 8. Soga Y, Saito T, N ishimura F, et al. Appearance o multidrug-resistant opportunistic bacteria on the gingiva during leukemia treatment. J Periodontol. 2008;79(1):181–186. 9. Wu J, Fantasia JE, Kaplan R. O ral mani estations o acute myelomonocytic leukemia: a case report and review o the classi cation o leukemias. J Periodontol. 2002;73(6):664–668. 10. Ryder M I, N ittayananta W, Coogan M , et al. Periodontal disease in H IV/AIDS. Periodontol 2000. 2012;60(1):78–97. 11. Ryder M I. An update on H IV and periodontal disease. J Periodontol. 2002;73(9):1071–1078. 12. Vastardis SA, Yukna RA, Fidel PL Jr., et al. Periodontal disease in H IV-positive individuals: association o periodontal indices with stages o H IV disease. J Periodontol. 2003;74(9):1336–1341. 13. Rylander H , Ericsson I. M ani estations and treatment o periodontal disease in a patient su ering rom cyclic neutropenia. J Clin Periodontol. 1981;8(2):77–87. 14. Amano A, Kishima T, Kimura S, et al. Periodontopathic bacteria in children with Down syndrome. J Periodontol. 2000;71(2):249–255. 15. Dababneh R, Al-Wahadneh AM , H amadneh S, et al. Periodontal mani estation o leukocyte adhesion de ciency type I. J Periodontol. 2008;79(4):764–768. 16. Cox DP, Weathers DR. Leukocyte adhesion de ciency type 1: an important consideration in the clinical di erential diagnosis o prepubertal periodontitis. A case report and review o the literature. O ral Surg O ral M ed O ral Pathol O ral R adiol Endod. 2008;105(1):86–90. 17. Cagli N A, H akki SS, Dursun R, et al. Clinical, genetic, and biochemical ndings in two siblings with Papillon-Le evre Syndrome. J Periodontol. 2005;76(12):2322–2329. 18. Delcourt-Debruyne EM , Boutigny H R, H ildebrand H F. Features o severe periodontal disease in a teenager with ChediakH igashi syndrome. J Periodontol. 2000;71(5):816–824. 19. Bailleul-Forestier I, M onod-Broca J, Benkerrou M , et al. Generalized periodontitis associated with Chediak-H igashi syndrome. J Periodontol. 2008;79(7):1263–1270. 20. Salapata Y, Laskaris G, Drogari E, et al. O ral mani estations in glycogen storage disease type 1b. J O ral Pathol M ed. 1995;24(3):136–139. 21. Saglam F, Atamer T, O nan U, et al. In antile genetic agranulocytosis (Kostmann type). A case report. J Periodontol. 1995;66(9):808–810. 22. Carlsson G, Andersson M , Putsep K, et al. Kostmann syndrome or in antile genetic agranulocytosis, part one: celebrating 50 years o clinical and basic research on severe congenital neutropenia. A cta Paediatr. 2006;95(12):1526–1532. 23. Alaluusua S, Kivitie-Kallio S, Wol J, et al. Periodontal ndings in Cohen syndrome with chronic neutropenia. J Periodontol. 1997;68(5):473–478. 24. Perez LA, Al-Shammari KF, Giannobile WV, et al. Treatment o periodontal disease in a patient with Ehlers-Danlos syndrome. A case report and literature review. J Periodontol. 2002;73(5):564–570. 25. Karrer S, Landthaler M , Schmalz G. Ehlers-Danlos type VIII. Review o the literature. Clin O ral Investig. 2000;4(2): 66–69. 26. Letourneau Y, Perusse R, Buithieu H . O ral mani estations o Ehlers-Danlos syndrome. J Can D ent A ssoc. 2001;67(6): 330–334. 27. M oore M M , Votava JM , O rlow SJ, et al. Ehlers-Danlos syndrome type VIII: periodontitis, easy bruising, mar anoid habitus, and distinctive acies. J A m A cad D erm atol. 2006;55(2 suppl):S41–S45. 28. M cKee M D, H oac B, Addison WN , et al. Extracellular matrix mineralization in periodontal tissues: noncollagenous matrix proteins, enzymes, and relationship to hypophosphatasia and X-linked hypophosphatemia. Periodontol 2000. 2013;63(1):102–122. 29. Watanabe H , Umeda M , Seki T, et al. Clinical and laboratory studies o severe periodontal disease in an adolescent associated with hypophosphatasia. A case report. J Periodontol. 1993;64(3):174–180. 30. O lsson A, M atsson L, Blomquist H K, et al. H ypophosphatasia a ecting the permanent dentition. J O ral Pathol M ed. 1996;25(6):343–347. 31. Loesche WJ, Syed SA, Laughon BE, et al. The bacteriology o acute necrotizing ulcerative gingivitis. J Periodontol. 1982;53(4):223–230. 32. Proctor DB, Baker CG. Treatment o acute necrotizing ulcerative gingivitis with metronidazole. J Can D ent A ssoc (Tor). 1971;37(10):376–380. 33. Shields WD. Acute necrotizing ulcerative gingivitis. A study o some o the contributing actors and their validity in an Army population. J Periodontol. 1977;48(6):346–349. 34. Stevens AW Jr., Cogen RB, Cohen-Cole S, et al. Demographic and clinical data associated with acute necrotizing ulcerative gingivitis in a dental school population (AN UG-demographic and clinical data). J Clin Periodontol. 1984;11(8):487–493. 35. da Silva AM , N ewman H N , O akley DA. Psychosocial actors in inf ammatory periodontal diseases. A review. J Clin Periodontol. 1995;22(7):516–526.

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36. H ildebrand H C, Epstein J, Larjava H . The inf uence o psychological stress on periodontal disease. J W est Soc Periodontol Periodontal A bstr. 2000;48(3):69–77. 37. Gaggl AJ, Rainer H , Grund E, et al. Local oxygen therapy or treating acute necrotizing periodontal disease in smokers. J Periodontol. 2006;77(1):31–38. 38. H orning GM , Cohen M E. N ecrotizing ulcerative gingivitis, periodontitis, and stomatitis: clinical staging and predisposing actors. J Periodontol. 1995;66(11):990–998.

STUDENT ANCILLAr y r ESOUr CES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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Cl n cal Appl cat o n.

Members of the dental team are equipped with a broad array of skills that can be called upon when caring for patients with periodontal disease. The dental hygienist is superbly trained to provide many of the therapies that are required during this care, and the hygienist needs to understand how to make decisions related to this care to be an effective member of the dental team. This chapter outlines guidelines for decision making including those related to arriving at a periodontal diagnosis, sequencing periodontal treatment, obtaining consent for treatment, and the ongoing need for decision making.

L arn ng O j ct v s • List the three fundamental diagnostic questions used when assigning a periodontal diagnosis. • Explain how to arrive at appropriate answers to each of the fundamental diagnostic questions. • Explain the difference between the terms signs of a disease and symptoms of a disease. • Explain the term silent disease. • Describe what is meant by the term clinical attachment loss. • Describe the elements of a well-written diagnosis for periodontitis. • List the phases of treatment. • Describe the importance of informed consent to treatment planning. • List guidelines for obtaining informed consent. • Describe two formats for documenting informed consent. • Describe the ADPIE nursing process. • Explain how the ADPIE nursing process might apply to periodontal decision making

C apt r 10

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Guidelines for Periodontal Decision Making

T rms

Signs of periodontal disease Symptoms of periodontal disease Silent disease Overt signs Hidden signs Natural level of gingival attachment

Clinical attachment loss Disease sites Master treatment plan Assessment and preliminary therapy phase Nonsurgical periodontal therapy phase Surgical therapy phase

Restorative phase Periodontal maintenance phase Informed consent Informed refusal ADPIE

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S ct o n 1

G d l n s R lat d to Arr v ng at a P r o do ntal D ag no s s The rst step in planning periodontal treatment is assigning a correct periodontal diagnosis (or correct diagnoses). Determination o a periodontal diagnosis can be simpli ed by asking and answering three undamental clinical questions in a systematic manner (Fig. 10-1). 1 Do e s the c linic a l a s s e s s m e nt ind ic a te he a lth o r d is e a s e ?

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F g r 10-1. D c s o n Tr . A decision tree illustrating the three fundamental questions for determining an initial periodontal diagnosis.

These three undamental questions can be used to guide the dental team through the diagnostic process. M any decisions, including assigning a periodontal diagnosis and planning nonsurgical therapy, revolve around the answers to these undamental questions. 1. Answering Fundamental Diagnostic Questions when Assigning a Periodontal Diagnosis A. The First Fundamental Diagnostic Question is: “ Does the clinical assessment indicate health or inf ammatory disease in the periodontium?” 1. The answer to the rst question should be based on the signs o inf ammation that are noted and recorded during the clinical assessment, and by its very nature is not usually di cult or members o the dental team to answer. a. Signs o Periodontal Disease. The dental team should be amiliar with the di erence between the signs o a disease and the sym ptom s o a disease. Signs of periodontal disease are the eatures o a disease that can be observed or are measurable by clinicians. 1. Examples o periodontal disease signs might include gingival erythema (redness), gingival edema (swelling), bleeding on gentle probing, loss o attachment, tooth mobility, or loss o alveolar bone support. 2. Some o these signs are easy to detect by the clinician (i.e., gingival erythema or gingival redness); some o these signs require care ul assessment by the dental team (i.e., loss o attachment). b. Symptoms o Periodontal Disease. Symptoms of periodontal disease are eatures o a disease that are noticed by the patient.

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1. Examples o symptoms o moderate to severe periodontitis might include di culty chewing, itching gums, blood on the bed pillow, or a bad taste in the mouth. 2. It should be noted that in many patients, periodontitis does not cause much in the way o obvious symptoms to the patients, and some clinicians re er to periodontitis as a silent disease because o this lack o or “ silence” o symptoms that are obvious to the patient. 3. Calling periodontitis a silent disease underscores the requent clinical observation that periodontitis can exist in patients who are totally unaware o its presence. c. It is critical or members o the dental team to realize that signs o inf ammation in the periodontium include both overt signs o inf ammation (i.e., those signs that are readily visible) and hidden signs o inf ammation (i.e., those signs that not readily visible) (Table 10-1). 1. Examples o overt signs o inf ammation are changes in the color, contour, and consistency o the gingival tissue. 2. Examples o hidden signs o inf ammation are alveolar bone loss, bleeding on probing, and sometimes purulence or exudate. 2. H ealth as an answer to the rst diagnostic question a. I the clinical periodontal assessment reveals no signs o inf ammation in the periodontium, then the answer to Q uestion #1 is health (i.e., an inf ammation- ree periodontium). b. This means that inf ammatory disease is not present and, though other problems in the periodontium m ay well be present, the patient certainly does not have either gingivitis or periodontitis. 3. Inf ammatory disease as an answer to the rst diagnostic question a. I the clinical periodontal assessment reveals either overt or hidden signs o inf ammation in the periodontium, then the answer to Q uestion #1 is, o course, inf ammatory disease. b. This means that some type o inf ammatory disease is present (i.e., some type o gingivitis or periodontitis) and that urther diagnostic decisions related to this inf ammatory disease will need to be made by the team. 4. Additional Diagnostic M easures a. N ote that even in the absence o any inf ammatory disease in the periodontium, some patients will require additional diagnostic measures. b. For example, a patient with no inf ammation in the periodontium at all but with severe gingival recession accompanied by cervical abrasion o the teeth may need to be evaluated or possible use o traumatic toothbrushing techniques.

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B. The Second Fundamental Diagnostic Question is: “I the clinical assessment indicates inf ammatory disease, is the disease gingivitis or is it periodontitis?” 1. Using Attachment Loss to Answer Fundamental Diagnostic Q uestion 2 a. The answer to this second undamental question is based on clinical evidence o attachment loss as determined rom the ndings recorded during the clinical assessment. 1. The natural level of gingival attachment to the tooth is slightly coronal to (or in a sense above) the level o the cementoenamel junction (CEJ). 2. Clinical attachment loss or attachment loss re ers to migration o the junctional epithelium to a position apical to (or in a sense below) the level o the CEJ (Fig. 10-2). b. Gingivitis. I the clinical assessment reveals no attachment loss in the presence o inf ammation, then the answer to Q uestion #2 is gingivitis. c. Periodontitis. I the clinical assessment revealed attachment loss in the presence o inf ammation, then the answer to Q uestion #2 is periodontitis. 2. It is important or the dental team to use dental radiographs as well as the clinical ndings during the clinical assessment process. a. In most patients with moderate to severe periodontitis, alveolar bone loss will be evident on the radiographs. b. H owever, even be ore radiographic changes occur, attachment loss will normally be detectable by alert clinicians. c. The members o the dental team must make every e ort to detect periodontitis be ore there is obvious radiographic evidence o alveolar bone loss. C. The Third Fundamental Diagnostic Question is: “ I the patient has gingivitis, what type o gingivitis?” or “I the patient has periodontitis, what type o periodontitis?” 1. The classi cation o various types o gingival disease and the various types o periodontitis will be discussed in many other chapters in this textbook (Chapters 5, 6, 7, 8, and 9). 2. The dentist will use these disease classi cations to assign a speci c periodontal diagnosis based on the clinical eatures outlined in those chapters.

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Guidelines for Periodontal Decision Making

2. Recognizing the N eed for Flexibility When Assigning a Periodontal Diagnosis. A. Flexibility. The members o the dental team must be aware o the need or some f exibility when assigning a periodontal diagnosis since more than one periodontal condition may be ound in a patient. 1. Flex ibility in this case re ers to a realization that the important undamental decision as to the presence o either gingivitis or periodontitis in a patient may not describe the total periodontal condition o that patient. 2. O ther periodontal conditions may indeed be present, and this nding must be noted when documenting a periodontal diagnosis in addition to any undamental decision about the presence o gingivitis or periodontitis. B. Other Findings. Examples o some o these other periodontal conditions might be recession o the gingival margin, occlusal trauma, or aberrant renum position. (M any o these other conditions will be discussed in Chapter 9.) 3. Thorough Documentation of the Periodontal Diagnosis. Documenting the periodontal diagnosis is a critical skill or the dental team, and adhering to a standard ormat or such documentation is help ul. The ollowing are some guidelines or documenting periodontal diagnoses. A. Diagnostic Term. As part o the diagnosis, include the correct diagnostic term as outlined in the classi cation scheme, such as chronic periodontitis or aggressive periodontitis (as discussed in Chapters 7 and 8). B. Disease Severity. When assigning a diagnosis, add descriptive modi ers such as slight (mild), moderate, or severe to describe the severity o the disease. 1. Table 10-2 shows how the terms slight, moderate, and severe should be used as part o documentation o a periodontitis diagnosis. 2. N ote that the term clinical attachm ent loss (CAL) is used to underscore that these measurements are clinical measurements and may not coincide exactly with precise histologic measurements. C. Disease Extent. When assigning a diagnosis, also include descriptive modi ers such as localized or generalized to describe the ex tent o the disease. 1. Table 10-2 also shows how the terms localized and generalized should be used as part o documentation o the extent o periodontal disease. 2. N ote that the term disease sites re ers to the individual teeth or speci c sur aces o a tooth that are experiencing periodontal destruction. 3. Examples o appropriate periodontal diagnoses might be generalized m oderate chronic periodontitis or localized severe aggressive periodontitis. Table 10-3 provides some examples o well-written periodontal diagnoses. 4. Using the Case Type System for Periodontal Patients A. Case Types 1. Although the case type system is somewhat limited in value, it has been standard practice in the United States to assign a periodontal case type to all periodontal patients. These case types are sometimes used in insurance reporting and in communication with third-party payers. 2. Assigning a periodontal case type is included in the initial decision-making process in most dental o ces and is included here as additional in ormation related to assigning a periodontal diagnosis. a. Case Type I. Patients with gingivitis only b. Case Type II. Patients with slight (mild) periodontitis c. Case Type III. Patients with moderate periodontitis d. Case Type IV. Patients with severe periodontitis

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B. Limited Value of Case System. The value o the case type system is very limited because the case type alone does not speci y the precise periodontal disease classi cation. 1. For example, a Case Type III patient could be a patient with either chronic periodontitis or a patient with aggressive periodontitis since the Case Type system does not speci y the precise type o periodontitis. 2. N ote that a designation o Case Type III only signi es that the disease is o moderate severity. 3. It is important or all members o the dental team to use the written periodontal diagnosis (e.g., generalized moderate chronic periodontitis) when describing the periodontal status o a patient and to use the case type only as a supplemental description i called or.

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Guidelines for Periodontal Decision Making

S ct o n 2

G d l n s R lat d to P r o do ntal Tr atm nt S q nc ng 1. The Periodontal Master Treatment Plan. The master treatment plan is a sequential outline o the measures to be carried out by the dentist, the dental hygienist, or the patient to eliminate disease and restore a healthy periodontal environment. • The master treatment plan can be used to coordinate and to sequence all treatment and educational measures employed. • Although some o the treatment included in the master treatment plan may not involve the dental hygienist directly, it is important that the hygienist understand how all phases o treatment contribute to the goal o restoring a healthy periodontal environment. 2. Understanding the Phases of Periodontal Treatment. The master treatment plan can be sequenced into phases. An overview o the sequence o phases o treatment is presented in Figure 10-3 as well as in the discussion below. Re er to Table 10-4 or examples o components o each o the phases in the management o periodontal patients. It should be noted that much overlap in these phases is required in the management o some patients, but understanding these basic phases can help the members o the dental team understand the entire scope o therapy needed or many patients. A. Assessment and Preliminary Therapy Phase 1. The assessment and preliminary therapy phase includes (1) assessment data collection and (2) needed care or any immediate treatment needs such as emergency dental care. Details o the clinical periodontal assessment are discussed in Chapters 19 and 20, and periodontal emergencies are discussed in Chapter 28. 2. This phase o care also has been re erred to as emergency therapy by some authors. B. N onsurgical Periodontal Therapy Phase 1. The nonsurgical periodontal therapy phase o treatment includes all the nonsurgical measures used to control gingivitis and periodontitis. a. This phase includes intensive dental hygiene care and comprehensive patient educational measures. b. This phase can also include measures to minimize the impact o local contributing actors. 2. The nonsurgical periodontal therapy phase has also been called initial periodontal therapy, Phase I therapy, bacterial control, and anti-in ective therapy. C. Surgical Therapy Phase 1. The surgical therapy phase o treatment includes any needed periodontal surgery and placement o dental implants. 2. The surgical therapy phase o care has also been called Phase II therapy. Periodontal surgical procedures are discussed in Chapter 27 o this book. 3. N ote that this phase o treatment is not needed or all patients. D. Restorative Therapy Phase 1. The restorative therapy phase o treatment may include placement o dental restorations and replacement o missing teeth by xed or removable prostheses. 2. The restorative therapy phase o care has also been called Phase III therapy. E. Periodontal Maintenance Phase 1. The periodontal maintenance phase o treatment includes all measures used by the dental team and by the patient to keep periodontitis rom recurring once the inf ammatory disease is brought under control.

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2. The objective o the periodontal maintenance phase is to maintain the teeth unctioning throughout the li e o the patient and may actually be needed or the rest o the patient’s li e. 3. The periodontal maintenance phase o care has also been called Phase IV therapy. Periodontal maintenance is discussed in detail in Chapters 30 and 31.

Patient evaluation, diagnos is , and urgent therapy

Nons urgical periodontal therapy (other name for this phas e = initial periodontal therapy)

Revaluation of res ults of nons urgical therapy

Surgical periodontal therapy including implant placement where needed

Res torative therapy

Periodontal maintenance

F g r 10-3. S q nc ng o Tr atm nt P as s. This flow chart provides an overview of the sequence of the normal phases of treatment for a patient.

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S ct o n 3

G d l n s R lat d to Co ns nt o r P r o do ntal Tr atm nt Periodontal treatment is always based upon the best available scienti c evidence, but many times there will be more than a single course o treatment that could bene t an individual patient. An appropriate plan or any individual patient must include input rom that patient and requires some detailed discussions with the patient. During dental hygiene treatment, it is requently the role o the dental hygienist to provide patients with the in ormation necessary to make in ormed decisions about their oral health. One important decision in patient care is how to manage these discussions with a patient prior to treatment. According to the American Dental Hygienists’ Association (ADHA) code o Ethics, a patient has the right to in ormed consent prior to treatment, and they have the right to ull disclosure o all relevant in ormation, so that they can make in ormed choices about their care (1). This makes the patient a critical participant in any plan involving periodontal therapy, and communications with the patient are vital as the treatment plan is developed. Studies demonstrate that patients who believe that they have been well in ormed regarding their condition and who have had their questions answered by members o the dental team are more compliant with treatment recommendations, have a higher trust in their healthcare providers, and are more satis ed with their care. These actors lead to better treatment outcomes and reduced malpractice risk. 1. Informed Consent for Periodontal Treatment. Informed consent is a patient’s voluntary agreement to proposed treatment. A patient can only give in ormed consent to treatment a ter achieving an understanding o the relevant acts, bene ts, and risks involved (2). In ormed consent requires that recommended treatment, alternate treatment options, and the likely consequences o declining treatment have been explained in language understood by the patient. A. What Constitutes Informed Consent? 1. An individual’s consent is in ormed only i the recommended treatment, alternate treatment options, and the bene ts and risks o treatment have been thoroughly described to the person in language understood by the patient (3). 2. In ormed consent must be voluntary, and this in ormed consent originates rom (a) a person’s legal right to direct what happens to his or her body and (b) the ethical duty o the dental healthcare provider to involve the individual in his or her own dental care. 3. In ormed consent is more than simply getting a patient to agree to a procedure or to sign a written consent orm. It is a process o communication between a patient and healthcare provider that allows the patient to make a knowledgeable decision about his or her own dental care. B. What are the Goals of Informed Consent? The most important goal o in ormed consent is to provide an individual an opportunity to be an in ormed participant in healthcare decisions, and it is generally accepted that complete in ormed consent includes a discussion o the ollowing elements: 1. The diagnosis and an explanation o the periodontal condition that warrants the proposed treatment. 2. An explanation o the purpose o the proposed periodontal treatment. 3. A description o the proposed treatment and the individual patient’s role and responsibilities during and a ter periodontal treatment. 4. A discussion o the known risks and bene ts o the proposed periodontal treatment.

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Guidelines for Periodontal Decision Making

5. An assessment o the likelihood that the proposed treatment will accomplish the desired objectives. a. N ote that when discussing treatment outcomes it is important not to appear to guarantee treatment outcomes to the patient. b. Dental healthcare providers should remember that individual patients may well respond di erently to similar treatments. 6. A presentation o alternative treatment options, i any, and the known risks and bene ts o these options. 7. The risks and bene ts o not receiving the proposed periodontal treatment. 8. A discussion o the prognosis (or outcomes expected) i no treatment is provided. 9. A discussion o the actual costs associated with the proposed treatment. 10. Rein orcement o the individual’s right to re use consent to the proposed treatment. a. Keep in mind that patients o ten eel powerless when dealing with healthcare providers. b. To encourage the patient’s voluntary consent, the dental healthcare provider should make it clear to the patient that she or he is participating in a decision, not merely signing a consent orm. 2. Informed Refusal for Periodontal Treatment. Informed refusal is a person’s right to re use all or a portion o the proposed treatment. In ormed re usal requires that recommended treatment, alternate treatment options, and the likely consequences o declining treatment have been explained in language understood by the patient. A patient always has a legal right to re use proposed periodontal care. 3. Obtaining Informed Consent from Patients. The doctrine o in ormed consent reminds dental healthcare providers to respect patients by ully and accurately providing in ormation relevant to their healthcare decisions. The ollowing are some guidelines to use when obtaining in ormed consent rom a patient. A. Use Understandable Language. In ormation should be provided in language that is easily understood by the patient. 1. Use simple, straight orward sentences. 2. Use commonly recognizable terms. 3. Avoid the use o pro essional jargon or technical terms, and explain any terms that may not be readily understood. 4. Use a translator i the patient does not speak English or speaks English with little understanding. B. Provide Opportunities for Patient Questions. An opportunity should be provided or the patient to ask questions. Foster an open exchange o in ormation and encourage the patient to ask questions. Using open-ended and nondirective questions such as those below can simpli y this process. 1. “W hat m ore would you lik e to k now ?” 2. “W hat are your concerns?” 3. “W hat is your nex t question?” C. Assess Patient Understanding. An assessment should be made o the patient’s understanding o in ormation provided. 1. A simple strategy to assess understanding is to let patient know that “many people have di f culty understanding the in ormation that I give them or have questions that they need answered. So, please let’s discuss anything you do not understand.” 2. Another strategy is to make a comment such as: “ M ost o my patients want to ex plain my treatm ent suggestions to another am ily m em ber. W hat additional in orm ation can I give you to help you ex plain this treatm ent to your spouse?”

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4. Legal Responsibilities Related to the Consent Process A. The Dental Hygienist’s Legal Responsibility Related to Consent 1. The dental hygienist has a legal responsibility or the services that he or she provides. Failure to obtain consent rom the patient or services can have serious legal consequences. 2. A patient could claim “ battery” (i.e., unconsented touching) or dental services provided without the patient’s consent. 3. Patients also can claim “ negligence” (i.e., lack o reasonable and prudent care resulting in harm) or ailure to provide su cient in ormation or the patient to make an in ormed decision. This type o negligence also is called malpractice. B. Basic Legal Requirement to Demonstrate Informed Consent. Basic requirements or demonstrating that in ormed consent has been obtained are listed below. I any element were missing, it would indicate that in ormed consent is not complete. • Patient’s periodontal diagnosis presented in language that is easily understood by the patient • Discussion o proposed periodontal treatment and bene ts diagnosis presented in language that is easily understood by the patient • Discussion o the risks and likelihood o success o the proposed periodontal therapy • Discussion o alternative treatments • Documentation that the patient was encouraged to ask questions and that answers were provided in language that is easily understood by the patient • Patient’s signature on the consent orm C. Legal Requirements N ecessary for a Patient to Give Informed Consent. There are certain legal requirements necessary or a patient to give in ormed consent. These legal requirements are listed below. • The patient is ully in ormed (as discussed in point “ B” above). • The patient is o legal age. Legal age is determined by state law—not ederal law—and so may vary rom state to state. Dental healthcare providers should know the legal age or the state in which they practice. • The patient is mentally competent (understands in ormation presented and is able to make a decision about the proposed treatment). • The patient is able to give voluntary consent (without coercion rom care providers, amily members, or others). 5. Format for the Consent Process. The ormat or the consent process may be either verbal or written. Some states have statutes or regulations requiring dentists to secure written in ormed consent rom patients (1). Dentists should ensure that they are amiliar with and in compliance with the in ormed consent laws in their states. A. Written Consent. M ost dental healthcare providers pre er to have the patient sign and date a written consent orm or documentation o the consent process. Figure 10-4 shows an example o a written in ormed consent/in ormed re usal orm. 1. In addition, the written consent document should be signed and dated by the dentist and a witness (generally, another sta member). 2. O nce signed, a written consent document becomes part o the individual’s permanent dental record. B. Verbal Consent. I a written consent document is not used, the patient’s verbal consent should be documented in the patient chart. An example o documentation o verbal consent would be a written entry in the patient’s chart that says, “ D iscussed the diagnosis; purpose, description, benef ts, and risk s o the proposed treatm ent; alternative treatm ent options; the prognosis o no treatm ent; and costs.

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T he patient asked questions and dem onstrated that he understood all in orm ation presented during the discussion. In orm ed consent was obtained or the attached treatm ent plan.”

S a m p le Info rm e d Co ns e nt/ Info rm e d Re fus a l Fo rm

1. I

, (na me) a gre e to the pro pos ed periodontal tre atment by , (na me) RDH. Yes

2. I fully unde rs tand the importanc e of the prop os ed tre atme nt. 3. I und ers ta nd that

No

is the exp ec te d o utc ome of the p rop os e d periodontal treatment.

4. I unde rs tand that the p os s ible ris ks and/or unanticipa te d outc omes of the pro pos ed periodontal . treatme nt are 5. The pos s ible treatment alte rnatives to the prop os ed treatment are

.

6. I have be en informed of the c os ts of the prop os ed a nd a lte rnative treatme nts .

Yes

7. I und e rs ta nd the p os s ible c ons eq ue nc e (s ) of refus al of the prop os e d periodontal treatment is /are . 8. I ha ve the c ap ac ity to c ons e nt to the prop os e d trea tme nt. 9. I refus e the p ropos ed tre atme nt.

Yes

Yes

No

No

10. I am refus ing the propos ed periodontal treatment for the following reas on(s ):

Patie nt Signature

Date

RDH Signature

Witness Signature

F g r 10-4. Sampl in o rm d Co ns nt/ in o rm d R

sal Fo rm o r P r o do ntal T

rap .

No

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S ct o n 4

G d l n s R lat d to t N Ong o ng D c s o n Mak ng

d or

1. The Ongoing N ature of the Decision-Making Process A. Since most patients are monitored or many years or even decades by the members o the dental team, clinical decision making and treatment planning is best described as an ongoing, evolving process over time. B. In addition, the periodontium consists o dynamic and continuously changing tissues (even in the absence o disease), and an individual’s plan or periodontal care requently requires adjustment over time because o these changes. C. The dental team must be aware that a per ectly sensible periodontal diagnosis and plan or therapy at one point in time may require modi cation at a later date, and this act must be communicated to the patient. 2. Applying Principles from the ADPIE N ursing Process to Periodontal Decisions A. Some nurses are trained to use a nursing process re erred to as ADPIE. ADPIE is an acronym or Assess, Diagnose, Plan, Implement, and Evaluate. B. In many ways, the ADPIE nursing process can be a help ul tool or members o the dental team to adopt. The process parallels most o the periodontal decisionmaking principles and underscores the need or constant reevaluation o the results o any therapy provided. C. Table 10-5 outlines the steps in the ADPIE process and shows an example o each step related as it might be related to the management o patients with periodontal disease. D. It can be help ul or members o the dental team to understand the principles o the ADPIE nursing process when dealing with patients with periodontal disease since this process seems to be ideally suited to the kinds o decisions the team must make when dealing with most patients with periodontal conditions.

TAb Le 1 0 -5 . Th e ADPie Nu RSiNG PROCe SS Acro n m

M an ng

e ampl o Parall l n D nt str

a

a ss ss

p

fo m in g

D

Di g n o s

a

ivin g

p

pl n

e s b lis in g

I

Im l m n

p

fo m in g

io d o n

e

e v lu

r

v lu

s ons

co m

n siv

io d o n

l v lu

io d o n

l d i g n o sis o d i g n o s s

m s

l n fo

in g

l

io d o n

l

y by o ny

io d o n

io n

y m mb l

s of y

Table 10-1. ADPIE N ursing Process. Table 10-5 provides an example o how the ADPIE process might be applied to the management o patients with periodontal disease.

C apt r S mmar Stat m nt This chapter outlines guidelines that can be help ul to the members o the dental team during the management o patients with periodontal diseases. These guidelines include those related to arriving at a periodontal diagnosis, periodontal treatment sequencing, consent or treatment, and the need or ongoing decision making.

m o vid d

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171

S ct o n 5

Fo c s o n Pat nts Cl n cal Pat nt Car CA S e

1

Periodontal assessment o a new patient reveals generalized bleeding on probing but very little gingival erythema (redness) and very little gingival edema (swelling). H ow would you answer the rst undamental diagnostic question or this patient?

CA S e

2

Periodontal assessment o a new patient reveals de nite signs o inf ammation in the periodontium. Explain how to answer the second diagnostic question or this patient.

CA S e

3

Periodontal assessment o a new patient reveals localized signs o gingival inf ammation but no attachment loss. The ndings also include a site o gingival recession and toothbrush abrasion on the acial sur ace o a canine tooth. At this site o recession, there is no sign o inf ammation o the gingiva. H ow should this site o gingival recession due to traumatic brushing a ect the basic diagnostic questions?

CA S e

4

Following thorough clinical assessment o the periodontal condition o a patient, you are convinced that the patient has periodontitis. Explain how you would determine the severity o the periodontitis?

e t cal Sc nar o M rs. E is the rst patient o the a ternoon in your periodontal o ce. She is new to the practice. She is a 50-year-old lady who has only lived in the United States or the last 3 years. H er English skills are minimal, but she works as a medical researcher, so you assume that she understands medical terminology. M rs. E has generalized moderate chronic periodontitis with generalized horizontal bone loss on her posterior teeth. You determine that periodontal instrumentation using local anesthesia is indicated. The next phase o treatment will be based on the ndings at the time o the reevaluation, and will be determined by Dr. Evans, one o the periodontists in the o ce.

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You review your dental hygiene treatment plan with her. She asks no questions and signs at the bottom o the consent or treatment orm, on the signature line. You tell her that you will begin the recommended treatment at today’s appointment. You prepare the anesthesia syringe and as you approach M rs. E, she becomes very agitated, screaming and covering her mouth with her hands. She re uses to allow any urther treatment today. She gets up abruptly, and leaves the o ce. 1. What could the hygienist have done di erently, to avoid the above situation? 2. What ethical principles are in conf ict in this dilemma? 3. N ow, that M rs. E’s experience has been a negative one or her; what is the best way to handle this ethical dilemma? 4. What changes might the hygienist make when explaining proposed treatment to uture patients?

R

r nc s

1. Bylaw s and Code o Ethics. Chicago, IL: American Dental H ygienists’ Association; 2009. 2. M cCombs G. Protect yoursel with in ormed consent. D im ensions D ent H yg. 2010;8(11):60–63. 3. S kas PM . A duty to disclose. Issues to consider in securing in ormed consent. J A m D ent A ssoc. 2003;134(10): 1329–1333.

S g g st d R ad ng s SC: Suit or malpractice & lack o consent: directed verdict-malpractice: trial on consent. Fletcher v. M edical University o South Carolina, 4732 SCCA (9/1/2010)-SC. N urs L aw R egan R ep. 2011;51(8):3. Baker JN , Leek AC, Salas H S, et al. Suggestions rom adolescents, young adults, and parents or improving in ormed consent in phase 1 pediatric oncology trials. Cancer. 2013;119(23):4154–4161. Brands WG, van der Ven JM , Brands-Bottema GW. [Dental and health law 4. The treatment o minors and o adults who are unable to give in ormed consent]. N ed Tijdschr Tandheelk d. 2013;120(7–8):394–398. Brands WG, van der Ven JM , Eijkman M A. [Dentistry and healthcare legislation 3: in ormed consent]. N ed Tijdschr Tandheelk d. 2013;120(6):327–332. Coulter A. International standards on in ormed patient consent are available. BM J. 2013;347: 5454. Eyal N . In ormed consent, the value o trust, and hedons. J M ed Ethics. 2014;40(7):447. Fullbrook S, Sanders K. Consent and capacity 2: the M ental Capacity Act 2005 and ‘living wills’. Br J N urs. 2007;16(8): 474–475. Glick M . In ormed consent: a delicate balance. J A m D ent A ssoc. 2006;137(8):1060. Govan P. Dental ethics case 5. Child consent and the Children’s Act (2005) as amended. SA D J. 2010;65(8):382. Greco PM . In ormed consent or in ormed re usal? A m J O rthod D ento acial O rthop. 2013;143(5):598. H odgson J, M endenhall T, Lamson A. Patient and provider relationships: consent, con dentiality, and managing mistakes in integrated primary care settings. Fam Syst H ealth. 2013;31(1):28–40. H udgins C, Rose S, Fi eld PY, et al. N avigating the legal and ethical oundations o in ormed consent and con dentiality in integrated primary care. Fam Syst H ealth. 2013;31(1):9–19. Ingravallo F, Gilmore E, Vignatelli L, et al. Factors associated with nurses’ opinions and practices regarding in ormation and consent. N urs Ethics. 2014;21(3):299–313. Jenkins VA, Anderson JL, Fallow eld LJ. Communication and in ormed consent in phase 1 trials: a review o the literature rom January 2005 to July 2009. Support Care Cancer. 2010;18(9):1115–1121. Lamont S, Jeon YH , Chiarella M . Assessing patient capacity to consent to treatment: an integrative review o instruments and tools. J Clin N urs. 2013;22(17–18):2387–2403. Lamont S, Jeon YH , Chiarella M . H ealth-care pro essionals’ knowledge, attitudes and behaviours relating to patient capacity to consent to treatment: an integrative review. N urs Ethics. 2013;20(6):684–707. M cQ uoid M ason D. Provisions or consent by children to medical treatment and surgical operations, and duties to report child and aged persons abuse: 1 April 2010. S A r M ed J. 2010;100(10):646–648. N ijhawan LP, Janodia M D, M uddukrishna BS, et al. In ormed consent: issues and challenges. J A dv Pharm Technol R es. 2013;4(3):134–140. Paasche-O rlow M K, Brancati FL, Taylor H A, et al. Readability o consent orm templates: a second look. IR B. 2013;35(4):12–19. Rait JL. In ormed consent in 2012. Clin Ex perim ent O phthalm ol. 2012;40(9):835–837. Richardson V. Patient comprehension o in ormed consent. J Perioper Pract. 2013;23(1–2):26–30. Robertson CG, Verco CJ. The quality o consent - what is the evidence? A ust N Z J O bstet G ynaecol. 2013;53(5):502–504. Sand K, Eik-N es N L, Loge JH . Readability o in ormed consent documents (1987–2007) or clinical trials: a linguistic analysis. J Em pir R es H um R es Ethics. 2012;7(4):67–78.

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Stoopler ET. The importance o in ormed consent. J Can D ent A ssoc. 2013;79:d81. Taylor JS. Introduction: children and consent to treatment. H EC Forum . 2013;25(4):285–287. Toumba KJ. Children and consent/assent to treatment. Eur A rch Paediatr D ent. 2013;14(4):195–196.

STu De NT ANCiLLARy Re SOu RCe S A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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11

Et o lo c Facto rs: R sk fo r Pe r o do t t s

Se ct o

1

R sk Facto rs fo r Pe r o do tal D se ase

175

Se ct o

2

Bala ce Be tw e e

177

Pe r o do tal He alth a d D se ase

Biologic Equilibrium Periodontal Risk Assessment

Se ct o

3

Fo c s o

Pat e ts

185

Ethical Dilemma Clinical Patient Care

Cl

cal Appl cat o .

It is always a challenge to explain why periodontal disease a ects some patients while others seem so resistant to its development. This chapter organizes in ormation about the risk actors or periodontal disease, in ormation about the biologic equilibrium involved with this disease, and the possible alterations to this equilibrium that can help clari y this perplexing issue. This in ormation is use ul when developing recommendations or a course o treatment or patients with periodontal diseases, as well as, when explaining the nature o these diseases to patients and other healthcare providers.

Le ar

Obje ct ve s

• Def ne the term biologic equilibrium and discuss actors that can disrupt the balance between health and disease in the periodontium. • Def ne and give examples o the term “ contributing risk actors.” • Discuss the importance o a periodontal risk assessment in periodontal treatment planning. • For a patient in your care with periodontitis, explain to your clinical instructor the actors that may have contributed to your patient’s disease progression.

Ke Te rms Multi actorial etiology Biologic equilibrium

Homeostasis Risk Assessment

Chapte r 11

Se ct o

Etiologic Factors: Risk or Periodontitis

175

1

R sk Facto rs fo r Pe r o do tal D se ase Research studies have clearly demonstrated that periodontal disease is a bacterial in ection o the periodontium and that bacteria are the primary etiologic agents in the initiation o periodontal disease (1–4). The presence o pathogenic bacteria, however, does not necessarily mean that an individual will experience periodontitis. Periodontitis has a multi actorial etiology, that is, periodontitis is a disease that results rom the interaction o many actors (Fig. 11-1). Some persons with abundant bio lm exhibit only mild disease while others with sparse amounts o bio lm su er severe disease. Untreated gingivitis does not always lead to periodontitis and everyone in ected with periodontal pathogens does not experience periodontitis. These ndings suggest that additional actors, other than the mere presence o bacteria, must play a signi cant role in determining why some individuals are more susceptible to periodontal disease than others (1,2,4–15). M any contributing actors help to determine the initiation and progression o periodontal disease. Table 11-1 lists some risk actors that may be involved in the etiology o periodontitis. Contributing etiologic actors negatively inf uence the periodontium as well as the host immune response. It is critical or the dental team to recognize contributing actors or periodontal disease during a periodontal assessment. Whenever possible, the dental team should eliminate or minimize the impact o contributing actors during the nonsurgical periodontal treatment (Table 11-2).

He re d ity - Immune d e c ie nc y - Ge ne tic s ynd rome s

Sys te m ic d is e a s e - Diabetes Me d ic a tio ns

P e rio d o nta l p a tho g e ns Actinobacillus actinomycetemcomitans Tannerella forsythia Porphyromonas gingivalis

P e rio d o ntitis

-

-

Ha b its Self-care (plaque control) Profes s ional care (recall) Smoking Alcohol Diet

So c ia l a tm o s p he re Family, upbringing Culture Socioeconomic factors Acces s to dental care Dental ins urance

F re 11-1. R sk Facto rs fo r Pe r o do tal D se ase . Periodontitis has a multi actorial etiology. Additional actors—other than the presence o bacteria—play a signi icant role in determining why some individuals are more susceptible to periodontal disease than others.

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TABLE 1 1 -1 . RiSK FACTORS FOR PERiODOn TAL DiSEASE

TABLE 1 1 -2 . MAn Ag EMEn T OF RiSK FACTORS

Po o r Se lf-Care pl q u b io film C lcu lu s d o si s

Po o r Se lf-Care Im o v d b io film co n o l F qu n o f ssio n l c

Fa lt De t str Ov ngs Su b g in g iv l m

Fa lt De t str Co c iv d n is y g in s

Smo k / To bacco F q u n cy Cu n is o y p s is o y n tr t o Di ig in f s fo o d s, ju n k fo o d s Me d cat o s Dil n in C lciu m c n n l b lo ck s Cyclo s o in D u g s kn o w n o c u s x o s o m i

Smo k / To bacco C ss io n co u n s lin g C mo u ics n tr t o Di ig

in f u i s/v g

Me d cat o s C n g m d ic io n s Wo k w i ysici n Go o d d ily s lf-c F qu n o f ssio n l c

D abe te s Du io n po o g lyc m ic co n o l

D abe te s Go o d g lyc m ic co n o l Wo k w i ysici n Go o d d ily s lf-c F qu n o f ssio n l c

Ho rmo al Var at o s pu b y p g n n cy M no us

Ho rmo al Var at o s Go o d d ily s lf-c F qu n o f ssio n l c C mo u ics

He re d t F m ily is o y G n ic s in g

He re d t C mo F qu n

imm o co mpro m se d N u o n i ( b n o m lly lo w l v ls o f

imm o co mpro m se d Co n su l w i ysici n C mo u ics

n u o

ils)

u ics o f ssio n l c

bl s

Chapte r 11

Se ct o

2

Bala ce Be tw e e

Etiologic Factors: Risk or Periodontitis

Pe r o do tal He alth a d D se ase

Bio l o g ic Eq u il iBr iu m 1. Biologic Equilibrium. The human body is continually working to maintain a state o balance in the internal environment o the body, known as biologic equilibrium or homeostasis. A. Periodontal Health 1. In the oral cavity, most o the time, things are in a state o balance between the bio lm bacteria and the host. 2. For the periodontium to remain healthy, the bacterial challenge must be contained at a level that can be tolerated by the host (2). 3. The situation can be thought o as a balance scale, with the disease-promoting actors on one side o the scale and the health-promoting actors on the other (Fig. 11-2). As long as the two sides o the scale are in balance, there will be no disease progression. B. Periodontal Disease 1. The intermittent pattern o disease activity seen in periodontitis is believed to result rom the changing balance between the pathogenic bacteria and the host’s inf ammatory and immune responses. 2. This balance also can be a ected by other risk actors, such as local or systemic variables. 2. The Delicate Balance Between Health and Disease. When active periodontal disease sites are present in the mouth, the goal is to return the oral cavity to a state o biologic equilibrium.

Reduction of ris k factors

Ris k factors (e.g., genetics , s moking, diabetes ) Overproduction of proin ammatory or des tructive mediators and enzymes (e.g., IL-1, IL-6, PGE2, TNF-α , MMPs ) Underactivity or overactivity of as pects of hos t res pons e Poor compliance Poor bio lm control

Dis e a s e

Subgingival bio lm

Expres s ion of hos t-derived anti-in ammatory or protective mediators and enzymes (e.g., IL-1, IL-6, PGE2, TNF-α , MMPs ) Hos t modulation therapy

Res olution of in ammation

OHI, perio. ins trumentation, s urgery, chemical agents to reduce bacterial challenge

He a lth

F re 11-2. Pe r o do tal Eq l br m. Equilibrium occurs when there is a balance between diseasepromoting actors and health-promoting actors.

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A. Periodontal Equilibrium and Dental Plaque Biof lm 1. Experienced dental hygienists will attest to the act that major di erences exist in the way that individuals respond to the plaque bio lm. a. M any patients return to the dental o ce year a ter year with generalized plaque bio lm. These patients exhibit gingivitis and yet, year a ter year, show no clinical signs o progression to periodontitis. For some reason, in these individuals, gingivitis never progresses to periodontitis. Perhaps these individuals have no systemic or acquired risk actors that add stress to the biologic equilibrium. Basically, i an individual’s immune system can e ectively deal with a mouth ul o periodontal pathogens, there will be no destructive periodontal disease (Fig. 11-3). b. In a ew individuals, gingivitis progresses to periodontitis. It is theorized that in these individuals the body’s immune response (host response) is responsible or the tissue destruction seen in periodontitis (Fig. 11-4). In addition, some individual possess systemic risk actors (such as genetic variables or systemic disease) that signi cantly increase their susceptibility to periodontitis (13). 2. There are many patients who are unable or unwilling to per orm the thorough sel -care necessary to control plaque bio lm. For these patients, it is necessary to increase the requency o pro essional care to compensate or the inadequate level o sel -care. Pro essional care at requent intervals can be e ective in restoring the balance between health and disease (Fig. 11-5).

Bio film

Ris k fac to rs

Immune re s po ns e Pro fe s s io nal Se lf-c are c a re HEALTH FACTORS

DIS EAS E FACTORS

F re 11-3. g vts the Pre se ce o f Plaq e B o f lms. In individuals with a low susceptibility to periodontitis, gingivitis may never progress to periodontitis.

Ho s t re s po ns e

Bio film

S e lf- c a re Pro fe s s io nal c a re HEALTH FACTORS

Ris k fa c to rs

DIS EAS E FACTORS

F re 11-4. Pe r o do t t s the Pre se ce o f Plaq e B o f lm. In susceptible individuals, the body’s immune response (host response) results in damage to the periodontal tissues and progression rom gingivitis to periodontitis.

Chapte r 11

Bio film

Ris k fac to rs

Se lf-c are

Etiologic Factors: Risk or Periodontitis

179

Pro fe s s io nal c are

HEALTH FACTORS

DIS EAS E FACTORS

F re 11-5. Fre q e t Pro fe ss o al Care . An individual who is unwilling or unable to obtain adequate bio ilm control on a daily basis. More requent periodontal instrumentation can help to control the development o mature plaque bio ilms.

S m o king

Bio film

Ris k fa c to rs

DIS EAS E FACTORS

s io nal S e lf-c a re Pro fec as re HEALTH FACTORS

F re 11-6. El m at a S ste m c R sk Facto r. Smoking cessation, combined with adequate sel -care and pro essional care, restores the balance.

B. Local Contributing Factors 1. It is possible to totally eliminate a local risk actor in many cases. A aulty restoration is a good example o a local actor that can be corrected, restoring the balance between local disease-promoting and health-promoting actors at the site. 2. In other cases, it is possible to compensate or a local risk actor by improving the patient’s sel -care and/or increasing the requency o pro essional care. For example, the patient may need to use tu ted dental f oss to clean around the abutment teeth o a xed bridge. This situation can be compared to adding more weight on the health side o the balance scale to equal or exceed the weight on the disease side o the scale. C. Systemic or Genetic Contributing Factors 1. Certain systemic or acquired risk actors are possible to control or eliminate i the patient is willing to do so (14). For example, the individual can work with a physician to keep diabetes well controlled. A smoker may decide to stop smoking. In both cases the individual has made a change that is health promoting, both systemically and or the periodontium (Fig. 11-6). 2. In the case o a contributing risk actor that cannot be controlled, it is necessary to add weight to the health side o the scale. For example, some individuals have a genetic risk actor—such as abnormal neutrophil unction— that causes them to be susceptible to severe periodontitis. At the present time, we are unable to eliminate or control genetic risk actors. It is possible, however, to assist the patient in maintaining health by increasing the extent o pro essional care. Frequent pro essional care will increase the weight on the health side o the scale (Fig. 11-7).

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S e lf- c a re Ge ne tic ris k fa c to rs Bio film

AntiPro fe s s io nal mic ro bials c are HEALTH FACTORS

DIS EAS E FACTORS

F re 11-7. Ma a e me t o f a g e e t c R sk Facto r. At the present time, there are some risk actors that cannot be eliminated or controlled. Pro essional care can help slow disease progression.

PEr io d o n t a l r is k a s s Es s m En t Dental healthcare providers are interested not only in diagnosing and treating periodontal disease but also in predicting which individuals are more likely to develop periodontitis. The process o identi ying risk actors that increase an individual’s probability o disease is called risk assessment (8,16–19). The American Academy o Periodontology (AAP) describes the risk assessment process as “ increasingly important in periodontal treatment planning and should be part o every comprehensive dental and periodontal evaluation” (16). It is becoming possible to consider an individual’s risk actors or periodontal disease (systemic disease, genetic in ormation, personal habits, and characteristics) and to classi y patients into high- or low-risk groups (19). For example, individuals who smoke have a higher risk o periodontitis than nonsmokers (12). Clinicians also use the risk assessment process to prevent disease (such as, identi ying smokers and o ering smoking cessation counseling). In ormation concerning individual risk or developing periodontal disease is obtained through care ul evaluation o the individual’s demographic data, medical history, dental history, and comprehensive periodontal clinical examination (Table 11-3). Risk assessment questionnaires are practical tools that can be help ul in identi ying individuals who are at a high risk or periodontal disease (19). Figure 11-8A,B shows an example o a simple two-page periodontal risk questionnaire that can elicit the presence o common periodontal risk actors. Dental hygienists can use risk questionnaires to initiate discussion with patients about periodontal risk actors.

Chapte r 11

Etiologic Factors: Risk or Periodontitis

181

TABLE 1 1 -3 . CLin iCAL RiSK ASSESSMEn T FOR PERiODOn TAL DiSEASE De mo raph c Data

ag Du

io n o f x o su

S lf-c

o co n ib u in g isk f c o s

( l q u co n o l)

F q u n cy o f

o f ssio n l c

M l g nd D n

l w

n ss

So cio co n o m ic s Me d cal H sto r

us

t o b cco u s Di b

s

Os o o o sis h IV/a IDS G n De tal H sto r

ic

d is o si io n o g g

F q u n cy o f

Cl

cal Exam at o

s

o f ssio n l c

F m ily is o y o f p

ssiv d is

ly o o

vio u s is o y o f

lo ss

io d o n

l d is

s

pl q u b io film ccu m u l io n n d m ic o b i l co m o si io n C lcu lu s d Bl

o si s

d in g o n

o b in g

Lo ss o f

c m n

pl q u

n iv

an

s

o m ic co n ib u in g f c o s

r so

iv co n ib u in g f c o s

182

Part 3

Risk Factors or Periodontal Diseases

Do yo u no w o r have yo u e ve r us e d the fo llo wing ? Am ount p e r d a y?

How m a ny ye a rs ?

If you q uit, wha t ye a r?

Cig a re tte Cig a r

Tob a c c o us e is the m os t s ignific a nt ris k fa c tor for gum d is e a s e .

P ip e Ch e w S n u ff

Do yo u have any o the r ris k fac to rs fo r he art dis e as e o r s tro ke ?

Untre a te d gum d is e a s e c a n inc re a s e your ris k for heart attack and stroke.

Fa m ily h is to ry o f h e a rt d is e a s e

To b a c c o us e

Hig h c h o le s te ro l

Hig h b lo o d p re s s u re

If yo u h a ve a n y o f th e s e o th e r ris k fa c to rs it is e s p e c ia lly im p o rta n t fo r yo u to a lwa ys ke e p yo u r g u m s a s h e a lth y a n d in fla m m a tio n fre e a s p o s s ib le to re d uc e yo u r o ve ra ll ris k fo r he a rt a tta c k a n d s tro ke .

Have yo u e ve r take n any o f the fo llo wing me dic atio ns ? Dila n tin a ntis e izu re m e d ic a tio n

A s id e e ffe c t of s om e m e d ic a tions c a n c a us e c ha nge s in your gum s .

Ca lc iu m c h a n ne l b lo c ke r b lo o d p re s s ure m e d ic in e (s u c h a s P ro c a rd ia , Ca rd ize m , No rva s c , Ve ra p a m il, e tc .) Cyc lo s p o rin im m un o s u p p re s s a n t th e ra p y

Has anyo ne o n yo ur s ide o f the family had g um pro ble ms (e .g ., yo ur mo the r, fathe r, o r s ibling s )? Ye s

The te nd e nc y for gum d is e a s e to d e ve lop c a n b e inhe rite d .

No

Has anyo ne in yo ur imme diate family be e n te s te d o r tre ate d fo r g um pro ble ms ? If s o , who m? S p o us e

The b a c te ria , whic h c a us e gum d is e a s e m a y b e s p re a d to othe r fa m ily m e m b e rs .

Child re n

The fo llo wing c an adve rs e ly affe c t yo ur g ums . Ple as e c he c k all that apply P re g n a n t

Nu rs in g

Os te o p o ro s is

Ta kin g b irth c o ntro l p ills

Fe m a le s c a n b e a t inc re a s e d ris k for gum d is e a s e a t d iffe re nt p oints in the ir life .

Ta kin g h o rm o n e s up p le m e n ts In fre q u e n t c a re d u rin g p re vio u s p re g n a n c ie s o ve r

A

F re 11-8A. S de 1 o f Pe r o do tal R sk Q e st o a re . Risk assessment questionnaires are practical tools that can be help ul in identi ying individuals who have a high susceptibility to periodontitis. Side one o a risk assessment questionnaire is shown here. See Figure 11-8B or side two o this questionnaire. (Courtesy o Timothy G. Donley, DDS, MSD, Bowling Green, KY.)

Chapte r 11

Etiologic Factors: Risk or Periodontitis

If yo u ARE diabe tic ... Fo r ho w m a n y ye a rs ? Ye s

Is yo u r d ia b e te s we ll c o n tro lle d ?

No

Wh o is yo u r p h ys ic ia n fo r d ia b e te s ?

Gu m d is e a s e is a c o m m o n c o m p lic a tio n o f d ia b e te s . Un tre a te d g um d is e a s e m a ke s it m o re d iffic u lt fo r in d ivid ua ls with d ia b e te s to c o n tro l th e ir b lo o d s u g a r.

If yo u ARE NOT diabe tic ... An y fa m ily h is to ry o f d ia b e te s ?

Ye s

No

Ha ve yo u h a d a n y o f th e s e wa rn ing s ig n s o f d ia b e te s ? Fre q u e n t urina tio n

Exc e s s ive th irs t

Exc e s s ive h u ng e r

Tin g lin g o r nu m b n e s s in e xtre m itie s

We a kne s s a n d fa tig u e

S lo w he a lin g o f c u ts

Un e xp la in e d we ig h t lo s s

An y c ha ng e o f vis io n

Do yo u have a he art m urm ur o r a rtific ia l jo int? Ye s

No

If s o , do e s yo ur phys ic ian re c o m me nd antibio tic s Ye s No prio r to de ntal vis its ? With the s lighte s t a m ount of gum infla m m a tion, b a c te ria from the m outh c a n e nte r the b lood s tre a m a nd c a us e a s e rious infe c tion of the he a rt m us c le or your a rtific ia l joint.

Na m e o f p h ys ic ia n : It is e s p e c ia lly im p o rta n t in yo u r c a s e to a lwa ys ke e p yo ur g u m s a s h e a lthy a n d in fla m m a tio n fre e a s p o s s ib le to re d u c e th e c h a n c e o f b a c te ria l in fe c tio n o rig in a ting in th e m o u th.

Have yo u be e n tre ate d fo r ulc e rs ? Ye s

No

Is the ulc e r a c tive no w ? When your gum s are inflamed, bacteria from the mouth can travel to the gut and cause ulcers to become active.

Ye s

No

Ulce rs a re ca used by bac teria . If yo u ha ve b e e n tre a te d fo r u lc e rs yo u s h o u ld m a ke s u re yo u r g u m s a re a s in fla m m a tio n fre e a s p o s s ib le .

Have yo u no tic e d any o f the fo llo w ing s ig ns o f g um dis e as e ? Ble e d in g g u m s d u rin g to o th b rus h ing

P u s b e twe e n the te e th a n d g u m s

Re d , s wo lle n , o r te n d e r g u m s

Lo o s e o r s e p a ra tin g te e th

Gu m s th a t ha ve p u lle d a wa y fro m the te e th

Ch a n g e in th e wa y yo u r te e th fit to g e th e r

P e rs is te nt b a d b re a th

Fo o d c a tc h in g b e twe e n te e th

Ye s Is it impo rta nt to yo u to ke e p yo ur te e th a s lo ng a s po s s ible ? Any pa rtic ular re a s o n w hy mis s ing te e th ha ve no t be e n re plac e d? Ye s No Do yo u like the appe aranc e o f yo ur s mile ? Ye s Do yo u like the c o lo r o f yo ur te e th? No Do yo ur te e th ke e p yo u fro m e ating any s pe c ific fo o d?

Ye s

No

No

B

F re 11-8B. S de 2 o f Pe r o do tal R sk Q e st o a re . Side 2 o a two-page risk assessment questionnaire. (Courtesy o Timothy G. Donley, DDS, MSD, Bowling Green, KY.)

183

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Chapte r S mmar State me t In the oral cavity, most o the time, things are in a state o balance between the bacteria in plaque bio lms and the host. • For the periodontium to remain healthy, the bacterial challenge must be contained at a level that can be tolerated by the host. • The situation can be thought o as a balance scale, with the disease-promoting actors on one side o the scale and the health-promoting actors on the other. • As long as the two sides o the scale are in balance, there will be no disease progression. • The intermittent pattern o disease activity seen in periodontitis is believed to result rom the changing balance between the pathogenic bacteria and the host’s inf ammatory and immune responses. Periodontal disease is a bacterial in ection o the periodontium. The presence o pathogenic bacteria, however, does not necessarily mean that an individual will experience periodontitis. • Additional actors play a role in determining why some individuals are more susceptible to periodontitis than others. • Contributing actors are actors that increase an individual’s susceptibility to periodontitis by modi ying the host response to bacterial in ection. • Contributing actors such as systemic disease, smoking, and genetic actors can play a signi cant role in determining the onset and progression o periodontitis. Thorough daily sel -care (plaque control) by the patient and routine pro essional care are the best methods or prevention o periodontal disease. O ther risk actors must be evaluated, however, to develop the best treatment plan or each individual.

Chapte r 11

Se ct o

3

Fo c s o

Etiologic Factors: Risk or Periodontitis

185

Pat e ts

Eth cal D le mma Your rst patient on M onday morning is Joyce Robbins. She is new to your practice. She has lled out a Periodontal Assessment Q uestionnaire to assist you in determining her risk assessment. She states that she has never lled one out be ore, and is concerned that she has received poor quality dental work as a result. As she enters your operatory, you notice that she is a very petite, well-dressed woman. H er medical history and Periodontal Assessment Q uestionnaire reveal the ollowing: Joyce is a 58-year-old college pro essor. She has stage 1 hypertension, and takes 20 mg o Lisinopril daily as a result. She has a amily history o cardiac disease ( rom both her mother and ather), and her ather developed type II diabetes at age 50. She takes Simvastatin or high cholesterol. She is a borderline diabetic, and her blood sugar levels have been rising at each primary care visit. She su ers rom osteoporosis o the spine and hip. She is presently a nonsmoker but did smoke while she was in college. H er oral exam and radiographs reveal that she has generalized slight recession, generalized horizontal bone loss, generalized 3-mm pockets, with some 4- and 5-mm pockets on the posterior teeth, little plaque bio lm, but generalized slight to moderate supragingival and subgingival calculus deposits. She f osses daily but hasn’t had her teeth cleaned in 5 years. She requently gets ood stuck between her teeth, and is increasingly becoming concerned about “ the way her teeth look and eel.” She wants to know what she can do to maintain her “ pretty smile,” and why no other o ce was as thorough with her care. 1. 2. 3. 4.

Cl

What do you think have may caused the patient’s generalized recession? What actors may have contributed to the patient’s disease progression? H ow will you discuss the balance between periodontal health and disease? Is there an ethical dilemma involved?

cal Pat e t Care CA S E 1 M r. Archie N ewcomer is a new patient in your dental o ce. M r. N ewcomer is 35 years o age and reports that this is his rst dental checkup in 5 or 6 years. Mr. Newcomer’s completed Periodontal Assessment Q uestionnaire is shown in Figure 11-9A,B on the next two pages of this module. Review M r. N ewcomer’s questionnaire, make a list o periodontal risk actors, and suggest strategies or managing these risk actors.

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QUESTIONNAIRE

Do yo u no w o r have yo u e ve r us e d the fo llo wing ? Am ount p e r d a y?

How m a ny ye a rs ?

If you q uit, wha t ye a r?

X Cig a re tte Cig a r

Tob a c c o us e is the m os t s ignific a nt ris k fa c tor for gum d is e a s e .

P ip e Ch e w S n uff

Do yo u have any o the r ris k fac to rs fo r he art dis e as e o r s tro ke ? Fa m ily his to ry o f he a rt d is e a s e Hig h c ho le s te ro l

Untre a te d gum d is e a s e c a n inc re a s e your ris k for heart attack and stroke.

X To b a c c o u s e Hig h b lo o d p re s s ure

If yo u h a ve a n y o f th e s e o th e r ris k fa c to rs it is e s p e c ia lly im p o rta n t fo r yo u to a lwa ys ke e p yo u r g u m s a s h e a lth y a n d in fla m m a tio n fre e a s p o s s ib le to re d u c e yo u r o ve ra ll ris k fo r h e a rt a tta c k a n d s tro ke .

Have yo u e ve r take n any o f the fo llo wing me dic atio ns ? Dila ntin a ntis e izure m e d ic a tio n

A s id e e ffe c t of s om e m e d ic a tions c a n c a us e c ha nge s in your gum s .

Ca lc iu m c h a nn e l b lo c ke r b lo o d p re s s ure m e d ic in e (s u c h a s P ro c a rd ia , Ca rd ize m , No rva s c , Ve ra p a m il, e tc .) Cyc lo s p o rin im m u no s up p re s s a nt the ra p y

Has anyo ne o n yo ur s ide o f the family had g um pro ble ms (e .g ., yo ur mo the r, fathe r, o r s ibling s )? X Ye s

The te nd e nc y for gum d is e a s e to d e ve lop c a n b e inhe rite d .

No

Has anyo ne in yo ur imme diate family be e n te s te d o r tre ate d fo r g um pro ble ms ? If s o , who m? X Sp ous e

The b a c te ria , whic h c a us e gum d is e a s e m a y b e s p re a d to othe r fa m ily m e m b e rs .

Ch ild re n

The fo llo wing c an adve rs e ly affe c t yo ur g ums . Ple as e c he c k all that apply P re g na nt

Nurs in g

Os te o p o ro s is

Ta kin g b irth c o n tro l p ills

Fe m a le s c a n b e a t inc re a s e d ris k for gum d is e a s e a t d iffe re nt p oints in the ir life .

Ta kin g h o rm o n e s u p p le m e n ts In fre q u e n t c a re d u rin g p re vio u s p re g n a n c ie s o ve r

A

F

re 11-9A. Pa e 1 o f Mr. n e w co me r’s R sk Q e st o

a re .

Chapte r 11

Etiologic Factors: Risk or Periodontitis

If yo u ARE diabe tic ... Fo r ho w m a ny ye a rs ? Is yo ur d ia b e te s we ll c o n tro lle d ?

Gum d is e a s e is a c o m m o n c o m p lic a tio n o f d ia b e te s . Untre a te d g u m d is e a s e m a ke s it m o re d iffic ult fo r in d ivid ua ls with d ia b e te s to c o n tro l the ir b lo o d s ug a r.

X Ye s

No

Wh o is yo u r p h ys ic ia n fo r d ia b e te s ?

If yo u ARE NOT diabe tic ... An y fa m ily his to ry o f d ia b e te s ?

Ye s

No

Ha ve yo u h a d a n y o f the s e wa rnin g s ig ns o f d ia b e te s ? Fre q u e n t u rin a tio n

Exc e s s ive th irs t

Exc e s s ive h u n g e r

Tin g ling o r n u m b ne s s in e xtre m itie s

We a kn e s s a n d fa tig u e

S lo w h e a lin g o f c uts

Une xp la ine d we ig h t lo s s

An y c h a n g e o f vis io n

Do yo u ha ve a he art m urmur o r artific ial jo int? Ye s

X No

If s o , do e s yo ur phys ic ia n re c o mm e nd a ntibio tic s Ye s No prio r to de nta l vis its ? With the s lighte s t a m ount of gum infla m m a tion, b a c te ria from the m outh c a n e nte r the b lood s tre a m a nd c a us e a s e rious infe c tion of the he a rt m us c le or your a rtific ia l joint.

Na m e o f p h ys ic ia n : It is e s p e c ia lly im p o rta n t in yo u r c a s e to a lwa ys ke e p yo u r g um s a s h e a lthy a n d in fla m m a tio n fre e a s p o s s ib le to re d u c e th e c h a n c e o f b a c te ria l in fe c tio n o rig ina tin g in th e m o u th .

Ha ve yo u be e n tre ate d fo r ulc e rs ? Ye s

X No

Is the ulc e r ac tive no w ? When your gums are inflamed, bacteria from the mouth can travel to the gut and cause ulcers to becom e active.

Ye s

No

Ulc ers are c ause d b y ba cte ria. If yo u h a ve b e e n tre a te d fo r u lc e rs yo u s h o uld m a ke s u re yo ur g u m s a re a s in fla m m a tio n fre e a s p o s s ib le .

Ha ve yo u no tic e d any o f the fo llo w ing s ig ns o f g um dis e as e ? X Ble e d in g g u m s d u rin g to o th b ru s hing

P u s b e twe e n th e te e th a n d g um s

Re d , s wo lle n , o r te n d e r g um s

Lo o s e o r s e p a ra tin g te e th

Gu m s th a t h a ve p u lle d a wa y fro m the te e th

Ch a n g e in the wa y yo u r te e th fit to g e th e r

P e rs is te n t b a d b re a th

X Fo o d c a tc h in g b e twe e n te e th

Ye s Is it im po rtant to yo u to ke e p yo ur te e th as lo ng as po s s ible ? Any partic ula r re as o n w hy m is s ing te e th have no t be e n re plac e d? No Do yo u like the appe a ranc e o f yo ur s m ile ? X Ye s Do yo u like the c o lo r o f yo ur te e th? X Ye s No Do yo ur te e th ke e p yo u fro m e a ting a ny s pe c ific fo o d?

B

F

re 11-9B. Pa e 2 o f Mr. n e w co me r’s R sk Q e st o

a re .

Ye s

X No

No

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Re fe re ce s 1. Armitage GC. Learned and unlearned concepts in periodontal diagnostics: a 50-year perspective. Periodontol 2000. 2013;62(1):20–36. 2. Bartold PM , Van Dyke TE. Periodontitis: a host-mediated disruption o microbial homeostasis. Unlearning learned concepts. Periodontol 2000. 2013;62(1):203–217. 3. Dick DS, Shaw JR. The in ectious and transmissible nature o the periodontal syndrome o the rice rat. A rch O ral Biol. 1966;11(11):1095–1108. 4. Wade WG. The oral microbiome in health and disease. Pharm acol R es. 2013;69(1):137–143. 5. Berezow AB, Darveau RP. M icrobial shi t and periodontitis. Periodontol 2000. 2011;55(1):36–47. 6. Cullinan M P, Seymour GJ. Understanding risk or periodontal disease. A nn R A ustralas Coll D ent Surg. 2010;20:86–87. 7. Ebersole JL, Dawson DR 3rd, M or ord LA, et al. Periodontal disease immunology: ‘double indemnity’ in protecting the host. Periodontol 2000. 2013;62(1):163–202. 8. Genco RJ, Borgnakke WS. Risk actors or periodontal disease. Periodontol 2000. 2013;62(1):59–94. 9. H ajishengallis G, Lamont RJ. Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model o periodontal disease etiology. M ol O ral M icrobiol. 2012;27(6):409–419. 10. M arsh PD, Devine DA. H ow is the development o dental bio lms inf uenced by the host? J Clin Periodontol. 2011;38 (suppl 11):28–35. 11. M arsh PD, M oter A, Devine DA. Dental plaque bio lms: communities, conf ict and control. Periodontol 2000. 2011;55(1):16–35. 12. M atthews JB, Chen FM , M ilward M R, et al. E ect o nicotine, cotinine and cigarette smoke extract on the neutrophil respiratory burst. J Clin Periodontol. 2011;38(3):208–218. 13. M ealey BL, O campo GL. Diabetes mellitus and periodontal disease. Periodontol 2000. 2007;44:127–153. 14. M ichalowicz BS, Diehl SR, Gunsolley JC, et al. Evidence o a substantial genetic basis or risk o adult periodontitis. J Periodontol. 2000;71(11):1699–1707. 15. Peruzzo DC, Benatti BB, Ambrosano GM , et al. A systematic review o stress and psychological actors as possible risk actors or periodontal disease. J Periodontol. 2007;78(8):1491–1504. 16. American Academy o Periodontology. American Academy o Periodontology statement on risk assessment. J Periodontol. 2008;79(2):202. 17. Douglass CW. Risk assessment and management o periodontal disease. J A m D ent A ssoc. 2006;137 Suppl:27S–32S. 18. Koshi E, Rajesh S, Koshi P, et al. Risk assessment or periodontal disease. J Indian Soc Periodontol. 2012;16(3):324–328. 19. Thyvalikakath TP, Padman R, Gupta S. An integrated risk assessment tool or team-based periodontal disease management. Stud H ealth Technol Inform . 2013;192:1150.

STu DEn T An CiLLARy RESOu RCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

r e t p a h C

12 Se ctio n 1

Oral Bio f lms and Pe rio do ntal In e ctio ns Bacte rial Bio f lms

191

Characteristics o Bacteria Bacterial Communities

Se ctio n 2

The Str ct re and Co lo nizatio n o De ntal Plaq e Bio f lms

194

Species Capable o Colonizing the Mouth The Complex Structure o Dental Plaque Bio lms Bacterial Colonization and Succession

Se ctio n 3

Co ntro l o Plaq e Bio f lms

203

Se ctio n 4

The Ro le o Bacte ria in Pe rio do ntitis

204

Changing Evidence or the Role o Bacteria Is There Such a Thing as a Periodontal Pathogen?

Se ctio n 5

Fo c s o n Patie nts

208

Clinical Patient Care Evidence in Action

Clinical Applicatio n.

Caring or patients with periodontal diseases requires a comprehensive understanding o the concept o oral bio lms and how individual types o bacteria interact as residents in these bio lms. This chapter discusses what is currently known about oral bio lms and sets the stage or the inevitable expansion o our knowledge about these bio lms as the results o additional research become available.

Le arning Obje ctive s • Explain the di erence in the cell membrane o a gram-positive versus a gram-negative bacterium. • De ne the term bio lm and explain the advantages o a bacterium living in a bio lm. • Describe the li e cycle o a bio lm. • Given a drawing o a mature bio lm, label the ollowing: bacterial microcolonies, f uid channels, extracellular slime layer, acquired pellicle, and tooth sur ace. • Explain the signi cance o the extracellular slime layer and f uid channels o a bio lm. • De ne coaggregation and explain its signi cance in bacterial colonization o the tooth sur ace. • Explain why systemic antibiotics and antimicrobial agents are not e ective in eliminating dental plaque bio lms.

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Part 3 Risk Factors or Periodontal Diseases

• State the most e ective ways to control dental plaque bio lms. • Name several reasons why newer microbe detection methods have brought Socransky’s microbial complexes and the speci c plaque hypothesis model into question. • Discuss the hypothesis that plaque bio lm is necessary but not su cient or periodontal destruction (microbial homeostasis–host response hypothesis). • Name the three bacteria designated by The World Workshop in Periodontology (1996) as periodontal pathogens.

Ke Te rms Bacterium/Bacteria Cell membrane Gram staining Gram-positive bacteria Gram-negative bacteria Bio ilm Acquired pellicle

Fimbriae Bacterial blooms Mushroom-shaped microcolonies Extracellular slime layer Fluid channels Coaggregation

Tooth-associated plaque bio ilms Tissue-associated plaque bio ilms Unattached bacteria Transmission Commensal organisms

Chapte r 12

Oral Bio lms and Periodontal In ections

Se ct io n 1

Bacte rial Bio ilms O ne human mouth is home to more microorganisms than there are people on the planet Earth. It is currently estimated that some 650 to 1,000 microbial species reside in the oral cavity (1–3). These microorganisms have evolved to survive in the environment o the tooth sur ace, gingival epithelium, and oral cavity. Though this is not a microbiology textbook, knowledge o several characteristics o bacteria is undamental to understanding many o the ideas presented in this chapter. The bacterial characteristics discussed in this section include cell membrane structure, Gram staining o bacteria, and the environments in which bacteria live.

Ch a r a Ct e r is t iCs o f Ba Ct e r ia 1. Characteristics o Bacteria A. Description 1. Bacterium (plural, bacteria). Bacteria are the simplest organisms and can be seen only through a microscope. 2. There are thousands o kinds o bacteria, most o which are harmless to humans. 3. Bacteria have existed on earth or longer than any other organisms and are still the most abundant type o cell. 4. Bacteria can replicate quickly. This ability to divide quickly enables populations o bacteria to adapt rapidly to changes in their environment. B. Structure o the Bacterial Cell Membrane. A tough protective layer called a cell membrane encloses nearly all bacteria. 1. The composition o the cell membrane is an important characteristic used in identi ying and classi ying bacteria. Gram staining is a laboratory method that reveals di erences in the chemical and physical properties o bacterial cell membranes. Depending on their permeability, the bacterial cell membranes appear either purple or red in color under a light microscope. 2. Gram staining divides bacteria into gram-positive (purple color) and gramnegative (red color) bacterial cell membrane types. a. Gram-positive bacteria (purple stain) 1. H ave a single, thick cell membrane 2. Retain a purple color when stained with a dye known as crystal violet and so, the bacterial cell membranes show a purple stain under a light microscope b. Gram-negative bacteria (red stain) 1. H ave double cell membranes 2. Do not stain purple with crystal violet and there ore, show a red stain under a light microscope

Ba Ct e r ia l Co m m u n it ie s Until recently, bacteria were studied as they grew on culture plates in a laboratory. Recent advances in research technology have allowed researchers to study bacteria in their natural environment. These studies have revealed that most bacteria live in complex communities called bio lms and that bio lms are ound everywhere in nature.

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1. Where Bacteria Live. Bacteria live almost everywhere, even in environments where other li e orms cannot survive. Bacteria are always present on the skin and in the digestive and respiratory systems o humans. A. Free-Floating Bacteria 1. Bacteria may be ree f oating. These ree-f oating bacteria are also known as planktonic bacteria. 2. Until recently, most research done on bacteria was conducted on ree-f oating bacteria. B. Attached Bacteria 1. Bacteria can attach to sur aces and to one another. Communities o bacteria that attach to each other and to a sur ace are described as living in a bio lm. 2. O nce a bacterium attaches to a sur ace, it activates a whole di erent set o genes that give the bacterium di erent characteristics rom those it had as a ree-f oating organism. 3. It has been estimated that more than 99% o all bacteria on earth live as attached bacteria. 2. Bio lms and Where They Form A. Description 1. A bio lm is a living lm—containing a well-organized community o microorganisms—that grows on a sur ace. Usually bio lms consist o many species o bacteria as well as other organisms and debris. 2. By some estimates 65% o all diseases may be bio lm induced. Bio lm-induced diseases include tuberculosis, cystic brosis, subacute bacterial endocarditis, and periodontal disease. B. Bio lm Environments 1. Bio lms are everywhere in nature (Fig. 12-1). “Bio lm” may seem like a new term, but everyone encounters bio lms on a regular basis. The plaque bio lm that orms on teeth, the slime in sh tanks, and the slime deposit that clogs the sink drain are all examples o bio lms. The slimy rocks in a stream are bio lm coated. 2. Bio lms can exist on any solid sur ace that is exposed to a bacteriacontaining f uid. 3. Bio lms thrive in dental unit water and suction lines and have been shown to be the primary source o contaminated water delivered by dental units. Stagnant f uid f ow allows ree-f oating bacteria to attach to the tubing walls in the dental unit and orm intricate bio lms.

Co ntac t le ns c as e

To o th Ro c ks in a s tre am

Artific ial hip implant

On g las s s ide s o f a fis h tank

Fig re 12-1. Bio ilm Enviro nme nts. Bio ilms are ound nearly everywhere in nature. They have a major impact on human health.

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3. Li e Cycle o a Bio lm. The bio lm li e cycle has three stages: attachment, growth, and detachment (Fig. 12-2). A. Attachment. Bacteria attach to a sur ace. B. Growth 1. The attached bacteria begin releasing substances that attract other ree-f oating bacteria to join the bio lm community. 2. The attached bacteria secrete a lm known as the extracellular slime layer. This slimy lm helps to keep the bacteria attached to the sur ace and acts as a protective shield or the bacteria. 3. The bacteria multiply rapidly and grow away rom the sur ace to orm threedimensional mushroom-shaped mature bio lms that attach to a sur ace at a narrow base. 4. M ovement o the f uid surrounding the mature bio lms results in extensions that stream rom the main body o the bio lm. C. Detachment 1. Clumps o the main bio lm break o and are carried away by the f uid surrounding the bio lm. 2. These detached clumps can attach to other portions o a sur ace and orm new bacterial colonies.

Attac hme nt 1

Gro wth 2

De tac hme nt 3

Fig re 12-2. Bio ilm Li e C cle . The three major stages in the li e cycle o a bio ilm: attachment, growth, and detachment in clumps.

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Se ct io n 2

Str ct re and Co lo nizatio n o De ntal Plaq e Bio ilms The pattern o dental plaque bio lm development can be divided into ve phases: (1) ormation o acquired pellicle, (2) attachment o early bacterial colonizers, (3) coaggregation o additional bacterial colonizers, and (4) ormation o an extracellular slime layer and microcolony ormation (Fig. 12-3). Phase 5 is a mature bio lm characterized by the bacterial microcolonies that orm complex groups with a primitive communication system and f uid channels (Fig. 12-4).

(Phas e 1) (Phas e 2)

(Phas e 3)

(Phas e 4)

Multip lic a tion

Continue d growth

(Phas e 5)

Flow

Cle a n s urfa c e

Film c oa ting

Bind ing of s ingle orga nis ms

Ma ture b iofilm

Fig re 12-3. Five Phase s in the Fo rmatio n o a Bio ilm. Phase 1, the acquired pellicle coats the tooth sur ace. Phase 2, initial colonizers attach to the tooth sur ace. Additional bacteria coaggregate with the initial colonizers in Phase 3. Phase 4 is signaled by the ormation o the extracellular slime layer. Phase 5 is a mature bio ilm.

Fig re 12-4. De ntal Plaq e Bio ilm. Scanning electron micrograph o dental plaque bio ilm showing bacteria (red and yellow stain) and extracellular matrix (orange stain). (Courtesy o Getty Images.)

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s p e Cie s Ca pa Bl e o f Co l o n iz in g t h e m o u t h M any di erent species and subspecies are capable o colonizing the mouth. Figure 12-5 lists some examples o over 600 cultivable species.

Gra m p o s itive

Fa c ulta tive a na e rob e s Coc c i

Rod s

+

Gra m ne g a tive

Ob liga te a na e rob e s

Stre p toc oc c us

Fa c ulta tive a na e rob e s

P e p tos tre p toc oc c us • Pm

–S. a nginos us (S. mille ri) –S. muta ns P e p toc oc c us –P. –S. s a nguis –S. a nginos us • Ss mic ros –S. ora (S. mille ri) lis –S. mitis –S. muta ns inte rme d ius –S. s–S. a nguis –S. ora lis –S. mitis –S. inte rme d ius

Ac tinomyc e s

P rop ionib a c te rium

–E. nod a tum • En –E. s a b urre um –E. timid um –E. b ra c hy –E. a la c tolytic um

Bifid ob a c te rium –B. d e ntium

Rothia –R. d e ntoc a rios a

Ve illone lla –V. p a rvula

Aggre tib a c te r m–A. a cga tinomyc e te

ns e te m–A. caomita c tinomyc c omita ns • Aa

Ca p noc ytop ha ga

–L. oris –L. a c id op hilus –L. s a liva rius –L. b uc c a lis

P orp hyromona s • Pg –P. gingiva lis –P. e nd od onta lis

P re vote lla –P. inte rme d ia • P i –P. nigre s c e ns

–C. oc hra c e a –C. gingiva lis –C. s p utige na

Ca mp ylob a c te r –C. re c tus • Cr –C. c urvus

–P. d e ntic ola –P. loe s c he ii –P. oris –P. ora lis

Ta nne re lla

–C. s howa e

La c tob a c illus

Ob liga te a na e rob e s

Bra nha me lla

Eub a c te rium

–A. na e s lund ii • An –A. vis c os us • Av –A. od ontolytic us –A. is ra e lii

Ne is s e ria

–

–T. fors ythia

Eike ne lla –E. c orrod e ns • Ec

Ha e mop hilus –H. a p hrop hilus –H. s e gnis

Fus ob a c te rium –F. nuc le a tum • Fn –F. p e riod ontic um

Se le ne mona s –S. s p utige na –S. noxia

Sp iroc he te s a nd myc op la s ms

Euka ryote s

Myc op la s m

Sp iroc he te s of ANUG

–M. ora le –M. s a liva rium –M. hominis

Ca nd id a

Tre p one ma s p . –T. d e ntic ola • Td –T. s oc ra ns kii –T. p e c tinovorum –T. vinc e ntii

Enta moe b a

–C. a lb ic a ns

Fig re 12-5. Example s o Micro o rg anisms Capable o Co lo nizing the Mo th.

• Tf

Tric homona s

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t h e Co m p l e x s t r u Ct u r e o f De n t a l p l a q u e Bio f il m s 1. Pattern o Plaque Bio lm Development A. Phase 1—Film Coating 1. Within minutes a ter cleaning the tooth sur ace, a lm orms over the tooth sur ace. This lm, the acquired pellicle, is composed o a variety o salivary glycoproteins (mucins) and antibodies. a. The purpose o the acquired pellicle is to protect the enamel rom acidic activity. b. Un ortunately, in addition to providing protection rom acids, the acquired pellicle also alters the charge and energy o the tooth sur ace, acilitating bacterial adhesion. c. A help ul analogy in understanding the role o acquired pellicle in plaque bio lm ormation is to think o the pellicle as “ double-sided adhesive tape.” The double-sided tape adheres to the tooth sur ace on one side and provides a sticky sur ace on the other side that acilitates attachment by bacteria to the tooth sur ace. B. Phase 2—Initial Attachment o Bacteria to Pellicle 1. Within a ew hours a ter pellicle ormation, bacteria begin to attach to the outer sur ace o the pellicle. 2. Some bacteria possess attachment structures, such as extracellular substances and hundreds o hair-like structures, which enable them to attach rapidly upon contact with the tooth sur ace. The hair-like structures are termed mbriae. C. Phase 3—New Bacteria Join In. Once bacteria stick to the tooth, they begin producing substances that stimulate other ree-f oating bacteria to join the community. D. Phase 4—Extracellular Slime Layer and Microcolony Formation 1. Production o an Extracellular Slime Layer a. It appears that the act o attaching to the tooth sur ace stimulates the bacteria to excrete a slimy, glue-like substance, called the extracellular slime layer. b. This extracellular slime layer helps to anchor bacteria to the tooth sur ace and provides protection or the attached bacteria. 2. M icrocolony Formation a. O nce the sur ace o the tooth has been covered with attached bacteria, the bio lm grows primarily through cell division o the adherent bacteria (rather than through the attachment o new bacteria). b. N ext, the proli erating bacteria begin to grow away rom the tooth. c. Bacterial blooms are periods when speci c species or groups o species grow at rapidly accelerated rates. E. Phase 5—Mature Bio lm: Mushroom-Shaped Microcolonies 1. The bacteria cluster together to orm mushroom-shaped microcolonies that are attached to the tooth sur ace at a narrow base. 2. The result is the ormation o complex collections o di erent bacteria linked to one another. 2. The Complex Structure o Mature Dental Plaque Bio lms A. Bacterial Microcolonies 1. The bacteria in a bio lm are not distributed evenly. As the bacteria attach to a sur ace and to each other, they cluster together to orm microcolonies (Fig. 12-6). 2. Each microcolony is a tiny independent community containing thousands o compatible bacteria. Di erent microcolonies may contain di erent combinations o bacterial species.

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Stre a me r Root s urfa c e

Ba c te ria l mic roc olony

Ac q uire d p e llic le

Extra c e llula r s lime la ye r Void

Ba c te ria l mic roc olony

Fluid c ha nne l

Sa liva a nd GCF

Fig re 12-6. Str ct re o Plaq e Bio ilm. The complex structure o dental plaque bio ilm includes clusters o bacterial microcolonies, streamers, and luid channels.

a. Environmental conditions within each microcolony o bacteria vary radically. The environmental conditions among several microcolonies may include di erences in oxygen concentration, pH , and temperature. b. The di ering environmental conditions within a bio lm mean that the bacterial population is very diverse—with each di erent bacterial species pre erring a certain environment within the bio lm. 1. This bacterial diversity helps to ensure the survivability o the plaque bio lm in widely varying oral conditions. 2. I the plaque bio lm had only one species o bacteria, it would be much more likely that a toxic agent or condition would destroy the bio lm. B. Extracellular Slime Layer 1. The extracellular slime layer is a dense protective barrier that surrounds the bacterial microcolonies (Fig. 12-6). 2. The slime layer acts like a shield protecting the bacterial microcolonies rom antibiotics, antimicrobials, and the body’s immune system. C. Fluid Forces 1. The f uid orces o the saliva surrounding the bio lm inf uence the shape o the plaque bio lm, as well as the spatial arrangement o the bacteria inside. 2. These f uid orces result in the development o extensions rom the main body o the bio lm. These bio lm extensions can break ree and be swallowed, expectorated, or orm new bio lm colonies in other areas o the mouth. 3. Fluid orces also result in cell-to-cell collisions o the bacteria within the bio lm.

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a. Bacterial cell collisions lead to a more rapid spread o genes among the bacteria than there would be i there were no f uid orces acting on the bio lm. b. This rapid trans er o genes rom bacterial cell to bacterial cell may result in enhanced bacterial virulence and antimicrobial resistance. c. The continuous exchange o genetic in ormation among bacteria means that the bacteria are constantly evolving. This makes the bacterial bio lm very di cult to eradicate and helps to ensure the survivability o the bio lm. D. Fluid Channels 1. As the plaque bio lm develops, a series o f uid channels are ormed that penetrate the extracellular slime layer (Fig. 12-6). 2. These f uid channels direct f uids in and around the bio lm bringing nutrients and oxygen to the bacteria and carrying bacterial waste products away. 3. The f uids include everything rom saliva to any beverages consumed. E. Cell-to-Cell Communication System 1. Direct cell-to-cell interaction occurs among the bacteria in the bio lm. 2. The bacterial microcolonies use chemical signals to communicate with each other. 3. This cell-to-cell communication also results in the trans er o genes among bacteria. F. Bacterial Signaling 1. Bacterial communication occurs when bacteria within the bio lm release and sense small proteins (signaling molecules). This type o communication among bacteria is termed quorum sensing. 2. Bacteria in the bio lm use quorum sensing to trigger events such as adhesion o additional bacteria to the bio lm and ormation o the extracellular slime layer that surrounds the bacteria.

Ba Ct e r ia l Co l o n iz a t io n a n D s u CCe s s io n 1. Microbial Complexes A. Internal Organization 1. The internal structure o plaque bio lm has been examined in a number o studies by light and electron microscopy (4–8). 2. The organization o bacteria within bio lms is not random; rather there are speci c associations among bacterial species (9). The bacteria within a bio lm no longer work as single entities, but rather, act as a unctioning system o interdependent parts. B. Bacterial Colonization o the Tooth Sur ace 1. Layers and Layers o Bacteria. The bio lm develops by stacking one bacterial species on top o another bacterial species. A mature dental bio lm does not consist o only one species o bacteria. 2. Coaggregation o Bacteria a. Coaggregation is the cell-to-cell adherence o one oral bacterium to another (Fig. 12-7). b. Coaggregation is not random; rather, each bacterial strain only has a limited set o bacteria to which they are able to adhere. c. The ability to adhere and coaggregate is an important determinant in the development o the bacterial bio lm.

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Fig re 12-7. Bacte rial Co ag g re g atio n. One example o coaggregation o bacteria has a corncob appearance that is created when a central rod-shaped bacterium becomes surrounded by many round cocci. (Courtesy o Ziedonis Skobe, PhD, Head, Biostructure Core Facility, The Forsyth Institute.)

2. Sequence o Colonization A. Early Bacterial Colonizers: Important to Bacterial Succession 1. The rst bacteria to colonize the tooth sur ace are nonpathogenic (Fig. 12-8). The ability o these species to attach to the tooth sur ace lays the oundation or the growth o dental plaque bio lms. 2. Early bacterial colonizers o the tooth sur ace include many streptococcal species, such as Streptococcus m itis and Streptococcus oralis that have the ability to attach to the tooth pellicle, as well as, to each other (10,11). Another early colonizer is A ctinomyces viscosus. 3. The early bacterial colonizers release chemical signals that indicate to the next group o bacteria that conditions are avorable or them to join the bio lm. 4. The early streptococcal colonizers are able to coaggregate with many o the other early colonizing bacteria and intermediate species. M any early and intermediate colonizing species are unable to attach to the tooth pellicle but have the ability to coaggregate with the streptococcal species. 5. Free-f oating bacteria cannot join the bio lm until the conditions are avorable (Box 12-1). The succession o bacteria joining the bio lm is comparable to elementary school students who are asked to line up in alphabetical order as their teacher calls out their names. Students whose last names start with the letter “ O ” cannot get in line until all the students whose last names start with “ M and N ” have taken their place in the line. B. Intermediate and Late Colonizers 1. As is the case with the early bacterial colonizers, the intermediate and late colonizers must join the bio lm in the proper sequence. 2. The intermediate species, such as Fusobacterium nucleatum , in turn coaggregate with the last colonizers. 3. A mature plaque bio lm is a very complex collection o multiple bacterial species (Fig. 12-9).

Bo x 12-1. The Impo rtance o Earl Co lo nize rs in Bio f lm S cce ssio n 1. F - o in g b c i c 2. I b io f lm is d q u b io f lm w ill lw ys b b c i l su cc ssio n s

n n o in i i io d o n l d is s . ly d is u d b y d ily s l -c n d o u in o o m in g . e v y im b io f lm is d is u d, s o v b g in n in g w i ly co lo n iz s.

ssio n l c , n i o c ss o

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Av

Ss

Av

Ss

A. Co lo nizatio n o Acq ire d Pe llicle . Early grampositive bacterial colonizers include Actinomyces viscosus (Av) and Streptococcus sanguis (Ss). S. sanguis is the most dominant.

Ac q uire d p e llic le

A

Ss

Av

Ss Av

B. Inte rme diate Co ag g re g atio n. Once an initial group o bacteria adhere to the pellicle, the bacteria begin to multiply.

Ss

Av

Ss

Ac q uire d p e llic le

B

Fn Pi

Ss

Fn Av

Pi

Ss

Av Ss

Av

Ss

C. Co ag g re g atio n o Gram-ne g ative Org anisms. Gram-negative bacteria join the bio ilm, such as Fusobacterium nucleatum (Fn) and Prevotella intermedia (Pi).

Ac q uire d p e llic le

C

Cg Cg Ai Fn

Pi

Ss

Fn Av

Pi

Ss Ss

Ai

Pg

Av

D. Dive rse Arra o Gram-Ne g ative Org anisms. As the bio ilm matures more gram-negative anaerobic bacteria colonize the bio ilm including Porphyromonas gingivalis (Pg) and Capnocytophaga gingivalis (Cg). Actinomyces israelii (Ai) is a grampositive organism.

Av Ss

Ac q uire d p e llic le

D

Fig re 12-8. Stag e s o Bacte rial Co lo nizatio n o the To o th S r ace . 0 hours

12 we e ks 6 hours

Ac q uire d p e llic le fo rm a tio n

Ba c te ria l a d he s io n

Da y 7

S up ra g ing iva l p la q ue

P la q ue m a tura tio n

Ac tino m yc e s S tre p to c o c c i

Fila m e nto us b a c te ria

We ll-d iffe re ntia te d s ub g ing iva l b io film

Fig re 12-9. Se q e nce o Bacte rial Attachme nt. Dental plaque bio ilm development always begins supragingivally and progresses subgingivally.

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3. Bacterial Attachment Zones. The zones o subgingival bacterial attachment (Fig. 12-10) are the tooth sur ace and the epithelial lining o the periodontal pocket. Bacteria also may attach to other bacteria that are attached to one o these sur aces. A. Tooth-Associated Plaque Bio lms—bacteria that are attached to the tooth sur ace. 1. Bacteria attach to an area o the tooth sur ace that extends rom the gingival margin almost to the junctional epithelium at the base o the pocket. 2. Subgingival bacteria appear to have the ability to invade the dentinal tubules o the cementum. 3. Filamentous microorganisms, cocci, and rods—including S. m itis, S. sanguis, and A . viscosus—dominate the tooth-associated plaque bio lms. B. Tissue-Associated Plaque Bio lms—bacteria that adhere to the epithelium. 1. The bacteria that adhere loosely to the epithelium o the pocket wall are distinctly di erent rom those o the tooth-associated plaque bio lms. 2. The layers closest to the so t tissue wall contain large numbers o spirochetes and f agellated bacteria. Gram-negative cocci and rods are also present. There is a predominance o species such as S. oralis, Streptococcus interm edius, Porphyrom onas gingivalis, Prevotella interm edia, Tannerella orsythia, and F. nucleatum . 3. Bacteria rom the tissue-attached plaque bio lms can invade the gingival connective tissue and be ound within the periodontal connective tissues and on the sur ace o the alveolar bone. C. Unattached Bacteria. In addition to the attached bacteria, the periodontal pocket also contains many ree-f oating bacteria that are not part o the bio lm.

Root s urfa c e Ep ithe lia l lining of p e riod ontic p oc ke t

Ac q uire d p e llic le

Fig re 12-10. S bg ing ival Plaq e Bio ilm Attachme nt Zo ne s. Within a periodontal pocket, bacteria attach to the tooth sur ace or the epithelial lining o the pocket.

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4. Transmission o Periodontal Bacteria A. M olecular epidemiology techniques that isolate DN A provide evidence that bacteria in the bio lm are transmissible. Transmission is the trans er o bacteria rom the oral cavity o one person to another. B. Transmission should not be con used with contagion. There is little or no evidence that periodontal in ections are communicable. The term communicable re ers to a disease that may be passed rom one person to another by direct or indirect contact via substances such as inanimate objects. C. Studies demonstrate that A . actinomycetem com itans (Fig. 12-11) and P. gingivalis strains isolated rom parents and children within the same amily exhibited identical restriction endonuclease DN A ragment patterns (12–15). Kissing is the primary means by which saliva and its bacterial contents are transmitted (14,16,17). D. Table 12-1 provides a pronunciation guide to bacteria commonly associated with plaque bio lms.

Fig re 12-11. Ag g re g a t ib a ct e r a ct in o m yce t e m co m it a n s (Aa). A three-dimensional image o A. actinomycetemcomitans taken with a scanning electron microscope (SEM). (Used with permission rom Dennis Kunkel Microscopy, Inc.)

TABLE 1 2 -1. PRONu NCIATION Gu IDE TO BACTERIAL TONGu E Tw ISTERS Name

Pro n nciatio n G ide

A g g re g at ib act e r

g -g

-g

act in o m yce t e m co m it an s

c - in -o -m y-s

Tan n e re lla

n n - - ll

f o rsyt h ia

w -sith-

Fu so b act e riu m n u cle at u m Po rp h yro m o n as g in g ivalis

-

-b c- m -co m b -

-u

u s -so -b ck- i -e e e -u m n u -kl

-

- um

o u - y- o -m o -n s g in g -ji -v l-lis

- ns

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Co ntro l o Plaq e Bio ilms 1. Mechanisms o Bacterial Survival. The bio lm provides the bacteria with an advantage that permits long-term survival within the sulcus or pocket environment. The protective extracellular slime layer makes bacteria extremely resistant to antibiotics, antimicrobial agents, and the body’s immune response. It is likely that several mechanisms are responsible or bio lm resistance to systemic antibiotics, antimicrobial agents, and the immune system. A. Resistance to Systemic Antibiotics and Antimicrobial Agents 1. Bacteria living in a bio lm are unusually resistant to systemic antibiotics (in dentistry, usually administered in pill orm) and antimicrobials (placed locally in the oral cavity). 2. Antibiotic doses that kill ree-f oating bacteria, or example, need to be increased as much as 1,500 times to kill plaque bio lm bacteria (and at these high doses, the antibiotic would kill the patient be ore the bio lm bacteria!) (18). 3. Antimicrobial agents work best when used in conjunction with mechanical cleaning that removes or disrupts the dental plaque bio lm (19). B. Protective Mechanisms o Bio lms 1. Extracellular Slime Layer a. The extracellular slime layer is very dense and may prevent the drugs rom penetrating ully into the depth o the bio lm. b. The thick slime layer may protect the bacteria against leukocytes (de ensive cells o the body’s immune system). The dense slime layer may block substances released by leukocytes. As a result the leukocyte substances end up causing more damage to the surrounding body tissue than to the bio lm bacteria. 2. Enzymes. Some bacteria produce enzymes that degrade antibiotics aster than the drug can penetrate into the bio lm. 3. Dormant Bacteria a. The bio lm is very thick and bacteria in the deepest layers become dormant—not dead—because they are cut o rom the sources o nutrients. Dormant bacteria are in an inactive state in order to survive adverse environmental conditions. b. Antibiotics only work on bacteria that are active and reproducing. c. When the course o antibiotics is nished, the dormant active bacteria within the bio lm reactivate. 2. Physical Removal o Dental Plaque Bio lms is Essential A. Control o bacteria in dental plaque bio lms is best achieved by the physical disruption (such as brushing, f ossing, and periodontal instrumentation). 1. It takes some time or the complex structure o a mature plaque bio lm to orm. 2. M echanical cleaning orces the bacteria to start over with initial attachment, initial colonization, secondary colonization, and nally to become a mature bio lm. 3. In areas that are cleaned regularly, a mature bio lm will not be able to develop. The cleaner the tooth sur ace, the less complex the bacterial ormation. B. Toothbrushes and f oss cannot reach the subgingival plaque bio lm located within pockets. For this reason, requent periodontal instrumentation o subgingival root sur aces by a dental hygienist or dentist is an essential component in the treatment o periodontitis.

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Se ct io n 4

The Ro le o Bacte ria in Pe rio do ntitis Ch a n g in g e v iDe n Ce f o r t h e r o l e o f Ba Ct e r ia In 1683, Antonie van Leeuwenhoek, using a homemade microscope, rst described oral microorganisms. Despite 330 years o scienti c investigation in the eld o oral microbiology, researchers have ailed to identi y bacterial pathogens that cause periodontitis (20). O ver the years, three main hypotheses have been proposed to explain the etiology o periodontal disease: (1) accumulation o bacterial bio lms leads to periodontal destruction, (2) speci c pathogenic bacteria and their products in the bio lm lead to periodontal destruction, and (3) bacterial plaque bio lm is necessary but not su cient or periodontal destruction. 1. Historical Perspective: Accumulation o Bacterial Bio lms Lead to Periodontal Destruction (N onspeci c Plaque Hypothesis) A. Hypothesis. This theory proposed that the accumulation o plaque bio lm adjacent to the gingival margin led to gingival inf ammation and subsequent periodontal destruction (21–23). B. Problems with the N onspeci c Plaque Hypothesis 1. A ailing o the nonspeci c hypothesis is that it ails to explain why most cases o gingivitis never progress to periodontitis. Some individuals with heavy amounts o plaque bio lm ail to develop periodontitis. Yet, ironically other individuals with very light amounts o bio lm su er rom aggressive orms o periodontitis (24). 2. This hypothesis cannot clari y why some sites in a particular individual’s periodontium experience considerable periodontal destruction while other sites are una ected. 2. Historical Perspective: Speci c Pathogenic Bacteria Lead to Periodontal Destruction (Speci c Plaque Hypothesis) A. Hypothesis. This theory proposed that speci c pathogenic bacteria present in subgingival bio lms and their toxic products resulted in destruction o the periodontal tissues (22,23). 1. An increase in the number o speci c pathogens was thought to be associated with periodontitis. 2. This model postulates that a microbial shi t occurs in which the bacteria in the bio lm change rom a predominantly gram-positive aerobic community to one consisting mainly o groups o gram-negative anaerobes (25). B. Socransky’s Microbial Complexes. As a result o the speci c plaque hypothesis, research e orts, over many years, ocused on identi ying speci c microorganisms associated with various periodontal diseases and conditions. 1. These studies identi ed speci c groups o bacteria—T. orsythia, P. gingivalis, and Treponem a denticola—that were signi cantly associated with periodontitis. It was noted that these bacteria were interdependent and o ten could not exist without the presence o the others (9,26). 2. Socransky grouped microorganisms into complexes and assigned each complex a color (Fig. 12-12) (9). The yellow, green, and orange complexes were thought to be compatible with gingival health. The orange and red complexes comprise the species that were thought to be the major etiologic agents o periodontal disease.

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3. The appeal o the concept o red and other color-coded complexes led to the theory’s widespread adoption until molecular-based approaches to microbe detection brought its validity into question.

Ac tinomyc e s Ac tinomyc e s s p e c ie s

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C. Problems with the Speci c Plaque Hypothesis 1. Recently the development o newer microbe detection methods brought the model o the speci c plaque hypothesis into question. First, it is established that red complex organisms can be ound in the absence o periodontal disease (27,28). The act that P. gingivalis and T. orsythia requently are ound in healthy periodontal sites brings into question whether these bacteria are true periodontal pathogens (29). 2. Second, the periodontal microbe population is more heterogeneous and diverse than previously thought (30–32). Over 600 organisms are recognized as possible oral inhabitants, o which around 200 can be present in any one individual and about 50 present at any one site (33). Many o these newly recognized organisms show as good or better correlation with disease as the classical red complex (34–36). The identi cation o so many more bacterial species in the oral cavity makes the concept o speci c bacteria causing periodontitis even more unlikely (37). 3. Contrary to the doctrine that gram-negative bacteria dominate disease sites in periodontitis, numbers o gram-positive anaerobic bacteria species are shown to exhibit a signi cant increase in deep periodontal pockets relative to healthy sites and can be detected in greater numbers than gram-negative species in some studies (35). 4. It is evident that the concept o a three-species red complex as representing the primary etiologic unit in periodontitis requires re nement (38).

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3. Current Perspective: Plaque Bio lm is N ecessary but not Su cient or Periodontal Destruction (Microbial Homeostasis–Host Response Hypothesis) A. Hypothesis. This theory proposes that while plaque bio lms are the cause o the initial inf ammatory response leading to gingivitis, it is the host response, not the type o bacteria, w hich determ ines w hether periodontal destruction progresses (39). 1. Evidence or the role o host response in periodontal destruction rst emerged in the landmark paper by Page and Schroeder (40). H ost and inf ammatory response is discussed in detail in Chapters 13 and 14. 2. Page and Schroeder noted that established gingivitis would not progress to periodontitis unless some other unknown actor tipped the delicate bio lm– host balance toward urther tissue destruction. 3. This hypothesis proposes that the subgingival environment determines the speci c bacteria that f ourish in the environment. T he in am m ation w ithin the tissues drives the changes in the m icrobial com position o the biof lm and not vice versa. B. Support or this Hypothesis 1. The bio lm microbe population associated with periodontal health appears to remain stable over time and exists in a state o biologic equilibrium or homeostasis. 2. Decades o research have ailed to identi y speci c bacterial pathogens that cause the tissue destruction seen in periodontitis. In the same time period, overwhelming evidence has amassed demonstrating that it is the uncontrolled host inf ammatory and immune responses that drive the tissue destruction (41).

is t h e r e s u Ch a t h in g a s a p e r io Do n t a l pa t h o g e n ? M ost organisms that colonize the human body are commensal. Commensalism is a relationship between individuals o two species in which one species—the commensal organisms—obtains bene ts rom the other species without either harming or helping the host species. The commensal organism may obtain nutrients, shelter, or locomotion rom the host species. The commensal relation o ten is between a larger host (the human body) and a smaller commensal organism. As with the human body as a whole, most organisms that colonize the oral cavity are commensal (3,42,43). A. What is a Bacterial Pathogen? How Do We De ne the Term “Periodontal Pathogen”? 1. A pathogen usually is de ned as a microorganism that causes or can cause a disease; a microbe that can cause damage in a host. 2. It is generally accepted that bacteria can cause disease in humans through three di erent pathways: (1) as a true pathogen that generally is not ound in humans and causes disease upon rst exposure, (2) as part o the indigenous (natural) f ora in one site—but when moved to another site in the body—cause disease, and (3) as a commensal organism, which can only cause disease i a change occurs in the host body that allows it to f ourish and cause disease (44). B. How do we de ne the term “periodontal pathogen”? 1. There is little evidence to support the concept that periodontal bacteria are true pathogens. a. Periodontal plaque bio lms are ound in the oral cavities throughout the general population and yet, not all individuals in ected with bio lms develop periodontitis. O n the contrary, most individuals do not develop periodontitis.

Chapte r 12

Oral Bio lms and Periodontal In ections

b. Studies have shown the inoculation o gingival sulci with periodontal pathogens rom periodontitis sites ailed to induce a success ul colonization and periodontitis at the recipient site (45). 2. The plaque bio lm community is an association o commensal organisms (3,42). Under certain circumstances, which are not ully understood, commensal organisms can trans orm to being pathogenic in nature (37). a. Under appropriate environmental conditions, commensal organisms in the plaque bio lm can become pathogenic and be associated with disease. H ajishengallis and Lamont (38) postulate that some organisms become what he terms “ keystone pathogens.” H ajishengallis suggests that the keystone pathogens—a minor constituent o the plaque bio lm—have the ability to tip the balance in avor o disease progression (1,38,46). b. H ajishengallis contends that key pathogens only can become virulent within a synergistic microbial bio lm community. The bio lm community has both gram-negative and gram-positive bacteria that can tolerate inf ammation or provide other use ul service to the bio lm community. 3. N o de nitive evidence exists in the literature that speci c bacteria are responsible or the progression and mani estation o periodontitis. a. In 1996, the World Workshop in Periodontology (Consensus Report, 1996) designated A . actinomycetem com itans, P. gingivalis, and T. orsythia as periodontal pathogens (47). b. It seems possible that these bacteria that have been noted to date as “ periodontal pathogens” are present as the result o the periodontal disease but did not cause the disease (20). 4. Despite the presence o plaque bio lms, bacteria do not appear to be the major determining actor in the progression o gingivitis to periodontitis.

Chapte r S mmar State me nt M ore than 600 bacterial strains have been identi ed in dental plaque bio lm. The recognition that dental plaque is a bio lm helps to explain why periodontal diseases have been so di cult to prevent and to treat. Bacteria within a bio lm environment behave very di erently rom ree-f oating bacteria. The protective extracellular slime matrix makes bacteria extremely resistant to systemic antibiotics, antimicrobial agents, and the body’s immune system. M echanical removal is the most e ective treatment or the control o dental plaque bio lms. To date, there is no de nitive evidence that speci c bacteria are responsible or the progression o periodontal disease. O ne theory suggests that the speci c bacteria noted to date are present as the result o the disease but do not cause the disease. Considerable evidence indicates that it is more likely to be the host response to plaque bio lm that leads to the tissue destruction seen in periodontitis. It seems that it is the host inf ammatory and immune responses that determine whether gingivitis progresses to periodontitis.

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Se ct io n 5

Fo c s o n Patie nts Clinical Patie nt Care CA S E 1 You have just completed a thorough cleaning o a tooth sur ace. Describe what deposits you might expect to orm on the tooth sur ace over the next ew days i the patient does absolutely no urther cleaning o the tooth sur ace.

CA S E 2 Imagine that you are holding an “ interview” o bacteria living in an oral bio lm. H ow might the bacteria respond to your question about advantages o living in a bio lm?

Evide nce in Actio n M r. and M rs. Jones have been patients in the dental o ce or several years. M r. Jones has mild gingivitis while M rs. Jones has chronic periodontitis that is slowly progressive. Today you are seeing M rs. Jones or her 3-month maintenance visit. You show M rs. Jones areas o her mouth that exhibit increased attachment loss. M rs. Jones begins to cry and asks: “ M y husband only comes every 6 months and only gives his teeth a quick brush. I come every 3 months and spend a lot o time on every single day f ossing, using that tiny brush (interdental brush) and care ully brushing. You tell me that I have more bone loss and yet, my husband has N O bone loss. H ow can this be?!!” H ow would you answer M rs. Jones?

Re e re nce s 1. Jenkinson H F, Lamont RJ. O ral microbial communities in sickness and in health. Trends M icrobiol. 2005;13(12):589–595. 2. Paster BJ, O lsen I, Aas JA, et al. The breadth o bacterial diversity in the human periodontal pocket and other oral sites. Periodontol 2000. 2006;42:80–87. 3. Wade WG. The oral microbiome in health and disease. Pharm acol R es. 2013;69(1):137–143. 4. Eastcott AD, Stallard RE. Sequential changes in developing human dental plaque as visualized by scanning electron microscopy. J Periodontol. 1973;44(4):218–224. 5. Lie T. Ultrastructural study o early dental plaque ormation. J Periodontal R es. 1978;13(5):391–409. 6. Ronstrom A, Attstrom R, Egelberg J. Early ormation o dental plaque on plastic lms. 1. Light microscopic observations. J Periodontal R es. 1975;10(1):28–35. 7. Saxton CA. Scanning electron microscope study o the ormation o dental plaque. Caries R es. 1973;7(2):102–119. 8. Theilade E, Theilade J, M ikkelsen L. M icrobiological studies on early dento-gingival plaque on teeth and M ylar strips in humans. J Periodontal R es. 1982;17(1):12–25. 9. Socransky SS, H a ajee AD, Cugini M A, et al. M icrobial complexes in subgingival plaque. J Clin Periodontol. 1998;25(2):134–144. 10. Bradshaw DJ, M arsh PD, Watson GK, et al. Role o Fusobacterium nucleatum and coaggregation in anaerobe survival in planktonic and bio lm oral microbial communities during aeration. In ect Im m un. 1998;66(10):4729–4732. 11. Li J, H elmerhorst EJ, Leone CW, et al. Identi cation o early microbial colonizers in human dental bio lm. J A ppl M icrobiol. 2004;97(6):1311–1318. 12. Alaluusua S, Saarela M , Jousimies-Somer H , et al. Ribotyping shows intra amilial similarity in Actinobacillus actinomycetemcomitans isolates. O ral M icrobiol Im m unol. 1993;8(4):225–229. 13. DiRienzo JM , Slots J. Genetic approach to the study o epidemiology and pathogenesis o Actinobacillus actinomycetemcomitans in localized juvenile periodontitis. A rch O ral Biol. 1990;(35 suppl):79S–84S.

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14. Petit M D, van Steenbergen TJ, Scholte LM , et al. Epidemiology and transmission o Porphyromonas gingivalis and Actinobacillus actinomycetemcomitans among children and their amily members. A report o 4 surveys. J Clin Periodontol. 1993;20(9):641–650. 15. Slots J, Feik D, Rams TE. Actinobacillus actinomycetemcomitans and Bacteroides intermedius in human periodontitis: age relationship and mutual association. J Clin Periodontol. 1990;17(9):659–662. 16. Petit M D, van Steenbergen TJ, Timmerman M F, et al. Prevalence o periodontitis and suspected periodontal pathogens in amilies o adult periodontitis patients. J Clin Periodontol. 1994;21(2):76–85. 17. Petit M D, van Winkelho AJ, van Steenbergen TJ, et al. Porphyromonas endodontalis: prevalence and distribution o restriction enzyme patterns in amilies. O ral M icrobiol Im m unol. 1993;8(4):219–224. 18. Elder M J, Stapleton F, Evans E, et al. Bio lm-related in ections in ophthalmology. Eye. 1995;9(Pt 1):102–109. 19. Costerton JW, Lewandowski Z , Caldwell DE, et al. M icrobial bio lms. A nnu R ev M icrobiol. 1995;49:711–745. 20. Bartold PM , van Dyke TE. Periodontitis: a host-mediated disruption o microbial homeostasis. Unlearning learned concepts. Periodontol 2000. 2013;62(1):203–217. 21. Loe H , Theilade E, Jensen SB. Experimental gingivitis in man. J Periodontol. 1965;36:177–187. 22. Loesche WJ. Chemotherapy o dental plaque in ections. O ral Sci R ev. 1976;9:65–107. 23. Theilade E. The non-speci c theory in microbial etiology o inf ammatory periodontal diseases. J Clin Periodontol. 1986;13(10):905–911. 24. Socransky SS, H a ajee AD. Evidence o bacterial etiology: a historical perspective. Periodontol 2000. 1994;5:7–25. 25. M arsh PD. M icrobial ecology o dental plaque and its signi cance in health and disease. A dv D ent R es. 1994;8(2):263–271. 26. Socransky SS, H a ajee AD. Dental bio lms: di cult therapeutic targets. Periodontol 2000. 2002;28:12–55. 27. M ayanagi G, Sato T, Shimauchi H , et al. Detection requency o periodontitis-associated bacteria by polymerase chain reaction in subgingival and supragingival plaque o periodontitis and healthy subjects. O ral M icrobiol Im m unol. 2004;19(6):379–385. 28. Ximenez-Fyvie LA, H a ajee AD, Socransky SS. Comparison o the microbiota o supra- and subgingival plaque in health and periodontitis. J Clin Periodontol. 2000;27(9):648–657. 29. Papapanou PN . Population studies o microbial ecology in periodontal health and disease. A nn Periodontol. 2002;7(1):54–61. 30. Curtis M A, Z enobia C, Darveau RP. The relationship o the oral microbiotia to periodontal health and disease. Cell H ost M icrobe. 2011;10(4):302–306. 31. Dewhirst FE, Chen T, Izard J, et al. The human oral microbiome. J Bacteriol. 2010;192(19):5002–5017. 32. Gri en AL, Beall CJ, Firestone N D, et al. CO RE: a phylogenetically-curated 16 S rDN A database o the core oral microbiome. PL oS O ne. 2011;6(4):e19051. 33. Aas JA, Paster BJ, Stokes LN , et al. De ning the normal bacterial f ora o the oral cavity. J Clin M icrobiol. 2005;43(11):5721–5732. 34. Gri en AL, Beall CJ, Campbell JH , et al. Distinct and complex bacterial pro les in human periodontitis and health revealed by 16 S pyrosequencing. ISM E J. 2012;6(6):1176–1185. 35. Kumar PS, Gri en AL, M oeschberger M L, et al. Identi cation o candidate periodontal pathogens and bene cial species by quantitative 16 S clonal analysis. J Clin M icrobiol. 2005;43(8):3944–3955. 36. Kumar PS, Leys EJ, Bryk JM , et al. Changes in periodontal health status are associated with bacterial community shi ts as assessed by quantitative 16 S cloning and sequencing. J Clin M icrobiol. 2006;44(10):3665–3673. 37. Avila M , O jcius DM , Yilmaz O. The oral microbiota: living with a permanent guest. D N A Cell Biol. 2009;28(8):405–411. 38. H ajishengallis G, Lamont RJ. Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model o periodontal disease etiology. M ol O ral M icrobiol. 2012;27(6):409–419. 39. Page RC, Kornman KS. The pathogenesis o human periodontitis: an introduction. Periodontol 2000. 1997;14:9–11. 40. Page RC, Schroeder H E. Pathogenesis o inf ammatory periodontal disease. A summary o current work. L ab Invest. 1976;34(3):235–249. 41. Page RC, O enbacher S, Schroeder H E, et al. Advances in the pathogenesis o periodontitis: summary o developments, clinical implications and uture directions. Periodontol 2000. 1997;14:216–248. 42. Darveau RP. The oral microbial consortium’s interaction with the periodontal innate de ense system. D N A Cell Biol. 2009;28(8):389–395. 43. Feng Z , Weinberg A. Role o bacteria in health and disease o periodontal tissues. Periodontol 2000. 2006;40:50–76. 44. H irsch RS, Clarke N G. In ection and periodontal diseases. R ev In ect D is. 1989;11(5):707–715. 45. Christersson LA, Slots J, Z ambon JJ, et al. Transmission and colonization o Actinobacillus actinomycetemcomitans in localized juvenile periodontitis patients. J Periodontol. 1985;56(3):127–131. 46. H ansen SK, Rainey PB, H aagensen JA, et al. Evolution o species interactions in a bio lm community. N ature. 2007;445(7127):533–536. 47. American Academy o Periodontology. A nnals o Periodontology. Chicago, IL: The Academy; 1996.

STu DENT ANCILLARy RESOu RCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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13 S ctio

Basic Co c pts o Imm it a d I f ammatio 1

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Introduction to the Immune System Components o the Immune System Cells o the Immune System The Complement System

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Periodontal diseases are in part the result o the body’s de ense mechanism reacting to a bacterial challenge in the oral cavity. It is critical or healthcare providers caring or patients with periodontal disease to have a basic understanding o immunity and in ammation. This chapter presents a brie outline o this complex topic that can prove invaluable during urther study o periodontal diseases and in understanding the undamental behavior o these diseases.

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• Def ne the term immune system and describe its unction. • Describe the role o polymorphonuclear leukocytes, macrophages, B lymphocytes, and T lymphocytes in the immune system. • Contrast the terms macrophage and monocyte. • Describe the three ways that antibodies participate in the host de ense. • Def ne complement system and explain its principle unctions in the immune response. • Describe the steps in the process o phagocytosis. • Give an example o a type o injury or in ection that would result in in ammation in an individual’s arm. Describe and contrast the symptoms o in ammation that the individual would experience due to acute in ammation versus chronic in ammation. • Def ne the term in ammatory mediator and give several examples o in ammatory mediators o importance in periodontitis.

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Immune system Host Host response Leukocyte Polymorphonuclear leukocytes (PMNs) Neutrophil Chemotaxis Lysosome Neutropenia Macrophage

Monocyte Lymphocyte B lymphocyte Antibody Immunoglobulin T lymphocyte Cytokine Complement system Membrane attack complex Opsonization Endothelium

Transendothelial migration Phagocytosis Phagosome Phagolysosome In lammation In lammatory biochemical mediator Chemokines Acute In lammation C-reactive protein (CRP) Chronic In lammation

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H umans are surrounded by millions o microorganisms, many o which may prove to be deadly. O ur hands, alone, harbor up to two million microorganisms. The only reason that the human body survives is that it has a protective de ense system that is remarkably e ective in recognizing and ghting disease-causing microorganisms. The immune system is a complex system that is responsible or de ending the body against millions o bacteria, viruses, ungi, toxins, and parasites.

In t r o d u c t Io n t o t h e Im m u n e Sy St e m 1. Description A. A Complex System o Responses 1. The immune system is a collection o responses that protects the body against in ections by bacteria, viruses, ungi, toxins, and parasites. 2. Bacteria, viruses, and other disease-causing microorganisms attack the human body over 100 million times a day. For this reason, the human immune system attempts to control quickly the spread o invading microorganisms. 3. The immune system is composed o two major subdivisions—the innate and adaptive immune systems (Table 13-1) (1). a. The innate immune system—which humans are born with—is the rst line o de ense against invading organisms while the adaptive immune system acts as a second line o de ense and also a ords protection against reexposure to the same pathogen. b. The adaptive immune system—which develops throughout li e—requires some time to react to an invading organism, whereas the innate immune system includes de enses that, or the most part, are present and ready to be mobilized upon in ection. c. The adaptive immune system demonstrates immunological memory. It “ remembers” that it has encountered an invading organism and reacts more rapidly on subsequent exposure to the same organism. In contrast, the innate immune system does not demonstrate immunological memory.

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B. Sel Versus N onsel . When the immune system encounters cells or molecules, it must determine whether these are self (part o the body) or oreign substances. M olecules might be harmless substances, such as pollen, or constitute part o a microorganism. M icroorganisms, in turn, might be innocuous or pathogenic. 2. Function A. Prime Purpose 1. The prime purpose o the human immune system is to de end the li e o the individual (host) by identi ying oreign substances in the body (bacteria, viruses, ungi, or parasites) and developing a de ense against them (Fig. 13-1) (1,2). 2. The body recognizes bacteria, viruses, ungi, and parasites as something oreign to itsel and responds by (1) sending certain types o cells to the in ection site and (2) producing biochemical substances to counteract the oreign invaders. B. The way that an individual’s body responds to an in ection is known as the host response. 3. Consequences o Loss o Immune Function. Loss o immune unction is deadly to the body. An example is the human immunode ciency virus (H IV), the virus that causes acquired immune de ciency syndrome (AIDS). H IV disables a speci c group o immune system cells responsible or coordinating immune responses. People in ected with H IV may develop in ections rom microorganisms that rarely cause in ection in individuals with normal, healthy immune systems. 4. Consequences o an Overzealous Immune Response. The immune system can sometimes become con used or so intense in its response that it begins to harm the body it is trying to protect. Rheumatic heart disease is an example o a con used immune response to in ection. The problem begins as an in ection o the skin or pharynx with streptococcal bacteria. Un ortunately, there are similarities between certain molecules o the streptococcal bacteria and molecules o human heart tissue. As a result o this molecular similarity, immune responses against the streptococcal bacteria also attack and damage the heart tissue o the in ected individual. Infe c tious orga nis ms ta king a d va nta ge of b re a c he s in the b od y’s b a rrie rs

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c o m p o n e n t S o f t h e Im m u n e Sy St e m Components o the immune system that play an important role in combating periodontal disease are the (1) cellular de enders (phagocytes, lymphocytes) and (2) the complement system (Fig. 13-2A–F in Table 13-2) (1,2).

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Fig ure 13-2D Immunoglob ulins IgG, IgM, IgA, IgD, IgE

Fig ure 13-2E Comp le me nt s ys te m

Fig ure 13-2F

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c e l l S o f t h e Im m u n e Sy St e m 1. Leukocytes. Leukocytes are white blood cells that act much like independent singlecell organisms able to move and capture microorganisms on their own (Fig. 13-3). A. Polymorphonuclear leukocytes. Polymorphonuclear leukocytes (PMN s) are phagocytes that play a vital role in combating the bacteria in plaque bio lms (Fig. 13-4). 1. PM N s, also known as neutrophils, are phagocytic cells that actively engul and destroy microorganisms. 2. These cells are the rapid responders and provide the rst line o de ense against many common microorganisms and are essential or the control o bacterial in ections. 3. O nce in the blood stream, PM N s can move through capillary walls and into the tissue. PM N s are attracted to bacteria by a process called chemotaxis. 4. The cytoplasm o a PM N contains many granules lled with strong bactericidal and digestive enzymes. These granules (called lysosomes) can kill and digest bacterial cells a ter phagocytosis. 5. PM N s are short-lived cells that die when they become engorged with the bacteria they phagocytize. The pus ormed at sites o inf ammation contains many dead and dying PM N s. PM Ns have a short li e span, generally less than 1 day. 6. The bacteria associated with periodontal disease are most e ectively phagocytized by PM N s. 7. N ormally, each milliliter o blood contains between 3,000 and 6,000 PM N s. A PM N count o less than 1,000 cells/mL is called neutropenia and indicates an increased risk o in ection. B. Monocytes/ Macrophages. Macrophages are large phagocytes with one kidneyshaped nucleus and some granules (Figs. 13-5 and 13-6). 1. These leukocytes are called monocytes when ound in the bloodstream and macrophages when they are located in the tissues.

Le uko c yte s

Ce lls

Lympho c yte s

B-c e lls

Phag o c yte s

T-c e lls La rge gra nula r Mononuc le a r p ha goc yte s lymp hoc yte s

Ne utrop hil Gra nuloc yte e os inop hil

Othe rs

He lpe r c e lls

Ba s op hil Ma s t c e ll

Blood p la te le ts Tis s ue c e lls

Solub le Antibo die s me d ia tors

Cyto kine s

Co mple me nt fac to rs

Inflammato ry me diato rs

Inte rfe ro n c yto kine s

Fig 13-3. C lls a d C mical M diato s o t Imm S st m. Immune system cells and the chemical mediators are closely related since the cells produce most o the mediators.

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2. M acrophages are highly phagocytic cells that actively engul and destroy microorganisms. M acrophages contain a ew lysosomes that are lled with bactericidal and digestive enzymes. 3. M acrophages are slower to arrive at the in ection site than PM N s. The slower, long-lived macrophages are o ten the most numerous cells in chronic inf ammation. 4. M acrophages present antigen to T cells. Together macrophages and T lymphocytes play an important role in chronic inf ammation.

Lys os ome Multilob e d nuc le us

Fig 13-4. Mo p olo g o a Po l mo p o cl a L ko c t . PMNs contain granules called lysosomes that are used to digest bacteria.

P ha gos ome

P ha gos ome Lys os ome Nuc le us

A Mo no c yte P s e ud op od ia

P ha gos ome

Lys os ome

B Mac ro phag e

P s e ud op od ia

Fig 13-5. Mo p o lo g o a Mo o c t a d a Mac o p ag . These phagocytic leukocytes are called monocytes (A) when ound in the bloodstream and macrophages (B) when they are located in the tissues. O the blood cells, macrophages are the largest— thus, the name “ macro.” Macrophages are ive- to ten old larger than monocytes and contain more lysosomes.

Fig 13-6. Se M o Mac o p ag . A scanning electron micrograph (SEM) o a human macrophage (gray) approaches a chain o Streptococcus pyogenes (orange). Riding atop the macrophage is a spherical lymphocyte. Both macrophages and lymphocytes are important in eliminating in ection. (SEM courtesy o Cells Alive.)

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2. Lymphocytes. Lymphocytes are small white blood cells that play an important role in recognizing and controlling oreign invaders. The two main types o lymphocytes that are important in de ense against the bacteria in plaque bio lm are B lymphocytes (B cells) and T lymphocytes (T cells). A. B Lymphocytes 1. Description a. B lymphocytes are small leukocytes that help in the de ense against bacteria, viruses, and ungi. b. B lymphocytes can urther di erentiate into one o the two types o B cells: plasma B cells and memory B cells. c. The principal unctions o B lymphocytes are to make antibodies. O nce a B cell has been activated, it manu actures millions o antibodies and pours them into the bloodstream (Fig. 13-7). 2. Antibodies a. Antibodies are Y-shaped proteins. O ne end o the Y binds to the outside o the B cell. The other end binds to a microorganism and helps to kill it. b. Antibodies are known collectively as immunoglobulins. The ve major classes o immunoglobulin are immunoglobulin M (IgM ), immunoglobulin D (IgD), immunoglobulin G (IgG), immunoglobulin A (IgA), and immunoglobulin E (IgE). c. Antibodies participate in host de ense in three main ways: 1. N eutralize bacteria or bacterial toxins to prevent bacteria rom destroying host cells. 2. Coat bacteria making them more susceptible to phagocytosis. 3. Activate the complement system. B. T lymphocytes 1. T lymphocytes are small leukocytes whose main unction is to intensi y the response o other immune cells—such as B lymphocytes and macrophages—to the bacterial invasion. 2. T cells can produce substances called cytokines, such as the interleukins (ILs), that urther stimulate the immune response. Cytokine is a general name or any protein that is secreted by cells and a ects the behavior o nearby cells.

Nuc le us

B-lympho c yte s

Y-s ha p e d a ntib od ie s

Fig 13-7. B l mp o c t s. Diagram o a B cell showing the Y-shaped antibody protein attached to the cell wall.

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t h e c o m p l e m e n t Sy St e m In addition to the cellular de enders, the other major component o the immune response is the complement system. The cellular de enders only respond a ter they encounter a microorganism. Pathogens, however, can avoid contact with the immune cells. I this happens, the complement system provides a second means o de ense. 1. De nition. The complement system is a complex series o proteins circulating in the blood that works to acilitate phagocytosis or kill bacteria directly by puncturing bacterial cell membranes. The complement proteins are activated by and work with (complement) the antibodies, hence the name. 2. Three Principal Functions o Complement. A ter activation, the complement proteins interact, in a highly regulated cascade, to carry out a number o de ensive unctions (Fig. 13-8): A. Destruction o Pathogens. Components o complement can destroy certain microorganisms directly by orming pores in their cell membranes. To accomplish this task, the complement system creates a protein unit called the membrane attack complex that is capable o puncturing the cell membranes o certain bacteria (lysis). B. Opsonization o Pathogens. The complement system acilitates the engul ment and destruction o microorganisms by phagocytes. This process, known as opsonization o pathogens, is the most important action o the complement system. Complement components coat the sur ace o the bacterium allowing the phagocytes to recognize, engul , and destroy the bacterium. C. Recruitment o Phagocytes. The complement system recruits additional phagocytic cells to the site o the in ection. D. Immune Clearance. Finally, the complement system per orms a “ housekeeping” unction, the removal o immune complexes rom circulation.

Lys is

Ops o nizatio n

Comp le me nt p rote ins Ba c te ria

Ac tivatio n o f inflammato ry re s po ns e

Cle aranc e o f immune c o mple xe s Ag-Ab c omp le x

Comp le me nt re c e p tor

De g ranulatio n Tis s ue Blood

Targ e t c e ll

Phag o c yte

Extravas atio n

Phag o c yte

Comp le me nt p rote ins

Fig 13-8. Acti iti s o t Co mpl m t S st m. In this diagram, complement proteins are represented by small red triangles. Complement proteins acilitate a number o immune activities: puncturing the cell membranes o certain bacteria (lysis), phagocytosis o bacteria (opsonization), urther activation o the in lammatory response by recruitment o additional phagocytic cells to the in ection site, and clearance o immune complexes rom circulation.

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219

mo taxis, a d P ag o c to sis

1. Leukocyte Migration rom the Blood Vessels A. Transendothelial Migration 1. In order to ght an in ection, the cells o the immune system travel through the bloodstream and into the tissues (Fig. 13-9). a. N ear the in ection site, the immune cells push their way between the endothelial cells lining the blood vessels (extravasation) and enter the connective tissue (3). b. The thin layer o epithelial cells that line the interior sur ace o the blood vessels is called the endothelium. For this reason, the process o immune cells exiting the vessels and entering the tissues is called transendothelial migration. 2. De ects in transendothelial migration are associated with aggressive periodontitis underscoring the importance o this process in the de ense against the bacteria ound in plaque bio lms. B. Leukocyte Migration to the In ection Site 1. O nce the leukocytes enter the connective tissue, the cells must migrate to the site o the in ection. 2. Chemotaxis is the process whereby leukocytes are attracted to the in ection site in response to biochemical compounds released by the invading microorganisms.

P rote in Che mokine s Cytokine s

A

Fluid s

B

C

Fig 13-9. L ko c t Mig atio to Co cti Tiss . A: Leukocytes travel through the bloodstream to the site o in ection. B: Leukocytes squeeze between the cells o the blood vessel wall. C: Leukocytes enter the connective tissue and are attracted to the invading bacteria.

2. Phagocytosis A. Description. Phagocytosis is the process by which leukocytes engul and digest microorganisms (4). 1. Steps in Phagocytosis a. First, the external cell wall o a phagocytic cell (such as a neutrophil or macrophage) adheres to the bacterium (Fig. 13-10). The phagocytic cell extends nger-like projections (pseudopodia) that surround the bacterium. b. N ext, a phagocytic vesicle called a phagosome surrounds the bacterium. c. Lysosome granules use with the vesicle to orm a phagolysosome. d. The bacterium is digested within the phagolysosome. e. Finally, the phagocytic cell discharges the contents o the phagolysosome into the surrounding tissue.

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Pa t 3 Risk Factors or Periodontal Diseases

2. Local Tissue Destruction rom Phagocytosis a. Lysosomal enzymes and other microbial products are released rom a leukocyte a ter phagocytosis or when the leukocyte dies. b. O nce released the lysosomal enzymes cause damage to tissue cells in the same manner that they destroy bacteria.

1 Ba c te rium b e c ome s a tta c he d to me mb ra ne e va gina tions c a lle d p s e ud op od ia

2 Ba c te rium is inge s te d , forming p ha gos ome

3 P ha go goss ome fus e s with lys os ome

4 Lys os oma l e nzyme s ddige ige s t c a p ture d ma te ria l

5 Dige s tion p rod uc ts a re re le a s e d from c e ll

Fig 13-10. P ag o c to sis. The steps involved in phagocytosis, the process by which leukocytes engul and digest microorganisms.

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I lammato

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P o c ss

Inf ammation is the body’s reaction to injury or invasion by disease-producing organisms. The inf ammatory response ocuses on host de ense components at the site o the in ection to eliminate microorganisms and heal damaged tissue. Inf ammation is part o the immune response. It is a process that depends both on the physical actions o leukocytes and the biochemical compounds that these cells produce (1,2).

m a j o r e v e n t S In t h e In f l a m m a t o r y r e Sp o n Se 1. The inf ammatory response is triggered by the invasion o pathogens or tissue injury. 2. Immediately, mast cells (located in the connective tissues near to blood vessels) release chemicals that dilate the capillaries and increase vascular permeability (Fig. 13-11). 3. M inutes a ter tissue injury, there is an increase in blood f ow to the area. H igher blood volume heats the tissue and causes it to redden. This increased blood f ow is needed to deliver immune “ cellular de enders” to the site. 4. Within hours, leukocytes pass through the walls o capillaries into the connective tissue. Plasma proteins leak rom the capillaries and accumulate in the tissues. 5. The leukocytes phagocytose invading pathogens and release inf ammatory mediators that contribute to the inf ammatory response. A. Inf ammatory biochemical mediators are biologically active compounds secreted by cells that activate the body’s inf ammatory response. B. Inf ammatory mediators o importance in periodontitis are the cytokines, prostaglandins, and matrix metalloproteinases. 1. Leukocytes secrete cytokines that play a major role in regulating the behavior o immune cells. 2. Chemokines, a major subgroup o cytokines, cause additional immune cells to be attracted to the site o in ection or injury (5).

4 P ha goc yte s d e s troy b a c te ria

1 Tis s ue d a m a ge trigge rs a loc a l inc re a s e in Ne utrop hils a nd othe r p ha goc yte s

b lood flow a nd c a p illa ry p e rme a b ility

Ba c te ria 2 P e rm e a b le c a p illa rie s a llow a n influx of fluid (e xud a te ) a nd c e lls into tis s ue

3 P ha goc yte s migra te to

Exud a te (c omp le me nt, C-re a c tive p rote in)

s ite of infla m ma tion (c he mota xis )

Extra va s a tion Ne utrop hil Ca p illa ry

Fig 13-11. I lammato r spo s . In this illustration, bacteria have entered the body through a wound created by a nail puncture. The entry o bacteria initiates an in lammatory response that begins with the release o chemical substances that attract phagocytic cells to the site o the bacterial invasion.

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Pa t 3 Risk Factors or Periodontal Diseases

t w o St a g e S o f In f l a m m a t Io n 1. Acute Inf ammation A. Description 1. Acute inf ammation is a short-term, normal process that protects and heals the body ollowing physical injury or in ection (Fig. 13-12). 2. In the absence o inf ammation, wounds and in ections would never heal and the progressive tissue destruction would threaten the li e o the individual. 3. The acute inf ammatory process is achieved by the increased movement o plasma and leukocytes rom the blood into the injured tissues.

Tis s ue in va s io n b y b a c te ria Re s u lts in

In ju ry to the b o d y Re a c tio n

Bo d y’s infla m m a to ry re s p o ns e : In c re a s e d b lo o d flo w d e live rs th e b o d y’s d e fe ns ive c e lls a nd p la s m a to the inva s io n s ite

Le u ko c yte s a nd p la s m a p ro te in s le a k fro m b lo o d ve s s e ls in to th e tis s u e a t th e s ite o f in fe c tio n

Le uko c yte s fig h t the inva d ing b a c te ria

S o m e tis s u e d e s tru c tio n o c c urs in the a re a s urro und ing the in fe c tio n s ite tha t is a s id e -e ffe c t o f the b o d y’s in fla m m a to ry re s p o ns e

Fig 13-12. Majo e ts i t Bo d ’s I lammato r spo s . In lammation is the body’s response to injury or invasion by disease-producing organisms. This response ocuses on the body’s de ense mechanisms at the site o an injury or in ection.

B. Five Classic Symptoms o Acute Inf ammation. To inf ame means “ to set on re,” which makes us think o red, heat, and pain. Clinically, there are ve classic symptoms o acute inf ammation (Box 13-1, Fig. 13-13) at the site o in ection or injury: 1. Heat—a localized rise in temperature due to an increased amount o blood at the site. 2. Redness—the result o increased blood in the area 3. Swelling—the result o the accumulation o f uid at the site. The leukocytes and plasma that collect at the site cause the swelling (edema) associated with inf ammation. 4. Pain—the result o pressure rom edema in the tissue. The excess f uid in the tissues puts pressure on sensitive nerve endings, causing pain. 5. Loss o unction—the result o swelling and pain. For example, inf ammation o a nger (swelling and pain) would cause you to avor that nger and not use it in a normal manner.

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Basic Concepts o Immunity and In ammation

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da e xampl o Ac t I f ammatio C lli L su s in d d cu o li l n g . S li d n n is ic c m n d co v d wound wi n d siv b nd g . a w ou s l , in ju d n g is q u i in u l. W n C lli li s ssu o n wound, i ls w m n d ssu o o u c is q u i in u l. t n g lo o ks d n d sw o ll n . W h at is t h e so u rce o f t h e re d n e ss? t d n ss is d u o in c s d b lo o d f o w

Fig

13-13.

W h at is t h e p rim ary so u rce o f t h e sw e llin g ? t im y so u c o sw llin g is c u s d b y f u id in o co n n c iv issu . C lls n in g issu lso co n ib u o sw llin g . W h at is t h e cau se o f t h e w arm t h ? t w m o n in f m d su l s o m in c f ow o b in g s w i i w m .

in ju y si .

n yo co n n c iv

s d b lo o d

C. The Acute Inf ammatory Process 1. Description. The process o acute inf ammation is initiated by the blood vessels, near the injured tissue, which alter to allow the release o plasma proteins and leukocytes into the surrounding tissue. 2. PM N s are the rst leukocytes to arrive at the injured site. a. These cells phagocytose and kill invading microorganisms through the release o nonspeci c toxins. These nonspeci c toxins kill pathogens as well as adjacent host cells, sick and healthy alike. b. The PM N s release cytokines, including IL and tumor necrosis actor (TN F). c. Such inf ammatory cytokines, in turn, induce the liver to synthesize various plasma proteins called acute phase reactant proteins. 1. The liver produces C-reactive protein (CRP), a type o acute phase protein, during episodes o acute inf ammation. The levels o CRP increase up to 50,000- old in acute inf ammation. 2. Periodontitis, as well as other systemic diseases—diabetes, hypertension, and cardiovascular disease—are associated with elevated levels o CRP (6,7). 3. A study published in the Journal o Periodontology, reports that the inf ammatory e ects rom periodontal disease cause oral bacterial by-products to enter the bloodstream and trigger the liver to make CRP that inf ames the arteries and promotes blood clot ormation (8). 3. PM N s are short lived and so are primarily involved in the early stages o inf ammation. 4. I the body succeeds in eliminating all microorganisms, the tissue will heal and the inf ammation will cease. 5. Inf ammation is the body’s rst line o de ense against injury and in ection, but it’s a double-edged sword. I the acute inf ammatory responses are not e ective in controlling the invading microorganisms, the inf ammatory response becomes chronic (Fig. 13-14).

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Pa t 3 Risk Factors or Periodontal Diseases

Infla m m a to ry re s p o ns e

HEAT!

REDNES S !

S WELLING!

Ba c te ria l infe c tio n o f 2 we e ks o r le s s

PAIN!

Ac u te infla m m a tio n Ba c te ria l infe c tio n o f lo ng e r tha n 2 we e ks

LOS S OF FUNCTION!

Chro n ic infla m m a tio n

NO S YMP TOMS !

P e rs is te nt o ns la ug ht o f b a c te ria

NO S YMP TOMS !

Exa g g e ra te d ho s t infla m m a to ry re s p o n s e

Fig 13-14. Tw o Stag s o I lammatio . Acute in lammation is o short duration, whereas chronic in lammation is a long-lived in lammatory response.

2. Chronic inf ammation A. Description 1. Chronic inf ammation is a long-lived, out-o -control inf ammatory response that continues or more than a ew weeks. a. It is a pathological condition characterized by active inf ammation, tissue destruction, and attempts at repair. b. The warning signs o acute inf ammation are absent in chronic inf ammation—such as periodontitis—and the problem may go unnoticed by the host (patient). Clinically, pain o ten is absent. 2. The inf ammatory response has one all-important goal: respond immediately to destroy in ectious microorganisms in the damaged tissue be ore they can spread to other areas o the body. a. Chronic inf ammation occurs when the body is unable to eliminate the in ection. In this stage, the invading microorganisms are persistent and stimulate an exaggerated response by the host’s immune system. b. In its zeal to protect the body, the inf ammatory response will destroy as much tissue as necessary to accomplish this goal. c. In cases where inf ammation becomes chronic, the inf ammation can become so intense that it inf icts permanent damage to the body tissues. This is the case in periodontitis. B. The Chronic Inf ammatory Process 1. The accumulation o macrophages characterizes chronic inf ammation. 2. M acrophages engul and digest microorganisms. 3. Leukocytes release several di erent inf ammatory mediators, including IL-1, TNFalpha, and prostaglandins that perpetuate the inf ammatory response (Fig. 13-15).

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a. O ne o the principle cytokines secreted by macrophages is TN F-alpha (9). Evidence indicates that TN F-alpha contributes to the tissue destruction that characterizes chronic inf ammation (Table 13-3). b. In act, tissue damage is the hallmark o chronic inf ammation. 4. I the in ection persists, inf ammation can last months or even years. 5. Chronic inf ammation is abnormal and does not bene t the body. Chronic inf ammation is an out-o -control response that can destroy healthy tissue and cause more damage than the original problem. a. Le t unchecked, a hyperactive inf ammatory response can even start attacking healthy tissue. b. Chronic inf ammation is associated with a number o disease states, including asthma, rheumatoid arthritis, diabetes, atherosclerosis, gingivitis, and periodontitis.

Blood ve s s e l

Tis s ue s Co mple me nt ac tivatio n

Ma c rop ha ge

Ba c te ria Che mota xis

Tis s ue d a ma ge Che mo kine s

P MN IL-1, IL-6, TNF-α IL-8

Pro s tag landins Le uko trie ne s Ma c rop ha ge

Lymp hoc yte

Endo the lial damag e

Fig 13-15. C ll la D d s a d M diato s i I lammato r spo s . The three primary cells involved in the in lammatory response are the polymorphonuclear leukocytes (PMNs), macrophages, and lymphocytes. The irst o these cells to migrate into the tissues are the PMNs, ollowed by macrophages, and then the lymphocytes. In addition, this illustration shows some o the many chemical mediators that play a part in the in lammatory response. These include chemokines, IL-1, IL-6, TNF-alpha, prostaglandins, and leukotrienes.

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Pa t 3 Risk Factors or Periodontal Diseases

TABLe 1 3 -3 . In FLAMMATOr y BIOCh e MICAL Me DIATOr S n am

e

IL-1

In c

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m

b ili y

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in , b y liv

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s d im m u n o g lo b u lin syn

sis

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o

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a llo w l u ko cy s o xi

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t NF- l

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c io n o pMNs o in

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The immune system is a collection o responses that is responsible or de ending the body against millions o bacteria, viruses, ungi, toxins, and parasites. The prime purpose o the human immune system is to de end the li e o the individual (host) by identi ying oreign substances and developing a de ense against them. The way that an individual’s body responds to in ection is known as the host response. Without an e ective immune system, human beings would not survive. Components o the immune system that play an important role in combating periodontal disease are the cellular de enders and the complement system. In order to ght an in ection, immune cells travel through the bloodstream and into the tissues (transendothelial migration). The process whereby leukocytes are attracted to the in ection site in response to the invading microorganisms is known as chemotaxis. Phagocytosis is the process by which leukocytes engul and digest microorganisms. Inf ammation is the body’s reaction to injury or invasion by disease-producing organisms. The inf ammatory response ocuses on host immune components at the site o an in ection to eliminate microorganisms and heal damaged tissue. It relies on both the physical actions o leukocytes and the biochemical compounds that these cells produce. Acute inf ammation is a short-term, normal process that protects and heals the body. Chronic inf ammation is a long-lived, out-o -control response that continues or more than a ew weeks. In chronic inf ammation, the immune system response can sometimes become so intense that it begins to harm the body that it is trying to protect. Tissue damage is the hallmark o chronic inf ammation. Periodontal disease is a bacterial in ection that induces an inf ammatory response in the periodontal tissues. Chapter 14 ocuses on the host immune response in periodontal disease.

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CASe 1 You accidentally injure your arm by accidentally stabbing it with an ice pick. Within minutes ollowing the injury, you note some changes in the tissues in the area o the injury. What changes in the tissues should you expect i your body responds with a typical inf ammatory response? CASe 2 A new patient in your o ce reports a history o rheumatic heart disease at a very early age on her health questionnaire. The patient explains that her physician at the time thought that the rheumatic heart disease was a result o a streptococcal skin in ection that she developed a ew months prior to the discovery o the heart disease, but the physician did not explain any o the details o these conditions to her. Explain how an in ection o the skin could result in damage to the heart tissue.

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r

c s

1. Janeway C, M urphy KP, Travers P, et al. Janeway’s Im m unobiology. 7th ed. N ew York: Garland Science; 2008: p.xxi, 887. 2. Paul WE. Fundam ental Im m unology. 6th ed. Philadelphia, PA: Wolters Kluwer H ealth/Lippincott Williams & Wilkins; 2008. xviii, 1603. 3. M arshall D, H askard DO. Clinical overview o leukocyte adhesion and migration: where are we now? Sem in Im m unol. 2002;14(2):133–140. 4. Greenberg S, Grinstein S. Phagocytosis and innate immunity. Curr O pin Im m unol. 2002;14(1):136–145. 5. Van H aastert PJ, Devreotes PN . Chemotaxis: signalling the way orward. N at R ev M ol Cell Biol. 2004;5(8):626–634. 6. Fitzsimmons TR, Sanders AE, Bartold PM , et al. Local and systemic biomarkers in gingival crevicular f uid increase odds o periodontitis. J Clin Periodontol. 2010;37(1):30–36. 7. M egson E, Fitzsimmons T, Dharmapatni K, et al. C-reactive protein in gingival crevicular f uid may be indicative o systemic inf ammation. J Clin Periodontol. 2010;37(9):797–804. 8. N oack B, Genco RJ, Trevisan M , et al. Periodontal in ections contribute to elevated systemic C-reactive protein level. J Periodontol. 2001;72(9):1221–1227. 9. Tieri P, Valensin S, Latora V, et al. Q uanti ying the relevance o di erent mediators in the human immune cell network. Bioinform atics. 2005;21(8):1639–1643.

STu De n T An CILLAr y r e SOu r Ce S A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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Factors Enhancing the Microbial Challenge In ammatory Biochemical Mediators Factors A ecting the Host Immune Response

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2

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R spo s a d P rio do titis

234

Histologic Stages in Development o Periodontal Disease Mechanism or Alveolar Bone Destruction

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3

Fo c s o

Pati

ts

243

Clinical Patient Care Evidence in Action Ethical Dilemma

Cli ical Applicatio .

Members o the dental team will encounter many, many patients with gingivitis and periodontitis. Recognizing the clinical eatures o these conditions will become second nature to all clinicians. However, understanding the underlying body de ense mechanisms that can both help protect patients and do damage to the periodontium will not always be so straight orward. This chapter ocuses on the host response to plaque biof lm and the tissue destruction that ensues when bacteria present in plaque biof lm elicit a response in the host.

L ar i g Obj ctiv s • Def ne the term host response and explain its primary unction. • Name actors that can enhance the microbial challenge to the periodontium. • Def ne the term biochemical mediator and name three types o mediators. • Describe the potential role o cytokines in the pathogenesis o periodontitis. • Describe the potential role o prostaglandins in the pathogenesis o periodontitis. • Describe the e ect o increased levels o MMPs on periodontal tissues. • Name three actors that can a ect host immune response. • For each o the histologic stages o gingivitis and periodontitis listed below name one change in the host immune response likely to be encountered:

K

Bacterial Accumulation

Established Gingivitis

Early Gingivitis

Periodontitis

Tr s

Host response Host Virulence actor Biochemical mediators

Cytokines Prostaglandins Prostaglandins o the E series (PGE)

Matrix metalloproteinases (MMPs)

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1

Th Ho st R spo s i P rio do tal Dis as Periodontal disease is a bacterial in ection that induces an in ammatory response in the periodontal tissues (1–3). For the progression o disease rom health to gingivitis to periodontitis, pathogenic bacteria must be present. Research f ndings indicate that although bacteria are essential or disease to occur, the presence o suspected periodontal pathogens alone is insu f cient to cause the tissue destruction seen in periodontitis. Rather, it appears to be the body’s response to the bacteria present in plaque biof lm that is the cause o nearly all the destruction seen in periodontal disease (1,3–8). The body’s response to bacteria is re erred to as the host response. The prime purpose o the host response is to de end the li e o the individual (i.e., the host). In the instance o periodontal disease, the immune system strives to de end the body against bacteria present in plaque biof lm. The body’s de enses are activated to eliminate the potential pathogens and limit the spread o in ection, not actually to preserve the tooth or its supporting periodontal tissues.

Fa c t o r s En h a n c in g t h E M ic r o b ia l c h a l l En g E The presence o bacteria is essential or the initiation and progression o periodontal disease. It is known that bacteria can activate the human immune and in ammatory system, which can subsequently lead to damage o the periodontium (1,2). The term virulence actor re ers to all o the mechanisms that enable biof lm bacteria to colonize and damage the tissues o the periodontium. Virulence actors may be either structural characteristics o the bacteria themselves or substances that are produced by the bacteria. The primary bacterial virulence actors that can enhance damage to the periodontium are: 1. The presence o lipopolysaccharide (LPS): Gram-negative bacteria are a component o mature plaque biof lm. LPS is an endotoxin that is present on the outer membrane o Gram-negative bacteria. LPS can be responsible or initiating in ammation in periodontal tissues. 2. The ability to invade tissues: Some o the periodontal bacteria—such as Porphyrom onas gingivalis and A ggregatibacter actinomycetem com itans—can invade host tissues. Penetration o tissues can to some degree allow the bacteria to escape host de ense mechanisms. 3. The ability to produce enzymes: Several periodontal bacteria can produce enzymes such as collagenases and proteases that can directly degrade host proteins that are a basic part o the structure o the periodontium. When pathogenic bacteria success ully in ect the periodontium, the body responds by mobilizing de ensive immune cells and releasing a series o biochemical mediators to combat the bacteria. Cells involved in immune and in ammatory processes include in ammatory cells, polymorphonuclear neutrophils (PM N s), antigen-presenting cells (macrophages and Langerhans cells), T and B lymphocytes, f broblasts, and epithelial cells. These cellular components o the immune and in ammatory processes were discussed in Chapter 13.

Chapt r 14

Host Immune Response to Plaque Biof lm

in Fl a M M a t o r y b io c h EM ic a l M Ed ia t o r s In response to a microbial challenge, host immune cells secrete biologically active compounds called biochemical mediators. These biochemical mediators are the “ middlemen” sent by the host cells to activate the in ammatory response. Biochemical mediators o importance in periodontitis are cytokines, prostaglandins, and M M Ps (Table 14-1). 1. Cytokines. Cytokines are power ul regulatory proteins released by host immune cells that in uence the behavior o other cells. The cytokine (literally “ cell protein” ) is a molecule that transmits in ormation or signals rom one cell to another. When released by host cells, cytokines signal the immune system to send additional phagocytic cells to the site o an in ection. A. Sources o Cytokines. M any di erent cells including PM N s, macrophages, B lymphocytes, epithelial cells, gingival f broblasts, and osteoblasts can produce cytokines in response to the bacterial challenge or in response to tissue injury. B. Functions o Cytokines 1. Cytokines can recruit cells such as PM N s and macrophages to the in ection site. 2. Cytokines can increase vascular permeability allowing immune cells and complement to move into the tissues at the in ection site. 3. Cytokines have the potential to initiate tissue destruction and bone loss in chronic inf ammatory diseases, such as periodontitis. 4. Cytokines that play an important role in periodontitis include interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis actor-α (TN F-α ) (5,9). 2. Prostaglandins. Prostaglandins are a group o power ul biochemical mediators derived rom atty acids. Biologically important prostaglandins are prostaglandin D, E, F, G, H , and I. Prostaglandins o the E series (PGE) play an important role in the bone destruction seen in periodontitis. A. Sources o Prostaglandins. M ost cells can produce prostaglandins, but PM N s and macrophages are particularly important sources. The major source o PGE in in amed periodontal tissues is the macrophage, although PM N s and gingival f broblasts also produce them. B. Functions o Prostaglandins 1. Prostaglandins can increase the permeability and dilation o the blood vessels, leading to redness and edema o the connective tissue. 2. Prostaglandins can trigger osteoclasts (i.e., bone-resorbing cells) to destroy alveolar bone. 3. Prostaglandins can promote the overproduction o destructive M M P enzymes. 4. Prostaglandins initiate most o the alveolar bone destruction in periodontitis. 3. Matrix Metalloproteinases. Matrix metalloproteinases (MMPs) are a amily o at least 12 di erent enzymes produced by various cells o the body. These enzymes can act together to break down the connective tissue matrix. A. Sources o MMPs. PM N s, macrophages, gingival f broblasts, and junctional epithelial cells can produce M M Ps. PM N s and gingival f broblasts are the major source o M M Ps in periodontitis. B. Functions o MMPs 1. MMPs E ects in Health. In the absence o disease, M M Ps acilitate the normal turnover o the periodontal connective tissue matrix. 2. MMPs E ects in Chronic In ection and Inf ammation

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a. In the presence o chronic bacterial in ection, large amounts o M M Ps are released in what appears to be an attempt to kill the invading bacteria. b. This overproduction o M M Ps results in the enhanced breakdown o the connective tissue o the periodontium. c. In the presence o increased MMP levels, extensive collagen destruction occurs in the periodontal tissues. It should be noted that collagen provides the structural ramework o all periodontal tissues. Without collagen, the tissues o the gingiva, periodontal ligament, and supporting alveolar bone degrade, resulting in gingival recession, pocket ormation, periodontal attachment loss, and tooth mobility.

TABLe 1 4 -1 . TISSu e De STRu CTIOn By BIOCHe m ICAL m e DIATORS In Pe RIODOn TITIS m diato rs

Lo cal e

C to ki

S im u l

IL-1

cts s o s o cl s

In d u c s b

c ivi y

kd o w n o co ll g n m

lig m n , n d lv o l C to ki

IL-6

S im u l

s bon

In ib i s b o n C to ki

C to ki

IL-8

Tn F-α

mmP e z

s

io d o n

l

io d o n

l

io n (5,14)

io n (5,15)

s co n n c iv

S im u l

s bon

so

io n (5,11,17,18)

S im u l

s bon

so

io n (5,12)

issu d s u c io n (5,16)

kd o w n o co ll g n m

lig m n , n d lv o l

b o n (5,12)

S im u l

s MMp s c

io n (8,19)

S im u l

s bon

In d u c b

io n (5,10–12)

b o n (10,13)

so

o m

so

ix in g in g iv ,

S im u l

In d u c s b

Pro stag la di e 2

su l in g in b o n

so

io n (12,20–22)

kd o w n o co ll g n m

lig m n , n d lv o l

ix in g in g iv ,

ix in g in g iv ,

io d o n

b o n (13,23)

Fa c t o r s a FFEc t in g t h E h o s t iM M u n E r Es p o n s E Certain actors may have an e ect on the host’s susceptibility to periodontal disease by modi ying the host response or modi ying tissue metabolism (24,25). These actors include: genetic actors, environmental actors, and acquired actors—all o which can play important roles in periodontal disease pathogenesis (Fig. 14-1). 1. Genetic Factors. Genetic actors appear to contribute to periodontal disease. Studies in twins and amilies reported an association between periodontal disease and genetic actors (26). Diseases with genetic origin such as Papillon Le evre Syndrome

l

Chapt r 14

Host Immune Response to Plaque Biof lm

or leucocyte adhesion def ciency (LAD) are associated with aggressive type o periodontal diseases. Also, variations in the genes controlling the ormation o biochemical mediators can modi y the immune response to the plaque biof lm enough to increase the susceptibility to periodontal disease (27–30). 2. Environmental Factors. Tobacco smoking is a known risk actor or periodontal diseases. It has a signif cant e ect on the immune and in ammatory system. Smoking has been shown to decrease PM N phagocytic capacity, decrease vascularity o gingival tissues, and a ect both T- and B lymphocyte response to periodontal pathogens (31–35). 3. Acquired Factors. Diabetes mellitus is a known risk actor or periodontal diseases and its progression (36–40). Diabetes mellitus a ects the host response by reducing PM N unction, increasing IL-1, TN F-α , and PGE2 levels in gingival crevicular uid and reducing growth and proli eration o periodontal ligament f broblasts and osteoblasts in periodontium (25).

Ge ne tic fa c to rs Enviro nm e nta l fa c to rs Ac q uire d fa c to rs

Mic ro b ia l c ha lle ng e fro m b a c te ria in p la q ue b io lm

Ho s t re s p o ns e to m ic ro b ia l c ha lle ng e (Inc lud ing re le a s e o f b io c he m ic a l m e d ia to rs )

Cytokines Pros ta gla ndins MMPs

Da m a g e to p e rio d o nta l tis s ue s

Clinic a l s ig ns o f p e rio d o nta l d is e a s e

sis. Periodontal disease may be the result o an imbalance between Fig r 14-1. Th o r o Patho g the microbial bio ilm challenge and the resulting host response. The host response increases numbers o polymorphonuclear neutrophils (PMNs), produces cytokines, prostaglandins, and matrix metalloproteinases (MMPs) that mediate the destruction o connective tissue and alveolar bone.

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Risk Factors or Periodontal Diseases

R spo s a d P rio do titis

h is t o l o g ic s t a g Es in d Ev El o p M En t o F p Er io d o n t a l d is Ea s E Researchers Page and Schroeder conducted the classic, landmark research on the histologic development o gingivitis and periodontitis (8,41,42). They described our distinct histologic stages in the development o periodontal disease: initial lesion, early lesion, established lesion, and advanced lesion. For clarity these terms appear in the discussion below, but more is understood today about the host immune response related to these stages than when these researchers initially published their descriptions (Boxes 14-1 to 14-4 and Figs. 14-2 to 14-5).

Bo x 14-1. Bact rial Acc

latio

(In it ia l Le sio n ) (Fig . 14-2)

1. Bact rial F at r s. B c i co lo n iz o o su c n g in g iv l m g in . s n c o G m -n g iv b c i n d i m b o lic o d u c s 2. C ll lar F at r s. t in i i s o s im m u n s ons . A. In s o n s o b c i l o g n s, ju n c io n l i li l c lls l s v io u s b io c m ic l m d i o s, in clu d in g cyt o kin e s, PGE2 , MMPs, n d TNF-a . B. t s m d i o s s im u l im m u n s o n s , c u i in g o lym o o n u cl l u ko cy s (pMNs) o si . g in g iv l co n n c iv issu . C. pMNs ss o m b lo o d v ss ls in o 1. t pMNs n d o c su lcu s in o d o g b c i l in c io n lo c d n d so m u s v l oug g in g iv l co n n c iv issu o w d ju n c io n l i liu m n d g in g iv l su lcu s. 2. a s y ss in o g in g iv l co n n c iv issu pMNs l s cy o kin s. Cyt o kin e s re le a se d b y t h e PMNs d e st ro y h e a lt h y g in g iva l co n n e ct ive t issu e cre a t in g a p a t h w a y t h a t a llo w s t h e PMNs t o m o ve q u ickly t h ro u g h t h e t issu e . go l o pMNs is o c b c i in su lcu s n d d s o y m. t 3. t d m g o l y co n n c iv issu is n o n o m lly co n c n . In l y b o d y, is issu d s u c io n w ill b i d b c i l in c io n is b o u g u n d co n o l. in o su lcu s n d g o cy iz b c i . D. pMNs m ig e. t s n c o G m -n g iv b c i c iv s co m l m n sys m . L v l F at r s 3. Tiss A. t l q u b io lm is in i i lly lo c d su g in g iv lly. is v scul dil ion o iol s, c ill i s, nd v nul s in d n ogingiv l com l x. B. t C. t g in g iv l c vicu l f u id in c s s in vo lu m . 4. Cli ical F at r s A. At t h is st a g e t h e g in g iva lo o ks h e a lt h y clin ica lly. B. t is in i i l l sio n s d v lo s 2 o 4 d ys o llo w in g l q u b io lm ccu m u l io n . o Ho st R spo s 5. O tco A. t os s o n s is su cc ss u l i m o s o b c i d s oy d. B. I b c i l in c io n is b o u g u n d co n o l— o u g o so im m u n sys m n d c iv l q u b io lm co n o l— b o d y is b l o i d s u c io n c us d by im m u n s ons . C. I b c i l og ns n o co n o ll d , o w v , ly g in g ivi is d v lo s.

Chapt r 14

Host Immune Response to Plaque Biof lm

235

Bio lm

ENAMEL

LPS Bacterial Virulence Factor

D

E

N

T

I

N

Sulcus depth

2 mm

J unctional epithelium CEJ

IL-8 IL-1α PGE2 MMP TNF-α

IL-8

Cementum

Blood ves s el

Bacteria

PMN

Fig r 14-2. Bact rial Acc latio (In it ia l Le sio n ). This irst phase is characterized by bacterial colonization near the gingival margin, increased vascular dilatation, and PMN migration to gingival sulcus. Although the host immune and in lammatory responses are activated, the gingival tissue looks clinically healthy in this phase.

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Bo x 14-2. e arl Gi g ivitis (Ea rly Le sio n ) (Fig . 14-3) 1. Bact rial F at r s. a s b c i l ccu m u l io n n d b io lm m u io n co n in u s, b c i l o xin s n d b y- o d u c s sily n ju n c io n l i liu m . 2. C ll lar F at r s: m ig ratio a d Ch o taxis o Pm n s A. Cyt o kin e s— l s d b y ju n c io n l i li l c lls in s o n s o in c s d b c i l c ll n g — c d d i io n l c llu l d nd s o si . s d m b ili y o b lo o d v ss ls llo w s l g n u m b s o pMNs o m o v o B. In c in o g in g iv l co n n c iv issu n in c io n si . C. t in c sin g n u m b s o pMNs d s o y d d i io n l l y g in g iv l co n n c iv issu s y us ow d b c i l in v d s in su lcu s. oug ju n c io n l i liu m o o m “ w ll o c lls” b w n D. pMNs m ig b io lm n d su lcu s w ll. t s pMNs co m is m o s im o n co m o n n o lo c l d n s g in s b c i . e . Cyt o kin e s l s d b y pMNs c u s lo c liz d d s u c io n o co n n c iv issu . t is issu d s u c io n llo w s pMNs o m ig oug co n n c iv issu ow d su lcu s. F. pMNs g o cy iz b c i in su lcu s in n o o o c o s issu s o m b c i l c ll n g . 3. m ig ratio o Additio al C ll lar D d rs g s c ui d o co n n c iv issu . t s c lls l s m n y A. M c o b io c m ic l m d i o s in clu d in g cyt o kin e s, PGE2 , n d MMPs. t s b io c m ic l m d i o s c u i d d i io n l im m u n c lls o in c io n si . B. Lym o cy s b co m vid n in co n n c iv issu n d lso o d u c cyt o kin e s n d n ib o d i s. 4. Tiss L v l F at r s A. Su lcu l i liu m n d d j c n co n n c iv issu c d mos . B. Su lcu l i liu m s s o m in g i li l id g s ( i li l x n io n s o ud in o co n n c iv issu ) d u o in f m m o y c n g s. C. Ju n c io n l i liu m c lls s o o li . 5. Cli ical F at r s A. In a m m a t o ry ch a n g e s su ch a s e d e m a a n d re d n e ss o g in g iva l m a rg in a l t issu e ca n b e o b se rve d clin ica lly. B. e ly l sio n s d v lo s 4 o 7 d ys o llo w in g l q u b io lm ccu m u l io n . C. Du io n o ly g in g ivi is c n v y b w n in d ivid u ls. o Ho st R spo s 6. O tco A. t l g n u m b o pMNs m y co n o l b c i l o g n s. B. In i i io n o g o o d i n s l -c c n d is u l q u b io lm n d su l in u n o l .I b c i l in c io n is b o u g u n d co n o l— o u g o so im m u n sys m n d c iv l q u b io lm co n o l— b o d y is b l o i d s u c io n c u s d b y im m u n s ons . C. I b c i l o g n s co n in u o o li , s ly l sio n c n g s w ill b co m s b lis d g in g ivi is— n x s o d is s o g ssio n .

Chapt r 14

Host Immune Response to Plaque Biof lm Bio lm

ENAMEL

LPS Bacterial Virulence Factor

IL-8

D

E

N

T

I

N

Sulcus depth

237

Formation of epithelial ridges

2 mm

IL-8 IL-1-α PGE2 MMP TNF-α

J unctional epithelium CEJ

IL-8

IL-1β IL-6 TNF-α PGE2

Cementum

Blood ves s el

Bacteria

PMN

Macrophage

T cell

Fig r 14-3. e arl Gi g ivitis (Ea rly Le sio n ). The bio ilm overgrowth phase is characterized by subgingival plaque bio ilm ormation and intensi ied immune and in lammatory response compared to plaque bio ilm accumulation phase. Early in lammatory changes are observed clinically as redness and swelling o the marginal gingiva.

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Bo x 14-3. e stablish d Gi g ivitis (Est a b lish e d Le sio n ) (Fig . 14-4) 1. Bact rial F at r s. t l q u b io lm x n d s su b g in g iv lly in o g in g iv l su lcu s, d is u in g c m n o co o n l m o s o io n o ju n c io n l i liu m o m o o su c . 2. C ll lar F at r s: m ig ratio o Additio al C ll lar D d rs to th Sit A. L g n u m b s o su b g in g iv l b c i s im u l i li l c lls o s c cyt o kin e s, su l in g in c u i m n o d d i io n l pMNs, m c o g s, n d lym o cy s. B. M acro p h ag e s an d lym p h o cyt e s b co m m o s n u m o u s c lls in issu . PM Ns, o w v , co n in u o g b c i in su lcu s. C. a c iv d lym o cy s o d u c l g q u n i i s o n ib o d i s o ssis in co n o llin g b c i l c ll n g . D. t im m u n sys m k s s n d in g m o im m u n c lls o g b c i . Mo o xic c m ic ls l s d n d d d i io n l l y co n n c iv issu is d s o y d . 1) M c o g s x o s d o G m -n g iv b c i o d u c cyt o kin e s, PGE2 , n d MMPs. g s n d lym o cy s o . 2) Cyt o kin e s c u i d d i io n l m c o 3) PGE2 n d MMPs in i i co ll g n d s u c io n . 4) Gin g iv l b o b l s s s im u l d o o d u c d d i io n l PGE2 n d MMPs. 3. Tiss L v l F at r s A. e i li l id g s x n d d in co n n c iv issu o m in in i li l in g i y. B. Ju n c io n l i liu m d o s n o clo s ly c o o o su c n d s s o ns o m in o o ck i liu m . po ck i liu m is in n nd mo m b l co m d o ju n c io n l i liu m . C. Co ll g n lo ss in co n n c iv issu c d by in f m m io n x n d s in l l nd ic l d i c io n s. 4. Cli ical F at r s A. All t h e u su a l clin ica l e a t u re s o g in g ivit is a re e vid e n t in t h is p h a se . B. e s b lis d g in g ivi is is g n lly o b s v d 21 d ys o llo w in g l q u b io lm ccu m u l io n . 5. O tco o Ho st R spo s os s o n s is d q u o co n in b c i l c ll n g A. In m n y in d ivid u ls, d u in g is s . B. p io d o n l in s u m n io n n d i n d u c io n , is o in , c n b l u l in co n o llin g b c i l c ll n g . t co m b in io n o o ssio n l m n nd good i n s l -c c nso b c i l c ll n g nd u n io d o n iu m o l . C. In c in su sc ib l in d ivid u ls i b c i l in c io n is n o co n o ll d , s b lis d g in g ivi is o g ss s o io d o n i is. Un o u n ly, n o o n c n d ic w n n d i s b lis d g in g ivi is w ill o g ss o io d o n i is. Mu c cu n s c is d i c d o yin g o d m in w ic in d ivid u ls isk o d v lo in g io d o n i is.

Chapt r 14

Host Immune Response to Plaque Biof lm Bio lm

ENAMEL

Sulcus depth

D

E

N

T

I

N

IL-8 IL-1α PGE2 MMP TNF-α

2 mm

Epithelial ridges

LPS Bacterial Virulence Factor IL-8

MMP LT IL-1β IL-6 IL-8 TNF-α

J unctional epithelium CEJ

IL-1 TNF-α

IgG IL-6 TNF-α

IL-1α , β TNF-α IL-8

Collagen MMP TIMP

Cementum

Blood ves s el

Bacteria

PMN

Macrophage

T cell

IL-1β IL-1ra IL-6 TNF-α

B cell

PGE2 IL-10 IL-12 MMP

Plas ma cell

Fibroblas t

Fig r 14-4. e stablish d Gi g ivitis (Est a b lish e d Le sio n ): Th S bg i g ival Plaq Phas . Subgingival plaque bio ilm extends to junctional epithelium. Increased cellular in iltrate and collagen breakdown in connective tissue is observed. All clinical characteristics o gingivitis are evident in this phase.

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Bo x 14-4. P rio do titis (Ad va n ce d Le sio n ) (Fig . 14-5) 1. Bact rial F at r s. t l q u b io lm g o w s l lly n d ic lly lo n g o o su c . t io d o n l o ck o vid s n id l o c d n vi o n m n o co n in u d g o w o su b g in g iv l b c i . t s b c i l og ns s n c o n ic, d c ll n g o os . 2. C ll lar F at r s: Ho st R spo s I t sif s b c i l in c io n b co m s c o n ic, l d in g o c o n ic in f m m io n . Th e im m u n e A. t re sp o n se b e co m e s so in t e n se t h a t it b e g in s t o h a rm t h e p e rio d o n t iu m t h a t it is t ryin g t o p ro t e ct ro m t h e b a ct e ria l p a t h o g e n s (5,23). B. C llu l d n d s in n si y i d n s g in s b c i l o g n s. ca u se t h e 1. pMNs, m c o g s, n d i li l c lls o d u c cyt o kin e s d e st ru ct io n o t h e g in g iva l co n n e ct ive t issu e a n d p e rio d o n t a l lig a m e n t f b e rs. 2. M c o g s o d u c ig co n c n io n s o cyt o kin e s, PGE2 , n d MMPs re su lt in d e st ru ct io n o co n n e ct ive t issu e a n d a lve o la r b o n e (12,23). s n in issu s. MMps m d i d s u c io n o 3. h ig l v ls o MMPs x c llu l m ix o g in g iv , c d co ll g n b s ic l d g o ju n c io n l i liu m , n d io d o n l lig m n . 4. PGE2 m d i s b o n d s u c io n b y s im u l in g l g n u m b s o o s o cl s s o so b c s o lv o l b o n . t g in g iv l o ck o g ss s o b co m io d o n l o ck . im m u n sys m k s yin g o lim in b c i , bu b c i no C. t lim in d. a s mo n d m o im m u n c lls u s o si , m o issu is d m g d . Th e t issu e d e st ru ct io n ca u se d b y t h e im m u n e re sp o n se n o w o ve rw h e lm s a n y t issu e re p a ir. Tissu e d e st ru ct io n b e co m e s t h e m a in o u t co m e o t h e im m u n e syst e m re sp o n se . 3. Tiss L v l F at r s (D str ctio o P rio do tal Tiss s e s s) ju n c io n l i liu m m ig ic lly o n o o su c su l in g in A. C lls o d v lo m n o p e rio d o n t al p o ck e t . B. Gin g iv l b o b l s s s i o s vo s d e st ru ct io n o t h e g in g ival co n n e ct ive t issu e an d p e rio d o n t al lig am e n t f b e rs (Fig . 14-5). C. Os o cl s s, s im u l d b y pGe 2 d e st ro y t h e cre st o t h e alve o lar b o n e (Fig . 14-5). 4. Cli ical F at r s A. Th is a d va n ce d le sio n p h a se is ch a ra ct e rize d b y: p e rio d o n t a l p o cke t o rm a t io n , b le e d in g o n p ro b in g , a lve o la r b o n e lo ss, u rca t io n in vo lve m e n t , a n d t o o t h m o b ilit y. liu m , co n n c iv issu B. t issu c n g s su c s ic l m ig io n o ju n c io n l i d s u c io n , io d o n l lig m n d s u c io n , n d lv o l b o n lo ss no v sib l . 5. O tco o Ho st R spo s A. C o n ic in c io n b y io d o n l o g n s in d u c s c o n ic in f m m o y s o n s . Th is ch ro n ic in a m m a t io n is a n o u t -o -co n t ro l re sp o n se t h a t d e st ro ys p e rio d o n t a l t issu e s a n d ca u se s m o re d a m a g e t o t h e p e rio d o n t iu m t h a n t h e b a ct e ria l in e ct io n . Tissu e d a m a g e is t h e h a llm a rk o p e rio d o n t it is. B. F c o s in f u n cin g o s ’s ilu o co n o l b c i l c ll n g m y in clu d : 1) a b n o m l pMN u n c io n . b io lm . 2) p sis n c n d vi u l n c o b c i in 3) a cq u i d n d n vi o n m n l c o s su c s sm o kin g n d s ss. 4) Sys m ic c o s su c s u n co n o ll d d i b s m lli u s o g n ic c o s.

Chapt r 14

Host Immune Response to Plaque Biof lm

ENAMEL

D

E

N

T

I

N

Bio lm

IL-1α , β TNF-α IL-8 Epithelial ridges Sulcus depth

CEJ

6 mm

IL-8

Collagen MMP TIMP

J unctional epithelium

Cementum

Bacteria

LPS Bacterial Virulence Factor

IL-1β IL-6 IL-8 TNF-α IL-8 IL-1α PGE2 MMP TNF-α

Blood ves s el

241

MMP IL-1β IL-1ra IL-6 IL-10 IL-12

IL-1β IL-6 IL-8 TNF-α

TNF-α PGE2 MMP

PMN

Macrophage

T cell

B cell

Plas ma cell

Fibroblas t

Fig r 14-5. P rio do titis (Ad va n ce d Le sio n ). This phase is characterized by periodontal pocket ormation, bleeding on probing, alveolar bone loss, urcation involvement, and tooth mobility.

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M Ec h a n is M Fo r a l v Eo l a r b o n E d Es t r u c t io n The precise mechanism or alveolar bone destruction is not completely understood, however, the cascade o events depicted in Figure 14-6 provides a reasonable explanation or this destruction. 1. In chronic periodontitis, macrophages produce high concentrations o cytokines (IL-L and TN F-α ), PGE2 , and M M P (43). 2. The biochemical mediators produced by macrophages stimulate the resident f broblasts to secrete both PGE2 and M M P. Gingival f broblasts shi t to a state that avors the destruction o the gingival connective tissue and periodontal ligament f bers (44). 3. Biochemical mediators produced by the macrophages and f broblasts result in destruction o : A. The extracellular matrix o the gingival connective tissue B. Gingival f bers at the apical edge o the junctional epithelium C. The periodontal ligament f bers. 4. PGE2 mediates bone destruction by stimulating large numbers o osteoclasts to resorb the crest o the alveolar bone (12).

Macrophage

IL-1β

TNF-α TNF-α IL-1β

Fibroblas t

MMP

MMP

PGE2

PGE2 Os teoclas t

Extracellular matrix

Alveolar bone

Fig r 14-6. D str ctio o Co ctiv Tiss m atrix a d Alv o lar Bo . The cascade o events postulated to result in destruction o the gingival connective tissue matrix and supporting alveolar bone.

Chapt r 14

Chapt r S

ar Stat

Host Immune Response to Plaque Biof lm

t

The immune system provides the body with a strong de ense against invading periodontal pathogens. In many cases, PM N s attracted to the site are able to contain the bacterial challenge and no tissue damage occurs. I the bacterial challenge is not contained, the plaque biof lm extends subgingivally and develops into a highly organized biof lm. In many cases, the host response still is able to contain the bacterial pathogens. In some individuals, however, the host resistance is insu f cient to contain the bacterial challenge. Biochemical mediators produced by immune cells are largely responsible or the tissue destruction seen in periodontitis. High levels o cytokines, MMPs, and PGE 2 characterize periodontitis. The unrelenting, chronic bacterial in ection triggers immune responses that (1) destroy the connective tissue o the gingiva, (2) destroy the periodontal ligament, and (3) resorb the alveolar bone. Page and Schroeder described our distinct stages in histologic development o gingivitis and periodontitis: (1) bacterial accumulation (initial lesion), (2) early gingivitis (early lesion), (3) established gingivitis (established lesion), and periodontitis (advanced lesion).

S ct io

3

Fo c s o

Cli ical Pati CA S e

Pati

ts

t Car

1

M rs. Smith is a new patient in the dental o f ce. M rs. Smith is 45 years o age and has not received regular dental care in the past. H er new employer provides dental insurance or his employees and she has come to your o f ce or oral health care. M rs. Smith has chronic periodontitis. H ow will you explain in ammatory periodontal disease to M rs. Smith?

CA S e

2

Two unrelated individuals who have exactly the same level o daily sel -care and exactly the same amount o plaque biof lm accumulation do not necessarily develop the same severity o periodontal disease. H ow do you explain this act?

e vid

c i Actio

CASe 1 In reading a dental journal you f nd an article that describes a new medication that is reported to stop collagen destruction by one o the M M Ps. I this new medication does indeed block such collagen destruction, what e ect might this medication have on a patient with periodontitis? Can you think o another biochemical mediator target that could be inhibited would benef t a patient with periodontitis?

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e thical Dil

Risk Factors or Periodontal Diseases

a

CASe 1 Your next two patients are identical twin sisters who are new to the practice, M ary and Katherine. They request that you review their health histories together. You learn that they are 68 years old, both widowed, and live together. They have received routine dental care rom their longtime riend and dentist, Dr. Lipman, who just retired at 80, so they have decided to become patients in your dental o f ce. They in orm you that their mother is still alive at 90, but is edentulous, as she lost all o her teeth due to “ gum disease.” They both state that they are in good health, however, M ary was diagnosed with type II diabetes a ew years back. She states that she hasn’t paid much attention to it. Your examination and radiographs o Katherine reveal that she has generally good oral health, with localized gingivitis on the mandibular anterior region. H er sel -care appears to be more than adequate, and you compliment her on it. M ary’s examination is quite the opposite. She presents with generalized periodontitis, and vertical bone loss on her mandibular posterior teeth. She exhibits attachment loss in the 4- to 5-mm range, with localized posterior readings o 6 to 7 mm. Some o her mandibular posterior teeth are mobile. She too has good sel -care but becomes very agitated when you present your f ndings to her. She states that she and Katherine “ always” went to Dr. Lipman together and received the same treatments. She questions why her outcome is so di erent than that o her sister and asks i you think Dr. Lipman provided substandard dental care. 1. What actors may have contributed to the patient’s disease progression? 2. H ow will you discuss the host immune response in periodontal disease and periodontitis with Katherine? 3. Are there any ethical dilemmas involved?

R

r

c s

1. Bartold PM , Van Dyke TE. Periodontitis: a host-mediated disruption o microbial homeostasis. Unlearning learned concepts. Periodontol 2000. 2013;62(1):203–217. 2. Darveau RP. Periodontitis: a polymicrobial disruption o host homeostasis. N at R ev M icrobiol. 2010;8(7):481–490. 3. Ebersole JL, Dawson DR 3rd, M or ord LA, et al. Periodontal disease immunology: ‘double indemnity’ in protecting the host. Periodontol 2000. 2013;62(1):163–202. 4. Deo V, Bhongade M L. Pathogenesis o periodontitis: role o cytokines in host response. D ent Today. 2010;29(9):60–62, 64–66. 5. Graves D. Cytokines that promote periodontal tissue destruction. J Periodontol. 2008;79(8 suppl):1585–1591. 6. O ringer RJ. M odulation o the host response in periodontal therapy. J Periodontol. 2002;73(4):460–470. 7. Page RC, Kornman KS. The pathogenesis o human periodontitis: an introduction. Periodontol 2000. 1997;14:9–11. 8. Page RC, O enbacher S, Schroeder H E, et al. Advances in the pathogenesis o periodontitis: summary o developments, clinical implications and uture directions. Periodontol 2000. 1997;14:216–248. 9. Page RC. The role o in ammatory mediators in the pathogenesis o periodontal disease. J Periodontal R es. 1991;26 (3 Pt 2):230–242. 10. M cDevitt M J, Wang H Y, Knobelman C, et al. Interleukin-1 genetic association with periodontitis in clinical practice. J Periodontol. 2000;71(2):156–163. 11. Q warnstrom EE, M acFarlane SA, Page RC. E ects o interleukin-1 on f broblast extracellular matrix, using a 3-dimensional culture system. J Cell Physiol. 1989;139(3):501–508. 12. Schwartz Z , Goultschin J, Dean DD, et al. M echanisms o alveolar bone destruction in periodontitis. Periodontol 2000. 1997;14:158–172. 13. Reynolds JJ, M eikle M C. M echanisms o connective tissue matrix destruction in periodontitis. Periodontol 2000. 1997;14:144–157. 14. Roodman GD. Interleukin-6: an osteotropic actor? J Bone M iner R es. 1992;7(5):475–478. 15. H ughes FJ, H owells GL. Interleukin-6 inhibits bone ormation in vitro. Bone M iner. 1993;21(1):21–28. 16. M eikle M C, Atkinson SJ, Ward RV, et al. Gingival f broblasts degrade type I collagen f lms when stimulated with tumor necrosis actor and interleukin 1: evidence that breakdown is mediated by metalloproteinases. J Periodontal R es. 1989;24(3):207–213.

Chapt r 14

Host Immune Response to Plaque Biof lm

17. Bertolini DR, N edwin GE, Bringman TS, et al. Stimulation o bone resorption and inhibition o bone ormation in vitro by human tumour necrosis actors. N ature. 1986;319(6053):516–518. 18. Thomson BM , M undy GR, Chambers TJ. Tumor necrosis actors alpha and beta induce osteoblastic cells to stimulate osteoclastic bone resorption. J Im m unol. 1987;138(3):775–779. 19. Gemmell E, M arshall RI, Seymour GJ. Cytokines and prostaglandins in immune homeostasis and tissue destruction in periodontal disease. Periodontol 2000. 1997;14:112–143. 20. Dietrich JW, Goodson JM , Raisz LG. Stimulation o bone resorption by various prostaglandins in organ culture. Prostaglandins. 1975;10(2):231–240. 21. O enbacher S, Farr DH , Goodson JM . M easurement o prostaglandin E in crevicular uid. J Clin Periodontol. 1981;8(4):359–367. 22. Z ubery Y, Dunstan CR, Story BM , et al. Bone resorption caused by three periodontal pathogens in vivo in mice is mediated in part by prostaglandin. Infect Im m un. 1998;66(9):4158–4162. 23. Giannobile WV. H ost-response therapeutics or periodontal diseases. J Periodontol. 2008;79(8 suppl):1592–1600. 24. Albandar JM . Global risk actors and risk indicators or periodontal diseases. Periodontol 2000. 2002;29:177–206. 25. Salvi GE, Lawrence H P, O enbacher S, et al. In uence o risk actors on the pathogenesis o periodontitis. Periodontol 2000. 1997;14:173–201. 26. Cagli N A, H akki SS, Dursun R, et al. Clinical, genetic, and biochemical f ndings in two siblings with Papillon-Le evre Syndrome. J Periodontol. 2005;76(12):2322–2329. 27. Baker PJ. Genetic control o the immune response in pathogenesis. J Periodontol. 2005;76(11 suppl):2042–2046. 28. H art TC, Kornman KS. Genetic actors in the pathogenesis o periodontitis. Periodontol 2000. 1997;14:202–215. 29. M ichalowicz BS. Genetic and heritable risk actors in periodontal disease. J Periodontol. 1994;65(5 suppl):479–488. 30. N ibali L, O ’Dea M , Bouma G, et al. Genetic variants associated with neutrophil unction in aggressive periodontitis and healthy controls. J Periodontol. 2010;81(4):527–534. 31. Barbour SE, N akashima K, Z hang JB, et al. Tobacco and smoking: environmental actors that modi y the host response (immune system) and have an impact on periodontal health. Crit R ev O ral Biol M ed. 1997;8(4):437–460. 32. Johnson GK, Guthmiller JM . The impact o cigarette smoking on periodontal disease and treatment. Periodontol 2000. 2007;44:178–194. 33. Kenney EB, Kraal JH , Saxe SR, et al. The e ect o cigarette smoke on human oral polymorphonuclear leukocytes. J Periodontal R es. 1977;12(4):227–234. 34. Rezavandi K, Palmer RM , O dell EW, et al. Expression o ICAM -1 and E-selectin in gingival tissues o smokers and nonsmokers with periodontitis. J O ral Pathol M ed. 2002;31(1):59–64. 35. Tomar SL, Asma S. Smoking-attributable periodontitis in the United States: f ndings rom N H AN ES III. N ational H ealth and N utrition Examination Survey. J Periodontol. 2000;71(5):743–751. 36. Diabetes and periodontal diseases. Committee on Research, Science and Therapy. American Academy o Periodontology. J Periodontol. 2000;71(4):664–678. 37. Botero JE, Yepes FL, Roldan N , et al. Tooth and periodontal clinical attachment loss are associated with hyperglycemia in patients with diabetes. J Periodontol. 2012;83(10):1245–1250. 38. Deshpande K, Jain A, Sharma R, et al. Diabetes and periodontitis. J Indian Soc Periodontol. 2010;14(4):207–212. 39. M ealey BL, O ates TW; American Academy o Periodontology. Diabetes mellitus and periodontal diseases. J Periodontol. 2006;77(8):1289–1303. 40. Preshaw PM , Bissett SM . Periodontitis: oral complication o diabetes. Endocrinol M etab Clin N orth A m . 2013;42(4): 849–867. 41. Page RC. The etiology and pathogenesis o periodontitis. Com pend Contin Educ D ent. 2002;23(5 suppl):11–14. 42. Page RC, Schroeder H E. Pathogenesis o in ammatory periodontal disease. A summary o current work. L ab Invest. 1976;34(3):235–249. 43. M cCauley LK, N ohutcu RM . M ediators o periodontal osseous destruction and remodeling: principles and implications or diagnosis and therapy. J Periodontol. 2002;73(11):1377–1391. 44. Dongari-Bagtzoglou AI, Ebersole JL. Gingival f broblast cytokine prof les in Actinobacillus actinomycetemcomitans-associated periodontitis. J Periodontol. 1996;67(9):871–878.

STu De n T An CILLARy Re SOu RCe S A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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r e t p a h C

15 Se ctio

S ste mic Co ditio s that Amplif Susce ptibilit to Pe rio do tal Dise ase 1

S ste mic Risk Facto rs fo r Pe rio do titis

248

Diabetes Mellitus Leukemia HIV In ection Hormonal Fluctuations During Puberty, Pregnancy, and Menopause

Se ctio

2

Ge e tic Risk Facto rs fo r Pe rio do titis

261

Se ctio

3

S ste mic Me dicatio s w ith Pe rio do tal Side Effe cts

265

Fo cus o

269

Se ctio

4

Patie ts

Clinical Patient Care Evidence in Action Ethical Dilemma

Cli ical Applicatio .

Plaque biof lm is the undamental etiology or periodontal disease, but evaluating patients with periodontal disease o ten can be quite con using. Frequently patients with minimal plaque biof lm challenge will be ound to have advanced disease or no readily apparent reason. Some o these patients will have systemic conditions that can ampli y their susceptibility to the periodontal disease, presenting a con using clinical presentation. All members o the dental team must be alert or the possibility o systemic risk actors when evaluating patients with the signs o periodontal disease. This chapter presents an interesting outline o these systemic conditions.

Le ar i g Obje cti e s • Name several systemic diseases/conditions that may modi y the host response to periodontal pathogens. • Discuss the potential implications o these systemic diseases on the periodontium: uncontrolled diabetes, leukemia, and acquired immunodef ciency syndrome. • Discuss how hormone alterations may a ect the periodontium. • Def ne the term osteoporosis and discuss the link between skeletal osteoporosis and alveolar bone loss in the jaw. • Discuss the implications o Down syndrome on the periodontium.

Chapte r 15

Systemic Conditions that Ampli y Susceptibility to Periodontal Disease

• Name three medications that can cause gingival enlargement. • For a patient in your care with periodontitis who is amplif ed by a systemic condition, explain to your clinical instructor the risk actors that may have contributed to the severity o your patient’s periodontitis.

Ke Te rms Systemic risk actors Diabetes mellitus Well-controlled diabetes Leukemia Oral mucositis Linear gingival erythema

Pregnancy gingivitis Pregnancy-associated pyogenic granuloma Menopausal gingivostomatitis

Drug-in luenced gingival enlargement Phenytoin Cyclosporine Ni edipine

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Risk Factors or Periodontal Diseases

1

S ste mic Risk Facto rs fo r Pe rio do titis Additional actors, other than the presence o bacteria, play a signi cant role in determining why some individuals are more susceptible to periodontal disease than others. Systemic risk actors are conditions or diseases that increase an individual’s susceptibility to periodontal in ection by modi ying or ampli ying the host response to the bacterial in ection. Proven systemic risk actors include diabetes mellitus, osteoporosis, hormone alteration, medications, tobacco use, and genetic inf uences. Tobacco use as a risk actor or periodontal disease is discussed in Chapter 18.

Dia b e t e s M e l l it u s 1. Characteristics o Diabetes Mellitus. Diabetes mellitus is a chronic disease in which the body does not produce or properly use insulin. Insulin is a hormone that is needed to convert sugar, starches, and other ood into energy that the body uses to sustain li e. The World H ealth O rganization (WH O ) estimates that the number o adults in the world with diabetes will rise to 366 million in the year 2030 (1). 2. Diabetes as a Risk Factor or Periodontitis A. Incidence o Periodontitis 1. Patients with well-controlled diabetes have no more periodontal disease than persons without diabetes. Diabetes is well controlled i the blood glucose levels are stabilized within the recommended range. The response o individuals with controlled diabetes to nonsurgical periodontal therapy is similar to that o nondiabetic persons, with similar trends in improved probing depth and attachment gain (2). 2. Individuals with undiagnosed or poorly controlled diabetes are at greater risk or severe periodontitis than are persons with controlled diabetes and nondiabetic individuals (Figs. 15-1–15-3). Periodontal disease is considered a complication o uncontrolled diabetes. a. Individuals with undiagnosed or poorly controlled diabetes have high blood glucose levels. There is a clear relationship between the degree o high blood sugar and the severity o periodontitis (3,4). As glucose levels increase, individuals with undiagnosed or poorly controlled diabetes experience a dramatic decline in periodontal health (4–7). b. A large number o epidemiologic studies demonstrate that periodontitis is more prevalent and severe in individuals with uncontrolled diabetes mellitus versus nondiabetic individuals. People with uncontrolled or undiagnosed diabetes are approximately three times more likely to develop periodontitis (3,4,8–12). c. Periodontal attachment loss (connective tissue destruction and bone loss) occurs more requently in individuals with poorly controlled diabetes than in individuals with well-controlled diabetes (5,7,13–15). A person with diabetes who smokes, and who is age 45 or older, is 20 times more likely than a nondiabetic, nonsmoking individual to experience severe periodontitis. d. An un avorable treatment outcome may occur in long-term maintenance therapy o individuals with poorly controlled diabetes (16). Individuals with poorly controlled diabetes have a poorer response to nonsurgical and surgical periodontal therapy, more rapid recurrence o deep pockets, and a less avorable long-term response to treatment.

Chapte r 15

Systemic Conditions that Ampli y Susceptibility to Periodontal Disease

249

Fig ure 15-1. I flammato r Re actio . Note the localized in lammatory swelling o the gingiva on the palatal sur ace o the maxillary lateral incisor. The patient has uncontrolled diabetes mellitus. This intense in lammatory reaction is typical or individuals with uncontrolled diabetes. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

Fig ure 15-2. Pe rio do titis Asso ciate d w ith Po o rl Co tro lle d Diabe te s. Marked tissue changes are evident in this individual with poorly controlled diabetes. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

Fig ure 15-3. Pe rio do titis Asso ciate d w ith U co tro lle d Diabe te s. Examination o this patient revealed pronounced tissue changes and loss o attachment. The patient stated that he has been diagnosed with diabetes but that he is not seeing a physician or taking any medications or diabetes. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

B. E ects o Increased Glucose Blood Levels on the Periodontium. An individual with uncontrolled or poorly controlled blood glucose levels has an increased risk or developing acute periodontal abscesses, more extensive attachment loss and progressive alveolar bone loss (Fig. 15-4). 1. Hyperglycemia (high blood sugar) in uncontrolled diabetics results in increased glucose in the gingival crevicular f uid and blood. Since many bacteria thrive on sugars, this glucose-rich crevicular f uid may result in altered bacterial composition within the bio lm microcolonies and inf uence the development o periodontal disease (17). Periodontal status—as estimated by degree o attachment loss—deteriorates signi cantly with poor glycemic control in diabetes (5–7).

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2. Reduced PM N unction and de ective chemotaxis in uncontrolled diabetics can contribute to impaired host de enses. Since PM N s are the rst line o de ense against periodontal pathogens, reduced PM N unction allows the bacteria to increase greatly in number (16). 3. Individuals who have both diabetes and periodontitis have signi cantly higher levels o IL-1β and PGE2 in gingival crevicular f uid compared to nondiabetic controls with a similar degree o periodontal disease (18). 4. H yperglycemia can a ect the synthesis, maturation, and maintenance o collagen and extracellular matrix. a. The hyperglycemic state results in the excessive ormation o accumulated glycation end-products (AGE). AGEs are derived rom the reaction o glucose and proteins. These substances are involved in biological processes relating to collagen turnover. b. Collagen is cross-linked by AGE ormation, making it less likely to be repaired or to be newly synthesized normally. Collagen in the gingival tissues o individuals with uncontrolled diabetes is aged and more susceptible to breakdown. C. Other Oral Complications o Poorly Controlled Diabetes Mellitus 1. Reduced salivary f ow and burning mouth or tongue are common complaints o patients with uncontrolled diabetes (19–21). Dental healthcare pro essionals should suspect undiagnosed diabetes as a likely cause o burning tongue and re er the patient to a physician or ollow-up care. 2. Reduced salivary f ow and xerostomia can encourage the growth o Candida albicans and the development o oral candidiasis (22). 3. Individuals with undiagnosed or poorly controlled diabetes requently present with multiple periodontal abscesses, leading to rapid destruction o periodontal bone support.

Tis s ue d e s truc tio n

Enzym e s elas tas e/collagenas e/β-glucuronidas e

Cyto kine s IL1, TNFα

PMNs

Monocyte/macrophage s timulation

Impaired chemotaxis

Chro nic hyp e rg lyc e m ia

Ad va nc e d g lyc a tio n e nd p ro d uc ts

Reduced migration

Capillary thickening

Altered connective tis s ue broblas t/os teoblas t

Im p a ire d ho s t d e fe ns e s

Fig ure 15-4. Po stulate d Effe cts o f U co tro lle d Diabe te s Me llitus o

P o o re r h e a ling

the Ho st Re spo se .

Chapte r 15

Systemic Conditions that Ampli y Susceptibility to Periodontal Disease

D. Diabetes Mellitus: Implications or the Dental Hygienist 1. The dental team can act as an important point o contact or early screening and diagnosis o undiagnosed diabetes. In 2007, it was estimated that 24 million people in the United States have diabetes and 24% o those are undiagnosed (about 5.8 million undiagnosed diabetics). For every 1,000 adult dental patients, approximately 120 would have diabetes and about 40 would be undiagnosed (23,24). Knowledge about the association between diabetes and periodontal disease should be increased among dental and medical practitioners to prevent, manage, and control periodontal disease e ectively (25). 2. The dental team is well placed to screen patients or diabetes since many people (70% o Americans) visit their dentist regularly (e.g., every 6 months) o ten more requently than they visit their medical practitioner (23,26). The level o diabetic control and the health status should be care ully monitored or all individuals with diabetes. 3. Educating patients with diabetes about the importance o good oral sel -care needs to become a priority or dental hygienists (27). Dental hygienists’ role in periodontal care and regular, ongoing involvement with these individuals places hygienists in an optimal position to provide this education (28). Dental hygienists are very adept and experienced in instituting behavioral changes in their patients and represent an untapped resource or medical colleagues in this role. 4. Patients with diabetes o ten are poorly in ormed about the relationship between periodontitis and diabetes. There ore, dental healthcare providers should be aware o this link and emphasize the importance o care ul sel care at home and requent pro essional care visits (27,29–31). People with poorly controlled diabetes (adults and children) must be considered at risk or periodontitis and should be in ormed o this risk. 5. Closer collaboration between medical and dental clinical teams is necessary or the joint management o people with diabetes and periodontitis (10,32). Collaboration o dental pro essionals with certi ed diabetes educators (CDEs) will improve the ability o CDEs to educate their clients about oral health topics (33). 6. Researchers at Columbia University reported on the largest study to date o 6- to 18-year-old individuals with diabetes and 350 individuals in the same age group without diabetes. The children and adolescents with diabetes showed signi cantly more periodontal disease than those without diabetes. Children and adolescents with diabetes had greater attachment loss than those without diabetes. Based on these ndings, children with diabetes should be examined or signs o periodontal disease and receive early intervention and prevention (2,34).

l e u k e M ia 1. Characteristics o Leukemia A. Leukemia is cancer that begins in blood cells. In people with leukemia, the bone marrow produces a large number o abnormal white blood cells that don’t unction properly. At rst, leukemia cells unction almost normally. In time, they may crowd out normal white blood cells, red blood cells, and platelets. This makes it hard or blood to do its work. The N ational Cancer Institute estimates that there were 48,610 new cases and 23,720 deaths rom leukemia in the United States in 2013. Leukemia is a disease o both children and adults and is more common in men and boys than girls and women.

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B. Types o Leukemia 1. Leukemia is classi ed on the duration (acute or chronic) and the type o cell involved (myeloid or lymphoid). a. Leukemia is either chronic (gets worse slowly) or acute (gets worse quickly). b. Leukemia that a ects the lymphoid cells is called lym phocytic. Leukemia that a ects the myeloid cells is called myelogenous leukemia. 2. Leukemia is the most common cancer in children younger than 15 years old (35). C. Medical Treatment o Leukemia 1. Treatment or leukemia is complex and is not the same or all patients. It varies with the type o leukemia, extent o the disease, and also on the patient’s age, symptoms, and general health. The physician plans the treatment to t each patient’s needs. 2. M ost patients with leukemia are treated with chemotherapy. Some also may have radiation therapy and/or bone marrow transplantation (BM T) or biological therapy. 3. Chemotherapy causes patients to su er rom severe suppression o the immune system. Chemotherapy unctions by suppressing the growth and spread o malignant cells; un ortunately, normal cells are also adversely a ected. N ormal cells with the highest rate o cell turnover (proli eration)—such as those o the mouth—are a ected because chemotherapy inter eres with cell production, maturation, and replacement. 4. Dental care is a vital component o treatment. Anticancer treatments or leukemia can make the mouth sensitive, easily in ected, and likely to bleed (35–40). 2. Oral Complications o Leukemia A. Leukemia-Associated Gingivitis 1. In ammation o the Gingiva. Signs o inf ammation in the gingiva include swollen, glazed, and spongy tissues that are red to deep purple in appearance (Fig. 15-5). Gingival bleeding is also a common sign. Areas o spontaneous bleeding usually are characterized by intermittent oozing o blood. a. In a study o 1,093 adult inpatients undergoing chemotherapy treatment or leukemia, 14.9% o patients mani ested gross bleeding rom the mouth during the course o chemotherapy (41). The most common oral bleeding sites were the lips, tongue, and gingiva. b. In children, the prevalence o gingival inf ammation is highest in the maintenance phase o chemotherapy ollowed by the induction phase with radiotherapy (36). 2. Gingival Enlargement. Gingival enlargement is a common characteristic, initially beginning at the interdental papilla ollowed by marginal and attached gingiva.

Fig ure 15-5. Le uke mia-Asso ciate d Gi g i itis. Note the swollen, red gingival tissues in this patient with leukemia. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

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B. Oral Mucositis 1. Oral mucositis is an inf ammation o the oral mucous membranes caused when chemotherapy attacks and kills the rapidly dividing cells o the mucous membranes. Cells o the oral mucosa have a li espan o only 10 to 14 days. There ore, during chemotherapy, mucosal cells are dying at a aster rate than new cells can be produced. 2. Sloughing o mucosal sur aces can be localized or generalized involving the buccal mucosa, palate, f oor o the mouth, gingiva, lips, and/or tongue. Ulcerations o the oral cavity also are a common complication o chemotherapy. C. Xerostomia 1. Xerostomia may occur due to damage o the salivary glands during radiation therapy. A reduction in salivary f ow alters the sel -cleaning mechanisms o the oral cavity resulting in rapid bio lm accumulation and the development o dental caries. 2. Lack o saliva also can result in diminished taste perception and/or di culty in swallowing and talking. 3. Reduced salivary f ow and xerostomia can encourage the growth o C. albicans and the development o oral candidiasis (42). 3. Leukemia: Implications or the Dental Hygienist A. The dental team can act as an important point o contact or early screening and diagnosis o undiagnosed leukemia. In some individuals, the rst signs o leukemia show up in the oral cavity (35,43). 1. When a dental patient has spontaneous gingival bleeding and/or gingival enlargement or no apparent reason—combined with symptoms such as acial swelling, tiredness, poor appetite, lethargy, musculoskeletal pain—the individual should be re erred to a medical specialist (35,43). 2. The act that leukemia requently presents with early oral mani estations emphasizes the need or dental pro essionals who are aware o the early oral signs o leukemia and can provide a timely re erral. B. Frequent un avorable oral conditions o individuals undergoing anticancer therapy or leukemia highlight the responsibility o the otolaryngologist to re er these patients to the dental o ce (36,44). The planning o anticancer therapy or leukemia should include dental pro essionals in the multidisciplinary oncology team. 1. Immune suppression during chemotherapy may cause serious oral in ections. There ore, pro essional diagnosis and elimination o oral in ection oci must be carried out as early as possible be ore chemotherapy. Aggressive chemotherapy causes xerostomia and as a consequence an increased risk or oral diseases. 2. Adequate oral care be ore, during, and a ter chemotherapy is necessary to prevent oral diseases and systemic complications o oral origin. Frequent dental care is essential or improvement in oral conditions that may diminish patient su ering and prevent the spread o serious in ections rom the oral cavity to other parts o the body (36). 3. Chemotherapy can cause a sore and sensitive mouth that bleeds easily. So t toothbrushes with gentle brushing should be recommended. I the mouth is too sensitive to tolerate toothbrushing, so t dental sponges (available rom a pharmacy) can be recommended. C. Pain rom oral mucositis a f icts rom 40% to 70% o patients receiving chemotherapy or radiation therapy. Current methods o clinical pain management (e.g., topical anesthetics, systemic analgesics) have limited success (45). 1. O ral mucositis is common in children undergoing chemotherapy. In 2011, a study by Soares et al. (40) suggest that the prophylactic use o 0.12% chlorhexidine gluconate reduces the requency o oral mucositis and oral pathogens in children with leukemia.

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2. In a pilot study, Berger examined the ability o oral capsaicin to provide temporary relie o oral mucositis pain. a. Capsaicin (cap-SAY-sin) is the active ingredient in chili peppers. Along with being very spicy, capsaicin also helps to relieve pain. It has antiinf ammatory e ects, much like aspirin or ibupro en. b. The oral capsaicin ta y recipe in Box 15-1, developed by nurses, uses just enough o the cayenne pepper to get the anti-inf ammatory e ects and produces temporary pain reduction (45). Clinicians should monitor patients with care, however, since this sugar containing candy may increase the risk o developing dental caries. D. Good nutrition can become challenging due to mouth sores and/or xerostomia during anticancer treatment or leukemia. Table 15-1 summarizes recommendations or good nutrition. E. Care should be coordinated with other health pro essionals. Interpro essional collaboration among pro essionals such as physicians, dental pro essionals, dieticians, and case managers is an essential component o patient-centered care (46).

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HiV in f e c t io n 1. Characteristics o Human Immunodef ciency Virus (HIV) In ection A. Acquired immunode ciency syndrome (AIDS) is a communicable disease caused by H IV. People with AIDS are at an increased risk or developing certain cancers and or in ections that usually occur only in individuals with a weak immune system. B. In most developed countries, the death rate rom AIDS among adults has declined largely because o newer antiretroviral therapies and improved access to these therapies (47,48). N evertheless, because o the large numbers o existing plus new cases o H IV in ection, dental and medical practitioners will still be required to treat oral and periodontal conditions in H IV-in ected adults and children (49). C. Periodontal diseases strongly associated with H IV in ection are classi ed as linear gingival erythema and necrotizing periodontal diseases (47,50). N ecrotizing periodontal diseases are discussed in Chapters 9 and 28. 2. Linear Gingival Erythema A. Characteristics 1. Gingival mani estations o H IV in ection were ormerly known as H IVassociated gingivitis but currently are designated as linear gingival erythema. Linear gingival erythema (LGE) is characterized by a 2- to 3-mm marginal band o intense erythema (redness) in the ree gingiva (Fig. 15-6) (51). 2. The band o gingival erythema may extend into the attached gingiva and/or extend beyond the mucogingival line into the alveolar mucosa (51). Linear gingival erythema may be localized to one or two teeth but is more commonly a generalized gingival condition. 3. The lack o response o linear gingival erythema to conventional sel -care and periodontal therapy is an important criterion in its diagnosis (52).

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Fig ure 15-6. Li e ar Gi g i al Er the ma. Gingival changes associated with linear gingival erythema. Note the marginal band o intense erythema in the ree gingiva.

4. The etiology o linear gingival erythema is not well understood. Research suggests that organisms not generally associated with gingivitis, such as Candida species, are associated with linear gingival erythema (51,53). 5. With the advent o antiretroviral therapy or H IV-positive patients, the prevalence o H IV-speci c lesions has been dramatically reduced (3,54,55). 3. HIV-In ected Individuals: Implications or the Dental Hygienist A. H IV-in ected individuals should be monitored to prevent irreversible periodontal damage. The need or early periodontal therapy and more requent maintenance visits should be stressed. Continuity o dental care remains important or H IVpositive patients even when they are being treated with antiretroviral therapies (55–58). Dental healthcare providers should emphasize the importance o care ul sel -care at home and requent pro essional care visits (56). B. The initial treatment or linear gingival erythema should be standard periodontal therapy plus the use o 0.12% chlorhexidine gluconate as a mouth rinse. Consideration may be given to the use o antibiotics (52). C. Care should be coordinated with other health pro essionals. Interpro essional collaboration among pro essionals such as physicians, dental pro essionals, social workers, dieticians, and case managers is an essential component o patientcentered care (46,59). D. Despite the bene cial e ects o antiretroviral therapies, drug interactions with other medications have been observed. For instance, f uconazole, ketoconazole, itraconazole, metronidazole, ciprof oxacin, midazolam, and triazolam can interact with some antiretroviral medications, such as zidovudine, nevirapine, and ritonavir. Dental pro essionals need to understand drug interaction in H IV in ection in order to establish a better control during periodontal treatment (47).

Ho r M o n a l f l u c t u a t io n s Du r in g Pu b e r t y , Pr e g n a n c y , a n D M e n o Pa u s e H ormonal f uctuations during puberty, pregnancy, and menopause impact the periodontal tissues. 1. Puberty A. Impact o Puberty on the Periodontium 1. During puberty there are increased levels o estradiol in emales and testosterone in males. Increased levels o sex hormones during puberty cause increased blood circulation to the gingival tissues and may cause an increased sensitivity to local irritants, such as plaque bio lms, resulting in pubertal gingivitis.

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2. Pubertal gingivitis occurs equally in girls and boys. The tendency or plaqueinduced gingivitis usually decreases as the young person progresses through puberty. 3. Clinical eatures o pubertal gingivitis include a. Accumulation o plaque bio lm b. Red, inf amed, swollen gingival tissue; bleeding upon probing c. Reversible with meticulous daily sel -care; reversible ollowing puberty B. Implications or the Dental Hygienist 1. Dental hygienists should stress that daily attention to bio lm control (sel -care) and requent pro essional care are very important or gingival health during puberty (60). 2. The American Dental Association (ADA) recommends the use o antimicrobial mouth rinses, antibiotic therapy, and aggressive periodontal therapy or any severe cases o puberty gingivitis. 2. Pregnancy A. Impact o Pregnancy on the Periodontium 1. Inf ammation o the gingiva increases in pregnant women in the presence o even small amounts o plaque bio lm. a. The likelihood o gingival inf ammation increases in the second and third trimesters when enhanced estrogen levels in the blood increase sensitivity to plaque bio lm and other local irritants (61). Pregnant women, near or at term, produce large quantities o estradiol, estriol, and progesterone. b. Elevated progesterone levels in pregnancy enhance capillary permeability and dilation resulting in increased gingival exudate and edema (62). c. During pregnancy pro ound changes in immune response impact the periodontal tissues (63). H igh levels o progesterone and estrogen associated with pregnancy have been shown to suppress the immune response to dental plaque bio lm. PM N chemotaxis and phagocytosis have been reported to be depressed in response to high levels o gestational hormones (64). 2. Gingival inf ammation initiated by plaque bio lms, and exacerbated by hormonal changes in the second and third trimesters o pregnancy, is re erred to as pregnancy gingivitis. a. The gingival tissue may be edematous and dark red, with bulbous interdental papillae (Figs. 15-7 and 15-8). b. In some cases, a gingival papilla can react so strongly to plaque bio lm that a large, localized overgrowth o gingival tissue called a pregnancyassociated pyogenic granuloma (pregnancy tumor), may orm on the interdental gingiva or on the gingival margin (Fig. 15-9). 1. These growths are benign and are generally not pain ul. 2. I the growth persists a ter delivery, it can be surgically removed. c. Probing depths, bleeding on probing, and crevicular f uid f ow are increased in pregnancy gingivitis. B. Expectant Patient: Implications or the Dental Hygienist 1. Dental pro essionals and gynecologists should educate pregnant patients about the importance o oral health. The perinatal period is an ideal time to educate and per orm dental treatment on expectant mothers (65,66). Pregnancy provides an opportunity to educate women regarding oral health with sel -care and uture child care (67).

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Fig ure 15-7. Pre g a c Gi g i itis. Clinical appearance o reddened, swollen tissues o pregnancy gingivitis. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

Fig ure 15-8. Ho rmo al Gi g i itis. Hormonal gingivitis is evident 3 weeks postpartum (a ter giving birth) in this emale patient. (Used with permission rom Langlais RP. Color Atlas of Common Oral Diseases. Philadelphia, PA: Wolters Kluwer; 2003.)

Fig ure 15-9. Pre g a c -Asso ciate d P o g e ic g ra ulo ma. The clinical appearance o a pyogenic granuloma (pregnancy tumor).

a. The e ects o pregnancy on the gingival tissues and the importance o thorough daily sel -care or plaque control in combination with regular pro essional care should be stressed. b. The dental hygienist should ask the expectant woman i she has any concerns about getting dental care while pregnant and be ready to address her concerns. c. Expectant women should be advised that prevention, diagnosis, and treatment o oral diseases—including needed dental x-ray and use o local anesthesia—is sa e, bene cial, and can be undertaken any time during pregnancy (68). Also, acute/emergency care may be provided at any time during pregnancy. d. H ygienists should encourage behaviors that support good oral health. 1. M eticulous daily sel -care or bio lm control.

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259

2. Prenatal vitamins, including olic acid to reduce the risk o birth de ects such as cle t lip and palate. 3. Chewing xylitol-containing gum to decrease caries risk. 2. Expectant women experiencing requent nausea and vomiting should be advised that erosion o tooth sur aces might be reduced by a. Eating more requent, smaller meals consisting o nutritious oods. b. Using a rinse comprised o one-teaspoon baking soda in a cup o water should be used to rinse and spit out a ter vomiting. Avoiding toothbrushing directly a ter vomiting as the e ect o erosion can be exacerbated. 3. A comprehensive periodontal treatment plan should be developed or preventive, treatment, and maintenance care throughout pregnancy. In addition, the importance o regular dental care during the postpartum period and therea ter should be emphasized. 4. Dental care should be coordinated with the expectant woman’s medical care pro essional to ascertain whether other risk actors—such as gestation diabetes—are present and to advise the medical pro essional o the periodontal status o the patient and any proposed treatment. 3. Menopause and Postmenopause A. Impact o Menopause on the Periodontium 1. A ter menopause, some women become more susceptible to periodontal disease. Dental healthcare providers o ten are the rst pro essionals to notice changes that occur during menopause. The periodontium is extremely susceptible to hormonal changes that take place just be ore menopause. A literature review by Dutt, Chaudhary, and Kumar compiled data on the major orodental complications observed during menopause. This review observed that the health o the periodontium is most severely a ected, ollowed by dry mouth and burning mouth; which, in turn, may increase the occurrence o oral mucosal and dental diseases, such as candidiasis (69). 2. I menopause does a ect the gingiva, it is called menopausal gingivostomatitis. M enopausal gingivostomatitis is characterized by gingivae that bleed readily, with an abnormally pale, dry, shiny erythematous appearance (70). 3. During menopause there is a decline in hormonal levels, most notably, a rapid decline in estrogen levels. Lack o estrogen during and a ter menopause may cause the loss o bone. The rapid decline in estrogen can lead to systemic bone loss. Osteoporosis is a reduction in bone mass that causes an increased susceptibility to ractures (Fig. 15-10). Osteopenia is a condition in which there is a lower than average bone density but not necessarily an increase in the risk or incidence o racture.

Fig ure 15-10. He alth Bo e v e rsus Bo e w ith Oste o po ro sis. The upper illustration depicts the structure o healthy bone. The lower illustration depicts the reduction in bone mass commonly seen in osteoporosis.

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4. Bisphosphonates are the most commonly prescribed medications to inhibit the bone resorption o systemic osteoporosis. In dentistry, there is concern about bisphosphonate-associated osteonecrosis o the jaw (71). O steonecrosis o the jaw is a rare disorder characterized by pain ul areas o exposed bone in the mouth that ail to heal a ter an extraction or oral surgery procedure. Bisphosphonates and osteonecrosis are discussed in Chapter 26, H ost M odulation. 5. The same processes that lead to loss o bone in the spine and hips can also lead to loss o alveolar bone. a. There may be a link between skeletal osteoporosis, alveolar bone loss in the jaw, and tooth loss (72–74). Preliminary studies report signi cant correlations between mandibular bone mineral density and hipbone mineral density (74,75). Some studies suggest that emales with osteoporosis are at an increased risk o periodontal attachment loss and tooth loss (72,75,76). b. The American Academy o Periodontology considers osteoporosis to be a risk actor or periodontal disease (77). The relationship between alveolar bone loss and systemic bone loss, however, is not yet ully understood (78). c. In and o itsel , however, osteoporosis does not initiate periodontitis. Loss o density o the alveolar bone, however, may exacerbate the bone resorption seen in pre-existing periodontitis. d. Estrogen replacement therapy improves bone density in postmenopausal women. In a 3-year study, hormone/estrogen replacement therapy signi cantly increased alveolar bone mass compared with placebo and tended to improve alveolar crest (79). 6. Genco and Grossi (80) have proposed a model or estrogen de ciency as a risk actor or periodontal disease (Fig. 15-11). B. Menopause: Implications or the Dental Hygienist 1. Dental hygienists and gynecologists should educate postmenopausal women about osteoporosis and interventions such as calcium supplements and weightbearing exercise. 2. M eticulous daily sel -care, combined with regular pro essional care, decreases the likelihood o periodontal problems during menopause.

Es tro g e n de fic ie nc y + buildup o f plaque bio film

Ho s t inflammato ry re s po ns e Inc re a s e d p rod uc tion of b one -re s orb ing c ytokine s p rod uc e d b y monoc yte s , ma c rop ha ge s , a nd os te ob la s ts

Co nne c tive tis s ue de s truc tio n

Fig ure 15-11. Po stulate d Effe cts o f Estro g e

Alve o lar bo ne re s o rptio n To o th lo s s

De ficie c o

the Pe rio do tium.

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Systemic Conditions that Ampli y Susceptibility to Periodontal Disease

261

2

Ge e tic Risk Facto rs fo r Pe rio do titis Periodontitis is widely recognized as a complex disease. For many years, clinical observations that severe periodontitis can occur in successive generations o some amilies led to speculation about the potential role o genetic actors in periodontitis. Research has begun to clari y the true role o genetics as a risk actor in this complex disease. 1. Rare Genetic Syndromes Associated with Periodontitis A. It is common knowledge today that genes within cell nuclei have a huge inf uence on most o our characteristics. M utations or variations within these genes can lead to speci c diseases, and sometimes these diseases can even a ect the periodontium. B. There are several rare genetic disorders that in addition to creating multiple medical problems or patients can also lead to very unusual orms o periodontitis. 1. Examples o some o these rare disorders include conditions such as Chédiak– H igashi syndrome, leukocyte adhesion de ciency syndrome, Job syndrome, Papillon–Le èvre syndrome, Crohn disease, acute monocytic leukemia, as well as cyclic and chronic neutropenia. 2. M any o these rare disorders are accompanied by a PM N mal unction that makes patients more susceptible to in ections such as periodontitis (Fig. 15-12). Abnormalities in PM N unction can lead to overwhelming systemic bacterial in ections and are o ten associated with increased susceptibility to severe periodontal destruction. 3. Dental hygienists are unlikely to encounter patients with most o these severe genetic disorders outside a hospital dentistry setting.

Fig ure 15-12. C clic n e utro pe ia. This individual with cyclic neutropenia exhibits pronounced gingival erythema. (Used with permission rom Langlais RP. Color Atlas of Common Oral Diseases. Philadelphia, PA: Wolters Kluwer; 2003.)

2. Down Syndrome and Periodontitis. Though most o these rare genetic syndromes are unlikely to be encountered by the dental hygienist outside a hospital setting, persons w ith Down syndrome are requently treated by members o the dental team in general and periodontal dental o f ces. Down syndrome is one o the most common birth de ects. A. Genetic Changes in Down Syndrome 1. N ormally, the nucleus o each cell contains 46 chromosomes. In Down syndrome, however, the nucleus contains 47 chromosomes. M ost cases o Down syndrome occur because there are three copies o the 21st chromosome. For this reason, Down syndrome is also re erred to as trisomy 21.

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2. Due to advances in medical treatment, individuals with Down syndrome are living longer. As the mortality rate associated with Down syndrome decreases, the prevalence o adults with Down syndrome in our society will increase. M ore and more dental healthcare providers will interact with individuals with this condition, increasing the need or education and acceptance. B. Oro acial Features Characteristic o People with Down Syndrome. Among the most common oro acial traits o individuals with Down syndrome are: 1. An underdeveloped mid acial region, a ecting the appearance o the lips, tongue, and palate. a. The maxilla, the bridge o the nose, and the bones o the mid ace region are smaller than in the general population, creating a prognathic occlusal relationship. M outh breathing may occur because o smaller nasal passages, and the tongue may protrude because o a smaller mid ace region. People with Down syndrome o ten have a strong gag ref ex due to placement o the tongue, as well as anxiety associated with any oral stimulation. b. The palate, although normal sized, may appear highly vaulted and narrow. This deceiving appearance is due to the unusual thickness o the sides o the hard palate. This thickness restricts the amount o space the tongue can occupy in the mouth and a ects the ability to speak and chew. c. The lips may grow large and thick. Fissured lips may result rom chronic mouth breathing. In addition, decreased muscle tone may cause the mouth to droop and the lower lip to protrude. Increased drooling, compounded by a chronically open mouth, contributes to angular cheilitis. d. The tongue also develops cracks and ssures with age; this condition can contribute to halitosis. 2. M alocclusion is ound in most people with Down syndrome because o the delayed eruption o permanent teeth and underdevelopment o the maxilla. A smaller maxilla contributes to an open bite, leading to poor positioning o teeth and increasing the likelihood o periodontal disease and dental caries. C. Medical and Developmental Problems o Patients with Down Syndrome 1. Children are at increased risk or congenital heart de ects, susceptibility to in ection, respiratory problems, gastrointestinal abnormalities, and childhood leukemia. 2. Abnormal PM N unction is seen in about hal o all patients with Down syndrome. 3. M ost individuals with Down syndrome have IQ s in the mild to moderate range o mental retardation. Those who receive good medical care and experience a supportive social environment can attend school, hold jobs, and participate in decisions that a ect them (Fig. 15-13).

Fig ure 15-13. I di iduals w ith Do w S dro me i the Wo rkfo rce . With appropriate training and support people with Down Syndrome can and do make a huge contribution to their workplace. (Courtesy o Getty Images.)

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Fig ure 15-14. Pe rio do titis a d Do w S dro me . A 25-year-old patient with Down syndrome exhibits severe periodontal destruction. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

D. Implications o Down Syndrome or the Periodontium 1. It is widely known that individuals with Down syndrome o ten develop severe, aggressive periodontitis. a. The prevalence o periodontal disease ranges rom 58% to 96% in young adults under 35 years o age with Down syndrome (81). b. Substantial plaque bio lm ormation, deep periodontal pockets, and extensive gingival inf ammation characterize periodontal disease in Down syndrome (Figs. 15-14 and 15-15A–C) (82). 2. Children experience rapid, destructive periodontal disease. Consequently, large numbers o them lose their permanent anterior teeth in their early teens. a. At least some children with Down syndrome are congenitally missing at least one salivary gland (83). b. Studies indicate that various periodontal pathogens colonize the gingival tissues in the very early childhood years o children with Down syndrome (84). 3. The etiology o periodontal disease in persons with Down syndrome is complex. The prevalence o periodontal disease cannot simply be attributed to poor daily sel -care. In recent years, much ocus has been placed on the altered immune response resulting rom the underlying genetic disorder (81,85). a. Impaired PM N chemotaxis and phagocytosis most likely explain the high prevalence and increased severity o periodontitis associated with Down syndrome. b. Impaired cellular motility o gingival broblasts that prevents wound healing and regeneration o periodontal tissues may be involved in the etiology o Down syndrome periodontitis (86). E. Down Syndrome: Implications or the Dental Hygienist 1. Early and requent pro essional treatment and meticulous daily care at home can mitigate the severity o periodontal disease in individuals with Down syndrome. a. Some people with Down syndrome can brush and f oss independently, but many need help rom caregivers. b. Encourage independence in daily sel -care in those individuals who are capable on their own. Involve patients in hands-on demonstrations o brushing and interdental cleaning aids. c. H ygienists should educate caregivers about daily sel -care. Dental healthcare providers should not assume that all caregivers know the basics; demonstrate proper brushing and f ossing techniques. A power toothbrush or a f oss holder can simpli y oral care.

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1. The hygienist can demonstrate techniques to caregivers on techniques to access the oral cavity, such as having the person close slightly or improved access to the posterior teeth and where to sit or stand to gain easier access to di erent areas o the dentition. 2. The hygienist should emphasize to the caregiver the importance o establishing a daily routine or oral care.

A

Fig ure 15-15. Pe rio do titis a d Do w S dro me . Photos A to C show an individual with Down syndrome. A: This patient exhibits pronounced attrition and localized loss o attachment. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC).

B

B: Pronounced attrition o the maxillary teeth in an individual with Down syndrome. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC).

C

C: This bitewing radiograph shows attrition and localized loss o attachment on the le t side o the mouth in an individual with Down syndrome. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

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S ste mic Me dicatio s w ith Pe rio do tal Side Effe cts M any medications used to treat systemic diseases can cause oral complications. E ects o medications can modi y oral hygiene habits, plaque bio lm composition, size o gingival tissues, level o bone, and salivary f ow. Educating patients about potential oral side e ects is critical to reducing the medication-related risks o periodontal disease. Commonly prescribed medications that can a ect the periodontium are summarized in Table 15-2.

TABLE 1 5 -2 . HARMFUL EFFECTS OF COMMOn Ly PRESCRIBED MEDICATIOn S On PERIODOn TIUM Me dicatio

Class

Ge e ric n ame (Bra d n ame )

Effe ct o

a n ico n vu ls n

p

Gin g iv l o v g o w

a n i n xi y g n s

al

an i y

en l

n siv

C lciu m b lo ck Im m u n o su

ssiv

n y o in (Dil n in ) zo l m (Zo lo ) il (V so

c)

D c In c

Pe rio do tium

s d b io ilm o m

io n

s d g in g iv l in l m m

Ni d i in (p o c d i )

Gin g iv l o v g o w

Cyclo s o in (S n d im m u n )

Gin g iv l o v g o w

1. Medications that Alter Plaque Biof lm Composition, pH, or Salivary Flow A. Plaque Biof lm Composition or pH 1. M any oral medications alter plaque bio lm composition and pH in ways that are harm ul to the periodontium. 2. Sugar is a major component o some cough drops, liquid medications, cough syrups, tonics, chewable vitamins, antacid tablets, and other medications. M edications that contain sugar add signi cantly to the alteration o pH and composition o the bio lm. 3. Sugar is metabolized by bacteria to orm acid, causing enamel to demineralize. The demineralized areas are rough and act as attachment sites or bacteria, keeping bacterial plaque bio lm against tissues and eventually resulting in inf ammation o the gingiva. 4. Some over-the-counter (OTC) preparations contain sugar and vitamin C. This combination delivers sugar and the vitamins cause an acid pH . 5. Products that alter the plaque bio lm pH signi cantly can cause root-sur ace caries in older adults and have an e ect on the metabolism o periodontal pathogens (87,88). B. Salivary Flow and pH 1. Adequate saliva f ow is necessary or the maintenance o healthy oral tissues. The ability o saliva to limit the growth o pathogens is a major determinant o systemic and oral health. a. The physical f ow o the saliva helps to dislodge microbes rom the teeth and mucosa sur aces. Saliva can also cause bacteria to clump together, so that they can be swallowed be ore they become rmly attached.

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b. Saliva is rich in antimicrobial components. Certain molecules in saliva can directly kill or inhibit a variety o microbes. 2. Patients with xerostomia su er rom an increase in the incidence o oral candidiasis, coronal and root-sur ace caries, as well as excess plaque bio lm ormation. Xerostomia is discussed more ully in Chapter 33, O ral M alodor and Xerostomia. 3. M ore than 400 OTC and prescription drugs have xerostomia as a possible side e ect (89). 4. Some o the more common groups o medications that cause xerostomia are cardiovascular medications (blood pressure, diuretics, calcium channel blockers); antidepressants; sedatives; anti-parkinsonism medications; allergy medications; and antacids (90). 2. Drug-In uenced Gingival Enlargement A. Introduction 1. Drug-in uenced gingival enlargement is an esthetically dis guring overgrowth o the gingiva that is a side e ect associated with certain medications. 2. Drugs associated with gingival enlargement can be broadly divided into three categories: anticonvulsants, calcium channel blockers, and immunosuppressants (Table 15-2). These three classes o medications inf uence gingival broblasts to overproduce collagen matrix when stimulated by gingival inf ammation (91). a. M ore than 20 medications have been shown to have the potential to induce gingival enlargement. b. Among longstanding and relatively newer pharmacologic agents involved in gingival enlargement, overall, the anticonvulsant phenytoin still has the highest prevalence rate with calcium channel blockers and immunosuppressant-associated enlargements about hal as prevalent (92). 3. The clinical characteristics o drug-inf uenced gingival enlargement include enlargement o the gingiva, tendency to occur more o ten in the anterior gingiva, prevalence in younger age groups, and onset within 3 months o use (93). B. Anticonvulsants 1. Phenytoin (FEN -i-toyn) is one o the most commonly used anticonvulsant medications used to control convulsions or seizures in the treatment o epilepsy. Phenytoin is marketed under various trade names including Dilantin 4, Dilantin Kapseals 4, and Phenytoin. Phenytoin is among the 20 most prescribed drugs in the world. 2. O vergrowth o the gingiva is one o the most common side e ects o phenytoin. It has been estimated that 40% to 50% o the millions o individuals who take phenytoin will develop gingival overgrowth to some extent (92). O vergrowths appear to be more common in children and young adults. 3. Gingival overgrowth begins with enlargement o the interdental papillae. a. The interdental papillae overgrow, orming rm triangular tissue masses that protrude rom the interdental area. b. Gradually the enlarged papillae may use mesially and distally and partially cover the anatomical crown with marginal gingiva (Fig. 15-16). O vergrowths are most commonly seen on the acial aspect o the anterior teeth. c. In the presence o good bio lm control, the enlarged tissue is pink in color and rm and rubbery in consistency. In the presence o poor bio lm control, the tissue appears red, edematous, and spongy.

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Fig ure 15-16. Phe to i -I flue ce d Gi g i al O e rg ro w th. Severe enlargement o the gingiva associated with phenytoin (Dilantin) medication in an individual with epilepsy. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

Fig ure 15-17. C clo spo ri e -I flue ce d Gi g i al O e rg ro w th. The clinical appearance o cyclosporineassociated gingival overgrowth resembles that o phenytoin-associated gingival enlargement. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

C. Immunosuppressants 1. Cyclosporine (SIGH -kloe-spor-een) belongs to the group o medicines known as immunosuppressive agents used or prevention o transplant rejection as well as or management o a number o autoimmune conditions such as rheumatoid arthritis. 2. The incidence o cyclosporine-associated gingival overgrowth a ects approximately 25% o patients taking the medication. 3. The clinical appearance o cyclosporine-associated gingival overgrowth resembles that o phenytoin-associated gingival enlargement (Fig. 15-17). D. Calcium Channel Blockers 1. Antihypertensive drugs in the calcium channel blocker group are used extensively in elderly patients who have angina or peripheral vascular disease. 2. The use o calcium channel blockers is associated with an increased risk o gingival hyperplasia (94,95). a. Ni edipine (nye-FED-I-peen), one type o calcium channel blocker, is used as a coronary vasodilator in the treatment o hypertension, angina, and cardiac arrhythmias. Calcium channel blockers are a class o drugs that block the inf ux o calcium ions through cardiac and vascular smooth muscle cell membranes. This results in the dilation o the main coronary and systemic arteries. b. Various other calcium channel blocking medications, such as diltiazem, elodipine, nitrendipine, and verapamil also may induce gingival enlargement. 3. The clinical appearance o gingival overgrowth associated with calcium channel blockers resembles that o phenytoin-associated gingival enlargement (Figs. 15-18 and 15-19).

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Fig ure 15-18. Gi g i al O e rg ro w th Asso ciate d w ith n ife dipi e . Gingival overgrowth in a patient who takes ni edipine or the treatment o cardiac arrhythmia. (Courtesy o Dr. Ralph Arnold, San Antonio, TX.)

Fig ure 15-19. Gi g i al E larg e me t Asso ciate d w ith Calcium Cha e l Blo cki g Drug s. Gingival enlargement o the papilla between the lateral incisor and canine induced by the calcium channel blocking medication Norvasc. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

E. Systemic Medications: Implications or the Dental Hygienist 1. Dental hygienists should be alert or patient medications that can alter bio lm composition, pH , or salivary f ow. a. Sugar-containing liquid or chewable medications are sometimes used in the treatment o children with chronic medical problems. Parents should be made aware o the oral health consequences o such medications. Giving the medications at mealtimes instead o between meals is help ul. b. Some OTC preparations contain sugar and vitamin C. This combination delivers sugar and the vitamins cause an acid pH . Examples o products containing sugar and vitamin C include chewable vitamin C tablets, certain cough drops, and certain liquid cough preparations. 2. Closer collaboration between medical and dental clinical teams is necessary or the joint management o individuals being treated with anticonvulsants, calcium channel blockers, or immunosuppressants (46). Patients receiving cyclosporine are usually medically compromised, requiring close consultation with the patient’s physician to assure sa e management o the patient’s periodontal condition. In addition to pro essional and at-home plaque bio lm control, it has been shown that azithromycin induced a striking reduction in cyclosporine-induced gingival hyperplasia (96). 3. Treatment o gingival enlargement should include consultation with the physician, substitution o the current medication or another whenever possible,

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nonsurgical periodontal therapy, requent periodontal maintenance, and surgical therapy, i needed (96). a. The hygienist should emphasize the importance o meticulous daily sel care and involve patients in hands-on demonstrations o brushing and interdental cleaning aids. b. Surgical elimination o the tissue overgrowth is o ten required. Un ortunately, the gingival overgrowth is likely to recur within 1 to 2 years even in the presence o good plaque bio lm control, especially i the patient is younger than 25 years. I plaque bio lm control is inadequate, the regrowth will occur rapidly. The patient should be advised o the likelihood o the recurrence o the gingival overgrowth ollowing surgery.

Chapte r Summar State me t The presence o dental plaque bio lm does not necessarily mean that an individual will experience periodontitis. Additional actors play a role in determining why some individuals are more susceptible to periodontitis than others. Signi cant systemic contributing actors include diabetes mellitus, leukemia, AIDS, hormonal f uctuations, genetic risk actors, and systemic medications. Contributing risk actors must be evaluated to develop the best treatment plan or each individual. Dental pro essionals should provide health promotion education that contributes to overall systemic and periodontal health and collaborate with medical team members or joint patient management.

Se ct io

4

Fo cus o

Patie ts

Cli ical Patie t Care CA S E 1 A patient, who has been previously treated or chronic periodontitis and has been ollowed by your dental team or several years, calls your dental o ce with a concern. She is scheduled to undergo a liver transplant and has been warned by her physician that the medications she will need will make her more susceptible to in ections. She asks i these medications might have an e ect on her continuing treatment or periodontitis. H ow might you respond to her concern?

CA S E 2 The parents o a young patient currently being treated by your dental team in orm you that ollowing a lengthy illness, their daughter has recently been diagnosed by her physician with a neutrophil de ect. N eutrophils are also known as polymorphonuclear leukocytes. They inquire about any dental implications o this diagnosis. H ow might you respond to this inquiry?

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E ide ce i Actio CASE 1 A new patient in your o ce reports that she has recently been diagnosed with diabetes mellitus and that her physician suggested that she should have a dental checkup. The patient con des in you that she eels like this disease is really changing her li estyle. She laughingly says “ I have always had such good reports rom my previous dentist, and I just don’t really see why I need to be worried about my teeth now.” Based upon what is known about the relationship between diabetes and periodontal disease, how might you explain the need or the recommended dental exam to the patient?

Ethical Dile mma You have just recently married and moved across the country to the city where your husband was raised. His parents helped you secure a ull-time dental hygiene position with their amily dentist, Dr. Ramos. You are quite happy working with the o ce sta , as well as meeting and getting to know many o your in-law’s amily and riends, who are patients o the practice as well. Today your mother-in-law, June, is scheduled or her 6-month recall appointment. This is the rst time you will be treating her. You review her medical history, and she states that lately she’s been eeling tired, lethargic, and has a poor appetite. She assumed she was just overtired rom all the wedding planning and estivities. She hasn’t been able to workout regularly, as she has musculoskeletal aches and pains. Your clinical examination reveals gingival enlargement and spontaneous gingival bleeding, despite excellent sel -care. H er tissues are swollen, glazed, and spongy, red to deep purple in appearance, and ooze blood intermittently. She also appears to have acial swelling. You review the notes rom her last appointment, which was 6 months ago, and see that her tissues were classi ed as normal and healthy. You become very concerned that June may have a serious medical condition, and you are not sure what to do. You eel that you need to discuss this with your husband be ore saying anything to June. 1. What systemic condition do you think could be causing June’s signs/symptoms? 2. What ethical principles are in conf ict in this dilemma? 3. What is the best way or you to handle this ethical dilemma?

Re fe re ce s 1. Wild S, Roglic G, Green A, et al. Global prevalence o diabetes: estimates or the year 2000 and projections or 2030. D iabetes Care. 2004;27(5):1047–1053. 2. Christgau M , Palitzsch KD, Schmalz G, et al. H ealing response to non-surgical periodontal therapy in patients with diabetes mellitus: clinical, microbiological, and immunologic results. J Clin Periodontol. 1998;25(2):112–124. 3. Deshpande K, Jain A, Sharma R, et al. Diabetes and periodontitis. J Indian Soc Periodontol. 2010;14(4):207–212. 4. Preshaw PM , Alba AL, H errera D, et al. Periodontitis and diabetes: a two-way relationship. D iabetologia. 2012;55(1):21–31. 5. Botero JE, Yepes FL, Roldan N , et al. Tooth and periodontal clinical attachment loss are associated with hyperglycemia in patients with diabetes. J Periodontol. 2012;83(10):1245–1250. 6. Demmer RT, H olt reter B, Desvarieux M , et al. The inf uence o type 1 and type 2 diabetes on periodontal disease progression: prospective results rom the Study o H ealth in Pomerania (SH IP). D iabetes Care. 2012;35(10):2036–2042. 7. H aseeb M , Khawaja KI, Ataullah K, et al. Periodontal disease in type 2 diabetes mellitus. J Coll Physicians Surg Pak . 2012;22(8):514–518.

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44. Thomaz EB, M ouchrek JC Jr., Silva AQ, et al. Longitudinal assessment o immunological and oral clinical conditions in patients undergoing anticancer treatment or leukemia. Int J Pediatr O torhinolaryngol. 2013;77(7):1088–1093. 45. Berger A, H enderson M , N adoolman W, et al. O ral capsaicin provides temporary relie or oral mucositis pain secondary to chemotherapy/radiation therapy. J Pain Sym ptom M anage. 1995;10(3):243–248. 46. Bridges DR, Davidson RA, O degard PS, et al. Interpro essional collaboration: three best practice models o interpro essional education. M ed Educ O nline. 2011;16. 47. Goncalves LS, Goncalves BM , de Andrade M A, et al. Drug interactions during periodontal therapy in H IV-in ected subjects. M ini R ev M ed Chem . 2010;10(8):766–772. 48. Ryder M I, N ittayananta W, Coogan M , et al. Periodontal disease in H IV/AIDS. Periodontol 2000. 2012;60(1):78–97. 49. H irnschall G, H arries AD, Easterbrook PJ, et al. The next generation o the World H ealth O rganization’s global antiretroviral guidance. J Int A ID S Soc. 2013;16:18757. 50. M ata tsi M , Skoura L, Sakellari D. H IV in ection and periodontal diseases: an overview o the post-H AART era. O ral D is. 2011;17(1):13–25. 51. Armitage GC. Development o a classi cation system or periodontal diseases and conditions. A nn Periodontol. 1999; 4(1):1–6. 52. Yin M T, Dobkin JF, Grbic JT. Epidemiology, pathogenesis, and management o human immunode ciency virus in ection in patients with periodontal disease. Periodontol 2000. 2007;44:55–81. 53. Velegraki A, N icolatou O, Theodoridou M , et al. Paediatric AIDS–related linear gingival erythema: a orm o erythematous candidiasis? J O ral Pathol M ed. 1999;28(4):178–182. 54. Kroidl A, Schaeben A, O ette M , et al. Prevalence o oral lesions and periodontal diseases in H IV-in ected patients on antiretroviral therapy. Eur J M ed R es. 2005;10(10):448–453. 55. Fricke U, Geurtsen W, Stau enbiel I, et al. 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Int J D ent H yg. 2007;5(4):211–217. 61. Gursoy M , Gursoy UK, Sorsa T, et al. H igh salivary estrogen and risk o developing pregnancy gingivitis. J Periodontol. 2013;84(9):1281–1289. 62. Straka M . Pregnancy and periodontal tissues. N euro Endocrinol L ett. 2011;32(1):34–38. 63. Armitage GC. Bi-directional relationship between pregnancy and periodontal disease. Periodontol 2000. 2013;61(1):160–176. 64. Lundgren D, M agnusson B, Lindhe J. Connective tissue alterations in gingivae o rats treated with estrogen and progesterone. A histologic and autoradiographic study. O dontol R evy. 1973;24(1):49–58. 65. Boggess KA, Society or M aternal-Fetal M edicine Publications C. M aternal oral health in pregnancy. O bstet G ynecol. 2008;111(4):976–986. 66. Silk H , Douglass AB, Douglass JM , et al. O ral health during pregnancy. A m Fam Physician. 2008;77(8):1139–1144. 67. Boggess KA, Edelstein BL. O ral health in women during preconception and pregnancy: implications or birth outcomes and in ant oral health. M atern Child H ealth J. 2006;10(5 suppl):S169–S174. 68. American College o O bstetricians and Gynecologists Women’s H ealth Care Physicians, Committee on H ealth Care or Underserved Women. Committee O pinion N o. 569: oral health care during pregnancy and through the li espan. O bstet G ynecol. 2013;122(2 Pt 1):417–422. 69. Dutt P, Chaudhary S, Kumar P. O ral health and menopause: a comprehensive review on current knowledge and associated dental management. A nn M ed H ealth Sci R es. 2013;3(3):320–323. 70. Friedlander AH . The physiology, medical management and oral implications o menopause. J A m D ent A ssoc. 2002;133(1):73–81. 71. Carey JJ, Palomo L. Bisphosphonates and osteonecrosis o the jaw: innocent association or signi cant risk? Cleve Clin J M ed. 2008;75(12):871–879. 72. Al H abashneh R, Alchalabi H , Khader YS, et al. Association between periodontal disease and osteoporosis in postmenopausal women in Jordan. J Periodontol. 2010;81(11):1613–1621. 73. Bertulucci Lde A, Pereira FM , de O liveira AE, et al. [Periodontal disease in women in post-menopause and its relationship with osteoporosis]. R ev Bras G inecol O bstet. 2012;34(12):563–567. 74. Vishwanath SB, Kumar V, Kumar S, et al. Correlation o periodontal status and bone mineral density in postmenopausal women: a digital radiographic and quantitative ultrasound study. Indian J D ent R es. 2011;22(2):270–276. 75. Je coat M . The association between osteoporosis and oral bone loss. J Periodontol. 2005;76(11 suppl):2125–2132. 76. Chang WP, Chang WC, Wu M S, et al. Population-based 5-year ollow-up study in Taiwan o osteoporosis and risk o periodontitis. J Periodontol. 2014;85(3):e24–e30. 77. American Dental Association. Council on Access, Prevention, and Interpro essional Relations. Women’s O ral H ealth Issues. Chicago, IL: American Dental Association, 2006, pp. 46 (O ral health care series). 78. Pilgram TK, H ildebolt CF, Yokoyama-Crothers N , et al. Relationships between longitudinal changes in radiographic alveolar bone height and probing depth measurements: data rom postmenopausal women. J Periodontol. 1999;70(8):829–833. 79. Civitelli R, Pilgram TK, Dotson M , et al. Alveolar and postcranial bone density in postmenopausal women receiving hormone/estrogen replacement therapy: a randomized, double-blind, placebo-controlled trial. A rch Intern M ed. 2002;162(12):1409–1415. 80. Genco RJ, Grossi SG. Is estrogen de ciency a risk actor or periodontal disease? Com pend Contin Educ D ent Suppl. 1998(22):S23–S29. 81. M organ J. Why is periodontal disease more prevalent and more severe in people with Down syndrome? Spec Care D entist. 2007;27(5):196–201.

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82. Barr-Agholme M , Dahllo G, M odeer T, et al. Periodontal conditions and salivary immunoglobulins in individuals with Down syndrome. J Periodontol. 1998;69(10):1119–1123. 83. O deh M , H ershkovits M , Bornstein J, et al. Congenital absence o salivary glands in Down syndrome. A rch D is Child. 2013;98(10):781–783. 84. Amano A, Kishima T, Kimura S, et al. Periodontopathic bacteria in children with Down syndrome. J Periodontol. 2000;71(2):249–255. 85. Cavalcante LB, Tanaka M H , Pires JR, et al. Expression o the interleukin-10 signaling pathway genes in individuals with Down syndrome and periodontitis. J Periodontol. 2012;83(7):926–935. 86. M urakami J, Kato T, Kawai S, et al. Cellular motility o Down syndrome gingival broblasts is susceptible to impairment by Porphyromonas gingivalis invasion. J Periodontol. 2008;79(4):721–727. 87. Steele JG, Sheiham A, M arcenes W, et al. Clinical and behavioural risk indicators or root caries in older people. G erodontology. 2001;18(2):95–101. 88. Touger-Decker R, van Loveren C. Sugars and dental caries. A m J Clin N utr. 2003;78(4):881S–892S. 89. Ciancio SG. M edications’ impact on oral health. J A m D ent A ssoc. 2004;135(10):1440–1448; quiz 68–69. 90. Guggenheimer J, M oore PA. Xerostomia: etiology, recognition and treatment. J A m D ent A ssoc. 2003;134(1):61–69; quiz 118–119. 91. Dongari-Bagtzoglou A; Research, Science and Therapy Committee, American Academy o Periodontology. Drug-associated gingival enlargement. J Periodontol. 2004;75(10):1424–1431. 92. M ohan RP, Rastogi K, Bhushan R, et al. Phenytoin-induced gingival enlargement: a dental awakening or patients with epilepsy. BM J Case R eports. 2013;2013. doi:10.1136/bcr-2013–008679. 93. Drug-induced gingival hyperplasia. Prescrire Int. 2011;20(122):293–294. 94. Sanz M . Current use o calcium channel blockers (CCBs) is associated with an increased risk o gingival hyperplasia. J Evid Based D ent Pract. 2012;12(3 suppl):147–148. 95. Parwani RN , Parwani SR. M anagement o phenytoin-induced gingival enlargement: a case report. G en D ent. 2013;61(6): 61–67. 96. Ramalho VL, Ramalho H J, Cipullo JP, et al. Comparison o azithromycin and oral hygiene program in the treatment o cyclosporine-induced gingival hyperplasia. R en Fail. 2007;29(3):265–270.

STUDEn T An CILLARy RESOURCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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As discussed in other chapters o this book, periodontal diseases are in ections. Many individuals, however, have local contributing actors that can (1) make it more likely that they will develop periodontal disease or (2) a ect the progress o existing periodontal disease. Members o the dental team must identi y these local actors when they exist and minimize the impact o these actors or periodontal therapy to be truly success ul. This chapter outlines these local contributing actors and explains how these actors can alter periodontal disease in patients.

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• Def ne the terms pathogenicity and local contributing actors. • Describe local etiologic actors that contribute to the retention and accumulation o microbial plaque biof lm. • Explain the meaning o the phrase “ pathogenicity o plaque biof lm.” • Identi y and di erentiate the location, composition, modes o attachment, mechanisms o mineralization, and pathologic potential o supra- and subgingival calculus deposits. • Describe local contributing actors that can lead to direct damage to the periodontium. • Explain the role o trauma rom occlusion as a possible contributing actor in periodontal disease.

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Local contributing actors Disease site Dental calculus Pellicle Morphology Overhanging restoration Palatogingival groove Pathogenicity Plaque bio ilm pathogenicity

Food impaction Tongue thrusting Mouth breathing Biologic width Embrasure space Encroaching on the embrasure space Prosthesis Removable prosthesis

Trauma rom occlusion Primary trauma rom occlusion Secondary trauma rom occlusion Functional occlusal orces Para unctional occlusal orces Clenching Bruxism Occlusal adjustment

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As will be discussed in subsequent chapters, it is clear that both gingivitis and periodontitis have bacterial plaque bio lm as their primary etiology. There are, however, certain local contributing actors that can increase the risk o developing gingivitis and periodontitis or that can increase the risk o developing more severe disease when gingivitis and periodontitis are already established (1–3). Local contributing actors or periodontal disease are oral conditions or habits that increase an individual's susceptibility to periodontal in ection or that can damage the periodontium in speci c sites within the dentition. Local contributing actors do not actually initiate either gingivitis or periodontitis, but these actors can contribute to the disease process previously initiated by bacterial plaque bio lm. It is critical or the dental team to recognize local contributing actors or periodontal disease during a periodontal assessment. The dental team should always eliminate or at least minimize the impact o existing local contributing actors during the nonsurgical periodontal treatment. The conditions discussed in this chapter re er to circumstances that avor periodontal breakdown and can contribute to gingivitis or periodontitis in individual sites in the mouth. In the context o this discussion, a disease site is an individual tooth or speci c sur ace o a tooth. For instance, a local contributing actor might increase the susceptibility to periodontal in ection on the distal sur ace o a maxillary premolar tooth. Examples o potential local contributing actors can include dental calculus, aulty dental restorations, developmental de ects in teeth, dental decay, certain patient habits, and trauma rom occlusion.

M e c h a n is M s f o r in c r e a s e d d is e a s e r is k Local contributing actors can increase the risk o developing gingivitis or periodontitis through several mechanisms or through combinations o these mechanisms. Table 16-1 summarizes mechanisms or increasing disease risk in local sites, and each o these mechanisms is discussed in detail in the ollowing sections o this chapter. There are three primary mechanisms by which local actors can increase the risk o developing periodontal disease or increase the severity o existing periodontal disease. 1. A local actor can increase plaque bio lm retention. 2. A local actor can increase plaque bio lm pathogenicity (disease-causing potential). 3. A local actor can cause direct damage to the periodontium.

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This section discusses local actors that can increase plaque bio lm retention. M ost o ten these local contributing actors include rough or irregular sur aces that decrease the e ectiveness o a patient' s sel -care and lead to the increased plaque bio lm retention. 1. Dental Calculus. Dental calculus is the most obvious example o a local contributing actor that can lead to increased plaque bio lm retention. Dental calculus is mineralized bacterial plaque bio lm, covered on its external sur ace by nonmineralized, living bacterial plaque bio lm. M ineralization o plaque bio lm can begin rom 48 hours up to 2 weeks a ter plaque bio lm ormation. A. E ects o Calculus on the Periodontium 1. The sur ace o a calculus deposit at the microscopic level is quite irregular in contour and is always covered with disease-causing bacteria. Thus, even calculus that has not built up enough to result in a ledge or grossly altered tooth contour can lead to plaque bio lm retention at the site simply because o the rough nature o the calculus sur ace and its tendency to harbor bacteria. 2. As dental calculus deposits build up, they can lead to even more irregular sur aces, ledges on the teeth, and other alterations o the contours o the teeth (Fig. 16-1). As calculus deposits accumulate, they create more and more areas o plaque bio lm retention that are di cult or impossible or a patient to clean. B. Pathologic Potential 1. Since a layer o living bacterial plaque bio lm always covers a calculus deposit, dental calculus plays a signi cant role as a local contributing actor in periodontal disease. 2. It is di cult to bring either gingivitis or periodontitis under control in the presence o dental calculus on a ected teeth, and the importance o removing these deposits in patients with gingivitis and periodontitis cannot be overemphasized. The removal o dental calculus is discussed in Chapter 22.

A

B

Fi ur 16-1. Irr ular Sur ac o Calculus D po sits. A: Heavy calculus deposits on the lingual sur aces o the mandibular anterior teeth. These deposits are so large that they inter ere with the patient's sel -care e orts. In addition, calculus deposits harbor living bacteria that can be in constant contact with the gingival tissue. B: Calculus deposit on the crown and root sur aces o an extracted mandibular canine. (Photograph B courtesy o Dr. Don Rol s, Periodontal Foundations, Wenatchee, WA.)

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C. Composition o Dental Calculus. Calculus comprises an inorganic (or mineralized) component and an organic component. 1. Inorganic Portion o Calculus a. The inorganic part o calculus makes up 70% to 90% o the overall composition o calculus. b. This inorganic part o dental calculus is primarily calcium phosphate, but the dental calculus also contains some calcium carbonate and magnesium phosphate. c. The inorganic part o calculus is similar to the inorganic components o bone. 2. O rganic Portion o Calculus a. The organic part o calculus makes up 10% to 30% o the overall composition o calculus. b. Components o the organic part include materials derived rom plaque bio lm, derived rom dead epithelial cells, and derived rom dead white blood cells. It can also include living bacteria within the deposits o calculus. D. Types o Dental Calculus 1. Crystalline Forms o Dental Calculus. As calculus ages on a tooth sur ace, the inorganic component changes through several di erent crystalline orms. It is interesting to note that some o these crystalline orms o calculus are quite similar to the crystal orms in the tooth itsel . a. N ewly ormed calculus deposits appear as a crystalline orm called brushite. b. In calculus deposits that are a bit more mature, but less than 6 months old, the crystalline orm is primarily octacalcium phosphate. c. In mature deposits that are more than 6 months old, the crystalline orm is primarily hydroxyapatite. 2. Location o Calculus Deposits a. Supragingival calculus deposits are calculus deposits located coronal to (above) the gingival margin. O ther terms that have been used to re er to deposits coronal to the gingival margin are supramarginal calculus and salivary calculus. 1. Though supragingival calculus deposits can be ound on any tooth sur ace, they usually are ound in localized areas o the dentition, such as lingual sur aces o mandibular anterior teeth, acial sur aces o maxillary molars, and on teeth that are crowded or in malocclusion. It is interesting to note that supragingival calculus is requently ound in areas adjacent to large salivary ducts (such as the lingual sur aces o mandibular anterior teeth and the acial sur aces o maxillary posterior teeth). 2. Though supragingival calculus can orm in any shape, these deposits most o ten are irregular, large deposits. b. Subgingival deposits are calculus deposits located apical to (below) the gingival margin. O ther terms that have been used or deposits apical to the gingival margin are submarginal calculus or serumal calculus. 1. The distribution o subgingival deposits may be localized in certain areas or generalized throughout the mouth. 2. The shape o subgingival deposits is most o ten f attened. It is thought that the shape o the deposit may be guided by pressure o the pocket wall against the deposit. E. Modes o Attachment to Tooth Sur aces. Dental calculus attaches to tooth sur aces through several di erent modes, and di erent attachment mechanisms can even exist in the same calculus deposit.

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1. Attachment by Means o Pellicle a. Calculus can attach to the tooth sur ace by attaching to pellicle on the sur ace. The pellicle is a thin, bacteria- ree membrane that orms on the sur ace o the tooth during the late stages o eruption. b. This mode o attachment occurs most commonly on enamel sur aces. c. Calculus deposits attached via the pellicle are usually removed easily because this attachment is on the sur ace o the pellicle (and not actually locked into the tooth sur ace). 2. Attachment to Irregularities in the Tooth Sur ace a. Calculus can also attach to irregularities in tooth sur aces. These irregularities include cracks in the teeth, tiny openings le t where periodontal ligament bers are detached, and grooves in cemental sur aces created as the result o aulty instrumentation during previous calculus removal procedures. b. Complete calculus removal in areas o irregularities in tooth sur aces is usually di cult since the deposits can be sheltered in these tooth de ects. 3. Attachment by Direct Contact o the Calcif ed Component and the Tooth Sur ace a. Calculus can also attach to tooth sur aces by attaching directly to the calci ed component o the tooth. In this mode o attachment, the matrix o the calculus deposit is interlocked with the inorganic crystals o the tooth. b. Deposits, rmly interlocked in the tooth sur ace, are usually di cult to remove. 2. Tooth Morphology. Morphology is the study o the anatomic sur ace eatures o the teeth. There are a variety o local contributing actors that relate to tooth morphology. Some o these variations in tooth morphology can occur when a tooth requires a restoration, and some o them occur simply because o variations in the way teeth orm. A. Poorly Contoured Restorations 1. When a dentist places a restoration, it is not always possible to contour the restoration per ectly smoothly with the existing tooth structure. When a restoration is not smoothly contoured with the tooth sur aces, this condition is re erred to as an overhanging restoration or overhang (Fig. 16-2). 2. Because o di culty o access to tooth sur aces protected by an overhanging restoration, it is o ten impossible or a patient to remove plaque bio lm e ectively rom the tooth sur ace. This leads to plaque bio lm retention at the site and can subsequently lead to increased severity o either gingivitis or periodontitis at the site. B. Dental Caries. Untreated tooth decay is another example o a local contributing actor that can increase plaque bio lm retention. Since tooth decay can result in de ects in tooth structure (dental cavities), these de ects (cavities) can also act as protected environments or bacteria that cause gingivitis and periodontitis to live and grow undisturbed (Fig. 16-3).

Fi ur 16-2. Radio rap ic e vid c o Po o rl Co to ur d R sto ratio s. Note that the restoration margins on the distal sur aces o the second premolar and irst molar are not smoothly contoured with the actual tooth sur aces. This leads to increased bio ilm retention o these areas. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

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C. Tooth Grooves or Concavities 1. N aturally occurring developmental grooves and concavities in tooth sur aces requently lead to di culty in sel -care at the site and can also be a local contributing actor or gingivitis and periodontitis because o the increase in plaque bio lm retention at the site. 2. During the natural development o some incisor teeth, a groove orms on the palatal sur ace o the tooth. This groove is a developmental de ect called a palatogingival groove and is most requently seen on maxillary lateral incisors. Plaque bio lm retention is a common problem associated with a palatogingival groove since the groove is o ten di cult or impossible to clean e ectively (Fig. 16-4). 3. Some tooth root sur aces have naturally occurring concavities or depressions that can lead to plaque bio lm retention (Fig. 16-5). The mesial sur ace o maxillary rst premolar teeth o ten has a pronounced concavity in the sur ace. This concavity is a natural contour or that tooth, but i exposed in the oral cavity, can make it extremely di cult or a patient to maintain e ective sel care at the site. Figure 16-6 illustrates how a tooth concavity can prevent thorough sel -care even or a patient skilled in use o dental f oss.

Fi ur 16-3. U tr at d D ca . Note that this untreated tooth decay leaves an actual hole (cavity) in the tooth sur ace that can then harbor periodontal pathogens and can allow them to grow undisturbed by sel -care e orts. (Courtesy o Dr. Ralph Arnold.)

Fi ur 16-4. Palato i ival g ro o v . A palatogingival groove on the lingual sur ace o this maxillary lateral incisor is revealed during a periodontal surgical procedure. The gingiva has been li ted o the bone and tooth root. The palatal side o the root and the alveolar bone level is clearly visible. The palatogingival groove allowed plaque bio ilm to mature undisturbed in the depth o the groove and has contributed to the extensive alveolar bone loss. (Courtesy o Dr. Ralph Arnold.)

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Fi ur 16-5. Ro ot Co cavit . The mesial root concavity on a maxillary irst premolar. This photograph was taken during a periodontal surgical procedure designed to allow better visualization and treatment o the root concavity. (Courtesy o Dr. Ralph Arnold.)

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Fi ur 16-6. Flo ssi a To o t Sur ac w it a Co cavit . Note that even i loss is closely adapted to the tooth sur aces, the loss will not dislodge the plaque bio ilm in the base o the concavity.

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Pathogenicity can be described as the ability o a disease-causing agent to actually produce the disease. In the dental context, pathogenicity can be thought o as the ability o the dental plaque bio lm to cause periodontal disease. Plaque bio lm pathogenicity relates to the character o the plaque bio lm rather than simply an increase in the amount o plaque bio lm. 1. Undisturbed Plaque Biof lm Growth A. Plaque Biof lm Maturation 1. Plaque bio lm allowed to grow undisturbed is said to “ mature.” As plaque bio lm matures, it becomes colonized with larger and larger numbers o bacteria. 2. Starting with a per ectly clean tooth sur ace, plaque bio lm bacteria accumulate in a predictable pattern on any tooth sur ace not being cleaned by the patient. a. Immediately a ter cleaning, salivary proteins attach to the tooth sur ace and orm the pellicle. b. Within the rst 2 days, the pellicle becomes colonized with gram-positive aerobic cocci and rods. These bacteria can cause gingivitis but do not cause periodontitis. c. O ver the next week, other bacteria enter the plaque bio lm. These new bacteria include those that can cause periodontitis. 1. The bacteria in this stage o plaque bio lm development include some gram-negative anaerobic cocci and gram-negative rods. 2. In addition, at this stage speci c periodontal pathogens can colonize the plaque bio lm including Fusobacterium species and Prevotella intermedia. d. Later, other bacteria including Porphyrom onas gingivalis colonize the plaque bio lm. Some o these other bacteria are also associated with periodontitis. B. Increased Plaque Biof lm Pathogenicity 1. The concept o plaque biof lm pathogenicity re ers to the ability o the bacteria in the dental plaque bio lm to produce periodontal disease. a. It is important to understand that all plaque bio lm that is le t undisturbed and allowed to mature (i.e., age) on a tooth sur ace is eventually colonized by bacteria known to cause periodontitis. b. As plaque bio lm matures into a true plaque bio lm it becomes more pathogenic than the plaque bio lm that rst developed on the tooth sur ace since it includes more o the bacteria that are the causative agents in periodontitis (Fig. 16-7). 2. Increased plaque bio lm pathogenicity is closely related to some plaque bio lm retention actors. Plaque bio lm retention actors not only allow an increase in the amount o plaque bio lm at the site but can also allow plaque bio lm to mature and increase in its pathogenicity.

Fi ur 16-7. Matur D tal Plaqu Bio ilm. Note the thick dental plaque bio ilm at the gingival margin o the teeth in this photograph. This plaque bio ilm has been present or several weeks and is more pathogenic than a less mature plaque bio ilm because it now harbors periodontal pathogens. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

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Lo cal Facto rs T at Caus Dir ct Dama This section discusses a ew o the local contributing actors that may actually cause direct damage to the periodontium. These actors also may alter the progress o periodontitis at individual sites. Some local contributing actors that can directly damage the periodontium include ood impaction, patient habits, and aulty restorations or appliances. 1. Direct Damage Due to Food Impaction A. Def nition. Food impaction re ers to orcing ood (such as pieces o tough meat) between teeth during chewing, trapping the ood in the interdental area. B. E ect o Food Impaction 1. Food orced into a tooth sulcus can strip the gingival tissues away rom the tooth sur ace and contribute to periodontal breakdown in addition to the more obvious danger o serving as nutrients or tooth decay–causing bacteria. 2. Food impaction not only damages the gingival tissues directly but can also lead to alterations in gingival contour that result in interdental areas that are di cult or patients to clean (Fig. 16-8). 2. Direct Damage rom Patient Habits. In some patients, habits such as tongue thrusting, mouth breathing, or the improper use o toothbrushes, toothpicks, and other dental cleaning aids can also cause direct damage to the periodontium. A. Improper Use o Plaque Biof lm Control Aids. Improper use o plaque bio lm control aids can result in direct damage to the gingival tissues causing alteration o the natural contours o the tissues (Fig. 16-9).

Fi ur 16-8. Food Impactio . Note the ood impaction between the two molar teeth. As this patient chews ood, the ood is orced between these teeth and produces direct damage to the periodontium. (Courtesy o Dr. Don Rol s, Periodontal Foundations, Wenatchee, WA.)

Fi ur 16-9. Misus o To o t pick. The interdental papilla between the two central incisors has been destroyed by the patient's habit o repeatedly orcing a toothpick between the teeth. This damage to the papillae is an example o direct damage to the periodontium.

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B. Tongue Thrusting. Tongue thrusting is the application o orce ul pressure against the anterior teeth with the tongue. 1. Tongue thrusting is o ten the result o an abnormal tongue positioning during the initial stage o swallowing. 2. This oral habit exerts excessive lateral pressure against the teeth and may be traumatic to the periodontium (Fig. 16-10). C. Mouth Breathing. Mouth breathing is the process o inhaling and exhaling air primarily through the mouth rather than the nose, and o ten occurs while the patient is sleeping. M outh breathing has a tendency to dry out the gingival tissues in the anterior region o the mouth. 3. Direct Damage Due to Faulty Restorations and Appliances A. Inappropriate Crown Placement. A crown is a metal, ceramic, or ceramic-bondedto-metal covering or a badly damaged tooth. Placing a crown on a damaged tooth is a common mechanism used to preserve a badly damaged tooth. 1. Crowns can sometimes be placed inappropriately when tooth structure is minimal. There can be direct damage to the periodontium when the edges o a crown (called margins) are placed below the gingival margin and too near the alveolar bone. 2. A crown margin that is closer than 2 mm to the crest o the alveolar bone can result in resorption o alveolar bone (Fig. 16-11).

A

B

Fi ur 16-10. To u T rust. A: Facial view o a patient with a tongue thrust. As this patient swallows, the patient applies lateral pressure with her tongue against the teeth. B: Side view o the tongue thrust. The tongue is visible in the canine region o the mouth as the patient presses her tongue orward when swallowing. (Courtesy o Dr. Don Rol s, Periodontal Foundations, Wenatchee, WA.)

to t P rio do tium. This radiograph reveals Fi ur 16-11. Dir ct Dama a crown with a margin that is approximately 1 mm rom the alveolar bone. This distance is too close to bone to allow or normal so t tissue attachment to the tooth.

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3. Biologic width re ers to the space on the tooth sur ace occupied by the junctional epithelium and the connective tissue attachment bers immediately apical to (below) the junctional epithelium (Fig. 16-12). This biologic width can be “ violated” or damaged by restoration margins. The drawings in Figure 16-13 show the biologic width and its relationship to a properly placed margin and a restoration margin that violates or damages the biologic width.

Gin g iva l s u lc u s 0 .6 9 m m J u n c t io n a l e p it h e liu m 0 .9 7 m m Bio lo g ic w id t h C o n n e c t ive 2 .0 4 m m t is s u e a tta c hm e nt 1 .0 7 m m

Fi ur 16-12. Bio lo ic Widt i h alt . Illustration showing the biologic width in health with average dimensions that have been reported in the literature.

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Fi ur 16-13. Mar i s o a R sto ratio . A: Illustration showing the placement o a restoration margin in a position that leaves the biologic width undamaged by the restoration. B: Illustration showing the placement o a restoration margin in a position that violates or damages the biologic width.

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B. Improperly Contoured Restorations 1. Bulky or overcontoured crowns or restorations can result in inadequate space between the teeth to accommodate the natural orm o the interdental papilla. 2. The open space apical to the contact area o two adjacent teeth is re erred to as an embrasure space. In health, the embrasure space is lled by an interdental papilla. 3. Bulky crowns reduce the size o the embrasure space, so that inadequate space exists between the teeth to accommodate the interdental papilla. In this situation, the bulky crowns are described as encroaching on the embrasure space (Fig. 16-14). C. Faulty Removable Prosthesis 1. A prosthesis is an appliance used to replace missing teeth. a. A removable prosthesis is one that the patient can remove or cleaning and be ore going to bed. A removable prosthesis that replaces a ew teeth is commonly called a removable partial denture. b. A removable prosthesis should be di erentiated rom a xed prosthesis. A xed prosthesis is a prosthesis that is cemented to the teeth (also known as a xed bridge). 2. A damaged or poorly tting removable prosthesis can impinge on gingival tissue and avor plaque bio lm accumulation and thus hasten the progress o periodontitis (Fig. 16-15).

Fi ur 16-14. Bulk Cro w e cro ac i o I t rd tal Spac . The crowns shown here are so bulky in contour on their proximal sur aces that they ill the embrasure space leaving no room or the natural orm o the papilla. Note the papilla between the central and lateral incisor appears enlarged because it is being pushed rom between the teeth.

A

B

Fi ur 16-15. Tissu Dama b a Poorl Fitti R movabl Prost sis. A: Clinical photograph showing a removable prosthesis (lower partial denture) that replaces extracted posterior teeth. B: With the prosthesis removed, the tissue damage to the mandibular canine is revealed. Gingival recession on the canine is due in part to the clasp o the aulty prosthesis impinging upon the gingival tissue. (Courtesy o Dr. Don Rol s, Wenatchee, WA.)

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4. Direct Damage From Occlusal Forces A. Trauma rom Occlusion 1. Direct damage to the periodontium can result rom excessive occlusal (or biting) orces on the teeth. 2. When excessive occlusal orces cause damage to the periodontium, this is re erred to as trauma rom occlusion. a. When trauma rom occlusion occurs, some alveolar bone resorption can result simply because o increased pressure placed on the surrounding alveolar bone. b. When there is loss o some alveolar bone due to pressures rom trauma rom occlusion, there can be a more rapid destruction by any existing periodontitis. 3. A thorough clinical exam and a thorough radiographic exam can requently reveal signs o trauma rom occlusion. a. Some o the clinical signs o trauma rom occlusion that have been reported include the ollowing: 1. Tooth mobility 2. Sensitivity to pressure 3. M igration o teeth b. Some o the radiographic signs o trauma rom occlusion that have been reported include the ollowing: 1. Enlarged, unnel-shaped periodontal ligament space. 2. Alveolar bone resorption. Figure 16-16 shows a radiograph o a tooth that has been subjected to excessive occlusal orces (trauma rom occlusion). 4. Trauma rom occlusion has been classi ed in the dental literature or many years as either primary trauma rom occlusion or secondary trauma rom occlusion. a. Primary trauma rom occlusion is de ned as excessive occlusal orces on a sound periodontium. 1. Examples o causes o primary trauma rom occlusion include accidental placement o a high restoration or insertion o a xed bridge or partial denture that places excessive orce on the supporting teeth. 2. The changes seen in primary occlusal trauma include a wider periodontal ligament space, tooth mobility, and even tooth and jaw pain. These changes are reversible i the trauma is removed. b. Secondary trauma rom occlusion is de ned as normal occlusal orces on an unhealthy periodontium previously weakened by periodontitis. 1. Secondary trauma rom occlusion occurs to a tooth in which the surrounding periodontium has experienced apical migration o the junctional epithelium, loss o connective tissue attachment, and loss o alveolar bone. In this type o trauma, the periodontium was unhealthy

Fi ur 16-16. Radio rap ic e vid c o Trauma ro m Occlusio . Note the dramatic widening o the periodontal ligament space along the lateral root sur aces on the mandibular right central incisor (center tooth on radiograph). The alveolar bone has been destroyed because o the pressures resulting rom trauma rom occlusion.

C apt r 16

Local Factors Contributing to Periodontal Disease

287

be ore experiencing excessive occlusal orces. Table 16-2 summarizes de nitions o some terms used to describe trauma rom occlusion. 2. A tooth with an unhealthy, inf amed periodontium that is subjected to excessive occlusal orces is thought to be subject to more rapid bone loss and pocket ormation. 3. Teeth can be tipped laterally easily when subjected to lateral occlusal orces. These tipping orces requently accompany trauma rom occlusion and can create areas o pressure and tension within the periodontal ligament (PDL) that are transmitted to the bone. Figure 16-17 illustrates how this tipping can occur. As alveolar bone loss progresses, this lateral tipping becomes even more likely because o the longer lever arm created by the part o the tooth out o the bone compared to the part o the tooth encased in bone. 4. Teeth with reduced alveolar bone support can have additional damage to the periodontium because o the tipping action o lateral orces placed on the teeth. Figure 16-18 shows a series o drawings that illustrate this concept. B. Para unctional Occlusal Forces 1. A series o other terms has been used to describe excessive occlusal orces. Two o these terms are unctional and para unctional occlusal orces. a. Functional occlusal orces are the normal orces produced during the act o chewing ood. b. Para unctional occlusal orces result rom tooth-to-tooth contact made when not in the act o eating. 1. Examples o these para unctional habits are clenching o the teeth together as a release o nervous tension or grinding the teeth together or the same release. a. Clenching is the continuous or intermittent orce ul closure o the maxillary teeth against the mandibular teeth. b. Bruxism is orce ul grinding o the teeth. c. These para unctional habits can occur without the person having conscious knowledge o the habit. Some individuals exhibit these habits while asleep. 2. Para unctional habits can exert excessive orce on the teeth and to the periodontium. 2. There are several clinical therapies that can be used by a dentist to help control the damage rom trauma rom occlusion. a. When the trauma is a result o a aulty bite (re erred to as a aulty occlusion), the dentist can make minor adjustments in the bite to minimize the damaging orces. This procedure is called an occlusal adjustment. b. When the trauma is a result o bruxism, the dentist can abricate an acrylic appliance known sometimes re erred to as a night guard appliance that can protect the teeth during part o each day.

TABLe 1 6 -2 . Te RMS ASSOCIATe D WITh TRAUMA FROM OCCLUSIOn T rm

D f itio

t

In ju y o

u m f o m o cclu sio n

p im

y

S co n d o cclu sio n

um f om occlusion y

um f om

Inju y o

io d o n iu m l y

su l in g f o m xc ssiv o cclu s l fo c s

io don ium

sul in g f om xc ssiv occlus l fo c s

In ju y f o m n o m l o cclu s l fo c s vio u sly d m g d b y

io d o n i is

li d o

io d o n iu m

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Tip p ing move me nt

T

P

Fi ur 16-17. Tippi Mo v m t ro m Lat ral Occlusal Fo rc s. Tipping o a tooth within the socket due to lateral occlusal orces o ten accompanies trauma rom occlusion. This tipping can result in areas o pressure and tension within the PDL. In the illustration, “ P” indicates an area o pressure in the PDL and alveolar bone. The letter “ T” indicates an area o tension. Bone under pressure tends to undergo resorption.

A

B

C

Fi ur 16-18. Dama to T t w it R duc d Bo h i t. A: Teeth with reduced bone height rom existing periodontitis. B: Teeth being subjected to lateral orces and being moved laterally by those orces. C: Additional bone loss to the periodontium as a result o pressure on bone rom the lateral tooth movement. This additional bone loss can be additive to the bone loss already occurring in a periodontitis patient.

C apt r Summar Stat m

t

Local contributing actors can increase the risk o developing gingivitis or periodontitis or increase the risk o developing more severe disease when gingivitis or periodontitis is already established. The three mechanisms in which local actors can increase the risk o periodontal disease are by (1) increasing plaque bio lm retention, (2) increasing plaque bio lm pathogenicity, and (3) causing direct damage to the periodontium. As will be discussed in Chapter 19, the dental team must identi y these local contributing actors during a clinical assessment, so that any local contributing actors can be eliminated or minimized during the nonsurgical periodontal treatment.

C apt r 16

S ct io

5

Fo cus o

Cli ical Pati CA S e

Pati

Local Factors Contributing to Periodontal Disease

ts

t Car

1

Examination o a patient reveals gingivitis. In addition, the patient has generalized calculus deposits and numerous restorations with overhangs. What steps might be necessary to bring the gingivitis under control in this patient?

CA S e

2

Examination o a patient reveals periodontitis. The patient also has a severe tooth-clenching habit. Explain how the tooth-clenching habit could be related to the progress o the periodontitis.

e vid

c i Actio

CASe 1 In a dental hygiene journal you nd an article that re ers to mature dental plaque bio lm. Explain what the author means by this term mature dental plaque bio lm.

R

r

c s

1. Genco RJ. Current view o risk actors or periodontal diseases. Journal of periodontology. 1996;67(10 Suppl):1041-9. doi: 10.1902/jop.1996.67.10.1041. PubM ed PM ID: 8910821. 2. Leknes KN . The inf uence o anatomic and iatrogenic root sur ace characteristics on bacterial colonization and periodontal destruction: a review. Journal of periodontology. 1997;68(6):507-16. doi: 10.1902/jop.1997.68.6.507. PubM ed PM ID: 9203093. 3. Pihlstrom B. Treatment o periodontitis: key principles include removing subgingival bacterial deposits; providing a local environment and education to support good home care; providing regular pro essional maintenance. Journal of periodontology. 2014;85(5):655-6. doi: 10.1902/jop.2014.140046. PubM ed PM ID: 24773135.

STUDe n T An CILLARy Re SOURCe S A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

289

r e t p a h C

17 S ctio n 1

N t itio n, Inf ammatio n, and P io do ntal Dis as Asso ciatio n B t n Ob sit and P io do ntal Dis as

291

Mic o n t i nts, Antio xidants, and P io do ntal Dis as

294

S ctio n 3

Mac o n t i nts and P io do ntal Dis as

297

S ctio n 4

Fo c s o n Pati nts

299

S ctio n 2

Clinical Patient Care Ethical Dilemma

Clinical Applicatio n.

Though the precise relationship between nutrition and periodontal disease is not ully understood, all members o the dental team must be aware o what is known about this relationship and understand how to apply this in ormation to guide patients with nutritional issues that may have an impact upon periodontal health. This chapter outlines emerging understanding related to the association between nutrition and periodontal disease and provides some practice in applying this in ormation to a clinical setting.

L a ning Obj ctiv s • Discuss the link between obesity and periodontal disease. • Discuss the role o polymorphonuclear leukocytes in the production o reactive oxygen species in response to plaque bio lm. • Discuss how antioxidants may inf uence periodontal disease onset and progression. • Describe the proposed roles o micronutrients and macronutrients in periodontal disease. • List some oral symptoms associated with ascorbic acid–de ciency gingivitis. • Explain the role o dental healthcare providers in addressing obesity and nutrition in the management o periodontal disease.

K

T ms

Body mass index (BMI) Reactive oxygen species (ROS) Micronutrients

Antioxidants Macronutrients Ascorbic acid–de iciency gingivitis

Chapt

17

Nutrition, Inf ammation, and Periodontal Disease

H istorically, periodontal disease has been seen as an in ammatory disease with limited associations to nutrition. M any early studies into the relationship between nutrition and periodontal disease ailed to show associations between nutritional status and periodontal disease. These studies, however, used poor methodologies, tended to study nutrients in isolation, and ailed to control or con ounding variables (such as smoking). Improved understanding o periodontal disease at the cellular level and more stringent nutritional methodologies have created a renewed interest in the relationship between nutrition and periodontal disease. Recent research is ocused on (1) the association between obesity and periodontal inf ammation and (2) the role o antioxidants in the prevention and treatment o periodontal disease.

S ct io n 1

Asso ciatio n B t n Ob sit and P io do ntal Dis as 1. Obesity Overview A. O besity is an excess amount o body at in proportion to lean body mass, to the extent that health is impaired (1). 1. The most commonly used measure o body at is the body mass index (BMI), which is def ned as a person’s weight in kilograms divided by the square o his/ her height in meters. The World H ealth O rganization and the N ational H eart, Lung, and Blood Institute def ne overweight as a body mass index o 25 to 29.9 and obesity as a BM I o equal to or greater than 30 (2). 2. M ore than 65% o the United States adult population has a body mass index o greater than or equal to 25 kg/m2 and 15.8% o children aged 6 to 11 years, and 16.1% o adolescents aged 12 to 19 years, are overweight (3). 3. M ore than a third o adults (35% ) and 17% o youth (age 2 to 19) were obese in 2011 to 2012, with no signif cant change or either group since 2003 to 2004, O gden et al. reported in the Journal of the A m erican M edical A ssociation. H owever, more women over 60 became obese with the prevalence rising to 38% rom 31.5% in that group during that time. The CDC data comes rom an analysis o the N ational H ealth and N utrition Examination Survey (N H AN ES) 2011 to 2012 involving 9,120 people in the United States (4). International trends are similar to those in the United States. The International O besity Task Force estimates that over 1 billion adults are overweight (5). B. Adipose tissue is a complex and metabolically active endocrine organ that secretes numerous immunomodulatory actors and plays a major role in regulating metabolic and vascular biology (6). O bese individuals are reported to have elevated levels o circulating TN F-α and IL-6 compared to normal weight controls (7,8). 2. The Obesity–Periodontal Disease Link A. Recent research indicates a link between obesity and periodontal disease (9–19). 1. An analysis o data rom The Third N ational H ealth and N utrition Examination Survey (N H AN ES III) involving over 13,000 individuals having one or more sites with clinical attachment loss ound a positive correlation between BM I and the severity o periodontal attachment loss (20). 2. Al-Z ahrani et al. conducted a study o a representative sample o participants in the N H AN ES III survey who were 18 years or younger and had undergone a periodontal examination.

291

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a. The purpose o the study was to examine the relation between body weight and periodontal disease in a representative United States sample. Body mass index and waist circum erence were used as measures o overall and abdominal at content, respectively. b. Study results indicate that even in a younger population, overall and abdominal obesity are associated with increased prevalence o periodontal disease while underweight (BM I < 18.5) is associated with decreased prevalence (9). 3. In another analysis o the N H AN ES III data, Al-Z ahrani et al. ound that individuals who maintained normal weight, exercised regularly, and ollowed a diet utilizing the U.S. Department o Agriculture Center or N utrition Policy and Promotions’ dietary guidelines were 40% less likely to have periodontitis (21). 4. In the United States, the Forsyth Institute conducted an ongoing case control study. The study reported that obesity is related to a marked increase in plaque biof lm accumulation, attachment loss, deep pockets, and bleeding on probing and an increase in the proportion o Tannerella forsythia (Bacteroides forsythus) (22). B. Among li estyle-related risk actors, smoking displays the greatest impact on periodontitis. Both smoking and obesity are independent risk indicators or periodontitis. Nishida et al. (23) suggested that obesity is second only to smoking as the strongest li estyle-related actor or in ammatory periodontal disease destruction. 3. Biological Mechanisms Linking Obesity with Periodontal Disease. The mechanism o how obesity modif es the pathogenesis o periodontal disease at the molecular level currently is poorly understood, but what is known is that obesity has several harm ul biological e ects that might be related to the pathogenesis o periodontitis (16). A. Release o Proin ammatory Cytokines rom Adipose Tissue. Further studies are needed to determine i obesity is a true risk actor or periodontal disease. Several researchers have suggested that the association most likely lies in the commonality o their in ammatory pathways. According to Genco (24), the relentless release o proin ammatory cytokines into the systemic circulation rom adipose tissue in obese individuals provides a “ systemic in ammatory overload.” The relentless release o cytokines provides a possible explanation o how obesity intensif es in ections, including periodontal disease. 1. Adipose tissue secretes several cytokines and hormones that are involved in in ammatory processes, suggesting that similar pathways are involved in the pathogenesis o obesity and periodontitis. The adverse e ect o obesity on the periodontium may be mediated through proin ammatory cytokines like interleukins (IL-1, IL-6, and TN F-α ), adipokines (leptin and adiponectin), and reactive oxygen species (RO S), which may a ect the periodontal tissues directly (25). 2. Adiponectin is a circulating hormone secreted by the adipose tissue involved in glucose and lipid metabolism. a. Adiponectin production is decreased in obese individuals. b. Low levels o adiponectin are associated with increased systemic in ammation (26). 3. Leptin is secreted rom adipose tissue and plays an important role in regulating appetite and metabolism. a. Leptin acts to suppress appetite and increase energy expenditure. b. M ost obese individuals have elevated leptin levels that do not suppress appetite. M any researchers consider leptin resistance to be one o the eatures contributing to obesity’s pathology (27). It has been demonstrated

Chapte r 17

Nutrition, Inf ammation, and Periodontal Disease

293

that human leptin is present within healthy gingival tissue and decreases in concentration with increased probing depths (28). 4. O besity-associated tumor necrosis actor-α (TN F-α ) is primarily secreted rom macrophages accumulated in abdominal adipose tissue. It is thought that increased circulating TN F-α rom adipose tissue contributes to general systemic in ammation (29). 5. Interleukin-6 (IL-6) is secreted by adipose tissue and is produced in greater amounts by abdominal at. B. Increased Levels of Reactive Oxygen Species 1. Reactive oxygen species (ROS) are chemically reactive molecules containing oxygen. RO S are products o normal cellular metabolism, but excessive production induces damage by oxidizing DN A, lipids, and proteins (30). RO S clearly can be toxic to cells. O ne o the best-known toxic e ects o oxygen radicals is damage to cellular membranes. 2. Emerging scientif c evidence indicates that obesity appears to play a role in the multi actorial etiology o periodontitis through the increased production o RO S and an increase in in ammatory cytokines (9–19). Figure 17-1 shows a suggested model or the link between obesity and periodontal disease. 3. N ormally, cells de end themselves against RO S damage with enzymes and small molecule antioxidants such as ascorbic acid (vitamin C), tocopherol (vitamin E), uric acid, and glutathione. 4. The Role of the Dental Team in Managing Obesity and Periodontal Disease. Periodontists and dental hygienists must be aware o the increasing numbers o obese persons and o the signif cance o obesity as a multiple risk actor or oral health. Addressing obesity in the management o periodontal disease is clearly important in patients who have both conditions. This necessitates the cooperation and collaboration o all healthcare pro essionals to educate patients regarding the implications o obesity and periodontitis and to encourage counseling, weight reduction, and treatment.

Ge ne tic fa c to rs

P e rio d o ntitis (bacterial factors )

Enviro nm e nta l fa c to rs (e.g., s moking, nutrition, and phys ical activity)

Ob e s ity adipos e tis s ue

Ele va te d p ro d uc tio n o f in a m m a to ry c yto kine s a nd Re a c tive Oxyg e n Sp e c ie s

Fig ure 17-1. Hypo the sis Linking Obe sity and Pe rio do ntal Dise ase . One hypothesis linking obesity and periodontal disease is that both conditions are associated with an elevated production o both in lammatory cytokines and reactive oxygen species. O course, both conditions are also a ected by other background actors such as genetic actors and environmental actors, which make identi ying a precise link between them di icult.

294

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Risk Factors or Periodontal Diseases

S ct io n 2

Mic o n t i nts, Antio xidants, and P io do ntal Dis as Nutrients are divided into six categories: vitamins, minerals, proteins, lipids, carbohydrates, and water. Micronutrients are nutrients that are needed in tiny quantities each day. Vitamins and calcium are two examples o micronutrients. Proteins, lipids, and carbohydrates are macronutrients, which provide energy or calories. 1. Micronutrients and Oxidation A. Oxidation. As oxygen interacts with cells o any type—a ripening banana or a cell in the body—oxidation occurs. O xidation produces some type o change in the cell. The banana may rot or in time, dead body cells are replaced with new cells. 1. O xidative stress occurs with the production o harm ul molecules called ree radicals. 2. Free radicals containing oxygen, known as reactive oxygen species (ROS), are the most biologically signif cant ree radicals. 3. It is impossible or the cells o the body to avoid damage by ree radicals. Free radicals arise rom sources both inside and outside the body. O xidants develop rom processes within the body as the result o normal metabolism and in ammation. O utside the body ree radicals orm rom environmental actors such as pollution, sunlight, smoking, and radiation. 4. In response to plaque biof lm, polymorphonuclear leukocytes (PMNs) produce reactive oxygen species during phagocytosis as part o the host response to in ection. a. Individuals with periodontal disease display increased PM N number and activity. b. It has been suggested that this proli eration results in a high degree o RO S release, culminating in heightened damage to gingival tissue, periodontal ligaments, and alveolar bone (31–34). c. Studies also have suggested the RO S stimulate osteoclast activation (35). Compared with healthy controls, patients with chronic periodontitis generate higher levels o many RO S. Several studies have demonstrated a correlation between RO S and periodontal disease activity (36,37). 5. The damage mediated by RO S can be mitigated by antioxidants (38). B. Antioxidants. Antioxidants are substances—such as vitamins—that are capable o counteracting the damaging e ects o the physiological process o oxidation in a living organism. 1. N ature provides thousands o di erent antioxidants in ruits, vegetables, nuts, whole grains, and legumes to help protect the body rom oxidation. 2. Dietary antioxidants include vitamins and minerals as well as enzymes (proteins in the body that assist in chemical reactions). 3. Data rom research suggests that there are mechanisms in which nutrition, particularly antioxidants, can in uence periodontal disease onset, progression, and wound healing (31). Antioxidants are thought to be important in the downregulation o proin ammatory responses. While additional in ormation is needed, nutrients can act as antioxidants that may modulate gingival in ammation (31,38). 2. Vitamins and Minerals A. Vitamins. Vitamins are organic antioxidants that are not synthesized by the body and are necessary or normal metabolism. Vitamin C is the most common water-soluble antioxidant while vitamin E is one o the most common at-soluble antioxidants.

Chapt

17

Nutrition, Inf ammation, and Periodontal Disease

295

1. Vitamin C a. Vitamin C has e ective antioxidant properties that are important or maintaining the integrity o cell membranes and protection against the RO S generated during in ammatory responses (39). b. In addition, vitamin C has the ability to enhance neutrophil, monocyte, and natural killer cell unctions (40,41). c. An epidemiologic study o vitamin C intake demonstrated an association between low vitamin C intake and periodontal disease, especially among smokers (42). d. Vitamin C is a water-soluble vitamin that cannot be stored by the body except in insignif cant amounts. 1. Since the human body lacks the ability to synthesize and make vitamin C, it depends on dietary sources to meet vitamin C needs. 2. Vitamin C is ound in resh ruits and vegetables such as oranges, berries, tomatoes, lea y greens, and kiwi ruit. Consumption o ruits and vegetables or orti ying diets with vitamin C supplements is essential to avoid ascorbic acid def ciency. e. Ascorbic acid–def ciency gingivitis is an in ammatory response o the gingiva caused by plaque biof lm that is aggravated by chronically low vitamin C (ascorbic acid) levels. 1. Ascorbic acid–def ciency gingivitis mani ests clinically as bright red, swollen, ulcerated gingival tissue that bleeds with the slightest provocation (43,44). 2. An example o in antile vitamin C def ciency is shown in Figures 17-2 and 17-3.

Fig 17-2. Asco bic Acid–D ici nc Ging ivitis. This 15-month-old boy had a history o unexplained gingival bleeding or several weeks and ever or 2 days. He had been ed only cow’s milk and oatmeal since age 4 months. Laboratory blood tests revealed that his vitamin C levels were low. (Used with permission rom Riepe FG, Eichmann D, Oppermann HC, et al. Special eature: picture o the month. Arch Pediatr Adolesc Med. 2001;155:607; copyright 2001 American Medical Association. All rights reserved.)

Fig 17-3. A t T atm nt ith Vitamin C. The same boy shown in Figure 17-2 a ter 3 days treatment with vitamin C. (Courtesy o Dr. Felix G. Riepe, MD, Christian Albrechts University, Kiel, Germany.)

296

Pa t 3

Risk Factors or Periodontal Diseases

2. Vitamin A a. Vitamin A appears to be essential or epithelial cell di erentiation, cellmediated immunity, and supporting a T-helper anti-in ammatory response (45). b. Vitamin A has a key role in epithelial maintenance. Severe vitamin A def ciency, however, is rare in industrialized nations. The NHANES III study ound no signif cant relationship between serum vitamin A and risk or periodontitis (46). c. Foods high in vitamin A include milk, eggs, liver, carrots, pumpkin, and mangoes. 3. Vitamin D a. Vitamin D promotes the di erentiation o monocytes to macrophages (47,48). b. Vitamin D may reduce susceptibility to gingival in ammation through its antiin ammatory e ects (49). Studies o gingival tissue suggest a mitigating e ect o vitamin E on periodontal in ammation and collagen breakdown. Lower gingival levels o vitamin E are associated with periodontal disease (34,50,51). c. Vitamin D is ound in some oods but is mostly produced within the skin in response to sunlight; good sources o dietary vitamin D include egg yolk, liver, and oily f sh. 4. Vitamin E a. Vitamin E is considered the most important at-soluble antioxidant that protects cell membranes rom oxidative damage and reduces the production o prostaglandin E2 in macrophages (52). b. Recent in vitro studies show vitamin E to have mitigating e ects on indicators o gingival in ammation (34,51). c. Several clinical studies have shown positive e ects o supplementation o vitamin E on the immune response, particularly in aged populations (53). d. Good dietary sources include nuts, seeds, and wheat germ. 5. Folic Acid a. Folic acid is a water-soluble vitamin belonging to the B-complex group o vitamins. With the exception o olic acid, there is little evidence that B vitamins are vital to periodontal health. b. Folic acid is involved with DN A synthesis. Cells with rapid turnover, such as those in the gingival epithelium, have high olic acid requirements. c. A def ciency o olic acid may reduce the ability o the gingival tissue to act as a barrier to bacteria. d. Recently published data rom the N H AN ES survey showed that low serum oliate was independently associated with periodontal disease in older adults (54). e. In Canada and the United States, grains marketed as enriched have been ortif ed with olic acid since 1998. O ther good dietary sources include broccoli, asparagus, Brussels sprouts, peas, and brown rice. B. Minerals: Calcium 1. The micronutrient calcium is intricately involved in the calcif cation process and, there ore, has a role in the ormation and maintenance o alveolar bone. N ishida et al. ound a 54% increased risk o periodontal disease in emales who ingested less than 499 mg/d o calcium and a 27% increased risk in those with intakes below 800 mg/d (42,55). 2. In another interesting longitudinal study, elderly adults with higher daily calcium intake had a decreased risk or tooth loss than adults who consumed lower calcium levels (56). 3. Consumption o milk, yogurt, and cheese (pre erably lower- at varieties) is important in ensuring adequate intakes o calcium.

Chapt

17

Nutrition, Inf ammation, and Periodontal Disease

S ct io n 3

Mac o n t i nts and P io do ntal Dis as Proteins, lipids, and carbohydrates are macronutrients, which provide energy or calories. M any o the pathways to in ammation are related to high caloric intake rom ref ned carbohydrates and oxidative stress, which is stimulated by changes in the metabolism o adipose tissue (57). 1. Proteins A. Protein def ciency can have an e ect on the host de enses that could modulate the progress o periodontitis. Cell-mediated immunity, the complement system, phagocyte activity, and production o cytokines are all impaired by protein def ciency (58). B. The e ect o protein–energy malnutrition on periodontal disease risk was extensively reviewed by Enwonwu (32), who observed that aggressive periodontal disease was more prevalent and severe in undernourished individuals than in well-nourished ones. The immune depression that occurs in protein–energy malnutrition promotes vulnerability o the periodontium to in ammatory stimuli rom the plaque biof lm. 2. Ref ned Carbohydrates and Lipids. Diets rich in ref ned carbohydrates and saturated ats may play a role in increasing the risk or periodontal disease. Excessive energy intake causes obesity, which has been shown to be associated with increased risk o periodontitis. A. Excess consumption o ref ned carbohydrates can a ect the immune response and may lead to continued destruction o the periodontium in patients with existing periodontitis through mechanisms such as the action o enzymes (i.e., collagenase) and proin ammatory mediators (i.e., interleukin-1 and interleukin-6) (57). These destructive mechanisms have been discussed in other chapters o this book. B. Diets high in ref ned carbohydrates and saturated ats cause rapid release o glucose into the bloodstream (Table 17-1). H igh blood glucose levels increase triglyceride levels and stimulate the release o insulin, which decreases the ability o the body to break down at stored in adipose depots (57). C. As discussed earlier in this chapter, obesity increases the circulation o RO S, which, in turn, causes oxidative damage, and progression o periodontal disease (10,17,38,59–61). 3. The Role o the Dental Team in Promoting Good N utrition A. M aking an appropriate connection between diet, nutrients, and periodontal disease can allow clinicians to make specif c suggestions to improve a patient’s diet. When indicated clinically, nutritional counseling, with an emphasis on periodontal health and root caries prevention, should be o ered to periodontal patients. Teaching patients good dietary habits can be accomplished using standard diet orms, counseling techniques, and analysis procedures (62). B. Table 17-1 contains a summary o potential ways that diet and nutrition may modi y periodontal disease.

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Risk Factors or Periodontal Diseases

TABLe 1 7 -1 . Su MMAr y OF THe ASSOCIATION Be Tw e e N Nu Tr ITION OF Pe r IODONTAL DISe ASe Di ta Di

Co mpo n nt

y n io xid n s

Asso ciatio n

ith P io do ntal Dis as

a n io xid n s

Vi m in C

an

u s is co m

id m io lo g ic s u d y d m o n s

lo w vi m in C in sm o k Vi m in e

k

nd

in fl m m Su

io d o n d

io d o n

l d is

o si iv

l d is

s (38,63)

sso ci io n b

s , s

w

ci lly m o n g

s (42)

In vi o s u d i s s o w

Fo lic cid

o m is d in

vi m in e c n d m

n g in g iv l

io n (37,53)

l m n

io n w i

fo lic cid

d u c s g in g iv l in fl m m

io n

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Though periodontal disease cannot be caused by nutritional def ciencies, some nutritional def ciencies do indeed appear to modi y the severity and extent o the periodontal disease. • Research links specif c nutrient def ciencies and oods high in ref ned carbohydrates to increased in ammation—the very kind that triggers the host-mediated in ammatory response seen in periodontal disease. • Reports o the relationship between obesity and periodontal disease are increasing. At this time, it is not possible to determine whether obesity predisposes an individual to periodontal disease or periodontal disease a ects lipid metabolism, or both. Future longitudinal studies with more precise measures o adiposity on large populations are needed to clari y whether obesity is one o the risk actors or periodontal disease or simply a risk indicator. • Data rom research suggests that there are mechanisms in which nutrition, particularly antioxidants, can in uence periodontal disease onset, progression, and wound healing. • It is wise to counsel patients with periodontal disease to be thought ul ood shoppers and to prepare meals and snacks that are rich in specif c nutrients.

n

Chapt

17

299

Nutrition, Inf ammation, and Periodontal Disease

S ct io n 4

Fo c s o n Pati nts Clinical Pati nt Ca Directions or Clinical Patient Cases: Analyze the in ormation and 24-H our Diet Recall (Tables 17-2 and 17-3) on the two f ctitious periodontal patients, to answer the ollowing questions: 1. Can you identi y any eating patterns (healthy or unhealthy)? I so, what are they? 2. List diet practices that have the potential to be most detrimental to the individual’s periodontal health. 3. List two diet behaviors that the individual could modi y to benef t his/her periodontal health.

CA S e

1

Fictitio s P io do ntal Pati nt—M . Phillip B g ss M r. Phillip Burgess is a 39-year-old male. M r. Burgess is 5′8″ in height and weighs 280 lb (173 cm and 127 kg). H is periodontal diagnosis is generalized mild chronic periodontitis.

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300

Pa t 3

CA S e

Risk Factors or Periodontal Diseases

2

Fictitio s P io do ntal Pati nt—M s. Gl nda Bissada M rs. Bissada is a 70-year-old emale. M rs. Bissada is 5′1″ in height and weighs 160 lb (155 cm and 73 kg). H er periodontal diagnosis is generalized severe chronic periodontitis.

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G

11:00

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Chapt

17

Nutrition, Inf ammation, and Periodontal Disease

301

e thical Dil mma Stuart Fisher, your next patient, is new to the practice. H e is a 48-year-old male, who is married with three young children. H e owns a success ul restaurant, where he works as the head che . As he is sel -employed, he doesn’t carry dental insurance. You review Stuart’s medical history, and he states that he is scheduled or lap band surgery next month. Stuart admits that he has neglected his general and oral health or many years, due to his busy li estyle. H e also notes that although he knows better, his diet is poor. A ter cooking in the restaurant all day and night, the last thing he wants to do is prepare ood or himsel . So, both be ore and a ter work, he stops or “ ast ood.” Your radiographs and examination reveal that Stuart presents with generalized chronic periodontitis and moderate bone loss throughout his mouth, as well as localized urcation involvement. You review the treatment plan with Stuart, which includes periodontal instrumentation with anesthesia, nutritional counseling, and re erral to a periodontist. Stuart re uses to agree with your suggestions, as he states that he doesn’t carry dental insurance. H e only scheduled this appointment, as his surgeon required it prior to his surgery. H e wants to receive the minimal dental treatment, and will not “ go or” anything more. 1. What is the best way or you to handle this ethical dilemma? 2. What is the best way to address/discuss Stuart’s treatment plan with him? 3. What ethical principles are in con ict in this dilemma?

r

nc s

1. Aronne LJ, Segal KR. Adiposity and at distribution outcome measures: assessment and clinical implications. O bes R es. 2002;10(Suppl 1):14S–21S. 2. Executive summary o the clinical guidelines on the identif cation, evaluation, and treatment o overweight and obesity in adults. A rch Intern M ed. 1998;158(17):1855–1867. 3. N ational Center or H ealth Statistics (U.S.). H ealth, United States, 2005: w ith Chartbook on Trends in the H ealth of A m ericans. H yattsville, M D: Dept. o H ealth and H uman Services, Centers or Disease Control and Prevention, N ational Center or H ealth Statistics; 2005:xix, 535. 4. O gden CL, Carroll M D, Kit BK, et al. Prevalence o childhood and adult obesity in the U.S., 2011–2012. JA M A . 2014;311(8):806–814. 5. James PT, Rigby N , Leach R; International O besity Task Force. The obesity epidemic, metabolic syndrome and uture prevention strategies. Eur J Cardiovasc Prev R ehabil. 2004;11(1):3–8. 6. Trayhurn P, Wood IS. Adipokines: in ammation and the pleiotropic role o white adipose tissue. Br J N utr. 2004;92(3):347–355. 7. Kern PA, Ranganathan S, Li C, et al. Adipose tissue tumor necrosis actor and interleukin-6 expression in human obesity and insulin resistance. A m J Physiol Endocrinol M etab. 2001;280(5):E745–E751. 8. Z iccardi P, N appo F, Giugliano G, et al. Reduction o in ammatory cytokine concentrations and improvement o endothelial unctions in obese women a ter weight loss over one year. Circulation. 2002;105(7):804–809. 9. Al-Z ahrani M S, Bissada N F, Borawskit EA. O besity and periodontal disease in young, middle-aged, and older adults. J Periodontol. 2003;74(5):610–615. 10. Dahiya P, Kamal R, Gupta R. O besity, periodontal and general health: relationship and management. Indian J Endocrinol M etab. 2012;16(1):88–93. 11. Gorman A, Kaye EK, N unn M , et al. Changes in body weight and adiposity predict periodontitis progression in men. J D ent R es. 2012;91(10):921–926. 12. Krejci CB, Bissada N F. O besity and periodontitis: a link. G en D ent. 2013;61(1):60–63. 13. Kumar PM , Kumar PA, Rao A, et al. Periodontal disease and obesity. J Stom at O cc M ed. 2013;6:1–5. 14. Lawande S. O besity and periodontal disease: a multidirectional relationship? J Pharm Biom ed Sci. 2012;25(25):252–256. 15. M orita I, O kamoto Y, Yoshii S, et al. Five-year incidence o periodontal disease is related to body mass index. J D ent R es. 2011;90(2):199–202. 16. Ritchie CS. O besity and periodontal disease. Periodontol 2000. 2007;44:154–163. 17. Saito T, Shimazaki Y, Koga T, et al. Relationship between upper body obesity and periodontitis. J D ent R es. 2001;80(7):1631–1636. 18. Shimazaki Y, Shirota T, Uchida K, et al. Intake o dairy products and periodontal disease: the H isayama Study. J Periodontol. 2008;79(1):131–137. 19. Wood N, Johnson RB, Streck us CF. Comparison o body composition and periodontal disease using nutritional assessment techniques: Third N ational H ealth and N utrition Examination Survey (N H AN ES III). J Clin Periodontol. 2003;30(4):321–327.

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20. Genco RJ, Grossi SG, H o A, et al. A proposed model linking in ammation to obesity, diabetes, and periodontal in ections. J Periodontol. 2005;76(11 Suppl):2075–2084. 21. Al-Z ahrani M S, Borawski EA, Bissada N F. Periodontitis and three health-enhancing behaviors: maintaining normal weight, engaging in recommended level o exercise, and consuming a high-quality diet. J Periodontol. 2005;76(8):1362–1366. 22. Socransky SS, H a ajee AD. Periodontal microbial ecology. Periodontol 2000. 2005;38:135–187. 23. N ishida N , Tanaka M , H ayashi N , et al. Determination o smoking and obesity as periodontitis risks using the classif cation and regression tree method. J Periodontol. 2005;76(6):923–928. 24. Genco R. The three-way street. In: O ral and W hole Body H ealth. N ew York, N Y: Scientif c American, Inc.; 2006. 25. Ylostalo P, Suominen-Taipale L, Reunanen A, et al. Association between body weight and periodontal in ection. J Clin Periodontol. 2008;35(4):297–304. 26. N isoli E, Carruba M O. Emerging aspects o pharmacotherapy or obesity and metabolic syndrome. Pharm acol R es. 2004;50(5):453–469. 27. Correia M L, H aynes WG. O besity-related hypertension: is there a role or selective leptin resistance? Curr H ypertens R ep. 2004;6(3):230–235. 28. Johnson RB, Serio FG. Leptin within healthy and diseased human gingiva. J Periodontol. 2001;72(9):1254–1257. 29. Berg AH , Scherer PE. Adipose tissue, in ammation, and cardiovascular disease. Circ R es. 2005;96(9):939–949. 30. Ahsan H , Ali A, Ali R. O xygen ree radicals and systemic autoimmunity. Clin Ex p Im m unol. 2003;131(3):398–404. 31. Chapple IL. Role o ree radicals and antioxidants in the pathogenesis o the in ammatory periodontal diseases. Clin M ol Pathol. 1996;49(5):M 247–M 255. 32. Enwonwu CO. Cellular and molecular e ects o malnutrition and their relevance to periodontal diseases. J Clin Periodontol. 1994;21(10):643–657. 33. Enwonwu CO, Phillips RS, Falkler WA Jr. N utrition and oral in ectious diseases: state o the science. Com pend Contin Educ D ent. 2002;23(5):431–434, 436, 438 passim; quiz 448. 34. O enbacher S, O dle BM , Green M D, et al. Inhibition o human periodontal prostaglandin E2 synthesis with selected agents. A gents A ctions. 1990;29(3–4):232–238. 35. H all TJ, Schaeublin M , Jeker H , et al. The role o reactive oxygen intermediates in osteoclastic bone resorption. Biochem Biophys R es Com m un. 1995;207(1):280–287. 36. Cao CF, Smith Q T. Crevicular uid myeloperoxidase at healthy, gingivitis and periodontitis sites. J Clin Periodontol. 1989;16(1):17–20. 37. M arton IJ, Balla G, H egedus C, et al. The role o reactive oxygen intermediates in the pathogenesis o chronic apical periodontitis. O ral M icrobiol Im m unol. 1993;8(4):254–257. 38. Ritchie CS, Kinane DF. N utrition, in ammation, and periodontal disease. N utrition. 2003;19(5):475–476. 39. Vojdani A, Bazargan M , Vojdani E, et al. N ew evidence or antioxidant properties o vitamin C. Cancer D etect Prev. 2000;24(6):508–523. 40. H euser G, Vojdani A. Enhancement o natural killer cell activity and T and B cell unction by bu ered vitamin C in patients exposed to toxic chemicals: the role o protein kinase-C. Im m unopharm acol Im m unotox icol. 1997;19(3):291–312. 41. Siegel BV, M orton JI. Vitamin C and immunity: natural killer (N K) cell actor. Int J Vitam N utr R es. 1983;53(2):179–183. 42. N ishida M , Grossi SG, Dun ord RG, et al. Dietary vitamin C and the risk or periodontal disease. J Periodontol. 2000;71(8):1215–1223. 43. M oran JR, Greene H L. The B vitamins and vitamin C in human nutrition. II. ‘Conditional’ B vitamins and vitamin C. A m J D is Child. 1979;133(3):308–314. 44. Riepe FG, Eichmann D, O ppermann H C, et al. Special eature: picture o the month. A rch Pediatr A dolesc M ed. 2001;155(5):607–608. 45. Stephensen CB. Vitamin A, in ection, and immune unction. A nnu R ev N utr. 2001;21:167–192. 46. Chapple IL, M ilward M R, Dietrich T. The prevalence o in ammatory periodontitis is negatively associated with serum antioxidant concentrations. J N utr. 2007;137(3):657–664. 47. Bikle DD. Vitamin D and the immune system: role in protection against bacterial in ection. Curr O pin N ephrol H ypertens. 2008;17(4):348–352. 48. Kreutz M , Andreesen R, Krause SW, et al. 1,25-dihydroxyvitamin D3 production and vitamin D3 receptor expression are developmentally regulated during di erentiation o human monocytes into macrophages. Blood. 1993;82(4):1300–1307. 49. Dietrich T, N unn M , Dawson-H ughes B, et al. Association between serum concentrations o 25-hydroxyvitamin D and gingival in ammation. A m J Clin N utr. 2005;82(3):575–580. 50. Asman B, Wijkander P, H jerpe A. Reduction o collagen degradation in experimental granulation tissue by vitamin E and selenium. J Clin Periodontol. 1994;21(1):45–47. 51. Cohen M E, M eyer DM . E ect o dietary vitamin E supplementation and rotational stress on alveolar bone loss in rice rats. A rch O ral Biol. 1993;38(7):601–606. 52. M eydani SN , Beharka AA. Vitamin E and immune response in the aged. Bibl N utr D ieta. 2001;(55):148–158. 53. H an SN , M eydani SN . Impact o vitamin E on immune unction and its clinical implications. Ex pert R ev Clin Im m unol. 2006;2(4):561–567. 54. Yu YH , Kuo H K, Lai YL. The association between serum olate levels and periodontal disease in older adults: data rom the N ational H ealth and N utrition Examination Survey 2001/02. J A m G eriatr Soc. 2007;55(1):108–113. 55. N ishida M , Grossi SG, Dun ord RG, et al. Calcium and the risk or periodontal disease. J Periodontol. 2000;71(7): 1057–1066. 56. Krall EA, Wehler C, Garcia RI, et al. Calcium and vitamin D supplements reduce tooth loss in the elderly. A m J M ed. 2001;111(6):452–456. 57. Chapple IL. Potential mechanisms underpinning the nutritional modulation o periodontal in ammation. J A m D ent A ssoc. 2009;140(2):178–184. 58. Woodward B. Protein, calories, and immune de enses. N utr R ev. 1998;56(1 Pt 2):S84–S92. 59. Boesing F, Patino JS, da Silva VR, et al. The inter ace between obesity and periodontitis with emphasis on oxidative stress and in ammatory response. O bes R ev. 2009;10(3):290–297. 60. Saito T, Shimazaki Y, Kiyohara Y, et al. Relationship between obesity, glucose tolerance, and periodontal disease in Japanese women: the H isayama study. J Periodontal R es. 2005;40(4):346–353.

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61. Tomo uji T, Yamamoto T, Tamaki N , et al. E ects o obesity on gingival oxidative stress in a rat model. J Periodontol. 2009;80(8):1324–1329. 62. Sroda R. N utrition for a H ealthy M outh. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010:xviii, 350. 63. Brock GR, Butterworth CJ, M atthews JB, et al. Local and systemic total antioxidant capacity in periodontitis and health. J Clin Periodontol. 2004;31(7):515–521. 64. Pack AR, Thomson M E. E ects o topical and systemic olic acid supplementation on gingivitis in pregnancy. J Clin Periodontol. 1980;7(5):402–414. 65. Vogel RI, Fink RA, Frank O, et al. The e ect o topical application o olic acid on gingival health. J O ral M ed. 1978;33(1):22–32.

STu De NT ANCILLAr y r e SOu r Ce S A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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r e t p a h C

18 Se ctio

To bacco , Smo ki g , a d Pe rio do tal Dise ase 1

To bacco as a Risk Facto r fo r Pe rio do tal Dise ase

305

Epidemiology o Tobacco in Periodontal Patients Smoking and Periodontitis

Se ctio

2

Me cha isms o f Smo ki g -Me diate d Pe rio do tal Dise ase

306

E ects o Smoking on the Periodontium E ects o Smoking on Periodontal Therapy

Se ctio

3

Smo ki g a d Pe ri-Impla t Dise ase

309

The Impact o Smoking on Dental Implants

Se ctio

4

To bacco Ce ssatio

fo r the Pe rio do tal Patie t

310

E ects o Tobacco Cessation on the Periodontium Tobacco Cessation Counseling in Periodontal Therapy A User-Friendly Model or Counseling the Periodontal Patient

Se ctio

5

Fo c s o

Patie ts

316

Clinical Patient Care

Cli ical Applicatio .

Smoking may be one o the most signif cant risk actors in the development and progression o periodontal disease. Dental hygienists have a pro essional responsibility to provide tobacco cessation services as a routine component o dental hygiene practice. Smoking cessation guidelines recommend that dental team members should check the smoking status o their patients at least once a year and should advise all smokers to stop smoking. This chapter summarizes what is known about tobacco as a risk or periodontitis and provides suggestions or brie , e ective tobacco cessation counseling in the dental setting.

Le ar i g Obje ctive s • Discuss the implications o smoking/the use o tobacco products on periodontal health status. • Discuss the implications o smoking on the host response to periodontal disease. • Discuss the e ects o smoking on periodontal treatment outcomes. • Discuss current theories as to why smokers have more periodontal disease than nonsmokers. • Explain why tobacco cessation counseling is a valuable part o patient care in the dental setting. • Value the importance o providing tobacco cessation counseling as a routine part o periodontal treatment.

Ke Te rms Dental implant Peri-implant mucositis

Peri-implantitis Environmental tobacco smoke

Tobacco cessation counseling

Chapte r 18

Se ct io

Tobacco, Smoking, and Periodontal Disease

305

1

To bacco as a Risk Facto r fo r Pe rio do tal Dise ase In ammation is a critical component o normal tissue repair, as well as being undamental to the body’s de ense against in ection. Environmental actors, such as smoking, have been reported to modi y the host response and hence modi y the progression, severity, and outcome o the in ammatory response. There ore, a comprehensive understanding o how smoking a ects in ammation is vital or preventive and therapeutic strategies on a clinical level.

Ep id Em io l o g y o f To b a c c o in p Er io d o n Ta l pa TiEn Ts • Evidence accumulated over the past three decades indicates that cigarette smoking is considered to be a very strong risk actor or periodontal disease (1–4). Cigarette smoking increases the risk or periodontal disease by at least 2 to 3 times (1). • Tooth loss is the ultimate outcome o untreated periodontitis. Smokers are at higher risk or tooth loss due to periodontal disease (3,5–7). • Cigar and pipe smoking are also signif cant risk actors or attachment loss (7–9). • Smokeless tobacco use is associated with severe recession and loss o attachment to buccal sur aces o teeth, where the smokeless tobacco was placed (10).

s m o k in g a n d p Er io d o n TiTis • There is a wealth o literature outlining the role that cigarette smoking has on periodontal disease and treatment, and a number o reviews cover this topic in detail (4,11,12). • Results rom the f rst N ational H ealth and N utrition Examination Survey (N H AN ES) demonstrated that smokers have greater periodontal destruction than ormer and never smokers (8). • More recently the NH AN ES III study concluded that approximately hal o periodontitis cases could be attributed to either current (42.9% ) smoking or ormer smoking (10.9% ) (8,13). Current estimates indicate smoking also increases the prevalence o periodontitis in excess o 20% in younger segments o the adult population (7). • The e ect o smoking and periodontal destruction are said to be dose dependent with total exposure to cigarette smoking being a widely used measure o dose (7). H eavy smokers (more than 10 cigarettes/day) have greater odds or more severe attachment loss compared to nonsmokers (Fig. 18-1) (14).

Fig re 18-1. Attachme t Lo ss Asso ciate d w ith Smo ki g . Clinical and radiographic evidence shows advanced periodontitis with horizontal and vertical bone loss in this 37-year-old male, cigarette smoker, with 20 pack-years o smoking.

306

Se ct io

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2

Me cha isms o f Smo ki g -Me diate d Pe rio do tal Dise ase M ore than 4,000 toxins are present in cigarette smoke including poisons such as carbon monoxide, oxidizing radicals, carcinogens (e.g., nitrosamines) and addictive psychoactive substances such as nicotine (3,7). O ral problems associated with smoking include halitosis, dry mouth, dental staining (Fig. 18-2), periodontal disease, and cancer (3,12,13). Smoking a ects the periodontium in several ways. Some o the possible mechanisms are highlighted in Figure 18-3.

Fig re 18-2. Oral Pro ble ms Asso ciate d With Smo ki g . Heavy tobacco staining and plaque bio ilm accumulation are evident in a smoker along with accompanying signs o periodontitis.

Ef f Ec Ts o f s m o k in g o n Th E p Er io d o n Tiu m Smoking a ects the periodontium in several ways. Some o the possible mechanisms are highlighted in Figure 18-3. S mo king

Impac t o n the o ral mic ro bial bio films

Impac t o n the immune s ys te m

Impac t o n bo ne me tabo lis m

Fig re 18-3. Me cha isms o f Smo ki g -Me diate d De str ctio .

1. Impact o Smoking on the Oral Microbial Biof lms A. There are con icting reports on how smoking a ects the oral micro ora. A ew studies indicate that there are no di erences in the subgingival bacteria between smokers and nonsmokers (15–17). 1. O ther investigations, however, show that the subgingival microbial prof le associated with periodontitis in smokers is diverse and distinct rom that o nonsmokers (16,18–20). 2. M ultiple studies have shown that plaque biof lm in smokers is more likely to be colonized by Porphyrom onas gingivalis and other potential periodontal pathogens (21–25).

Chapte r 18

Tobacco, Smoking, and Periodontal Disease

B. Cigarette smoking is associated with a lower oxygen tension in the periodontal pocket and thus is avorable or the growth o anaerobic bacteria (13). C. A recent study by Kumar et al. (18) examined the impact o smoking on composition and proin ammatory characteristics o the biof lm during ormation. The authors reported that smoking avors early acquisition and colonization o periodontal pathogens in oral biof lms. 2. Impact o Smoking on the Immune system A. From both a biological and epidemiological viewpoint, numerous studies suggest that smoking enhances the risk o periodontal disease (3,12,26). Smoking a ects both the human immune system and cellular and humoral in ammatory response systems (3,27,28). B. Smokers have decreased signs o in ammation and a decreased gingival crevicular blood ow that is indicative o impaired gingival blood ow in smokers. This is due to the vasoconstrictor properties o nicotine. C. Although smokers have a higher number o neutrophils, neutrophil unction in the peripheral circulation is impaired. N eutrophils have shown decreased adherence, chemotaxis, and phagocytosis in smokers (29). D. Antibody production is another protective mechanism impacted by smoking (29). Smoking generally decreased IgG2 antibody production that, in turn, leads to decreased serum immunoglobulin G (IgG) concentrations. IgG2 antibody production is also reported to occur in patients with aggressive periodontitis (23,29,30). 3. Smoking and Bone Metabolism A. Bone is one o the tissues most a ected by smoking (31). Smoking is associated with a greater amount o alveolar bone destruction in comparison to nonsmokers (29,31–33). In a 10-year longitudinal study, reduction in bone height was 2.7 times greater in adult smokers compared to nonsmokers (31). 1. At least one longitudinal cohort study has reported the bone mineral content among smokers was 10% to 30% lower compared to nonsmokers (2). 2. Bone loss in smokers also appears to be dose dependent with odds ratios ranging rom 3.25 or light smokers to 7.28 or heavy smokers (34). B. Although the mechanisms o how nicotine contributes to alveolar bone damage are not ully understood, several pathways have been proposed. 1. In vitro studies have shown that nicotine suppresses osteoblasts while stimulating alkaline phosphatase activity (35,36). 2. N icotine also increases the secretion o interleukin-6 (IL-6) and tumor necrosis actor alpha (TN F-α ) in osteoblasts (37). 3. Lastly, nicotine is also known to alter normal bone remodeling by increasing the release o matrix metalloproteinases (33). 4. Impact o Environmental Tobacco Smoke A. N onsmokers exposed to environmental tobacco smoke—“ secondhand smoke” or “ passive smoking” —are at increased risk or periodontitis. An analysis o N H AN ES III data concluded that the odds o having periodontitis are 1.6 times higher or nonsmoking adults who are exposed to environmental tobacco smoke than adults who are not exposed to passive smoke (38). 1. Sanders et al. (39) conclude that exposure to environmental tobacco smoke and presence o severe periodontitis among nonsmokers had a dosedependent relationship. Their research f ndings show that individuals exposed to environmental tobacco smoke or 1 to 25 hours per week have a 29% increased risk o severe periodontitis. For those exposed to environmental

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Part 3

Risk Factors or Periodontal Diseases

tobacco smoke or 26 hours or more per week, the odds were twice as high or severe periodontitis as individuals not exposed. 2. A more recent investigation o 3,137 subjects evaluated the association between environmental tobacco smoke and periodontitis in nonsmokers. This study concluded that adults with high environmental tobacco smoke exposure had two times the odds o periodontitis in comparison with subjects with negligible exposure (40). B. N ishida et al. (26) determined that passive smoke exposure was correlated to an elevation o interleukin-1β, albumin, and aspartate aminotrans erase (AST) levels in the saliva. 5. Electronic Cigarettes (E-cigarettes) A. The electronic cigarette was introduced to the United States market in 2007. “ E-cigarettes” don’t contain tobacco. Instead, there’s a mechanism that heats up liquid nicotine, which turns into a vapor that smokers inhale and exhale. 1. Laboratory analysis o electronic cigarette conducted by the U.S. Food and Drug Administration shows quite clearly that the uid and aerosol in e-cigarettes contains known toxins, including propylene glycol, heavy metals, volatile organic compounds, and tobacco-specif c nitrosamines. (http://www. da.gov/N ewsEvents/ PublicH ealthFocus/ucm173146.htm. Accessed February 12, 2014.) 2. At this time, the possible side e ects o inhaling nicotine vapor, as well as other health risks e-cigarettes may pose—both to users and to the public—are unknown. B. The environmental tobacco smoke generated rom a single cigarette is 32 µg/m 3 compared to 3.3 µg/m 3 rom a single e-cigarette. Thus, it may be that e-cigarettes have proportionally less impact ( actor o 10 times) on the periodontium than would exposure to environmental tobacco smoke rom a cigarette (41).

Ef f Ec Ts o f s m o k in g o n p Er io d o n Ta l Th Er a p y 1. Impact o Chemical Products and Toxins in Cigarette Smoke on Periodontal Therapy A. Chemical products and toxins in tobacco smoke may delay wound healing by impairing the biologic progression o healing and by inhibiting the basic cellular unctions necessary or the initiation o wound healing (29). B. Volatile components o cigarette smoke—namely acrolein and acetaldehyde—may inhibit gingival f broblast attachment and proli eration. Fibroblasts exposed to nicotine produce less extracellular matrix, less collagen, and more collagenase. These negative e ects on f broblast unctions in uence wound healing and progression o periodontitis (3,12). 2. Smoking and Response to Periodontal Treatment. Smoking not only increases the risk or developing periodontal disease, but it also impacts the response to periodontal treatment. Smokers show a poorer response to periodontal therapy compared to nonsmokers (42–44). A. Smokers exhibit less reduction in probing depth and less gain in clinical attachment a ter treatment compared to ex-smokers or nonsmokers (45). B. In a 6-year longitudinal study, nonsmokers had approximately a 50% higher rate o improvement in probing depth and clinical attachment levels a ter periodontal therapy than did active smokers (34). C. Periodontal treatment in smokers, both surgical and nonsurgical therapies, has been associated with improvements in periodontal outcomes. Comparison o the outcomes, however, showed signif cantly less improvement in smokers compared with nonsmokers (45–52).

Chapte r 18

Se ct io

Tobacco, Smoking, and Periodontal Disease

309

3

Smo ki g a d Pe ri-Impla t Dise ase A dental implant is a nonbiologic (artif cial) device surgically inserted into the jawbone to (1) replace a missing tooth or (2) provide support or a prosthetic denture. The periimplant tissues are the tissues that surround the dental implant. In many ways, the periimplant tissues are similar to the periodontium o a natural tooth. Dental implants are discussed in detail in Chapter 31, M aintenance o the Dental Implant. • Peri-implant mucositis (also called peri-implant gingivitis) is plaque-induced gingivitis (with no loss o supporting bone) that is localized in the gingival tissues surrounding a dental implant and is characterized by edema, change in color (red or red-blue), bleeding and/or purulence on probing, with probing depts o equal to or greater than 4 mm, and no evidence o radiographic peri-implant bone loss (53). • Peri-implantitis is a more advanced in ammatory disease—essentially chronic periodontitis—that exhibits deep probing depths (5 mm or greater), bleeding on probing (BOP) and/or purulence, and radiographic evidence o loss o alveolar bone (54).

Th E im pa c T o f s m o k in g o n d En Ta l im p l a n Ts • H eat produced by smoking, as well as, the toxic by-products o cigarette smoking, such as nicotine, carbon monoxide, and hydrogen cyanide, have been implicated as risk actors or impaired healing a ter implant surgery (55). • Smokers experience almost twice as many implant ailures compared with nonsmokers and are more prone to show peri-implant bone loss in the maxilla (56–63). • Risk indicators associated with increased peri-implant mucositis and peri-implantitis include poor plaque biof lm control, a history o periodontitis, diabetes, and smoking (55,59,61–63). • The combination o smoking and a history o periodontitis (treated or untreated) increases the risk o peri-implant bone loss (Figs. 18-4 and 18-5) (56,62).

Fig re 18-4. Pe ri-impla t M co sitis. Clinical signs o peri-implant mucositis o the mandibular irst molar.

Fig re 18-5. Pe ri-impla titis. Radiographic evidence o peri-implantitis eaturing circum erential angular bone loss.

310

Se ct io

Part 3

4

Risk Factors or Periodontal Diseases

To bacco Ce ssatio

fo r the Pe rio do tal Patie t

Ef f Ec Ts o f To b a c c o c Es s a Tio n o n Th E p Er io d o n Tiu m There have been ew publications in the periodontal literature to specif cally address the impact o smoking cessation on the periodontium, most probably because o the common challenges in motivating patients to quit smoking. Fiorini et al. conducted a systematic review o the literature to evaluate the e ect o smoking cessation on periodontitis progression and response to periodontal therapy. Based on the limited available evidence, Fiorini et al. (1) concluded that smoking cessation seems to have a positive in uence on periodontitis occurrence and periodontal healing. 1. The E ect o Smoking Cessation on Periodontal Status A. Current smokers usually have signif cantly worse periodontal conditions (greater probing depths, more attachment loss, and alveolar bone loss) than either never smokers or ormer smokers. The N H AN ES III study concluded that approximately hal o periodontitis cases could be attributed to either current (42.9% ) smoking or ormer smoking (10.9% ) (8,13). B. In general, the periodontal health status o ormer smokers is not as good as that o never smokers but is better than that o current smokers (64). These f ndings suggest that while the past e ects o smoking on the periodontium cannot be reversed, smoking cessation is benef cial to periodontal health (65). C. The American Academy o Periodontology strongly recommends that inclusion o tobacco cessation counseling is an integral part o periodontal therapy (66). 2. The E ect o Smoking Cessation on Periodontal Treatment Outcomes A. Studies have conf rmed that treatment outcomes in ormer smokers are generally similar to those that can be expected in never smokers but are usually better than those that can be expected in current smokers (65). B. The benef ts o smoking cessation on the periodontium likely result rom (1) a reduction in pathogenic bacteria in the subgingival plaque biof lm, (2) improved circulation in the gingiva, and (3) improvements in the host’s immunein ammatory response.

To b a c c o c Es s a Tio n c o u n s El in g in p Er io d o n Ta l Th Er a p y 1. Smoking Cessation and the Prevention o Periodontal Disease A. The knowledge that smoking is a signif cant risk actor suggests that in smokers, smoking cessation might prevent more periodontal disease than daily plaque control sel -care. All patients should be assessed or smoking status and smokers should be given smoking cessation counseling (67). B. Tobacco cessation counseling includes in ormation on smoking cessation and prevention o tobacco use, as well as re errals to other health pro essionals or tobacco cessation programs. 2. The Role o the Dental Team in Tobacco Cessation Counseling A. The World H ealth O rganization (WH O ) advocates that all health providers must be involved in tobacco cessation e orts, including oral health pro essionals who reach a large proportion o the healthy population (68).

Chapte r 18

Tobacco, Smoking, and Periodontal Disease

B. Dental team members have regular contact with patients, are the f rst to see the e ects o tobacco in the mouth, and are the only health pro essionals who requently see “ medically healthy” patients. Dental hygienists, thus, are in an ideal position to rein orce the antitobacco message, as well as being able to motivate and support smokers willing to quit. C. Dental hygienists have a pro essional responsibility to provide tobacco cessation services as a routine component o dental hygiene practice. Smoking cessation guidelines recommend that all health pro essionals, including dental team members, should check the smoking status o their patients at least once a year, and should advise all smokers to stop smoking (1,68,69).

a u s Er -f r iEn d l y m o d El f o r c o u n s El in g Th E p Er io d o n Ta l pa TiEn T 1. Counseling Time Commitment. In the vast majority of cases, dental teams will only be involved in delivering brief advice to smokers. This should take less than 5 minutes of their time. 2. Key Elements in Providing Brie Advice A. All patients should have their smoking/tobacco use status (current, ex-, never smoked) established and checked at regular intervals. This in ormation should be recorded in the patient’s chart. B. Smokers should then be asked some simple questions, in order to assess their degree o interest in stopping smoking/tobacco use. C. All smokers and chewers o tobacco should be advised both o the value o stopping, and o the health risks o continuing. The advice should be clear, f rm, and personalized. D. Although most people know o the risks o tobacco use in relation to cancers and heart disease, ewer are aware o the detrimental e ects on the mouth. Dental teams, thus, have a unique opportunity to highlight the dangers o tobacco use. The early signs o tobacco use—such as tooth staining, changes to the so t tissues and halitosis—are easily identif ed and are reversible, and these provide a use ul means o motivating smokers to stop. E. All smokers and chewers o tobacco should be advised o the value o the support o ered by quitlines. Quitlines are toll- ree telephone centers sta ed by trained tobacco cessation experts. It takes as little as 30 seconds to re er a patient to a quitline. Smokers who are interested and motivated to stop should be re erred to these services. The U.S. Department o H ealth & H uman Services has a national quitline number: 1–800-QUIT-N OW (1–800–784–8669). 3. A Pathway and Sample Dialogs or Cessation Counseling. A tobacco cessation care pathway or dental practice is summarized in Figure 18-6 (70). Boxes 18-1 to 18-3 provide sample dialogs or cessation counseling.

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Chapte r 18

Bo x 18-1. Sample Ce ssatio

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Tobacco, Smoking, and Periodontal Disease

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Ms. W is 22-y -o ld d io lo g y c n ici n w o s co m o d n lo fc o b i n n u l x m . Ms. W s n o sig n if c n l is o y. S s io d o n i is o n x m . Ms. W b g n sm o kin g g 12 n d s sm o k d ¾ o 1 ck d y o lm o s 10 y s. S is v y xci d b c u s s s ju s b co m n g g d b u d m i s f n cé w ill no s w d d in g d u n il s s q u i sm o kin g . o m sm o kin g . h o w d o yo u l bou Clin ici n : Yo u o l x m s o w s vid n c o d m g q u i in g ? Ms. W: I w n o q u i . My f n cé s I m sm o kin g . e v y d y I ll m ys l n o o sm o k b u I ju s c n n o s m o q u i . Clin ici n : W is m o s d i f cu l b o u q u i in g ? W is yo u b ig g s b i ? Ms. W: I l lik cig s m y b s i n d s! t o n ly im I l x is w n I sm o k —o w n I m o u d in kin g n d sm o kin g w i m y i n d s. a lm o s ll m y i n d s sm o k . i d o qui ? Clin ici n : h v yo u v n m y f n cé y lls m , so I l wo s nd Ms. W: e v y d y!! Bu n o in g w o ks! a n d n d u sm o kin g m o . I l so g u il y n d so m b ss d ! in vicio u s ci cl is o b b ly m kin g i d o qui . Clin ici n : I so u n d s lik yo u L ’s u is in s c iv . O ll d d ic io n s, i is d o k co n o l o v n ico in d d ic io n n ny o . I is lso d o wom n o qui n o m n . Bu good n w s is mo in g s v il b l o l sm o k s q u i n v b o . a nd q u i in g yo u yo u n g g w ill b so b n f ci l in v y w y—in clu d in g yo u o l l ! t lo n g w d o n y in g , d i is o s o . So s o in g n o w w o u ld b b s in g yo u w ill v d o o yo u s l n d w il i w ill b v y d i f cu l , i w ill d f n i ly b si n i yo u co n in u o sm o k o n o 20 y s. is b s w y o qui ? Ms. W: W Clin ici n : p o b b ly m o s im o n in g o yo u o d o is m k d cisio n o q u i . t is v n m o im o n n w n in g o q u i . r n llin g yo u s l , “ o d y I m n o g o in g o sm o k ,” s f m qui d w i in 1 o 2 w ks o is o in m n n d m k l n s o n o w n o o sm o k . t in k o q u i in g s kin g o n n w jo b . Wi ll o s o n sib ili i s yo u v , q u i in g s o b yo u io i y o b o u 3 m o n s. a n d g l — m o su o yo u v b . kin d o l ? My f n cé lls m o ju s s o — i I lly w n d o q u i I Ms. W: W co u ld . Clin ici n : a lo o o l in k sm o k s s o u ld ju s s o . Bu is lik llin g n lco o lic o ju s s o d in kin g n d w w o u ld n ’ d o .W ll o d d ic s o g q u i y nd ’s w sm o k s s o u ld d o ! I is b o u l n in g o w o q u i . W ly g w w w n in li u n l ss w w o k i. Ms. W: I n v oug o i w y. I o u g I co u ld n ’ s o b c u s I m w k o ju s don’ v n y w ill o w . ll. I w o u ld su g g s c llin g 1 800 QUIt NOW. t is is Clin ici n : No s vic o vid s co u n s lin g o n o w o q u i . t is q u i lin c n lso ll yo u b o u og ms n yo u i yo u in s d in m o in n siv m n . a n d s yo u o vid I w ill ssis yo u in n y w y I c n —in clu d in g d u c yo u b o u m d ic io n s l o l qui . Ms. W: t n k yo u . I w ill c ll q u i lin n d l yo u kn o w w I d cid o d o . Clin ici n : Go o d o yo u . Yo u w ill m iss yo u “ b s i n d ” b u yo u li w ill b so m u c b o n c yo u v m d b k!

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Bo x 18-2. Sample Ce ssatio Ms. G is 50-y -o ld g n w s y 2 di b s, COpD (c mos o v b n nd s sm o k d ck d y co n su m io n o l ck.

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i w o s co m o d n l o f c o o llo w -u c . Ms. G o n ic b o n c i is), n d s v noug io d o n l d is s x c d in s wy s. Ms. G b g n sm o kin g g 13 o mos o li . a b o u y go s d c s d d ily

Clin ici n : Co n g u l io n s o n b in g b l o cu d o w n o n yo u sm o kin g ! h v yo u o u g b o u q u i in g co m l ly? W m ig b b l o s v yo u m in in g i yo u bl o qui . Ms. G: I kn o w I s o u ld q u i b u I lly lo v m y cig s. Clin ici n : h s i b n d o yo u o cu d o w n ? Ms. G: a c u lly i ’s b n o ib l . Clin ici n : W sb n m o s d i f cu l o yo u ? in kin g b o u m y n x cig . I f n d m ys l in kin g b o u w n I c n Ms. G: I c n ’ s o g n x cig in s so o n s I u o n o u ! Clin ici n : I lm o s so u n d s lik cig s v b co m v n m o im o n o yo u sin c yo u cu d o w n ! W il q u i in g is m o s d i f cu l in g yo u m ig v d o , i m ig in c m k yo u li si o no v o w o y b o u w n yo u c n g in yo u n x cig . Ms. G: t ’s u —i w o u ld b so n ic o n o o v o in k b o u m n ym o . s b u d o n ’ lo v yo u sm o kin g ! Clin ici n : So yo u s ill lo v yo u cig Ms. G: Y s is x c ly i . I I m s ill sm o kin g . I kn o w i is so b d o m y l . I l I mus qui bu I v i d o qui b o nd lo n g s I v v g o n wi ou cig s o n ly b n 4 o u s! Cig s o n ly in g s c lm m down. Clin ici n : h o w so o n d o yo u sm o k w n yo u f s g u in m o n in g n d d o yo u v sm o k i yo u w k d u in g n ig ? Ms. G: I sm o k b o m y i g o u n d v y m o n in g n d I o n k co u l o d g s i I w k u d u in g n ig . Clin ici n : I so u n d s lik yo u v s ong ysic l d d ic io n s w ll s sig n if c n syc o lo g ic l d d ic io n . h v yo u co n sid d u sin g m d ic io n o l yo u q u i ? Yo u w o u ld b g o o d c n d id o m co y. Ms. G: No . I k in su lin o m y d i b s n d I d o n ’ w n o k n y in g w o u ld in wi . Clin ici n : a c u lly, sm o kin g in s w i co n o llin g yo u d i b s muc mo n qui sm o kin g m d ic io n . a n d w yo u w wi v y cig yo u b lo o d su g g o s u ? So yo u d i b s w o u ld b m u c si o co n o l i yo u q u i . Ms. G: I d n o id w s c s . q u i in g s m w y yo u lo o k vin g Clin ici n : On su g g s io n w o u ld b o lo o k di b s. a n ico in d d ic io n is c o n ic co n d i io n ju s s d i b s is. Yo u d o w v yo u c n o co n o l yo u b lo o d su g w i d i , x cis , n d m d ic io n in o d o n n c yo u q u li y o li nd d c s isks— v n o u g yo u m y n o w n o d o ll os in g s. t y o lo o k q u i in g w y. e v n o u g yo u lo v cig s, yo u w ill b n f b y kin g co n o l! Lo o k q u i in g s so m in g yo u d o in g o yo u s l n o yo u s l . t o c m ym k i si o l g o o sm o kin g . Ms. G: I lik . I u s m in co n o l o si u io n — n l in g cig s co n o l m ! M yb I w ill co n sid yin g m d ic io n o l m .

Chapte r 18

Bo x 18-3. Sample Smo ki g Ce ssatio

Tobacco, Smoking, and Periodontal Disease

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M . r is 48-y -o ld o n yw o s co m o d n l o f c o is c .M.r s y n sio n n d ig c o l s o l. h s io d o n l d is s o n x m . M . r . b g n sm o kin g g 17 n d s sm o k d 2 cks d y o 30 y s. Clin ici n : a s yo u kn o w, yo u o l x m s o w s sig n if c n d m g o m sm o kin g n d yo u b lo o d ssu is l v d o d y. h v yo u i d o q u i sin c o u l s visi ? M . r : No lly. a n d I d o n ’ w n o lk b o u i . e v yo n is o n m . My d o c o s, m y w i , m y kid s, n d n o w I su o s yo u g o in g o g iv m d im o o . d im . Bu I d o w n o n co u g yo u o l s y Clin ici n : I d o n ’ w n o g iv yo u nd qui . t mo im s yo u y, m o c n c yo u v o su cc ss. I m n o g o in g o ll yo u o w d n g o u s i is o sm o k . Bu I m g o in g o m in d yo u b y q u i in g yo u c n v s so m u c o d m g cig s v c u s d in yo u . lly d o n ’ w n o q u i . I x cis n d I w c w I . I’ll k co m in g o M . r : Lo o k I yo u o m y n d k m d icin o m y obl ms nd o o b s. Clin ici n : Yo u su c “ k c g ” so n in v y o s c o yo u li . h o w b o u kin g co n o l o v is d d ic io n n o in g o b s? M . r : I w ill q u i w n I m d y. I kn o w m ys l . W n I d cid o d o so m in g , i g s don . Clin ici n : t k d v n g o ! Co n sid w is v il b l o l yo u q u i n o w. I is o ssib l o q u i v n i yo u d o n ’ w n o q u i o d o n ’ l d y. o l o m y b ck n yw y. My kid s n g m v y d y. M . r : I w o u ld g Clin ici n : p o l in yo u li co n c n d b o u yo u . Bu yo u c n n o q u i o m . Yo u c n us c yo u w ill v lo n g , b q u li y li w i yo u kid s s m o iv io n , oug d cisio n o q u i is yo u s. No o n , n o in g , c n m k yo u q u i b u l n y o us w o c n l yo u q u i . M . r : I I d o is, I m d o in g i o n m y o w n . o c . h o w v , i w o u ld b so m u c Clin ici n : I u n d s n d yo u w n in g o k si i yo u u s m d ic io n . Yo u v b n sm o kin g o lo n g im n d m d ic io n w o u ld in c s yo u c n c o m n n su cc ss. M . r : Is i o k o k so m in g w i ll m y o b l m s? Clin ici n : a b so lu ly. In c m d ic io n , C n ix, s ig s su cc ss s. I s o u ld b s d 1 o 2 w ks b o q u i in g n d o n c is u ic d o s in yo u sys m , yo u s o u ld n o ic sig n if c n d c s in yo u d si o sm o k . I c n o vid yo u w i m o in o m io n n d ng o sc i io n . M.r:I v d m k s yo u ld ss d . is b n o d b u o n ly in in y m in o i y. F lin g d ss d is v y co m m o n Clin ici n : t w i q u i in g ! I w ill s o w yo u lis o m o s co m m o n w i d w l sym o m s, so yo u w ill b w o w o x c . a n d lso g iv yo u in o m io n o n o six FDa ov d m d ic io n s, so yo u w ill v ll o io n s. t in k b o u s in g q u i d w i in co u l o w ks n d l m kn o w o w I c n b s ssis yo u oug o c ss. I w ill k w o kin g w i yo u u n il yo u bl o qui . M . r : OK I w ill y b u is is ju s b w n yo u n d m . Clin ici n : I u n d s n d n d w ill s c . a so m o in o l in yo u li w ill b w yo u yin g o q u i n d i m ig l yo u o l m kn o w w y c n do o l yo u —in clu d in g NOt n g yo u ! I m v y o u d o yo u o m kin g m . Yo u w ill n o g i!

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Chapte r S mmar State me t Tobacco use is a major risk actor or the onset and progression o periodontal disease. Smoking a ects the periodontium in several ways by impacting oral biof lms, host immune response, and bone metabolism. There is su f cient evidence or the benef ts o tobacco cessation on a wide variety o oral health outcomes, including periodontal treatment. Advice and assistance on tobacco cessation is there ore an integral part in the management o all patients seeking periodontal care.

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Cli ical Patie t Care CA S E 1 A new patient with severe chronic periodontitis has a history o smoking one to two packs o cigarettes each day. The patient in orms you that he will do “ anything” to save his teeth, but that he cannot quit smoking. What counsel would you provide this patient about the e ect o the smoking habit on the likelihood o long-term control o his periodontitis?

Re fe re ce s 1. Fiorini T, M usskop M L, O ppermann RV, et al. Is there a positive e ect o smoking cessation on periodontal health? A systematic review. J Periodontol. 2014;85(1):83–91. 2. Gelskey SC. Cigarette smoking and periodontitis: methodology to assess the strength o evidence in support o a causal association. Com m unity D ent O ral Epidem iol. 1999;27(1):16–24. 3. Johannsen A, Susin C, Gusta sson A. Smoking and in ammation: evidence or a synergistic role in chronic disease. Periodontol 2000. 2014;64(1):111–126. 4. Johnson GK, Guthmiller JM . The impact o cigarette smoking on periodontal disease and treatment. Periodontol 2000. 2007;44:178–194. 5. Ahlqwist M , Bengtsson C, H ollender L, et al. Smoking habits and tooth loss in Swedish women. Com m unity D ent O ral Epidem iol. 1989;17(3):144–147. 6. H olm G. Smoking as an additional risk or tooth loss. J Periodontol. 1994;65(11):996–1001. 7. Tonetti M S. Cigarette smoking and periodontal diseases: etiology and management o disease. A nn Periodontol. 1998;3(1):88–101. 8. Albandar JM , Streck us CF, Adesanya M R, et al. Cigar, pipe, and cigarette smoking as risk actors or periodontal disease and tooth loss. J Periodontol. 2000;71(12):1874–1881. 9. Tomar SL, Asma S. Smoking-attributable periodontitis in the United States: f ndings rom N H AN ES III. N ational H ealth and N utrition Examination Survey. J Periodontol. 2000;71(5):743–751. 10. Anand PS, Kamath KP, Bansal A, et al. Comparison o periodontal destruction patterns among patients with and without the habit o smokeless tobacco use–a retrospective study. J Periodontal R es. 2013;48(5):623–631. 11. H easman L, Stacey F, Preshaw PM , et al. The e ect o smoking on periodontal treatment response: a review o clinical evidence. J Clin Periodontol. 2006;33(4):241–253. 12. Johnson GK, H ill M . Cigarette smoking and the periodontal patient. J Periodontol. 2004;75(2):196–209. 13. Johnson GK, Slach N A. Impact o tobacco use on periodontal status. J D ent Educ. 2001;65(4):313–321. 14. Grossi SG, Genco RJ, M achtei EE, et al. Assessment o risk or periodontal disease. II. Risk indicators or alveolar bone loss. J Periodontol. 1995;66(1):23–29. 15. Bostrom L, Bergstrom J, Dahlen G, et al. Smoking and subgingival micro ora in periodontal disease. J Clin Periodontol. 2001;28(3):212–219. 16. Preber H , Bergstrom J. O ccurrence o gingival bleeding in smoker and non-smoker patients. A cta O dontol Scand. 1985;43(5):315–320. 17. Stoltenberg JL, O sborn JB, Pihlstrom BL, et al. Association between cigarette smoking, bacterial pathogens, and periodontal status. J Periodontol. 1993;64(12):1225–1230. 18. Kumar PS, M atthews CR, Joshi V, et al. Tobacco smoking a ects bacterial acquisition and colonization in oral biof lms. Infect Im m un. 2011;79(11):4730–4738.

Chapte r 18

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19. Shchipkova AY, N agaraja H N , Kumar PS. Subgingival microbial prof les o smokers with periodontitis. J D ent R es. 2010;89(11):1247–1253. 20. van Winkelho AJ, Bosch-Tijho CJ, Winkel EG, et al. Smoking a ects the subgingival micro ora in periodontitis. J Periodontol. 2001;72(5):666–671. 21. Bagaitkar J, Daep CA, Patel CK, et al. Tobacco smoke augments Porphyromonas gingivalis-Streptococcus gordonii biof lm ormation. PL oS O ne. 2011;6(11):e27386. 22. Eggert FM , M cLeod M H , Flowerdew G. E ects o smoking and treatment status on periodontal bacteria: evidence that smoking in uences control o periodontal bacteria at the mucosal sur ace o the gingival crevice. J Periodontol. 2001;72(9):1210–1220. 23. H a ajee AD, Socransky SS. Relationship o cigarette smoking to attachment level prof les. J Clin Periodontol. 2001;28(4):283–295. 24. Kamma JJ, N akou M , Baehni PC. Clinical and microbiological characteristics o smokers with early onset periodontitis. J Periodontal R es. 1999;34(1):25–33. 25. Z ambon JJ, Grossi SG, M achtei EE, et al. Cigarette smoking increases the risk or subgingival in ection with periodontal pathogens. J Periodontol. 1996;67(10 suppl):1050–1054. 26. N ishida N , Yamamoto Y, Tanaka M , et al. Association between passive smoking and salivary markers related to periodontitis. J Clin Periodontol. 2006;33(10):717–723. 27. Kinane DF, Chestnutt IG. Smoking and periodontal disease. Crit R ev O ral Biol M ed. 2000;11(3):356–365. 28. Palmer RM , Wilson RF, H asan AS, et al. M echanisms o action o environmental actors–tobacco smoking. J Clin Periodontol. 2005;32(suppl 6):180–195. 29. Jacob V, Vellappally S, Smejkalova J. The in uence o cigarette smoking on various aspects o periodontal health. A cta M edica. 2007;50(1):3–5. 30. M ooney J, H odge PJ, Kinane DF. H umoral immune response in early-onset periodontitis: in uence o smoking. J Periodontal R es. 2001;36(4):227–232. 31. Bergstrom J, Eliasson S. Cigarette smoking and alveolar bone height in subjects with a high standard o oral hygiene. J Clin Periodontol. 1987;14(8):466–469. 32. Kerdvongbundit V, Wikesjo UM . E ect o smoking on periodontal health in molar teeth. J Periodontol. 2000;71(3):433–437. 33. Razali M , Palmer RM , Coward P, et al. A retrospective study o periodontal disease severity in smokers and non-smokers. Br D ent J. 2005;198(8):495–498. 34. Grossi SG, Z ambon JJ, H o AW, et al. Assessment o risk or periodontal disease. I. Risk indicators or attachment loss. J Periodontol. 1994;65(3):260–267. 35. Fang M A, Frost PJ, Iida-Klein A, et al. E ects o nicotine on cellular unction in UM R 106–01 osteoblast-like cells. Bone. 1991;12(4):283–286. 36. Rosa GM , Lucas GQ, Lucas O N . Cigarette smoking and alveolar bone in young adults: a study using digitized radiographs. J Periodontol. 2008;79(2):232–244. 37. Kamer AR, El-Ghorab N , M arzec N , et al. N icotine induced proli eration and cytokine release in osteoblastic cells. Int J M ol M ed. 2006;17(1):121–127. 38. Yamamoto Y, N ishida N , Tanaka M , et al. Association between passive and active smoking evaluated by salivary cotinine and periodontitis. J Clin Periodontol. 2005;32(10):1041–1046. 39. Sanders AE, Slade GD, Beck JD, et al. Secondhand smoke and periodontal disease: atherosclerosis risk in communities study. A m J Public H ealth. 2011;101(suppl 1):S339–S346. 40. Sutton JD, Ranney LM , Wilder RS, et al. Environmental tobacco smoke and periodontitis in U.S. non-smokers. J D ent H yg. 2012;86(3):185–194. 41. Goniewicz M L, Kuma T, Gawron M , et al. N icotine levels in electronic cigarettes. N icotine Tob R es. 2013;15(1):158–166. 42. James JA, Sayers N M , Drucker DB, et al. E ects o tobacco products on the attachment and growth o periodontal ligament f broblasts. J Periodontol. 1999;70(5):518–525. 43. M achuca G, Rosales I, Lacalle JR, et al. E ect o cigarette smoking on periodontal status o healthy young adults. J Periodontol. 2000;71(1):73–78. 44. Preber H , Bergstrom J. The e ect o non-surgical treatment on periodontal pockets in smokers and non-smokers. J Clin Periodontol. 1986;13(4):319–323. 45. Kaldahl WB, Johnson GK, Patil KD, et al. Levels o cigarette consumption and response to periodontal therapy. J Periodontol. 1996;67(7):675–681. 46. Ah M K, Johnson GK, Kaldahl WB, et al. The e ect o smoking on the response to periodontal therapy. J Clin Periodontol. 1994;21(2):91–97. 47. Grossi SG, Skrepcinski FB, DeCaro T, et al. Response to periodontal therapy in diabetics and smokers. J Periodontol. 1996;67(10 suppl):1094–1102. 48. Kinane DF, Radvar M . The e ect o smoking on mechanical and antimicrobial periodontal therapy. J Periodontol. 1997;68(5):467–472. 49. M iller PD Jr. Root coverage with the ree gingival gra t. Factors associated with incomplete coverage. J Periodontol. 1987;58(10):674–681. 50. Preber H , Bergstrom J. E ect o cigarette smoking on periodontal healing ollowing surgical therapy. J Clin Periodontol. 1990;17(5):324–328. 51. Rosen PS, M arks M H , Reynolds M A. In uence o smoking on long-term clinical results o intrabony de ects treated with regenerative therapy. J Periodontol. 1996;67(11):1159–1163. 52. Tonetti M S, Pini-Prato G, Cortellini P. E ect o cigarette smoking on periodontal healing ollowing GTR in in rabony de ects. A preliminary retrospective study. J Clin Periodontol. 1995;22(3):229–234. 53. Sanz M , Chapple IL; Working Group 4 o the VEWoP. Clinical research on peri-implant diseases: consensus report o Working Group 4. J Clin Periodontol. 2012;39(suppl 12):202–206. 54. Tomasi C, Derks J. Clinical research o peri-implant diseases–quality o reporting, case def nitions and methods to study incidence, prevalence and risk actors o peri-implant diseases. J Clin Periodontol. 2012;39(suppl 12):207–223. 55. Levin L, Schwartz-Arad D. The e ect o cigarette smoking on dental implants and related surgery. Im plant D ent. 2005;14(4):357–361.

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56. Anner R, Grossmann Y, Anner Y, et al. Smoking, diabetes mellitus, periodontitis, and supportive periodontal treatment as actors associated with dental implant survival: a long-term retrospective evaluation o patients ollowed or up to 10 years. Im plant D ent. 2010;19(1):57–64. 57. Cavalcanti R, O reglia F, M an redonia M F, et al. The in uence o smoking on the survival o dental implants: a 5-year pragmatic multicentre retrospective cohort study o 1727 patients. Eur J O ral Im plantol. 2011;4(1):39–45. 58. Charalampakis G, Rabe P, Leonhardt A, et al. A ollow-up study o peri-implantitis cases a ter treatment. J Clin Periodontol. 2011;38(9):864–871. 59. H eitz-M ayf eld LJ. Peri-implant diseases: diagnosis and risk indicators. J Clin Periodontol. 2008;35(8 suppl):292–304. 60. H eitz-M ayf eld LJ, H uynh-Ba G. H istory o treated periodontitis and smoking as risks or implant therapy. Int J O ral M ax illofac Im plants. 2009;24(suppl):39–68. 61. Klokkevold PR, H an TJ. H ow do smoking, diabetes, and periodontitis a ect outcomes o implant treatment? Int J O ral M ax illofac Im plants. 2007;22(suppl):173–202. 62. Koldsland O C, Scheie AA, Aass AM . Prevalence o implant loss and the in uence o associated actors. J Periodontol. 2009;80(7):1069–1075. 63. Rodriguez-Argueta O F, Figueiredo R, Valmaseda-Castellon E, et al. Postoperative complications in smoking patients treated with implants: a retrospective study. J O ral M ax illofac Surg. 2011;69(8):2152–2157. 64. Bolin A, Eklund G, Frithio L, et al. The e ect o changed smoking habits on marginal alveolar bone loss. A longitudinal study. Swed D ent J. 1993;17(5):211–216. 65. Preshaw PM , H easman L, Stacey F, et al. The e ect o quitting smoking on chronic periodontitis. J Clin Periodontol. 2005;32(8):869–879. 66. Position paper. tobacco use and the periodontal patient. Research, Science and Therapy Committee o the American Academy o Periodontology. J Periodontol. 1999;70(11):1419–1427. 67. Binnie VI. Addressing the topic o smoking cessation in a dental setting. Periodontol 2000. 2008;48:170–178. 68. The world health report: report o the Director-General / 2003. Shaping the Future. Geneva: WH O ; 2003. XV, 193. 69. West R, M cN eill A, Raw M . Smoking cessation guidelines or health pro essionals: an update. H ealth Education Authority. T horax . 2000;55(12):987–999. 70. N eedleman I, Warnakulasuriya S, Sutherland G, et al. Evaluation o tobacco use cessation (TUC) counselling in the dental o f ce. O ral H ealth Prev D ent. 2006;4(1):27–47.

STu DEn T An CILLARy RESOu RCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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Clinical Patient Care Ethical Dilemma

Cli ical Applicatio .

Clinical periodontal assessment is a critical step in the care o all patients with periodontal diseases. This step serves as the oundation or assigning a periodontal diagnosis, the oundation or developing plans or treating patients, and the oundation or monitoring the success or ailure o periodontal treatment per ormed. The rigorous standards or care in e ect today require every clinician participating in patient care to be amiliar with the details o per orming and documenting a clinical periodontal assessment. This chapter describes how to per orm a clinical periodontal assessment, how to document the f ndings o the assessment, and how to per orm calculations needed during the assessment.

Le ar i

O je ctive s

• Compare and contrast a periodontal screening examination and a comprehensive periodontal assessment. • Describe how to per orm one type o periodontal screening examination. • List the components o a comprehensive periodontal assessment. • Describe how to evaluate each component o a comprehensive periodontal assessment. • Explain how to calculate the width o attached gingiva. • Explain how to calculate clinical attachment level given several di erent clinical scenarios. • Given a clinical scenario, calculate and document the clinical attachment levels or a patient with periodontitis.

Ke Te rms Clinical periodontal assessment Baseline data Periodontal screening examination Periodontal Screening and Recording (PSR)

World Health Organization (WHO) probe PSR Code Comprehensive periodontal assessment Exudate Horizontal tooth mobility

Vertical tooth mobility Fremitus Furcation probes Gingival crevicular luid Attached gingiva Clinical attachment level (CAL)

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1

Assessment and Planning or Patients with Periodontal Disease

I tro uctio

to Pe rio o tal Asse ssme t

Ov e r v ie w Of t h e As s e s s m e n t Pr Oc e s s 1. Clinical periodontal assessment is a act-gathering process designed to provide a comprehensive picture o the patient’s periodontal health status. A. Importance o Periodontal Assessment 1. This assessment is one o the most important duties per ormed by any dental team. a. The dental team is obligated to per orm and document ndings o a periodontal assessment or every patient when the patient rst enters the dental practice and periodically therea ter (1). b. Periodontal assessment requires meticulous attention to detail since success ul patient care is dependent on a thorough and accurate periodontal evaluation. 2. The in ormation gathered during the clinical periodontal assessment orms the basis o both a periodontal diagnosis and an individualized treatment plan or the patient. B. Objectives o Periodontal Assessment. The objectives o the clinical periodontal assessment process include the ollowing: 1. Detect clinical signs o inf ammation in the periodontium. 2. Identi y damage to the periodontium already caused by disease or trauma. 3. Provide the dental team with data used to assign a periodontal diagnosis. 4. Document eatures o the periodontium to serve as baseline data or long-term patient monitoring. C. Two Types o Periodontal Assessment. Two commonly used types o periodontal assessment are periodontal screening examinations and comprehensive periodontal assessments. 1. Periodontal Screening Examination. Periodontal screening examination is a rapid in ormation-gathering process that may be used to determine i a periodontium appears healthy, displays signs o gingivitis, or displays signs o periodontitis. 2. Comprehensive Periodontal Assessment. Comprehensive periodontal assessment is an intensive in ormation-gathering process used to gather the detailed data needed to document the complete periodontal health status o a patient. 2. Standard o Care A. The standard o care is or dentists and dental hygienists to complete an accurate and thorough periodontal assessment on every patient. B. Without a thorough clinical periodontal assessment, periodontal diseases are o ten not diagnosed or are misdiagnosed, inevitably leading to either undertreatment or overtreatment o the patient. 3. Documentation o Assessment Findings A. The clinical periodontal assessment is not complete until all o the in ormation gathered during the assessment has been accurately recorded in the patient’s dental chart. B. The importance o the accuracy o the documentation cannot be overstated. 1. Findings documented during the clinical periodontal assessment serve as baseline data used to evaluate the success or ailure o an episode o periodontal therapy. Baseline data re ers to clinical in ormation gathered prior to periodontal therapy that can be used or comparison to clinical in ormation gathered at a subsequent appointment. 2. Documented ndings also provide the baseline data used in the long-term monitoring o the patient’s periodontal health status. An example o when patient monitoring may occur is at periodontal maintenance visits ollowing success ul treatment.

C apte r 19

Se ct io

2

Pe rio o tal Scre e i

Clinical Periodontal Assessment

Exami atio

In some dental o ces a periodontal screening examination is used as one o the rst steps in evaluating the periodontal status o a patient. A periodontal screening examination is a rapid in ormation-gathering process that may be used to determine i a periodontium appears healthy, displays signs o gingivitis, or displays signs o periodontitis. The Periodontal Screening and Recording (PSR) is one example o an easy-to-use screening system that can aid in the detection o periodontal disease. 1. Periodontal Screening and Recording (PSR) A. Characteristics o Periodontal Screening and Recording (PSR) 1. The PSR can help separate patients into broad categories: those who seem to have periodontal health, gingivitis, or periodontitis. 2. When the PSR screening examination indicates the presence o periodontal health or gingivitis, in a very ew instances no urther clinical periodontal assessment may be needed beyond the PSR. It is important to note that individual states have di erent rules related to the use o this screening examination. B. Techniques or Per orming the PSR Screening Examination 1. Special Probe. A World Health Organization (WHO) probe is used or this examination. The WH O probe has a colored band (called the re erence mark) located 3.5 to 5.5 mm rom the probe tip. This color-coded re erence mark is used when per orming the PSR screening examination. 2. One Code Per Sextant. Each sextant o the mouth is examined and assigned an individual PSR code. The unique aspects o the PSR screening system are the manner in which the probe is read and the minimal amount o in ormation that needs to be recorded. a. Instead o reading and recording six precise measurements per tooth, the clinician only needs to observe the position o the color-coded re erence mark in relation to the gingival margin and a ew other clinical eatures such as the presence o bleeding on probing, the presence o calculus, or the presence o an overhang on a restoration. b. Each o the sextants is examined as a separate unit during the PSR screening (i.e., only one PSR code number will be assigned to the entire sextant). c. O nly one PSR code is recorded or each sextant in the mouth. Each sextant is assigned a single PSR code; the highest code obtained or the sextant is recorded. d. An “ X” is recorded instead o a PSR code i the sextant is edentulous. 3. Probing Technique a. The probe is “ walked” circum erentially around each tooth in the sextant being examined. Walking a periodontal probe re ers to moving the probe in small increments circum erentially around a tooth. b. The color-coded re erence mark is monitored continuously as the probe is walked around each tooth. At each site probed, the color-coded re erence mark will be (a) completely visible, (b) partially visible, or (c) not visible at all. 2. The PSR Codes A. Use o PSR Codes 1. A PSR code is assigned to each sextant according to the criteria shown in Table 19-1. The code assigned to a sextant should represent the most advanced periodontal f nding on any tooth in that sextant. 2. The PSR codes are used to guide urther clinical documentation.

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a. For some patients with low PSR codes in all sextants (codes 0, 1, or 2), the PSR screening may be adequate documentation o the patient’s periodontal health status. N ote, however, that the dentist may request a comprehensive periodontal assessment even when low PSR codes are ound, since many periodontal conditions must be monitored in more detail than that included in the PSR. b. For patients with higher PSR codes in one or more sextants (codes 3 or 4), a comprehensive periodontal examination should be per ormed as outlined in Section 3 o this chapter. B. Cautions or Interpreting PSR Codes. The PSR codes can mislead a clinician in certain patients. As already pointed out, lower codes usually mean periodontal health or gingivitis, and higher codes usually mean periodontitis. When interpreting the results o the PSR, the clinician must be alert or teeth with gingival enlargement or with gingival recession. In the presence o either o these conditions the PSR can give misleading results.

TAb LE 1 9 -1 . CRITERIA FOR ASSIg n In g PSR COd ES COd E 0:

• Co lo -co d d

nc m

k is co m p le t e ly visib le in d

s su lcu s o

o ck

o

s x n • No c lcu lu s o d

c iv m

• Gin g iv l issu s COd E 1:

l

• Co lo -co d d

g in s o n y wi

so

no bl

io n s

s n

d in g vid n o n g n l

k is co m p le t e ly visib le in d

nc m

o b in g

s su lcu s o

o ck

o

o ck

o

s x n • No c lcu lu s o d • Bl COd E 2:

c iv m

d in g is e vid e n t o n

• Co lo -co d d

g in s o n

so

io n s

s n

o b in g

nc m

k is co m p le t e ly visib le in d

s su lcu s o

s x n • Su COd E 3:

g in g iv l o su b g in g iv l c lcu lu s n d /o d

• Co lo -co d d o

k is o n ly p art ially visib le in

g in s d

d

c d

s su lcu s o

s x n

• Co d 3 in d ic COd E 4:

nc m

c iv m

s

• Co lo -co d d

o b in g d nc m

b

w

n 3.5 n d 5.5 m m

k is n o t visib le in

d

s su lcu s o

o ck

o

s x n • Co d 4 in d ic COd E *:

• t

* (s

s

o b in g d

o g

) sym b o l is d d d o

n 5.5 m m

co d o

ny s x n

x ib i s n y o

o llo w in g : 1. Fu c io n in vo lv m n 2. Mo b ili y 3. Mu co g in g iv l

obl ms

4. r c ssio n x n d in g in o • t

* (s

) sym b o l is

co lo

co d d n x

d o

o

ob

s x n co d . Fo

x m l , “ 4*”

o ck

C apte r 19

Se ct io

Clinical Periodontal Assessment

323

3

Co mpre e sive Pe rio o tal Asse ssme t A comprehensive periodontal assessment is an intensive clinical periodontal evaluation used to gather in ormation about the periodontium. This section o the chapter outlines the clinical eatures that should be noted and documented during a comprehensive periodontal assessment. It is important to note that special precautions are necessary when examining dental implants. These examination techniques are presented in Chapter 31. The comprehensive periodontal assessment normally includes clinical eatures such as probing depth measurements, bleeding on probing, presence o exudate, level o the ree gingival margin, level o the mucogingival junction, tooth mobility, urcation involvement, presence o calculus, presence o plaque bio lms, gingival inf ammation, radiographic evidence o alveolar bone loss, and presence o local contributing actors. It should be noted that there are a number o excellent electronic tools that can be used during parts o a comprehensive periodontal assessment; or example, periodontal probes are available that can record probing depths directly in computer so tware. The discussion in this chapter ocuses only on the basic concepts underlying each o the clinical actors being assessed with the knowledge that a clinician who understands the basic concepts can easily apply any o the available electronic tools appropriately. 1. Components o the Comprehensive Periodontal Assessment A. Probing Depth Measurements. Probing depth measurements are made rom the ree gingival margin to the base o the pocket (or base o the sulcus). 1. Probing depths are recorded to the nearest ull millimeter. M easurements are normally rounded up to the next higher whole number (e.g., a reading o 3.5 mm is recorded as 4 mm, and a 5.5 mm reading is recorded as 6 mm). 2. Probing depth measurements are recorded or six speci c sites on each tooth: (i) disto acial, (ii) middle acial, (iii) mesio acial, (iv) distolingual, (v) middle lingual, and (vi) mesiolingual. B. Bleeding on Probing 1. Bleeding on gentle probing represents bleeding rom the so t tissue wall o a periodontal pocket where the wall o the pocket is ulcerated (i.e., where portions o the epithelium have been destroyed) (Fig. 19-1). 2. Bleeding can occur immediately a ter the site is probed or can be slightly delayed in occurrence. An alert clinician will observe each site or a ew seconds be ore moving on to the next site.

Fi ure 19-1. A ble e i Site . Bleeding rom the so t tissue wall is a sign o disease. This bleeding was evident upon gentle probing. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

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C. Presence o Exudate 1. Exudate (sometimes re erred to as suppuration) is pus that can be expressed rom a periodontal pocket. Pus is composed mainly o dead white blood cells and can occur in response to any in ection, including periodontal disease. 2. Exudate can be recognized as a pale yellow material oozing rom the ori ce o a pocket. It is usually easiest to detect when the gingiva is manipulated in some manner. For example, light nger pressure on the gingiva can reveal exudate when it is present (Fig. 19-2). Figure 19-3 illustrates the clinical appearance o exudate in a patient with periodontitis.

Exud a te

A

B

Fi ure 19-2. Usi Fi e r Pre ssure to d e te ct Exu ate . Exudate can be detected in a periodontal pocket by placing an index inger on the so t tissue in the area o the pocket and exerting slight pressure. This slight pressure can orce the exudate out o the pocket, making it readily visible to the clinician.

C

Fi ure 19-3. Exu ate . A: Pressure with the clinician’s inger on the gingiva reveals exudate rom the gingival tissue adjacent to the central incisor. b: Exudate also is visible during probing. C: Radiograph o the incisor shown in A and B. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

C apte r 19

Clinical Periodontal Assessment

D. Level o the Free Gingival Margin 1. The level o the ree gingival margin in relationship to the cementoenamel junction (CEJ) should be recorded on the dental chart. This level can simply be drawn on the acial and lingual sur aces o the dental chart. 2. Several possible relationships exist between the ree gingival margin and the CEJ: a. Free gingival margin can be slightly coronal to (above) the CEJ. This is the natural level o the gingival margin and represents the expected position o the gingival margin in the absence o disease or trauma. b. Free gingival margin can be signi cantly coronal to the CEJ. The gingival margin can be signi cantly coronal to the CEJ due to (1) swelling (edema), (2) overgrowth (as seen in patients taking certain medications), or (3) increase in brous connective tissue (as seen in long-standing inf ammation o tissue). c. Free gingival margin can be apical to the CEJ. This relationship, known as gingival recession, results in exposure o a portion o the root sur ace. 3. Box 19-1 outlines the technique or determining the ree gingival margin level. 4. When the gingival margin is apical to the CEJ (i.e., gingival recession is present), the severity o gingival recession can be classi ed using the M iller classi cation system or gingival recession. This system is outlined in Figure 19-4A–D.

bo x 19-1. Te c ique o r d e te rmi i g i ival Mar i

t e Le ve l o t e

W n issu sw llin g o c ssio n is s n , io d o n l o b is u s d o m su d is n c g in g iv l m g in is ic l o co o n l o Ce J. K in m in d n u lo x c d l v lo g in g iv l m g in in b s n c o d is s o u m is slig ly co o n l o Ce J. s n , d is n c b w n Ce J n d 1. Fo r i ival re ce ssio . I g in g iv l c ssio n is g in g iv l m g in is m su d u sin g c lib d io d o n l o b . t is d is n c is co d d s g in g iv l m g in l v l. s n , d is n c b w n 2. Fo r i ival e lar e me t. I g in g iv l n l g m n is Ce J n d g in g iv l m g in is lso m su d u sin g c lib d io d o n l o b . t is d is n c is s im d u sin g o llo w in g c n iq u : a. po si io n i o ob 45-d g ngl o o o su c . ob i b n g in g iv l m g in u n il ju n c io n b w n . Slo w ly m o v n m l n d c m n u m is d c d s slig d isc n cy in sm o o n ss o o o su c . c. M su d is n c b w n g in g iv l m g in n d Ce J. t is d is n c is co d d s g in g iv l m g in l v l.

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A Clas s I

Fi ure 19-4A: Mille r Class I d e e ct. In a Miller Class I gingival de ect the recession is isolated to the acial sur ace and the interdental papillae ill the adjacent interdental spaces. Class I recession does not extend to the mucogingival line. These Class I de ects can be urther subdivided into narrow or wide.

B Clas s II

Fi ure 19-4b: Mille r Class II d e e ct. In a Miller Class II gingival de ect the recession is isolated to the acial sur ace and the papillae remain intact and ill the interdental spaces. Class II recession does extend beyond the mucogingival line into the mucosa.

C Clas s III

Fi ure 19-4C: Mille r Class III d e e ct. In a Miller Class III gingival de ect the recession is quite broad with the interdental papillae missing due to damage rom disease. The Class III de ect extends beyond the mucogingival line into the mucosa.

D Clas s IV

Fi ure 19-4d : Mille r Class IV d e e ct. In a Miller Class IV gingival de ect the recession extends to or beyond the mucogingival junction with loss o alveolar bone resulting in open interdental areas.

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327

E. Level o Mucogingival Junction 1. The level o the mucogingival junction represents the junction between the keratinized gingiva and the nonkeratinized mucosa. The level o the mucogingival junction is used in calculation o the width o the attached gingiva as will be described in Section 4 o this chapter. 2. The mucogingival junction is usually readily visible since the keratinized gingiva is normally pale pink and opaque while the sur ace o the mucosa consists o thin, translucent tissue (Fig. 19-5). 3. O ccasionally, the mucogingival junction can be di cult to detect visually. In this case, the tissue can be manipulated by pulling on the patient’s lip or pushing on the tissue with a blunt instrument to distinguish the movable mucosa rom the more rmly attached gingiva.

Fi ure 19-5. Muco i ival Ju ctio . The mucogingival junction represents the junction between the keratinized gingiva and nonkeratinized mucosa and is usually readily visible.

F. Tooth Mobility and Fremitus 1. Horizontal tooth mobility, movement o a tooth in a acial to lingual direction, is assessed by trapping the tooth between two dental instrument handles. a. Alternating moderate pressure is applied in the acial–lingual direction against the tooth rst with one, then the other instrument handle. b. M obility can be observed by using an adjacent tooth as a stationary point o visual re erence during attempts to move the tooth being examined. 2. Vertical tooth mobility, the ability to depress the tooth in its socket, can be assessed using the end o an instrument handle to exert pressure against the occlusal or incisal sur ace o the tooth (Fig. 19-6). 3. Even though the periodontal ligament allows some slight movement o the tooth in its socket, the amount o this natural tooth movement is so slight that it cannot normally be seen with the naked eye. Thus, when visually assessing mobility, the clinician should expect to nd no visible movement in a periodontally healthy tooth. 4. There are many rating scales or recording clinically visible tooth mobility. O ne use ul scale is indicated in Table 19-2. 5. In some dental o ces, the dentist may also wish to assess remitus. a. Fremitus is a palpable or visible movement o a tooth when in unction. b. Fremitus can be assessed by gently placing a gloved index nger against the acial aspect o the tooth as the patient either taps the teeth together or simulates chewing movements. Fremitus is easy to detect i the nger pressure is gentle.

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A

B

Fi ure 19-6. Ve rtical To o t Mo ilit . A: The patient came to the dental o ice complaining o a loose tooth. Note the position o the maxillary le t central incisor. b: The patient then demonstrated how he could push this tooth upward by applying pressure with his index inger against the incisal edge. This central incisor has vertical mobility. (Courtesy o Dr. Don Rol s, Wenatchee, WA.)

TAb LE 1 9 -2 . SCALE FOR RATIn g VISIb LE TOOTh MOb ILITy Classif catio

d e scriptio

Cl ss I

Slig

Cl ss II

Mo d

m o b ili y, u

m o b ili y, g

d is l c m n in Cl ss III

S v v

o 1 mm o

o izo n

l d is l c m n in

n 1 m m b u l ss

ci l–lin g u l d i c io n

n 2 mm o

o izo n

l

ci l–lin g u l d i c io n

m o b ili y, g ic l d is l c m n ( o o

n 2 m m o d is l c m n in d

ssib l in

so ck

ci l–lin g u l d i c io n o

)

G. Furcation Involvement 1. A urcation probe is used to assess urcation involvement on multirooted teeth. M ost molar teeth are multirooted, but some maxillary premolar teeth also develop with two roots creating the potential or a urcation involvement on some premolars also. 2. Furcation probes are curved, blunt-tipped instruments that allow easy access to the urcation areas; straight periodontal probes cannot be relied upon to detect urcation involvements accurately. 3. Furcation involvement occurs on a multirooted tooth when periodontal in ection invades the area between and around the roots, resulting in a loss o attachment and loss o alveolar bone between the roots o the tooth. a. M andibular molars are usually bi urcated (with mesial and distal roots), with potential urcation involvement on both the acial and lingual aspects o the tooth (Fig. 19-7A,B). b. M axillary molar teeth are usually tri urcated (with mesiobuccal, distobuccal, and palatal roots) with potential urcation involvement on the acial, mesial, and distal aspects o the tooth. c. M axillary rst premolars that have bi urcated roots (buccal and palatal roots) have the potential or urcation involvement on the mesial and distal aspects o the tooth.

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4. Furcation involvement requently signals a need or periodontal surgery a ter completion o nonsurgical therapy, so detection and documentation o urcation involvement is a critical component o the comprehensive periodontal assessment. 5. Furcation involvement should be recorded using a scale that quanti es the severity (or extent) o the urcation invasion. Table 19-3 shows a commonly used scale or rating urcation invasions o multirooted teeth.

A

B

Fi ure 19-7. Furcatio I vo lve me t. A: Furcation involvement as viewed rom the acial aspect o a mandibular irst molar. b: The radiograph o the same molar shows bone loss between the roots o this molar.

TAb LE 1 9 -3 . SCALE FOR RATIn g FURCATIOn In VOLVEMEn T Classif catio

d e scriptio

Cl ss I

Cu v u

o

co n c vi y l

ow v , Cl ss II

t

ob

co m l Cl ss III

ob

t

ob

In m n d ib u l b

Cl ss IV

w

n

n ly

n

s

s in o oug

u c io n n o m o

l wi

ob

i ;

n 1 mm n 1 mm bu do s no

ss

u c io n

ss s co m l

ly

m o l s,

oug ob

u c io n .

ss s co m l

ly

oug

u c io n

m si l n d d is l o o s. ob

o o s n d w ill o u c

l

ss s b

s nc o

w

n

m sio b u cc l n d d is o b u cc l

l oo .

s Cl ss III u c io n , xc

b c us o

u c io n c n b

u c io n g

In m xill y m o l s,

S m

d in g o

n

d v n c d g in g iv l

nc

o

c ssio n .

u c is clin ic lly visib l

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H. Presence o Calculus Deposits on the Teeth 1. The presence o dental calculus on the teeth should be noted since these deposits must later be identi ed and removed as part o the nonsurgical therapy. 2. Calculus is a local contributing actor in both gingivitis and periodontitis; thus, the identi cation and removal o these deposits is a critical component o success ul patient treatment. 3. Calculus deposits can be located through several techniques that include the ollowing: a. Direct visual examination using a mouth mirror to locate supragingival deposits. b. Visual examination while using compressed air to dry the teeth to aid in locating supragingival deposits. c. Tactile examination using an explorer to locate subgingival calculus deposits. I. Presence o Plaque Bio lm on the Teeth 1. The presence o plaque bio lm on the teeth should be noted during a comprehensive periodontal assessment since these deposits contain living periodontal pathogens that can lead to both gingivitis and periodontitis. 2. Plaque bio lm can be identi ed using disclosing dyes or by moving the tip o an explorer or a periodontal probe along the tooth sur ace adjacent to the gingival margin. 3. There are many ways to record the presence o plaque bio lms, but most dental o ces record the results o the plaque assessment in terms o the percentage o tooth sur aces with plaque bio lm evident at the gingival margin. A use ul ormula or recording plaque percentages is shown in Box 19-2. a. N ote that in using the calculation shown in Box 19-2, a plaque score o 90% indicates that 90% o the total available tooth sur aces have plaque bio lm at the gingival margin. b. O ne goal o therapy would be or the patient to learn and per orm plaque bio lm control measures that would bring the plaque score as close to 0% as possible (or at least to bring the percentage o tooth sur aces with plaque bio lm as low as possible). 4. As discussed previously in this book, plaque bio lm is the primary etiologic actor or both gingivitis and periodontitis. Identi cation o the presence and distribution o plaque bio lm on the teeth is a critical piece o in ormation needed when planning appropriate therapy and patient education.

bo x 19-2. Fo rmula o r Calculati Nu m b o o o t o l numb

su c s w i o o o su

Plaque Pe rce ta e s l qu c s

× 100 =

c n

g sco

J. Gingival Inf ammation 1. A thorough periodontal assessment includes recording the overt signs o inf ammation. The overt signs o inf ammation o the gingiva include erythema (redness) and edema (swelling) o the gingival margins resulting in readily identi able changes in gingival color and contour. 2. It is always important to be aware that inf ammation can be present in the deeper structures o the periodontium without necessarily involving any obvious clinical signs o inf ammation o the gingival margin.

C apte r 19

Clinical Periodontal Assessment

a. When assessing the presence o inf ammation, it is important to remember that bleeding on probing also can be a sign o inf ammation. b. Thus, when a clinician is identi ying gingival inf ammation or purposes o planning treatment, the visible signs such as color, contour, and consistency changes in the gingiva must be correlated with the other signs such as bleeding on probing or the presence o exudate. K. Radiographic Evidence o Alveolar Bone Loss. Radiographic interpretation is discussed in Chapter 20. 1. It is important or the clinician to remember, however, that radiographs play an important role in arriving at the periodontal diagnosis and in developing an appropriate plan or nonsurgical periodontal therapy. 2. Radiographic evidence o alveolar bone loss is always an important part o a clinical periodontal assessment. L. Presence o Local Contributing Factors 1. A thorough periodontal assessment will always include identi cation o local contributing actors. 2. These actors are discussed in Chapter 16. The plan or treatment or any periodontal patient will always include measures to eliminate or to minimize the impact o these local actors. 2. Supplemental Diagnostic Tests A. Overview o Supplemental Diagnostic Tests 1. Clinical periodontal assessment using the parameters discussed in Section 3 will result in an accurate periodontal diagnosis and can serve as a sound basis or designing an appropriate plan or therapy or the patient with gingival or periodontal disease. There are, however, a number o supplemental diagnostic tests that can be used or certain patients. 2. Clinicians might consider using some o these supplemental tests or patients who have periodontitis that is ailing to respond to conventional periodontal therapy or periodontitis that shows other unusual signs o disease progression. 3. There are a number o supplemental tests that have been suggested or use, and much research is continuing related to these types o tests. M ost o these tests all into three general types: a. Tests related to bacteria b. Tests that analyze gingival crevicular f uid content c. Tests or genetic susceptibility to periodontal disease. 4. It is critical or the clinician to realize that based upon current research, none o these supplemental diagnostic tests should be ordered routinely on all patients with periodontal disease. B. Tests Related to Bacteria. Table 19-4 presents an overview o the tests related to bacteria. It is important to keep in mind that conventional periodontal therapy brings periodontal pathogens to low enough levels that disease progression can be halted without the need or identi ying speci c periodontal pathogens in most patients. C. Tests that Analyze Gingival Crevicular Fluid Content 1. Gingival Crevicular Fluid a. Gingival crevicular f uid is the f uid that f ows into the sulcus rom the adjacent gingival connective tissue; the f ow is slight in health and increases in the presence o inf ammatory disease. b. Gingival crevicular f uid originates in connective tissue and f ows into periodontal pockets. It has long been believed that this gingival crevicular

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f uid can contain markers or periodontal disease progression, and quite a bit o research time has been devoted to the study o this f uid. 2. Examples o Gingival Crevicular Contents That H ave Been Studied a. Collagenase (an enzyme that breaks down collagen) is an example o one o the gingival crevicular f uid contents that has been studied, though no test or this is currently in widespread use. b. Prostaglandin E2 is another such gingival crevicular f uid ingredient that has been studied. Prostaglandin E2 is associated with arachidonic acid that is involved with inf ammatory reactions such as those seen in periodontal disease. D. Tests or Genetic Susceptibility to Periodontal Disease 1. Genetic Susceptibility a. It is obvious that a patient’s genetic makeup a ects susceptibility to many diseases including periodontal disease. b. This genetic makeup is inherited and cannot normally be altered. 2. Tests or Interleukin-1 a. O ne test or genetic susceptibility to periodontal disease has been studied extensively and has resulted in a test that has been marketed to clinicians. The rst version o this test was the PST Genetic Susceptibility Test rom Interleukin Genetics Incorporated, Waltham, M A. A new version o this genetic susceptibility test, called PerioPredict is scheduled to be released. b. Both o these tests identi y patients with genetic programming to produce high levels o interleukin-1 (an inf ammatory mediator produced in response to the presence o periodontal pathogens). 1. H igher levels o interleukin-1 in patients tend to predispose the patients to more inf ammation in the periodontium and have been associated with increased risk or severe and progressive periodontal disease. 2. It has been reported that 30% o the people in the United States have the genetic makeup to produce high levels o interleukin-1 in response to periodontal pathogens. E. The Future. It would be extremely help ul i clinicians had access to a diagnostic test that could indicate which patients are undergoing or are likely to undergo attachment loss. It is sa e to assume that as more research is completed additional use ul clinical tests will be developed in this area.

TAb LE 1 9 -4 . TESTS RELATEd TO b ACTERIA Te st n ame p

s co n

s udy o Cu l u

s m ic o sco ic l qu s m l

n d s n si ivi y

Purpo se o Te st

Spe cial Co si e ratio s

Us d o

t s c n n o id n i y s

i n

d u c io n n d

m o iv io n

s

Us d o d

m in

s n si ivi y o b c s DNa (d o xy ib o n u cl ic cid )

ob

n lysis

Us d o id n i y s

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i n ’s m o u

ci ic

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is

nd

c n iq u s o

ns o

o

ci ic n ib io ics

i l

ci s

S m lin g i

ci ic b c

On ly

o b c

o y

i ls m l s o

d i icu l

wb c

id n i i d b y

s

i ls is

s

ci s c n b

C apte r 19

Se ct io

Clinical Periodontal Assessment

333

4

Cli ical Fe ature s t at Re quire Calculatio s Some judgments that are made as part o the clinical periodontal assessment may require some calculations. The most common eatures that may require some calculations are the width o the attached gingiva and clinical attachment level. 1. Calculating the Width o Attached Gingiva A. Description. The attached gingiva is the part o the gingiva that is rm, dense, and tightly connected to the cementum on the cervical-third o the root or to the periosteum (connective tissue cover) o the alveolar bone. The attached gingiva lies between the ree gingiva and the alveolar mucosa, extending rom the base o the sulcus (or pocket) to the mucogingival junction. 1. The unctions o the attached gingiva are to keep the ree gingiva rom being pulled away rom the tooth and to protect the gingiva rom trauma. 2. The width o the attached gingiva is not measured on the palate since it is not possible to determine where the attached gingiva ends and the palatal mucosa begins. 3. The attached gingiva does not include any portion o the gingiva that is separated rom the tooth by a crevice, sulcus, or periodontal pocket. B. Signi cance. The width o the attached gingiva on a tooth sur ace is an important clinical eature or the dentist to keep in mind when planning many types o restorative procedures. I there is no attached gingiva on a tooth sur ace, the dentist is limited in the types o restorations that can be placed. There ore, it is important to use the in ormation collected during the comprehensive periodontal assessment to calculate this clinical eature. C. Method o Calculation. The method o calculation o the width o attached gingiva is shown in Box 19-3. Note that the in ormation needed to calculate the width o the attached gingiva already would have been recorded during the periodontal assessment.

bo x 19-3. Calculati

t e Wi t o Attac e

To t a l w id t h o f g in g iva

A

iva

Wid t h o f a t t a c h e d g in g iva

B

Fo rmula: t o c lcu l g in g iv n d su b

w id c

o

Ste p 1: M su ju n c io n . Ste p 2: M su Ste p 3: C lcu l o l w id

l w id

o

o

gi

o b in g d w id o o g in g iv .

c d g in g iv o b in g d om g in g iv

om

s ci c si , m su o l w id u sin g g in g iv l m

( om g in g iv l m g in o c d g in g iv b y su b c in g

g in o

s

w id o s b lo w : m u co g in g iv l

b s o o ck ). o b in g d om

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2. Calculating the Clinical Attachment Level (CAL) A. De nition. The clinical attachment level (CAL) is a clinical measurement o the true periodontal support around the tooth as measured with a periodontal probe. Box 19-4 outlines a comparison o probing depths and clinical attachment levels. B. Signi cance o Clinical Attachment Levels 1. An attachment level measurement is a more accurate indicator o the periodontal support around a tooth than is a probing depth measurement. a. Probing depths are measured rom the ree gingival margin to the base o the sulcus or pocket. The position o the gingival margin may change with tissue swelling, overgrowth o tissue, or recession o tissue. Since the position o the gingival margin can change (move coronally or apically), probing depths do not provide an accurate means to monitor changes in periodontal support over time in a patient. b. CAL provides an accurate means to monitor changes in periodontal support over time. The CAL is calculated rom measurements made rom a xed point on the tooth that does not change (i.e., the CEJ o the tooth). 2. The presence o loss o attachment is a critical actor in distinguishing between gingivitis and periodontitis. a. Inf ammation with no attachment loss is characteristic o gingivitis. b. Inf ammation with attachment loss is characteristic o periodontitis.

bo x 19-4. Co mpariso o Pro i Attac me t Le ve ls

d e pt s a

Cli ical

Mo n i o in g io d o n l su o o ov im is vi l co m o n n o lo n g - m c o i n s wi io d o n l d is s . t w o m su m n s u s d o d sc ib moun o io d o n l su o o : (1) o b in g d s n d (2) clin ic l c m n l v ls (Ca Ls). p o b in g d s q u n ly u s d , w s clin ic l c m n l v ls l ss co m m o n ly u s d . Clin ici n s s o u ld b w us o o b in g d s lo n m y n o b in so m i n s’ b s in s s. • Pro i e pt s lo n no mos li b l in d ic o s o moun o io d o n l su o o o o . p o b in g d s m su d o m g in g iv l m g in ; o si io n o g in g iv l m g in o n c n g s o v im . C n g s in l v lo g in g iv l m g in o ccu w i g in g iv l sw llin g , o v g o w o g in g iv , o g in g iv l c ssio n . So , c n g in o b in g d ov im m y in d ic c n g in moun o io d o n l su o o o o , b u i m y lso o n ly in d ic s b n so m c n g in l v lo g in g iv l m g in (w ic m y w ll b u n l d o cu l io d o n l su o o o o ). • Cli ical attac me t le ve ls (CALs) d nd mo ccu in d ic o o c u l moun o io d o n l su o o o o . Ca L m su m n s m d om x d o in d o s n o c n g (i. ., Ce J o o o ). t o ,w n is c n g in Ca L o v im , is c n g f c s n ccu m su m n o u c n g in io d o n l su o o oo .

C apte r 19

Clinical Periodontal Assessment

C. Calculating the Clinical Attachment Level 1. When the gingival margin is near the CEJ. When the gingival margin is at its natural location (i.e., near the CEJ o the tooth), the probing depth and the clinical attachment level readings are the same or all practical purposes. 2. When the gingival margin is apical to the CEJ (i.e., there is gingival recession). When gingival recession is present, a straight calibrated periodontal probe is used to measure the distance the gingival margin is apical to the CEJ (Fig. 19-8A–C), and the same probe is used to measure the probing depth at the site. Both o these measurements will have been made and recorded as part o the comprehensive periodontal assessment. To calculate the CAL, simply add these two measurements (i.e., the amount o gingival recession plus the amount o the probing depth at the site). 3. When the gingival margin is signi cantly coronal to the CEJ (i.e., there is gingival enlargement). When gingival enlargement is present, a straight calibrated periodontal probe is used to measure the distance the gingival margin is coronal to the cementoenamel junction (Fig. 19-8A–C). Remember that the natural position or the gingival margin is either at or slightly coronal to the CEJ, but there are many instances when the gingival margin will be ound to be signi cantly (several millimeters) coronal to the CEJ. I the gingival margin is signi cantly coronal to the CEJ, the distance between the margin and the CEJ is estimated using the ollowing technique: a. Position the tip o the straight calibrated probe at a 45-degree angle to the tooth sur ace. b. With light orce, slowly move the probe beneath the gingival margin until the junction between the enamel and cementum is detected. c. M easure the distance between the gingival margin and the cementoenamel junction, and measure the probing depth at this site. d. Subtract the distance rom the gingival margin to the CEJ rom the probing depth to determine the CAL at the site. D. Recording the Gingival Margin on a Periodontal Chart. Customarily, the notations 0, −, or + are used to indicate the position o the gingival margin on a periodontal chart (Box 19-5).

bo x 19-5. n o tatio s t at I g i ival Mar i

icate t e Po sitio

o t e Fre e

s g in g iv l m g in is slig ly co o n l o Ce J. • a z o (0) in d ic • a n g iv n u m b (- ) in d ic s g in g iv l m g in sig n i c n ly co v s Ce J. s g in g iv l m g in is ic l o Ce J ( c ssio n ). • a o si iv n u m b (+) in d ic

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Fi ure 19-8A: Calculati Cli ical Attac me t Le ve l w e t e g i ival Mar i is Sli tl Co ro al to t e Ce me to e ame l Ju ctio . When the gingival margin is slightly coronal to the CEJ, no calculations are needed since the probing depth and the clinical attachment level are equal. For example: Probing depth measurement: 6 mm Gingival margin level: 0 mm Clinical attachment loss: 6 mm

A

3 mm 6 mm

9 mm

Fi ure 19-8b: Calculati Cli ical Attac me t Le ve l w e t e g i ival Mar i is Si i ica tl Co ro al to t e Ce me to e ame l Ju ctio . When the gingival margin is signi icantly coronal to the CEJ, the CAL is calculated by SUBTRACTING the gingival margin level rom the probing depth. B C EJ

Dis t a n c e g i m a rg in is c o ro n a l t o C EJ

P ro b in g d e p t h

C lin ic a l a t t a c h m e n t lo s s

For example: Probing depth measurement: 9 mm Gingival margin level: −3 mm Clinical attachment loss: 6 mm

2 mm 6 mm

4 mm

Cli ical Attac me t Le ve l i t e Fi ure 19-8C: Calculati Pre se ce o g i ival Re ce ssio . When recession is present, the CAL is calculated by ADDING the probing depth to the gingival margin level. C CEJ

Clin ic a l a t t a c h m e n t lo s s

P ro b in g d e p t h

Re c e s s io n

For example: Probing depth measurement: 4 mm Gingival margin level: +2 mm Clinical attachment loss: 6 mm

C apte r 19

Clinical Periodontal Assessment

337

C apte r Summar State me t The in ormation gathered by the members o the dental team during the clinical periodontal assessment orms the basis or an individualized treatment plan or the patient. This chapter discusses two types o clinical periodontal assessment: a periodontal screening examination and the comprehensive periodontal assessment. The Periodontal Screening and Recording (PSR) is an example o an e cient periodontal screening system or the detection o periodontal disease. The comprehensive periodontal assessment is a complete clinical periodontal assessment used to gather in ormation about the periodontium. The in ormation collected in a comprehensive periodontal assessment includes probing depth measurements, bleeding on probing, presence o exudate, level o the ree gingival margin, level o the mucogingival junction, tooth mobility, urcation involvement, presence o calculus, presence o plaque bio lm, gingival inf ammation, radiographic evidence o alveolar bone loss, and presence o local contributing actors. Supplemental diagnostic tests are indicated or certain patients. Some judgments made during a clinical periodontal assessment require calculation. These include the width o attached gingiva and clinical attachment levels. Detection o clinical attachment level is important in determining whether gingivitis or periodontitis is present at a site o inf ammation.

Se ct io

5

Fo cus o

Patie ts

Cli ical Patie t Care CA S E 1 While visiting a dental o ce, you observe a member o the dental team per orming a periodontal assessment. You note that while searching or urcation invasion, the clinician is using a straight calibrated periodontal probe. What critical in ormation might be lost because o instrument selection or this step in a periodontal assessment?

CA S E 2 During a comprehensive periodontal assessment you note severe inf ammation o the gingiva over the acial sur ace o a lower right molar tooth. O n the dental chart you are using there is no obvious mechanism to record this important piece o periodontal in ormation. H ow should you proceed?

CA S E 3 During a periodontal assessment o a periodontitis patient, you are trying to determine the clinical attachment level on the acial sur ace o a canine tooth. O n the acial sur ace o the canine tooth you have measured 3 mm o gingival recession and a probing depth o 6 mm. H ow much attachment has been lost on the acial sur ace o this canine tooth?

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Et ical d ile mma Your next patient is M arlene Perkins, who is a new patient to your practice. She is a 37-yearold married mother o two small daughters, who works part-time as a lawyer. H er chie complaint is “ bleeding gums.” She le t her last dental practice because she questioned i she was receiving quality dental services. The radiographs, you have taken today, show that there is very slight horizontal bone loss on her anterior teeth. M arlene’s pocket readings range rom 1 to 4 mm throughout her mouth, and there is generalized bleeding on probing. She presents with heavy plaque bio lm and moderate supragingival and subgingival calculus, although states that she had her teeth cleaned 4 months ago. She states that she “ isn’t a very good f osser, and was always reprimanded by the hygienist at her ormer dental practice, to do a better job.” She notes that she has a history o periodontal disease in her amily, as both her mother and ather have had “ extensive gum surgeries.” She asked the dentist and hygienist in her last practice i periodontal disease was hereditary and i there was a way to predict i she also would have periodontal disease. She was told that each person is an individual, and that i she “ took care o her teeth and gums,” she would be just ne. 1. What is the best way or you to handle this ethical dilemma? 2. What is the best way to address/discuss M arlene’s treatment plan? 3. What ethical principles are in conf ict in this dilemma?

Re e re ce 1. American Academy o Periodontology. Comprehensive periodontal therapy: a statement by the American Academy o Periodontology. J Periodontol. 2011;82(7):943–949.

STUd En T An CILLARy RESOURCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

r e t p a h C

20

Radio raphic Anal sis o f the Pe rio do ntium

Se ctio n 1

Radio raphic Appe arance o f the Pe rio do ntium

340

Se ctio n 2

Use o f Radio raphic Ima e s fo r Pe rio do ntal Evaluatio n

343

Fo cus o n Patie nts

350

Se ctio n 3

Clinical Patient Care Ethical Dilemma

Clinical Applicatio n.

Interpretation o radiographic images is an integral part o the diagnosis or patients with most types o periodontal diseases. Members o the dental team will need to rely on their skills in radiographic interpretation on a daily basis. This chapter outlines some in ormation about radiographic image interpretation that all members o the dental team will f nd help ul.

Le arnin Obje ctive s • Recognize the radiographic characteristics o normal and abnormal alveolar bone. • Recognize and describe early radiographic evidence o periodontal disease. • Distinguish between vertical and horizontal alveolar bone loss. • Recognize potential etiologic agents or periodontal disease radiographically. • Gain practical experience in radiographic assessment by applying in ormation rom this chapter in the clinical setting.

Ke Te rms Radiolucent Radiopaque

Cortical bone Lamina dura

Crestal irregularities Triangulation

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Se ct io n 1

Radio raphic Appe arance o f the Pe rio do ntium Dental radiographs are an important adjunct to the clinical assessment o the periodontium. To recognize disease, the dental hygienist must be able to recognize the normal radiographic appearance o the periodontium. Periodontal anatomy visible on radiographic images includes the alveolar bone, periodontal ligament space, and cementum. The gingiva is a noncalci ed so t tissue that cannot usually be seen on a radiograph. 1. Radiolucent and Radiopaque Structures and Materials A. Radiolucent materials and structures are easily penetrated by x-rays. 1. M ost o the x-rays will be able to pass through these objects and structures to expose the radiograph. Radiolucent areas appear as dark gray to black on the radiograph. 2. Examples o radiolucent structures are the tooth pulp, periodontal ligament space, a periapical abscess, marrow spaces in the bone, and bone loss de ects. B. Radiopaque materials and structures absorb or resist the passage o x-rays. 1. Radiopaque areas appear light gray to white on the radiograph. These structures absorb most o the x-rays, so that very ew x-rays reach the radiograph. 2. Examples o radiopaque structures and materials are metallic silver (amalgam restorations) and newer composite restorations, enamel, dentin, pulp stones, and compact or cortical bone. 2. Identif cation o the Periodontium on Radiographic images. The components o the periodontium that can be identi ed on radiographic images include the alveolar bone, periodontal ligament space, and cementum (Fig. 20-1). A. Cortical Bone 1. Cortical bone is the outer sur ace o the bone and is composed o layers o bone closely packed together. a. O n the maxilla, the cortical bone is a thin shell. b. O n the mandible, the cortical bone is a dense layer. 2. Radiographic Appearance o Cortical Bone a. In erior border o the mandible appears on the radiograph as a thick white border. b. Interdental alveolar crests between the teeth o both jaws appear on the radiograph as a thin white line on the outside o crestal bone. c. The lattice-like pattern o the cancellous bone that lls the interior portion o the alveolar process appears on the radiograph as a pattern o delicate white tracings within the bone.

Ename l (E) Metal res toration (MR)

Pulp (P) Dentin (D)

PDL

Bone

Lamina dura (LD)

A

B

Fi ure 20-1. Radio raphic Structure s o f the Pe rio do ntium.

Chapte r 20

Radiographic Analysis o the Periodontium

341

B. Alveolar Crest. The normal level of the alveolar bone is located approximately 2 mm apical to (below) the cementoenamel junction (CEJ). 1. I the coronal bone level is within 3 mm o the CEJ, the bone level is considered normal. 2. It is unlikely that bone loss less than 3 mm can be detected on a radiograph. C. Crestal Contour o the Interdental Bone 1. The contour o the crest o the interproximal bone is a good indicator o periodontal health. The contour of the interproximal crest is parallel to an imaginary line drawn between the CEJs of adjacent teeth. 2. In posterior sextants, the contour o the interproximal crest is parallel to an imaginary line drawn between the CEJs o the adjacent teeth. a. H orizontal crest contour. The crest o the interproximal bone will have a horizontal contour when the CEJs o the adjacent teeth are at the same level (Fig. 20-2). b. Angular crest contour. The crest o the interproximal bone will have a vertical contour when one o the adjacent teeth is tilted or erupted to a di erent height (Fig. 20-3).

Ho rizo n ta l c o n to u r

A

B

Fi ure 20-2. A: No rmal Alve o lar Bo ne He i ht. This radiograph shows a normal alveolar bone height that is 1.5 to 2 mm below and parallel to the cementoenamel junction. In this example, alveolar crest is a dense radiopaque line similar in density to the lamina dura surrounding the root o the tooth. B: Ho rizo ntal Cre st Co nto ur. The crest o the interproximal bone will have a horizontal contour when the CEJs o the adjacent teeth are at the same level.

An g u la r c o n to u r

A

B

Fi ure 20-3. An ular Cre st Co nto ur. The crest o the interproximal bone will have a vertical contour when one o the adjacent teeth is tilted or erupted to a di erent height.

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D. Alveolar Crestal Bone 1. Alveolar bone is the part o the jawbone that supports the teeth. 2. The sur aces o the bony crests are smooth and covered with a thin layer o cortical (dense, hard) bone that may be seen as a thin, white line on a radiograph. 3. The most important radiographic feature of the alveolar crest is that it forms a smooth intact surface between adjacent teeth with only the width of the periodontal ligament space separating it from the adjacent root surface. a. The crest o the interdental septa between incisors is thin and pointed. b. The crest o the interdental septa between the posterior teeth is rounded or f at (Fig. 20-4). E. Lamina Dura 1. The alveolar bone proper is the thin layer o dense bone that lines a normal tooth socket. In radiographic images, the alveolar bone proper is identi ed as the lamina dura. O n a radiograph, the lamina dura appears as a continuous white (radiopaque) line around the tooth root (Fig. 20-5). 2. O n a radiograph, the lamina dura is continuous with the cortical bone layer o the crest o the interdental septa. F. Periodontal Ligament Space 1. The space between the tooth root and the lamina dura o the socket is lled with the periodontal ligament tissue. The periodontal ligament tissue unctions as the attachment o the tooth to the lamina dura o the socket. 2. Periodontal ligament tissue does not resist penetration o x-rays and, there ore, appears on the radiograph as a thin radiolucent black line surrounding the tooth root (Fig. 20-5). 3. In most cases, a widening o the periodontal ligament space (PDLS) on the radiograph indicates tooth mobility (Fig. 20-6).

Fi ure 20-4. Alve o lar Cre st. The alveolar crest (indicated by an arrow) orms a smooth intact sur ace between adjacent teeth.

Fi ure 20-5. Lamina Dura and Pe rio do ntal Li ame nt Space . The lamina dura (ld) appears as a continuous white line around the tooth root.

Fi ure 20-6. Wide nin o f the PDL Space . This maxillary second premolar has a uni ormly widened periodontal ligament space (PDL) that is characteristic o tooth mobility.

Chapte r 20

Radiographic Analysis o the Periodontium

Se ct io n 2

Use o f Radio raphic Ima e s fo r Pe rio do ntal Evaluatio n 1. Techniques or Good Radiographic Quality A. Long-Cone Paralleling Technique. The long-cone paralleling technique provides a radiograph that is more anatomically accurate when compared with other intraoral techniques such as bisecting angle. B. Long Gray Scale Low Contrast Images. Long-scale contrast radiographic images have many visible shades o gray that make it easier to see subtle changes such as bone loss in periodontal disease. These images can be obtained using high kVp exposures (70 to 100 kVp) or using digital imaging so tware adjustments to maximize the gray scale o normally exposed images. M any so tware programs now provide presets to optimize or detection o periodontal disease. 2. Limitations o Radiographs or Periodontal Evaluation. There are limitations in the use o the radiograph in the diagnosis o periodontal disease. A. A Two-Dimensional Image. A radiograph provides a two-dimensional image o a complex three-dimensional structure. The act that the radiograph is a twodimensional image can be misleading to the viewer. For example, the buccal alveolar bone can hide bone loss on the lingual aspect o a tooth, and the palatal root makes it di cult to detect urcation involvement o a maxillary molar. B. In ormation Limited to Noncalcif ed Structures. In addition, radiographic images do not provide any in ormation about the noncalci ed components o the periodontium. C. Limited In ormation on Periodontium. Radiographic images do not reveal the ollowing: the presence or absence o periodontal pockets, early bone loss, exact morphology o bone destruction, tooth mobility, early urcation involvement, condition o the alveolar bone on the buccal and lingual sur aces, or the level o the epithelial attachment. 1. Periodontal Pockets a. The only reliable method of locating a periodontal pocket and evaluating its extent is by careful periodontal probing. b. The periodontal pocket is composed o so t tissue, so it will not be visible on the radiograph. 2. Early Bone Loss a. The very earliest signs of periodontitis must be detected clinically, not radiographically. By the time periodontal bone loss becomes detectable on the radiograph, it usually has progressed beyond the earliest stages o the disease. 1. Interseptal bony de ects smaller than 3 mm usually cannot be seen on radiographic images. 2. Bone height on the acial and lingual aspects is di cult to evaluate radiographically because the teeth are superimposed over the bone. b. A radiograph cannot accurately display the shape of bone deformities because it is not three dimensional. c. A radiograph with poor technique and excessive vertical angulation can obscure bone loss. Periapical radiographs may over- or underestimate the actual outline o the alveolar bone (Fig. 20-7) (1). 1. For this reason the bitewing radiograph should be the primary radiograph used to evaluate crestal bone height rather than the periapical radiograph. 2. Proper long-cone paralleling technique can prevent distortion o crestal bone height on periapical radiographic images and improve their use ulness.

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A

Fi ure 20-7A: Exce ssive Ve rtical An ulatio n. Note how the crestal bone height is exaggerated in the periapical radiograph shown here as opposed to the bitewing radiograph shown below. B

Fi ure 20-7B: Bite w in Radio raph. The bitewing shown here reveals the true bone height o the teeth shown in Figure 20-7A.

Fi ure 20-8. Furcatio n Invo lve me nt. The radiolucency on the mandibular irst molar should be evaluated using a urcation probe.

3. Early Furcation Involvement a. Radiographic images usually show more interradicular bone—bone between the roots o the teeth—than is actually present. The acial and lingual aspects o the alveolar bone will o ten be superimposed over the urcation and hide bone loss rom view. b. Variations in alignment of the x-ray beam may conceal the presence or extent of furcation involvement. c. Furcation involvement (bone loss between the roots) is detected by clinical examination with a urcation probe. The urcation area o a tooth should be examined with a urcation probe even i the radiograph shows a very small radiolucency or an area o diminished radiodensity at the urcation (Fig. 20-8). 4. Extensive Bone Loss a. Crestal bone loss of 5 mm or greater may cause the coronal bone to be poorly visualized or not seen at all on normal bitewing radiographic images. b. Vertically oriented bitewings may be used in these situations. c. An adaptor is available or most lm holders to accomplish this. d. The long axis o the lm is rotated 90 degrees to be perpendicular to the occlusal plane instead o the short axis (Fig. 20-9).

Chapte r 20

Radiographic Analysis o the Periodontium

345

e. Vertical bitewing radiographic images show more o the coronal bone than regular bitewings especially when the teeth are widely separated by the lm holder (Fig. 20-10). 5. Disease Activity a. Just as clinical attachment levels only indicate past disease destruction, radiographic im ages do not show disease activity, but only the effects of the disease. b. Because of these lim itations, the radiographic ex am ination is never a satisfactory substitute for a clinical periodontal assessm ent.

Fi ure 20-9. Film Place me nt fo r Ve rtical Bite w in . A #2 periapical ilm positioned or taking a vertical bitewing radiograph. Note how the ilm is rotated 90 degrees rom the usual orientation.

Fi ure 20-10. Fo ur Film Ve rtical Bite w in Se rie s. Note how much coronal bone is visible on these vertical bitewings despite the separation o the teeth by the positioning device.

3. Benef ts o Radiographs or Periodontal Evaluation. Despite the radiograph’s limitations, the periodontal examination is incomplete without accurate radiographic images. Radiographs will demonstrate the ollowing: most o the bony changes associated with periodontitis, the tooth root morphology, relationship o the maxillary sinus to the periodontal de ormity, widening o periodontal ligament space, advanced urcation involvement, periodontal abscesses, and local actors such as overhanging restorations, marginal ridge height discrepancies, open contacts, and calculus (Table 20-1) (1). A. Assessment o Bony Changes. Early radiographic signs o periodontitis are (1) uzziness at the crest o the alveolar bone, (2) a widened periodontal ligament space (PDLS), and (3) radiolucent areas in the interseptal bone (Fig. 20-11). 1. Crestal Irregularities. Crestal irregularities are the appearance o breaks or uzziness instead o a nice clean line at the crest o the interdental alveolar bone.

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TABLE 2 0 -1 . BENEFITS OF RADIOg RAPHS IN THE DETECTION OF PERIODONTAL DISEASE Co nditio n e

ly b o n y c

Radio raphic Si n(s) ng s

B

k o fu zzin ss

Wid n in g o f p

c s of io d o n

s n c o f fin g

-lik

in

l lig m n s

d io lu c n

d n

l lv o l

c

c s lm

o j c io n s in o

bon g in

in

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Fi ure 20-11. Earl Radio raphic Si ns. Sequence o radiographic changes that occur in periodontitis.

2. Triangulation (Funneling). Triangulation is the widening o the PDLS caused by the resorption o bone along either the mesial or distal aspect o the interdental (interseptal) crestal bone (Fig. 20-12). 3. Interseptal Bone Changes a. Another radiographic sign o periodontitis is the existence o nger-like radiolucent projections extending rom the crestal bone into the interdental alveolar bone (Fig. 20-13). b. These nger-like radiolucent lines represent a reduction o mineralized tissue (bone) adjacent to blood vessel channels within the alveolar bone.

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c. I chronic periodontitis goes untreated and much o the alveolar bone around the tooth is destroyed, the tooth will seem to “ f oat in space” on the radiograph. This represents the “ terminal stage” o the disease process. B. Extent or Direction o Bone Loss. The extent or direction o bone loss is determined using the cementoenamel junction (CEJ) o adjacent teeth as the points o re erence. 1. H orizontal Bone Loss. H orizontal bone loss is bone destruction that is parallel to an imaginary line drawn between the CEJs o adjacent teeth (Fig. 20-14). 2. Vertical Bone Loss. Vertical (or angular) bone loss occurs when there is greater bone destruction on the interproximal aspect o one tooth than on the adjacent tooth, so that the bone meets the tooth at an acute angle (Fig. 20-15). C. Assessment o Bone Loss 1. The radiograph is an indirect method o detecting bone loss. Periodontitis is a disease process with active and inactive periods, so the radiograph is only a snapshot of an instant in time in the disease process. 2. The radiograph reveals the bone remaining rather than the amount o bone actually lost. Bone loss occurs on all sur aces; however, the tooth root tends to mask (or hide) bone loss on the acial and lingual sur aces o the tooth. 3. M esial or distal bone loss is evaluated primarily by examining the interproximal septal bone on the radiograph. The amount o bone loss is estimated as the di erence between the level o the remaining bone and the normal bone height.

Fi ure 20-12. Trian ulatio n. The crestal bone between these mandibular teeth demonstrates triangulation, a pointed, triangular appearance.

Fi ure 20-13. Fin er-Like Radio lucent Projections. The nutrient canals within the bone are seen as ingerlike projections extending between and beyond the roots o the mandibular incisors on this radiograph.

Fi ure 20-14. Ho rizo ntal Bo ne Lo ss. Horizontal bone loss is parallel to an imaginary line drawn between the CEJs o adjacent teeth.

Fi ure 20-15. Ve rtical Bo ne Lo ss. The arrow points to vertical bone loss on the mesial sur ace o the mandibular irst molar.

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Fi ure 20-16. Furcatio n Invo lve me nt. The urcation involvement is easily visible on the mandibular irst molar in this radiograph.

D. Assessment o Furcation Involvement 1. Furcation involvement will not be seen on the radiograph until the bone resorption extends past the urcation area. a. Furcation involvement o mandibular molars is easier to detect on a radiograph than is urcation involvement o maxillary molars. This is because mandibular molars have only two roots, a mesial root and a distal root (Fig. 20-16). b. Furcation involvement on maxillary molars is more di cult to detect on a radiograph. M axillary molars have three roots, a mesiobuccal, distobuccal, and palatal root. The palatal root is o ten superimposed over the urcation o the tooth on the radiograph and masks (hides) any radiolucency there. 2. It is a general rule that urcation involvement is o ten greater than what the radiograph reveals. 3. I using the radiograph to aid in the detection o urcation involvement, the ollowing rules should be kept in mind: a. I there is a slight thickening o the periodontal ligament space in the urcation area, the area should be examined clinically with a urcation probe. b. I severe bone loss is evident on the mesial or distal sur ace o a multirooted tooth (especially maxillary molars), urcation involvement should be suspected. E. Recognition o Local Contributing Risk Factors. Several local contributing risk actors that may be revealed by the radiograph are calculus deposits, aulty restorations, and ood packing areas. 1. Calculus Deposits a. T he only accurate way to detect calculus deposits is w ith an ex plorer, however, large calculus deposits may be visible on a radiograph. 1. The radiograph may show large, heavy interproximal calculus deposits. 2. Calculus deposits may be visible on the acial and lingual sur aces o the anterior teeth (smooth sur ace calculus or calci ed plaque) 3. Calculus deposits may be visible on the acial and lingual sur aces o teeth when there is severe bone loss on these sur aces. b. The ability to visualize calculus radiographically depends on the degree o mineralization within the calculus and the angulation actors o the x-ray beam. 2. Faulty Restorations. Inadequate dental restorations and prostheses are common causes o gingival inf ammation, periodontitis, and alveolar bone resorption. In many cases, aulty restorations can be detected on a radiograph (Fig. 20-17). 3. Trauma rom O cclusion a. The radiograph is used only as a supplemental aid in recognizing trauma rom occlusion.

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b. Radiographic signs o trauma rom occlusion include the ollowing: 1. Increased width o the periodontal ligament spaces on the mesial and distal sides o the tooth due to resorption o the lamina dura. 2. Vertical or angular bone destruction o ten times wider at the crestal margins where maximum orce is directed during trauma.

A

B

Fi ure 20-17. Fault Re sto ratio ns. A: The distal sur ace o the mandibular irst molar, indicated by the arrow, has a aulty restoration that creates a ood trap and harbors plaque bio ilm. B: The distal proximal tooth sur ace o the maxillary irst molar and the mesial tooth sur ace o the second molar have not been restored to their original shape and contour. These aulty contours create an open contact that can allow ood impaction.

Chapte r Summar State me nt When the limitations o radiographic images are recognized, they can be an important diagnostic aid in the examination and diagnosis o patients with periodontitis. Radiographic images are extremely use ul tools in the detection o bony changes due to periodontitis such as crestal irregularities, triangulation, interseptal bone loss, assessment o bone de ects, and urcation involvement.

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Se ct io n 3

Fo cus o n Patie nts Clinical Patie nt Care CA S E 1 M r. Jones is a new patient in your dental o ce. H e brings with him some recent ull-mouth radiographs that reveal no evidence o alveolar bone loss. While studying a copy o the patient’s dental chart, you note that there is a diagnosis o chronic periodontitis. H ow might you explain the apparent discrepancy between the lack o radiographic evidence o bone loss and the diagnosis o periodontitis?

CA S E 2 During a periodontal assessment or a new patient, you detect clinical attachment loss. When you suggest that the patient needs dental radiographs, the patient objects because she does not want to be exposed to “ unnecessary x-rays.” H ow should you respond?

CA S E 3 While reviewing a new set o dental radiographs or a patient, you note numerous sites o obvious bone loss. The bone loss appears to be vertical (or angular), where there is much more bone loss on one tooth sur ace compared with the immediately adjacent tooth sur ace. H ow might the dental team use this vertical pattern o bone loss when developing the periodontal diagnosis?

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Ethical Dile mma Philomena C is your rst patient o the morning. She was born in Italy, and moved to the United States with her amily when she was 10. She is a 60-year-old homemaker, who appears slightly overweight, and admits to high blood pressure and high cholesterol, both controlled by medication. She has been a patient in the practice o your dentist’s sister, Dr. Lynne, who has an o ce across town, or the last 30 years. She recently decided to change dental practices as our o ce is near her residence. Philomena has been aith ul with her recall visits and has ollowed all the treatments that Dr. Lynne and the various hygienists have suggested during her years as a patient in that practice, including routine radiographs. You begin probing and Philomena questions what you are doing. She states that “ no one has ever done that to her teeth and gums,” and quite rankly nds it very uncom ortable. Philomena says that she thought her oral health could be evaluated by the “ ull set o x-rays” that she received every ew years. Your clinical exam reveals that Philomena presents with generalized tooth mobility and early urcation involvement, especially on the maxillary molars. H er probe readings are generalized 4 to 6 mm in the posterior sextants. She assumed that her mouth was in good health and is shocked to nd out otherwise. 1. What ethical principles are in conf ict in this dilemma? 2. What is the best way or you to handle this ethical dilemma? 3. What is the best way to address/discuss Philomena’s treatment plan?

Re fe re nce 1. Bragger U. Radiographic parameters: biological signi cance and clinical use. Periodontol 2000. 2005;39:73–90.

STUDENT ANCILLARy RESOURCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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All clinicians ace the daunting problem o making sure that they are providing the best possible care or their patients. Dental hygienists must continuously update their knowledge about periodontal diseases and about the care patients with these diseases require. Faced with the act that there is continuous publication o scientif c in ormation about these topics, keeping up-to-date can be di f cult. This chapter outlines strategies that any dental hygienist (or any member o the dental team) can employ to ensure that he or she is indeed able to provide patient care based upon the latest scientif c in ormation available.

Le ar i g Obje cti e s • Summarize how the explosion o knowledge is impacting practitioners and patients. • Identi y the three components o evidence-based decision making. • Discuss the benef ts and limitations o experience. • Describe the role o the patient in the evidence-based model. • List locations or accessing systematic reviews. • Explain the di erence between a peer-reviewed journal and trade magazine. • State three desired outcomes rom attending continuing education courses. • Formulate a question using the PICO process.

Ke Te rms Best practice Best evidence Databases Association Levels o evidence

Cochrane Collaboration Causal actor Systematic review MEDLINE (PubMed) Evidence-based practice

PICO process Peer-reviewed journals Con irmation bias

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What is Be st Practice ? Providing the best possible care to patients is the oremost goal o all dental healthcare providers. Yet it is generally acknowledged that periodontal care may vary rom o ce to o ce and even by regions o the country. A s new procedures and techniques becom e available, hygienists com m itted to ex cellence m ust regularly update and adapt their strategies or providing patient care. The approach known as “ best practice” is an important tool in helping hygienists provide high quality care to their patients. 1. Overview o the Concept o Best Practice A. Def nition. Best practice re ers to practices/treatments/therapies that are based on the best available evidence (1). B. Goals and Considerations 1. The goal o best practice is consistent, superior patient outcomes. a. The outcomes should be measurable such as a reduction in probing depths. b. The outcome should be reproducible. For example, i a technique produces a certain result on one patient, it is reasonable to expect a similar outcome when the technique is used with other patients. 2. Best practice is derived rom evidence-based care. It is the process o using the best available evidence in patient interventions (1). 2. Circumstances That Prompted the Best Practice Approach to Patient Care A. Direct Access to Rapidly Emerging Clinical Research In ormation 1. Explosion o In ormation a. In ormation about new techniques, tests, procedures, and products or periodontal care is emerging at an astonishing rate. H undreds o articles are published in dental journals each year. b. In addition to the in ormation in dental journals, relevant articles are published each year in medical and specialty journals. An example o articles in other disciplines that are relevant to periodontal health are those on the topic o the oral/systemic link. Important research on this topic can be ound in journals such as the N ew England Journal o M edicine or D iabetes Care. 2. Direct Access to In ormation a. In the past, dental healthcare providers relied on what they learned in school and the advice o recognized experts to determine how to provide care. Patients had little or no input into this process. Knowledge o new or cutting edge research was limited to a ew practitioners with access to an educational or healthcare institution. b. Today, with the Internet, clinicians and patients have instant access to the results o ederally unded clinical trials on treatment methods, equipment, and materials. PubM ed, a gateway to more than 23 million research citations, can be accessed by anyone or ree. c. Practicing dental hygienists are ex pected to rem ain current w ith new techniques, devices, and m aterials that w ill result in im provem ents in periodontal care. Dental hygienists in private practice cannot continue to use the same treatments and techniques learned in dental hygiene school year a ter year. The best practice 2 years ago may not represent the highest standard o care today.

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B. Active Patient Role in Decision Making 1. Today’s patient expects to be a partner in the decision-making process about his or her own periodontal care. Patients may arrive at the dental o ce with in ormation downloaded rom the Internet. 2. Be ore the widespread use o in ormation technology, patients depended on the expertise o a healthcare provider or advice, and in most cases accepted that advice without question. 3. Patients who are more engaged in their healthcare experience report a better experience and 3 to 5 times greater satis action with their providers (2). 3. Ability to Interpret the Literature A. N ot All Studies are Signif cant to Clinical Care. Even though hundreds o studies are published yearly, very ew are signi cant enough on their own to merit a change in clinical care. 1. The merit or weight o study is inf uenced by its design. For example, a randomized clinical trial is considered a higher level o evidence than a case series. 2. N o study is completely ree o bias. Reputable journals require investigators to declare a conf ict o interest and disclose corporate nancial support or studies. 3. M any studies either are not designed to provide an answer to the needs o the clinician or provide results that are too weak to merit implementation. B. N ew Does N ot N ecessarily Mean Better 1. N ew treatments and products need to demonstrate consistent superiority to established methods. 2. Some new products and therapies are also signi cantly more costly to implement, and these costs are ultimately passed down to patients. C. Associations Are N ot the Same as Cause and E ect 1. An association is a relationship between an exposure and a disease that implies the exposure might cause the disease (3). 2. A causal actor (causality) is an event or condition that plays a role in producing an occurrence o a disease. An example o a causal actor is exposure to the bacterium called M ycobacterium tuberculosis. Exposure to this bacterium may cause an individual to develop the in ectious disease tuberculosis (TB). a. Investigations/studies are undertaken to demonstrate a link—relationship or association—between an agent and a disease. O n a population basis: 1. An increase in the level o a causal actor will be accompanied by an increase in the incidence o disease (all other things being equal). So, i a population—such as, a large group o people in the con ned area o re ugee camp—is exposed to many persons in the camp who are in ected with the bacterium M . tuberculosis, then it is likely that there will be an increase in the number o new cases o tuberculosis. 2. I the causal actor is eliminated or reduced, the requency o tuberculosis will decline. 3. Finding an association between an event and a disease does not make it causal. a. O ver the past several years, many studies have looked at the relationship between periodontal disease and a host o systemic conditions. b. For instance, while many studies do show that periodontal disease is associated with cardiovascular disease, at the time o this writing, periodontal disease cannot be said to be a causal actor or cardiovascular disease (4).

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Best Practices or Periodontal Care

Maki g

1. Introduction to Evidence-Based Decision Making. Knowledge o the most recent and relevant evidence is the oundation or best practice. The ADH A advocates evidencebased, patient-/client-centered dental hygiene practice. A. Def nition. The ADH A de nes evidence-based practice as the conscientious, explicit, and judicious use o current best evidence in making decisions about the care o individual patients. The practice o evidence-based dental hygiene requires the integration o individual clinical expertise and patient pre erences with the best available external clinical evidence rom systematic research (5). B. Why is there a need or evidence-based decision making? 1. The Journal o Evidence-Based Dental Practice states “ Care that is important is o ten not delivered; care that is delivered is o ten not important.” Whether this stems rom lack o knowledge on the part o the provider or lack o support or implementation within the dental practice, the ultimate result is that the patient does not receive the highest level o care (6). 2. Studies o appropriateness o dental and dental hygiene care con rm that there is a lag time between the discovery o new scienti c ndings and implementation into private practice (7). Studies on dental hygienists’ knowledge and practices relating to oral cancer detection and caries prevention showed variation in knowledge and practices (8–10). 3. A recent study identi ed several key barriers or dental hygienists in the implementation o evidence-based care. These included a lack o support by the dentist employer, nonclinical personnel dictating care, a monetary preoccupation, and level o com ort in continuing to do procedures the same way (7). 4. Dental hygienists were more likely to utilize evidence-based decision making when there was an aligned practice philosophy that included supportive leadership and common goals. A commitment to continuing education also is important (7). C. About Evidence-Based Decision Making 1. Evidence-based decision making emerged rom the work o Dr. David Sackett and others at M cM aster University in O ntario, Canada. In 1981, this group began publishing articles to help clinicians critically appraise the literature, so the best evidence could be identi ed to help solve patient problems (11). 2. Evidence-based decision making includes three oundational elements: (1) incorporation o the best scienti c evidence with (2) the healthcare provider’s clinical expertise and judgment, and (3) patient’s pre erences and values. Figure 21-1 illustrates these three oundational elements o evidencebased health care. Box 21-1 provides an example o evidence-based practice. 3. Evidence is not meant to replace experience or clinical skills. The addition o evidence to decision making brings balance to the process. It helps close the gap between “ what we do” and science. It has the ability to enhance patient care and outcomes (12).

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Scienti c evidence

C lin ic a l e xp e rie n c e a nd ju d g m e n t

P a tie n t p re fe re n c e s o r va lu e s

Fig re 21-1. The Thre e Fo datio al Ele me ts o f E ide ce -Base d He alth Care . Evidence-based care has three equal components: scienti ic evidence, clinical experience, and patient pre erences or values.

Bo x 21-1. E ide ce -Base d Practice : A Example e vid n c -b s d c ic is b u il o n in o m io n o b in d o m s c . Fo x m l , s d n l yg i n is w s u g in sc o o l u l so n ic in s u m n io n s o u ld b u s d s in g ly n d o n ly o m o v l o l g su g in g iv l c lcu lu s d o si s. In d d i io n , yg i n is l n d in sc o o l n d in s u m n s o d u c b s su l s o io d o n l in s u m n io n . • a d in g cu n s c o n u l so n ic in s u m n io n , yg i n is l ns m o d n slim - i d u l so n ic in s u m n s c n b u s d su b g in g iv lly n d co m b in io n o u l so n ic n d n d in s u m n io n l d s o xc ll n su l s. • t is vid n c m o iv s d n l yg i n is o n d co n in u in g d u c io n co u s o n u l so n ic in s u m n io n n d o in co o u l so n ic in s u m n io n in in g i n s wi io d o n i is.

D. Foundational Elements o Evidence-Based Decision Making 1. Evidence-based care recognizes that essential skills are needed in order to engage in evidence-based decision making and obtain the best health outcomes (12). a. O ver time, healthcare providers gain clinical expertise by engaging in clinical experiences (i.e., treating patients and observing the results). b. Patients’ pre erences may be the result o many actors including past dental experiences, current medical and dental status, perceived needs, health values, and economic considerations. c. The most challenging essential skill or a healthcare pro essional to develop is the ability to assess “ evidence.” 2. Clinical experience is both valuable and limiting. It signi es the ability o a clinician to grow in skill and knowledge through experience. a. Experience helps the practitioner make thought ul clinical judgments about the applicability o research ndings to individual patient situations. Yet all patients are di erent, they may present with complicated or complex medical and dental histories. b. Experience is valuable when it is used as a learning rather than rein orcement tool. Ideally, a clinician uses his or her clinical experiences in making better treatment decisions.

Chapte r 21

Best Practices or Periodontal Care

c. Experience can be limiting. The limitation is that not all individuals are able to learn and grow rom experience. To acquire “practical wisdom” the clinician needs to learn how to be ref ective and analyze his or her own per ormance. 1. There is a human tendency to look or or interpret in ormation that con rms our belie s. This tendency is called conf rmation bias. 2. Con rmation bias can lead practitioners to misinterpret in ormation based on belie s, positive or negative, about a treatment or device. 3. Patient pre erence or values is an important consideration in treatment selection. I due consideration is not given to the individual patient’s pre erences, values, and concerns as well as their unique clinical circumstances, the likelihood o the patient ully accepting the clinician’s recommendation is diminished. a. It is the dental hygienist’s responsibility to understand the evidence and its implications or periodontal treatment and communicate it e ectively to a patient. Ultimately, it will be the patient who chooses which therapy he or she pre ers. b. In helping a patient decide which periodontal treatment is right or him or her, there are several elements that should be discussed, including: 1. The evidence about a particular treatment option. 2. The treatment o choice based on the evidence. 3. All possible treatment alternatives. 4. The risks o no treatment at all. c. In addition to the e cacy o a proposed treatment, a patient may place equal weight on other aspects o treatment such as: 1. Cost. Patients usually are concerned about what a treatment will cost. In addition, patients decide i the treatment has bene ts that they perceive as being worth the cost. 2. Pain. Assurances about pain control and management help lessen these concerns. 3. Time lost rom work. Di erent jobs and work environments have varying levels o f exibility in allowing employees time o or healthrelated matters. 4. Impact on amily. Caregivers o young children or elderly amily members may eel that they do not have the time to devote to periodontal treatment. Individuals with chronic health problems may believe that periodontal care is no longer a priority. 5. Insurance bene ts. A practice reality is that patients will sometimes choose care based on what insurance will pay or versus the ull treatment recommendation. 2. Evaluation o Scientif c Evidence. All scientif c evidences are not created equal. A. Levels o Evidence. Best evidence is the highest level o evidence available or a speci c clinical question. 1. Levels o evidence is a ranking system used in evidence-based care to describe the strength o the results measured in a clinical trial or research study. In simple terms, one way o looking at levels o evidence is as ollows (the higher the level, the better the quality; the lower, the greater the bias). Figure 21-2 illustrates the levels o evidence. 2. Based on a hierarchy o levels o evidence, systematic reviews o randomized controlled trials constitute the highest level o current best evidence, and expert opinion is lower-level evidence. 3. The highest level o evidence available represents the current best evidence or a speci c clinical question.

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B. Systematic Reviews: The Highest Ranked Source o Evidence 1. A systematic review is a concise summary o individual research studies on a treatment or device to determine the overall validity and clinical applicability o that treatment or device. a. The systematic review process strives to identi y and track down all the literature on a given topic. O nce the literature is complied, the review process strives to summarize, appraise, and communicate the results and implications in a concise orm or healthcare pro essionals who need this in ormation to keep up-to-date. b. Internationally, the stimulus or systematic reviews has come rom the Cochrane Collaboration, a worldwide group o subject and methodological specialists who aim to identi y and synthesize the research in all aspects o health care. 2. Systematic reviews are, by their very nature, e cient. As an in ormation management tool, they provide a way o coping with large volumes o data in a concise and manageable orm. a. With more than two million articles published in medical and dental journals annually, it is impossible or any one healthcare provider to read and utilize all the new in ormation. b. Systematic reviews o randomized clinical trials represent one o the highest levels o evidence (13). c. Systematic reviews also acilitate the development o clinical practice guidelines by bringing together all that is known about a given topic in a nonbiased manner. This provides use ul mechanisms or bringing research to practice (13). 3. Because o the emphasis on evidence-based care, there are more systematic reviews conducted in dentistry than ever be ore. 4. The systematic review makes incorporating evidence-based care easier. In the past, practitioners were encouraged to do their own searching or research. Since most busy practitioners do not have the time or expertise to do this, the systematic review lls this gap.

S ys t e m a t ic re vie w s S in g le ra n d o m iz e d c o n t ro lle d t ria l (RC T)

C o h o rt s t u d ie s

C a s e - c o n t ro lle d s t u d ie s , c a s e s e rie s / re p o rt s

Exp e rt o p in io n

Fig re 21-2. Le e ls o f E ide ce . The importance or merit o a research study usually is evaluated through its design. Systematic reviews and randomized controlled trials represent the best levels o evidence. Case reports and expert opinion are the lowest levels o evidence.

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Fi di g Cli icall Re le a t I fo rmatio Today, all that is required to have access to research in ormation is a computer with Internet access. Determining which studies are o the highest evidence and the most clinically relevant or a particular need is much more challenging. The most comprehensive process or nding and critically evaluating clinical evidence involves a ve-step process. This ve-step process is summarized in Box 21-2. Steps 1 to 3 o this ve-step process are discussed below.

Bo x 21-2. Fi e -Ste p Pro ce ss fo r Fi di g a d E al ati g Cli ical E ide ce 1. 2. 3. 4. 5.

D v lo n n sw b l clin ic l q u Co n d u c co m u iz d s c o C i ic lly is vid n c o a ly su l s o yo u icu l e v lu o c ss n d su l

s io n o m i n obl m o n lo c b s v il b l vid n c clin ic l lic b ili y clin ic l si u io n s

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ad d o m Fo s JL. e vid n c -b s d d cisio n m kin g : In o d u c io n n d o m u l in g g o o d clin ic l q u s io n s. 2012. a v il b l o n lin : ://w w w.d n lc .co m / n -US/d n l- d u c io n /co n in u in g - d u c io n /c 311/c 311. s x?Mo d u l N m =in o d u c io n &p ID=−1&S c io n ID=−1. a cc ss d a il 30, 2014.

1. Developing an Answerable Question. A clinical question may develop rom questions that arise relative to patient care or rom an area in which the hygienist wants updated knowledge. In order to nd the best in ormation to help patients, it is undamental to learn how to ask the “ right questions.” This is more challenging than it seems. It involves converting problems into answerable questions. A. Use Four Components to Structure the Question. The structure or asking a clear and ocused question entails our critical components, known as the PICO Process (12). The PICO process involves the combination o our separate components to orm an answerable question: “ Patient, Intervention, Comparison, and Outcome.” 1. P (Patient or Problem). An example o the P component might be “ A periodontal m aintenance patient with bleeding and gingivitis.” 2. I (Intervention) a. An intervention is a speci c diagnostic test, treatment, adjunctive therapy, medication, product, or clinical procedure. b. An example o an intervention being questioned is “ brushing and daily hom e irrigation.” 3. C (Comparison) a. Identi es the speci c alternative therapy or device that you wish to compare to the main intervention. b. An example o the “ C” segment o the question is “ com pared to brushing and ossing.” 4. O (O utcome) a. Identi es the measurable outcome you plan to accomplish, improve, or inf uence. b. An example o the “ O ” segment o the question is “ reduce gingivitis and bleeding w ithin 4 week s.”

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B. Formulate the Question. O nce each o the PICO components has been determined, the clinician combines them into an answerable question. Using the above examples, the question would read “ For a periodontal m aintenance patient w ith bleeding and gingivitis, w ill brushing and daily hom e irrigation O R brushing and ossing provide a better reduction in bleeding and gingivitis w ithin 4 week s?” 2. Conduct a computerized search to f nd the best evidence A. Databases 1. The most e cient way to go about nding relevant research is to use an online index o published articles, such as PubM ed, M EDLIN E, or CIN AH L (Cumulative Index o N ursing and Allied H ealth Literature). 2. These indexes—known as databases—list all articles published in a given period o time by journals in a particular pro ession or group o pro essions. 3. MEDLIN E is the U.S. N ational Library o M edicine’s (N LM ) premier database that contains over 19 million re erences to journal articles in li e sciences with a concentration on biomedicine. M EDLIN E enables quick access to locate relevant clinical evidence in the published dental/periodontal literature (Fig. 21-3). a. A distinctive eature o M EDLIN E is that the records are indexed with N LM M edical Subject H eadings (M eSH ). b. Anyone can access M EDLIN E or ree using PubMed—a gateway hosted by the N ational Library o M edicine.

Fig re 21-3. P bMe d We bsite . PubMed search results or the topic “ chronic periodontitis.” (Courtesy o the U.S. National Library o Medicine, Bethesda, MD.)

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B. Systematic Reviews. M any healthcare providers do not have the time or expertise needed to do their own systematic reviews o a question. Fortunately, there are numerous trustworthy resources or busy practitioners who want to implement high-quality science into patient care. 1. The Cochrane Collaboration Database o Systematic Reviews a. The Cochrane Collaboration was established in 1993 by a British epidemiologist, who recognized that ready access to systematic reviews o available evidence would acilitate better-in ormed decisions by healthcare providers. b. T he Cochrane D atabase o System atic R eview s includes systematic reviews o healthcare interventions that are produced and disseminated by The Cochrane Collaboration, a global not- or-pro t organization. 1. The Cochrane Library is published online. Abstracts o reviews are ree. 2. Also, many health science libraries subscribe to the Cochrane databases, so that aculty and students have online access. c. The Cochrane review group relevant to periodontics is the “ O ral H ealth Review Group.” An example o a systematic review conducted by the O ral H ealth Group is on the topic o psychological interventions to improve adherence to oral hygiene instructions in adults with periodontal diseases. d. A complete listing o topics and abstracts can be accessed at http://www. cochrane.org/reviews/index.htm 2. The PubMed Clinical Query: The N ational Library o Medicine a. O ne eature o the M EDLIN E database is the PubM ed Clinical Q uery, which provides specialized searches using an evidence-based lter. b. An online tutorial or the PubM ed Clinical Q uery tool can be accessed online at http://www.nlm.nih.gov/bsd/disted/pubmedtutorial/020_570.html 3. Systematic Reviews by Pro essional Organizations. M any pro essional organizations are developing systematic reviews. The American Dental Association recently developed a web-based Center or Evidence-Based Dentistry (http://ebd.ada.org). 4. Systematic Reviews in Evidence-Based Journals a. Evidence-based journals publish summaries o valid research studies to simpli y the evidence-based process or dental healthcare providers. b. For example, The Journal o Evidence-Based Dental Practice scans the top dental journals and a panel reviews the selected articles or clinical relevance to practice. c. O ther examples o evidence-based journals include Evidence-Based Dentistry, Evidence-Based M edicine, Evidence-Based H ealthcare, and Evidence-Based N ursing. 5. Appraisal o the Evidence or Clinical Applicability. In medicine, the use o point-o -care electronic databases and algorithms are emerging to help practitioners evaluate and implement evidence-based decision making (11). a. The use o electronic records is integral to this process as it allows individual patient characteristics to be automatically linked to the best evidence (1). b. Table 21-1 outlines preappraised evidence resources including interactive drug databases that are a key part o clinical care decision support systems (11). 3. Using the PICO Process to Find Clinically Relevant In ormation. Figure 21-4 shows how the PICO process can be incorporated in a three-step approach to nding clinically relevant in ormation.

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Fig re 21-4. Strate g fo r Fi di g Cli icall Re le a t E ide ce . The Center or Evidence-Based Medicine recommends a straight orward approach based on (1) ormulating a PICO question, (2) searching evaluated (secondary) resources, and (3) then examining primary text documents.

Cl in iCa l Ca s e e x a m p l e A dental hygienist used the ollowing steps to nd evidence-based clinically relevant in ormation. 1. Step 1: Formulate a PICO Q uestion • Patient: adult em ale patient w ith chronic periodontitis; new patient in the dental o f ce • Intervention: periodontal instrum entation • Comparison: ull-m outh disin ection versus quadrant instrum entation • O utcome: resolution o in am m ation • Q uestion: For a patient w ith chronic periodontitis, w ill ull-m outh disin ection O R quadrant instrum entation provide a better reduction in in am m ation? 2. Step 2: Search O nline Evidence-Based Sources a. ADA Center or Evidence-Based Dentistry at http://ebd.ada.org b. PubM ed at http://pubmed.gov 3. The results o the search suggest that both the traditional quadrant approach and the newer the ull-mouth debridement could be equally e ective (Box 21-3). 4. In this instance, the dental hygienist presented both options to the patient, explaining that both treatment options are equally e ective. 5. The patient chose ull-mouth debridement because it would be less disruptive or her to be away rom work or 1 day rather than our shorter appointments over a period o several weeks.

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s c id n if d 216 b s c s. r vi w o s b s c s su l d in 12 u b lic io n s o il d vi w. Fin lly, s v n n d o m iz d co n o ll d i ls (r Ct s) w ic m ci i o lig ib ili y w in d n d n ly s l c d b y w o vi w u o s. No n o s u d i s in clu d d o d o n o o lo ss. a ll m n m o d li i s l d o sig n if c n im o v m n s in clin ic l m s o llo w -u o l s 3 m o n s. Fo s co n d y o u co m , d u c io n in obing d , m n di nc b w n ull-mou disin c ion nd con ol w s 0.53 mm (95% co n f d n c in v l (CI) 0.28 o 0.77) in m o d ly d o ck s o sin g l - o o d n d o g in in o b in g c m n 0.33 m m (95% CI 0.04 o 0.63) in m o d ly d sin g l - n d m u l i o o d . Co m in g FMD n d FMS, m n di n c in o n s u d y o g in in o b in g c m n m o u n d o 0.74 m m in vo o FMS (95% CI 0.17 o 1.31) o d o ck s in m u l i o o d , w il n o s udy o d m n di nc o d u c io n in b l d in g o n o b in g o 18% in vo o FMD (95% CI −34.30 o −1.70) o d o ck s o sin g l - o o d . No sig n if c n d i nc s w obs v d o ny o o u co m m su s, w n co m in g u ll-m o u d isin c io n n d co n o l.

A tho rs’ Co cl sio s In i n s w i c o n ic io d o n i is in m o d ly d o ck s slig ly m o vo b l o u co m s o o ck d u c io n n d g in in o b in g c m n w o u n d o llo w in g u llm o u d isin c io n co m d o co n o l. h o w v , s d d i io n l im o v m n s w o n ly mod s nd w o n ly v y lim i d n u m b o s u d i s v il b l o co m iso n , u s lim i in g g n l co n clu sio n s b o u clin ic l b n f o u ll-m o u d isin c io n .

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4

Life lo g Le ar i g Skills fo r Be st Practice O ne o the most challenging but important aspects o getting to best practices involves sel -evaluation. Practitioners continually need to think about whether the care they are providing is still the best level care. There are several questions a dental hygienist should think about on a regular basis. 1. How sure am I that what I do is right? A. Do I know where to access systematic reviews? Do I keep up with journal reading? 1. Peer-Reviewed Journals. Peer-reviewed journals (also called re ereed journals) use a panel o experts to review research articles or study design, statistics, and conclusions. Peer-reviewed journals: a. Are good sources or randomized clinical trials, and learning about new research ndings. Sometimes will publish systematic reviews. b. M ay be expensive to purchase a subscription; some highly ranked peerreviewed journals rom pro essional associations have begun to allow ree access to ull studies 6 months a ter publication. c. Are a good source o higher levels o evidence—systematic reviews and randomized clinical trials. 2. Practice or Trade M agazines a. Can be commercial in nature b. M ay or may not be peer reviewed; generally provide more o the “ expert” opinion c. M ay or may not be supported with re erences d. Vary widely in quality e. Provide the lowest quality o evidence 3. Textbooks a. Provide a broad overview o a subject b. M ay not provide speci cs on the research c. M ay be dated because o the amount o time involved in writing and publishing a textbook; always check the publication date B. Do I attend continuing education courses? How do I decide which courses to attend? 1. Content: Is the subject matter something you like or something that you need? It is important to take the time to evaluate learning/practice needs. Con erring with coworkers or your employer can acilitate more objective choices. 2. Speaker: Is he or she an expert, a acilitator, or both? A well-rounded speaker will provide in ormation on the latest research ndings along with providing some practical advice based on experience. 3. O utcomes: A well-rounded continuing education course will do three things (14): a. Rea rm: The course in ormation provides support or your current ways o providing treatment. b. Reenergize: The course supports changes in areas that you have previously identi ed and provides the motivation and impetus to begin making those changes. c. Reexamine: The course addresses new research ndings that merit urther study and investigation as to the appropriateness o incorporation into practice. C. Am I active in my pro essional association? 1. N etworking with colleagues exposes dental hygienists to other practicing pro essionals who can provide guidance and mentoring to younger members.

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2. M embership in a pro essional organization can provide ree access to peer-reviewed journals. 3. Active membership provides the opportunity to help shape evidence-based policies and guidelines or the organization. 4. Provides immediate access to any Clinical Practice Guidelines the association may develop. How well developed is my clinical judgment? Am I able to combine evidence and clinical experience to make a good decision? Do I take into consideration what my patient wants? 1. Do I listen to my patients? 2. Do I provide them with enough in ormation and direction to make a good decision? 3. Do I respect their autonomy and choices? Are there things that I should stop doing? 1. Am I holding on to what I do because “ that’s what I learned in school” even though it was several years ago? 2. Is what I am doing making the best use o o ce and patient resources, both nancial and human? Are there things I need to change? 1. Are there better, more e cient, or cost-e ective tools available such as speci c diagnostic tests, treatments, adjunctive therapies, medications, products, or procedures than what I am currently using? 2. Do I have the appropriate amount o time scheduled or equipment provided or the highest level o patient care?

Chapte r S mmar State me t Best practice is a process o care with the goal o achieving consistent, superior patient outcomes. Best practice is ounded on evidence-based data. The highest ranked level o evidence today is the systematic review, an evaluation o a body o research on a treatment or device through rigorous scienti c methods to determine the overall validity and clinical applicability o that treatment or device. In addition to scienti c data, best practice incorporates sound clinical judgment and patient values into the process. Achieving best practice requires that dental hygienists question and think about what they are doing and be open to learning new techniques. By using this approach to periodontal care, hygienists can meet the challenges o continuing to provide quality care in a rapidly changing eld o dental health care.

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Patie ts

Cli ical Patie t Care CA S E 1 You have just started working in a new o ce and nd that the other dental hygienist in the practice, Debbie, “ doesn’t believe” in using the ultrasonic equipment. Debbie states she has been practicing or 20 years, that is what she learned in school and she knows what she sees, good results with hand scaling. It is a little intimidating since you have less experience (only 5 years) but have routinely used ultrasonic instruments and mention to her “ that is what you learned in school.” For a while you pass it o as no big deal, a di erence o opinions, but because Debbie didn’t use the ultrasonic equipment, the equipment in the o ce is old and doesn’t unction at the level it should. You speak to your employer about getting a new machine, but he said, “ Debbie doesn’t use it, why do you?” 1. 2. 3. 4. 5.

H ow would you answer your employer? What types o evidence would you try to locate to justi y your position? Where would you search? What types o key words would you use? H ow would you manage your conf ict with Debbie?

CA S E 2 Your patient, M s. Karen Jones, is a healthy, nonsmoking 30-year-old. H er only medication is birth control pills o 5 years duration, and a daily multivitamin. She has been coming in or regular maintenance every 6 months. She brushes two times per day and f osses when she remembers, perhaps once a week and she states she nds the procedure di cult. The exam shows some 4-mm probing depths and signi cant bleeding. As you have done several times in the past, you show the patient how to use the manual brush and f oss and really “ lay it on the line” about improving oral health and warn her she will need to come in more requently i her habits do not improve. The patient states that “ she tries” and is visibly upset when she leaves o ce. While you hate to see her upset, you hope she nally got the message. About a month a ter her visit, you get a message that Karen Jones would like you call her. When you reach Karen, she tells you she has been “researching” her gum problem, and she has ound out she has several alternatives to a manual toothbrush and f oss. Karen reports she has looked on the Internet and talked to a relative who is also a dental hygienist. She has learned about automatic toothbrushes, automatic f ossing devices, and oral irrigators, and how they could help her. In act, she has purchased one o everything and eels her mouth is improving. Not only that, the power-f ossing device makes the task so much easier. “ Why didn’t you tell me about this!” she demands. “I am unhappy, and going to have my records trans erred elsewhere!” 1. What are some o the reasons the dental hygienist may have or not telling Karen about these products? 2. Ethically, is not telling a patient about all sel -care products that have evidence to support their use the same as not telling a patient about all available pro essional treatment options? Why or why not? 3. What steps could the dental hygienist take to improve her knowledge on sel -care products?

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Ethical Dile mma You have been working as a hygienist in the same periodontal practice or the last 10 years and are quite happy there. There are our dentists in the group, so you have a very ull schedule, which allows you to work 4 10-hour days. The practice is very f exible and generous with their resources and bene ts. They pay or continuing education courses or all sta members. Un ortunately, you haven’t taken any courses since you have worked there, even though you know you are in violation o your state practice act. You have been very busy in your personal li e over the last number o years, as you got engaged, married, had two children within the span o 2 years, and are now caring or your aging parents. You just can’t squeeze anything else into your li e. Your next patient Richie G, is a 63-year-old real estate agent, who was re erred to your practice or a periodontal evaluation 3 months ago. Richie comes armed with questions, articles, and in ormation that he has downloaded rom the Internet. Although Dr. Willis, the periodontist, suggested periodontal surgery or Richie’s treatment, Richie is inquiring about laser procedures as well as bone and tissue regeneration. H e asks or your opinion on the articles and studies he has in hand, and i you think there are superior options to “ gum surgery.” While you want Richie to be a partner in the decision about his periodontal care, you eel very uncom ortable discussing this with him. You know you are not current in your dental knowledge, and do not know how to accurately interpret the literature Richie presents to you. Un ortunately, you have not updated or adapted your own treatment strategies, and still rely on what you learned in school over 10 years ago. 1. What ethical principles are in conf ict in this dilemma? 2. What is the best way or you to handle this ethical dilemma?

Re fe re ce s 1. H art ord Center or Geriatric N ursing Excellence. Best practices or healthcare pro essionals. Available online at: http://www. nursing.uiowa.edu/hart ord/best-practices- or-healthcare-pro essionals. 2. Alston C, Paget L, H alvorson G, et al. Com m unicating w ith Patients on H ealth Care Evidence. Washington, DC: Institute o M edicine; 2012. Available online at: http://www.iom.edu/evidence. 3. Bhopal R. Causes in epidemiology: the jewels in the public health crown. J Public H ealth (O x ). 2008;30(3):224–225; discussion 32–33. 4. Brunette DM . Causation, association and oral health–systemic disease connections. In: Glick M , ed. T he O ral-System ic H ealth Connection: A G uide to Patient Care. Chicago, IL: Q uintessence Publishing Co.; 2014:312. 5. American Dental H ygienists’ Association. A D H A Policy M anual. 2013. Available online at: http://www.adha.org/ resources-docs/7614_Policy_M anual.pd . 6. Building a business case or evidence-based medicine. J Evid Based D ent Pract. 2013;13(2):74–76. 7. Asadoorian J, H earson B, Satyanarayana S, et al. Evidence-based practice in healthcare: an exploratory cross-discipline comparison o enhancers and barriers. J H ealthc Q ual. 2010;32(3):15–22. 8. Forrest JL, Drury TE, H orowitz AM . U.S. dental hygienists’ knowledge and opinions related to providing oral cancer examinations. J Cancer Educ. 2001;16(3):150–156. 9. Forrest JL, H orowitz AM , Shmuely Y. Caries preventive knowledge and practices among dental hygienists. J D ent H yg. 2000;74(3):183–195. 10. Forrest JL, H orowitz AM , Shmuely Y. Dental hygienists’ knowledge, opinions, and practices related to oral and pharyngeal cancer risk assessment. J D ent H yg. 2001;75(4):271–281. 11. Forrest JL, O verman P. Keeping current: a commitment to patient care excellence through evidence based practice. J D ent H yg. 2013;87(Suppl 1):33–40. 12. Forrest JL. Evidence-based decision making: Introduction and ormulating good clinical questions. 2012. Available online at: http://www.dentalcare.com/en-US/dental-education/continuing-education/ce311/ce311.aspx?M oduleN ame= introduction& PartID=−1& SectionID=−1. Accessed April 30, 2014. 13. Prato GP, Pagliaro U, Buti J, et al. Evaluation o the literature: evidence assessment tools or clinicians. J Evid Based D ent Pract. 2013;13(4):130–141. 14. Jahn CA. Product ocus: continuing education. A ccess. 2008;22:30–32.

STu DEn T An CILLARy RESOu RCES A wide variety o resources to enhance your learning and understanding o this chapter are available on .

r e t p a h C

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Understanding Nonsurgical Periodontal Therapy Nonsurgical Therapy Related to the Periodontal Diagnosis Goals o Nonsurgical Periodontal Therapy Types o Procedures Included in Nonsurgical Therapy Typical Treatment Plans or Nonsurgical Periodontal Therapy

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Overview o Instrumentation in Nonsurgical Therapy End Point or Instrumentation During Nonsurgical Therapy Dentinal Hypersensitivity Associated with Nonsurgical Therapy

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The Reevaluation Appointment Options or Treatment Following Reevaluation How Reevaluation o Nonsurgical Therapy Relates to other Steps in Treatment The Relationship Between Nonsurgical Therapy and Periodontal Surgery

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Clinical Patient Care Ethical Dilemma

Clinical Applicatio n.

Treating patients with periodontal diseases is a dynamic process that requires constant monitoring and reorientation o ongoing therapy. Periodontal therapy is o ten divided into phases and one o the f rst phases o therapy ollowing comprehensive periodontal assessment is the nonsurgical therapy phase. Members o the dental team need to have a clear understanding o the importance o nonsurgical periodontal therapy and the decisions that are required ollowing this therapy. This chapter provides an overview o nonsurgical periodontal therapy, discusses some o the problems that can arise during this therapy and outlines the decisions needed ollowing reevaluation o the nonsurgical therapy.

L arning Obj ctiv s • Explain the term and name our goals or nonsurgical periodontal therapy. • Write a typical plan or nonsurgical therapy or (1) a patient with plaque-induced gingivitis and (2) a patient with slight chronic periodontitis. • Describe the type o healing to be expected ollowing instrumentation o root sur aces.

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• Explain strategies or managing dental hypersensitivity during nonsurgical therapy. • Explain why reevaluation is an important step during nonsurgical therapy. • List steps in an appointment or reevaluation o the results o nonsurgical therapy.

K

T rms

Nonsurgical periodontal therapy Periodontal instrumentation Long junctional epithelium

Dentinal hypersensitivity Dentinal tubules Odontoblastic process Smear layer

Reevaluation Nonresponsive disease sites

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o f No ns rg ical P rio do ntal Th rap

Un d e r s t a n d in g n o n s Ur g ic a l Pe r io d o n t a l t h e r a Py 1. N onsurgical Periodontal Therapy Def ned A. N onsurgical periodontal therapy is a term used to describe the many nonsurgical steps used to eliminate in ammation in the periodontium o a patient with periodontal disease in an attempt to return the periodontium to a healthy state that can then be maintained by a combination o both pro essional care and patient sel -care. 1. M any terms have been used to describe nonsurgical periodontal therapy, and this act may create some con usion. Some o the other terms that have been used to describe this same phase o treatment include initial periodontal therapy, initial therapy, hygienic phase, anti-in ective phase, cause-related therapy, phase I treatment, and so t tissue management. 2. N onsurgical periodontal therapy, however, is one o the most requently used terms or this phase o periodontal care. 3. It is convenient to view nonsurgical periodontal procedures as the initial step in the periodontal treatment or a patient, but or many patients this initial step is all that is needed to bring periodontal disease under control. B. Philosophy or N onsurgical Periodontal Therapy 1. The basic philosophy or developing a sensible plan or nonsurgical periodontal therapy should be to plan treatment that will provide or the control, elimination, or minimization o (1) primary etiologic actors or periodontal disease, (2) local risk actors or periodontal disease, and (3) systemic risk actors or periodontal disease. 2. Procedures included in a plan or nonsurgical periodontal therapy should be selected to meet the needs o each individual patient; there ore, nonsurgical therapy plans can vary rom patient to patient.

n o n s Ur g ic a l t h e r a Py r e l a t e d t o t h e Pe r io d o n t a l d ia g n o s is N onsurgical periodontal therapy is indicated or many patients but not all patients. It may be help ul to view some common periodontal diagnoses and to see how nonsurgical periodontal therapy normally relates to these diagnoses. 1. A Diagnosis o Plaque-Induced Gingivitis A. N onsurgical periodontal therapy is the primary type o care provided or most patients with plaque-induced gingivitis. B. Thorough nonsurgical therapy can normally bring plaque-induced gingivitis under control and bring it to a point that periodontal health can be maintained by a combination o both pro essional care and patient sel -care. C. This general relationship between nonsurgical therapy and a diagnosis o plaque-induced gingivitis should not be interpreted to mean that patients with this diagnosis never need periodontal surgery, since periodontal surgery is sometimes needed to correct other existing problems (i.e., gingival recession or gingival overgrowth) in gingivitis patients.

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2. A Diagnosis o Slight to Moderate Chronic Periodontitis A. Thorough nonsurgical therapy can also bring many cases o slight to moderate chronic periodontitis under control and bring it to a point that periodontal health can be maintained by a combination o both pro essional care and patient sel -care (1–4). B. It should be noted that some patients with a diagnosis o moderate chronic periodontitis will require periodontal surgery to correct damage done by the disease (i.e., urcation involvement or attachment loss) (5). C. It should also be noted that periodontal surgery is sometimes used to correct other problems (i.e., gingival recession) and may indeed be indicated in any patient. 3. A Diagnosis o Severe Chronic Periodontitis A. For most patients with more advanced periodontal disease, such as severe chronic periodontitis, control o the periodontitis will not only require thorough nonsurgical periodontal therapy, but it will also require more advanced periodontal procedures such as periodontal surgery. B. Although periodontal surgery is requently indicated or patients with more advanced periodontitis, it should be understood that most patients with chronic periodontitis can benef t rom undergoing nonsurgical therapy prior to periodontal surgical intervention. C. N onsurgical periodontal therapy is requently success ul in minimizing the extent o any surgery subsequently needed and may be needed to improve the outcomes o that periodontal surgery. 4. A Diagnosis o One o the Other Forms o Periodontitis A. M embers o the dental team should be aware that nonsurgical periodontal therapy may not be the treatment o choice or all patients with other types o periodontitis. B. For example, nonsurgical periodontal therapy is not necessarily the best therapy or patients with other types o periodontitis, such as aggressive periodontitis.

g o a l s o f n o n s Ur g ic a l Pe r io d o n t a l t h e r a Py The goals o nonsurgical periodontal therapy are discussed below and summarized in Box 22-1. 1. Goal 1: To minimize the bacterial challenge to the patient A. Control o the bacterial challenge usually involves intensive training o the patient in appropriate techniques or sel -care in combination with requent pro essional care or the removal o calculus deposits and bacterial products rom tooth sur aces (6). B. Removal o calculus deposits and bacterial products contaminating the tooth sur aces is an important step in achieving control o the bacterial challenge. Calculus deposits are always covered with living bacterial biof lms that are associated with continuing in ammation i not removed (7). 2. Goal 2: To eliminate or control local contributing actors or periodontal disease A. Local contributing actors can increase the risk o developing periodontitis in localized sites. For example, de ective restorations with overhangs can lead to plaque biof lm retention in a localized area. Local contributing actors are discussed in Chapter 16. B. Biof lm retention at a site over time allows periodontal pathogens to live, multiply, and lead to damage o the periodontium. C. A thorough plan or nonsurgical periodontal therapy will always include minimizing the impact o local environmental contributing actors.

Chapt r 22

Nonsurgical Periodontal Therapy

3. Goal 3: To minimize the impact o systemic actors or periodontal disease A. It is apparent that there are certain systemic diseases or conditions that can increase the risk o developing periodontitis or can increase the risk o developing more severe periodontitis where periodontitis already exists. Two examples o systemic actors are uncontrolled diabetes mellitus and smoking. Systemic actors are discussed in Chapter 15 o this book. B. A thorough plan or nonsurgical therapy always includes measures to minimize the impact o systemic risk actors. For example, a periodontitis patient with a amily history o diabetes mellitus should be evaluated to rule out undiagnosed diabetes as a contributing systemic actor to the periodontitis. This medical evaluation should occur as part o the nonsurgical periodontal therapy. Another example would be that a patient who smokes should receive smoking cessation counseling. 4. Goal 4: To stabilize the attachment level A. The ultimate goal o nonsurgical periodontal therapy in chronic periodontitis patients is to stabilize the level o attachment by eliminating in ammation in the periodontium. B. Stabilization o the attachment level by eliminating in ammation involves control o all o the actors listed in the other goals o nonsurgical periodontal therapy.

Bo x 22-1. Go als o f No ns rg ical P rio do ntal Th rap Go al 1: t o Go al 2: t o Go al 3: t o Go al 4: t o

m in im iz lim in m in im iz s b iliz

b c i l c ll n g o i n o co n o l lo c l n vi o n m n l isk c o s o io d o n l d is im c o sys m ic isk c o s o io d o n l d is s c m n l v l b y lim in in g in m m io n

s

t y Pe s o f Pr o c e d Ur e s in c l Ud e d in n o n s Ur g ic a l t h e r a Py Box 22-2 lists o some o the nonsurgical therapy procedures that the dental team may utilize or patients. The list o procedures that may be included in nonsurgical therapy is lengthy, but it should be evident that while some o the procedures are included in the treatment o all patients, other procedures are utilized only rarely. Since each patient presents unique treatment challenges, members o the dental team will need to customize the selection o the nonsurgical procedures included or each individual. 1. Customized Sel -Care Instructions. O ne important aspect o nonsurgical periodontal therapy is e ective daily sel -care by the patient. Thus, patients need to be taught sel -care skills and also be motivated to use those skills. These important topics are discussed in Chapters 23, 24, and 25. 2. Instrumentation o Tooth Sur aces. Periodontal instrumentation is always an important component o nonsurgical periodontal therapy. The thoroughness o the per ormance o this step can determine the overall success o nonsurgical periodontal therapy in most patients. 3. Use o antimicrobial agents. A variety o antimicrobial agents are available in the orm o irrigation solutions and gel applications. Antimicrobial agents are discussed in Chapter 25. 4. Correction o Local Contributing Factors. Correction o local contributing actors such as overhanging margins on restorations or control o ood impaction is a critical component o nonsurgical periodontal therapy in many patients. Local contributing actors are discussed in Chapter 16.

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5. Correction o Systemic Risk Factors. Correction o systemic risk actors such as undiagnosed diabetes is also a critical component o nonsurgical periodontal therapy in some patients. This component o ten demands care ul coordination o care with other healthcare providers such as physicians. Systemic risk actors are discussed in Chapter 15. 6. Modulation o Host De enses. When indicated, modulation o host de enses can also be a component o nonsurgical periodontal therapy. M odulation o host de enses is discussed in Chapter 26.

Bo x 22-2. Pro c d r s that Ma b Incl d d in No ns rg ical P rio do ntal Th rap 1. Cu s o m iz d s l -c in s u c io n s in clu d in g a. M c n ic l l q u b io f lm co n o l b. C m ic l l q u b io f lm co n o l 2. p io d o n l in s u m n io n o o o su c s 3. Us o n im ic o b i l g n s 4. Co c io n o lo c l co n ib u in g c o s 5. Co c io n o sys m ic isk c o s 6. Mo d u l io n o o s d ns s

t y Pic a l t r e a t m e n t Pl a n s f o r n o n s Ur g ic a l Pe r io d o n t a l t h e r a Py A treatment plan or nonsurgical therapy is a list o nonsurgical procedures or interventions that addresses a patient’s periodontal health needs as identif ed during the periodontal assessment. Although it is critical or a treatment plan or nonsurgical therapy to meet the needs o each individual patient, beginning clinicians o ten f nd it help ul to view examples o typical treatment plans. A properly designed treatment plan or nonsurgical periodontal therapy could include procedures to be carried out by the dental hygienist, by the dentist, or by the patient. 1. Examples o Typical Treatment Plans A. Plaque-Induced Gingivitis. A typical plan or nonsurgical therapy or a patient with moderate plaque-induced gingivitis might include the ollowing: 1. Customized sel -care instructions including patient education and motivation. 2. Periodontal instrumentation (typically a dental prophylaxis in American Dental Association terminology). 3. Elimination o plaque-retentive actors such as overhanging restorations, caries, or ill-f tting dental prostheses. 4. Reevaluation o the patient’s periodontal status. a. Response to nonsurgical therapy is normally delayed, since it takes some time or the body’s de ense mechanisms to respond to individual treatment steps. b. Because o this delay time in healing, the dental team is obligated to reevaluate the results o nonsurgical periodontal therapy a ter a period o healing to ensure that all appropriate measures have been included and to identi y any other measures that might be needed.

Chapt r 22

Nonsurgical Periodontal Therapy

c. It is wise or the dental team to include this reevaluation step in the plan or nonsurgical therapy, so that the patient has a clear understanding rom the outset how uture treatment decisions will be made. B. Slight to Moderate Chronic Periodontitis. As already discussed, it is always important to customize the nonsurgical therapy or the needs o each patient, but again it may be help ul to look at a typical nonsurgical plan or a patient with slight to moderate chronic periodontitis. This typical plan might include the ollowing: 1. Customized sel -care instructions including patient education and motivation. 2. Periodontal instrumentation (typically scaling and root planing in American Dental Association terminology). 3. Control o local risk actors to include steps such as removal o overhanging restorations, restoration o caries, or minimizing excessive occlusal orces. 4. Correction o systemic risk actors to include steps such as smoking cessation counseling or re erral or control o diabetes. 5. Reevaluation o patient’s periodontal status. C. Severe Chronic Periodontitis. M ost patients with severe chronic periodontitis can include complicating actors such as advanced attachment loss, deep probing depths, advanced alveolar bone loss, urcation involvements, or mucogingival problems that require some more advanced treatment procedures later in therapy. 1. A typical treatment plan or nonsurgical therapy or a patient with severe chronic periodontitis would look much like a treatment plan or a patient with moderate periodontitis. 2. Periodontal surgery would not normally be part o a plan or the nonsurgical periodontal therapy, but the dental team would be wise to document the possible need or this more advanced treatment and in orm the patient when the need or such treatment appears likely. This can avoid con usion on the part o the patient later in the therapy. a. The members o the dental team should be aware o the possible need or periodontal surgical intervention in patients with more advanced periodontitis. b. As the severity o periodontitis increases, it becomes more likely that some periodontal surgery will be needed to bring the disease under control. c. The need or periodontal surgical therapy should be reevaluated a ter the completion o nonsurgical periodontal therapy. Surgical periodontal therapy is discussed in Chapter 27.

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S ct io n 2

Instr m ntatio n D ring No ns rg ical Th rap o v e r v ie w o f in s t r Um e n t a t io n in n o n s Ur g ic a l t h e r a Py 1. Objective o Periodontal Instrumentation During N onsurgical Therapy A. The objective o the mechanical removal o calculus and plaque biof lm is the physical removal o microorganisms and their products to prevent and treat periodontal in ections. 1. Because o the structure o biof lms, physical removal o plaque biof lm is the most e ective mechanism o control, though chemical agents are sometimes used to improve the patient response to these procedures. 2. M ost subgingival biof lm within pockets cannot be reached by brushes, oss, or antibacterial rinses. a. For this reason, requent periodontal instrumentation o subgingival root sur aces to remove or disrupt plaque biof lms mechanically is an essential component o the treatment o most patients with periodontitis. b. In act, periodontal instrumentation is likely to remain an important component o nonsurgical periodontal therapy or the oreseeable uture. B. Removal o deposits rom tooth sur aces is a critical component in any plan or nonsurgical periodontal therapy. 1. Calculus deposits harbor living bacterial biof lms; thus, i the calculus remains, so do the bacteria, making it impossible to reestablish periodontal health. 2. Calculus removal is always a undamental part o nonsurgical periodontal therapy. 2. Evolving Instrumentation Terminology. There has been some evolution in the terminology associated with dental calculus and biof lm removal over the past years. The care ul reader will be wise to note the terminology that appears in many dental hygiene journals and textbooks compared to the terminology in dental journals and textbooks. The di erences in this terminology are described below. A. Traditional Instrumentation Terminology 1. Scaling is instrumentation o the crown and root sur aces o the teeth to remove plaque biof lm, calculus, etc. 2. A dental prophylaxis includes scaling and polishing procedures to remove coronal plaque biof lm, calculus, and stains. This procedure usually is used or healthy patients and patients with gingivitis. 3. Root planing is a treatment procedure designed to remove cementum or sur ace dentin that is rough, impregnated with calculus, or contaminated with toxins or microorganisms. Root planing is a undamental treatment procedure or patients with chronic periodontitis. a. As traditionally described, root planing involves the routine, intentional removal o cementum and the instrumenting o all root sur aces to a glassy smooth texture. b. At one time it was thought that bacterial products were f rmly held in cemental sur aces exposed by attachment loss occurring as a result o periodontitis. It was believed that vigorous root planing with intentional removal o most cementum was always needed to ensure the removal o all calculus as well as all bacterial products rom the root sur aces. c. It is now understood that vigorous root planing is not universally needed to reestablish periodontal health in all sites o periodontitis. Rather than vigorous root planing and removal o most or all o the cementum, it is now known that the bacterial products can be removed rom the root sur aces with a minimal amount o deliberate cementum removal.

Chapt r 22

Nonsurgical Periodontal Therapy

B. Emerging Instrumentation Terminology 1. Recently in the dental hygiene literature, increasing numbers o authors are using new terminology that re ects modern therapy better than the traditional terminology. The term “ periodontal instrumentation” or “ periodontal debridement” is suggested to replace the older terms “ dental prophylaxis,” “ scaling,” and “ root planning.” 2. Periodontal instrumentation (periodontal debridement) is def ned as the removal or disruption o plaque biof lm, its by-products, and biof lm-retentive calculus deposits rom coronal tooth sur aces and tooth root sur aces to the extent needed to reestablish periodontal health and restore a balance between the bacterial ora and the host’s immune responses. 3. Periodontal instrumentation includes instrumentation o every square millimeter o root sur ace or removal o plaque biof lm and calculus but does not include the deliberate, aggressive removal o cementum. a. Conservation o cementum is one goal o periodontal instrumentation. It is currently believed that conservation o cementum enhances periodontal healing in the orm o either repair or regeneration. In periodontal health an important unction o cementum is to attach the periodontal ligament f bers to the root sur ace. During the healing process a ter disease, cementum is thought to contribute to repair o the periodontium. b. During periodontal instrumentation, the extent o instrumentation should be limited to that needed to obtain a avorable tissue response. Root sur aces should be instrumented only to a level that results in resolution o tissue in ammation in the periodontal tissues. C. Considerations Regarding Emerging Terminology and Insurance Codes 1. Insurance codes are numeric codes to identi y di erent dental procedures. The most important use o codes is or insurance billing purposes. Insurance codes are entered on insurance orms indicating the dental treatment listed by the appropriate procedure code number. In the United States, insurance codes are published in the A m erican D ental A ssociation Current D ental Term inology. These codes are very specif c and should be reviewed care ully be ore specif c dental treatment is coded. 2. The ADA Current Dental Terminology continues to use the traditional terms “ prophylaxis” and “ scaling and root planing” to describe periodontal instrumentation. This di erence in terminology can be con using to clinicians. a. Although the term periodontal instrumentation/debridement as def ned in the dental hygiene literature may describe modern periodontal therapy better than older terms, this terminology has not yet replaced the older terms as recognized by the ADA. For this reason, many dentists have been reluctant to embrace the new terminology without changes in ADA codes. b. Some authors and clinicians have redef ned the term “ root planing,” so that its meaning is similar to that o periodontal instrumentation/debridement. This approach o redef ning the term root planing can be con using, however, because it is di f cult to determine which def nition o “ root planing” any one person is using. c. At this time, dental team m em bers should use the currently accepted insurance codes w hen f lling out insurance orm s and in com m unications w ith insurance com panies or other third-party payers.

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e n d Po in t f o r in s t r Um e n t a t io n d Ur in g n o n s Ur g ic a l t h e r a Py The end point o periodontal instrumentation is to return the tissues o the periodontium to a state o health. In this context health means periodontal tissues that are ree o in ammation. 1. Healing Following N onsurgical Instrumentation A. A ter thorough periodontal instrumentation, some healing o the periodontal tissues will normally occur. 1. The primary type o healing in a site o attachment loss a ter periodontal instrumentation is through the ormation o a long junctional epithelium. a. As in ammation in the periodontium resolves, epithelial cells can readapt to the root sur ace as shown in Figure 22-1. b. This adaptation o the epithelial cells to the root sur ace is re erred to as a long junctional epithelium. 2. It is important to realize that ollowing periodontal instrumentation, there normally is no ormation o new alveolar bone, new cementum, or new periodontal ligament.

A

B En a m e l

De n t in 2 mm

C EJ Ce m e ntum 2 mm

G in g iva l m a rg in P o c ke t e p it h e liu m

2 mm P o c ke t C EJ 2 mm

P o c ke t 4 mm Ce m e ntum

4 mm 6 mm 8 mm P DL

Alve o la r c re s t Alve o la r b one

Lo n g ju n c t io n a l e p it h e liu m C o n n e c t ive t is s u e a tta c hme nt

6 mm 8 mm

Fig r 22-1. H aling aft r No ns rg ical P rio do ntal Instr m ntatio n. A: Be ore therapy, the periodontal pocket has a probing depth o 6 mm. B: A ter periodontal therapy the tissue healing is through the ormation o a long junctional epithelium. This results in a probing depth o 3 mm. Note that there is no ormation o new bone, cementum, or periodontal ligament during the healing process that occurs a ter periodontal instrumentation in this example.

B. Clinically, nonsurgical periodontal therapy, including instrumentation, may certainly result in reduced probing depths. Figure 22-2 shows examples o various so t tissue responses to thorough periodontal instrumentation. 1. The reduced probing depths result rom the ormation o a long junctional epithelium combined in many instances with resolution o gingival edema that is usually a part o the in ammatory process. Figure 22-3 shows how some o this reduction in probing depth can occur at the base o a periodontal pocket.

Chapt r 22

Nonsurgical Periodontal Therapy

379

2. Thus, one important clinical eature to monitor ollowing periodontal instrumentation in addition to clinical attachment loss is the probing depths. 3. It should be noted at this point that there are other clinical signs that can correlate with in ammation that can be expected to change ollowing periodontal instrumentation (i.e., bleeding on probing). 2. Assessing Tissue Healing. Tissue healing does not occur overnight, and in many patients it is not possible to assess the true tissue response or at least 1 month a ter the completion o periodontal instrumentation. Assessing tissue healing during and ollowing nonsurgical therapy is discussed in Section 3 o this chapter.

A

B

C

Fig r 22-2. So ft Tiss R spo ns s to Tho ro g h P rio do ntal Instr m ntatio n. This igure shows some o the possible tissue changes that can occur ollowing thorough periodontal debridement o a root sur ace. A: There can be complete resolution o the in lammation resulting in shrinkage o the tissue and a shallow probing depth. B: There can be readaptation o the tissues to the root sur ace orming a long junctional epithelium resulting in shallow probing depths. C: There can be very little change in the level o the so t tissues resulting in a residual periodontal pocket.

Reces s ion 0.8 mm Res idual depth 4.3 mm

Initial depth 6.5 mm

Probing attachment gain 1.4 mm

Be fo re the rapy

Afte r the rapy

Fig r 22-3. D tails o f H aling at th Bas o f a Po ck t Fo llo ing P rio do ntal Instr m ntatio n. Since the tip o a periodontal probe can easily penetrate in lamed so t tissue in the base o periodontal pocket, the probing depth can decrease a small amount ollowing instrumentation because the tissues at the base o the pocket can be much more resistant to accidental penetration by the probe. This igure also depicts slight gingival recession resulting rom resolution o in lammation in the tissue.

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d e n t in a l h y Pe r s e n s it iv it y a s s o c ia t e d w it h n o n s Ur g ic a l t h e r a Py Dentinal hypersensitivity as described in this section is not really a periodontal disease or a periodontal condition. However, dentinal hypersensitivity appears so requently during success ul nonsurgical periodontal therapy that clinicians need to be aware o this condition, need to understand its origin and need to understand therapies or the condition. 1. Description o Dental Hypersensitivity A. Dentinal hypersensitivity is a short, sharp, pain ul reaction that occurs when areas o exposed dentin are subjected to mechanical, thermal, or chemical stimuli. For example, an individual might experience sensitivity while brushing, when eating cold oods such as ice cream, or when eating sweet, sour, or acidic ood such as grape ruit. In some patients simply breathing in cold air while walking outside on a cold day can produce this pain ul reaction. B. Dentinal hypersensitivity is associated with exposed dentin. 1. Exposed dentin is dentin that is visible in the oral cavity due to the recession o the gingiva or to an absence o some tooth enamel due to damage to the tooth crown. 2. Dentin may be exposed in a small area or exposed in an extensive area o a tooth; small areas o exposed dentin can occasionally lead to severe pain. 3. Since gingival recession is a very common condition, it is ortunate that not all exposed dentin displays hypersensitivity. 2. Precipitating Factors or the Hypersensitivity A. As already stated, dentinal hypersensitivity is usually associated with gingival recession, though exposure o dentin can also result because o tooth racture or destruction o enamel. B. Resolution o in ammation in the periodontium ollowing success ul nonsurgical periodontal therapy in periodontitis patients requently results in gingival recession that is related to resolution o the in ammatory swelling o the gingiva. This exposure o small areas o the tooth roots can result in dentinal hypersensitivity. C. It is common or dentinal hypersensitivity to appear ollowing some types o periodontal surgical therapy, but sensitivity can also be associated with the nonsurgical periodontal therapy being discussed in this chapter. D. In the patient’s eyes the development o the tooth sensitivity could well appear to be simply a result o the nonsurgical treatment. In reality most o ten the sensitivity results rom areas where clinical attachment loss has previously occurred as a result o existing periodontitis. 3. Theory About the Origin o Hypersensitivity A. The origin o dentinal hypersensitivity is o ten explained by the hydrodynamic theory. Important elements o the hydrodynamic theory o dental hypersensitivity are outlined below. 1. The dentinal tubules penetrate the dentin like long, miniature tunnels extending throughout the thickness o the dentin. Figure 22-4 shows some details o these dentinal tubules. 2. The part o a dentinal tubule closest to the pulp normally contains an odontoblastic process, which is a thin tail o cytoplasm rom a cell in the tooth pulp called an odontoblast (Fig. 22-5). 3. The part o a dentinal tubule not f lled by an odontoblastic process is f lled by uids. Stimulation o the root sur ace may result in uid ow within the tubules which is theorized to activate the nerve endings near the pulp leading to a pain ul

Chapt r 22

Nonsurgical Periodontal Therapy

381

sensation experienced by the patient. The stimulation o the sur ace o the tooth root can arise rom mechanical, thermal, or chemical stimuli, as already mentioned. 4. When dentinal tubules are exposed slowly in the oral cavity (as seen in the development o most gingival recession), root sur aces can undergo a natural process o calcif cation or occlusion (blocking) o the open dentinal tubules; the sealing o the dentinal tubules in this natural process prevents sensitivity rom developing. Dentin with calcif ed tubules has been re erred to as sclerosed dentin. 5. In addition, slow exposure o a tooth root can allow or secondary dentin ormation within the pulp. Secondary dentin ormation can in e ect thicken the dentin layer. 6. The occlusion or blocking o dentinal tubules does not always occur, and sometimes the occlusion o the tubules occurs very slowly. B. Dentinal hypersensitivity may arise ollowing instrumentation during periodontal instrumentation. 1. It should be noted that most dentinal hypersensitivity resulting ollowing periodontal instrumentation is mild and resolves within a ew weeks i the ex posed root sur aces are k ept biof lm ree by thorough sel -care. 2. In its more severe orms, however, dentinal hypersensitivity can result in so much discom ort that it can prevent a patient rom per orming thorough sel -care. 3. It is ortunate that most commonly instrumentation o root sur aces does not result in the development o dentinal hypersensitivity. 4. Sensitivity may not occur in some instances because instrumentation o root sur aces can result in a smear layer o dentin that covers the root sur aces and blocks the tubules. 5. This so-called smear layer re ers to crystalline debris rom the tooth sur ace that covers or plugs the dentinal tubules during the instrumentation; this smear layer blocks the tubules, inhibits uid ow, and prevents the development o sensitivity.

Ena me l

De ntin De ntina l tub ule s Ce me ntum

A

B

Fig r 22-4. D ntinal T b l s. A: Diagram showing the numerous dentinal tubules that penetrate the dentin. B: A scanning electron micrograph o the cross section o dentinal tubules adjacent to the pulp chamber o a human tooth. The black line engraved in the lower right is 10 µm long. (Used by permission rom Mel i RC. Permar’s Oral Embryology and Microscopic Anatomy. 10th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000:120, Figure 5–8.)

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Od o nto b la s ts Ce ll b o d y

De ntin

Ce m e ntum

P ro c e s s

P u lp

Fig r 22-5. Odo nto blastic Pro c ss. The odontoblastic cell process in the dentinal tubule o ten ills the part o the dentinal tubule closest to the pulp but can extend arther rom the pulp toward the junction o the dentin with the enamel or cementum.

4. Strategies or Managing Patients with Dentinal Hypersensitivity There are a number o strategies that have been recommended or dealing with dentinal hypersensitivity. These strategies range rom simply allowing the open dentinal tubules to seal themselves to per orming periodontal surgery. Each o the strategies has proved success ul or some patients. A. Periodontal Instrumentation in Patients with Existing Dental Hypersensitivity 1. For teeth with existing dentinal hypersensitivity, instrumentation o hypersensitive root sur aces can result in eliciting the sharp pain during a clinical procedure such as periodontal instrumentation. 2. Since many patients have existing dentinal hypersensitivity, it is critical or dental hygienists to ask patients about hypersensitive teeth be ore attempting a clinical procedure such as periodontal instrumentation. 3. For patients with existing hypersensitivity, local anesthesia can be used to control any discom ort that might arise during thorough instrumentation. B. Patient Education—A Critical Element in Patient Management An appropriate strategy or managing patients undergoing nonsurgical periodontal therapy would include educating patients about the possibility o developing hypersensitivity ollowing the procedure. This warning should be given be ore beginning any treatment and should be part o the discussion preceding in ormed consent. It may be help ul to provide the patient with the ollowing acts be ore initiating instrumentation: 1. Sensitivity to cold can increase ollowing periodontal instrumentation. 2. I sensitivity resulting rom periodontal instrumentation occurs, it will usually gradually disappear over a ew weeks. 3. T horough daily plaque biof lm rem oval during sel -care is one o the m ost im portant actors in the prevention and control o sensitivity. It should be noted that without meticulous sel -care, treatments or dentinal hypersensitivity are usually not success ul. 4. I dentinal hypersensitivity becomes an ongoing problem, recommendations or in-home therapies can be made that can enhance its resolution, but immediate results should not be expected.

Chapt r 22

Nonsurgical Periodontal Therapy

C. Occluding Patent (Open) Dentinal Tubules with In-Home Therapies 1. O ne important strategy or managing patients with dentinal hypersensitivity involves applying chemicals to the exposed root sur ace that can help occlude (or block) the dentinal tubules. 2. The chemicals used to occlude the dentinal tubules o ten eliminate or minimize associated sensitivity. The mechanism o action o these chemicals has been reported to be precipitating minerals or precipitating proteins within open dentinal tubules resulting in sealing the openings o the tubules. 3. M any o these chemical agents are available in special ormulations o toothpastes, and there are a variety o toothpastes specif cally ormulated to aid in desensitizing teeth (8–12). M any chemical agents have been reported to help in some patients. Examples o some o the more common chemical agents in toothpaste ormulations or dentinal hypersensitivity are potassium nitrate, strontium chloride, sodium citrate, and uorides. Table 22-1 includes an overview o some o the chemical agents that have been investigated or control o hypersensitivity by blocking dentinal tubules. 4. The reported e f cacy o the chemical agents in controlling dentinal hypersensitivity varies, but this strategy remains the most commonly utilized treatment or this condition. D. Occluding Patent Tubules with In-O f ce Therapies 1. There are also pro essionally applied in-o f ce products that contain chemicals that also have been reported to decrease dentinal hypersensitivity. 2. A variety o chemical agents have been utilized in in-o f ce remedies or dentinal hypersensitivity. Examples o chemicals that have been reported to decrease hypersensitivity ollowing in-o f ce applications are potassium oxalate, erric oxalate, and uorides solutions, or uoride varnishes. 3. Note that Table 22-1 includes an overview o some o the chemical agents that have been investigated or control o hypersensitivity by blocking dentinal tubules. E. Desensitizing N erves Associated with the Tubules It has also been reported that applying certain chemicals to the root sur ace can block the nerve receptors in or near the tooth pulp rom activating the pain ul response. 1. The chemical agents that can be used to block the nerve receptors rom activating a pain ul response include potassium salts (such as potassium nitrate); potassium nitrate is the active ingredient ound in some desensitizing toothpastes and has been shown to be e ective in decreasing sensitivity in some patients. 2. It is thought that potassium depolarizes the nerve f bers associated with the odontoblastic processes, thus preventing pain signals rom traveling to the brain. F. Treating Exposed Dentin Sur aces with Lasers 1. Lasers have been used to treat exposed hypersensitive dentin sur aces with some success. 2. The mechanism o action o lasers in decreasing dentinal hypersensitivity is not clear at this point. G. Blocking Dentinal Tubules with Restorative Materials 1. O ne strategy or blocking some dentinal tubules is to cover the exposed dentin sur ace with a bonding agent—the same kinds o materials that can sometimes be used to restore caries. 2. Since the exposure o dentin at some sites can be associated with missing tooth structure resulting rom abrasion or erosion o the root sur ace, bonding a restorative material over that sur ace can not only block exposed dentinal tubules, it can also restore any missing tooth structure.

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3. Examples o restorative materials that have been used to block dentinal tubules include: oxalic acid and resin, glass ionomer cements, composites, and dentin bonding agents. H. Blocking Dentinal Tubules with a Periodontal Surgical Procedure 1. Another strategy or blocking the open dentinal tubules is to cover the root sur ace with a gingival gra ting material. 2. This approach can result in rebuilding the gingiva to a more natural level that covers an exposed tooth root, covering the dentinal tubules. I. Overview o Dentinal Hypersensitivity 1. Figure 22-6 illustrates the wide range o possibilities or dentinal tubules that become exposed in the oral cavity. 2. Figure 22-7 illustrates the various possibilities or dentinal tubules ollowing therapy. 3. Table 22-1 provides an overview o chemical agents that have been investigated or the control o dentinal hypersensitivity by occluding dentinal tubules.

1 Open tubules

2 Normal

3 Tubular s cleros is

4 Secondary dentin

Fig r 22-6. Th Vario s Po ssibiliti s fo r D ntinal T b l s B fo r Th rap and Fo llo ing Th rap . Dentinal tubules prior to therapy may be open, sclerosed, or insulated rom the pulp itsel by the ormation o secondary dentin.

1 Remaining cementum 2 Treated root s urface K+ K+ K+ K+ K+ K+

3 Potas s ium-containing dentifrice 4 Flouride-containing dentifrices or gel 5 Bonding and lling materials

Odontoblas t

6 Covering the root s urface by means of mucogingival s urgery

Fig r 22-7. Th Vario s Po ssibiliti s fo r D ntinal T b l s Fo llo ing Th rap . Chemicals can be used to occlude the dentinal tubules and to eliminate or minimize associated dentinal sensitivity.

Chapt r 22

Nonsurgical Periodontal Therapy

TABLe 2 2 -1 . OVe RVIe w OF AGe NTS THAT HAVe Be e N INVe STIGATe D FOR THe CONTROL OF Hy Pe RSe NSITIVITy By OCCLu DING De NTINAL Tu Bu Le S Ag nts that can pr cipitat pro t ins that can o ccl d t b l s • Glu • Silv

ld

yd

ni

• Zin c c lo id • S o n iu m c lo id Ag nts that can pr cipitat min rals that can o ccl d d ntinal t b l s • So d iu m lu o id • S n n o u s lu o id • S o n iu m c lo id • po

ssiu m o x l

• C lciu m

os

• C lciu m c b o n • a g in in • Bio c iv g l ss

S ct io n 3

D cisio ns Fo llo

ing No ns rg ical Th rap

t h e r e e v a l Ua t io n a PPo in t m e n t Reevaluation re ers to a ormal step a ter the completion o nonsurgical therapy. During the reevaluation appointment, the members o the dental team per orm another periodontal assessment to gather in ormation about the patient’s periodontal status. A ter comparison with the periodontal status at the time o the initial assessment, the team members make several critical clinical decisions regarding management o the patient’s periodontal condition. The reevaluation is described in detail below. 1. Timing o a Reevaluation A. Periodontal tissue healing does not occur immediately, and in most cases it is not possible to determine the true tissue response or at least 1 month a ter the completion o nonsurgical periodontal therapy. B. M embers o the dental team should usually schedule an appointment or a reevaluation o a chronic periodontitis patient 4 to 6 weeks a ter completion o nonsurgical therapy. 2. Understanding the Steps in a Reevaluation The steps in a typical reevaluation appointment usually include those listed below (Box 22-3). A. The f rst step in the reevaluation appointment is to do a medical status update or the patient. O course, this is the f rst step in any patient appointment. B. The second step is to per orm a thorough periodontal assessment; the nature o a periodontal assessment has already been described in Chapter 19.

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C. The third step is to do a comparison o the results o the patient’s initial periodontal assessment with the results o the patient’s reevaluation assessment. D. The ourth step is to make appropriate decisions related to the next steps in therapy. O ptions or treatment ollowing nonsurgical therapy are discussed in the next section.

Bo x 22-3. St ps in a T pical R 1. 2. 3. 4.

val atio n Appo intm nt

U d m d ic l s u s o i n . p o m io d o n l clin ic l ss ssm n . Co m in i i l io d o n l ss ssm n w i M k d cisio n s l d o n x s s in io d o n

v lu l

io n ss ssm n . y.

o Pt io n s f o r t r e a t m e n t f o l l o w in g r e e v a l Ua t io n 1. Managing N onresponsive Disease Sites. During the reevaluation, members o the dental team may identi y nonresponsive disease sites. A. N onresponsive disease sites are areas in the periodontium that show deeper probing depths, continuing loss o attachment, or continuing clinical signs o in ammation in spite o the nonsurgical therapy provided. B. N onresponsive sites should be care ully rechecked or thoroughness o sel -care and rechecked or the presence o residual calculus deposits. C. I plaque biof lm is discovered at a nonresponsive site, the site should be thoroughly deplaqued with an ultrasonic instrument (unless ultrasonic instrumentation is contraindicated or this patient), and the patient should receive additional sel -care motivation and training. D. I calculus is ound at a nonresponsive site, additional periodontal instrumentation should be per ormed. E. When nonresponsive sites are encountered, the members o the dental team should also consider the possibility that other actors might be contributing to the disease process (such as undiagnosed diabetes or smoking). F. In some patients, the nonresponsive disease sites may also require the use o antimicrobial agents. G. Some nonresponsive sites represent areas o more advanced destruction rom the disease process that will need more advanced care such as periodontal surgery. 2. Per orming Additional N onsurgical Therapy. It is common or the reevaluation step to indicate the need or additional nonsurgical periodontal therapy by the dental team, and there are several reasons or this. A. Sel -care e orts by the patient, though improved, may not be adequate or control o in ammation in the periodontium. B. Subgingival calculus deposits are di f cult to remove especially in the presence o in ammation resulting in edematous tissue. C. An unsuspected systemic condition may be contributing to the disease process. 3. Establishing a Program or Periodontal Maintenance A. Following appropriate treatment, all patients with periodontitis should be placed on a program o periodontal maintenance.

Chapte r 22

Nonsurgical Periodontal Therapy

387

B. Periodontal maintenance includes all measures used by the dental team and the patient to keep periodontitis under control; periodontal maintenance is discussed in Chapters 30 and 31. C. The goal o periodontal maintenance is to prevent the recurrence o periodontal diseases. 4. Recognizing the N eed for Periodontal Surgery A. The need or some types o periodontal surgery can o ten be determined at the time o the initial periodontal assessment. B. Periodontal surgery to control chronic periodontitis or to regenerate damaged periodontal tissues, however, is requently best identif ed at the time o the reevaluation; periodontal surgery and its indications are discussed in Chapter 27.

Ho w Re e v a l u a t io n o f n o n s u Rg ic a l t He Ra p y Re l a t e s t o o t He R s t e p s in t Re a t m e n t Figure 22-8 illustrates how reevaluation o nonsurgical periodontal therapy relates to the other steps in the overall management o a periodontal patient.

Clinic a l P e riod onta l As s e s s me nt to Es ta b lis h a P e riod onta l Dia gnos is

Nons urgic a l P e riod onta l The ra p y

Re e valuatio n o f No ns urg ic al Pe rio do ntal The rapy

P e riod onta l S urge ry Whe re Ne e d e d (P e rform or Re fe r)

Ad d itiona l Nons urgic a l The ra p y

Es ta b lis h a P rogra m of P e riod onta l Ma inte na nc e

Fig ure 22-8. Diag ram illustrating ho w re e valuatio n o f no nsurg ical pe rio do ntal the rapy re late s to o the r ste ps in the o ve rall manag e me nt o f a pe rio do ntal patie nt. Reevaluation of nonsurgical therapy would be performed following the therapy. Decisions made at the reevaluation will primarily involve additional nonsurgical therapy, periodontal surgery, and periodontal maintenance. Periodontal surgery and periodontal maintenance are discussed in Chapters 27, 30, and 31.

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t h e r e l a t io n s h iP Be t w e e n n o n s Ur g ic a l t h e r a Py a n d Pe r io d o n t a l s Ur g e r y Periodontal surgery can play an important role in therapy or certain patients, and this topic will be discussed in other chapters o this textbook. H owever, at the time o reevaluation members o the dental team should be aware o the general relationship between nonsurgical periodontal therapy and periodontal surgery and should be able to discuss the possible need or periodontal surgery with patients. 1. Indications or Surgical Therapy. As a general rule, periodontal surgery will be needed by patients with more advanced periodontal conditions. Table 22-2 shows an overview o the general relationship o nonsurgical periodontal therapy to surgical periodontal treatment or patients with various periodontal conditions. A. Patients with plaque-induced gingivitis. For most patients with plaque-induced gingivitis, the gingivitis can be controlled with nonsurgical therapy alone, and only rarely will periodontal surgery be a part o the treatment recommended. B. Patients with slight periodontitis. For most patients with slight (mild) chronic periodontitis, the periodontitis can be controlled with nonsurgical therapy alone, and only occasionally will periodontal surgery be a part o the treatment recommended. C. Patients with Moderate Chronic Periodontitis. For some patients with moderate periodontitis, the periodontitis can be controlled with nonsurgical therapy alone. For other patients with moderate chronic periodontitis, control o the periodontitis will require thorough nonsurgical periodontal therapy ollowed by periodontal surgery. D. Patients with Severe Chronic Periodontitis. For most patients with severe periodontitis, control o the periodontitis will require thorough nonsurgical periodontal therapy ollowed by periodontal surgery. 2. Exceptions. There will always be exceptions to the general guidelines described above. A. O ne example o an exception would be a patient with moderate plaque-induced gingivitis where the gingivitis has resulted in gingival enlargement. It is common or some types o gingival enlargement to require periodontal surgery to reshape the enlargement to improve aesthetics or to provide or improved access or e ective sel -care.

TABLe 2 2 -2 . INDICATIONS FOR NONSu RGICAL AND Su RGICAL THe RAPy Dis as Stat s

No ns rg ical Th rap

S rg ical Th rap

pl q u - sso ci

d g in g ivi is

a lw ys in d ic

d

Usu lly n o in d ic

d

io d o n i is

a lw ys in d ic

d

Usu lly n o in d ic

d

a lw ys in d ic

d

So m

d

a lw ys in d ic

d

Usu lly in d ic

Slig

c

Mo d S v

o n ic c

c

o n ic

o n ic

io d o n i is io d o n i is

im s in d ic d

Chapt r 22

Nonsurgical Periodontal Therapy

389

B. Another example o an exception to the guidelines would be a patient with slight chronic periodontitis accompanied by severe gingival recession on a tooth. Though surgery is not normally needed in patients with slight chronic periodontitis, periodontal surgery may well be needed to correct the gingival recession.

Chapt r S mmar Stat m nt N onsurgical periodontal therapy re ers to all the initial steps used by the dental team to bring gingivitis and periodontitis under control. The goals o nonsurgical periodontal therapy are to control the bacterial challenge to the patient, to minimize the impact o systemic risk actors, to eliminate or control local environmental risk actors, and to stabilize the attachment level. The precise steps included in nonsurgical periodontal therapy should depend on the specif c needs o each individual patient. A vital component o a plan or nonsurgical periodontal therapy is periodontal instrumentation. Biof lms are resistant to topical chemical control; there ore, mechanical periodontal instrumentation o subgingival root sur aces is an essential component o success ul nonsurgical periodontal therapy. Dentinal hypersensitivity may occur in some areas o exposed dentin. Thorough daily sel -care is the most important actor in the prevention and control o hypersensitivity, but some patients with dentinal hypersensitivity will need additional measures. Reevaluation is an important step in nonsurgical periodontal therapy. During reevaluation the dental team determines the patient’s need or additional nonsurgical therapy or periodontal surgery and establishes a program or periodontal maintenance.

S ct io n 4

Fo c s o n Pati nts Clinical Pati nt Car CA S e

1

A new patient or your dental team has obvious clinical signs o moderate chronic periodontitis with generalized plaque biof lm and dental calculus deposits. Though the patient denies having diabetes, the patient does report having several close amily members with this disease. M ake a list o steps your dental team might include in an appropriate plan or nonsurgical periodontal therapy or this new patient.

CA S e

2

At the time o reevaluation or a patient with a diagnosis o generalized moderate chronic periodontitis, your dental team identif es a ew sites o residual subgingival calculus deposits and documents totally ine ective patient sel -care. H ow should the members o your dental team manage the oral health needs o this patient?

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CA S e

Implementation o Therapy or Patients with Periodontal Disease

3

O ne o your patients who has been undergoing nonsurgical periodontal therapy seems a bit upset when he comes in another appointment. A ter being seated in your treatment room, he states that he gets a sharp pain in his teeth when he tries to eat his avorite desert, ice cream. H ow should you proceed based upon the patient’s complaint?

e thical Dil mma You are a retired librarian who just recently lost your husband. You grew up, went to college, married and raised a amily all in the same town in which you were born. You are ortunate to be surrounded by many amily members and long-time riends. You are currently a patient in Dr. J. Jay M ack’s periodontal practice, and have been or the last 15 or so years. You see Evelyn, the older o the two hygienists in the practice, every 3 months, and have so since you can remember. The only supplemental aids she has suggested that you use, in addition to toothbrushing, are “ tu ted oss and a tongue scraper.” You are very active in your church and community. At your weekly bridge club gathering, a number o the other participants mention that they also are patients in Dr. Mack’s practice. Further discussions revealed that all the patients who saw Evelyn were instructed to use tu ted oss and tongue scrapers, or their sel -care. However, those patients who saw Anne, the younger hygienist, were instructed to use a variety o sel -care aids. It sounds like Anne recommends di erent aids based on each individual patient’s needs. Your bridge partner, Florence who also sees Evelyn, the hygienist, says her teeth are very sensitive to hot, cold, and sweets, yet has only been instructed and educated in the use o tu ted oss and a tongue scraper as well. You wonder why so many patients with di ering needs receive the same instructions rom the dental hygienist, Evelyn. 1. What ethical principles are in con ict in this dilemma? 2. Should you meet with Dr. M ack to discuss your concerns? 3. H ow should this ethical dilemma be handled?

R f r nc s 1. Badersten, A., R. N ilveus, and J. Egelberg, E ect o nonsurgical periodontal therapy. I. M oderately advanced periodontitis. J Clin Periodontol, 1981. 8(1): p. 57-72. 2. Cobb, C.M ., Clinical signif cance o non-surgical periodontal therapy: an evidence-based perspective o scaling and root planing. J Clin Periodontol, 2002. 29 Suppl 2: p. 6-16. 3. Greenstein, G., N onsurgical periodontal therapy in 2000: a literature review. J A m D ent A ssoc, 2000. 131(11): p. 1580-92. 4. Lowenguth, R.A. and G. Greenstein, Clinical and microbiological response to nonsurgical mechanical periodontal therapy. Periodontol 2000, 1995. 9: p. 14-22. 5. Stambaugh, R.V., et al., The limits o subgingival scaling. Int J Periodontics R estorative D ent, 1981. 1(5): p. 30-41. 6. Drisko, C.H ., N onsurgical periodontal therapy. Periodontol 2000, 2001. 25: p. 77-88. 7. Rabbani, G.M ., M .M . Ash, Jr., and R.G. Ca esse, The e ectiveness o subgingival scaling and root planing in calculus removal. J Periodontol, 1981. 52(3): p. 119-23. 8. Kimura, Y., et al., Treatment o dentine hypersensitivity by lasers: a review. J Clin Periodontol, 2000. 27(10): p. 715-21. 9. Li, R., et al., E f cacy o a desensitizing toothpaste containing arginine and calcium carbonate on dentin sur ace pore structure and dentin morphology. A m J D ent, 2012. 25(4): p. 210-4.

Chapt r 22

Nonsurgical Periodontal Therapy

10. Li, Y., Innovations or combating dentin hypersensitivity: current state o the art. Com pend Contin Educ D ent, 2012. 33 Spec N o 2: p. 10-6. 11. Schwarz, F., et al., Desensitizing e ects o an Er:YAG laser on hypersensitive dentine. J Clin Periodontol, 2002. 29(3): p. 211-5. 12. Verma, S.K., et al., Laser in dentistry: An innovative tool in modern dental practice. N atl J M ax illo ac Surg, 2012. 3(2): p. 124-32.

STu De NT ANCILLARy Re SOu RCe S A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

391

r e t p a h C

23

Patie nt’s Ro le in No nsurg ical Pe rio do ntal The rap

Se ctio n 1

Patie nt Se lf-Care in No nsurg ical The rap

393

Se ctio n 2

Se lf-Care Challe ng e s fo r Patie nts w ith Pe rio do ntitis

394

Se ctio n 3

To ng ue Cle aning as an Adjunct

403

Se ctio n 4

Fo cus o n Patie nts

404

Clinical Patient Care Evidence in Action Ethical Dilemma

Clinical Applicatio n.

For nearly every patient with periodontal disease, the patient plays a major role in nonsurgical periodontal therapy through the patient’s own e orts at sel -care. Sometimes the sel -care techniques required or a patient with periodontitis are ar more complicated than the sel -care e orts required by a patient with a healthy periodontium. Sel -care or a periodontal patient must accommodate changes in the periodontium due to disease—examples o such changes include open embrasure spaces, exposure o root concavities, and attachment loss. This chapter provides guidance or clinicians in both selecting appropriate sel -care techniques and training patients with periodontal disease in appropriate sel -care.

Le arning Obje cti e s • In a classroom or laboratory setting, explain the criteria or selection and correctly demonstrate the use o the ollowing to an instructor: power toothbrush and interdental aids presented in this chapter. • Explain why interdental care is o special importance or a patient with periodontitis. • In a clinical setting, recommend, explain, and demonstrate appropriate interdental aids to a patient with type III embrasure spaces. Assist the patient in selecting an appropriate interdental aid that the patient is willing to use on a daily basis. • Explain how the presence o exposed root concavities in a dentition would inf uence your selection o e ective sel -care aids. • State the rationale or tongue cleaning and, in the clinical setting, recommend and teach tongue cleaning to an appropriate patient.

Ke Te rms Cotherapist Volatile sul ur compounds

Gingival embrasure space (types I, II, III) Root concavity

Chapte r 23

Patient’s Role in Nonsurgical Periodontal Therapy

Se ct io n 1

Patie nt Se lf-Care in No nsurg ical The rap N onsurgical periodontal therapy includes all nonsurgical treatment and educational measures used to help control gingivitis and periodontitis, such as patient sel -care, periodontal instrumentation, and chemical plaque control. 1. Patient as Cotherapist. Because the primary etiologic actor or periodontitis is plaque bio lm, much o nonsurgical periodontal therapy must be directed toward its daily control by the patient. A. Success ul nonsurgical periodontal therapy always involves the patient in an intensive training program on sel -care techniques. B. The patient’s e orts at sel -care are so critical to the control o periodontitis that some dental teams re er to the patient as having the role o cotherapist in the process o nonsurgical periodontal therapy. 1. This concept o the patient as cotherapist is used to underscore the vital role the patient plays in establishing control o periodontitis. 2. The patient should be actively involved in making decisions about his or her own health care and be willing to make a long-term commitment to meticulous sel -care and regular pro essional care. C. M echanical bio lm removal includes sel -care e orts by the patient on a daily basis and subgingival periodontal instrumentation by the dental hygienist at regular intervals. 2. Sel -Care A. What is Sel -Care? There is no single accepted de nition o sel -care. According to one medical dictionary, it is the personal care per ormed by the patient usually in collaboration with and a ter instruction by a healthcare pro essional (1). This may include activities related to both disease prevention and health maintenance. 1. Sel -care involves instruction on the use and requency o a product. For example, suggesting the addition o a product such as interdental aid to the daily routine. 2. Sel -care includes collaboration between the dental hygienist and the patient. a. The dental hygienist needs to provide input and support while at the same time encouraging patient participation in the nal decision on sel -care devices. b. The optimal device must take patient pre erence into consideration. Recommending a device that the clinician likes, but that the patient dislikes will not contribute to patient motivation and compliance. c. Collaboration hinges on good communication, so the dental hygienist needs to provide education and instruction using words that the patient understands. B. Goals o Sel -Care. The goal o sel -care is improved oral health via optimal bio lm removal and the elimination o bleeding and inf ammation. C. Sel -Care Aids Employed in Biof lm Control 1. Toothbrushing is the most requently used aid or bio lm removal. Un ortunately, it is o ten the only used device by most patients or daily sel -care. Interdental aids are necessary or most patients and critical or periodontal maintenance patients as the interdental area is generally not accessible to toothbrushing (2). 2. Tongue cleaning on a daily basis helps control halitosis and may contribute to a healthy periodontal environment.

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Se ct io n 2

Se lf-Care Challe ng e s fo r Patie nts w ith Pe rio do ntitis 1. Anatomical Challenges or the Patient with Periodontitis. Due to attachment loss, the dentition o an individual with periodontitis o ten presents anatomical challenges to e ective bio lm control, such as recession o the gingival margin, type o embrasure spaces and exposed root concavities. A. Gingival Embrasure Spaces. The gingival embrasure space is the small triangular open space (apical to the contact area) between the curved proximal sur aces o two teeth. The three types o embrasure spaces are shown in Figures 23-1 to 23-3. 1. In health, the interdental papilla lls the gingival embrasure space. Dental f oss is e ective in areas o normal gingival contour. 2. The tissue destruction characterized by periodontitis usually results in an interdental papilla that is reduced in height or missing, resulting in an open embrasure space. Dental f oss is not e ective in areas with open embrasure spaces. 3. Analysis o the gingival embrasure spaces is critical in determining which interdental aid is likely to be most e ective in control o plaque bio lms. Table 23-1 summarizes aids or interdental bio lm removal.

Type I e mbras ure s pac e

Fig ure 23-1. T pe I Embrasure —Space Fille d b the Inte rde ntal Papilla. For the patient with excellent sel -care compliance and good manual dexterity, dental loss is an e ective means o bio ilm control.

Type II e mbras ure s pac e

Fig ure 23-2. T pe II Embrasure —He ig ht o f Inte rde ntal Papilla is Re duce d. Interdental brushes and wooden toothpicks are e ective means o bio ilm control.

Type III e mbras ure s pac e

Fig ure 23-3. T pe III Embrasure —the Inte rde ntal Papilla is Missing . Interdental brushes and end-tu t brushes are e ective means o bio ilm control.

Chapte r 23

Patient’s Role in Nonsurgical Periodontal Therapy

395

B. Exposed Root Concavities. A root concavity is a trench-like depression in the root sur ace. Root concavities commonly occur on the proximal sur aces o anterior and posterior teeth and the acial and lingual sur aces o molar teeth. 1. In health, root concavities are covered with alveolar bone and help to secure the tooth in the bone. 2. Periodontitis results in the apical migration o the junctional epithelium, loss o connective tissue, and destruction o alveolar bone. This tissue destruction results in the exposure o root concavities to the oral environment (either in the presence o tissue recession or, requently, within a periodontal pocket). 3. Figure 23-4 shows the root sur ace o a mandibular canine covered in a colored powder; the colored powder represents plaque bio lm. Figures 23-5A,B and 23-6 demonstrate the ine ectiveness o dental f oss in cleaning the root concavity o a maxillary premolar. 4. Figures 23-5C,D and 23-6 demonstrate the e ectiveness o an interdental brush in cleaning the root concavity o a maxillary premolar. Note that only the interdental brush is e ective in reaching the concave sur ace o the root concavity.

Fig ure 23-4. Anato mical Challe ng e : Bio film Re mo al fro m Ro o t Co nca it . The proximal sur ace o this mandibular canine is covered with colored powder representing plaque bio ilm. Figures 23-5A,B compare the e ectiveness o dental loss and an interdental brush in removing bio ilm rom an exposed root cavity.

A

C

B

D

Fig ure 23-5A,B: Use o f De ntal Flo ss fo r Bio film Re mo al. As seen in igures (A,B), dental loss is not e ective in removing the powder (simulated bio ilm) rom the exposed root concavity.

Fig ure 23-5C,D: Use o f an Inte rde ntal Brush fo r Bio film Re mo al. As seen in igures (C,D), an interdental brush e ectively removes the powder (simulated bio ilm) rom the root concavity.

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Part 5

Implementation o Therapy or Patients with Periodontal Disease

A

B

C

Fig ure 23-6. Applicatio n o f Inte rde ntal Aids to Ro o t Co nca it in Cro ss Se ctio n. A: A maxillary premolar (side view) is cut to expose a cross section o the root. B: The root o the same maxillary premolar viewed in cross section; dental loss is unable to clean the root concavity. C: The bristles o the interdental brush extend into the root cavity or success ul bio ilm removal.

TABLE 2 3 -1 . AIDS FOR INTERDENTAL PLAq UE BIOFILM REMOv AL Inte rde ntal Aid

De scriptio n/ Example

D n

Un w x d o w x d

l flo ss

silk, n ylo n , o fib Flo ss o ld

s

Indicatio ns fo r Use d m d of

a

i n wi

y

I mb

n d xc ll n co m li n c

l s ic m o n o fil m n

s

su

s

c s

o s lf-c

g im

h nd

ld d vic

o

o ld

flo ss

o sin g l -u s d vic co n s gm n of d n

in in g

l flo ss (r

c

a

i n wi

y

w o is m o iv

I mb

d bu

su

sd x

s

c s

iy

issu s

a cc ss Flo ss , Glid Flo ss picks) t uf

dd n

l flo ss

t ick n d y n -lik d n (J & J Su

l flo ss

ty

II m b

su

s

d is l su f c o f l s

flo ss)

c s, fix d b id g s, oo

in

c ,

o xim l su f c s o f w id ly s In

d n

l b us

t in y n ylo n b u s (Bu l b

s on

ndl

Gu m p o x b u s ), so m

n d s co m in v yin g siz s

(t p In

d n

l B us

s)

ty

II o

y

III m b

d is l su f c o f l s

su oo

x o s d fu c io n in s

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Chapte r 23

Patient’s Role in Nonsurgical Periodontal Therapy

2. Selecting Interdental Aids or the Patient with Periodontal Disease A. Dental Floss 1. Description. Dental f oss is unwaxed or waxed thread made o silk, nylon, or plastic mono lament bers used to remove dental plaque bio lm rom the proximal sur aces o teeth. 2. E ectiveness. While f oss tends to be the primary recommendation o most dental hygienists, patient compliance is low. It has also been shown that a signi cant number o those that do f oss are not able to per orm the unction e ectively (3). a. Evidence indicates that a variety o alternative interdental aids are as e ective or more e ective than dental f oss in removing bio lm and in reducing bleeding and gingivitis (4). 1. When added to toothbrushing, a study ound that dental f oss has been shown to signi cantly reduce bleeding compared to toothbrushing alone (5). 2. Two systematic reviews o dental f oss added to manual toothbrushing ound in most cases, the addition o dental f oss does not increase bio lm removal or reduce gingivitis (6,7). The authors conclude that practitioners need to determine on an individual basis whether e ective f ossing is a reasonable and achievable goal (6). 3. Even though conventional wisdom has long advocated or f ossing to reduce decay, the scienti c evidence does not bear this out with two systemic reviews nding no studies supporting the e ectiveness o f ossing in reducing decay in adults (7,8). 4. It may be easier or some individuals to use f oss via a f oss holder. Flossing via f oss holder has been shown to be as e ective as handheld f oss and a mechanism or increasing the development o a f ossing habit (9). There are many variations o f oss holder. Some require manually wrapping the f oss onto the holder. Others may be single-use devices with the f oss already in place (Fig. 23-7). b. When given a choice, patients o ten pre er other types o interdental cleaners to dental f oss (4). c. Flossing may not be as e ective or periodontal patients; recession, attachment loss, and size o the gingival embrasure space are limiting actors (4). d. A water f osser has also been shown to be an e ective alternative to dental f oss, appropriate or patients with many types o oral anatomy and conditions (4). The topic o irrigation is discussed in detail in Chapter 24. e. Some mouthrinses have been shown to be an e ective alternative to dental f oss. M outhrinses are discussed in detail in Chapter 25. 3. Indications or Recommendation o Dental Floss a. Type I embrasures. Dental f oss is e ective in removing bio lm rom tooth crowns and the convex root sur aces in the region o the cementoenamel junction (CEJ). Dental f oss is not e ective in removing bio lm rom root concavities and grooves. b. Recommended or patients with excellent compliance with sel -care. Patient compliance with dental f ossing is low with many patients being unable or unwilling to per orm daily f ossing (3). c. Patients who participate in cra ting hobbies such as knitting, crocheting, needlepoint, or woodworking may be good candidates or dental f oss as they are likely more adept and com ortable at using their hands.

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Fig ure 23-7. Te chni ue fo r Use o f Flo ss Ho lde r. Flossing via a loss holder is as e ective as handheld lossing provided the patient uses proper technique. The dental loss should be wrapped around the proximal tooth sur ace in a similar manner to the technique employed with handheld loss.

Flu y oss

Thin oss

Fig ure 23-8. Tufte d De ntal Flo ss. This aid is a specialized type o loss consisting o a lu y segment o yarnlike loss attached to a segment o thin loss.

B. Tu ted Dental Floss 1. Description. A specialized type o dental f oss that has a segment o ordinary f oss attached to a thicker, f u y, yarn-like segment o f oss (Fig. 23-8). 2. Indications a. For type II embrasures. b. To clean under the pontic o a xed bridge. c. To clean the distal sur ace o the last tooth in the arch. d. To remove plaque bio lm rom the proximal sur aces o widely spaced teeth. 3. Technique a. For interdental proximal sur aces, the f u y part o the f oss is used interdentally in a C-shape against the tooth, applying pressure with a slight sawing motion against rst one proximal sur ace and then the adjacent proximal tooth sur ace. b. For xed bridges, the tu ted f oss is threaded under the pontic and used to clean the undersur ace o pontic. N ext, the distal sur ace o the mesial abutment tooth and the mesial sur ace o the distal abutment tooth are cleaned using the tu ted f oss.

Chapte r 23

Patient’s Role in Nonsurgical Periodontal Therapy

399

C. Interdental Brush 1. Description. Tiny conical-shaped or “ pine tree” –shaped nylon bristle brush attached to a handle (Fig. 23-9). Brushes are available in di erent diameters, so that the best size can be selected. The size o the embrasure space determines the correct diameter o the bristle part o the brush. There should be a slight bit o resistance as the brush is moved back and orth between the teeth. O ten it is necessary to use di erent size brushes within one mouth. 2. Indications a. A systematic review o interdental brushes ound they remove more bio lm than brushing alone (10). b. The systematic review also ound when compared to dental f oss, interdental brushes removed more plaque bio lm. Both f ossing and interdental brush use resulted in a similar reduction in inf ammation (10). c. Excellent or bio lm removal in type II and III embrasure spaces (Fig. 23-10). Interdental brushes should not be used where the interdental papilla lls the interdental space. d. The bristles o an interdental brush are very e ective at cleaning root concavities. 3. Technique. The brush is inserted into the open interdental space and slid in and out o the embrasure space or several strokes. Always use the interdental brush without toothpaste. Figure 23-11A–D show techniques or use o interdental brushes.

Fig ure 23-9. Inte rde ntal Brushe s. Interdental brushes are one o the most use ul aids or cleaning root concavities.

Fig ure 23-10. Use o f Inte rde ntal Brush. (Courtesy o Dr. Deborah Milliken, South Florida Community College.)

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Fig ure 23-11. Pro ce dure fo r Use o f an Inte rde ntal Brush.

A

A: The brush handle is held between the thumb and index inger and the brush gently pushed between the teeth. The brush should be maintained at a 90-degree angle to the long axis o the tooth.

B

B: The bristles can be adapted to tooth sur aces with slight pressure and varying the angle o insertion. For optimal bio ilm removal, the brush is slid in and out o the space using the entire length o the bristle part o the brush.

C

C: By changing the angle o insertion, the bristles can be adapted to the mesial sur ace o the irst premolar. Slight pressure with the brush against the gingiva allows the bristles to clean slightly beneath the gingival margin.

D

D: For posterior areas, advise the patient to close his or her mouth slightly to relax the cheek. The brush may be bent to acilitate insertion between posterior teeth.

Chapte r 23

Fig ure 23-12. End-Tuft Brushe s. End-tu t brushes are used to clean areas that are di icult to access with a standard brush.

Patient’s Role in Nonsurgical Periodontal Therapy

Fig ure 23-13. Use o f End-Tuft Brush. Endtu t brush used around crowded anterior teeth. (Courtesy o Dr. Deborah Milliken, South Florida Community College.)

D. End-Tu t Brush 1. Description. An end-tu t brush is similar to a standard toothbrush except that the brush head has only a small tu t o bristles (Fig. 23-12). A standard toothbrush easily can be modi ed to create a customized end-tu t brush by removing some o the bristles. 2. Indications a. E ectively reaches sites around teeth that are di cult or patients to clean, such as the distal sur ace o the last tooth in the arch, lingual sur aces o mandibular teeth and crowded or misaligned teeth (Fig. 23-13). b. Works well to remove bio lm rom type III embrasure spaces. c. Use ul in removing bio lm rom an exposed urcation area since the small size o the bristle tu ts allows them to partially enter the urcation site. 3. Technique a. The end o the tu t is directed into the embrasure space or urcation area. Gentle circular strokes are used to clean the area. b. For di cult-to-reach mandibular lingual tooth sur aces, the brush is used like a standard brush with a sulcular brushing technique. E. Wooden Toothpick in a Holder 1. Description. This device consists o a round toothpick in a plastic handle. 2. Indications a. The toothpick in a holder has been shown to reduce bio lm and bleeding as e ectively as dental f oss (11). b. It can be used gently along or slightly below the gingival margin or directed into exposed urcation areas or bio lm removal. c. E ective in type II embrasures i the toothpick is easily inserted between the teeth; however, this aid is not e ective in cleaning root concavities unless the teeth are widely spaced. 3. Technique or Use o a Wooden Toothpick in a H older a. A toothpick is secured in the holder and the long end is broken o f ush with the holder, so that it will not scratch the inside o the cheek (Fig. 23-14). b. The end o toothpick is moistened with saliva.

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c. The toothpick tip is applied at right angles to the tooth or directed just beneath the gingival margin at a less than 45-degree angle. The tip should not be directed against the epithelial attachment. The tip is used to trace the gingival margin around each tooth. d. Where space permits, the tip is angled into embrasure spaces or exposed urcation areas and moved gently back and orth to remove accumulated bio lm. F. Wooden Wedge 1. Description. This aid is a short wooden stick usually made o so twood. These wedges are triangular, wedge-shaped sticks and should not be con used with round or rectangular toothpicks. 2. Indications. A systematic review o triangular wooden wedges ound they did not increase the amount o visible bio lm removal beyond toothbrushing, but they did improve interdental inf ammation better than brushing alone (12). To use a wedge, there must be su cient interdental space available to allow easy placement o the wooden wedge. Long-term use o wooden wedges in type I embrasures may cause a permanent loss o the papillae. 3. Technique or Use o Wooden Wedge a. The wooden wedge should be moistened thoroughly in the mouth to so ten the wood prior to use. b. The wedge is inserted between the teeth with the f at side next to the gums (Fig. 23-15). c. The wedge is used with gentle in and out motion to clean between the teeth. The wedge should not be orced into tightly spaced teeth. The wedge should be discarded as soon as the rst signs o splaying are evident.

Fig ure 23-14. To o thpick Ho lde r. To prepare this aid or use, secure a toothpick in the holder and break o the long end, so that it is lush with the plastic holder.

Fig ure 23-15. Use o f Wo o de n We dg e . The wedge is held between the thumb and index inger with the lat side toward the gingiva. In the upper arch the lat sur ace aces up, and in the lower arch the lat sur ace aces down.

Chapte r 23

Patient’s Role in Nonsurgical Periodontal Therapy

Se ct io n 3

To ng ue Cle aning as an Adjunct M any patients have coated tongues that make it di cult to maintain resh breath and cause a lessened sense o taste. Periodontal patients have been shown to have signi cantly higher prevalence o tongue coating (13). Daily tongue cleaning controls halitosis and may help to maintain a healthy periodontal environment. 1. Tongue Coating and the Role o Volatile Sul ur Compounds in Halitosis The tongue coating is made up o bacteria and other putre ed debris that produces hydrogen sul de and methyl mercaptan. A. Volatile sul ur compounds (VSCs) are a amily o gases that are responsible or halitosis. 1. Two members o the VSC amily o gases, hydrogen sul de and methyl mercaptan, are principally responsible or mouth odor. M ethyl mercaptan is produced primarily by periodontal pathogens. Some studies have suggested that low concentrations o these gases may be toxic to tissues; however, the research in this area is limited (14). 2. M ost patients are concerned about controlling halitosis and, there ore, are receptive to the introduction o tongue cleaning to their sel -care routine. 3. Tongue coating can contribute to a lessened sense o taste. Tongue cleaning should be recommended to geriatric patients who have a low desire to eat due to depressed taste sensation. B. Tongue cleaning is recommended because the bulk o bacteria and debris— especially the periodontal pathogens that produce methyl mercaptan—accumulate mostly within the li orm papillae and on the back o the tongue. The practice o tongue cleaning may not only make a patient eel more con dent but may actually help in maintaining a healthy periodontal environment. 2. Technique or use o Manual Tongue Cleaners. M anual tongue cleaners come in a variety o styles. The two most common types are specialized toothbrushes and tongue scrapers (Fig. 23-16). A. The tongue brush or scraper is positioned as ar back on the tongue as possible. B. O nce the brush or scraper is in position, it is pulled orward gently over the tongue. This procedure is repeated two or three times or until the tongue is clean. C. When rst learning tongue cleaning, some individuals gag and nd the process unpleasant. In the beginning, encourage the patient to place the cleaner wherever it is most com ortable on the tongue. With regular use, most patients become accustomed to the sensation o the tongue brush or scraper and are able to clean urther back on the tongue. Over time, most patients become skilled at tongue cleaning.

Fig ure 23-16. Manual To ng ue Scrape r. Daily tongue cleaning controls halitosis and may help to maintain a healthy periodontal environment.

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Chapte r Summar State me nt The patient’s e orts at sel -care are critical to the control o periodontitis. Since the importance o mechanical bio lm control is quite high or the patient with periodontitis, the dental hygienist should be knowledgeable about bio lm control measures and be prepared to recommend appropriate aids based on the individual needs o each patient. Due to attachment loss, the dentition o an individual with periodontitis o ten presents anatomical challenges to e ective bio lm control, such as recession o the gingival margin, type II or III embrasure spaces, and exposed root concavities. Interdental aids that are especially use ul or patients with type II or III embrasure spaces include interdental brushes and end-tu t brushes. Daily tongue cleaning results in reduced amounts o tongue coating and improvements in breath reshness.

Se ct io n 4

Fo cus o n Patie nts Clinical Patie nt Care CA S E 1 A patient with slight (or mild) chronic periodontitis has generalized recession o the interdental gingival papillae. What options would you have or training this patient in interdental plaque bio lm control?

CA S E 2 You are discussing sel -care or bio lm removal with a patient with chronic periodontitis. You point out to the patient how the bio lm control on the acial and lingual sur aces o his teeth is greatly improved and praise him or this success. The patient comments that he likes using his powered toothbrush and has been brushing longer. Un ortunately, you note that there is heavy plaque bio lm on the proximal sur aces o most teeth. The patient tells you that there is “ N o way that I am going to use that string. It is just too hard to use.” The patient has type II embrasure spaces throughout his mouth. What suggestions might you make or interdental bio lm control?

CA S E 3 A patient with chronic periodontitis has generalized bone loss and gingival recession, so that the cervical-thirds o the roots are exposed to the oral cavity. What interdental aid would you recommend to clean interproximally (between the roots)?

Chapte r 23

Patient’s Role in Nonsurgical Periodontal Therapy

405

E ide nce in Actio n You recently began working as the dental hygienist in an established periodontal practice. The previous hygienist retired a ter a 20-year career in dental hygiene. Today is M rs. J’s rst maintenance appointment with you. M rs. J has had periodontal surgery and has type III embrasure spaces throughout her dentition. She also has extensive restorative work in her dentition. According to her patient record, at the past several maintenance visits, M rs. J has had very little plaque bio lm on the acial and lingual sur aces o her teeth, but moderate bio lm accumulation on the mesial and distal sur aces o her teeth. Today, your assessment reveals a similar pattern o plaque bio lm ormation. You ask M rs. J about her current sel -care program and she explains that she has been instructed to use an electric toothbrush and dental f oss daily. She says that she really likes the electric toothbrush but simply cannot use the f oss. She complaints that the f oss breaks when she tries to get it between her “ llings” and that it is just simply too rustrating to use. Based on what you know about plaque bio lm control with type III embrasure spaces what suggestions might you o er to M rs. J as other options or her sel -care regimen?

Ethical Dile mma As a 50-year-old woman who runs a home day care center, you have been re erred to Dr. Rogers’ periodontal practice by your general dentist Dr. Patel. You now alternate your periodontal maintenance appointments between the two o ces, with appointments every 3 months. Six months ago, the hygienist at Dr. Rogers’ o ce, Khoa, a recent graduate, recommended that you use an interdental brush, due to the recession and large spaces between your teeth. H e spent much time educating you in the proper technique, and even watched you use it e ectively in your own mouth. H owever, at home, you nd it di cult to use, and due to the osteoarthritis in your ngers, nd changing the small nylon brushes on the handle almost impossible. As a result, you have not been using the aid. You are sitting in ront o Khoa again today, and he reviews your medical history and home care regime. You explain that it has been di cult or you to be compliant with the interdental brush, and ask or an alternative periodontal aid. Khoa eels that the interdental brush is the best device or mechanical bio lm control in your situation. You eel very rustrated and do not think that Khoa is being sensitive to your needs. 1. H ow should this ethical dilemma be handled? 2. What ethical principles are in conf ict in this dilemma?

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Re fe re nce s 1. O ’Toole M T. M osby’s M edical D ictionary. 9th ed. St. Louis, M O : Elsevier/M osby; 2013; xiv: A-43, 1921. 2. Jahn CA. Evidence or sel -care products: power brushing and interdental aids. J Pract H yg. 2004;13:24–29. 3. Lang WP, Ronis DL, Farghaly M M . Preventive behaviors as correlates o periodontal health status. J Public H ealth D ent. 1995;55(1):10–17. 4. Asadoorian J. Flossing: Canadian dental hygienists’ association position statement. CJD H . 2006;40(3):1–10. 5. Graves RC, Disney JA, Stamm JW. Comparative e ectiveness o f ossing and brushing in reducing interproximal bleeding. J Periodontol. 1989;60(5):243–247. 6. Berchier CE, Slot DE, H aps S, et al. The e cacy o dental f oss in addition to a toothbrush on plaque and parameters o gingival inf ammation: a systematic review. Int J D ent H yg. 2008;6(4):265–279. 7. Sambunjak D, N ickerson JW, Poklepovic T, et al. Flossing or the management o periodontal diseases and dental caries in adults. Cochrane D atabase Syst R ev. 2011;(12):CD008829. 8. H ujoel PP, Cunha-Cruz J, Banting DW, et al. Dental f ossing and interproximal caries: a systematic review. J D ent R es. 2006;85(4):298–305. 9. Kleber CJ, Putt M S. Formation o f ossing habit using a f oss-holding device. J D ent H yg: JD H /A m erican D ental H ygienists’ A ssociation. 1990;64(3):140–143. 10. Slot DE, Dor er CE, Van der Weijden GA. The e cacy o interdental brushes on plaque and parameters o periodontal inf ammation: a systematic review. Int J D ent H yg. 2008;6(4):253–264. 11. Lewis M W, H older-Ballard C, Selders RJ Jr., et al. Comparison o the use o a toothpick holder to dental f oss in improvement o gingival health in humans. J Periodontol. 2004;75(4):551–556. 12. H oenderdos N L, Slot DE, Paraskevas S, et al. The e cacy o woodsticks on plaque and gingival inf ammation: a systematic review. Int J D ent H yg. 2008;6(4):280–289. 13. Yaegaki K, Sanada K. Volatile sul ur compounds in mouth air rom clinically healthy subjects and patients with periodontal disease. J Periodontal R es. 1992;27(4 Pt 1):233–238. 14. Ratcli PA, Johnson PW. The relationship between oral malodor, gingivitis, and periodontitis. A review. J Periodontol. 1999;70(5):485–489.

STUDENT ANCILLARy RESOURCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

r e t p a h C

24

S p ag i g i al a d S bg i g i al I ig atio

S ctio

1

Pati

t-Appli d Ho m I ig atio

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2

P o f ssio al S bg i g i al I ig atio

415

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3

Fo c s o

417

Pati

ts

408

Clinical Patient Care Evidence in Action Ethical Dilemma

Cli ical Applicatio .

This chapter addresses the role o supragingival and subgingival irrigation in the treatment o periodontal diseases. The primary objective o supragingival irrigation is to diminish gingival in ammation by disrupting bacterial biof lms. The goal o subgingival irrigation is to reduce the number o bacteria in the periodontal pocket space.

La

i g Obj cti

s

• Discuss the oral health benef ts o a water osser or the patient with periodontitis. • Distinguish the depth o the delivery among the water osser, a toothbrush, dental oss, and other interdental aids. • Name the types o agents that can be used in a water osser. • In a clinical setting, instruct a patient with periodontitis in the use o a water osser. • Summarize research f ndings that relate to using pro essional irrigation to deliver chemicals to periodontal pockets.

K

T ms

Water losser Hydrokinetic activity Impact zone

Flushing zone Standard irrigation tips Subgingival irrigation tips

Orthodontic irrigation tips Filament-type irrigation tips Pro essional subgingival irrigation

408

S ct io

Pati

Pa t 5 Implementation o Therapy or Patients with Periodontal Disease

1

t-Appli d Ho m I ig atio

1. What is a Water Flosser? The water osser is a generic term or a device that delivers a pulsed irrigation o water or other solution around and between teeth (supragingivally) and into the gingival sulcus or periodontal pocket (subgingivally). This process is commonly re erred to as home or oral irrigation. A water osser jet may also be re erred to as a dental water irrigator, home irrigator, or dental water jet. A. Mechanism o Action o a Water Flosser 1. A water osser creates a pulsating uid stream to ush an area with water or an antimicrobial agent. Figure 24-1 shows examples o devices used or home oral irrigation. a. The pulsating uid delivered by a water osser incorporates a compression and decompression phase that e f ciently displaces biof lm, bacteria, and debris (1,2). b. The pulsating uid creates two zones o uid movement termed hydrokinetic activity (Fig. 24-2). 1. The area o the mouth o initial uid contact is called the impact zone. 2. The depth o uid penetration within a subgingival sulcus or pocket is called the ushing zone (3). 2. H ydrokinetic uid movement results in subgingival and interdental uid penetration. B. Fluid Penetration 1. A water osser produces subgingival uid penetration regardless o the type o tip or attachment used (4,5). 2. A water osser has the greatest potential or reaching deeper into a sulcus or pocket over other types o devices including toothbrushes and interdental aids (Table 24-1) (4,5).

A

B

Fig 24-1. Wat Flo ss s. A: A countertop dental water jet that plugs into an electrical outlet. B: A portable dental water jet that works o o a rechargeable battery. (Courtesy o Water Pik, Inc., Fort Collins, CO.)

Chapt

24

409

Supragingival and Subgingival Irrigation

2. Benef ts o Home Oral Irrigation. Studies demonstrate that the water osser is clinically proven to remove biof lm and reduce bleeding, gingivitis, periodontal pathogens, and in ammatory mediators (6–21). A. Removal o Biof lm. A water osser used in combination with manual toothbrushing has been shown to remove 29% more biof lm than traditional brushing and ossing (15). B. Reduction in Bleeding. Studies consistently show that the water osser is a valuable tool or helping patients reduce bleeding (6–10,12,13,17,19,20). 1. Daily irrigation with water signif cantly reduced bleeding in 14 days (10). 2. Daily irrigation with water was signif cantly better than rinsing with 0.12% chlorhexidine at reducing marginal bleeding and bleeding on probing (13).

Fig 24-2. Th Impact a d Fl shi g Zo s. A water losser creates a pulsating water stream to lush an area with luid. The area o the mouth where the luid initially contacts is called the impact zone. The depth o luid penetration within the subgingival sulcus or pocket is called the lushing zone. (Courtesy o Water Pik, Inc., Fort Collins, CO.)

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In

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ts

ls

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no

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c

3 mm

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c in o d

6 m m n d b yo n d (4,5)

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pik, In c., Fo

Co llin s, CO.

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410

Pa t 5 Implementation o Therapy or Patients with Periodontal Disease

C. Reduction in Gingival In ammation. The water osser has been shown to reduce the clinical signs o gingivitis (6–8,10,12,13,16,17,21–23). 1. A water osser used in combination with manual toothbrushing is more e ective in the reduction o gingivitis than manual toothbrushing and ossing (7). 2. Daily irrigation with water signif cantly reduces the clinical signs o gingivitis (8). D. Reduction o Periodontal Pathogens. Studies show the dental water jet can reduce subgingival bacteria (3,8,11,18). 1. The water osser has demonstrated the ability to reduce periodontal pathogens at up to a 6-mm level within a periodontal pocket (3,11). 2. Daily irrigation with either water or 0.04% chlorhexidine signif cantly reduces subgingival bacteria compared to toothbrushing and 0.12% chlorhexidine rinsing (8). E. Reduction in In ammatory Mediators and Destructive Host Response 1. Recent studies show that home oral irrigation is e ective in signif cantly reducing in ammatory cytokines Il-1β and PGE2 (8,10). These cytokines have been implicated in attachment loss and alveolar bone loss (24,25). 2. Irrigation may produce these e ects by ushing out loosely adherent plaque and toxins or in ammatory substances, although the exact mechanism o action o irrigation is still speculative (8,17). 3. Indications or Recommending Home Oral Irrigation A. Individuals on Periodontal Maintenance. Studies have shown that daily use o the water osser may be benef cial or patients with gingivitis or or those in periodontal maintenance (6–10,12,13,17,21). Patients with 5-mm pockets and bleeding who added daily irrigation to traditional home care achieved signif cant reductions in gingival in ammation and bleeding on probing when compared to patients using only traditional sel -care methods (17). B. Individuals N oncompliant with Dental Floss. While previously considered an adjunctive to brushing and ossing, new in ormation indicates that home oral irrigation can be considered an e ective alternative to daily ossing. 1. The addition o a water osser once daily with plain water to either a manual or power brushing routine was an e ective alternative to dental oss or the reduction o bleeding, gingivitis, and biof lm (7,19). 2. The water osser and a manual toothbrush were 29% more e ective at plaque removal than a manual toothbrush and oss (15). C. Individuals with Special N eeds. H ome irrigation has been shown to be sa e and e ective or patients with special needs. 1. Dental Implants. For improving the health o peri-implant tissues, daily irrigation using a tip with three so t f laments and water at medium pressure was signif cantly more e ective at reducing bleeding than manual brushing and ossing (16). 2. Individuals with Diabetes. For individuals living with diabetes, twice-daily water irrigation using the so t rubber tip provided a 44% better reduction in bleeding over routine oral hygiene (6). 3. Individuals with O rthodontic Appliances. For those with orthodontic appliances, the dental water jet with the orthodontic tip provided 3.76 times better biof lm removal and 26% better bleeding reduction than ossing using a oss threader (20,25). 4. Prosthetic Bridgework and Crowns. For individuals with bridgework and/or crowns, daily irrigation produced signif cant reductions in in ammation (26).

Chapt

24

Supragingival and Subgingival Irrigation

4. Patient Instruction A. Considerations or Irrigator Use: Product Sa ety 1. Water ossers have been extensively studied on thousands o people with more than 60 studies since the 1960s. Examination with a scanning electron microscope o chronic periodontal pockets immediately ollowing irrigation ound no evidence o trauma or injury to the tissue (3). 2. The incidence o bacteremia rom a dental water jet is similar to other healthcare devices (27). a. The American College o Cardiology/American H eart Association 2008 Guideline Update on Valvular H eart Disease: Focused Update on In ective Endocarditis states “ M aintenance o optimal oral health and hygiene may reduce the incidence o bacteremia rom daily activities and is more important than prophylactic antibiotics or a dental procedure to reduce the risk o in ective endocarditis” (28). b. Be ore recommending a water osser or any device to a patient who is at high risk or in ective endocarditis, it is imperative that dental healthcare providers consider both the patient’s overall medical and oral health status. Consultation with a physician is advisable in order to assess the patient’s overall risk or in ective endocarditis. B. Irrigant Solutions. M ost solutions can be used in a water osser. The most e ective agent is one that is acceptable to the patient. 1. Water a. Simple tap water has been demonstrated as highly e ective in numerous clinical trials (3,6,7,10,12,14–16,19,20). There ore, the addition o any antimicrobial agent or home oral irrigation should be considered care ully. b. Water has several advantages; it is readily available, cost-e ective, and has no side e ects. 2. Antimicrobial Solutions a. Chlorhexidine (CH X) 1. For home irrigation, chlorhexidine can be diluted with water. Use o diluted solutions o chlorhexidine has been studied in concentrations rom 0.02% to 0.06% (8,13,18,21). 2. Because o better interproximal and subgingival penetration with irrigation compared to rinsing, a diluted solution o chlorhexidine is acceptable or daily irrigation. In some cases, dilution can minimize staining. 3. CH X is available by prescription only. In the United States, the maximum strength is 0.12% . In Europe, it is available at 0.2% . b. Essential O ils 1. For home irrigation, the e ectiveness o an essential oil mouth rinse has been demonstrated only when used at ull strength (9). 2. Essential oil mouthrinses are available over the counter in both brand name and generic orms. C. Criteria or Equipment Selection. Selection o an irrigation device may be con using because there are many types on the market. The commercial and scientif c claims o some devices have yet to be evaluated. O nly pulsating water ossers have clinical research supporting sa ety and e f cacy. As each device operates di erently in respect to pressure and pulsation, outcomes rom studies on one brand o product cannot be trans erred to another product brand. There ore, be ore recommending any device, it is important to evaluate the research unique to that brand o product.

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Pa t 5 Implementation o Therapy or Patients with Periodontal Disease

5. Technique or Use o Irrigation Tips A. General Instructions 1. It is important or both dental healthcare providers and patients to read all instructions thoroughly be ore using a water osser. 2. The uid reservoir can be f lled with water, a solution o water and mouthwash, or a solution o an antimicrobial and water. The irrigating solution should be at warm temperature or maximum patient com ort. 3. The unit should be ushed a ter using any solution other than water. A ter using a diluted solution, such as diluted chlorhexidine, the unit is cleaned by f lling the reservoir with warm water and running the unit while holding the handle in the sink until the reservoir is empty. 4. M ost patients seem to comply with recommendations to use a water osser and f nd a standard irrigation tip easy to use or supragingival irrigation (12). For subgingival irrigation, it is important to provide patients with clear instructions on its use including the specif c areas where the tip should be used. B. Irrigation Tips. Irrigation is accomplished using a standard irrigation tip, a subgingival so t rubber tip, a so t-tapered brush orthodontic tip, or a tip with three f ne f laments.

A

B

C

D

Fig 24-3. I ig atio Tips. Four examples o irrigation tip designs. A: Standard irrigation tip. B: Subgingival tip. C: Orthodontic tip. D: Filament-type tip.

1. Standard irrigation tips are usually made o a plastic material (Fig. 24-3A). a. This type o tip is recommended or generalized, ull-mouth irrigation. b. Water osser devices with standard irrigation tips may deliver solution that penetrates a depth o 50% or more o the pocket (5). 2. Subgingival irrigation tips usually have a so t rubber-tipped end (Fig. 24-3B). a. Subgingival irrigation tips are recommended or use in areas such as deep pockets, urcation areas, dental implants, or areas that are di f cult to access with a standard tip. b. Subgingival placement o the tip allows the water or antimicrobial agent to penetrate deeper into a pocket. 1. In periodontal pockets 6 mm or less in depth, the subgingival tip may deliver water that penetrates up to 90% o the pocket depth (4).

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24

Supragingival and Subgingival Irrigation

2. In deeper pockets—7 mm or more—depth o penetration is somewhat less at 64% o the depth o the pocket (4). 3. Orthodontic irrigation tips have a so t-tapered brush end that enhances biof lm removal and provides or simultaneous irrigation (Fig. 24-3C). a. O rthodontic tips can be used or ull-mouth irrigation and are recommended or people with orthodontic appliances, implants, or who need additional help with biof lm removal. b. The bristles should come in light contact with the tooth or orthodontic appliances to acilitate biof lm removal. 1. The orthodontic tip when used in conjunction with toothbrushing was 3.76 times as e ective as dental oss at removing plaque. 2. When compared to toothbrushing only, the toothbrushing and orthodontic tip combination was 5.83 times as e ective (20). 4. Filament-type irrigation tips have three so t f laments surrounding a standard jet tip. This can enhance plaque removal and is sa e or use around dental implants (Fig. 24-3D). a. The f lament-type tip has also been shown to remove plaque biof lm (14). b. The f lament-type tip used around an implant was 145% better at reducing bleeding than manual brushing and ossing (16). C. Procedure or Use o a Standard Tip 1. Initially the pressure setting should be adjusted to its lowest setting. O ver time as the condition o the gingival tissue improves, pressure should be increased to at least the medium setting as this setting is where clinical e f cacy has been demonstrated (1,2). 2. The water spray is used to “ trace” along the gingival margin with the tip positioned at a 90-degree angle almost touching the gingiva (Fig. 24-4). The tip should be held brie y at each interproximal area. D. Procedure or Use o a Subgingival Irrigation Tip 1. The dental hygienist should instruct the patient on the areas o his or her mouth where use o a subgingival irrigation tip would be benef cial, such as pockets, dental implants, or urcation areas. The patient should be instructed on use o the tip in each area or these areas. 2. The pressure setting is adjusted to its lowest setting. The subgingival tip is designed for use only at the lowest pressure setting. 3. The tip should be placed at the site be ore starting the irrigation unit. The subgingival tip is directed at a 45-degree angle and placed at the gingival margin or slightly beneath the gingival margin as recommended by the manu acturer (Fig. 24-5). 4. O nce the tip is in place, the irrigation unit is turned on and the uid is allowed to ow brie y in the area. 5. A ter a site has been irrigated, the unit is paused and the subgingival tip is repositioned in the next area o the mouth. E. Procedure or the Use o Orthodontic and Filament Tips 1. Initially, the pressure setting should be adjusted to its lowest setting. O ver time as the condition o the gingival tissue improves, pressure should be increased to at least the medium setting as this setting is where clinical e f cacy has been demonstrated (1,2). 2. The water spray is used to “ trace” along the gingival margin with the tip positioned at a 90-degree angle touching the gingiva (Figs. 24-6 and 24-7). The tip should be held brie y in each interproximal area. 3. This tip can also be placed around orthodontic brackets or wires, or implants to enhance cleaning.

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Pa t 5 Implementation o Therapy or Patients with Periodontal Disease

Fig 24-4. Plac m t o f th Sta da d I ig atio Tip. The water spray is used to “ trace” along the gingival margin with the tip positioned at a 90-degree angle almost touching the gingiva.

Fig 24-5. Plac m t o f th S bg i g i al I ig atio Tip. The tip should be placed at the site be ore starting the irrigation unit. The subgingival tip is directed at a 45-degree angle and placed at the gingival margin or slightly beneath the gingival margin as recommended by the manu acturer.

Fig 24-6. Plac m t o f th O tho do tic Tip. The special orthodontic tip is used with the tip positioned at a 90-degree angle.

Fig 24-7. Plac m t o f th Filam t-T p Tip. The ilament-type tip is used with the tip positioned at a 90-degree angle.

Chapt

S ct io

24

Supragingival and Subgingival Irrigation

415

2

P o f ssio al S bg i g i al I ig atio 1. Introduction to Pro essional Irrigation A. Description o Subgingival Irrigation. Pro essional subgingival irrigation is the in-o f ce ushing o pockets per ormed by the dental hygienist or dentist using one o three systems: 1. A blunt-tipped irrigating cannula that is attached to a handheld syringe (Fig. 24-8) 2. Ultrasonic unit equipped with a reservoir (Fig. 24-9) 3. A specialized air-driven handpiece that connects to the dental unit airline B. Goal o Subgingival Irrigation. The purpose o supragingival irrigation is the disruption and dilution o bacteria and their products rom within periodontal pockets.

Fig 24-8. Ha dh ld S i g . Close-up view o the tip o a handheld syringe used or subgingival irrigation. The tip is positioned subgingivally or delivery o an antimicrobial solution.

Fig 24-9. r s o i fo u lt aso ic u it. This ultrasonic device has an optional reservoir system or dispensing irrigant solutions—such as chlorhexidine gluconate—to an ultrasonic tip. (Courtesy o Hu-Friedy, M g.)

C. Irrigant Solutions. Solutions used or subgingival irrigation include chlorhexidine gluconate, povidone-iodine and water, stannous uoride oral rinse, tetracycline dilutions, or Listerine. 2. E ectiveness o Pro essional Subgingival Irrigation A. Single Pro essional Application 1. The status o pro essional subgingival irrigation in the treatment o periodontitis remains controversial (29,30). 2. In-o f ce subgingival irrigation with an antimicrobial agent has been shown to have only limited or no benef cial e ects over nonsurgical periodontal instrumentation alone. a. Several research studies indicate that irrigation did not enhance the therapeutic e ect over that attained by nonsurgical periodontal instrumentation alone (31–36). b. O ther studies ound a minimal improvement. H owever, a ter 6 months, there was no signif cant di erence between irrigation and nonsurgical periodontal instrumentation regarding probing depths or in ammatory status (37–41).

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Pa t 5 Implementation o Therapy or Patients with Periodontal Disease

3. There is no long-lasting substantivity o the antimicrobial agent in the periodontal pocket due to the continuous ow o gingival crevicular uid rom the pocket, and the presence o serum and proteins in the pocket. A substantive antimicrobial agent, such as chlorhexidine gluconate, would have to be retained in the pocket and be released slowly over a period o time to inter ere with the repopulation o bacteria within the pocket. B. Conclusions Regarding Pro essional Irrigation. A position paper (42) on the role o supra- and subgingival irrigation in the treatment o periodontal diseases concludes: 1. “ . . . there currently is insu f cient evidence to indicate that subgingival irrigation routinely should be used as a supplemental in-o f ce procedure.” 2. “ H owever, preliminary data using high concentrations (37,40) and prolonged or multiple applications (31,34,35,40,43,44) o antimicrobials have shown some promise in improving periodontal status. Consequently, additional studies are needed to ascertain the ull potential o subgingival irrigation as an adjunct to periodontal therapy” (42). 3. Subgingival irrigation per ormed be ore periodontal instrumentation may reduce the incidence o bacteremia and reduce the number o microorganisms in aerosols.

Chapt

S mma

Stat m

t

When used daily or at home sel -care, supragingival and subgingival irrigation via a water osser can be benef cial or periodontal patients. A well-established body o evidence indicates that pulsating devices have the ability to remove biof lm and reduce bleeding, gingivitis, periodontal pathogens, and in ammatory mediators. Irrigation via a water osser also benef ts patients with special oral health needs and considerations including those in periodontal maintenance or with implants, crowns, bridges, orthodontic appliances, and diabetes. The status o pro essional subgingival irrigation in the treatment o periodontitis remains controversial. In-o f ce subgingival irrigation with an antimicrobial agent has been shown to have only limited or no benef cial e ects over nonsurgical periodontal instrumentation alone.

Chapt

S ct io

3

Fo c s o

Cli ical Pati CA S e

Pati

24

Supragingival and Subgingival Irrigation

417

ts

t Ca

1

You have just recommended a water osser to your patient, and he has accepted, but he has no idea how to use the product. The patient is in periodontal maintenance, has two 5-mm pockets (#3M and #18D), one 6-mm pocket (#14M ), and a urcation area on #30. H e also has an implant replacing #19. What type o instructions would you provide or the patient?

e id

c i Actio

A new patient comes to your practice rom another state. She has had periodontal therapy in the past. The patient uses a power toothbrush and osses irregularly. Supragingival plaque control looks good, but several areas o the mouth bleed upon probing. The medical history indicates that the patient has had type 2 diabetes or 7 years. How would you make a recommendation or the water osser to this patient?

e thical Dil mma Your next patient is Darren, a 26-year-old male, who just recently returned rom a 3-year stint in the Peace Corps. Prior to his Peace Corps experience, Darren had received routine and regular dental care but has not been to a dentist in the last 3 years. As you review his medical history, he states that he thinks that he may have su ered rom a bout o “ in ective endocarditis” while away, but as he was working in an underdeveloped third world country, his def nitive diagnosis was unclear. You start your periodontal assessment, and discover that his periodontal probe readings have signif cantly increased rom 1 to 3 mm at his last appointment, to generalized 4- to 5-mm probe readings. H is tissues appear moderately in amed, as he presents with substantial supragingival biof lm and subgingival calculus. H owever, his radiographs show no signs o bone loss. You recently attended a continuing education course on the use o “ water ossers,” and eel that this will be an ideal adjunctive periodontal aid or Darren, based on your clinical f ndings. You start explaining the device and demonstrating its use to Darren, who becomes quite agitated and says that he absolutely re uses to use it. While working in the Peace Corps, clean water was extremely scarce and considered a luxury. There is no way, he states, that he will “ waste water” in this ashion. You are not sure how to proceed. 1. What ethical principles are in con ict in this dilemma? 2. What is the best way or you to handle this ethical dilemma? 3. Do you have an ethical obligation to treat this patient?

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Pa t 5 Implementation o Therapy or Patients with Periodontal Disease

r f

c s

1. Bhaskar SN , Cutright DE, Gross A, et al. Water jet devices in dental practice. J Periodontol. 1971;42(10):658–664. 2. Selting WJ, Bhaskar SN , M ueller RP. Water jet direction and periodontal pocket debridement. J Periodontol. 1972;43(9): 569–572. 3. Cobb CM , Rodgers RL, Killoy WJ. Ultrastructural examination o human periodontal pockets ollowing the use o an oral irrigation device in vivo. J Periodontol. 1988;59(3):155–163. 4. Braun RE, Ciancio SG. Subgingival delivery by an oral irrigation device. J Periodontol. 1992;63(5):469–472. 5. Eakle WS, Ford C, Boyd RL. Depth o penetration in periodontal pockets with oral irrigation. J Clin Periodontol. 1986;13(1):39–44. 6. Al-M ubarak S, Ciancio S, Aljada A, et al. Comparative evaluation o adjunctive oral irrigation in diabetics. J Clin Periodontol. 2002;29(4):295–300. 7. Barnes CM , Russell CM , Reinhardt RA, et al. Comparison o irrigation to oss as an adjunct to tooth brushing: e ect on bleeding, gingivitis, and supragingival plaque. J Clin D ent. 2005;16(3):71–77. 8. Chaves ES, Kornman KS, M anwell M A, et al. M echanism o irrigation e ects on gingivitis. J Periodontol. 1994;65(11): 1016–1021. 9. Ciancio SG, M ather M L, Z ambon JJ, et al. E ect o a chemotherapeutic agent delivered by an oral irrigation device on plaque, gingivitis, and subgingival micro ora. J Periodontol. 1989;60(6):310–315. 10. Cutler CW, Stan ord TW, Abraham C, et al. Clinical benef ts o oral irrigation or periodontitis are related to reduction o pro-in ammatory cytokine levels and plaque. J Clin Periodontol. 2000;27(2):134–143. 11. Drisko CL, White CL, Killoy WJ, et al. Comparison o dark-f eld microscopy and a agella stain or monitoring the e ect o a Water Pik on bacterial motility. J Periodontol. 1987;58(6):381–386. 12. Flemmig TF, Epp B, Funkenhauser Z , et al. Adjunctive supragingival irrigation with acetylsalicylic acid in periodontal supportive therapy. J Clin Periodontol. 1995;22(6):427–433. 13. Flemmig TF, N ewman M G, Doherty FM , et al. Supragingival irrigation with 0.06% chlorhexidine in naturally occurring gingivitis. I. 6 month clinical observations. J Periodontol. 1990;61(2):112–117. 14. Gorur A, Lyle DM , Schaudinn C, et al. Biof lm removal with a dental water jet. Com pend Contin Educ D ent. 2009;30 Spec N o 1:1–6. 15. Goyal CR, Lyle DM , Q aqish JG, et al. Evaluation o the plaque removal e f cacy o a water osser compared to string oss in adults a ter a single use. J Clin D ent. 2013;24(2):37–42. 16. M agnuson B, H arsono M , Stark PC, et al. Comparison o the e ect o two interdental cleaning devices around implants on the reduction o bleeding: a 30-day randomized clinical trial. Com pend Contin Educ D ent. 2013;34 Spec N o 8:2–7. 17. N ewman M G, Cattabriga M , Etienne D, et al. E ectiveness o adjunctive irrigation in early periodontitis: multi-center evaluation. J Periodontol. 1994;65(3):224–229. 18. N ewman M G, Flemmig TF, N achnani S, et al. Irrigation with 0.06% chlorhexidine in naturally occurring gingivitis. II. 6 months microbiological observations. J Periodontol. 1990;61(7):427–433. 19. Rosema N A, H ennequin-H oenderdos N L, Berchier CE, et al. The e ect o di erent interdental cleaning devices on gingival bleeding. J Int A cad Periodontol. 2011;13(1):2–10. 20. Sharma N C, Lyle DM , Q aqish JG, et al. E ect o a dental water jet with orthodontic tip on plaque and bleeding in adolescent patients with f xed orthodontic appliances. A m J O rthod D entofacial O rthop. 2008;133(4):565–571; quiz 628 e1–e2. 21. Walsh TF, Glenwright H D, H ull PS. Clinical e ects o pulsed oral irrigation with 0.2% chlorhexidine digluconate in patients with adult periodontitis. J Clin Periodontol. 1992;19(4):245–248. 22. Felo A, Shibly O, Ciancio SG, et al. E ects o subgingival chlorhexidine irrigation on peri-implant maintenance. A m J D ent. 1997;10(2):107–110. 23. Lainson PA, Bergquist JJ, Fraleigh CM . A longitudinal study o pulsating water pressure cleansing devices. J Periodontol. 1972;43(7):444–446. 24. O enbacher S, H easman PA, Collins JG. M odulation o host PGE2 secretion as a determinant o periodontal disease expression. J Periodontol. 1993;64(5 suppl):432–444. 25. Tsai CC, H o YP, Chen CC. Levels o interleukin-1 beta and interleukin-8 in gingival crevicular uids in adult periodontitis. J Periodontol. 1995;66(10):852–859. 26. Krajewski J, Giblin J, Gargiulo AW. Evaluation o a water pressure cleaning device as an adjunct to periodontal treatment. J A m er Soc Periodont. 1964;2:76–78. 27. Wilson W, Taubert KA, Gewitz M , et al. Prevention o in ective endocarditis: guidelines rom the American H eart Association: a guideline rom the American H eart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Q uality o Care and O utcomes Research Interdisciplinary Working Group. Circulation. 2007;116(15):1736–1754. 28. N ishimura RA, Carabello BA, Faxon DP, et al. ACC/AH A 2008 guideline update on valvular heart disease: ocused update on in ective endocarditis: a report o the American College o Cardiology/American H eart Association Task Force on Practice Guidelines: endorsed by the Society o Cardiovascular Anesthesiologists, Society or Cardiovascular Angiography and Interventions, and Society o Thoracic Surgeons. Circulation. 2008;118(8):887–896. 29. H allmon WW, Rees TD. Local anti-in ective therapy: mechanical and physical approaches. A systematic review. A nn Periodontol. 2003;8(1):99–114. 30. Shiloah J, H ovious LA. The role o subgingival irrigations in the treatment o periodontitis. J Periodontol. 1993;64(9): 835–843. 31. Braatz L, Garrett S, Cla ey N , et al. Antimicrobial irrigation o deep pockets to supplement non-surgical periodontal therapy. II. Daily irrigation. J Clin Periodontol. 1985;12(8):630–638. 32. H erzog A, H odges KO. Subgingival irrigation with Chloramine-T. J D ent H yg. 1988;62(10):515–521. 33. Krust KS, Drisko CL, Gross K, et al. The e ects o subgingival irrigation with chlorhexidine and stannous uoride. A preliminary investigation. J D ent H yg. 1991;65(6):289–295. 34. Listgarten M A, Grossberg D, Schwimer C, et al. E ect o subgingival irrigation with tetrapotassium peroxydiphosphate on scaled and untreated periodontal pockets. J Periodontol. 1989;60(1):4–11.

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35. M acAlpine R, M agnusson I, Kiger R, et al. Antimicrobial irrigation o deep pockets to supplement oral hygiene instruction and root debridement. I. Bi-weekly irrigation. J Clin Periodontol. 1985;12(7):568–577. 36. Shiloah J, Patters M R. DN A probe analyses o the survival o selected periodontal pathogens ollowing scaling, root planing, and intra-pocket irrigation. J Periodontol. 1994;65(6):568–575. 37. Christersson LA, N orderyd O M , Puchalsky CS. Topical application o tetracycline-H Cl in human periodontitis. J Clin Periodontol. 1993;20(2):88–95. 38. Khoo JG, N ewman H N . Subgingival plaque control by a simplif ed oral hygiene regime plus local chlorhexidine or metronidazole. J Periodontal R es. 1983;18(6):607–619. 39. Rosling BG, Slots J, Webber RL, et al. M icrobiological and clinical e ects o topical subgingival antimicrobial treatment on human periodontal disease. J Clin Periodontol. 1983;10(5):487–514. 40. Southard SR, Drisko CL, Killoy WJ, et al. The e ect o 2% chlorhexidine digluconate irrigation on clinical parameters and the level o Bacteroides gingivalis in periodontal pockets. J Periodontol. 1989;60(6):302–309. 41. Wol LF, Bakdash M B, Pilhlstrom BL, et al. The e ect o pro essional and home subgingival irrigation with antimicrobial agents on gingivitis and early periodontitis. J D ent H yg. 1989;63(5):222–225, 241. 42. Greenstein G. Position paper: the role o supra- and subgingival irrigation in the treatment o periodontal diseases. J Periodontol. 2005;76(11):2015–2027. 43. M acaulay WJ, N ewman H N . The e ect on the composition o subgingival plaque o a simplif ed oral hygiene system including pulsating jet subgingival irrigation. J Periodontal R es. 1986;21(4):375–385. 44. Wennstrom JL, Dahlen G, Grondahl K, et al. Periodic subgingival antimicrobial irrigation o periodontal pockets. II. M icrobiological and radiographical observations. J Clin Periodontol. 1987;14(10):573–580.

STu De n T An CILLAr y r e SOu r Ce S A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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25

C mical A ts i P io do tal Ca

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Us o S st mic A tibio tics to Co t o l Bio f lm

424

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427

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mical A

ts

ts

437

Clinical Patient Care Ethical Dilemma

Cli ical Applicatio .

As discussed in other chapters o this textbook, it is clear that periodontal diseases are caused by bacterial in ections and that bacteria ound in dental plaque biof lm are the primary causative agents in these diseases. Many bacterial in ections that have a ected mankind have been brought under control using various chemical agents to attack bacteria that cause those diseases. It is quite natural or researchers and clinicians alike to search or chemical agents or medications to help in the di f cult task o controlling periodontal diseases. This chapter discusses some o the more important chemical agents that can be used in biof lm control.

La

i

Obj cti

s

• Describe the di erence between systemic delivery and topical delivery o chemical agents. • Explain the term systemic antibiotic. • Explain why systemic antibiotics are not used routinely in the treatment o patients with plaque-associated gingivitis and patients with chronic periodontitis. • Describe three examples o mouthrinse ingredients that can help reduce the severity o gingivitis. • List three antimicrobial agents that can be delivered with controlled-release delivery devices. • Explain why toothpastes are nearly ideal delivery mechanisms or chemical agents. • List two toothpaste ingredients that can reduce the severity o gingivitis.

K

T ms

Systemic delivery Topical delivery Microbial reservoir Systemic antibiotics Antibiotic resistance

Conventional mechanical periodontal therapy Controlled-release delivery device Therapeutic mouth rinses E icacy

Stability Substantivity Sa ety Active ingredien t Inactive ingredient Essential oils

C apt

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25

Chemical Agents in Periodontal Care

ts i Bio ilm Co t o l

As discussed in other chapters o this textbook, it is clear that periodontal diseases are caused by bacterial in ections, and that bacteria ound in dental plaque bio lm are the primary causative agents in these diseases. Research indicates 1,000 species o bacteria have been ound in dental plaque bio lm. M any bacterial in ections that have a ected mankind have been brought under control using various chemical agents to attack bacteria that cause those diseases. 1. Delivery o Chemical Agents in Periodontal Patients. Chemical agents use ul in bio lm control can be delivered by using either systemic delivery or topical delivery. A. Systemic Delivery 1. In dentistry, systemic delivery usually re ers to administering chemical agents in the orm o a tablet or capsule. When a tablet is taken by the patient, the chemical agent contained is released as the tablet dissolves, and the agent subsequently enters the blood stream—thus the chemical agent is circulated “ systemically” throughout the body. 2. As the chemical agent circulates throughout the body, it is also incorporated into the tissues o the periodontium including the gingival crevicular f uids where it can come into contact with bacteria causing periodontal diseases. 3. An example o systemic delivery o a chemical agent would be or a patient to take a tablet or capsule o the antibiotic penicillin. The penicillin passes through the wall o the gastrointestinal tract and enters body tissues. In medical care, systemic delivery o chemical agents can also be administered by injection into a muscle or blood vessel, although this mode o systemic delivery has little to do with the control o dental bio lm. B. Topical Delivery 1. In dentistry, topical delivery usually re ers to intraoral placement o a chemical agent or local delivery using controlled-release devices into a periodontal pocket where the chemical agent then comes into contact with bio lm orming either on the teeth or in the periodontal pocket. 2. Examples o topical delivery in dentistry would be using a mouth rinse or toothpaste that contains a chemical agent that can kill bacteria growing in dental bio lm. In this instance the chemical agent would come into contact with the teeth, oral mucous membranes, and the sur ace o dental bio lm. 3. It should be noted that when chemical agents come into contact with oral mucous membranes, some o the agents enter the bloodstream by passing through the mucous membranes, but the bulk o the agent contacts the bacteria topically. See Table 25-1 or an overview o topical and systemic delivery mechanisms or chemical agents used in dental bio lm control. 2. Considerations or Use o Chemical Agents in Periodontal Patients A. Resistance o the Biof lm to the Delivery o Chemical Agents 1. Research shows that the sur ace o dental plaque bio lm is covered by a slime layer that can act as a barrier preventing some chemical agents rom actually contacting bacteria that are a part o the plaque bio lm.

421

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Pa t 5 Implementation o Therapy or Patients with Periodontal Disease

TABLe 2 5 -1 . De LIv e r y Me Ch An ISMS FOr Ch e MICAL Ag e n TS D li

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c io n s

s

i l l q u b io f lm in o c d si s su c s u c io n s i in sid u l c lcu lu s d o si s no m o v d d u in g n o n su g ic l i livin g w i in co n n c iv issu dj c n o io d o n l o ck i v n d d n in l u b u l s i o c d b y i g u l i i s in o o su c s m c n ic l m n i o c d b y o o ly d f n d s o io n m g in s

2. Because o the protective nature o the sur ace slime layer, mechanical bio lm control—to disrupt the structure o the bio lm—is still important to allow the chemical agents to reach the bacteria themselves. B. Microbial Reservoirs or Periodontal Pathogens. In the oral cavity, there are a variety o microbial reservoirs that can lead to rapid repopulation o bacterial pathogens in a treated periodontal patient. 1. A microbial reservoir is a niche or secure place in the oral cavity that can allow periodontal pathogens to live undisturbed during routine therapy and subsequently repopulate periodontal pockets quickly. 2. An example o a microbial reservoir would be a residual calculus deposit ollowing periodontal instrumentation. Living bacteria ound within the calculus deposit can reproduce in periodontal pockets and continue to promote disease even a ter what appears to be thorough nonsurgical therapy. 3. Box 25-1 provides an overview o some o the many microbial reservoirs or periodontal pathogens in the oral cavity. 3. Criteria or E ective Chemical Agents. For chemotherapy to be e ective, it must meet three requirements: (1) reach the site o disease activity, namely the base o the pocket, (2) be delivered at a bacteriostatic or bactericidal concentration, and (3) remain in place long enough to be e ective (1). See Table 25-2 or a comparison o the e ectiveness o common drug delivery systems or management o periodontitis.

y

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423

4. Chemical Agents E ective Against Periodontitis. Periodontal instrumentation is an e ective mechanical therapy or periodontitis (2,3). In deep or tortuous pockets or sites that do not respond to nonsurgical periodontal therapy, however, it may be bene cial to use adjunctive chemical agents (4,5). At this point, there is no bio lm control chemical agent that can halt periodontitis, but there are a number o di erent chemical agents that can be used as part o comprehensive treatment or patients with periodontal diseases. An overview o some o the types o chemical agents that have been suggested or use in bio lm control in periodontal patients is presented in Table 25-3.

TABLe 2 5 -2 . COMPAr ISOn OF Dr Ug De LIv e r y Sy STe MS FOr MAn Ag e Me n T OF Pe r IODOn TITIS Ad quat D u Co c t atio

r ac s Sit o Dis as Acti it

Ad quat Tim i Plac to b e cti

Go o d

po o

po o

Go o d

Go o d

po o

Sys m ic d liv y

F i

Go o d

F i

Co n o ll d - l

Go o d

Go o d

Go o d

Mo u

in sin g

Su b g in g iv l i ig

io n

s

d liv y

TABLe 2 5 -3 . Ov e r v Ie w OF SOMe OF Th e Ch e MICAL Ag e n TS USe D In BIOFILM COn Tr OL T p o A

t

e ampl o A

a n ib io ics

t

t

cyclin s

M a s o Admi ist atio t b l /c

su l

Lo c l d liv y m c Bisb ig u n id

n is

ics

C lo

xid in

Mo u

in s

Lo c l d liv y m c Flu o id s

M

ls l s

Oxyg n p Qu t

S n n o u s lu o id

in g g n s

n o lic co m o u n d s n

y m m o n iu m

i y m in su

Mo u

in s

t oo

s

Mo u

in s

t oo

s

Mo u

in s

e ss n i l o ils

Mo u

in s

C yl y id in iu m c lo id

Mo u

in s

D lm o in o l

Mo u

in s

t in /zin c

c n

h yd o g n

o xid

n ism

n ism

424

Pa t 5 Implementation o Therapy or Patients with Periodontal Disease

S ct io

2

Us o S st mic A tibio tics to Co t o l Bio ilm 1. Overview o Systemic Antibiotics A. Def nitions 1. Antibiotics are medications used to help ght in ections either because they kill bacteria or because they can inhibit the growth o bacteria. 2. Systemic antibiotics re er to those antibiotics that can be taken orally or that can be injected and are in widespread use in ghting bacterial in ections throughout the world. In N orth America, healthcare providers such as physicians and dentists have access to a broad range o antibiotic drugs or use in patients with in ections. These drugs have been used or many years to help the body ght certain bacterial in ections and have undoubtedly been responsible or saving countless lives. B. Systemic Antibiotics Studied or Use in Periodontal Diseases. Systemic antibiotics have also been studied or their use in controlling periodontal diseases. Box 25-2 lists some examples o systemic antibiotics that have been studied by researchers or use in periodontal patients. C. Plaque-Induced Gingivitis and Chronic Periodontitis 1. For most patients with the more common orms o periodontal diseases (i.e., either plaque-induced gingivitis or chronic periodontitis), current recommendations are or clinicians to avoid the routine use o systemic antibiotic drugs to control these diseases. There are two major reasons or recommendations to avoid their routine use in these patients. a. One reason dentists do not use systemic antibiotics routinely to control the more common orms o periodontal diseases is antibiotic resistance (6–8). Antibiotic resistance re ers to the ability o a bacterium to withstand the e ects o an antibiotic by developing mechanisms to protect the bacterium rom the killing or inhibiting e ects o the antibiotic. Most species o subgingival bacteria are considerably more resistant in bio lms than in planktonic cultures. Resistance appeared to be age related because bio lms demonstrated progressive antibiotic resistance as they matured with maximum resistance coinciding with the steady-state phase o bio lm growth (9). 1. According to the N ational Science Foundation and the Centers or Disease Control, antibiotic resistance is a serious public health problem throughout the world, and the problem is increasing in scope. When antibiotic resistant strains o bacteria develop, they are generally not a ected by the antibiotic, survive, and continue to cause more damage. 2. An example o how antibiotic resistance can be a public health problem is the high incidence o penicillin-resistant microorganisms that have already limited the use ulness o this important drug. As more and more bacteria develop resistance to the antibiotic penicillin, the use ulness o this antibiotic as a li esaving drug will continue to decrease.

Bo 25-2. e ampl s o S st mic A tibio tics Studi d o Us i P io do tal Ca • p n icillin n d m o xicillin cyclin s • t • e y o m ycin

• M o n id zo l • Clin d m ycin

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b. Another reason dentists do not use systemic antibiotics routinely to control periodontal diseases is that studies indicate that in most patients these diseases respond to conventional mechanical periodontal therapy just as well as they respond to the systemic administration o antibiotics. Conventional mechanical periodontal therapy is a term that re ers to sel care, periodontal instrumentation (scaling and root planing), and control o local contributing actors. 2. When antibiotics are being considered or use in periodontal patients, care ul patient selection is necessary. a. When tempted to use systemic antibiotics to control either plaque-induced gingivitis or chronic periodontitis, dental healthcare providers must weigh potential bene ts and disadvantages. At this point, most clinicians have decided that the potential harm outweighs the bene ts. b. In patients with chronic periodontitis the e cacy o using antibiotic therapy is not completely clear, and antibiotic therapy in these patients should usually be limited to those patients who have continued periodontal breakdown a ter thorough conventional mechanical periodontal therapy. c. It should be noted that even though systemic antibiotics are rarely indicated or routine treatment o patients with plaque-induced gingivitis or chronic periodontitis, they are requently indicated in the treatment o patients with rarer orms o periodontitis, such as aggressive periodontitis. 3. Patient education. Even though systemic antibiotic drugs are not normally used or patients with plaque-induced gingivitis or chronic periodontitis, systemic antibiotics are discussed here because periodontal patients can ask why antibiotics are not being recommended or them. a. This question may arise when the patient learns that periodontitis is a bacterial in ection. This is a natural question or a patient to ask given the widespread use o antibiotics in ghting in ections o all sorts. b. When con ronted with a question rom a patient about why antibiotics are not being recommended, the dental hygienist can explain the ollowing acts: 1. M ost cases o gingivitis and periodontitis can be readily controlled with treatments that do not require the use o systemic antibiotics. 2. O veruse o systemic antibiotics o ten results in the development o antibiotic-resistant strains o bacteria, simply compounding a complex dental problem. This is a major public health concern, since many antibiotics can be rendered useless or li esaving measures through the development o antibiotic resistance. D. Aggressive Periodontitis 1. The use o antibiotics in conjunction with mechanical therapy is usually indicated in patients with aggressive orms o periodontitis (10–13). 2. When antibiotics are being considered or use, microbiologic analysis is a wise clinical step. M icrobiologic analysis involves sampling the bacteria associated with the disease process and testing cultures o the bacteria or speci c antibiotic susceptibility. Utilizing microbiologic analysis can avoid prescribing inappropriate antibiotics that can lead to a poor clinical response. Figure 25-1 illustrates the relationship between periodontal diagnoses and the use o systemic antibiotics.

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426

Pa t 5 Implementation o Therapy or Patients with Periodontal Disease P e rio d o nta l Dia g no s is

Chronic periodontitis

Aggres s ive periodontitis

• Self-care training

• Microbial analys is and

• Periodontal ins trumentation • Periodontal s urgery

antibiotics PLUS • Self-care training • Periodontal ins trumentation • Periodontal s urgery

Microbial analys is at s ites unres pons ive to nons urgical therapy

Periodontal maintenance

Pos s ible us e of antibiotics

Periodontal maintenance

Fi u 25-1. T r latio s ip B t P io do tal Dia o sis a d t Us o S st mic A tibio tics.

2. Use o Tetracyclines in Periodontal Patients. O ne o the antibiotic groups, the group o drugs called tetracyclines, has received special attention by researchers because it has some speci c properties that make it attractive to consider or use in selected periodontal patients. A. Tetracyclines Tend to be Concentrated in the Gingival Crevicular Fluids. When tetracycline drugs are administered orally, the drugs permeate body tissues and reach a certain concentration in the blood serum. The level o tetracycline drugs, however, is more concentrated within the gingival crevicular f uids f owing into periodontal pockets than the level ound in the blood serum. This results in a higher concentration o the drug in exactly the site it might be needed in a periodontal patient. B. The Tetracyclines are E ective Against Most Strains o Aggregatibacter Actinomycetemcomitans. A ggregatibacter actinomycetem com itans is one o the periodontal pathogens thought to be a primary player in many patients with periodontitis. C. The Tetracyclines Have Other E ects in Addition to Their Antimicrobial Properties 1. Tetracyclines inhibit the action o collagenase—one o the enzymes responsible in part or breakdown o the periodontium in periodontitis patients. 2. Any drug that can inhibit the action o collagenase can be expected to slow the progress o breakdown o the periodontium that is seen in periodontitis. D. Certain Tetracyclines are E ective in Subantimicrobial Doses 1. A subantimicrobial dose (SDD) o the doxycycline (20 mg twice a day) signi cantly improved clinical parameters associated with periodontal health in patients with periodontitis when used as an adjunct to a maintenance schedule o periodontal instrumentation (10,11,13). 2. Several studies accessed whether long-term SDD o doxycycline produces doxycycline-resistant oral microf ora in adults with periodontitis. These studies ound no evidence o antibiotic resistance in the SDD doxycycline treatment groups (11,13).

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3

Us o To picall D li

dC

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Chemical Agents in Periodontal Care

mical A

ts

1. Controlled Release o Antimicrobial Chemicals A. Overview o Controlled-Release Mechanisms 1. A controlled-release delivery device usually consists o an antibacterial chemical that is imbedded in a carrier material. It is designed to be placed directly into the periodontal pocket where the carrier material attaches to the tooth sur ace and dissolves slowly, producing a steady release o the antimicrobial agent over a period o several days within the periodontal pocket (14). 2. The earliest version o these products involved coating carrier bers with chemical agents that would be released ollowing placement o the bers within periodontal pockets. Use o this early example o these products involved a return patient o ce visit or removal o the bers. 3. The latest versions o these products involve imbedding antimicrobial agents into carrier materials, which dissolve slowly over approximately 1 week. The carrier material can be placed into a periodontal pocket, and as it dissolves it slowly releases the antimicrobial agent. 4. Antimicrobial agents currently used in controlled-release delivery devices include chlorhexidine and some o the antibiotic drugs such as the tetracyclines. In the uture, other drugs may be used or this purpose. B. Rationale or Use. The goal o the use o these controlled-release delivery devices is to subject subgingival bacteria to therapeutic levels o an antibacterial drug or a sustained period. M ost o these controlled-release devices continue to deliver chemicals into the pockets or approximately 1 week. C. Benef ts o Controlled-Release Delivery Devices 1. Use o controlled-release delivery devices has been shown to result in a small increase in attachment level in a periodontal pocket (about a 2-mm reduction ound in probing depths). 2. Controlled studies are available to guide dental healthcare providers in the appropriate use o these new devices. a. Controlled-release devices may be indicated or use in localized periodontal pockets that are nonresponsive a ter thorough nonsurgical and surgical periodontal therapy. b. When these products were used along with periodontal instrumentation, they can result in both an improvement in probing depth reduction and a clinical attachment gain. The clinical signi cance o the small amount o improvement is unclear at this point. Routine use o controlledrelease delivery devices as an adjunct to periodontal instrumentation and periodontal maintenance may show improved results in uture phase III designed clinical studies. c. Current guidelines support the use o controlled-release devices in combination with periodontal instrumentation (3–5,15–18). D. Controlled-Release Mechanisms. Several controlled-release delivery products have been introduced in the United States over the last ew years, and it is likely that more will be available within the next ew years. The chemical agents that have been incorporated into these devices and marketed over the past ew years are outlined next.

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Pa t 5 Implementation o Therapy or Patients with Periodontal Disease

1. Tetracycline H ydrochloride–Containing Fibers a. O ne o the rst o these products released or use involved tetracycline hydrochloride–containing bers that were to be inserted into the periodontal pocket to deliver a high concentration o tetracycline to the site or several days. 1. M arketed under the brand name Actisite, this product is no longer available in the United States. 2. T his m echanism represents the f rst success ul product o this type, and is discussed here or historical purposes. b. Technique or Fiber Placement and Stabilization 1. A gingival retraction cord-packing instrument was used to insert the tetracycline-containing bers into a pocket, but the insertion was timeconsuming. 2. The ber was placed under the gingival margin around an entire tooth, and the pocket was lled by layering the ber back and orth upon itsel (Fig. 25-2). 3. Finally, adhesive was applied along the gingival margin to keep the ber in the pocket. 4. A return patient visit to the dental o ce was needed or ber removal. c. Adverse reactions that were reported or this product included discom ort on ber placement, oral candidiasis, allergic response, gingival inf ammation, and pain. 2. M inocycline H ydrochloride M icrospheres a. M arketed under the brand name Arestin. b. Another example o a controlled-release mechanism delivers the antibiotic minocycline hydrochloride in a powdered microsphere orm. M inocycline hydrochloride is a broad-spectrum, semisynthetic tetracycline derivative that is bacteriostatic. c. Application 1. A cannula tip is used to expel the microspheres into the pocket (Fig. 25-3) where it binds to the tooth sur ace because o the sticky nature o the carrier material. 2. O ver 5 to 7 days, the powdered microspheres dissolve releasing the imbedded minocycline, so there is nothing to remove rom the pocket. d. Studies demonstrate that repeated subgingival administration o minocycline microspheres in the treatment o adult periodontitis is sa e and is more e ective than periodontal instrumentation alone in reducing probing depths in periodontitis patients (19,20). e. Adverse reactions. Possible adverse reactions include oral candidiasis or an allergic response. In addition, the use o antibiotic preparations may result in the development o resistant bacteria. . Contraindications or use. This product is a tetracycline derivative, and should not be used in patients who are hypersensitive to any tetracycline or in women who are pregnant or nursing. 3. Doxycycline hyclate gel a. M arketed under the brand name Atridox. b. This product is a gel system that delivers the antibiotic doxycycline (also a tetracycline derivative) to the periodontal pocket.

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Chemical Agents in Periodontal Care

c. Application o doxycycline hyclate gel 1. The gel is expressed into the pocket with a cannula (Fig. 25-3), and a ter placement the gel solidi es into a wax-like substance. 2. The cannula tip is placed near the pocket base and gel is expressed using a steady pressure until the gel reaches the top o the gingival margin. 3. A limitation to this delivery system is that the gel tends to cling to the cannula when withdrawn rom the pocket, which can be reduced by using a moistened dental hand instrument to hold the gel in place while slowly withdrawing the cannula tip rom the pocket. 4. The gel is biodegradable (it dissolves), so there is nothing to remove rom the pocket. d. In a 6-month multicenter trial, results indicate that periodontal instrumentation combined with local application o doxycycline in deep periodontal sites can be considered as a justi ed approach or nonsurgical treatment o chronic periodontitis (21). e. Adverse reactions 1. Possible adverse reactions include oral candidiasis or an allergic response. 2. The use o antibiotic preparations may result in the development o resistant bacteria. . Contraindications or use. This product is a tetracycline derivative, and should not be used in patients who are hypersensitive to any tetracycline or in women who are pregnant or nursing. 4. Chlorhexidine gluconate chip a. M arketed under the brand name PerioChip. b. Another example o a controlled-release device is a tiny gelatin chip containing the antiseptic chlorhexidine that is inserted into a periodontal pocket that is 5 mm or greater in depth (Fig. 25-4). c. Investigations indicate that the chlorhexidine gluconate chip, when used as an adjunct to periodontal instrumentation, signi cantly reduces loss o alveolar bone (22). d. Application 1. The gelatin chip is inserted into the periodontal pocket. 2. The gelatin chip can be di cult to insert into some pockets due to the size and shape o the chip. 3. The gelatin chip is bioabsorbed, so there is no need to have it removed a ter placement. e. Since chlorhexidine is not an antibiotic, there is no risk o antibiotic resistance with the use o the chlorhexidine gluconate gelatin chip. . A 1-year clinical trial by H enke et al. (23) suggest that a chlorhexidine chip may reduce periodontal surgical needs at little additional cost.

429

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Pa t 5 Implementation o Therapy or Patients with Periodontal Disease

Fi u 25-2. Fib s I s t d i to t Po ck t. One o the irst local delivery mechanisms used involved a tetracycline-containing iber. The tetracyclinecontaining iber was inserted into the periodontal pocket, and the entire pocket was illed by layering the iber back and orth upon itsel . The iber released the tetracycline slowly over several days, and required removal a ter 5 to 7 days. Th is p ro d u ct is n o lo n g e r a va ila b le in t h e Un it e d St a t e s.

Fi u 25-3. P o ducts e p ll d i to t Po ck t. Some local delivery mechanisms involve placing the carrier material into a periodontal pocket with a cannula tip. Minocycline hydrochloride–containing microspheres and doxycycline gel are examples o such products. These carrier materials adhere to the tooth sur aces and dissolve slowly—releasing the antimicrobial agents trapped in the carrier material.

Fi u 25-4. g lati C ip I s t d i to Po ck t. The gelatin chip is inserted into periodontal pockets 5 mm or greater in depth. The gelatin chip adheres to the tooth sur ace and dissolves slowly—releasing the chlorhexidine antimicrobial agent trapped in the gelatin.

2. Mouth Rinses as Aids in Biof lm Control A. Introduction to Mouth Rinses 1. M any mouth rinses available today are therapeutic mouth rinses. Therapeutic mouth rinses are mouth rinses that have some actual bene t (provide some therapeutic action) to the patient in addition to the simple goal o breath reshening and halitosis reduction. a. In the context o this chapter therapeutic mouth rinses would be rinses that decrease dental bio lm enough to also decrease the severity o gingivitis. Figure 25-5 pictures two examples o therapeutic mouth rinses. b. Clinical studies support the e ectiveness o therapeutic mouth rinses used in addition to proper home care or the reduction o dental bio lm and the control o gingivitis. Insu cient evidence is available to support the claim that therapeutic mouth rinses can reduce the risk o developing periodontitis or the rate o progression o periodontitis (24,25). O ver the last ew decades, researchers are still searching or chemicals that can be added to mouth rinses that might actually reduce or halt periodontitis.

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431

Fi u 25-5. T ap utic Mo ut r i s s. Two examples o therapeutic mouth rinses used to aid in dental bio ilm control. The mouth rinse pictured on the le t contain chlorhexidine gluconate as its active ingredient. The mouth rinse pictured on the right contains essential oils as the active ingredient and is available over the counter.

2. It should be noted that in addition to therapeutic mouth rinses that can aid in the control o bio lm and gingivitis, there are other therapeutic mouth rinses available that can bene t the patient in a variety o ways such as decreasing the risk o developing dental caries and treatment o dentinal hypersensitivity. B. Characteristics That an Ideal Mouth Rinse Should Possess. Investigations into chemical bio lm control have not yet produced a bio lm control mouth rinse that can be used as a total substitute or mechanical bio lm control. H owever, these investigations have indeed produced mouth rinses that can be use ul components o a comprehensive program o patient sel -care. An ideal mouth rinse would possess our characteristics that are described below. 1. E f cacy. The active ingredient in the rinse should be e ective in inhibiting (bacteriostatic) or killing periodontal pathogens (bactericidal). 2. Stability. The ingredients in the mouth rinse should be stable at room temperature and have a reasonable shel li e. 3. Substantivity (sub-stan-tiv-ity). The active ingredient in the rinse should display the property o substantivity. This means that the active ingredient would be retained in the oral cavity or a while ollowing rinsing and would be released slowly over time (usually several hours), resulting in a continuing antimicrobial e ect against periodontal pathogens. a. Substantivity is an important characteristic, since dental bio lm grows and matures continuously. b. An active ingredient that displays the property o substantivity would continue to kill periodontal pathogens over an extended number o hours ollowing rinsing. 4. Sa ety. The ingredients in the mouth rinse should not produce any harm ul e ects to the tissues in the oral cavity or systemically to the patient. C. Ingredients o Mouth Rinses 1. Products such as mouth rinses contain both active ingredients and inactive ingredients. a. An active ingredient is a component that produces some bene t or the patient (such as a reduction in the severity o gingival inf ammation associated with gingivitis). b. All mouth rinses also contain inactive ingredients. 1. Inactive ingredients are included in mouth rinse ormulations simply to add other properties such as color enhancement, taste improvements, increase in shel li e, or to keep components in a liquid state.

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Pa t 5 Implementation o Therapy or Patients with Periodontal Disease

2. Though these ingredients are called “ inactive,” there can be associated side e ects with some o these ingredients in certain patients. It is important that clinicians maintain amiliarity with the inactive ingredients o rinses as well as the active ingredients. 2. M any chemicals that might be placed in mouth rinses have been investigated or their e ect against both bio lm and gingivitis. a. Chemicals that reduce bio lm ormation to only a minor degree usually have little or no clinically signi cant e ect against gingivitis, and there ore may not be very use ul in controlling a disease such as gingivitis. M any mouth rinses marketed today all into this category. b. Among the many ingredients tested or e cacy against gingivitis, our mouthrinse ingredients that have some e ect against gingivitis have been studied extensively. These ingredients are listed below. 1. Chlorhexidine gluconate 2. Essential oils 3. Cetylpyridinium chloride 4. Delmopinol D. Mouth Rinses Containing Chlorhexidine Gluconate 1. O ne group o mouth rinses currently available contains chlorhexidine gluconate as the active ingredient. These rinses are only available through prescriptions in the United States, but they can be purchased over the counter in some other countries. a. M outh rinses containing chlorhexidine gluconate as the active ingredient have been demonstrated to reduce the severity o gingivitis in numerous clinical studies. b. In the United States the concentration o chlorhexidine gluconate used in prescription mouth rinses is 0.12% , but it should be noted that a higher concentration is used in mouth rinses in some other countries. 2. At this point, chlorhexidine is the most e ective antimicrobial agent or longterm reduction o bio lm and gingivitis. For this reason, it is o ten regarded as the standard against which all other topical chemical bio lm control agents are judged (26,27). a. The e ectiveness o chlorhexidine gluconate mouth rinses is due to the ollowing characteristics. 1. Chlorhexidine is bactericidal agent that is e ective against both grampositive and gram-negative bacteria. 2. Chlorhexidine binds with oral tissues in the mouth and is slowly released over time (several hours) in a concentration that will continue killing bacteria. Thus, these rinses display the property o substantivity (27). 3. Chlorhexidine has a very low level o toxicity and shows no permanent retention in the body. 3. The primary mechanism o action or chlorhexidine gluconate is disruption o the integrity o the cell walls o bacteria. 4. Chlorhexidine-containing mouth rinses are use ul adjuncts to bio lm control in many patients. Current recommendations or use o this mouth rinse (0.12% chlorhexidine gluconate) are to rinse with one-hal ounce or 30 seconds twice daily, 30 minutes a ter toothbrushing.

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5. There are several groups o patients that should be considered or use o chlorhexidine gluconate mouth rinse. Some o these are outlined below: a. Special needs patients. The use o a chlorhexidine mouth rinse is suggested or speci c groups o patients who have special needs. Two examples o such patients are those with immunode ciencies that might be more susceptible to in ections in general and patients who are unable to per orm bio lm control because o some impairment. b. Postsurgical care patients. Following periodontal surgery, it is requently di cult or patients to per orm adequate mechanical bio lm control during the healing period without damaging the surgical site. In these patients, chlorhexidine mouth rinses can be used or postsurgical rinsing as a temporary adjunct to mechanical bio lm control. Use o a chlorhexidine mouth rinse ollowing periodontal surgery or 4 to 6 weeks can be e ective in many patients to promote healing. c. Patients with Candida in ections. It should be noted that a variety o medications are used to control Candida in ections, but chlorhexidine mouth rinses can be used as a disin ectant or dental appliances such as complete dentures or partial dentures in patients with these in ections. d. Patients with high caries risk. Chlorhexidine is also e ective against the bacteria responsible or dental caries. Rinsing with chlorhexidine mouth rinses has been used to reduce the counts o caries causing bacteria in certain patients. e. Patients with oral piercings or dental implants. Chlorhexidine mouth rinses have also been recommended or use by patients or a tercare o oral piercings and dental implants. . Patients who are immunocompromised. Chlorhexidine rinsing is recommended or patients being treated with radiation therapy or immunosuppressive drugs. 6. Chlorhexidine mouth rinses do have their limitations (27–29). a. Chlorhexidine is an antiplaque agent that can prevent plaque ormation, but its mode o action does not allow it to remove plaque already present on tooth sur aces e ciently. In a randomized split-mouth study, Z anatta ound that a 0.12% chlorhexidine gluconate mouth rinse had little antiplaque and antigingivitis e ect on previously plaque-covered sur aces. These results con rm the diminished e ect o chlorhexidine on structured bio lm and rein orce the necessity o mechanical bio lm disruption be ore the initiation o chlorhexidine mouth rinse (29). b. Also, the chlorhexidine molecule reacts with anionic sur actants (sodium lauryl sul ate) present in certain toothpaste ormulations, thus reducing the e ectiveness o the chlorhexidine (26). 7. Chlorhexidine mouth rinses have been evaluated related to their e ectiveness as a preprocedural rinse or dental o ce procedures producing aerosols. Studies suggest that a preprocedural chlorhexidine rinse eliminates the majority o bacterial aerosols generated by the use o an ultrasonic unit (30,31). E. Mouth Rinses Containing Essential Oils 1. Chemicals re erred to as essential oils have been used as active ingredients in some mouth rinses or many years. Chemical agents included in the group o chemicals called essential oils include thymol, menthol, eucalyptol, and methyl salicylate.

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Pa t 5 Implementation o Therapy or Patients with Periodontal Disease

2. M outh rinses containing essential oils are available over the counter (i.e., available without a prescription). Listerine mouth rinse is one example o a rinse containing essential oils, but there are other products on the market with similar ingredients. 3. There are numerous investigations related to the e cacy o essential oils in controlling gingivitis published in the literature. a. This group o chemicals can indeed help control bio lm, and they have received the Seal o Acceptance rom the American Dental Association or their e ect against gingivitis. b. A 6-month controlled clinical study demonstrated that the essential oil mouth rinse and the chlorhexidine mouth rinse had comparable antiplaque and antigingivitis activity (32). c. Several investigations ound no signi cant di erence with respect to reduction o gingival inf ammation between an essential oil mouth rinse and a chlorhexidine mouth rinse. In long-term use, the essential oil mouth rinse appears to be a reliable alternative to chlorhexidine mouthwash with respect to parameters o gingival inf ammation (33,34). d. The mechanism o action o essential oils appears to be disruption o the integrity o the cell wall and inhibition o certain bacterial enzymes. e. Essential oil mouth rinses are much less expensive than chlorhexidine mouth rinses and can be purchased without a prescription. Inso ar as the side e ects associated with chlorhexidine mouth rinses—staining, taste alteration—may limit patient compliance, essential oil mouth rinses can have a distinct role in the management o patients with periodontal diseases. F. Mouth Rinses Containing Quaternary Ammonium Compounds 1. Some mouth rinses currently marketed contain the quaternary ammonium compound cetylpyridinium chloride as the active ingredient. 2. This sur ace active agent also kills bacteria by disrupting bacterial cell walls. 3. This chemical agent binds to oral tissues but is released so rapidly that it has very limited substantivity, limiting its e ectiveness in controlling dental bio lm. 4. Investigations have shown that cetylpyridinium chloride can reduce the severity o gingivitis and supragingival bio lm, but the level o reduction is less than either chlorhexidine gluconate or essential oils (35,36). G. Mouth Rinses Containing Delmopinol 1. Some mouth rinses currently marketed contain delmopinol as the active ingredient, which is a third-generation morpholinoethanol derivative and tertiary amine sur actant. 2. This chemical agent orms a barrier preventing bio lm rom adhering to the tooth sur ace and gingiva. Delmopinol inter eres with the enzymes responsible or the ormation o bio lm and inhibits bio lm. 3. Tooth- and tongue-staining side e ects have been reported with delmopinol but were not ound to be comparable with the staining associated with chlorhexidine gluconate. 4. Investigations have shown that delmopinol e ectively reduces the severity o gingivitis and bio lm when used adjunctively with mechanical bio lm removal and is a good alternative to chlorhexidine gluconate or some patients who cannot tolerate the associated side e ects and allergies (37,38).

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Chemical Agents in Periodontal Care

H. Problems With Mouthrinse Ingredients 1. N o chemicals are completely sa e or all patients, and most mouth rinses have produced unwanted side e ects in some patients. Reported side e ects or some o the active ingredients discussed above are outlined in Table 25-4. 2. As already discussed, in addition to the active ingredients mouth rinses contain inactive ingredients such as f avoring agents and preservatives that can create problems or some patients. Two o these ingredients are listed below. a. Alcohol. Some mouth rinses have rather high levels o alcohol content, and these should be avoided in patients addicted to alcohol. b. Salt. Some mouth rinses have rather high levels o sodium, making them questionable or use in certain patients with hypertension (high blood pressure).

TABLe 2 5 -4 . POSSIBLe SIDe e FFe CTS OF MOUTh r In Se S e ss

tial Oils r i s s

• Bu n in g s n s io n in • Bi

C lo • a ll g ic

mou

g luco at r i s s

c io n

• e x in sic s in in g o

s

• D yin g o u o m u co u s m m b

idi

n s

• Disco lo • al • In c • t

io n o io n s o

ongu s

s in c lcu lu s o m n si n

n s

io n

si

3. Toothpastes as Delivery Mechanisms or Biof lm Control Agents. Denti rices such as toothpastes and gels would appear to be nearly ideal delivery mechanisms or chemical agents that might bene t patients, since most patients use these products daily. O riginally denti rices were simply aids to brushing, but today there are a variety o chemical agents that can be added to toothpastes that may actually bene t some patients in other ways. A. Categories o Toothpastes. The American Dental Association loosely classi es toothpastes as alling into one o the ollowing categories: 1. Antitartar activity 2. Caries prevention 3. Cosmetic e ects 4. Gingivitis reduction 5. Bio lm ormation reduction 6. Reduction o tooth sensitivity B. Active Chemical Ingredients. This American Dental Association classi cation o toothpastes underscores the broad range o bene ts that can be derived rom active ingredient chemical agents added to some toothpastes. 1. Some o these chemical agents are added to impart special bene ts to periodontal patients. See Table 25-5 or some examples o the chemical agents that can be used as active ingredients in toothpastes or their periodontal bene ts. 2. Stannous f uoride has been used success ully as an anticaries agent or many years. Studies indicate that stannous f uoride also a ects dental bio lm and can also reduce the severity o gingivitis when used as an active ingredient in toothpastes.

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3. Triclosan is a topical antimicrobial agent used in many products and is now available as the active ingredient in toothpaste. a. Triclosan can be combined with copolymers to enhance its substantivity (binding and subsequent slow release), which has been ound to be retained in the oral cavity or 12 hours. b. Studies indicate that when combined with copolymers, triclosan (when delivered in toothpaste orm) can decrease the severity o gingivitis more than denti rice with stannous f uoride (39,40). c. Triclosan can also be combined with zinc citrate to reduce dental calculus ormation. C. The Future. Toothpastes appear to be ideal delivery mechanisms or chemical agents that might be expected to control certain periodontal conditions, such as gingival inf ammation. It is reasonable to expect that additional research in this area will result in additional toothpaste ormulations that target periodontal conditions such as gingivitis.

TABLe 2 5 -5 . e x AMPLe S OF TOOTh ACTIv e In g r e DIe n TS USe D FOr Pe r IODOn TAL Be n e FITS I

di

py o

os

ts

Actio s s

r d u c s su p ra g in g iv l c lcu lu s

S n n o u s lu o id

r d u c s su p ra g in g iv l b io ilm r d u c s g in g iv l in l m m

r d u c s su p ra g in g iv l c lcu lu s

t iclo s n

r d u c s g in g iv l in l m m Zin c ci

C apt

io n

io n

r d u c s su p ra g in g iv l c lcu lu s

Summa

Stat m

t

Chemical agents that can be used to control dental bio lm can be delivered both systemically and topically. Since dental bio lm is covered by a protective slime layer, chemical agents will not necessarily contact all o the targeted bacteria, and their use must be accompanied by mechanical bio lm control that can disrupt the structure o the bio lm. Systemic antibiotics are not normally used to control dental bio lm in patients with the most common periodontal conditions (plaque-associated gingivitis and chronic periodontitis) because o the high risk o developing antibiotic-resistant strains. M outh rinses can be use ul adjuncts in the treatment o patients with periodontal diseases. Thus, ar the most e ective ingredients to control bio lm that can be incorporated into mouth rinses include chlorhexidine and the essential oils. Controlled-release delivery devices are also available to help control bacterial bio lm in periodontal patients. Toothpastes are widely used by patients and appear to be an ideal mechanism or delivery o chemical agents to aid in bio lm control. In selecting the appropriate delivery system, the clinician has to weigh the e cacy o the products, ease o use, availability, and cost. Although local delivery systems do not replace existing periodontal therapies, they do have a place in the treatment o periodontitis and o er the dental team additional methods to aid in the control o periodontal diseases.

C apt

S ct io

4

Fo cus o

Cli ical Pati CA S e

Pati

25

Chemical Agents in Periodontal Care

437

ts

t Ca

1

A patient shows you a bottle o mouth rinse and asks you i it would be all right to use this mouth rinse instead o brushing and f ossing so requently. You study the label on the bottle o mouth rinse and nd that the active ingredients are the essential oils. H ow should you respond to this patient about substituting this rinse or other sel -care e orts such as brushing and f ossing?

CA S e

2

A patient being treated by the members o your dental team has generalized chronic periodontitis. Following your thorough explanation o the nature o chronic periodontitis and your emphasis that this disease is indeed a bacterial in ection, the patient asks this question, “ I periodontitis is an in ection, can you ask the dentist to give me a prescription or an antibiotic?” H ow should you respond to this patient’s question?

CA S e

3

A new patient being seen by your dental team has recently moved into your city. She has previously been treated or chronic periodontitis and has been on periodontal maintenance or several years. She is now having trouble with mechanical bio lm control because o increasing dexterity problems. What chemical agents can you recommend that might help reduce the patient’s gingival inf ammation?

e t ical Dil mma Your patient, Sandy L, is a 24-year-old woman who has come to your o ce or a second opinion. H er chie complaint is that she eels that her periodontal health is not improving, and i anything, getting worse. You review her health history, and she states that she has been under the care o her uncle, who is a 70-year-old periodontist. She has been taking tetracycline or the last 5 years, and is concerned with her periodontal and overall health. She did not bring any radiographs, as she doesn’t want her uncle to know about this appointment. Your examination reveals that Sandy has relatively good oral hygiene, with slight supragingival visible calculus between her mandibular anterior teeth. H owever, she presents with generalized severe gingival recession, and her attachment level readings range rom 3 to 6 mm, with localized 7-mm readings on her posterior teeth. continued on nex t page

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It is hard to get a ull picture due to the lack o radiographs. Sandy’s periodontal status is troubling and you are not sure i the antibiotics that she is taking are actually helping her. You ask i she ever had a microbiologic analysis, to sample her oral bacteria susceptibility. She is not sure o any procedures, as she “ just le t all o that stu to her uncle, the periodontal expert.” 1. What do you think have may caused the patient’s generalized recession? 2. What actors may have contributed to the patient’s disease progression? 3. What ethical principles are in conf ict in this dilemma?

r

c s

1. Finkelman RD, Polson AM . Evidence-based considerations or the clinical use o locally delivered, controlled-release antimicrobials in periodontal therapy. J D ent H yg. 2013;87(5):249–264. 2. Cobb CM . Clinical signi cance o non-surgical periodontal therapy: an evidence-based perspective o scaling and root planing. J Clin Periodontol. 2002;29 (suppl 2):6–16. 3. Drisko CL, Cochran DL, Blieden T, et al. Position paper: sonic and ultrasonic scalers in periodontics. Research, Science and Therapy Committee o the American Academy o Periodontology. J Periodontol. 2000;71(11):1792–1801. 4. H anes PJ, Purvis JP. Local anti-in ective therapy: pharmacological agents. A systematic review. A nn Periodontol. 2003;8(1):79–98. 5. Greenstein G. The role o local drug delivery in the treatment o chronic periodontitis. Things you should know. D ent Today. 2004;23(3):110–115. 6. M ah TF, O ’Toole GA. M echanisms o bio lm resistance to antimicrobial agents. Trends M icrobiol. 2001;9(1):34–39. 7. Rams TE, Degener JE, van Winkelho AJ. Antibiotic resistance in human chronic periodontitis microbiota. J Periodontol. 2014;85(1):160–169. 8. Walker CB. The acquisition o antibiotic resistance in the periodontal microf ora. Periodontol 2000. 1996;10:79–88. 9. Sedlacek M J, Walker C. Antibiotic resistance in an in vitro subgingival bio lm model. O ral M icrobiol Im m unol. 2007;22(5):333–339. 10. Caton JG, Ciancio SG, Blieden TM , et al. Treatment with subantimicrobial dose doxycycline improves the e cacy o scaling and root planing in patients with adult periodontitis. J Periodontol. 2000;71(4):521–532. 11. Ciancio S, Ashley R. Sa ety and e cacy o sub-antimicrobial-dose doxycycline therapy in patients with adult periodontitis. A dv D ent R es. 1998;12(2):27–31. 12. Slots J; Research, Science and Therapy Committee. Systemic antibiotics in periodontics. J Periodontol. 2004;75(11): 1553–1565. 13. Thomas J, Walker C, Bradshaw M . Long-term use o subantimicrobial dose doxycycline does not lead to changes in antimicrobial susceptibility. J Periodontol. 2000;71(9):1472–1483. 14. Ciancio SG. Site speci c delivery o antimicrobial agents or periodontal disease. G en D ent. 1999;47(2):172–178. 15. Finkelman RD. Re: role o controlled drug delivery or periodontitis (position paper). The American Academy o Periodontology (2000;71:12–40). J Periodontol. 2000;71(12):1929–1933. 16. Greenstein G. Local drug delivery in the treatment o periodontal diseases: assessing the clinical signi cance o the results. J Periodontol. 2006;77(4):565–578. 17. Greenstein G, Tonetti M . The role o controlled drug delivery or periodontitis. The Research, Science and Therapy Committee o the American Academy o Periodontology. J Periodontol. 2000;71(1):125–140. 18. Killoy WJ. The clinical signi cance o local chemotherapies. J Clin Periodontol. 2002;29 Suppl 2:22–29. 19. van Steenberghe D, Rosling B, Soder PO, et al. A 15-month evaluation o the e ects o repeated subgingival minocycline in chronic adult periodontitis. J Periodontol. 1999;70(6):657–667. 20. Williams RC, Paquette DW, O enbacher S, et al. Treatment o periodontitis by local administration o minocycline microspheres: a controlled trial. J Periodontol. 2001;72(11):1535–1544. 21. Wennstrom JL, N ewman H N , M acN eill SR, et al. Utilisation o locally delivered doxycycline in non-surgical treatment o chronic periodontitis. A comparative multi-centre trial o 2 treatment approaches. J Clin Periodontol. 2001;28(8):753–761. 22. Je coat M K, Palcanis KG, Weather ord TW, et al. Use o a biodegradable chlorhexidine chip in the treatment o adult periodontitis: clinical and radiographic ndings. J Periodontol. 2000;71(2):256–262. 23. H enke CJ, Villa KF, Aichelmann-Reidy M E, et al. An economic evaluation o a chlorhexidine chip or treating chronic periodontitis: the CH IP (chlorhexidine in periodontitis) study. J A m D ent A ssoc. 2001;132(11):1557–1569. 24. Barnett M L. The role o therapeutic antimicrobial mouthrinses in clinical practice: control o supragingival plaque and gingivitis. J A m D ent A ssoc. 2003;134(6):699–704. 25. O sso D, Kanani N . Antiseptic mouth rinses: an update on comparative e ectiveness, risks and recommendations. J D ent H yg. 2013;87(1):10–18. 26. Jones CG. Chlorhexidine: is it still the gold standard? Periodontol 2000. 1997;15:55–62. 27. M athur S, M athur T, Shrivastava R, et al. Chlorhexidine: the gold standard in chemical plaque control. N atl J Physiol Pharm Pharm acol. 2011;1(2):45–50. 28. Li W, Wang RE, Finger M , et al. Evaluation o the antigingivitis e ect o a chlorhexidine mouthwash with or without an antidiscoloration system compared to placebo during experimental gingivitis. J Investig Clin D ent. 2014;5(1):15–22.

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29. Z anatta FB, Antoniazzi RP, Rosing CK. The e ect o 0.12% chlorhexidine gluconate rinsing on previously plaque- ree and plaque-covered sur aces: a randomized, controlled clinical trial. J Periodontol. 2007;78(11):2127–2134. 30. Gupta G, M itra D, Ashok KP, et al. E cacy o preprocedural mouth rinsing in reducing aerosol contamination produced by ultrasonic scaler: a pilot study. J Periodontol. 2014;85(4):562–568. 31. Klyn SL, Cummings DE, Richardson BW, et al. Reduction o bacteria-containing spray produced during ultrasonic scaling. G en D ent. 2001;49(6):648–652. 32. Charles CH , M ostler KM , Bartels LL, et al. Comparative antiplaque and antigingivitis e ectiveness o a chlorhexidine and an essential oil mouthrinse: 6-month clinical trial. J Clin Periodontol. 2004;31(10):878–884. 33. Stoeken JE, Paraskevas S, van der Weijden GA. The long-term e ect o a mouthrinse containing essential oils on dental plaque and gingivitis: a systematic review. J Periodontol. 2007;78(7):1218–1228. 34. Van Leeuwen M P, Slot DE, Van der Weijden GA. Essential oils compared to chlorhexidine with respect to plaque and parameters o gingival inf ammation: a systematic review. J Periodontol. 2011;82(2):174–194. 35. H aps S, Slot DE, Berchier CE, et al. The e ect o cetylpyridinium chloride-containing mouth rinses as adjuncts to toothbrushing on plaque and parameters o gingival inf ammation: a systematic review. Int J D ent H yg. 2008;6(4):290–303. 36. Versteeg PA, Rosema N A, H oenderdos N L, et al. The plaque inhibitory e ect o a CPC mouthrinse in a 3-day plaque accumulation model - a cross-over study. Int J D ent H yg. 2010;8(4):269–275. 37. Addy M , M oran J, N ewcombe RG. M eta-analyses o studies o 0.2% delmopinol mouth rinse as an adjunct to gingival health and plaque control measures. J Clin Periodontol. 2007;34(1):58–65. 38. M oran J, Addy M , Wade WG, et al. A comparison o delmopinol and chlorhexidine on plaque regrowth over a 4-day period and salivary bacterial counts. J Clin Periodontol. 1992;19(10):749–753. 39. Ciancio S, Panagakos FS. Superior management o plaque and gingivitis through the use o a triclosan/copolymer denti rice. J Clin D ent. 2010;21(4):93–95. 40. H araszthy VI, Z ambon JJ, Sreenivasan PK. Evaluation o the antimicrobial activity o denti rices on human oral bacteria. J Clin D ent. 2010;21(4):96–100.

STUDe n T An CILLAr y r e SOUr Ce S A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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26

Ho st Mo d latio n The rap

Se ctio n 1

Intro d ctio n to the Ho st Mo d latio n The rap

441

Se ctio n 2

Po te ntial Ho st Mo d lating The rapie s in Pe rio do ntal Patie nts

443

Ho st Mo d latio n The rap as a Part o Co mpre he nsive Pe rio do ntal Patie nt Manag e me nt

447

Fo c s o n Patie nts

449

Se ctio n 3

Se ctio n 4

Evidence in Action Ethical Dilemma

Clinical Applicatio n.

Host modulation therapy is currently one o the most exciting areas o research related to periodontal diseases. Though recommended clinical applications o this topic are limited, everyone who is involved in the care o patients with periodontal disease will read more and more publications devoted to this topic. To interpret these publications correctly, dental hygienists will need to understand what host modulation therapy can include and will need to be prepared to accept this modality as a valid part o patient care. This chapter provides an outline o the topic o host modulation therapy.

Le arning Obje ctive s • Explain the term host modulation therapy. • Explain the potential importance o host modulation therapy. • Name some anti-inf ammatory mediators. • Name some proinf ammatory mediators. • List three types o drugs that have been studied or use as possible host modulating agents. • Explain why low-dose doxycyclines are use ul as host modulating agents. • Explain the term subantibacterial dose. • Make a list o treatment strategies or a periodontitis patient that includes host modulation.

Ke Te rms Host modulation therapy Osteoporosis Biochemical mediators Anti-in lammatory mediators

Proin lammatory mediators Doxycycline Subantibacterial doses

Nonsteroidal Anti-in lammatory Drugs (NSAIDs) Bisphosphonates

Chapte r 26

Host Modulation Therapy

Se ct io n 1

Intro d ctio n to the Ho st Mo d latio n The rap For several decades the ocus o therapy or patients with in ammatory periodontal diseases has been directed toward controlling the microbial etiology o these diseases; minimizing the bacterial challenge to the periodontium has been a success ul strategy or the treatment o many patients with both gingivitis and periodontitis. Beyond any doubt, plaque biof lm control strategies will continue to play a major role in the therapy or patients with periodontal disease. Based upon current knowledge o the underlying pathology involved in periodontal diseases, additional strategies or therapy are emerging that may also be employed or patients with in ammatory periodontal diseases. O ne o these additional strategies relates to the concept o host modulation therapy (1–4). 1. Host Modulation Therapy De ned. Host modulation therapy can be def ned as altering a patient’s (i.e., the host’s) de ense responses to help the body de enses limit damage caused by a disease. In dentistry the concept o host modulation therapy ocuses on how the body responds to the bacterial challenge rather than simply reducing that bacterial challenge posed by plaque biof lm. 2. Examples o Host Modulation Therapy in Medicine A. H ost modulation therapy is not a new concept in medicine, and it has been a part o the medical care or patients with a variety o systemic diseases or many years. O ne example o a common systemic disease or which physicians requently use host modulation is osteoporosis. B. Osteoporosis is a progressive bone disease that is characterized by a decrease in both bone mass and bone density that can lead to an increased risk o bone ractures. O steoporosis a ects millions o patients in the United States. C. Treatments or osteoporosis can be broadly divided into two categories based upon how the treatment medications a ect the bone. O ne group o medications reduces bone resorption while the second group o medications stim ulates bone orm ation. 1. Antiresorptive agents, which include medications such as estrogen, selective estrogen receptor modulators, and bisphosphonates, reduce bone resorption and help to preserve bone mineral density. 2. Bone- orming agents stimulate bone ormation, thereby increasing overall bone mineral density. D. Patients who receive the types o medications discussed above are said to be receiving host modulation therapy, that is, the host response to the disease (loss o bone mass and density) is modulated to minimize the e ects o the disease to prevent bone ractures. 3. Importance o Host Modulation Therapy in Dentistry. The potential importance o host modulation as one strategy in managing periodontitis patients is huge. A. As already discussed in other chapters, many adults show signs o periodontal or gingival disease with severe periodontitis a ecting approximately 15% o the adult population in the United States. Because so many patients have in ammatory periodontal diseases, there is a continuing need or cost-e ective strategies or managing periodontitis patients. B. As the population in the United States ages, it is reasonable to expect the prevalence o periodontitis to increase, making the need or the most cost-e ective therapy even greater.

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C. In addition, there is mounting evidence that periodontal health and several systemic conditions (such as diabetes and cardiovascular disease) are linked, again making it likely that the demand or periodontal therapy will increase over the upcoming decades. 4. Review o Host Responses That Can Be Modulated A. The undamental pathologic processes or periodontitis have been outlined in other chapters o this book; in those chapters the ollowing issues have been discussed. 1. Bacteria (and bacterial products) that are a part o the plaque biof lm initiate an in ammatory response in the periodontium. The bacteria stimulate the immune cells to produce biochemical mediators (i.e., biologically active compounds) that activate this in ammatory response. 2. The in ammatory response unctions as a protective response that keeps the bacterial in ection rom doing serious harm to the periodontium in many patients partly through the production o chemicals called anti-in ammatory mediators. Anti-inf ammatory mediators are biochemical mediators that are protective and help keep the bacterial in ection rom doing serious harm to the periodontium. These anti-in ammatory mediators include the cytokines IL-4 (interleukin-4) and IL-10 (interleukin-10). 3. Box 26-1 shows an overview o some o the anti-in ammatory biochemical mediators that have been discussed in other chapters. 4. I the bacterial challenge is great enough, however, the nature o the protective responses changes, resulting in the production o additional biochemical mediators that can lead to actual damage within the periodontium. a. Some biochemical mediators (re erred to as proinf ammatory mediators) can damage the periodontium. These proin ammatory biochemical mediators include chemicals such as matrix metalloproteinases (M M Ps), certain cytokines, prostanoids, and other less well-understood mediators (5–9). b. Specif c examples o these proin ammatory mediators include prostaglandin E2 IL-1α (interleukin-1 alpha), IL-1β (interleukin-1 beta), IL-6 (interleukin-6), and tumor necrosis actor alpha. c. For example, one o the M M Ps is an enzyme called collagenase that can actually break down collagen. Collagen is one o the major building blocks in the periodontium, and its breakdown is part o the undamental pathology in periodontitis. d. Box 26-2 shows some o the proin ammatory biochemical mediators. 5. In the periodontium these altered host de ense responses can result in both breakdown o connective tissue f bers and resorption o alveolar bone (the precise type o tissue destruction seen in periodontitis). 6. M uch o the destruction o the periodontium that accompanies periodontitis is thought to be a result o these altered processes that occur as part o the host de enses (the host in ammatory and immune responses). B. Fundamentally, the concept o host modulation therapy as a strategy in treating periodontitis patients is to limit the damaging e ect o the altered host responses by modi ying (or modulating) the e ect o these destructive biochemical mediators. M odulation o host de enses is currently an important ocus or periodontal research, and host modulation therapy will undoubtedly play a ar larger part in periodontal therapy in the uture.

Chapte r 26

Host Modulation Therapy

Bo x 26-1. Example s o Anti-Inf ammato r Bio che mical Me diato rs t s b io c m ic l m d i o s • IL-4 (in l u kin -4) • IL-10 (in l u kin -10)

l

body f g o c so • IL-1 ( c o n g o n is ) • t IMps ( issu in ib i o s o m

b c ix m

i lc llo

o

ll n g : in s s)

Bo x 26-2. Example s o Pro inf ammato r Bio che mical Me diato rs t s b io c m ic l m d i o s c n l • IL-1 (in l u kin -1) • IL-6 (in l u kin -6) • pGe 2 ( o s g l n d in e 2 )

d o d s u c io n o issu s o io d o n iu m : • t NFα ( u m o n c o sis c o l ) • MMps (m ix m llo o in s s)

Se ct io n 2

Po te ntial Ho st Mo d lating The rapie s in Pe rio do ntal Patie nts 1. Use o Tetracycline Medications A. Doxycycline 1. Doxycycline is a tetracycline antibiotic drug that has been used to treat a variety o in ections. a. As with other antibiotic medications, doxycycline must be given in doses high enough to a ect the targeted bacteria to help the body f ght an in ection. b. Antibiotic doses high enough to inhibit or kill bacteria are sometimes called antibacterial doses. A typical antibacterial dose or doxycycline would be 50 to 100 mg every 12 hours. 2. Doxycycline has other e ects besides its antibiotic e ect that is seen with the higher doses described above. a. I this medication is given even at low doses (below that needed or any antibacterial e ect), it decreases the e ects o the enzyme collagenase (one o the matrix metalloproteinases or M M Ps). b. As already discussed, M M Ps (such as collagenase) can be released in in amed periodontal tissues and can cause breakdown o the connective tissue. Prevention o the action o collagenase can inhibit the progress o periodontitis. c. Doses o an antibiotic that are below the normal bacterial killing or inhibiting doses are re erred to as subantibacterial doses. d. Since doxycycline at low doses (or subantibacterial doses) alters the body de enses by inhibiting part o the destruction that can occur in periodontitis, it is considered one example o a host modulating agent (10–22).

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e. The FDA (U. S. Food and Drug Administration) has approved subantibacterial doses o doxycycline (20-mg tablets) or use in treating patients with periodontitis. 1. Low doses o doxycycline must be taken twice daily in tablet orm to be e ective in periodontitis patients. 2. N o antibacterial e ects on the oral bacteria or bacteria in other parts o the body have been ound with the use o low-dose doxycycline. 3. Studies o this drug have also shown a clinical benef t when used as an adjunct to periodontal instrumentation. 4. Though tetracyclines used at antibacterial doses can have side e ects (including nausea, vomiting, photosensitivity, and hypersensitivity reactions), doxycycline at low doses appears to be accompanied by a very low incidence o adverse e ects. 3. Studies have shown reductions in probing depths and gains in clinical attachment levels as well as the prevention o periodontal disease progression with the use o subantibacterial doses o doxycycline in periodontitis patients. B. Use o Chemically Modi ed Tetracyclines 1. Chemically modif ed tetracyclines are derivatives o tetracycline group o drugs that lack antimicrobial action but have potent host modulating e ects. 2. Though these drugs lack antimicrobial action, they can inhibit elevated matrix metalloproteinases, proin ammatory cytokines, and other destructive mediators (23). 3. Bone resorption can also be suppressed by these drugs. 4. Development o resistant bacteria and gastrointestinal toxicity seen with antibacterial doses o the tetracyclines is not produced by chemically modif ed tetracyclines (23). 5. Chemically modif ed tetracyclines are currently being investigated as potential host modulation therapeutic agents in the management o chronic diseases like periodontitis, but only urther research may demonstrate their e f cacy and sa ety in periodontal patients. 2. Use o N onsteroidal Anti-inf ammatory Drugs A. N onsteroidal anti-inf ammatory drugs (N SAIDs) have been used or many years in medical care to treat pain, acute in ammation, and chronic in ammatory conditions. 1. Box 26-3 shows examples o drugs included in the group called N SAIDS. 2. N SAIDs can reduce tissue in ammation by inhibiting the action o prostaglandins including PGE2 . B. In periodontal studies systemically administered N SAIDs have been evaluated or their e ect on periodontitis (a disease intimately associated with in ammation). 1. In the periodontium N SAIDs can both reduce in ammation and inhibit osteoclast activity. 2. Some N SAIDs, when administered daily over 3 years, have been shown to slow the rate o alveolar bone loss associated with periodontitis. 3. M ore research is needed in this area to clari y the e f cacy and sa ety o using N SAIDs as host modulating agents in periodontal patients. C. Long-term use o N SAIDs in periodontitis patients is not recommended because o signif cant side e ects that can develop with the use o these drugs. 1. Side e ects rom N SAIDs can include gastrointestinal problems, hemorrhage (bleeding), and kidney or liver impairment. 2. In addition, when a patient with periodontitis stops taking daily doses o N SAIDs, there can be an acceleration o bone loss seen be ore taking the drugs. 3. At present no N SAIDs are approved or the treatment o periodontal disease.

Chapte r 26

Host Modulation Therapy

Bo x 26-3. Example s o NSAID Me dicatio ns • • • • •

S licyl s ( s i in ) In d o m cin Ib u o n Flu b i o n N ox n

D. Even though N SAIDs are not currently recommended or use in host modulation in periodontitis patients, they have been discussed here because o the extensive dental research that has involved these drugs. E. In addition to systemically administered N SAIDs, topically applied N SAIDs have been studied or their possible benef ts to periodontitis patients. 1. Topical N SAIDs have also been shown to reduce PGE2 (prostaglandin E2 ) in gingival crevicular uid in periodontitis patients (24–27). 2. Topically administered N SAIDs have not been approved or the management o periodontitis, but more study o the possible use o topical N SAIDs is warranted. 3. Use o Bisphosphonate Medications A. Bisphosphonates are drugs that can inhibit the resorption o bone by altering osteoclastic activity, though the mechanism o action or these drugs is not ully understood. B. Early research indicates there may be some benef t to periodontitis patients rom the ability o bisphosphonates to alter osteoclastic activity (bone resorption activity) (25,28). C. Some o the bisphosphonates have side e ects that may limit their use in periodontitis patients, but they are discussed in this section because o the interest that has been shown in these drugs over the last ew years. D. O ne o the possible side e ects o these drugs is osteonecrosis o the jaws ollowing their extended use (29). O steonecrosis is the destruction and death o bone tissue, in this case the bone tissue o the jaw. Studies are under way to clari y the precise risk and etiology o this serious side e ect o bisphosphonates. E. A t present there are no bisphosphonate drugs that are approved or the treatm ent o periodontal disease. 4. Use o Statin Medications A. Recently it has been suggested that statin drugs that are normally used to control elevated cholesterol levels may have an e ect upon periodontitis. B. There are quite a ew statin medications available, but only a ew such as simvastatin and atorvastin have been suggested as possible host modulation agents in periodontal patients. C. Statin medications have several e ects including o ering some protection against systemic in ammation (30). D. At this point the e f cacy o these drugs in periodontal patients needs to be clarif ed with additional research studies. 5. Dietary Supplementation A. Dietary supplementation is another avenue that may hold promise or developing strategies to modi y the host response to chronic periodontitis, especially i it is possible to enhance the resolution o in ammation through dietary supplements.

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B. The possibility o supplementing the diet with specif c biomolecules, such as essential atty acids, is currently being investigated or its e ect upon periodontitis (31–33). C. Using supplements o omega-3 atty acids to modi y the host response to chronic periodontitis and reduce the severity o periodontal disease would certainly be a straight orward strategy or host modulation therapy i studies demonstrate the e f cacy o such supplements. 6. Use o Other Types o “Host Modulation Agents” A. Several potential agents have been investigated or use as adjuncts to periodontal surgical procedures. B. These drugs do not produce the same types o e ects discussed or the other potential host modulating agents, but they are mentioned here because some authors have re erred to them as “ host modulating agents.” C. These agents are generally applied topically during periodontal surgical procedures and have been suggested or use or possible enhancement o wound healing or possible enhancement o regeneration o periodontal tissues ollowing the surgery. D. Some agents o this type that have been investigated are enamel matrix proteins, bone morphogenetic proteins (BM P-2, BM P-7), and certain growth actors. E. Currently the only local host modulation agent approved or adjunctive use during periodontal surgery is an enamel matrix protein called Emdogain, and this agent is under continuing study. F. M embers o the dental team should expect additional host modulation products to be investigated and to appear on the market; care ul evaluation o each o the products will be needed (2).

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Host Modulation Therapy

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Ho st Mo d latio n The rap as a Part o Co mpre he nsive Pe rio do ntal Patie nt Manag e me nt 1. Periodontal therapy based upon minimizing the bacterial challenge has been a primary therapeutic modality or many years, and this therapy has proved to be success ul in many patients. A. Studies indicate, however, that markers o periodontal disease in patients with periodontitis undergo little change ollowing conventional mechanical periodontal therapy, in spite o its success ul outcomes. B. It appears that even though conventional periodontal therapy based upon minimizing the bacterial challenge is usually success ul, the underlying disease processes may indeed be diminished in severity, but they may remain undamentally unchanged. C. These observations should not distract rom a clinician’s enthusiasm or recommending conventional periodontal therapy, but they should make clinicians eager or more therapies to be developed and to be added to those currently available. 2. Employing host modulation therapy in the comprehensive management o some periodontal patients seems to be a promising strategy to employ in the uture. A. It should be reemphasized that at present the only host modulation therapy agent currently being recommended is the low-dose tetracyclines, but as discussed, investigations have indicated that at least theoretically other possible host modulation therapies may one day be employed in periodontal patients. B. It must also be noted that when used in periodontitis patients, sound clinical practice dictates that the use o low-dose doxycycline therapy be accompanied by all o the usual treatment strategies such as risk actor reduction (i.e., smoking cessation counseling) and bacterial challenge reduction (i.e., sel -care training and periodontal instrumentation). 3. Box 26-4 lists the array o therapeutic strategies that can be employed when managing a patient with periodontitis to illustrate that host modulation therapy may be viewed as another therapy among the long list o options available or a patient with periodontal disease. 4. Figure 26-1 shows some theoretical possibilities or host modulation as a part o overall management o periodontitis patients.

Bo x 26-4. The rape tic Optio ns o r a Pe rio do ntitis Patie nt 1. 2. 3. 4. 5. 6. 7. 8. 9.

p i n d u c io n n d in in g in s l -c . e m lo ym n o m o iv io n l s gi s o i n s l -c . r d u c io n o b c i l c ll n g b y io d o n l in s u m n Us o lo c l d liv y sys m s o n im ic o b i l g n s. e lim in io n o lo c l co n ib u in g c o s. Sys m ic isk c o d u c io n . h o s m o d u l io n y. p io d o n l su g y. p io d o n l m in n n c .

io n .

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Cas c ade o f e ve nts in the de ve lo pme nt o f c hro nic pe rio do ntitis P la q ue b io lm with a s s oc ia te d b a c te ria a nd b a c te ria l p rod uc ts

Applic atio n o f po te ntial ho s t mo dulatio n the rapie s to vario us s te ps in the de ve lo pme nt o f pe rio do ntitis

Ac tiva tion of hos t re s p ons e to b a c te ria l c ha lle nge

Hos t mod ula tion the ra p y might b e us e d to e nha nc e the hos t’s p rote c tive re s p ons e

P rod uc tion of a nti-in a mma tory me d ia tors (p rote c tive re s p ons e )

Hos t mod ula tion the ra p y might b e us e d to mod ify the ove ra ll in a mma tory re s p ons e

Fa ilure of p rote c tive re s p ons e to c ontrol c ha lle nge (p e rha p s d ue to ina d e q ua te s e lf-c a re or p re s e nc e of loc a l fa c tors s uc h a s c a lc ulus )

P rod uc tion of p roin a mma tory me d ia tors (d a ma ging re s p ons e )

Hos t mod ula tion the ra p y might b e us e d to nullify the e ffe c t of s p e c i c p roin a mma tory me d ia tors

P ros ta gla nd ins , Cytokine s , MMP s le a d to b re a kd own of c onne c tive tis s ue in p e riod ontium a nd re s orp tion of a lve ola r b one

Hos t mod ula tion the ra p y might b e us e d to b loc k the b re a kd own of c olla ge n or to b loc k b one re s orp tion

Chro nic pe rio do ntitis

Fig re 26-1. Applicatio n o Po te ntial Ho st Mo d latio n The rapie s. Potential host modulation therapies can be applied to a cascade o events starting with plaque bio ilm and ending with chronic periodontitis. This igure shows the wide range o potential applications that research may make possible in the uture.

Chapte r S mmar State me nt H ost modulation therapy in periodontal patients (i.e., altering the body’s de ense mechanisms to limit damage rom the oral bacterial challenge) is an interesting and ongoing line o investigation. H ost modulation therapy has been suggested as an additional therapeutic strategy in periodontitis patients. At this point, low-dose doxycycline has been approved or use as a host modulating agent in humans with periodontitis. When used in subantimicrobial doses, this drug can help inhibit the progress o periodontitis. M embers o the dental team will undoubtedly encounter much research activity related to additional host modulating therapies over the next several decades.

Chapte r 26

Host Modulation Therapy

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Fo c s o n Patie nts Evide nce in Actio n CASE 1 A new patient in your dental team’s o f ce has a periodontal diagnosis o generalized severe chronic periodontitis. Explain how host modulation therapy might be included among other treatment strategies used to help control the damage to the periodontium that normally accompanies periodontitis.

Ethical Dile mma Tammy is a 60-year-old artist, who you see every 3 months or periodontal maintenance, as she su ers rom generalized chronic periodontitis. As you review her health history today, she states that she is now taking Fosamax, which was prescribed by her primary care physician, Dr. James. She states that she has been diagnosed with osteoporosis and has been taking Fosamax or the last 2 months. Dr. James also told Tammy that the medication would be help ul in stabilizing her periodontal disease, which was a side benef t. H e assured her that there was no down side in taking the medication. Tammy has done some research on line and has ound some disturbing evidence o the possible side e ects o Fosamax. She asks or your thoughts and opinion. 1. Are bisphosphonate drugs approved or the treatment o periodontal disease? 2. What would you tell Tammy about the possible side e ects o the use o bisphosphonate drugs? 3. Are there ethical principles in con ict with this dilemma?

Re e re nce s 1. Bhatavadekar N B, Williams RC. N ew directions in host modulation or the management o periodontal disease. J Clin Periodontol. 2009;36(2):124–126. 2. Gokhale SR, Padhye AM . Future prospects o systemic host modulatory agents in periodontal therapy. Br D ent J. 2013;214(9):467–471. 3. Salvi GE, Lang N P. H ost response modulation in the management o periodontal diseases. J Clin Periodontol. 2005;32 Suppl 6:108–129. 4. Tonetti M S, Chapple IL; Working Group 3 o Seventh European Workshop on Periodontology. Biological approaches to the development o novel periodontal therapies–consensus o the Seventh European Workshop on Periodontology. J Clin Periodontol. 2011;38 Suppl 11:114–118. 5. Birkedal-H ansen H . Role o matrix metalloproteinases in human periodontal diseases. J Periodontol. 1993;64(5 Suppl):474– 484. 6. Deo V, Bhongade M L. Pathogenesis o periodontitis: role o cytokines in host response. D ent Today. 2010;29(9):60–62, 64–66; quiz 68–69. 7. Golub LM , Lee H M , Greenwald RA, et al. A matrix metalloproteinase inhibitor reduces bone-type collagen degradation ragments and specif c collagenases in gingival crevicular uid during adult periodontitis. Inf am m R es. 1997;46(8):310–319. 8. Kornman KS. H ost modulation as a therapeutic strategy in the treatment o periodontal disease. Clin In ect D is. 1999; 28(3):520–526. 9. O enbacher S, H easman PA, Collins JG. M odulation o host PGE2 secretion as a determinant o periodontal disease expression. J Periodontol. 1993;64(5 suppl):432–444.

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10. Caton J, Ryan ME. Clinical studies on the management o periodontal diseases utilizing subantimicrobial dose doxycycline (SDD). Pharm acol R es. 2011;63(2):114–120. 11. Choi DH , M oon IS, Choi BK, et al. E ects o sub-antimicrobial dose doxycycline therapy on crevicular uid M M P-8, and gingival tissue M M P-9, TIM P-1 and IL-6 levels in chronic periodontitis. J Periodontal R es. 2004;39(1):20–26. 12. Emingil G, Atilla G, Sorsa T, et al. The e ect o adjunctive low-dose doxycycline therapy on clinical parameters and gingival crevicular uid matrix metalloproteinase-8 levels in chronic periodontitis. J Periodontol. 2004;75(1):106–115. 13. Golub LM , M cN amara TF, Ryan M E, et al. Adjunctive treatment with subantimicrobial doses o doxycycline: e ects on gingival uid collagenase activity and attachment loss in adult periodontitis. J Clin Periodontol. 2001;28(2):146–156. 14. Golub LM , Suomalainen K, Sorsa T. H ost modulation with tetracyclines and their chemically modif ed analogues. Curr O pin D ent. 1992;2:80–90. 15. Gu Y, Walker C, Ryan M E, et al. N on-antibacterial tetracycline ormulations: clinical applications in dentistry and medicine. J O ral M icrobiol. 2012;4. 16. N ovak M J, Dawson DR 3rd, M agnusson I, et al. Combining host modulation and topical antimicrobial therapy in the management o moderate to severe periodontitis: a randomized multicenter trial. J Periodontol. 2008;79(1):33–41. 17. N ovak M J, Johns LP, M iller RC, et al. Adjunctive benef ts o subantimicrobial dose doxycycline in the management o severe, generalized, chronic periodontitis. J Periodontol. 2002;73(7):762–769. 18. Preshaw PM , H e ti AF, Bradshaw M H . Adjunctive subantimicrobial dose doxycycline in smokers and non-smokers with chronic periodontitis. J Clin Periodontol. 2005;32(6):610–616. 19. Preshaw PM , H e ti AF, Jepsen S, et al. Subantimicrobial dose doxycycline as adjunctive treatment or periodontitis. A review. J Clin Periodontol. 2004;31(9):697–707. 20. Subramanian S, Emami H , Vucic E, et al. H igh-dose atorvastatin reduces periodontal in ammation: a novel pleiotropic e ect o statins. J A m Coll Cardiol. 2013;62(25):2382–2391. 21. Thomas JG, M etheny RJ, Karakiozis JM , et al. Long-term sub-antimicrobial doxycycline (Periostat) as adjunctive management in adult periodontitis: e ects on subgingival bacterial population dynamics. A dv D ent R es. 1998;12(2):32–39. 22. Walker C, Preshaw PM , N ovak J, et al. Long-term treatment with sub-antimicrobial dose doxycycline has no antibacterial e ect on intestinal ora. J Clin Periodontol. 2005;32(11):1163–1169. 23. Agnihotri R, Gaur S. Chemically modif ed tetracyclines: novel therapeutic agents in the management o chronic periodontitis. Ind J Pharm acol. 2012;44(2):161–167. 24. H owell TH , Williams RC. N onsteroidal antiin ammatory drugs as inhibitors o periodontal disease progression. Crit R ev O ral Biol M ed. 1993;4(2):177–196. 25. Reddy M S, Geurs N C, Gunsolley JC. Periodontal host modulation with antiproteinase, anti-in ammatory, and bone-sparing agents. A systematic review. A nn Periodontol. 2003;8(1):12–37. 26. Salvi GE, Lang N P. The e ects o non-steroidal anti-in ammatory drugs (selective and non-selective) on the treatment o periodontal diseases. Curr Pharm D es. 2005;11(14):1757–1769. 27. Williams RC, Je coat M K, H owell TH , et al. Altering the progression o human alveolar bone loss with the non-steroidal anti-in ammatory drug urbipro en. J Periodontol. 1989;60(9):485–490. 28. Weinreb M , Q uartuccio H , Seedor JG, et al. H istomorphometrical analysis o the e ects o the bisphosphonate alendronate on bone loss caused by experimental periodontitis in monkeys. J Periodontal R es. 1994;29(1):35–40. 29. Thumbigere-M ath V, M ichalowicz BS, H odges JS, et al. Periodontal disease as a risk actor or bisphosphonate-related osteonecrosis o the jaw. J Periodontol. 2014;85(2):226–233. 30. Price U, Le H O, Powell SE, et al. E ects o local simvastatin-alendronate conjugate in preventing periodontitis bone loss. J Periodontal R es. 2013;48(5):541–548. 31. Dawson DR 3rd, Branch-M ays G, Gonzalez OA, et al. Dietary modulation o the in ammatory cascade. Periodontol 2000. 2014;64(1):161–197. 32. Elkhouli AM . The e f cacy o host response modulation therapy (omega-3 plus low-dose aspirin) as an adjunctive treatment o chronic periodontitis (clinical and biochemical study). J Periodontal R es. 2011;46(2):261–268. 33. Sculley DV. Periodontal disease: modulation o the in ammatory cascade by dietary n-3 polyunsaturated atty acids. J Periodontal R es. 2014;49(3):277–281.

STu DENT ANCILLARy RESOu RCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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As members o dental teams, dental hygienists must understand the undamental concepts related to periodontal surgery so that they can discuss this important topic with both patients and other healthcare providers. In addition, hygienists o ten play a primary role in the management o patients ollowing periodontal surgery. A basic understanding o periodontal surgical procedures can provide the ramework or improved patient care during critical stages o healing o periodontal surgical wounds. This chapter provides oundation in ormation about basic concepts associated with periodontal surgery.

Le ar i

Obje cti e s

• List the objectives or periodontal surgery. • Explain the term relative contraindications or periodontal surgery. • De ne the terms repair, reattachment, new attachment, and regeneration. • Explain the di erence between healing by primary intention and secondary intention. • Explain the term elevation o a f ap. • Explain two methods or classi cation o periodontal f aps. • Describe two types o incisions used during periodontal f aps. • Describe healing ollowing f ap or access and open f ap debridement.

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• Describe the typical outcomes or apically positioned f ap with osseous surgery. • De ne the terms ostectomy and osteoplasty. • De ne the terms osteoinductive and osteoconductive. • Explain the terms autogra t, allogra t, xenogra t, and alloplast. • Name two types o materials available or bone replacement gra ts. • Explain why a barrier material is used during guided tissue regeneration. • Explain the term periodontal plastic surgery. • List two types o crown lengthening surgery. • List some disadvantages o gingivectomy. • Describe the technique or a gingival curettage. • Explain what is meant by biological enhancement o periodontal surgical outcomes. • Name two broad categories o materials used or suturing periodontal wounds. • Explain the term interrupted interdental suture. • List general guidelines or suture removal. • Describe the technique or periodontal dressing placement. • List general guidelines or periodontal dressing management. • Explain the important topics that should be covered in postsurgical instructions. • List steps in a typical postsurgical visit.

Ke Te rms Resective Osseous de ect Relative contraindications Repair Reattachment New attachment Regeneration Primary intention Secondary intention Tertiary intention Periodontal lap Elevation Full-thickness lap Blunt dissection Partial-thickness lap Sharp dissection Nondisplaced lap Displaced lap Horizontal incision

Crevicular incision Internal bevel incision Vertical incision Flap or access Open lap debridement Osseous resective surgery Ostectomy Osteoplasty Apically positioned lap with osseous resective surgery Bone replacement gra t Osteogenesis Osteoconductive Osteoinductive Autogra t Allogra t Xenogra t Alloplast Guided tissue regeneration

Periodontal plastic surgery Mucogingival surgery Free gingival gra t Subepithelial connective tissue gra t Laterally positioned lap Coronally positioned lap Semilunar lap Frenectomy Crown lengthening surgery Functional crown lengthening Esthetic crown lengthening Gingivectomy Gingivoplasty Gingival curettage Periodontal microsurgery Nonabsorbable suture Absorbable suture Periodontal dressing

Chapte r 27

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to Pe rio do tal Sur e r

All busy general dental practices encounter many patients who can bene t rom periodontal surgery. O ne undamental overreaching goal or most periodontal surgical procedures is to provide an environment in the periodontium that can be maintained in health and com ort throughout the li e o the patient. In most instances as the severity o periodontitis increases, controlling periodontal disease with nonsurgical therapy alone becomes more and more di cult, and the need or periodontal surgery as part o comprehensive patient care becomes increasingly likely.

Ev o l u t io n o f Co n CEp t s REl a t Ed t o p ERio d o n t a l s u Rg ERy 1. Historical Perspective or Periodontal Surgery. Various types o periodontal surgery have been recommended or dental patients with periodontitis and other periodontal conditions or many years. A. H istorically, periodontal surgery was recommended mainly to remove what was thought to be dead or in ected tissue in the periodontium; these early periodontal surgical procedures were mainly resective procedures. The term resective surgery re ers to those procedures that simply cut away and remove some o the periodontal tissues. This concept o resecting or cutting away tissues lead to a variety o surgical techniques that have little in common with most modern periodontal surgery. B. There are a ew o the resective periodontal surgical procedures that still have a limited use in modern periodontal care (i.e., the gingivectomy as discussed in subsequent chapter sections), but most modern periodontal surgical procedures have moved away rom this early concept o simply resecting tissues. 2. Move Toward Modern Periodontal Surgical Techniques A. During the past ew decades, as more research data has become available, an evolution o both the objectives and techniques or periodontal surgery has taken place. B. The emphasis in periodontal surgery has shi ted rom the resective types o periodontal surgery to periodontal surgical procedures that rebuild or regenerate periodontal tissues damaged or lost because o disease.

in d iCa t io n s a n d Co n t Ra in d iCa t io n s f o R p ERio d o n t a l s u Rg ERy 1. Indications or Periodontal Surgery. Periodontal surgeons can employ an array o surgical techniques that are directed toward di erent outcomes. The most common indications or periodontal surgery are outlined below and in Box 27-1. A. To Provide Access or Improved Periodontal Instrumentation o Root Sur aces 1. Periodontal surgery can provide access or more thorough periodontal instrumentation. Since instrumentation o root sur aces in the presence o deep periodontal pockets is so very di cult, the improved access that can be provided by periodontal surgery can be a huge advantage or clinicians. 2. Even though clinicians can select rom a wide array o hand and ultrasonic instruments, as probing depths in the dentition increase, it becomes more and more di cult to reach root sur aces or thorough periodontal instrumentation. 3. Periodontal surgery involving care ully planned incisions through the gingiva can allow or temporary li ting o the so t tissue o the tooth sur ace. M ore

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details about this type o surgery are presented under ap or access in the ollowing descriptions o periodontal surgery.

Bo x 27-1. I dicatio s fo r Pe rio do tal Sur e r • • • • • • • • •

To To To To To To To To To

p ro vid e a cce ss fo r im p ro ve d p e rio d o n t a l in st ru m e n t a t io n o f ro o t su rfa ce s re d u ce p o cke t d e p t h s p ro vid e a cce ss t o p e rio d o n t a l o sse o u s d e fe ct s re se ct o r re m o ve t issu e re g e n e ra t e t h e p e rio d o n t iu m lo st d u e t o d ise a se g ra ft b o n e o r b o n e -st im u la t in g m a t e ria ls in t o o sse o u s d e fe ct s im p ro ve t h e a p p e a ra n ce o f t h e p e rio d o n t iu m e n h a n ce p ro st h e t ic d e n t a l ca re a llo w fo r t h e p la ce m e n t o f a d e n t a l im p la n t

B. To Reduce Pocket Depths 1. As pocket depth increases, it can become increasingly di cult or patients to per orm e ective sel -care techniques, and plaque bio lms that thrive in the protected environment o the deep pocket can make it impossible to stop the progress o periodontitis. 2. Periodontal surgical procedures can reduce the pocket depths, so that a combination o daily sel -care and periodic pro essional periodontal maintenance increases the chance o maintaining the periodontium in health throughout the li e o the patient. C. To Provide Access to Periodontal Osseous De ects 1. An osseous de ect is a de ormity in the tooth-supporting alveolar bone usually resulting rom periodontitis. Figure 27-1 shows an example o an osseous de ect as viewed during a periodontal surgical procedure. a. As periodontitis advances, alveolar bone loss results in changes in the normal contour and structure o the supporting alveolar bone. b. The pattern o bone loss can vary rom one tooth to the next and even on di erent aspects o the same tooth, creating an array o de ects in alveolar bone contours re erred to as osseous de ects.

Fi ure 27-1. Pe rio do tal Osse o us De fe ct Expo se d Duri Sur e r . The so t tissues have been incised and temporarily moved away rom the teeth to reveal the bone contour. Note the extensive alveolar bone loss around one o the central incisor teeth creating a moat-like de ect around this tooth. This type o bone de ect would be an ideal site or bone replacement gra t discussed later in the chapter.

Chapte r 27

D.

E.

F.

G.

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Periodontal Surgical Concepts or the Dental Hygienist

2. Periodontal surgery to modi y the alveolar bone level or contour is called periodontal osseous surgery. a. Bone de ects can be managed surgically through a variety o techniques discussed later in this chapter. b. In ormation about how osseous de ects can be managed using periodontal surgery is presented under the topics osseous resective surgery, apically positioned ap w ith osseous surgery, bone replacem ent gra t, and guided tissue regeneration in other sections o this chapter. To Resect or Remove Tissue 1. Enlarged gingival tissues can be unsightly and can also inter ere with proper sel -care; in some patients, enlarged gingiva can even inter ere with com ortable mastication. 2. Even though the ocus o most modern periodontal surgery is not resection o tissues, this surgical approach can still be indicated in some instances. 3. Periodontal surgery can be used to remove and reshape enlarged gingiva; additional in ormation on this type o periodontal surgery is ound in the chapter section that discusses the gingivectomy. To Regenerate the Periodontium Lost Due to Disease 1. O ne o the long-range goals in periodontics is to be able to regenerate the periodontium predictably; the term regenerate implies growing back o lost cementum, lost periodontal ligament, and lost alveolar bone to reconstruct the periodontium damaged by periodontitis. 2. Periodontal regenerative procedures can reconstruct some o the damage by periodontitis through regenerating lost bone and other tissues. 3. Although it is not possible to regenerate the periodontium in all instances, it is possible to achieve this regeneration in many sites using some sophisticated periodontal surgical techniques; in ormation on periodontal surgery that can be expected to regenerate the periodontium is presented under guided tissue regeneration in another section o this chapter. To Gra t Bone or Bone-Stimulating Materials into Osseous De ects 1. Some periodontal osseous de ects o er the opportunity or the periodontal surgeon to gra t either bone or bone-stimulating materials into the de ects. 2. Although this surgery may seem quite similar to periodontal regeneration surgery, gra ting bone does not necessarily imply regeneration o other parts o the periodontium such as cementum and periodontal ligament. M ore in ormation on this interesting topic is located under bone replacem ent gra t in another section o this chapter. To Improve the Appearance o the Periodontium 1. Some patients have gingival levels or gingival contours that result in an unattractive smile; periodontal surgery also includes a variety o techniques or improving the appearance o the gingiva and improving the quality o a patient’s smile. 2. There are, o course, many restorative techniques or improving the appearance o the teeth themselves, but in many patients, alteration o the appearance o the gingiva must be coordinated with restorative dentistry and orthodontics to achieve a truly pleasing appearance. M ore in ormation on this topic is ound in the other sections o this chapter under periodontal plastic surgery and crow n lengthening surgery. To Enhance Prosthetic Dental Care 1. M odern prosthetic dental care has created the need or a variety o periodontal surgical procedures such as altering alveolar ridge contours, lengthening tooth

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crowns, augmenting the amount o gingiva, or augmenting the bone in an edentulous site prior to implant placement. 2. M odern periodontal surgery includes many procedures directed toward enhancing some aspect o restorative dentistry and enhancing prosthetic dental care. These surgical procedures may involve combinations o all types o periodontal surgery. I. To Allow or the Placement o a Dental Implant 1. Replacement o missing teeth with a dental implant is an option that must be considered when natural teeth are lost. The topic o dental implants is discussed in Chapter 31 but is listed here as one o the indications or periodontal surgery or completeness. 2. Periodontal surgery can also be used to prepare sites or dental implants. a. O ne o the basic tenets o dental implant placement is that the implant must be surrounded by sound alveolar bone. b. It is not at all unusual or edentulous sites—where implants are to be placed—to be de cient in the amount o alveolar bone needed to surround the implant. Such sites can require some type o bone gra ting procedure prior to implant placement. 2. Contraindications or Periodontal Surgery A. The Concept o Relative Contraindications. M ost contraindications or periodontal surgery are relative contraindications rather than absolute contraindications. 1. Relative contraindications are conditions that may make periodontal surgery inadvisable or some patients when the conditions or situations are severe or extreme, but at the same time, these conditions may not be contraindications when the conditions are mild. 2. An example o this concept o relative contraindications or periodontal surgery might be patients with hypertension (high blood pressure). a. A patient with uncontrolled severe hypertension would not be a candidate or periodontal surgery as long as the blood pressure remains severely elevated. b. At the same time, a patient with only mildly elevated blood pressure may be a suitable candidate or periodontal surgery. B. Common Relative Contraindications or Periodontal Surgery. Box 27-2 outlines a list o the more common relative contraindications or periodontal surgery; each o these relative contraindications is discussed brief y below. 1. Patients Who Have Certain Systemic Diseases or Conditions a. Systemic diseases or conditions that can be relative contraindications or periodontal surgery include conditions such as the ollowing: 1. Uncontrolled hypertension 2. Recent history o myocardial in arction (heart attack) 3. Uncontrolled diabetes 4. Certain bleeding disorders 5. Kidney dialysis 6. H istory o radiation to the jaws 7. H IV in ection b. It should be noted that consultation with a patient’s physician is always indicated i there is any doubt about the patient’s health status or i there is any doubt about how that status might a ect planned periodontal surgical intervention.

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Periodontal Surgical Concepts or the Dental Hygienist

Bo x 27-2. Co mmo Re lati e Co trai dicatio s fo r Pe rio do tal Sur e r • • • •

Pa t ie n t s Pa t ie n t s Pa t ie n t s Pa t ie n t s

who who who who

h a ve ce rt a in syst e m ic d ise a se s o r co n d it io n s a re t o t a lly n o n co m p lia n t w it h se lf-ca re h a ve a h ig h risk fo r d e n t a l ca rie s h a ve t o t a lly u n re a list ic e xp e ct a t io n s fo r su rg ica l o u t co m e s

2. Patients Who Are Totally N oncompliant with Sel -Care a. The outcomes o many types o periodontal surgery are at least in part dependent upon the level o plaque bio lm control maintained by the patient’s daily e orts at sel -care ollowing the surgical procedure. b. Lack o compliance with sel -care instructions can be a relative contraindication or some types o periodontal surgery i that lack o compliance is so poor that it precludes the possibility o achieving acceptable periodontal surgical outcomes. 3. Patients Who Have a High Risk or Dental Caries a. Some types o periodontal surgery result in exposure o portions o tooth roots. In a patient with uncontrolled dental caries where the risk or dental caries will remain quite high, it may not be wise to per orm the types o periodontal surgery that increase root exposure due to the potentially devastating e ect o root caries. b. M ost o ten, a high risk or dental caries can be altered, but when bringing the caries risk to an acceptable level is impossible, this risk can be a relative contraindication or some types o periodontal surgery. 4. Patients Who Have Totally Unrealistic Expectations or Surgical Outcomes a. Periodontitis damages the tissues that support the teeth, and surgical correction o that damage does not always result in a per ectly restored periodontium even when per ormed by the most skilled periodontal surgeon. b. I a patient cannot understand the nature o periodontal surgery and cannot develop realistic expectations or the outcomes o any planned periodontal surgery, it would not be wise to proceed with a plan or periodontal surgery. Thus, patient expectations can also be a relative contraindication or periodontal surgery.

p o s s ib l E o u t Co m Es f o R p ERio d o n t a l s u Rg ERy Table 27-1 illustrates possible outcomes that may result rom success ul periodontal surgery: (1) ormation o a long junctional epithelium (as can be seen in response to nonsurgical therapy), (2) resolution o inf ammation and the associated periodontal pocket (as can be seen in response to nonsurgical therapy), and (3) regeneration (which is an expectation or some types o periodontal surgery but not expected as a result o nonsurgical therapy alone).

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TABLE 2 7 -1 . POSSIBLE OUTCOMES FROM SUCCESSFUL PERIODOn TAL SURg ERy A

Ac tive

A: Pe rio do tal Po cke t Prio r to The rap . Th e p e rio d o n t a l p o cke t w it h b a ct e ria l p la q u e a n d in fla m m a t io n w it h in t h e t issu e s p rio r t o t h e ra p y. B

He ale d

B: He ali

b Lo

Ju ctio al Epithe lium. He a lin g in t h e a re a o f

t h e fo rm e r p o cke t a t t h e sit e b y fo rm a t io n o f a lo n g ju n ct io n a l e p it h e liu m . C

He ale d

C: He ali

ith Tissue Shri ka e . He a lin g a t t h e sit e b y re so lu t io n o f

t h e in fla m m a t io n in t h e t issu e s a n d sh rin ka g e o f t h e t issu e s. D

Re s to re d pe rio do ntium

D: He ali

b Re e e ratio . He a lin g a t t h e sit e b y re g e n e ra t io n o f t h e

p e rio d o n t a l t issu e s.

Chapte r 27

Periodontal Surgical Concepts or the Dental Hygienist

t ERm in o l o g y u s Ed t o d Es CRib E HEa l in g a f t ER p ERio d o n t a l s u Rg ERy Terminology used to describe healing ollowing periodontal surgery can be quite con using. Two sets o terminology are requently used to describe healing o periodontal surgical wounds. O ne set o terms attempts to describe the various types o wound healing that can result rom the surgery, and the second set o terms describes the degree o wound closure achieved at the time o surgery. The dental hygienist needs to have an accurate understanding o both sets o terms, since all members o the dental team are likely to encounter some o these terms requently. 1. Terminology Describing Types o Wound Healing. All periodontics textbooks present our terms that are used in describing the types o healing o the periodontium ollowing periodontal surgery: repair, reattachm ent, new attachm ent, and regeneration. These terms are used to convey very speci c concepts when describing the results o periodontal surgery. A. Healing by REPAIR 1. Repair is healing o a wound by orm ation o tissues that do not precisely restore the original architecture or original unction o the body part. a. An example o healing by repair would be the ormation o a scar during the healing o an accidental cut involving a nger. b. Certainly the healing o the nger wound is complete ollowing ormation o the scar, but the scar tissue is not precisely the same type o tissue in appearance or unction that existed on that part o the nger be ore the cut. 2. Repair is a per ectly natural type o healing or many types o wounds, including some wounds created during periodontal surgery. a. An example o repair in the periodontium is the healing that occurs ollowing periodontal instrumentation (scaling and root planing). 1. The usual healing o the wound created by periodontal instrumentation results is a close readaptation o epithelium to the tooth root. 2. This readaptation o epithelium has been re erred to as ormation o a long junctional epithelium and has been discussed and illustrated in Chapter 22. b. A long junctional epithelium is a per ectly legitimate type o healing, but it does not duplicate the precise periodontal tissues that were originally anatomically close to the tooth root. W ith the orm ation o a long junctional epithelium , there is no orm ation o new bone, new cem entum , or new periodontal ligam ent during the healing process. B. Healing by REATTACHMENT 1. Reattachment is healing o a periodontal wound by the reunion o the connective tissue and roots w here these two tissues have been separated by incision or injury but not by disease (1). 2. Frequently it is necessary to move healthy tissue away rom the tooth root or bone temporarily during some types o periodontal surgery. For example, moving the tissue may be necessary to allow access to damaged parts o the periodontium on adjacent teeth. The expected healing or this type o incision is healing by reattachment. C. Healing by NEW ATTACHMENT 1. N ew attachment is a term used to describe the union o a pathologically ex posed root w ith connective tissue or epithelium . 2. H ealing by new attachment occurs when the epithelium and connective tissues are newly attached to a tooth root w here periodontitis had previously destroyed this attachm ent (i.e., where attachment loss has occurred) (2,3).

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3. N ew attachment di ers rom reattachment because new attachment only occurs in an area ormerly damaged by disease, whereas reattachment occurs when tissues are separated in the absence o disease ( requently as a result o the surgical procedure). 4. Figure 27-2 illustrates the speci c area on a tooth that must have newly attached epithelium and connective tissue or the healing to be called new attachment.

A B C D

Fi ure 27-2. Are a o f the To o th Ro o t I o l e d i n e Attachme t. This drawing shows a site on a tooth where attachment loss has occurred. A: Enamel sur ace. B: Area o attachment loss. C: Junctional epithelium. D: Connective tissue attachment. To be quali ied as new attachment the tissues must be attached to the tooth sur ace in the area labeled B in this drawing.

D. Healing by REGENERATIO N 1. Regeneration is the biologic process by which the architecture and unction o lost tissue is com pletely restored. 2. H ealing by regeneration results in the regrowth o the precise tissues that were present be ore the disease or damage occurred. 3. For healing o the periodontium to be described as regeneration, the healing would have to result in the re ormation o lost cementum, lost periodontal ligament, and lost alveolar bone. 4. Regeneration o the periodontium is indeed possible with modern periodontal surgical procedures, but un ortunately the periodontium cannot be regenerated predictably in all sites with current periodontal surgical techniques. 2. Terminology Describing the Degree o Wound Closure. A second set o terms has also been used to describe events ollowing periodontal surgery. These terms describe the degree o wound closure (i.e., how the margins or edges o the surgical wound relate to each other ollowing the surgery but be ore healing). These terms include healing by primary intention, secondary intention, and tertiary intention. A. Healing by Primary Intention 1. H ealing by primary intention occurs when the wound margins or edges are closely adapted to each other. 2. An example o primary intention healing would be seen in a small wound in a nger that required stitches. To adapt the margins o the wound closely, a physician places stitches. 3. H ealing by primary intention is usually aster than the other types o healing, but it is not always possible to create wounds where the wound margins are closely adapted when per orming periodontal surgery. 4. It should be noted that healing by primary intention in the periodontium may pose challenges or the healing that di er rom healing by primary intention in other sites in the body—such as, healing o a cut nger.

Chapte r 27

Periodontal Surgical Concepts or the Dental Hygienist

a. O ne edge o a surgical wound in the periodontium may be a tooth root that is, o course, avascular and cannot contribute any living cells to the wound healing process. b. This would di er rom healing by primary intention or a wound such as a cut nger, because both edges o the wound in nger would be able to contribute living cells to the healing process. B. Healing by Secondary Intention 1. H ealing by secondary intention takes place when the margins or edges o the wound are not closely adapted (i.e., the two wound edges are not in close contact with each other). 2. When healing by secondary intention takes place, granulation tissue must orm to close the space between the wound margins prior to growth o epithelial cells over the sur ace o the wound. 3. Healing by secondary intention is generally slower than healing by primary intention, since more vascular and cellular events are required in this type o healing. 4. Ideally, all wounds created during periodontal surgery would be wounds that would be expected to heal by primary intention, but in reality, many o the wounds created during this type o surgery involve some wound healing by secondary intention. C. Healing by Tertiary Intention 1. An example o healing by tertiary intention would be healing o a wound that is temporarily le t open with the speci c intent o surgically closing that wound at a later date. 2. Healing by tertiary intention is not normally a type o healing that applies to healing o periodontal surgical procedures and is mentioned here only or completeness.

Se ct io

2

U de rsta di

the Pe rio do tal Flap

Many modern periodontal surgical techniques begin by per orming a periodontal f ap, and the periodontal f ap is an important step in most periodontal surgical procedures. As periodontitis progresses, it damages the attachment o the connective tissue to tooth roots and it destroys supporting alveolar bone. Treating patients with periodontitis and repairing damage done to the underlying periodontium requires gaining access to both tooth roots and alveolar bone. As attachment loss associated with periodontitis progresses, access to tooth roots with conventional nonsurgical periodontal therapy becomes di cult i not impossible. Elevating a periodontal f ap is the mechanism or gaining access to the underlying periodontal structures and to the tooth roots a ected by the disease; any overview o periodontal surgery requires some understanding o the principles involved in per orming a periodontal f ap. This chapter section discusses the techniques and the associated terminology related to per orming some o the many variations o a periodontal f ap. 1. Introduction to Periodontal Flaps A. Description o Procedure 1. A periodontal ap is a surgical procedure in which incisions are made in the gingiva or mucosa to allow or separation o the sur ace tissues (epithelium and connective tissue) rom the underlying tooth roots and underlying alveolar bone. 2. Separating the sur ace tissues rom the underlying tooth root and alveolar bone is commonly re erred to as elevation or raising o the f ap; the term elevation is used to convey the concept o li ting the sur ace tissues away rom the tooth roots and the alveolar bone.

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3. O nce the sur ace gingiva or mucosa is elevated o the underlying roots and bone, it can be replaced at its original position or it can be displaced to di erent locations that will be discussed in upcoming sections under some o the speci c types o surgery. 4. Table 27-2 shows a series o drawings that illustrate a typical periodontal f ap surgical procedure used to gain access to the underlying tooth roots and alveolar bone.

TABLE 2 7 -2 . Ty PICAL PERIODOn TAL FLAP SURg ICAL PROCEDURE USED TO g AIn ACCESS TO Un DERLy In g TOOTH ROOTS An D ALv EOLAR BOn E

A: Ma kin g a n in cisio n t o a llo w fo r se p a ra t io n o f t h e so ft t issu e fro m t h e ro o t s a n d a lve o la r A

B

bone.

B: Ele va t in g (o r ra isin g ) t h e so ft t issu e fla p fro m t h e ro o t s o f t h e t e e t h a n d a lve o la r b o n e .

C: Im p ro ve d visu a liza t io n o f b o t h t h e t o o t h C

ro o t s a n d a lve o la r b o n e co n t o u rs w it h t h e fla p e le va t e d .

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463

B. Indications or a Periodontal Flap 1. M ost modern periodontal surgical procedures require per orming periodontal f aps as a part o the procedure. 2. Basically, the f ap elevation is done to provide access or some treatment either to tooth roots or the alveolar bone, or to both o these structures. a. Periodontal f aps can be elevated simply to provide access to tooth root sur aces or completion o meticulous periodontal instrumentation (scaling and root planing) that was begun as a part o nonsurgical periodontal therapy. Use o a periodontal f ap or improved access to tooth roots is discussed in more detail later in this chapter under the heading ap or access. b. Periodontal f aps may also be used to provide access to reshape or treat alveolar bone de ects resulting rom periodontitis. In the ollowing sections o this chapter, the topic o apically positioned aps w ith osseous resective surgery provides an example o this type o procedure. 2. Classif cation o Periodontal Flaps. There are several classi cation schemes used to describe periodontal f aps. Two o the most common include (1) the degree o bone exposure provided by the f ap and (2) the location o the margin (or edge) o the f ap when it is sutured back into place. A. Degree o Bone Exposure. O ne method o classi cation o periodontal f aps is to describe the f ap based upon the degree o exposure o alveolar bone ollowing f ap elevation. Using this method o classi cation, f aps would be described as being either ull thickness or partial thickness. 1. A ull-thickness ap, or mucoperiosteal f ap as it is also called, includes elevation o entire thickness o the so t tissue (including epithelium, connective tissue, and periosteum). The periosteum is a dense membrane composed o brous connective tissue that closely wraps the outer sur ace o the alveolar bone. a. The ull-thickness f ap provides the complete access to underlying bone that might be needed when bone replacement gra ting or periodontal regeneration procedures are anticipated. b. The ull-thickness f ap is elevated with what is generally re erred to as a blunt dissection. 1. Blunt dissection means that the tools used to elevate (or raise) the f ap are not sharpened on the edge (i.e., blunted or slightly rounded on the edge); blunt dissection minimizes the chance o accidental damage to the f ap. 2. In this type o f ap elevation, the f ap is li ted or pried up using surgical tools called periosteal elevators, and it is elevated in a manner quite similar to li ting the peeling o o an orange. Figure 27-3 illustrates a ull-thickness f ap (or mucoperiosteal f ap) elevated during a periodontal surgical procedure.

Fi ure 27-3. Full-Thick e ss o r Muco pe rio ste al Flap. This photograph taken during a typical periodontal lap surgery shows a ull-thickness or mucoperiosteal lap (i.e., a lap o so t tissue that includes epithelium, underlying connective tissue, and the periosteum elevated o the teeth and alveolar bone). Note the exposure o the underlying alveolar bone margin and osseous de ects associated with that bone interdentally.

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2. A partial-thickness ap, or split-thickness f ap as it is also called, includes elevation o only the epithelium and a thin layer o the underlying connective tissue rather than the entire thickness o the underlying so t tissues. a. The partial-thickness f ap is elevated with sharp dissection; sharp dissection requires incising the underlying connective tissue in such a manner as to separate the epithelial sur ace plus a small portion o the connective tissue rom the periosteum. Use o this technique would leave the periosteal tissues covering the bone. b. To per orm the sharp dissection needed in a partial-thickness f ap, a surgeon must limit this approach to areas o gingiva that are relatively thick; care ul inspection o gingiva will reveal that gingiva is quite thin in some patients but somewhat thicker in others. c. Research data indicates that when alveolar bone is exposed during a f ap procedure, there is a potential loss o a very small sur ace layer o the bone ollowing the procedure. Whereas this change in the sur ace o the alveolar bone does not a ect nal healing, this act can make use o a ull-thickness f ap inadvisable in certain instances. B. Location o the So t Tissue Margin. Another method o classi ying periodontal f aps is to describe f aps based upon the location o the margin o the so t tissue when it is sutured back in place. Using this method o classi cation, f aps would be described as being either nondisplaced or displaced. 1. A nondisplaced ap is a f ap that is sutured with the margin o the f ap at its original position in relationship to the CEJ on the tooth. 2. A displaced ap is a f ap that is sutured with the margin o the f ap placed at a position other than its original position in relationship to the CEJ o the tooth. N ote that a displaced f ap can be positioned either apically, coronally, or laterally in relationship to its original position. a. For a displaced f ap to be moved to a new position (such as coronally or laterally), the surgeon must per orm the f ap elevation in such a manner that the base o the f ap extends into the movable mucosal tissues. b. Displaced f aps are generally not possible to per orm on the palatal sur ace o the teeth because o the absence o movable mucosa in this anatomical location. C. Common Terminology. Box 27-3 provides an overview o common terminology used to classi y periodontal f aps.

Bo x 27-3. Co mmo Te rmi o lo Use d to Classif Pe rio do tal Flaps

Bo x 27-4. T pe s o f I cisio s Utili e d Duri Pe rio do tal Flaps

1. Te rm in o lo g y Ba se d Up o n Bo n e Exp o su re • Fu ll-t h ickn e ss a p • Pa rt ia l-t h ickn e ss a p 2. Te rm in o lo g y Ba se d o n Lo ca t io n o f Fla p Ma rg in • No n d isp la ce d a p • Disp la ce d a p

1. Ho rizo n t a l In cisio n s • Cre vicu la r in cisio n s • In t e rn a l b e ve l in cisio n s 2. Ve rt ica l In cisio n s • Ve rt ica l re le a sin g in cisio n

Chapte r 27

Periodontal Surgical Concepts or the Dental Hygienist

3. Types o Incisions Used During Periodontal Flap Surgeries. M ost o the incisions made prior to elevation o a periodontal f ap are made with surgical scalpel blades, but there are a variety o special periodontal knives that can be used to per orm some o these incisions. Several basic types o incisions are utilized during periodontal f ap surgery. Some amiliarization with terminology related to f ap incisions could be use ul to the dental hygienist in understanding speci c types o periodontal surgery. These incisions can be broadly classi ed as either horizontal or vertical incisions. Box 27-4 provides an overview o the types o incisions utilized during periodontal f aps. A. Horizontal Incisions. Horizontal incisions run parallel to the gingival margins in a mesiodistal direction. 1. O ne type o horizontal incision commonly employed during f ap surgery is the crevicular incision (or sulcular incision as it is sometimes called). 2. In the crevicular incision the surgical scalpel is care ully placed into the gingival crevice or sulcus and the tissues are incised apically to bone. 3. A second type o horizontal incision is the internal bevel incision. 4. In an internal bevel incision the surgical scalpel enters the marginal gingiva but is not placed directly into the crevice or sulcus; the scalpel blade enters the gingival margin approximately 0.5 to 1.0 mm away rom the margin and ollows the general contour o the scalloped marginal gingiva. 5. Using an internal bevel incision results in leaving a small collar o so t tissue around the tooth root (including the lining o the pre-existing periodontal pocket); this collar o tissue is removed during most periodontal f ap procedures. 6. Terminology related to these incisions can be quite con using. a. The internal bevel incision has also been re erred to as a “ reverse bevel incision” or the “ initial incision,” since it is usually made as a rst step during a routine periodontal f ap procedure. b. The sulcular incision has also been re erred to as the “ second incision,” since it is usually made as the second step during a routine f ap procedure. B. Vertical Incisions. Vertical incisions run perpendicular to the gingival margin in an apicoocclusal direction. 1. Vertical incisions are primarily used to allow elevation o the f ap during the surgical procedure without stretching or damaging the so t tissues during f ap elevation. 2. The primary type o vertical incisions have also been re erred to as vertical releasing incisions, since once this type o incision passes the mucogingival junction, the f ap is “ released” or has possibilities or movement in relationship to the underlying bone and adjacent so t tissues.

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Implementation o Therapy or Patients with Periodontal Disease

De scriptio s o f Co mmo o f Pe rio do tal Sur e r

T pe s

1. Flap or Access A. Procedure Description 1. Flap or access (or modi ed Widman f ap surgery) is used to provide access to the tooth roots or improved root preparation (1,4–6). In this surgical procedure the gingival tissue is incised and temporarily elevated (li ted away) rom the tooth roots. Figure 27-4 shows a f ap or access with the f ap elevated and partial removal o collar o tissue. 2. There are two main advantages o f ap or access. a. Flap or access surgery provides excellent access to the tooth roots or thorough instrumentation in sites where deep pocket depths may have hindered periodontal instrumentation during nonsurgical therapy. b. Flap or access surgery also provides an intimate adaptation o healthy connective tissues to the debrided tooth roots ollowing suturing o the wound to allow or healing by primary intention. 3. The tissues are elevated only enough to allow good access or periodontal instrumentation o the tooth roots. Following root treatment, the gingival tissue is replaced at its original position (i.e., a nondisplaced f ap) and stabilized with sutures. B. Steps in a Typical Flap or Access. The usual steps ollowed during f ap or access surgery are outlined below. 1. An internal bevel incision is begun through the sur ace o the gingiva surrounding the teeth; the incision is made approximately 0.5 to 1 mm away rom the gingival margin and ollows the scallop o the marginal gingiva. 2. The internal bevel incision that was begun as the rst incision through the sur ace gingiva is retraced and extended apically all the way to the alveolar bone. 3. The f ap is elevated ar enough to provide good access to the tooth roots. 4. A crevicular or sulcular incision is then made rom the base o the pocket to the bone to acilitate removal o the small collar o tissue remaining around the necks o the teeth. 5. I needed, an incision may be made at the base o remaining tissue collar to completely ree this tissue, and the tissue collar is removed. 6. With the f ap elevated tooth roots are instrumented to remove remaining plaque, calculus deposits, root contaminants, and root irregularities. While

Fi ure 27-4. Flap fo r Acce ss i Pro re ss. This photograph was taken during a lap or access. In the photograph, the lap has been incised and elevated. Partial removal o the collar o tissue has been per ormed.

Chapte r 27

Periodontal Surgical Concepts or the Dental Hygienist

per orming the debridement, residual periodontal ligament bers adhering to the tooth root near the base o the pocket are le t undisturbed. 7. The f aps may be thinned i needed to allow or intimate adaptation o the gingiva to the necks o the teeth; alveolar bone contour is not altered unless minor recontouring is needed to allow or proper adaptation o the f ap. 8. The f ap is repositioned and sutured at its original position (nondisplaced); special e ort is made to insure that the tips o the acial and lingual papillae are in actual contact to promote healing by primary intention at this critical interdental site. C. Healing A ter Flap or Access 1. The type o healing expected rom f ap or access surgery is healing by repair and usually involves ormation o a long junctional epithelium . 2. Research shows that f ap or access surgery can result in a stable dentogingival unit that can be maintained in health with periodic periodontal maintenance by the dental team and proper sel -care by the patient. D. Special Considerations or the Dental Hygienist 1. During routine nonsurgical periodontal instrumentation, it may not be possible to per orm thorough calculus removal i the pocket depths are deeper than 6 mm. Flap or access surgery provides greatly improved access to root sur aces in areas o deeper pockets where the results o conventional nonsurgical periodontal instrumentation alone would be limited. 2. Even in patients where f ap or access surgery is part o the treatment plan, every e ort should be made to minimize the inf ammation associated with chronic periodontitis by per orming complete nonsurgical therapy prior to the surgical intervention. a. The dental hygienist plays a critical role in promoting patient understanding o how nonsurgical and surgical treatment are related— rst, nonsurgical therapy ollowed by surgical therapy i needed. b. Thorough and meticulous nonsurgical therapy even in areas o deep pockets can reduce the extent o any planned periodontal surgical treatment and is always an important part o patient care. 2. Open Flap Debridement A. Procedure Description 1. Open ap debridement is a term that describes a periodontal surgical procedure quite similar in concept and execution to f ap or access surgery. In the periodontal literature another term that has been used interchangeably with open f ap debridement is f ap curettage. 2. H istorically, the term open f ap debridement was used to describe some o the original f ap procedures that were rst developed by periodontal surgeons many years ago. 3. Today open f ap debridement (or f ap curettage) is usually per ormed with steps quite similar to f ap or access with the ollowing exceptions: a. Exception #1. O pen f ap debridement usually includes more extensive f ap elevation than f ap or access—providing access not only to the tooth roots but also to all o the alveolar bone de ects. Remember that during f ap or access surgery the f ap is elevated only ar enough to provide good access to the tooth roots. b. Exception #2. Whereas f ap or access includes a nondisplaced f ap, open f ap debridement may include displacing the f ap margin to a new location (i.e., during an open f ap debridement the f ap margin may be sutured in a position more apical to its original position).

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B. Steps in Typical Open Flap Debridement 1. The procedure begins with horizontal incisions that can be either crevicular or internal bevel incisions; vertical releasing incisions can be included as needed to allow or atraumatic f ap elevation. 2. Full-thickness (mucoperiosteal) f aps are elevated to provide access to both tooth roots and the underlying alveolar bone de ects. 3. Granulation tissue is removed rom existing osseous de ects and interdental areas. 4. Tooth roots are instrumented to remove remaining plaque, calculus deposits, root contaminants, and root irregularities. 5. O steoplasty, which is not normally included in open f ap debridement, is per ormed only i it is needed to allow or readaptation o the tissues to the tooth roots. 6. Flaps are sutured either at their original level (nondisplaced) or at a level more apical to their original position (displaced). 7. Figure 27-5 illustrates critical steps in a typical open f ap debridement. C. Healing Expected A ter Open Flap Debridement 1. H ealing rom open f ap debridement is typically resolution o much o the existing inf ammation within the periodontal tissues. 2. The ormation o a long junctional epithelium can occur along with slight remodeling o some o the osseous bone de ects caused by periodontitis. 3. Typically little i any bone regrowth occurs ollowing open f ap debridement. 4. It is common or residual periodontal pockets to remain in some sites ollowing this procedure—thus, complicating both patient sel -care and pro essional periodontal maintenance.

A

B

C

Fi ure 27-5. Critical Ste ps Duri a T pical Ope Flap De bride me t. A: Incisions being made to bone rom within the crevice or pocket base. B: Flap elevation to expose tooth roots and alveolar bone. C: Periodontal instrumentation o the roots o the teeth.

3. Osseous Resective Surgery. The word “ osseous” is de ned as ‘having to do with bone.” Thus, periodontal osseous surgery is surgery involving the alveolar bone. A. Description o Procedure 1. Periodontal osseous resective surgery (or periodontal osseous surgery) is a term used to describe periodontal surgery employed to correct many o the strange de ormities o the alveolar bone that o ten result rom advancing periodontitis (7,8).

Chapte r 27

Periodontal Surgical Concepts or the Dental Hygienist

2. The undamental goal or this type o periodontal surgery is to eliminate periodontal pockets, and this goal can be achieved when osseous surgery is combined with an apically displaced f ap as discussed in the next section. B. Rationale or Periodontal Osseous Surgery 1. Gingiva has a tendency to ollow its natural architecture with or without the support o underlying alveolar bone; the natural architecture o gingiva includes a scalloped contour where the gingiva over the acial and lingual sur aces o teeth is apical to the level o the interdental papillae. 2. As periodontitis progresses, the contours o alveolar bone are altered by the ormation o osseous de ects re erred to with names such as osseous craters, one-walled, two-walled, and three-walled osseous de ects, which have been discussed in other chapters o this textbook. In areas where these osseous de ects orm, attachment loss accompanies the alveolar bone contour changes and periodontal pockets orm. 3. O sseous surgery attempts to reestablish alveolar bone contours that mimic the predictable eventual contours o the gingiva ollowing healing rom periodontal surgery. Thus, periodontal osseous surgery can be used to minimize the discrepancy between the bone contour and the gingival contour to eliminate periodontal pockets ollowing complete healing. 4. Periodontal osseous resective surgery is commonly per ormed in patients with moderate periodontitis where the bone de ects created by the periodontitis are primarily osseous craters; as discussed in other chapters o this book, osseous craters are the most common type o periodontal osseous de ect in periodontitis patients. C. Special Terminology Associated with Osseous Surgery—Ostectomy and Osteoplasty O sseous surgery is requently employed in the treatment o patients with moderate periodontitis, and this topic is discussed in detail in all periodontal textbooks. Two terms requently arise during discussions o osseous surgery (ostectomy and osteoplasty), and these terms can be a bit con using. 1. O ne o these terms is ostectomy. Ostectomy or osteoectomy re ers to the removal o alveolar bone that is actually attached to the tooth (i.e., that is still providing some support or the tooth). a. O stectomy results in the immediate loss o a small amount o attachment at certain sites, and or that reason ostectomy must be used with appropriate caution by the surgeon. b. In spite o the slight attachment loss that occurs during ostectomy, this is an excellent method o eliminating periodontal pockets associated with certain commonly occurring osseous de ects such as osseous craters. The removal o small amounts o supporting bone is justi ed by the attainment o alveolar bone contours that are compatible with the natural contours o the gingiva. c. Figure 27-6 illustrates technique or ostectomy that might be per ormed during periodontal osseous resective surgery. 2. The second o these terms is osteoplasty. Osteoplasty re ers to reshaping the sur ace o alveolar bone without actually removing any o the supporting bone. 3. In reality, most periodontal osseous resective surgery involves both ostectomy and osteoplasty, and when per ormed with precision, these procedures can result in alveolar bone contours that mimic the contours o the gingiva ollowing complete healing. 4. Box 27-5 outlines the special terminology associated with periodontal osseous surgery.

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A

B

Fi ure 27-6. Oste cto m Te ch ique . A: Following exposure o the interdental osseous crater, one o the crater walls ( acial wall in this illustration) is being removed with a special surgical bur. B: Based upon the newly established bone level at the site, the surrounding bone is contoured in an attempt to reestablish a more natural bone contour.

Bo x 27-5. Spe cial Te rmi o lo Osse o us Sur e r

Asso ciate d

ith Pe rio do tal

• Ost e ct o m y—re m o va l o f so m e t o o t h -su p p o rt in g b o n e • Ost e o p la st y—re sh a p in g o f t h e su rfa ce b o n e co n t o u rs

D. Steps in Periodontal Osseous Resective Surgery 1. Incisions are made and f aps are elevated to provide access to the osseous de ects and the surrounding alveolar bone; these incisions typically are done on both the acial and lingual sur aces o the teeth and typically include both horizontal and vertical releasing incisions. 2. Granulation tissue associated with the osseous de ects is thoroughly debrided to allow ull visualization to the extent and shape o the osseous de ects. 3. All remaining so t tissue tags in the surgical site are identi ed and removed usually using a combination o hand and ultrasonic instrumentation. 4. Tooth root sur aces are debrided to remove all plaque, calculus, root contaminants, and root irregularities. 5. O steoplasty is per ormed to remove thick bone ledges where they exist on the acial and lingual sur aces o the alveolar bone. 6. O stectomy is per ormed to eliminate interproximal osseous de ects. 7. Bone contours are re ned with hand instruments and surgical burs. 8. The gingiva is sutured into place (usually at a more apical position than the original level as discussed in the next section). E. Healing A ter Periodontal Osseous Resective Surgery 1. When periodontal osseous resective surgery is per ormed in areas o the dentition where osseous craters exist, it is normally possible or the surgeon to recreate a natural contour to the alveolar bone. 2. When this osseous resective surgery is combined with the apically positioned f ap as discussed in the next section o this chapter, it is requently possible to reestablish a normal crevice or sulcus depth without the presence o residual periodontal pockets ollowing the surgery. 3. For most patients with moderate periodontitis, once periodontal pockets are eliminated using this type o surgery, with reasonable sel -care by the patient and periodontal maintenance by the dental team, it is possible to maintain the dentition in health.

Chapte r 27

Periodontal Surgical Concepts or the Dental Hygienist

4. Apically Positioned Flap with Osseous Resective Surgery A. Procedure Description 1. An apically positioned ap with osseous resective surgery is a periodontal surgical procedure involving a combination o a displaced f ap (displaced in an apical direction) plus resective osseous surgery. a. As already discussed, correction o altered alveolar bone contours to mimic the contours o healthy alveolar bone is usually re erred to as periodontal osseous resective surgery. b. Following contouring o the alveolar bone, the f ap in this procedure is sutured at a position that is more apical to its original position in relationship to the tooth CEJs (apically positioned or apically displaced f ap). 2. This periodontal surgical procedure is ideal or minimizing periodontal pocket depths in patients with osseous craters caused by moderate periodontitis. a. An apically displaced f ap can result in a gingival margin that is apical to the CEJ o the tooth. This new position o the gingival margin means that more o the root o the tooth is visible in the mouth. b. The reduced pocket depth can acilitate both sel -care by the patient and periodontal maintenance by the dental team. B. Steps in an Apically Positioned Flap with Osseous Resective Surgery 1. This procedure normally begins with an internal bevel incision. The internal bevel incision can preserve the width o keratinized tissue that is important to the overall procedure, because this width o keratinized tissue will be displaced apically as a nal step. 2. The internal bevel incision is ollowed by f ap elevation and crevicular incision prior to removal o the collar o tissues around the necks o the teeth. 3. Vertical releasing incisions are made as needed to avoid damage to the f ap. 4. Granulation tissues are debrided, and osseous de ects are exposed as discussed in the previous section. 5. Periodontal osseous resective surgery is per ormed to mimic the contours o healthy alveolar bone; this osseous surgery normally includes both ostectomy and osteoplasty. 6. The f ap is sutured at a position apical to its original position (usually near the tooth–bone junction). 7. The surgical site is covered with periodontal dressing to stabilize the f ap at its apical location. 8. Table 27-3 illustrates the critical steps in an apically positioned f ap with osseous resective surgery.

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TABLE 2 7 -3 . CRITICAL STEPS In An APICALLy POSITIOn ED FLAP w ITH OSSEOUS RESECTIv E SURg ERy

A: In t e rn a l b e ve l in cisio n a n d ve rt ica l re le a sin g in cisio n b e in g A

B

m a d e a ro u n d t h e t e e t h .

B: Re m o va l o f t h e co lla r o f so ft t issu e fo llo w in g fla p e le va t io n .

C: Ost e ct o m y b e in g p e rfo rm e d a ft e r id e n t ifica t io n o f o sse o u s C

d e fe ct s.

D: In sp e ct io n o f t h e fin a l b o n e co n t o u rs a ft e r o st e ct o m y a n d D

o st e o p la st y.

E: Su t u rin g o f b o t h t h e fla p m a rg in s a n d t h e ve rt ica l re le a sin g in cisio n s. No t e t h a t t h e le ve l o f t h e fla p m a rg in is d isp la ce d in E

a n a p ica l p o sit io n co m p a re d t o it s o rig in a l p o sit io n .

F: Pla ce m e n t o f p e rio d o n t a l d re ssin g t o st a b ilize t h e fla p a t it s F

n e w p o sit io n d u rin g t h e e a rly p h a se o f h e a lin g .

C. Healing o an Apically Positioned Flap with Osseous Resective Surgery 1. Final healing o this type o surgery results in a normal attachment (both junctional epithelium and connective tissue attachment) at a position more apical on the tooth root. 2. It should be emphasized that apically positioned f ap with osseous resection cannot eliminate all periodontal osseous de ects, especially where the de ects are quite severe. 3. Research has shown that an apically positioned f ap combined with periodontal osseous surgery can result in a stable dentogingival junction

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that can be maintained in health with reasonable sel -care by the patient and periodic periodontal maintenance by the dental team. 4. Figure 27-7 illustrates the results o a healed apically positioned f ap used to treat a urcation involvement on a molar tooth. D. Special Considerations or the Dental Hygienist 1. During surgery to minimize periodontal pockets, it is common or the gingival margin to be positioned at a more apical level to the CEJ than it originally occupied. a. This apical positioning results in exposure o a portion o the root to the oral cavity. b. Visibility o a portion o the root may be an esthetic concern or the patient. c. In patients with a high caries risk, exposure o root sur ace in the oral cavity can lead to root caries. There ore, this type o surgery may be contraindicated in patients with a high risk or dental caries. 2. Temporary dentinal hypersensitivity is a requent patient postsurgical complaint ollowing this type o surgery. As discussed in other chapters, dentinal hypersensitivity usually diminishes over time i the patient maintains good plaque control. 3. Be ore surgery, the members o the dental team should in orm the patient about anticipated changes in appearance and about the potential or dentinal hypersensitivity. The dental hygienist should also assure the patient that i sensitivity does occur, measures could be taken to minimize the sensitivity.

Fi ure 27-7. Re sults o f a Apicall Po sitio e d Flap. This apically positioned lap was per ormed to treat a large urcation involvement on the molar tooth. Note that in this case the healed gingival margin leaves the tooth CEJ coronal to the gingival margin.

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5. Bone Replacement Gra ts A. Procedure Description 1. Bone replacement gra t is a surgical procedure used to encourage the body to rebuild alveolar bone that has been lost usually as a result o periodontal disease. 2. Bone gra ting has been commonplace in medicine or many years, but gra ting bone replacement materials into the periodontium o ers some unique challenges di erent rom bone gra ting in medicine. a. Bone gra ts placed into periodontal de ects are subject to constant contamination rom bacteria and saliva traveling along the existing tooth roots adjacent to the gra t site; this constant potential or contamination rom bacteria would not be the case in many bone gra ts in medicine (such as a bone gra t done during a hip replacement). b. In addition, the healing o bone gra ts in periodontal de ects can be disrupted by the growth o epithelium into the wound that can lead to gra t ailure; this potential disruption by the growth o epithelium would also not be the case in most medical bone gra ts. B. Terminology Associated with Bone Replacement Gra ts 1. Osteogenesis is the term that is used to describe the potential or new bone cells and new bone to orm ollowing bone gra ting (9). Bone replacement gra t materials requently are re erred to based on their osteogenic potential. a. Some gra ting materials have been described as osteoconductive. O steoconductive gra ting materials are gra ts where the gra ting materials orm a ramework or bone cells existing outside the gra t to use to penetrate the gra t during the ormation o the new bone. b. Other gra ting materials have been described as osteoinductive. Osteoinductive gra ting materials are gra ts where the actual cells within the gra ting material are converted into bone- orming cells, and these cells then orm the new bone (i.e., when the material can induce new bone ormation). 2. Using this terminology, the ideal bone replacement gra t material would be one that is osteoinductive and one that has a high osteogenic potential. C. Broad Categories o Materials Used or Bone Replacement Gra ting. M any potential gra ting materials have been studied in relationship to their osteogenic potential. In general, these gra ting materials can be described as alling into one o the our broad categories: autogra ts, allogra ts, xenogra ts, and alloplasts. These our categories o bone gra t material have widely varying osteogenic potentials. 1. Autogra ts are bone replacement materials taken rom the patient who is receiving the gra t. Periodontal autogra ts can be taken rom sites in the patient’s own jaws or occasionally rom other areas o the patient’s body. 2. Allogra ts are bone replacement gra ts taken rom individuals who are genetically dissimilar to the donor (i.e., another human). O course when allogra ts are used, these gra ting materials must be modi ed to eliminate the potential or rejection. 3. Xenogra ts are bone replacement gra ts taken rom another species, such as bovine bone replacement gra t material, which can be placed in a human. Again, these materials must be modi ed to eliminate the potential or rejection. 4. Alloplasts are bone replacement gra ts that are synthetic materials or inert oreign materials. 5. Autogra ts have the highest osteogenic potential, and alloplasts have the least osteogenic potential with osteogenic potential or allogra ts and xenogra ts between those two extremes.

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6. Though autogra ts have the most osteogenic potential, it is not always possible to obtain enough autogenous bone rom a patient to ll all o the osseous de ects that need gra ting. This creates the need during many periodontal surgical procedures or a bone gra t material rom a source other than the patient being treated. 7. In some instances these gra ting materials can be used in combinations such as mixing autogenous bone with an allogra t material to obtain the needed volume o gra ting material or a particular gra ting site. 8. Box 27-6 provides an overview o materials used or bone replacement gra ts.

Bo x 27-6 Mate rials Use d fo r Bo e Re place me t g rafts • • • •

Au t o g ra ft —b o n e t a ke n fro m p a t ie n t ’s o w n b o d y Allo g ra ft —b o n e t a ke n fro m a n o t h e r h u m a n Xe n o g ra ft —b o n e t a ke n fro m a n o t h e r sp e cie s Allo p la st —syn t h e t ic b o n e -like m a t e ria l

D. Examples o Specif c Materials Used or Bone Replacement Gra ting. N umerous materials have been studied or possible use o bone replacement gra ting over the past several decades. N one o the materials is ideal, but many o them have been shown to have some osteogenic potential. The discussion below describes some examples o the types o bone replacement gra t materials that have been studied. 1. Autogenous bone gra ts rom intraoral sites a. As already discussed, autogra ts are gra t materials taken rom the patient’s own body. b. Autogra ts rom intraoral sites have been used in periodontics or many years, and currently these autogenous gra ts are considered the gold standard when comparing other gra ting materials or their osteogenic potential. c. It should not be surprising that autogenous bone is the most e ective gra ting material, since it already contains living bone cells and viable bone growth actors rom the patient—in contrast to some o the other gra ting materials such as alloplasts, which are usually manu actured materials. d. Intraoral sources or the autogra t material can be rom sites such as bone removed during ostectomy or osteoplasty, exostoses removed during surgery, bone removed rom edentulous ridges, bone taken rom healing extraction sites, bone taken rom the chin, and bone harvested rom the jaws distal to the teeth in a dental arch. e. A variety o techniques or harvesting the gra t material and insuring its osteogenic potential have been advocated. These techniques usually include exposing the alveolar bone by elevating a periodontal f ap, removing granulation tissue associated with an osseous de ect, treating the tooth root adjacent to the de ect, placing the gra t material into the de ect, and closing the f ap by suturing it at its original level on the teeth. . In addition to harvesting particles or larger pieces o bone, autogenous bone gra ts include the use o materials such as osseous coagulum. O sseous coagulum is a mixture o bone dust and blood taken rom the patient made by removing small particles o cortical bone and mixing it with blood rom the surgical site.

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g. O ne technique or collecting autogenous gra t material rom a patient during a periodontal surgical procedure involves the bone blend technique. This technique involves collecting bone in a plastic capsule and pestle and triturating the material into a workable mass o bone blend that can be gra ted into osseous de ects. h. Though small particles or pieces o cortical bone are usually selected as autogenous gra ting material, cancellous bone marrow may also be used. O ne common intraoral site to harvest bone marrow is rom a maxillary tuberosity. i. O ne disadvantage to using autogenous bone gra ts is that when they are used, they requently require a second surgical site or harvesting the gra t material, increasing the potential or postsurgical problems. 2. Autogenous bone rom extraoral sites a. Iliac (or hip) cancellous marrow has been studied as an autogenous bone replacement gra t material. b. When used in periodontal de ects this material does result in bone ormation in osseous de ects. Today marrow rom the hip is rarely used or autogenous gra ting into periodontal de ects, however, because o the potential or root resorption adjacent to the gra ting site, the potential or postoperative problems associated with the donor site, and the di culty in obtaining this type o donor material. 3. Freeze-dried bone allogra ts. Bone allogra ts (taken rom another human and processed) are attractive surgical options as bone replacement gra t materials. There has been a lot o interest in periodontics in identi ying an ideal bone allogra t. I the ideal bone allogra t could be identi ed or use in periodontal patients, there would be no need or a second surgical site to obtain an autogenous gra t. In addition, i the ideal bone allogra t could be identi ed, there would be no worry about limitation o the availability o the amount o gra t material needed. a. As already discussed, allogra ts are gra t materials taken rom another individual o the same species (i.e., another human who is recently deceased). b. Freeze-dried bone allogra ts (both calci ed and decalci ed) have been used success ully as bone replacement allogra ts, and bone allogra t products have been available commercially or some time (10–16). 1. Bone allogra t materials are obtained rom the cortical bone o a donor within a ew hours o death, de atted, washed in alcohol, and rozen. 2. The gra t material is then demineralized, ground into particles, and stored in sterile vials until used in a clinical setting. c. Since allogra ts are materials that are oreign to the body o the patient receiving the gra t and since potential deceased donors may have diseases that could be transmitted to the patient being treated, steps must be taken to maximize the sa ety o this type o gra ting material. These steps usually include the ollowing: 1. Excluding potential donors that are members o disease high-risk groups, 2. Testing o cadaver tissues to exclude donors with in ection or malignant disease, and 3. Treating the allogra t with chemical agents or with other techniques to inactivate viruses. d. Whereas the risk o disease transmission using allogra t materials is not zero, the risk o viral transmission by the use o allogra t bone replacement material has been described as highly remote.

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e. Allogra t products or use in periodontal de ects are available in two types based on how they are processed: reeze-dried bone allogra ts and decalci ed reeze-dried bone allogra ts. 1. Freeze-dried bone allogra t (FDBA) a. Freeze-dried bone allogra t or FDBA is an osteoconductive allogra t gra t material that has been reported to result in some bone ll. b. Bone ll rom FDBA can be improved i the material is mixed with some autogenous bone at the time o placement. 2. Decalci ed reeze-dried bone allogra t (DFDBA) a. Decalci ed reeze-dried bone allogra t or DFDBA is an osteoinductive gra t material that has a higher osteogenic potential than FDBA, and DFDBA is pre erred by many clinicians. b. The osteogenic potential or DFDBA has been shown to vary depending upon several actors such as the extent o demineralization as well as other actors. 4. Bovine-derived bone a. Bovine-derived bone is an example o a xenogra t material; xenogra ts are materials taken rom another species. b. Xenogra ts such as bovine-derived bone have also been used as bone replacement gra ts in periodontal de ects (17). c. An anorganic bovine bone has been tested and marketed, and studies have shown success ul regrowth o some bone with this material. 1. Anorganic bovine bone is bovine bone that has been treated to remove all o its organic components to eliminate the risk o rejection. 2. Removing the organic components rom bovine bone leaves a porous structure, similar in structure to human bone. 3. It has been suggested that the porous structure o anorganic bovine bone can act as sca olding or new bone and that it can act through this mechanism as an osteoinductive material. 5. Plaster o Paris a. Plaster o Paris has been used as an alloplastic bone replacement gra ting material (18). b. Plaster o Paris is actually calcium sul ate, which is porous and biocompatible when placed in periodontal wounds; when calcium sul ate is placed in a periodontal wound, it resorbs within a ew weeks. c. Though this material has been studied and used in humans as a bone replacement gra t material, its e cacy related to osteogenic potential has not been proven. 6. Bioactive glass a. Bioactive glass ceramics have been studied and used as alloplastic bone replacement gra ting materials (19–21). b. This ceramic material consists o calcium salts, phosphates, and silicone dioxide; when used as an alloplastic bone replacement gra t, bioactive glass is used in particulate orm. c. When bioactive glass comes in contact with periodontal tissues, the particulate sur aces can incorporate proteins and can attract osteoblasts that can subsequently orm bone.

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7. Calcium phosphate a. Calcium phosphate biomaterials have been used as alloplastic gra ting materials or several decades. Calcium phosphate is osteoconductive and is well tolerated by body tissues. b. Two types o calcium phosphate materials have been used: hydroxyapatite and tricalcium phosphate. c. Though these materials can result in some clinical repair o periodontal de ects, they are either poorly resorbable (tricalcium phosphate) or not resorbable at all (hydroxyapatite) and can remain encapsulated by collagen within the periodontal tissues. E. Healing A ter Bone Replacement Gra ting 1. Final healing expected rom bone replacement gra ting usually includes a partial rebuilding o alveolar bone lost because o periodontitis. a. It is not known, however, i success ul bone gra ting always results in the re ormation o cementum and periodontal ligament in addition to the alveolar bone. b. In spite o what appears to be good radiographic and clinical healing, the re ormed bone in some cases may not actually be attached to the cementum by periodontal ligament bers. 2. Research has shown that a success ul bone gra t combined with reasonable sel -care by the patient and periodic periodontal maintenance by the dental team can result in retaining a severely compromised tooth over time. F. Special Considerations or the Dental Hygienist 1. The site o a bone replacement gra t should be le t undisturbed or many months and should not be probed until an appropriate interval has elapsed. The dental hygienist should consult with the dentist to determine when a gra ted site may be probed sa ely. 2. M eticulous plaque control in any gra ted site is critical. In the early stages o the healing, the dental team maintains some o the responsibility or plaque control at the site, because the patient may temporarily be unable to per orm adequate sel -care. 6. Guided Tissue Regeneration A. Procedure Description 1. Guided tissue regeneration (GTR) is a periodontal surgical procedure employed to encourage regeneration o lost periodontal structures (i.e., to regrow lost cementum, lost periodontal ligament, and lost alveolar bone). a. When a periodontal surgical wound is created such as the elevation o a f ap, the healing o the wound may involve cells rom several di erent sources surrounding the wound. b. Figure 27-8 illustrates the potential sources o cells that could contribute to healing tissues within a periodontal surgical wound. c. Guided tissue regeneration techniques involve the use o a barrier membrane to delay the normally rapid ingrowth o epithelium into a healing periodontal wound; the rapid growth o epithelium into the wound can inter ere with the slower growth o other cells critical to the healing process (22–35). d. Figure 27-9 illustrates how a barrier membrane might be placed under a periodontal f ap at the time o surgery to delay the ingrowth o unwanted types o cells into the healing o the wound. e. Delay o the ingrowth o epithelium into a healing periodontal wound can allow or undi erentiated cells rom the periodontal ligament to populate the root area and di erentiate into the tissues that normally comprise the periodontium (i.e., cementum, PDL, and alveolar bone).

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. The barrier membranes used during a GTR procedure can also be used in conjunction with bone gra t materials in some instances. g. As the name implies, guided tissue regeneration can result in a true regeneration o the periodontium. 2. Goal o guided tissue regeneration a. When the entire array o types o periodontal surgery is viewed, periodontal regeneration is the ultimate goal, and there is much ongoing research related to GTR. b. Although regeneration o the cementum, periodontal ligament, and alveolar bone is the ultimate goal o periodontal therapy, regeneration o the periodontium is not completely predictable with techniques in use today.

1

2

3 4

Fi ure 27-8. Po te tial So urce s o f Ce lls i a He ali Pe rio do tal Sur ical w o u d. There are our potential sources o cells that can contribute to the healing o a periodontal surgical wound such as a lap: 1. Gingival epithelial cells, 2. Gingival connective tissue cells, 3. Bone cells, and 4. Periodontal ligament cells. O these our types o cells the most rapidly growing o them are the gingival epithelial cells.

Fi ure 27-9. Use o f Barrie r Mate rial to I hibit the Rapid g ro th o f the g i i al Epithe lial Ce lls. Note that the barrier has been placed to inter ere with the growth o the epithelial cells rom the lap margin along the tooth root to give the undi erentiated cells a chance to populate the wound and contribute to the healing.

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B. Steps in a Typical Guided Tissue Regeneration Procedure 1. The rst step in guided tissue regeneration is to make appropriate incisions and elevate a f ap. In this procedure, the f ap usually is elevated one to two teeth beyond the site o the osseous de ects. 2. The osseous de ects are thoroughly debrided and the roots in the site are planed. 3. The selected membrane is trimmed to the size needed or the site; during this membrane trimming, the membrane is allowed to extend several millimeters beyond the de ect in all directions. 4. The membrane is sutured into place with a sling suture placed around the tooth. 5. The f ap is sutured into place ( requently slightly coronally), so that the f ap covers the membrane completely. 6. Table 27-4 illustrates the use o a barrier membrane during a guided tissue regeneration procedure used to treat a urcation involvement in a molar tooth.

TABLE 2 7 -4 . USE OF BARRIER MATERIAL DURIn g g UIDED TISSUE REg En ERATIOn In THE TREATMEn T OF A MOLAR TOOTH w ITH DEEP FURCATIOn In v OLv EMEn T

A: Fla p is in cise d a n d e le va t e d p rio r t o d e b rid e m e n t A

B

C

o f t h e o sse o u s d e fe ct a n d d e b rid e m e n t o f t h e t o o t h ro o t .

B: A b a rrie r is se le ct e d , cu st o m t rim m e d t o size , a n d su t u re d in t o p la ce .

C: Fla p is su t u re d in t o p la ce co m p le t e ly co ve rin g t h e b a rrie r m a t e ria l.

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C. Barrier Materials Used During Guided Tissue Regeneration 1. Some o the barrier materials in current use require removal ollowing healing o the wound, so their use necessitates a second surgical procedure to remove the barrier material. a. Expanded polytetraf uoroethylene (ePTFE) is the most commonly used nonresorbable membrane material. b. These nonresorbable membranes are also available commercially with embedded titanium strips to prevent collapse o the membrane into larger osseous de ects. 2. O ther barrier materials in current use are resorbable and thus do not require removal at some later date; bioresorbable membranes are pre erred by many clinicians or most surgical applications. a. There are several types o bioresorbable membranes; these types include polyglycoside synthetic polymers, bovine and porcine collagen, and calcium sul ate. b. O ne disadvantage o bioresorbable membranes are that they lack rigidity that can be provided by titanium rein orcements available in some nonresorbable membranes. D. Use o Guided Tissue Regeneration with Bone Replacement Gra ts 1. The simultaneous use o barrier membranes to promote regeneration along with bone replacement gra ts is one clinical option. 2. At this point, most o the studies have been directed toward the use o barrier materials combined either with decalci ed reeze-dried bone allogra t (DFDBA) or calcium sul ate. 3. Available studies suggest that regeneration e orts can be improved by the combined use o both barrier materials and bone replacement gra ting. E. Healing Following Guided Tissue Regeneration 1. The healing expected rom guided tissue regeneration is regeneration o part or all o the periodontium that was destroyed by periodontitis. 2. As already mentioned, guided tissue regeneration requires the use o a barrier material. a. During surgery, a barrier material is placed under the f ap to stop the rapidly growing epithelium rom migrating along the root sur ace and inter ering with the connective tissue regrowth on the root. (It is the connective tissue components rom the periodontal ligament space that actually provide the cells needed to regrow cementum, periodontal ligament, and alveolar bone.) b. It is im portant to rem em ber that i a barrier m aterial were not used, the epithelial tissue would regrow very rapidly, covering the tooth root and block ing access to the root by the slower grow ing connective tissue and undi erentiated cells. T he epithelial grow th covering the root block s the connective tissue cells o the periodontal ligam ent rom m ak ing contact w ith the root sur ace. F. Special Considerations or the Dental Hygienist 1. During the GTR surgical procedure, every e ort is made to close the wound to cover the barrier material completely. a. I exposure o part o the barrier material is noted at any o the postsurgical visits, measures should be instituted to minimize bacterial contamination o the barrier material. b. For example, a patient with exposed barrier materials may need special sel care instructions or the topical application o antimicrobial agents to the surgical site.

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2. Sites treated by guided tissue regeneration should not be probed or several months ollowing the procedures. The dental hygienist should consult with the dentist to determine when each individual site can be probed sa ely. 7. Periodontal Plastic Surgery A. Description 1. Periodontal plastic surgery is the term most commonly used in modern dentistry to describe periodontal surgery that is directed toward correcting problems with attached gingiva, aberrant renum, or vestibular depth. 2. The term periodontal plastic surgery includes an array o periodontal surgical procedures that can be used to improve esthetics o the dentition and to enhance prosthetic dentistry as well as to deal with damage resulting rom periodontitis. 3. Some o these procedures include techniques that have been used in medical plastic surgery or many years. Periodontal plastic surgery can be used to alter the tissues surrounding both natural teeth and dental implants (36–41). B. Terminology Relating to Periodontal Plastic Surgery 1. Readers o periodontal literature can sometimes be con used by the terminology associated with periodontal plastic surgery, since some other terms have also been used to describe procedures currently included under this term. 2. The term mucogingival surgery has been used in the past to describe periodontal surgical procedures that alter the relationship between gingiva and mucosa. Some o the periodontal plastic surgical procedures utilized in modern dentistry were previously described as mucogingival surgical procedures, and this older terminology can still be encountered. 3. Another term that has been used to describe some o these types o procedures is reconstructive surgery; the term reconstructive surgery underscores that the goal o some o these procedures is to reconstruct (or rebuild) periodontal tissues such as gingiva. C. Goals o Periodontal Plastic Surgery 1. M any periodontal plastic surgical procedures are designed to alter components o the attached gingiva, and that type o procedure can dramatically alter the appearance o the tissues. M ost patients want a pleasing smile, and because the gingiva is readily visible in many patients, patients requently seek improvements in the appearance o the gingiva. 2. In addition to altering the appearance o the tissues, some periodontal plastic surgical procedures improve unction. Function can be compromised when lack o attached gingiva on a tooth limits the options or restoration o a tooth by contraindicating the intracrevicular placement o restoration margins. 3. This chapter part includes an overview o some o the more common types o procedures included under the heading periodontal plastic surgery. Box 27-7 provides an overview o the types o procedures commonly included in periodontal plastic surgery.

Bo x 27-7. O e r ie o f Pro ce dure s Co mmo l I clude d i Pe rio do tal Plastic Sur e r • • • •

Fre e g in g iva l g ra ft Su b e p it h e lia l co n n e ct ive t issu e g ra ft La t e ra lly p o sit io n e d a p Co ro n a lly p o sit io n e d a p

• Se m ilu n a r a p • Fre n e ct o m y • Cro w n le n g t h e n in g su rg e ry

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8. Free Gingival Gra t A. Description o a Free Gingival Gra t 1. A ree gingival gra t is a type o periodontal plastic surgery that was one o the rst procedures used to augment the width o attached gingiva. 2. The ree gingival gra t requires harvesting a donor section o tissue, usually rom the palate, so there are two intraoral wounds that are created during this surgery: the donor site and the recipient site. a. The donor tissue or a ree gingival gra t includes both the sur ace epithelium and som e o the underlying connective tissue. b. Taking the tissue or a ree gingival gra t rom a donor site leaves a wound that is an open connective tissue sur ace that must be allowed to heal by secondary intention, and healing o this donor wound can be troublesome or the patient. 3. Figure 27-10 shows a ree gingival gra t sutured in place on the acial sur ace o a mandibular incisor tooth root. 4. The ree gingival gra t has been used to provide root coverage in areas o gingival recession but augmentation o the width o attached gingiva can also be per ormed without the need or obtaining any root coverage. 5. The ree gingival gra t is an example o an autogra t, since the donor tissue is taken rom the same individual that is to receive that donor tissue. 6. O ne complicating actor or the ree gingival gra t that is used or root coverage is that the gra t is completely severed rom its blood supply and at least a portion o the gra t is then placed over an avascular root sur ace; special care is required to encourage di usion o nutrients to the gra t to maintain its viability during the early stages o healing.

Fi ure 27-10. Fre e g i i al g raft Place d o Facial Surface o f To o th Ro o t. The gra t is placed over an area o root previously exposed by advanced gingival recession. Note the sutures that have been placed to immobilize the gra t during healing.

B. Steps in a Typical Free Gingival Gra t 1. The root sur aces in the area o gingival recession are planed to remove plaque, calculus, root contaminants, and root irregularities. 2. H orizontal and vertical incisions are made at the recipient site a ter planning the precise location o the needed gra t; sur ace epithelium is removed to prepare a rm connective tissue bed to receive the gra t material. 3. A template ( requently made rom oil) is prepared to provide a pattern or the exact size and shape o the donor gra t that will be needed. 4. Using the template as a guide or the size and shape, the gra t is obtained rom the donor site (usually the palate) by incising through the epithelium and through a thin layer o connective tissue beneath the epithelium; the gra t is removed rom the site using sharp dissection.

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5. The gra t is sutured at the recipient site; during suturing, care is taken to prevent a blood clot rom orming between the gra t and the recipient vascular bed. 6. Both the donor site and recipient site are protected with periodontal dressing; in some instances the donor site on the palate is covered with a previously prepared acrylic retainer to hold the dressing over the donor site. C. Healing Expected with a Typical Free Gingival Gra t 1. Success ul healing o a ree gingival gra t depends upon survival o the connective tissue part o the gra t. In most instances, the epithelium sloughs o during the healing period, later to be replaced by new epithelium. 2. Survival o the tissues depends initially upon di usion o nutrient-containing f uid rom the vascular recipient tissues ollowed by growth o new blood vessels into the gra ted material. Immobilization o the gra t during the healing phase is a critical element in allowing the di usion o nutrients, reconnection o existing blood vessels, and ormation o new blood vessels. 3. Success ul augmentation o gingiva as well as success ul root coverage has been reported ollowing the use o the ree gingival gra t. 4. Un ortunately, ollowing complete healing o the ree gingival gra t, there is normally a less than ideal color match between the healed gra t and the adjacent gingiva. 9. Subepithelial Connective Tissue Gra t A. Description o Subepithelial connective tissue gra t 1. The subepithelial connective tissue gra t is a periodontal plastic surgical procedure that can also be used to augment the width o attached gingiva and to cover areas o gingival recession. 2. In addition to gingival augmentation, the subepithelial connective tissue gra t is used to alter the contour o alveolar ridges to improve the esthetics o some types o dental prostheses. 3. This procedure uses an autogra t o connective tissue (without epithelium) that can be harvested rom a variety o intraoral sites, but that is usually taken rom the patient’s palate. B. Typical steps in a Subepithelial Connective Tissue Gra t 1. A partial-thickness f ap is elevated at the recipient site using sharp dissection; the f ap normally extends one-hal to one tooth to the mesial and distal o the site o recession to be covered. 2. The exposed tooth root is thoroughly planed to remove plaque, calculus, root contaminants, and root irregularities. 3. The connective tissue gra t is obtained by incising through the epithelium o the palate and li ting a segment o connective tissue rom beneath the epithelium using sharp dissection. The sur ace tissues at the donor site can then be sutured to allow or healing by primary intention. 4. The gra t tissue is placed over the denuded tooth root and under the partialthickness f ap at the recipient site. 5. The outer portion o the partial-thickness f ap is placed over the gra t and sutured into place, making sure that at least hal o the gra t is covered by the outer portion o the f ap. 6. Periodontal dressing is placed to protect the gra ted site; since the donor site will heal by primary intention, normally no dressing is needed at the donor site.

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C. Healing Expected A ter a Subepithelial Connective Tissue Gra t 1. When root coverage is attempted with the subepithelial connective tissue gra t, it is reasonable to expect coverage, though not all sites result in complete root coverage. 2. The subepithelial connective tissue gra t results in excellent esthetics, since the color o the healed tissues o ten mimics the natural pre-existing tissue color precisely. D. Acellular Dermal Matrix Allogra t 1. As a substitute or autogenous connective tissue, an acellular dermal matrix allogra t material is now available. 2. Following harvesting, the allogra t is treated to remove cellular components, but it retains blood vessel channels, collagen, elastin, and proteoglycans. 3. This dermal matrix allogra t material can be used in some periodontal surgical procedures in place o autogenous connective tissue, but when used it must be completely covered by a partial-thickness f ap. 10. Laterally Positioned Flap A. Description o a Laterally Positioned Flap 1. The laterally positioned ap is a periodontal plastic surgery technique that can be used to cover root sur aces with gingiva in isolated sites o gingival recession. 2. The laterally positioned f ap involves a displaced f ap (displaced laterally in this case). 3. Use o this technique requires an adequate donor tissue (gingiva) on a tooth root adjacent to the site o recession. 4. Since the gingiva to be displaced laterally will be taken rom an adjacent tooth, the site o the donor tissue must have thick, healthy covering o gingiva to allow the donor tissue to be taken without resulting in harm to the donor site. B. Steps in a Typical Laterally Positioned Flap 1. The recipient site is prepared by thoroughly planing the exposed tooth root and by removing epithelium rom the sur ace o the gingiva surrounding the area o recession, thus exposing some connective tissue to serve as a vascular recipient bed or the displaced f ap. 2. A partial-thickness f ap is elevated rom the donor site using a series o care ully planned vertical incisions to provide mobility in the f ap a ter elevation. 3. The elevated f ap is rotated laterally so as to cover the recipient site including both the prepared bed o connective tissue and the prepared tooth root. 4. The f ap is stabilized at its new location using a combination o interrupted sutures and sling sutures. 5. The surgical site is covered with aluminum oil and periodontal dressing to protect the healing wound. C. Healing Expected A ter a Laterally Positioned Flap 1. With care ul selection o donor sites and skill ul manipulation o the tissues, little recession will occur on the donor site. 2. The laterally positioned f ap can result in excellent root coverage in many instances, since the f ap maintains part o its own blood supply (unlike the ree gingival gra t, which is completely severed rom its blood supply). 11. Coronally Positioned Flap A. Description o a Coronally Positioned Flap 1. The coronally positioned ap is a periodontal plastic surgical procedure that can be used to repair gingival recession i the recession is not advanced. 2. As the name implies the coronally positioned f ap is a displaced f ap (displaced in a coronal direction in this case).

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3. O ne advantage to this procedure compared to a ree gingival gra t or a subepithelial connective tissue gra t is that it does not require a second surgical site to provide the donor tissue. 4. O ne disadvantage to this procedure is that it can be di cult to stabilize the f ap with sutures at a more coronal position. 5. In some instances the coronally positioned f ap requires a two-stage procedure. a. I the thickness o the gingiva at the proposed donor site is inadequate, gingiva must be augmented at the donor site with a surgical procedure prior to advancement o the coronally positioned f ap. b. When indicated, this gingival augmentation may be accomplished with a ree gingival gra t prior to the coronal positioning. B. Steps in a Typical Coronally Positioned Flap 1. Exposed tooth roots are planed to remove plaque, calculus, root contaminants, and root irregularities. 2. Internal bevel and vertical releasing incisions are made at the site to be coronally positioned; the vertical releasing incisions extend into the alveolar mucosa to allow or mobility o the f ap margin in a coronal direction. 3. Sur ace epithelium is removed rom the site to create a vascular recipient bed. 4. The f ap is elevated; the elevation can be ull thickness or split thickness or a combination o the two depending upon the overall thickness o the tissues being elevated. 5. The f ap is advanced in a coronal direction and sutured using a combination o interrupted and sling sutures. 6. Periodontal dressing is placed to prevent movement o the f ap during healing. C. Healing Expected with a Typical Coronally Positioned Flap. The coronally positioned f ap can be used success ully to cover areas o gingival recession when the gingival recession is not advanced. 12. Semilunar Flap A. Description o a Semilunar Flap. The semilunar ap is a periodontal plastic surgical procedure that can be used to cover gingival recession where the recession is not ar advanced and where the keratinized tissues have an adequate thickness. The semilunar f ap is a variation o a coronally positioned f ap. B. Steps in a Typical Semilunar Flap 1. The level o the alveolar bone is sounded (located) to insure that coronal positioning o the semilunar f ap does not inadvertently expose alveolar bone at the base o the f ap. 2. A semilunar, curved incision is made rom one interdental area to the adjacent interdental area over the tooth root. a. The interdental sites or the incisions are selected to be slightly coronal to the position anticipated or the f ap advancement. b. This incision begins in the gingiva and arcs into the mucosa and then back into the gingiva. 3. A split-thickness f ap is per ormed using sharp dissection to ree the sur ace o the f ap rom the underlying connective tissue. 4. The semilunar f ap is displaced coronally and stabilized with gentle pressure or several minutes; i needed, the f ap can be stabilized with interrupted sutures, but sometimes suturing is not required.

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13. Frenectomy A. Description o a Frenectomy 1. Frenectomy is a periodontal plastic surgical procedure that results in removal o a renum, including removal o the attachment o the renum to bone. a. Some authors use the term renotomy to indicate a variation o the renectomy. b. The renotomy includes only incision o the renum but does not remove the attachment o the renum rom the bone sur ace. 2. I a renum is attached too close to the gingival margin, it can result in repeated pulling o the gingival margin away rom the tooth sur ace and can contribute to persistent inf ammation in the tissues; in addition, a renum too close to the gingival margin can inter ere with daily sel -care. a. An aberrant renum position that requires a renectomy occurs most o ten in the renum between the maxillary central incisors and mandibular central incisors. b. An aberrant renum position can also occur in other locations such as on the acial sur ace o premolar and canine teeth and on the lingual sur ace o the mandibular central incisors. B. Steps in a Typical Frenectomy 1. The renum is grasped with a hemostat placed to the depth o the vestibule. 2. Incisions are made through the tissues on both the under sur ace and the upper sur ace o the beaks o the hemostat. 3. The triangular piece o tissue held by the hemostat is removed exposing connective tissue over the sur ace o the bone. 4. The connective tissue covering the bone is incised and dissected. 5. Periodontal dressing is applied to the wound. C. Alternative Techniques or the Frenectomy 1. Frequently the renectomy is per ormed in conjunction with other types o periodontal surgery, and a variety o techniques have been described. 2. O ther techniques or per orming a renectomy include removing the tissue o the renum with electrosurgery or with a laser. D. Healing Following a Frenectomy. Expected healing ollowing a renectomy is elimination o the gingival margin movement caused by the renum. 14. Crown Lengthening Surgery A. Description o Procedure. Crown lengthening surgery re ers to periodontal plastic surgery designed to create a longer clinical crown or a tooth by removing some o the gingiva and usually by removing some alveolar bone rom the necks o the teeth (42). B. Terminology. Two terms requently used when describing crown lengthening surgery are unctional crown lengthening and esthetic crown lengthening 1. Functional crown lengthening re ers to crown lengthening per ormed on a tooth where the remaining tooth structure is inadequate to support a needed restoration. a. Functional crown lengthening surgery can be used to make a restorative dental procedure (such as a crown) possible when the only sensible alternative might be to remove the tooth. b. Crown lengthening surgery may be necessary when a tooth is decayed or broken below the gingival margin. 1. When a badly damaged tooth is to be restored, the dentist will evaluate the tooth and surrounding tissues to determine i the nal restoration o the tooth will damage the so t tissue attachment (i.e., encroach upon the biologic width). 2. I such damage can be expected, crown lengthening surgery is usually indicated prior to the placement o the nal restoration.

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2. Esthetic crown lengthening re ers to crown lengthening per ormed on teeth to improve the appearance o the teeth where there is excessive gingiva or a “ gummy smile” as it is sometimes called. a. Crown lengthening surgery can be used to improve the esthetics o the gingiva, especially on anterior teeth with short clinical crowns. 1. An individual’s smile may be unattractive because o the height or lack o symmetry o the gingiva surrounding the teeth. 2. In some cases tooth crowns are actually the correct length, but they appear too short in the mouth because there is an excess o gingival tissue covering the teeth. b. During esthetic crown lengthening, the gingival tissues are incised and reshaped to expose more o the natural crown o the tooth; requently some o the alveolar bone must also be removed to insure healing o the tissues at a more apical position. C. Surgical Procedure. The actual surgical procedure ollowed during crown lengthening surgery usually involves an apically positioned f ap (displaced f ap) with osseous resective surgery much like that already discussed. 1. Unlike the typical apically positioned f ap with osseous surgery, crown lengthening surgery may be indicated in the presence o a per ectly healthy periodontium simply to allow or improved esthetics or to allow or exposure o more tooth structure prior to restoration. 2. Also, unlike the typical apically positioned f ap with osseous surgery, esthetic crown lengthening requently requires the use o a template prepared to guide the surgeon in positioning the tissues during the surgery. 3. O ccasionally, esthetic crown lengthening may require only a gingivectomy type procedure to be discussed later in this chapter, but most o ten, esthetic crown lengthening requires some alveolar bone removal, so an apically positioned f ap with osseous surgery is most o ten indicated instead o a gingivectomy. D. Healing A ter Crown Lengthening Surgery 1. H ealing o crown lengthening surgery is similar to that described or the apically positioned f ap with osseous surgery. 2. Final healing o crown lengthening surgery results in a normal attachment (both junctional epithelium and connective tissue attachment) at a position more apical on the tooth root. E. Special Considerations or the Dental Hygienist 1. Since crown lengthening surgery usually involves exposure o additional tooth sur ace to the oral environment, temporary dentinal hypersensitivity is also a common result o this type o periodontal surgery; it is imperative or the dental team to warn patients in advance that they may experience temporary dentinal hypersensitivity ollowing crown lengthening surgery. 2. As already discussed, when dentinal hypersensitivity results, the dental hygienist may need to institute measures to help the patient deal with the sensitivity. 3. Control o dentinal hypersensitivity requires meticulous plaque control during the healing phase, and this can be a problem, since mechanical plaque control must be restricted ollowing most surgical procedures. 4. It is the responsibility o the members o the dental team to aid the patient in plaque control until healing allows the patient to resume routine sel -care.

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15. Gingivectomy A. Description o a Gingivectomy 1. The gingivectomy is a surgical procedure designed to excise and remove some o the gingival tissue. H istorically, the gingivectomy was used or many years in periodontics as a primary treatment modality, but it plays a greatly reduced role in modern dentistry. 2. When a gingivectomy is per ormed, the tissues are excised (cut away), removing some o the gingiva that would normally be attached to the tooth sur ace, thus the gingivectomy is a resective procedure. 3. The gingivectomy results in a more apical position o the marginal gingiva in relationship to the CEJ o the tooth. 4. Terminology related to gingivectomy can be con using because o the overlapping use o two terms: gingivectomy and gingivoplasty. a. In contrast to the gingivectomy described above, gingivoplasty is a term used to describe a surgical procedure that simply reshapes the sur ace o the gingiva to create a natural orm and contour to the gingiva. b. Unlike the gingivectomy, gingivoplasty implies reshaping the sur ace o the gingiva without removing any o the gingiva actually attached to the tooth sur ace. c. In reality, during almost all gingivectomy type procedures, a certain amount o gingivoplasty is also per ormed, so the precise distinction between these two companion terms can be a bit cloudy. 5. There is still a limited place in modern dentistry or the gingivectomy procedure. a. Periodontal diseases can produce de ormities o the gingiva including conditions such as gingival enlargements, gingival craters, and gingival cle ts. b. O ccasionally, even in the absence o periodontal pockets, these de ormities occur and need to be altered to allow or improved esthetics, improved mastication, or enhanced ease o patient sel -care. 6. Figure 27-11 illustrates the types o incisions involved when per orming a gingivectomy.

A

B

Fi ure 27-11. g i i e cto m I cisio s. A: The placement o a special gingivectomy kni e to incise the excess gingival tissue. Note that the direction o the tissue bevel being created is approximately 45 degrees to the tooth sur ace. B: The excess tissue has been excised and removed creating a more natural level and contour o the gingiva on the tooth sur ace.

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B. Disadvantages o Gingivectomy 1. In modern periodontal therapy, the gingivectomy is usually limited to removing enlarged gingiva to improve esthetics or to allow or better access or sel -care in isolated sites. 2. Though gingivectomy can be used to reshape more extensive areas o enlarged gingiva as might be seen in gingival overgrowth in response to certain medication use, periodontal surgeons have other more e ective surgical options today. 3. As a surgical technique, gingivectomy has several disadvantages: a. O ne disadvantage to gingivectomy is that it leaves a large open connective tissue wound that results in a somewhat slower sur ace healing than most other periodontal surgical procedures; this generally results in the expectation o more discom ort or the patient during the healing phase. b. Figure 27-12 illustrates the type o connective tissue wound that occurs ollowing a gingivectomy. c. Another disadvantage o gingivectomy is that ollowing healing it invariably results in a longer appearing tooth because o the excision o some o the gingiva. d. A third disadvantage to the gingivectomy is that it does not provide access to the underlying alveolar bone, so when access to the alveolar bone is needed, the surgeon must select another type o surgical approach. e. A ourth disadvantage to the gingivectomy is that it does not conserve keratinized tissue (gingiva); in many surgical sites it is unwise to remove keratinized tissue, since it may already be minimal in width. . In spite o these disadvantages, the gingivectomy can be a use ul surgical procedure in selected sites. C. Steps in Per orming a Typical Gingivectomy 1. Existing periodontal pockets are explored and the levels o the bases o the pockets are marked on the sur ace o the gingiva by punching a hole through the sur ace o the gingiva. 2. Using special gingivectomy knives (both broad bladed and narrow bladed), gingiva is excised at the levels o the bases o the pockets. 3. As the incision is made, care is taken to produce a 45-degree bevel o the gingiva against the tooth to mimic the natural contour o the sur ace o the gingiva in relationship to the tooth. 4. The excised portion o the gingiva is removed (which also removes the so t tissue wall o existing periodontal pockets).

Fi ure 27-12. Co e cti e Tissue w o u d Cre ate d b g i i e cto m . Note that the gingivectomy results in a rather large wound that exposes connective tissue. This large wound usually results in protracted healing, since the healing requires that the epithelium grows across the wound created by the gingivectomy.

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5. The wound sur ace is inspected, remaining tissue tags are removed and gingival contours are re ned as needed. 6. The tooth sur aces are inspected and debrided to remove plaque, calculus, root contaminants, and root irregularities. 7. The surgical wound is covered with periodontal dressing. D. Healing Expected A ter a Gingivectomy 1. H ealing o the gingivectomy requires healing by secondary intention, since the gingivectomy incisions invariably leave an exposed connective tissue sur ace. 2. The approximate rate that gingiva grows across a connective tissue wound in the oral cavity is 0.5 mm each day; since the gingivectomy normally leaves many millimeters o connective tissue exposed, the healing time can be protracted. 3. The nal healing o the wound created by a gingivectomy is a normal attachment o the epithelium and connective tissues to the tooth root at a level that is more apical in position than the original gingival level. 4. Following a gingivectomy, the teeth in the surgical area will appear to be longer since more o the root is exposed where the tissue was excised. a. O course, i more tooth exposure is the desired result o the procedure, this procedure can result in an acceptable outcome. b. H owever, i the exposure o more root structure is not esthetically desirable in a particular site in the oral cavity, another surgical approach would be selected by the surgeon. E. Special Considerations or the Dental Hygienist 1. As already mentioned, the gingivectomy wound leaves a broad connective tissue sur ace exposed that can be very uncom ortable or the patient during the healing phase. 2. Postsurgical discom ort can be managed by placing a periodontal dressing over the wound to provide protection and by prescribing analgesics (pain medications) or use ollowing surgery. 3. At the time o the dressing removal at the rst postsurgical visit ollowing a gingivectomy, the dental hygienist will requently need to replace the periodontal dressing to enhance wound com ort until total epithelialization o the wound has occurred. 4. H ealing o the wound created by a gingivectomy procedure progresses in a predictable manner. a. As already discussed, research studies have shown that oral epithelium grows across the exposed connective tissue at an approximate rate o 0.5 mm per day. b. Thus, it is possible or the clinical team to predict approximate healing times by estimating the wound size; this o course is use ul when counseling patients about what to expect during the postsurgical phase. 16. Gingival Curettage A. Procedure Description 1. Gingival curettage is an older type o periodontal surgical procedure that involves an attempt to scrape away the lining o the periodontal pocket usually using a periodontal curet, o ten a Gracey curet. a. During periodontal instrumentation, some unintentional curettage o the gingiva always occurs, but the term gingival curettage re ers to a separate surgical procedure per ormed a ter routine periodontal instrumentation has removed most o the plaque, calculus, and root contaminants.

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b. Research has demonstrated that normally the same bene ts rom gingival curettage can be derived rom thorough periodontal instrumentation by the clinician plus meticulous sel -care by the patient. Thus, curettage is rarely needed as a separate periodontal surgical procedure in modern dentistry. 2. Variations o the gingival curettage. Although the gingival curettage is no longer routinely recommended as a separate periodontal surgical procedure, some clinicians have advocated variations on this technique. a. O ne variation is per orming gingival curettage with caustic chemicals. 1. Examples o some chemicals that have been used or a chemical curettage include sodium hypochlorite and phenol. 2. The extent o tissue destruction that ollows the use o caustic chemicals cannot be controlled, and studies have ailed to show any e cacy or this type o curettage. b. Another variation is per orming gingival curettage with ultrasonic devices. 1. In this technique, ultrasound is used to debride the epithelial lining o periodontal pockets. 2. Some authors have ound the use o ultrasound as e ective as manual curets in removing the pocket linings, but since the undamental premise or gingival curettage is not sound, this technique is not advocated today either. c. A third variation o the gingival curettage is the excisional new attachment procedure (known as EN AP). 1. The excisional new attachment procedure was developed as a de nitive curettage per ormed with a surgical scalpel. 2. During an EN AP, a surgical scalpel is used to incise away the lining o a periodontal pocket, including the linings o interproximal pockets. 3. Sutures are placed only i the tissues do not rest against the necks o the teeth passively. B. Indications or Gingival Curettage in Modern Dentistry 1. Studies have shown that healing o so t tissues ollowing periodontal instrumentation is not normally improved by subsequent gingival curettage, so the indications or this procedure today are quite limited. 2. Though gingival curettage is not normally recommended as part o modern periodontal therapy, a ew indications or this procedure still exist; these indications include the ollowing: a. Gingival curettage can be per ormed in lieu o more de nitive types o surgery when the more de nitive procedures are contraindicated because o health concerns in the patient. b. Gingival curettage can be per ormed during periodontal maintenance in sites o persistent inf ammation where de nitive periodontal surgery has already been per ormed. C. Steps in a Typical Gingival Curettage 1. Curets are used to scrape away the lining o the so t tissue wall o the periodontal pockets. 2. Care is taken to place the cutting edge o the curet in direct contact with the so t tissue rather than away rom the so t tissue as might be done during routine periodontal instrumentation.

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3. A horizontal stroke with the curet is used to engage the lining o the pocket. 4. Light nger pressure can be used against the sur ace o the gingiva to stabilize the tissue during the scraping motion. D. Healing Following Gingival Curettage 1. H ealing expected ollowing gingival curettage would be healing by repair and the ormation o a long junctional epithelium. 2. This is the same type o healing you would expect ollowing thorough periodontal instrumentation. 3. Figure 27-13 illustrates the type o healing that would be expected ollowing a gingival curettage.

CEJ

Probing depth

A

Reces s ion

CEJ

CAL Probing depth

In ltrate

B

Fi ure 27-13. He ali Fo llo i g i i al Cure tta e . A: Periodontal pocket prior to treatment showing in lammation and calculus on the roots. B: Healing ollowing gingival curettage and root instrumentation. Healing includes resolution o in lammation and readaptation o some junctional epithelium.

17. Dental Implant Placement. Dental implants are discussed in Chapter 31, but they are brief y mentioned in this section to underscore that the placement o dental implants can utilize many periodontal surgical techniques. The planning and surgical placement o dental implants is quite complex and the interested reader is directed toward the many excellent textbooks devoted to that topic. In addition to the surgery involved in placing dental implants, periodontal surgical procedures can help prepare sites or the placement o dental implants. A. Description o Dental Implant Placement 1. As discussed in Chapter 31, a dental implant is an arti cial tooth root that is placed into the alveolar bone to hold a replacement crown or prosthesis (denture or bridge). 2. M ost dental implants in current use are endosseous implants that are placed in alveolar bone and protrude through the mucoperiosteum. a. Dental implant placement usually requires exposure o alveolar bone using the principles o periodontal f ap surgery, drilling a precise hole in the alveolar bone, insertion o a metallic implant into the site, and suturing o the wound created. b. There are a variety o dental implants in current use including various lengths, diameters, and designs; most types o dental implants have threads much like a screw has threads.

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3. Some dental implants are designed to be covered with gingiva during healing, and others are designed to leave a portion o the implant exposed in the oral cavity during healing. Those that are covered require a second surgical procedure ollowing healing to expose the top o the implant. 4. When preparing a site to receive a dental implant and during dental implant placement any o the periodontal surgical procedures already discussed may be employed. B. Healing Expected Following Dental Implant Placement 1. H ealing ollowing placement o a dental implant results in bone growth in such close proximity to the implant sur ace that the implant is stable enough to support a tooth-shaped restoration or a dental prosthetic appliance. 2. It should be noted that though dental implants are not surrounded by cementum and periodontal ligament (as are natural teeth), these implants are subject to periodontal disease that can result in the loss o supporting bone just like the natural tooth. C. Special Considerations or the Dental Hygienist 1. Patient sel -care ollowing placement o a dental implant is as critical as it is ollowing every periodontal surgical procedure, and the members o the dental team must assume responsibility or helping the patient with plaque control during the critical healing period. 2. O nce an implant site heals, the gingiva surrounding the implant can be maintained in health using sel -care techniques similar to what is required to keep tissues around a natural tooth healthy. 3. Implant maintenance and the role played by the dental hygienist are discussed in detail in Chapter 31. 18. Periodontal Microsurgery. Periodontal microsurgery is a term used to describe periodontal surgery per ormed with the aid o a surgical microscope. Principles o microsurgery have had a good deal o inf uence in medicine and will continue to inf uence the per ormance o certain periodontal surgical procedures, especially periodontal plastic surgery. Periodontal surgery per ormed using microsurgery techniques can result in procedures per ormed with increased precision on the part o the surgeon. 19. Laser Therapy. The use o lasers (light ampli cation by stimulated emission o radiation) to ocus a beam o light o a single wavelength at periodontal site has become an important topic in dentistry and periodontics. A. There is much debate related to some aspects o this topic among clinicians and scientists (43–50). Lasers can cut or coagulate so t tissues with e ciency, and this act makes the use o lasers during some surgical procedures such as gingivectomy, gingivoplasty, biopsy o so t tissues, ablation o lesions, vestibuloplasty, and renectomies use ul adjuncts. B. H owever, in periodontal patients lasers have also been used to remove pocket epithelium and decontaminate periodontal pockets in an e ort to attain improved attachment levels, but the precise e cacy o these types o therapies in periodontitis patients is not clear at this point. C. Current statements by the American Academy o Periodontology and the American Dental Association caution that there is insu cient evidence to support the use o lasers as a single orm o treatment in periodontitis patients at this time (51,52). Studies that may clari y the e cacy o this type o treatment will continue to be published.

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4

Bio lo ical E ha ce me t o f Sur ical Outco me s M any attempts have been made to enhance the outcomes o periodontal surgery by using chemical or biologic mediators to inf uence the healing ollowing periodontal surgical procedures. This chapter section provides a brie overview o some o the biologic mediators that have been studied. There is much ongoing research into this topic, and it is reasonable to expect that this ongoing research will reveal undamental mechanisms or enhancing periodontal surgical outcomes that will prove use ul in a clinical setting. 1. Root Sur ace Modif cation A. Mechanical Root Preparation 1. M any years o observation o the healing o periodontal surgical wounds demonstrate that gingival tissues adjacent to tooth roots—that have previously been exposed because o attachment loss—heal better when the roots are ree o plaque, calculus, and root contaminants. 2. These observations have lead to the incorporation o mechanical root preparation as a routine part o most periodontal surgical procedures. H and and ultrasonic instruments have been used extensively or this purpose. B. Chemical and Biologic Mediators. Chemical and biologic mediators also have been used in attempts to enhance the healing o the gingiva adjacent to the tooth roots beyond what can be achieved by periodontal instrumentation alone. Several chemical mediators have been studied or possible bene ts to the gingival healing process (53,54). 1. EDTA (ethylenediamine tetraacetic acid) has been used to decalci y the sur ace o the root ollowing mechanical root preparation. a. Possible bene ts o using EDTA on roots include removal o the dentin smear layer, exposure o ends o embedded collagen bers in remaining cemental sur ace, and removal o endotoxin buried deeper below the root sur ace. b. Though some clinicians have used this chemical to enhance root preparation, most o the evidence indicates that there is very little positive e ect on the outcomes o any surgery by the use o this chemical to prepare tooth roots. 2. A second chemical agent that has been re erred to as a biologic mediator, again to enhance the outcomes o periodontal root preparation, is tetracycline. a. Tetracyclines are a amily o antibiotics with varied properties in addition to their antibiotic e ects. It has been suggested that tetracyclines applied to roots during surgery may enhance the migration o broblasts to the root sur aces during healing in addition to slightly decalci ying the sur aces o the roots. b. M ost studies indicate that using this biologic mediator on root sur aces during surgery has little e ect on the outcomes o the surgical procedures. 2. Growth Factors. Growth actors are naturally occurring proteins that regulate both cell growth and development. Several growth actors are being studied or their e ect in enhancing the predictability o periodontal regeneration and studies o these potential biologic mediators are continuing (27,55). These growth actors include PDGF (platelet-derived growth actor) and IGF (insulin-derived growth actor). It is reasonable to expect that continued research into the use o growth actors to improve periodontal surgical outcomes might lead to clinical application o some o these actors in the uture.

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3. Enamel Matrix Derivative (EMD) A. Periodontal Regeneration Factors 1. It is clear that periodontal regeneration depends upon the type o cells that rst populate the periodontal surgical wound. 2. As already discussed, using barrier materials to insure that the correct cells enter the healing surgical wound without the early inter erence o epithelium can result in more predictable periodontal regeneration. The use o barriers to insure periodontal regeneration, however, has not been very success ul in all sites o more advanced osseous de ects. B. Protein Preparations. Research into using protein preparations and growth actors to enhance periodontal regeneration by mimicking natural healing processes has shown some promising results. 1. Enamel matrix derivative (EM D) has been used to enhance periodontal regeneration. 2. Enamel matrix derivative (EM D) is a preparation o proteins extracted rom porcine tooth buds; EM D is the tooth bud extract mixed with a propylene glycol alginate carrier (56–60). 3. The major constituents o this extract appear to be proteins called amelogenins and enamelin. 4. At this point it appears that EM D may indeed enhance periodontal regeneration and that the sa ety o this material is quite high when used in conjunction with periodontal surgery. 5. EM D is currently being used by clinicians in an attempt to improve outcomes o some types o periodontal surgery. 6. Studies into the precise constituents in this protein extract that can enhance healing are continuing. 4. Platelet-Rich Plasma (PRP). Another example o a biologic mediator is platelet-rich plasma (PRP). Using platelet-rich plasma requires obtaining a sample o the patient’s blood and separating the blood sample into three separate ractions: platelet-rich plasma (PRP), red blood cells, and platelet poor plasma. The PRP raction o blood contains high numbers o platelets plus PDGF (platelet-derived growth actor), TGF-β (trans orming growth actor-beta), and brinogen. Clinically both calcium and thrombin are added to the PRP to activate the production o brin be ore the preparation is applied in the surgical site. Though some studies indicate some enhancement o the healing process ollowing the use o this preparation, it is not clear that the growth actors are present in high enough concentrations to have much e ect on the actual surgical outcomes, and additional studies o this material are underway (61,62). 5. Bone Morphogenetic Proteins (BMP). Bone morphogenetic proteins (BM Ps) are a group o regulatory glycoproteins that have been studied or possible use in the eld o periodontal regeneration because o their known osteoinductive e ects. Both puri ed and recombinant BM Ps are currently being studied, and early results indicate possible enhancement o regeneration in some treated sites. Un ortunately using BM P to enhance surgical outcomes has resulted in tooth ankylosis and much urther study o this material is indicated. Investigations into the use o bone morphogenetic proteins to enhance periodontal regeneration are continuing.

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5

Patie t Ma a e me t Fo llo

i

Pe rio do tal Sur e r

The dental hygienist plays a major role in supporting the management o patients ollowing periodontal surgery. This chapter section discusses components o postsurgical management including use o sutures, use o periodontal dressings, delivery o postsurgical instructions, and organizing postsurgical visits. It is important to realize that the management o the patient during the healing phase ollowing periodontal surgery can be as important to the surgical outcomes as the skill o the surgeon per orming the surgery.

u s E o f s u t u REs in p ERio d o n t a l s u Rg iCa l Wo u n d s 1. Overview o the Use o Sutures in Periodontal Wounds. Many periodontal surgical procedures such as periodontal f aps require the placement o sutures to stabilize the position o the so t tissues during the early phases o healing; a suture, or stitch as it is sometimes called, is a device placed by a surgeon to hold tissues together during healing. A. Characteristics o Suture Material 1. To be use ul in periodontal wounds suture materials need to be nontoxic, f exible, and strong. 2. Some suture materials have been reported to have a “wicking” e ect (i.e., they can allow bacteria to travel down the suture and contaminate the surgical wound); this wicking e ect is believed to have a negative e ect on the surgical outcomes. 3. When placing sutures, periodontal surgeons take great care not to put tension on a f ap with sutures (i.e., to insure that the f ap lies passively at the intended position be ore suturing); sutures are used to stabilize the f ap in its passive position. 4. I a suture places tension on a f ap, the suture material will pull out o the tissues during healing and will ail to serve the purpose o stabilizing the tissues. B. Types o Suture Material. In general two types o suture material are used: nonabsorbable and absorbable. Box 27-8 provides an overview o some o the suture materials available or use in periodontal wounds. 1. N onabsorbable suture is a suture made rom a material that does not dissolve in body f uids. A clinician must remove the nonabsorbable sutures a ter some healing o the wound has occurred. 2. Absorbable suture is a suture made rom a material designed to dissolve harmlessly in body f uids over time; though absorbable sutures do not normally require removal by the dental team, some absorbable sutures do not dissolve particularly well in saliva.

Bo x 27-8. Example s o f Suture Mate rials No n a b so rb a b le : • Bra id e d silk • Mo n o la m e n t n ylo n • Exp a n d e d p o lyt e t ra u o ro e t h yle n e (e PTFE) • Bra id e d p o lye st e r

Ab so rb a b le : • Pla in a n d ch ro m ic g u t • Po lyg la ct in 910 • Po lyg le ca p ro n e 25

Bo x 27-9. O e r ie o f g e e ral I dicatio s fo r Co mmo Suture Te ch ique s 1. In t e rru p t e d su t u re : clo su re o f ve rt ica l in cisio n s, clo su re o f n o n d isp la ce d a p s 2. Slin g su t u re : clo su re o f d isp la ce d a p s 3. Co n t in u o u s slin g su t u re : clo su re o f d isp la ce d a p s, clo su re o f n o n d isp la ce d a p s

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2. Suture Placement Techniques. Familiarity with some general techniques or suturing can guide the hygienist assigned the task o suture removal at a postsurgical appointment. Box 27-9 provides an overview o general indications or some o the more common suturing techniques or periodontal surgical wounds. Three o the most common suture placement techniques are discussed and illustrated below. A. Interrupted Interdental Suture 1. During most periodontal f ap surgery, f aps are elevated on both the acial and lingual (or palatal) sur aces o the teeth; an interrupted interdental suture usually involves suturing the acial and lingual papillae together, but this technique is also ideal or closing vertical incisions. 2. When interrupted interdental sutures are placed to close a periodontal f ap procedure, a separate suture is placed and tied in each o the interdental sites. 3. An interrupted interdental suture that might be utilized during a periodontal f ap or access procedure is illustrated in Figures 27-14 and 27-15. 4. When removing interrupted interdental sutures, the clinician must cut each o the interdental sutures be ore pulling out the suture material.

Fi ure 27-14. I te rrupte d I te rde tal Suture s. Interrupted interdental sutures have been placed in each interdental site on the maxillary arch. Note that there is a knot associated with each o these interrupted sutures that would need to be cut prior to removal. (Courtesy o Dr. John S. Dozier, Tallahassee, FL.)

A

B

C

D

Fi ure 27-15. I te rrupte d I te rde tal Suture . In these drawings the most mesial tooth has been removed to allow or visualization o the path o the interrupted interdental suture. A: Suture placed through papilla on the acial. B: Suture placed through the papilla on the lingual. C: Suture returned to acial sur ace. D: Knot tied in suture on the acial.

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B. Continuous Loop Suture 1. The continuous loop suture is pre erred by many clinicians or suturing many types o periodontal f aps. 2. When continuous loop sutures are used, ollowing placing the suture material through two interdental papillae, the end o the suture is looped around the teeth to reach the next interdental site rather than being tied at each interdental site; the suture is tied ollowing placement o the loop around the terminal tooth. 3. A continuous loop suture that might be utilized during an apically positioned f ap is illustrated in Figures 27-16 and 27-17. 4. Removal o a continuous loop suture can requently be accomplished with a single cut through the suture near the knot be ore pulling out the suture material. C. Sling Suture 1. Some periodontal surgical wounds require the placement o a sling suture; the sling suture is used to sling or suspend the tissues around the cervical area o a tooth rather than to tie so t tissue to other so t tissue. 2. The sling suture is requently used when a f ap is displaced in an apical direction. Figure 27-18 illustrates a sling suture. 3. It should be noted that when acial and lingual f aps are sutured using the sling suture technique, a separate sling suture must be placed on both the acial and lingual sur aces. 4. Removal o the sling suture only requires locating the individual knots, cutting the suture near the knot, and care ul extraction o the suture.

A

B

Fi ure 27-16. Co ti uo us Lo o p Suture . Note that the suture is looped around each o the cervical areas o the teeth and passed through the tissues associated with each interdental area (A), but that it is tied only at the end o the continuous loop (B).

Fi ure 27-17. Co ti uo us Lo o p Suture . Continuous loop suture has been placed on the segment o teeth in maxillary arch. Note that the only knot visible is associated with the most distal tooth. (Courtesy o Dr. Don Rol s, Periodontal Foundations, Wenatchee, WA.)

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A

B

C

D

Fi ure 27-18. Sli Suture . In these drawings the most mesial tooth has been removed to allow or visualization o the path o the sling suture. A: Suture placed through the acial papilla. B: Suture looped around the lingual sur ace o the tooth without engaging the lingual so t tissues. C: Suture continues back to the acial sur ace under the contact and engages the acial papilla on the distal o the tooth. D: Suture continues back on same path and is tied on the sur ace where it irst penetrated the acial papilla.

Bo x 27-10. g e e ral g uide li e s fo r Suture Re mo al Gu id e lin e Gu id e lin e Gu id e lin e Gu id e lin e Gu id e lin e

1: Re m o ve su t u re s in a t im e ly m a n n e r. 2: Re a d t h e su rg ica l n o t e in t h e p a t ie n t ’s ch a rt . 3: Un d e rst a n d t h e t yp ica l sizin g syst e m fo r su t u re s. 4: Ne ve r a llo w t h e kn o t t o b e p u lle d t h ro u g h t h e t issu e s. 5: Alw a ys co n rm t h a t a ll o f t h e su t u re s h a ve b e e n re m o ve d .

3. Suture Removal A. Removal o N onabsorbable Sutures 1. N onabsorbable sutures placed during surgical procedures are removed as part o routine postsurgical visits. Frequently remnants o absorbable sutures can also be removed at the routine postsurgical visits to avoid unnecessary tissue inf ammation that can be caused by retained absorbable suture material that does not dissolve in a timely manner. 2. Guidelines or timing o removal vary, but in general, sutures should be removed when wound healing has progressed to the point at which the sutures are no longer needed to stabilize the tissues. M any sutures are loose and no longer needed to stabilize the tissues at the time o the 1-week postsurgical visit. 3. M ost periodontal sutures should not be le t in place longer than 2 weeks because they can act as irritants i the suture material remains in the tissues too long. It should be noted that sutures in some periodontal wounds are routinely le t in place or much longer periods. 4. Each periodontal surgical procedure is unique, and removal procedures can vary, but some general guidelines or suture removal are outlined below and in Box 27-10.

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B. General Guidelines or Suture Removal 1. Guideline 1: Remove sutures in a timely manner. N onabsorbable sutures are generally removed a ter 1 week o healing; most absorbable sutures can be le t in place 1 to 3 weeks. 2. Guideline 2: Read the surgical note in the patient’s chart prior to suture removal. a. The number and type o sutures placed should be a routine part o the chart entry recorded or each periodontal surgery. b. Knowing the number o sutures placed during the actual surgical procedure can help the dental hygienist con rm that all sutures have been located and removed during a postsurgical visit. 3. Guideline 3: Understand the typical sizing system used or periodontal sutures. a. Though there are numerous sizes o sutures used in a medical setting, typical designations or suture sizes used in periodontal surgery are sizes 3-0, 4-0, and 5-0. 1. In this sizing system, the 3-0 size is larger than the 4-0 size, and 4-0 is larger than 5-0. 2. In the mouth, 5-0 can be more di cult to locate than a 4-0 size, especially in the posterior part o the mouth. b. The dental hygienist should learn the precise abbreviations used in the chart entries in the individual clinical setting. A typical example o an abbreviation would be “ 4-0 BSS.” This would mean the size o the suture is 4-0, and BSS stands or black silk suture, a commonly used nonabsorbable suture material. c. Table 27-5 outlines designations or typical suture sizes used during periodontal surgery as they might appear in a patient’s chart. 4. Guideline 4: N ever allow the knot to be pulled through the tissues. a. Sutures should be removed by cutting the suture material near the knot and grasping the knot with sterile cotton pliers. b. When the suture is gently pulled rom the tissue, care should be taken not to orce the knot itsel through the tissue. This technique is illustrated in Figure 27-19. c. It should be noted that suture removal is rarely pain ul or the patient i care is taken not to create unnecessary tissue movement. 5. Guideline 5: Always con rm that all o the sutures have been removed. a. Following suture removal, it is imperative to inspect the wound with care to insure that all o the sutures have indeed been located and removed. b. Remember that the patient chart entry made on the day o the surgery usually will contain in ormation about how many sutures were actually placed.

TABLE 2 7 -5 . Ty PICAL DESIg n ATIOn S FOR SUTURE SIz ES USED In PERIODOn TAL SURg ERy Suture Si e

Appro ximate Diame te r o f Suture

3-0

0.20 m m

4-0

0.15 m m

5-0

0.10 m m

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C

Fi ure 27-19. Suture Re mo al. A: Suture in place. B: Grasp the suture material and cut it near the knot. C: Gently pull the suture material rom the tissue taking care not to pull the knot through the tissue.

u s E o f p ERio d o n t a l d REs s in g 1. Purpose o Periodontal Dressing A. Periodontal dressing, or periodontal pack as it sometimes called, is a protective material applied over a periodontal surgical wound. Periodontal dressings are used somewhat like using a bandage to cover a nger wound. B. Though the placement o periodontal dressings ollowing periodontal surgery used to be routine, modern surgical techniques may or may not require placement o a periodontal dressing. 1. The surgical wound created by the gingivectomy procedure leaves a raw connective tissue sur ace exposed that always requires a periodontal dressing. 2. Periodontal f aps that are well adapted to the alveolar bone and tooth roots may not always require a periodontal dressing. 3. Periodontal dressings can be placed to acilitate f ap adaptation and are requently indicated when the surgical procedures have created varying tissue levels or when displaced f aps are used. 4. The periodontal surgeon will determine the need or dressing placement at the time o the surgical procedure. 2. General Guidelines or Management o Periodontal Dressings A. Proper Placement 1. Remember that the periodontal dressing does not normally adhere to the teeth or gingiva and is retained primarily by pushing some o the material into the embrasure spaces to lock the dressing around the necks o the teeth mechanically. 2. The use o less periodontal dressing is better than more dressing during placement; the proper amount o dressing is only enough to cover the wound. 3. The dressing should be placed, so that there is no contact between the dressing and the teeth in the opposing arch when the patient bites down; occlusal contact with teeth in the opposing arch will quickly dislodge the dressing. 4. Table 27-6 illustrates the proper placement o a periodontal dressing. 5. It should be noted that suture material could accidentally become trapped within the periodontal dressing. When removing dressings, it may be necessary to loosen the dressing slightly and cut the suture be ore completely removing the dressing rom the necks o the teeth. 6. Periodontal dressings should be replaced every 5 to 7 days until the surgical wound is healed enough to be exposed.

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TABLE 2 7 -6 . STEPS In PERIODOn TAL DRESSIn g PLACEMEn T

A: Dre ssin g is p re sse d in t o t h e in t e rd e n t a l sp a ce s w it h A

g e n t le fin g e r p re ssu re o n t h e fa cia l.

B: Dre ssin g is lo o p e d a ro u n d t h e m o st d ist a l t o o t h a n d p re sse d in t o t h e in t e rd e n t a l sp a ce s o n t h e p a la t a l. C: Ge n t le fin g e r p re ssu re is co n t in u e d t o jo in t h e d re ssin g in t e rd e n t a lly o n t h e fa cia l a n d p a la t a l B

C

a sp e ct s.

D

D: Dre ssin g ca n b e b rid g e d a cro ss e d e n t u lo u s a re a s. E

E: Dre ssin g a m o u n t sh o u ld b e m in im a l t o a vo id co n t a ct o f t h e d re ssin g w it h t h e t e e t h in t h e o p p o sit e a rch .

3. Types o Periodontal Dressing. There are two types o modern periodontal dressings commonly available or use today. Both types o periodontal dressing are held in place primarily by mechanical retention around the necks o the teeth. A. Chemical Cure Paste. O ne type is a two-paste chemical cure material that requires the mixing o paste rom two tubes to orm a dressing with a putty-like consistency. 1. This type usually contains zinc oxide, mineral oils, and rosin plus a bacteriostatic or ungicidal agent. 2. M ixing o these two-paste dressings is either by hand or in an automix cartridge. 3. Examples o two-paste dressings are Coe-Pak manu actured by GC America, Inc. and PerioCare manu actured by Pulpdent Corp.

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B. Light-Cured Paste. A second type is a light-cured gel that contains polyether urethane dimethacrylate resin. 1. The dental hygienist must study the manu acturer’s instructions with care and must practice placement o the dressing on a typodont (model) be ore using it in a patient’s mouth. 2. This type o dressing is available as a clear, translucent material that is pre erred or use by some clinicians in esthetic areas o the dentition. 3. An example o a light-cured gel periodontal dressing is Barricaid VLC periodontal surgical dressing manu actured by Dentsply Caulk Co.

p o s t s u Rg iCa l in s t Ru Ct io n s a n d f o l l o W-u p v is it s A member o the dental team should provide postsurgical instructions to the patient ollowing periodontal surgery. Usually the patient is provided with both written and verbal instructions to minimize con usion and to maximize compliance. Typical postsurgical instructions are outlined in Box 27-11. For patients where sedation was required, the companion who accompanied the patient to the o ce is included when postsurgical instructions are given.

Bo x 27-11. T pical Po stsur ical I structio s 1. If yo u h a ve q u e st io n s o r co n ce rn s, ca ll t h e o f ce o r t h e o f ce e m e rg e n cy n u m b e r rig h t a w a y. Of ce : 555-1111; e m e rg e n cy 555-2222. 2. Do t a ke m e d ica t io n s a s p re scrib e d . Re p o rt a n y p ro b le m s w it h t h e m e d ica t io n s im m e d ia t e ly. 3. Do t a ke it e a sy fo r se ve ra l d a ys. Lim it yo u r a ct ivit y t o m ild p h ysica l e xe rt io n . 4. Exp e ct so m e b le e d in g fo llo w in g t h e p ro ce d u re . If h e a vy b le e d in g p e rsist s, ca ll t h e o f ce e m e rg e n cy n u m b e r. 5. Exp e ct so m e sw e llin g . In t e rm it t e n t u se o f a n ice p a ck o n t h e fa ce in t h e a re a o f t h e su rg e ry d u rin g t h e rst 8 t o 10 h o u rs fo llo w in g su rg e ry ca n m in im ize sw e llin g . 6. Die t Re co m m e n d a t io n s: a. So ft fo o d o n ly o n t h e d a y o f t h e su rg e ry b. No h o t b e ve ra g e s o n t h e d a y o f su rg e ry c. Avo id ch e w in g o n t h e su rg ica l sit e 7. Ora l Se lf-Ca re : a. Rin se w it h re co m m e n d e d m o u t h rin se st a rt in g t h e d a y a ft e r su rg e ry b. If d re ssin g w a s p la ce d , it m a y a lso b e b ru sh e d lig h t ly

1. Postsurgical Instructions to the Patient A. Restrictions on Sel -Care. M ost periodontal surgical procedures require some restrictions on sel -care during the early phase o healing. 1. It is common practice to prescribe 0.12% chlorhexidine mouth rinse to be used twice daily to aid with sel -care until the patient can sa ely resume mechanical plaque control. 2. In most cases ollowing routine f ap surgery and gingivectomy, manual sel -care can be resumed by the patient in 10 to 14 days.

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3. For selected surgical procedures (such as guided tissue regeneration or bone gra ting procedures) the surgical sites should not be cleaned with routine mechanical plaque control or up to 4 to 6 weeks. 4. Areas o the dentition not involved by the periodontal surgery may be cleaned with routine sel -care techniques. B. Postsurgical Medications. Patients should be encouraged to take medications as prescribed. 1. I systemic antibiotics are prescribed, it is particularly important or the patient to understand that all o this prescribed antibiotic medication should be taken. 2. Common postsurgical medications include either nonsteroidal or narcotic pain medications, but usually, these pain medications should only be taken as long as needed. C. Dietary Changes. Chewing requently must be limited to areas not involved by the surgery until healing has progressed to an acceptable level. 1. M any o these periodontal procedures require that the surgical site be undisturbed or an extended period o time. 2. Recommendations or a so t or liquid diet or 24 to 48 hours are routine ollowing most periodontal surgical procedures. 3. Chewing should be limited to the side o the mouth not involved by the surgery, especially during the early phases o healing. 2. Postsurgical Complications A. Facial swelling: It is common or the patient to experience some acial swelling ollowing most types o periodontal surgery. 1. Swelling can arise rom the tissue trauma incurred during the procedure and can even occur during the second and third day ollowing the surgery. 2. Although this swelling can be disconcerting to the patient, it is usually not a sign that healing is compromised. 3. Swelling can be minimized by the intermittent use o ice packs or the rst 8 to 10 hours ollowing the surgery. B. Postsurgical bleeding: Some bleeding ollowing periodontal surgery is to be expected. 1. Patients should be reassured that minor bleeding is not a cause or alarm. 2. Postsurgical instructions should be clear, however, that i excessive bleeding occurs the emergency number should be contacted immediately. C. Smoking: Surgical patients, who have elected to continue smoking, should be cautioned to re rain during the healing phase. 3. Organizing Postsurgical Visits. It is the dentist’s responsibility to manage postsurgical problems, such as extreme pain or in ection. The dental hygienist, however, can per orm much o the routine postsurgical patient management. Following periodontal f ap surgery, the patient is most o ten reappointed in 5 to 7 days or the rst postsurgical visit. Postsurgical care or the various types o periodontal surgery varies; however, steps to be ollowed at a typical postsurgical visit are outlined below. A. Steps Involved in a Typical Postsurgical Visit 1. Step 1. Patient interview: An interview is conducted with the patient to determine what the patient experienced during the days ollowing the surgery. The patient interview should be detailed enough to provide the dental hygienist with an overview o possible problems to investigate and solve at the postsurgical visit. The ollowing are some o the items that would normally be included in this interview. It is imperative that the dental hygienist alerts the dentist i any unusual conditions are reported by the patient or are observed during the postsurgical visit.

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a. Analgesics: Following periodontal surgery, analgesics (pain control medications) are used to control patient discom ort. The patient should be asked about the current level o discom ort and i another prescription is needed. b. Antibiotics: I antibiotics were needed ollowing a surgical procedure, remind the patient that all o the antibiotic tablets should be taken. It is also important to nd out i the patient experienced any unusual reactions to the antibiotic. c. Antimicrobial mouth rinse: An antimicrobial mouth rinse such as 0.12% chlorhexidine gluconate may have been prescribed or the patient to use during healing, since mechanical plaque control must be restricted at the surgical site ollowing periodontal surgery. Ask about the amount o mouth rinse remaining. During the course o the visit, it may be necessary to provide the patient another prescription or this mouth rinse. d. Swelling: Following periodontal surgery, it is common or the patient to experience some acial swelling. Remember that although this swelling can be disconcerting to the patient, it is common and usually not a sign that healing is compromised. e. Postsurgical bleeding: Inquire about postsurgical bleeding. It is common or patients to experience a little bleeding ollowing periodontal surgery, but heavy bleeding should not have occurred ollowing the procedure. I abnormal bleeding is suspected, the dentist should be alerted be ore planning any additional periodontal surgical intervention. . Sensitivity to cold: Sensitivity to cold ollowing root exposure during many types o periodontal surgery is quite common. Although this is an annoying postsurgical occurrence, the sensitivity normally disappears within the rst ew weeks ollowing the surgery i excellent plaque control is maintained. 2. Step 2. Vital signs: The patient’s vital signs including blood pressure, pulse, and temperature are assessed. An elevated temperature at the rst postsurgical visit can indicate a developing in ection. 3. Step 3. Periodontal dressing: Any periodontal dressing placed at the time o surgery is removed, so that the surgical site can be examined. The surgical site is rinsed with warm sterile saline and cotton-tipped applicators are used to remove any debris adherent to the teeth, so t tissues, or sutures. Suture material can become trapped within the periodontal dressing. When removing dressings, it might be necessary to loosen the dressing slightly and cut the suture be ore completely removing the dressing rom the necks o the teeth. Figure 27-20 shows interrupted interdental sutures ready or removal at the 1-week postsurgical visit.

Fi ure 27-20. I te rrupte d I te rde tal Suture s Re ad fo r Re mo al. At the 1-week postsurgical visit the periodontal dressing has been removed, the sutures have been cleaned with sterile saline, and the sutures are ready or removal.

Chapte r 27

Periodontal Surgical Concepts or the Dental Hygienist

4. Step 4. Examination o surgical site: Examine the surgical site with care. Tissue swelling or exudate such as pus can indicate a developing in ection. Excessive granulation tissue that occasionally orms in the surgical site should be removed with a sharp curet. 5. Step 5. Suture removal: The sutures are cut and removed using sterile scissors and cotton pliers. Remember to pull the suture out o the tissue w ithout draw ing the k not through the tissue. 6. Step 6. Plaque removal: All plaque on the teeth in the area o the surgery is removed. It is usual that patients cannot per orm per ect plaque control during the days ollowing periodontal surgery, so plaque accumulation is likely. Part o the responsibility o the dental team is to help the patient with plaque control during the critical stages o healing. 7. Step 7. Replacement o periodontal dressing: I indicated, the periodontal dressing is replaced. For most surgical procedures, the periodontal dressing should be discontinued as soon as the patient can resume some mechanical plaque control. In a ew instances the tissues will not be well adapted to the necks o the teeth, and replacement o the periodontal dressing should be considered to protect the continuing healing o the wound or at least another week. 8. Step 8. Sel -care instructions: The patient is instructed in sel -care. M echanical plaque control should be resumed as soon as possible ollowing periodontal surgery, but special instructions may be necessary during the rst ew weeks ollowing the surgery. a. Special tools such as brushes with very f exible bristles may be required during early stages o healing. b. During postsurgical healing, it is requently necessary to continue to modi y the patient’s plaque control techniques as the tissues heal and mature. Gingival margin contours usually are altered to some degree by the surgery, and this may necessitate the introduction o additional sel -care aids that were not necessary prior to the surgery. M onitoring and modi cation o the patient’s sel -care e orts during the healing phase is one o the most important responsibilities o the dental team and can help assure success o the surgical procedure. 9. Step 9. Reappointment: The patient is reappointed or the second postsurgical visit. This second visit should occur 2 to 3 weeks ollowing the surgery. B. Follow-Up Visits 1. Following the initial postsurgical visit, additional postsurgical visits must be scheduled based upon the extent o healing o the surgical wound. 2. Pro essional tooth polishing should be per ormed every 2 weeks until the patient can sa ely resume routine sel -care. 3. When healing is deemed complete by the dental team, the patient is always placed on a program o periodontal maintenance. 4. Attachment o the f ap back to the alveolar bone is usually complete within 3 weeks ollowing the surgery, and or many surgical procedures it is sa e to proceed with restorative care in the surgical site a ter at least 6 weeks o healing. N ote that some periodontal surgical procedures (such as bone replacement gra t and periodontal regeneration) will require much longer periods o healing prior to restoration placement. 5. Remodeling o the so t tissue can continue, however, or up to 6 months, so the dentist may wait quite a while prior to nal restoration placements in esthetic zones such as on anterior teeth.

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Chapte r Summar State me t Periodontal surgery is a critical element in the care o most patients with moderate to severe periodontitis and a critical element in the care o many patients in need o restorative dental procedures. The periodontal f ap is a undamental part o most periodontal surgical procedures, and a basic understanding o the principles o periodontal f ap surgery is important to the dental hygienist. The healing o periodontal surgical wounds is a complex process, and the terminology that has been used to describe the various types o healing that can occur in the periodontium can be con using. A variety o speci c types o periodontal surgery are being used; these techniques include procedures such as f ap or access, osseous resective surgery, bone replacement gra ting, periodontal regeneration, and periodontal plastic surgery among others; the dental hygienist should be amiliar with the common types o periodontal surgery employed. Current research into enhancing the outcomes o periodontal surgery by using biologic mediators is ongoing. Postsurgical care ollowing periodontal surgery is vital to success ul surgical outcomes, and dental hygienists play a key role in the management o patients ollowing periodontal surgery.

Se ct io

6

Fo cus o

Patie ts

CA S E 1 You are assigned the task o providing nonsurgical therapy or a periodontitis patient. During routine nonsurgical periodontal therapy, you encounter multiple sites where the probing depths exceed 6 mm. During periodontal instrumentation, you are unable to instrument the root sur aces thoroughly in the areas o the deepest pockets. What should you tell the patient related to this clinical observation?

CA S E 2 During nonsurgical periodontal therapy, a patient with chronic periodontitis in orms you that the dentist had previously discussed the possibility o periodontal surgery. The patient expresses deep concern and ear over the thought o agreeing to any periodontal surgery. The patient tells you about an aunt who had periodontal surgery many years ago and had many problems ollowing the surgery. H ow should you proceed?

CA S E 3 At the time o the rst week postsurgical visit, you note that a patient who had undergone f ap or access surgery has a temperature o 101.5°F and a pulse rate o 70 beats/min. Clinical examination o the surgical site reveals that the sutures are in place, but there appears to be a good deal o swelling in one part o f ap. H ow should you proceed?

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Periodontal Surgical Concepts or the Dental Hygienist

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CA S E 4 You are assigned the task o managing the rst week postsurgical visit or a patient who had an apically positioned f ap with osseous resective surgery. Following removal o the periodontal dressing and removal o the sutures, you note that there are several areas where the healing is progressing by secondary intention because the f ap could not be adapted to the teeth per ectly at the time o surgery. Though healing is progressing satis actorily, it is apparent that not all o the connective tissue wound around the teeth is completely covered by epithelium yet. H ow should you proceed?

Re fe re ce s 1. Caton, J. and S. N yman, H istometric evaluation o periodontal surgery. I. The modi ed Widman f ap procedure. J Clin Periodontol, 1980. 7(3): p. 212-23. 2. N yman, S., et al., N ew attachment ollowing surgical treatment o human periodontal disease. J Clin Periodontol, 1982. 9(4): p. 290-6. 3. Polson, A.M ., S. Ladenheim, and P.J. H anes, Cell and ber attachment to demineralized dentin rom periodontitis-a ected root sur aces. J Periodontol, 1986. 57(4): p. 235-46. 4. Gantes, B.G. and S. Garrett, Coronally displaced f aps in reconstructive periodontal therapy. D ent Clin N orth A m , 1991. 35(3): p. 495-504. 5. Graziani, F., et al., Clinical per ormance o access f ap surgery in the treatment o the intrabony de ect. A systematic review and meta-analysis o randomized clinical trials. J Clin Periodontol, 2012. 39(2): p. 145-56. 6. Ram jord, S.P. and R.R. N issle, The modi ed widman f ap. J Periodontol, 1974. 45(8): p. 601-7. 7. Caton, J. and S. N yman, H istometric evaluation o periodontal surgery. III. The e ect o bone resection on the connective tissue attachment level. J Periodontol, 1981. 52(8): p. 405-9. 8. O chsenbein, C., A primer or osseous surgery. Int J Periodontics R estorative D ent, 1986. 6(1): p. 8-47. 9. Reynolds, M .A., et al., The e cacy o bone replacement gra ts in the treatment o periodontal osseous de ects. A systematic review. A nn Periodontol, 2003. 8(1): p. 227-65. 10. Bowen, J.A., et al., Comparison o decalci ed reeze-dried bone allogra t and porous particulate hydroxyapatite in human periodontal osseous de ects. J Periodontol, 1989. 60(12): p. 647-54. 11. Guillemin, M .R., J.T. M ellonig, and M .A. Brunsvold, H ealing in periodontal de ects treated by decalcif ed reeze-dried bone allogra ts in com bination w ith ePT FE m em branes (I). Clinical and scanning electron m icroscope analysis. J Clin Periodontol, 1993. 20(7): p. 528-36. 12. Guillemin, M .R., et al., H ealing in periodontal de ects treated by decalci ed reeze-dried bone allogra ts in combination with ePTFE membranes. Assessment by computerized densitometric analysis. J Clin Periodontol, 1993. 20(7): p. 520-7. 13. M ellonig, J.T., Freeze-dried bone allogra ts in periodontal reconstructive surgery. D ent Clin N orth A m , 1991. 35(3): p. 505-20. 14. O reamuno, S., et al., Comparative clinical study o porous hydroxyapatite and decalci ed reeze-dried bone in human periodontal de ects. J Periodontol, 1990. 61(7): p. 399-404. 15. Rummelhart, J.M ., et al., A comparison o reeze-dried bone allogra t and demineralized reeze-dried bone allogra t in human periodontal osseous de ects. J Periodontol, 1989. 60(12): p. 655-63. 16. Sanders, J.J., et al., Clinical evaluation o reeze-dried bone allogra ts in periodontal osseous de ects. Part III. Composite reeze-dried bone allogra ts with and without autogenous bone gra ts. J Periodontol, 1983. 54(1): p. 1-8. 17. M ellonig, J.T., H uman histologic evaluation o a bovine-derived bone xenogra t in the treatment o periodontal osseous de ects. Int J Periodontics R estorative D ent, 2000. 20(1): p. 19-29. 18. Bier, S.J. and M .C. Sinensky, The versatility o calcium sul ate: resolving periodontal challenges. Com pend Contin Educ D ent, 1999. 20(7): p. 655-61; quiz 662. 19. Froum, S.J., M .A. Weinberg, and D. Tarnow, Comparison o bioactive glass synthetic bone gra t particles and open debridement in the treatment o human periodontal de ects. A clinical study. J Periodontol, 1998. 69(6): p. 698-709. 20. Lovelace, T.B., et al., Clinical evaluation o bioactive glass in the treatment o periodontal osseous de ects in humans. J Periodontol, 1998. 69(9): p. 1027-35. 21. Low, S.B., C.J. King, and J. Krieger, An evaluation o bioactive ceramic in the treatment o periodontal osseous de ects. Int J Periodontics R estorative D ent, 1997. 17(4): p. 358-67. 22. Caton, J., S. N yman, and H . Z ander, H istometric evaluation o periodontal surgery. II. Connective tissue attachment levels a ter our regenerative procedures. J Clin Periodontol, 1980. 7(3): p. 224-31. 23. Chambrone, L., et al., Root-coverage procedures or the treatment o localized recession-type de ects: a Cochrane systematic review. J Periodontol, 2010. 81(4): p. 452-78. 24. Christgau, M ., et al., Periodontal regeneration o intrabony de ects with resorbable and non-resorbable membranes: 30-month results. J Clin Periodontol, 1997. 24(1): p. 17-27. 25. Cortellini, P., et al., Guided tissue regeneration with di erent materials. Int J Periodontics R estorative D ent, 1990. 10(2): p. 136-51. 26. Cortellini, P., G. Pini Prato, and M .S. Tonetti, Periodontal regeneration o human intrabony de ects with titanium rein orced membranes. A controlled clinical trial. J Periodontol, 1995. 66(9): p. 797-803. 27. Darby, I.B. and K.H . M orris, A systematic review o the use o growth actors in human periodontal regeneration. J Periodontol, 2013. 84(4): p. 465-76. 28. Eickholz, P. and E. H ausmann, Evidence or healing o interproximal intrabony de ects a ter conventional and regenerative therapy: digital radiography and clinical measurements. J Periodontal R es, 1998. 33(3): p. 156-65. 29. Garrett, S., Periodontal regeneration around natural teeth. A nn Periodontol, 1996. 1(1): p. 621-66.

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30. Gottlow, J., Guided tissue regeneration using bioresorbable and non-resorbable devices: initial healing and long-term results. J Periodontol, 1993. 64(11 Suppl): p. 1157-65. 31. Khojasteh, A., et al., The e ectiveness o barrier membranes on bone regeneration in localized bony de ects: a systematic review. Int J O ral M ax illo ac Im plants, 2013. 28(4): p. 1076-89. 32. M cClain, P.K. and R.G. Schallhorn, Long-term assessment o combined osseous composite gra ting, root conditioning, and guided tissue regeneration. Int J Periodontics R estorative D ent, 1993. 13(1): p. 9-27. 33. M urphy, K.G. and J.C. Gunsolley, Guided tissue regeneration or the treatment o periodontal intrabony and urcation de ects. A systematic review. A nn Periodontol, 2003. 8(1): p. 266-302. 34. Stoecklin-Wasmer, C., et al., Absorbable collagen membranes or periodontal regeneration: a systematic review. J D ent R es, 2013. 92(9): p. 773-81. 35. Tu, Y.K., et al., A Bayesian network meta-analysis on comparisons o enamel matrix derivatives, guided tissue regeneration and their combination therapies. J Clin Periodontol, 2012. 39(3): p. 303-14. 36. Consensus report. M ucogingival therapy. A nn Periodontol, 1996. 1(1): p. 702-6. 37. Cairo, F., M . N ieri, and U. Pagliaro, E cacy o periodontal plastic surgery procedures in the treatment o localized acial gingival recessions. A systematic review. J Clin Periodontol, 2014. 41 Suppl 15: p. S44-62. 38. Camargo, P.M ., P.R. M elnick, and E.B. Kenney, The use o ree gingival gra ts or aesthetic purposes. Periodontol 2000, 2001. 27: p. 72–96. 39. H arris, R.J., Root coverage with connective tissue gra ts: an evaluation o short- and long-term results. J Periodontol, 2002. 73(9): p. 1054-9. 40. Langer, B. and L. Langer, Subepithelial connective tissue gra t technique or root coverage. J Periodontol, 1985. 56(12): p. 715-20. 41. M iller, P.D., Jr. and E.P. Allen, The development o periodontal plastic surgery. Periodontol 2000, 1996. 11: p. 7–17. 42. Bragger, U., D. Lauchenauer, and N.P. Lang, Surgical lengthening o the clinical crown. J Clin Periodontol, 1992. 19(1): p. 58-63. 43. Aoki, A., et al., In vitro evaluation o Er:YAG laser scaling o subgingival calculus in comparison with ultrasonic scaling. J Periodontal R es, 2000. 35(5): p. 266-77. 44. Christensen, G.J., So t-tissue cutting with laser versus electrosurgery. J A m D ent A ssoc, 2008. 139(7): p. 981-4. 45. Frentzen, M ., A. Braun, and D. Aniol, Er:YAG laser scaling o diseased root sur aces. J Periodontol, 2002. 73(5): p. 524-30. 46. Gold, S.I. and M .A. Vilardi, Pulsed laser beam e ects on gingiva. J Clin Periodontol, 1994. 21(6): p. 391-6. 47. Israel, M . and J.A. Rossmann, An epithelial exclusion technique using the CO 2 laser or the treatment o periodontal de ects. Com pend Contin Educ D ent, 1998. 19(1): p. 86-8, 90, 92-5. 48. N eill, M .E. and J.T. M ellonig, Clinical e cacy o the N d:YAG laser or combination periodontitis therapy. Pract Periodontics A esthet D ent, 1997. 9(6 Suppl): p. 1-5. 49. Sgolastra, F., et al., E cacy o Er:YAG laser in the treatment o chronic periodontitis: systematic review and meta-analysis. L asers M ed Sci, 2012. 27(3): p. 661-73. 50. Yukna, R.A., R.L. Carr, and G.H . Evans, H istologic evaluation o an N d:YAG laser-assisted new attachment procedure in humans. Int J Periodontics R estorative D ent, 2007. 27(6): p. 577-87. 51. American Academy o Periodontology statement on the e cacy o lasers in the non-surgical treatment o inf ammatory periodontal disease. J Periodontol, 2011. 82(4): p. 513-4. 52. A airs, C.o.S. Statement on lasers in dentistry. 53. M ariotti, A., E cacy o chemical root sur ace modi ers in the treatment o periodontal disease. A systematic review. A nn Periodontol, 2003. 8(1): p. 205-26. 54. O liveira, G.H . and E.A. M uncinelli, E cacy o root sur ace biomodi cation in root coverage: a systematic review. J Can D ent A ssoc, 2012. 78: p. c122. 55. Cochran, D.L. and J.M . Wozney, Biological mediators or periodontal regeneration. Periodontol 2000, 1999. 19: p. 40–58. 56. Esposito, M ., et al., Enamel matrix derivative (Emdogain) or periodontal tissue regeneration in intrabony de ects. A Cochrane systematic review. Eur J O ral Im plantol, 2009. 2(4): p. 247-66. 57. H ammarstrom, L., Enamel matrix, cementum development and regeneration. J Clin Periodontol, 1997. 24(9 Pt 2): p. 658-68. 58. H eijl, L., et al., Enamel matrix derivative (EM DO GAIN ) in the treatment o intrabony periodontal de ects. J Clin Periodontol, 1997. 24(9 Pt 2): p. 705-14. 59. Koop, R., J. M erheb, and M . Q uirynen, Periodontal regeneration with enamel matrix derivative in reconstructive periodontal therapy: a systematic review. J Periodontol, 2012. 83(6): p. 707-20. 60. O kuda, K., et al., Enamel matrix derivative in the treatment o human intrabony osseous de ects. J Periodontol, 2000. 71(12): p. 1821-8. 61. Lynch, S.E., et al., A combination o platelet-derived and insulin-like growth actors enhances periodontal regeneration. J Clin Periodontol, 1989. 16(8): p. 545-8. 62. M arx, R.E., et al., Platelet-rich plasma: Growth actor enhancement or bone gra ts. O ral Surg O ral M ed O ral Pathol O ral R adiol Endod, 1998. 85(6): p. 638-46.

STUDEn T An CILLARy RESOURCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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Pe io do ntal Eme g e ncie s

Se ctio n 1

Int o ductio n to Acute Pe io do ntal Co nditio ns

512

Se ctio n 2

Absce sse s o f the Pe io do ntium

512

Se ctio n 3

Ne c o tizing Pe io do ntal Dise ase s

521

Se ctio n 4

P ima

525

Se ctio n 5

Fo cus o n Patie nts

He pe tic Ging ivo sto matitis

528

Clinical Patient Care Evidence in Action Ethical Dilemma

Clinical Applicatio n.

There are several periodontal conditions that can bring a patient to a dental o f ce on an emergency basis or relie o pain or discom ort. Occasionally in the early stages o some o these conditions, dental hygienists may encounter them during a routine patient appointment. Dental hygienists need to be amiliar with these conditions, so that the patient’s needs can be managed in a timely manner. This chapter outlines some o the more common periodontal emergency conditions and o er suggestions or management o the patients with these conditions.

Le a ning Obje ctive s • Name and describe the three types o abscesses o the periodontium. • List the possible causes o abscesses o the periodontium. • Compare and contrast the abscess o the periodontium and the pulpal abscess. • Outline the typical treatment steps or a gingival abscess and a periodontal abscess. • Describe the clinical situation that can result in a pericoronal abscess. • Outline the typical treatment or a pericoronal abscess (pericoronitis). • Describe the characteristics o necrotizing ulcerative gingivitis. • Outline the typical treatment steps or necrotizing ulcerative gingivitis. • Describe the symptoms o primary herpetic gingivostomatitis.

Ke Te ms Acute periodontal conditions Abscess o the periodontium Pus Suppuration Circumscribed

Pulpal abscess Gingival abscess Periodontal abscess Pericoronal abscess Pericoronitis Operculum Trismus

Necrosis Ulceration Punched-out papillae Pseudomembrane Sequestrum Primary herpetic gingivostomatitis

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Implementation o Therapy or Patients with Periodontal Disease

Se ct io n 1

Int o ductio n to Acute Pe io do ntal Co nditio ns 1. M ost periodontal diseases are chronic in nature and progress rather slowly; they can take years or decades to destroy the periodontium and lead to tooth loss. These diseases are rarely pain ul, especially in their earlier stages. There are a ew periodontal diseases, such as aggressive periodontitis, that progress more rapidly. H owever, even aggressive periodontitis can take several years to lead to tooth loss, and it is not usually associated with pain in the early stages. A. There are several periodontal conditions that can bring patients to a dental o ce or hospital emergency room or relie o pain or other more dramatic symptoms (1). B. The emergency conditions described in this chapter are normally considered examples o acute periodontal conditions. C. The term “ acute periodontal conditions” re ers to conditions that are commonly characterized by having a sudden onset and a rapid course o progression. These acute conditions are requently accompanied by pain and discom ort, and they may be unrelated to the presence o any pre-existing gingivitis or periodontitis (Box 28-1). D. It is imperative that all members o the dental team be alert or these conditions because their recognition and early intervention can limit subsequent permanent damage to the periodontium (2,3). E. Some o these acute conditions can be encountered in their earliest stages by the dental hygienist during routine treatment or recall appointments. 2. This chapter outlines some o the more common periodontal emergency conditions and brief y describes the treatment that may be recommended and per ormed by the dentist or the dental hygienist or by other healthcare providers.

Bo x 28-1. Cha acte istics o f Acute Pe io do ntal Co nditio ns • • • •

Su d d e n o n se t o f t h e co n d it io n Ra p id co u rse o f p ro g re ssio n Acco m p a n ie d b y p a in a n d d isco m fo rt Ma y b e u n re la t e d t o p re -e xist in g g in g ivit is o r p e rio d o n t it is

Se ct io n 2

Absce sse s o f the Pe io do ntium 1. Overview o Abscesses o the Periodontium A. Abscesses o the Periodontium Def ned 1. An abscess o the periodontium may be de ned as an acute in ection involving a circumscribed collection o pus in the periodontium. 2. Abscesses o the periodontium are collections o pus within the periodontal tissues. Pus consists primarily o dead and dying neutrophils, bacteria, cellular debris, and f uid leaked rom blood vessels; pus can result when body de ense mechanisms are involved in attempting to control an in ection. The process o orming pus is called suppuration.

Chapte 28

Periodontal Emergencies

513

3. In its earliest stages, the abscess o the periodontium can be discovered by the dental hygienist during an oral inspection at a routine treatment visit; but in more advanced stages, the abscess o the periodontium can bring the patient to the dental o ce or relie o pain. 4. Abscesses o the periodontium are usually described as being circumscribed. The term circumscribed means that the abscess is localized or con ned to a speci c site (i.e., the acial sur ace o a single tooth or perhaps the gingival margin on a speci c tooth). Figure 28-1 illustrates a typical example o an abscess o the periodontium. 5. The precise bacterial etiology o the abscess o the periodontium is not clear, but it is known that most o these lesions contain microf ora that are predominantly gram negative and anaerobic. M ost studies indicate that the bacteria seen in these abscesses are similar to the bacteria seen in periodontitis patients with deeper pockets.

Fig u e 28-1. Absce ss o f the Pe io do ntium. Note the localized swelling between the mandibular right canine and lateral incisor. Palpation o the swelling would reveal what eels like a luid- illed sack. Pus can be ound in this site.

Bo x 28-2. Cha acte istics o f an Absce ss o f the Pe io do ntium • • • • •

Pa in t h a t is co n st a n t a n d lo ca lize d Circu m scrib e d (lo ca lize d ) sw e llin g in t h e p e rio d o n t iu m Po ssib le in cre a se in t o o t h m o b ilit y Ra d io g ra p h ic lo ss o f a lve o la r b o n e n o t in vo lvin g t h e t o o t h a p e x To o t h u su a lly h a s a vit a l p u lp

B. Characteristics o an Abscess o the Periodontium 1. Typical patient complaints related to an abscess o the periodontium include dental pain and swelling in the gingiva at a speci c location (Box 28-2). a. Pain resulting rom an abscess o the periodontium is usually described by the patient as a constant pain (as opposed to intermittent). Patients requently report that the pain is easy or them to localize (i.e., the patient can point to the exact spot that hurts). N ote that in some other conditions, a patient can report pain that is not at all localized to a speci c location. b. In addition to pain and swelling, the patient may report di culty in mastication and a bad taste in the mouth.

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2. O ral examination will usually reveal the presence o a circumscribed swelling o the so t tissue. This swelling may involve the gingiva only, or it may involve both the gingiva and the mucosa. 3. M any teeth with an abscess o the periodontium can also exhibit a temporary increase in mobility. 4. Dental radiographs o a tooth with an abscess o the periodontium requently reveal alveolar bone loss in the area o the abscess, but the bone loss does not usually involve the tooth apex. Figure 28-2 is a radiograph o a tooth with an abscess o the periodontium. a. Alveolar bone loss resulting rom an abscess o the periodontium can occur extremely rapidly when compared with the rate o alveolar bone loss usually associated with all orms o either chronic or aggressive periodontitis. b. Although a dental radiograph o an abscess o the periodontium may reveal alveolar bone loss, in a periodontitis patient, it is not always possible to tell what part o the missing bone actually resulted rom the acute in ection and what part o the missing bone was caused by chronic periodontitis that was present be ore the abscess ormed.

Fig u e 28-2. Absce ss if the Pe io do ntium Invo lving Mandibula Se co nd Mo la To o th. The clinical photograph shows circumscribed swelling and in lammation o the gingival tissue on the acial sur ace o a mandibular second molar with an abscess o the periodontium. The radiograph o the site reveals loss o bone density between the roots o the molar tooth a ected by the abscess. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

Fig u e 28-3. Path o f D ainag e . The abscess o the periodontium shown in this igure has broken through the sur ace tissues, establishing a path o drainage or the pus on its own.

Chapte 28

Periodontal Emergencies

5. Teeth a ected by an abscess o the periodontium are usually vital (have healthy pulp tissue) and respond positively i pulp testing is per ormed. 6. Another clinical sign o an abscess o the periodontium can be an elevated body temperature; an elevated body temperature would not normally be present unless the abscess o the periodontium is spreading, so this would represent a serious sign i present. Since many abscesses o the periodontium are circumscribed (localized), they are not associated with an elevated body temperature. 7. When there is delay in treating an abscess o the periodontium, there can be additional oral changes (4). The collection o pus can break through the sur ace tissues, thus establishing a path o drainage or the pus on its own. Figure 28-3 illustrates an abscess o the periodontium that has drained spontaneously by breaking through the sur ace tissues. C. Causes o Abscesses o the Periodontium. Several causes o abscesses o the periodontium have been reported (5,6). Theories about the origin o the abscess o the periodontium vary, but most investigators attribute ormation o this type o abscess to one o the ollowing scenarios. 1. Blockage o the Orif ce o a Pocket. Blockage o the ori ce (or opening) o a pre-existing periodontal pocket has been suggested as a cause o some abscesses o the periodontium. M ost periodontal pockets have readily accessible openings that give easy access to a periodontal probe. Some authors have theorized that in certain instances, the opening o a periodontal pocket can become restricted in size because o temporary improvement o the sur ace tissue tone. This improvement o tissue rmness could result in trapping bacteria and f uids in a pre-existing periodontal pocket, leading to an abscess that begins within this existing periodontal pocket. 2. Accidentally Forcing a Foreign Object into the Tissues. It has also been suggested that an abscess o periodontium can be caused by accidentally orcing a oreign object into the supporting tissues o a tooth. a. A variety o oreign objects have been implicated in the ormation o some abscesses o the periodontium. For example, an abscess could result when a patient accidentally punctures the gingiva with a toothpick, orcing bacteria into the tissue. b. Another common event that can result in an abscess o the periodontium is accidentally orcing some ood product like a husk rom a kernel o popcorn or a peanut skin into the tissues associated with the tissue inf ammation as part o a periodontal pocket. 3. Incomplete Calculus Removal in a Periodontal Pocket. Incomplete calculus removal in a periodontal pocket has also been suggested as one cause o an abscess o the periodontium. a. When this occurs, it is usually thought to be in a site with a very deep probing depth where the calculus deposits are removed only in the most coronal aspects o the pocket near the gingival margin, but the calculus deposits deeper in the pocket are not completely removed because o di culty o access or instrumentation o the tooth sur ace. b. It is theorized that removal o the more coronal calculus deposits allows the gingival margin to heal somewhat and to tighten around the tooth, like a drawstring o a pouch, preventing drainage o bacterial toxins and other waste products rom the pocket. Bacteria remaining in the deeper aspects o the periodontal pocket could result in the ormation o an abscess o the periodontium.

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2. Comparison Between the Periodontal Abscesses and the Pulpal Abscesses. The clinical recognition and diagnosis o a periodontal abscess can be complicated in some instances because o the possible overlap o signs o a periodontal abscess with the signs o a pulpal abscess. A. Abscesses a ecting the tissues around a tooth can result or two di erent sources: (1) the periodontium itsel , which surrounds the tooth or (2) the pulpal tissues that are within the pulp chamber o the tooth (7). 1. It is help ul or the dental hygienist to be amiliar with the characteristics o these two types o abscesses, since the periodontal abscess and the pulpal abscess sometime appear to have somewhat similar clinical characteristics. 2. The characteristics o each o these types o abscesses are outlined in Table 28-1. B. As already discussed, a periodontal abscess is an abscess that results rom an acute in ection o the periodontium. C. O n the other hand, a pulpal abscess is an abscess that results rom an in ection o the tooth pulp that can sometimes extend into the periodontium. 1. A pulpal abscess can be caused by death o the tooth pulp rom trauma to the tooth or rom deep dental decay; a dead tooth pulp is requently re erred to as a nonvital pulp. 2. M anagement o a patient with a pulpal abscess usually requires root canal treatment and will not be discussed in this chapter.

TABLE 2 8 -1 . DIFFEr ENTIATION OF THE Ty PES OF ABSCESS Cha acte istic

Pe io do ntal Absce ss

Pulpal Absce ss

Vit a lit y t e st re su lt s

Usu a lly vit a l p u lp

Usu a lly n o n vit a l p u lp

Ra d io g ra p h ic a p p e a ra n ce

Bo n e lo ss p re se n t (n o t a t a p e x)

Bo n e lo ss a t t o o t h ro o t a p e x

Sym p t o m s

Lo ca lize d , co n st a n t p a in

Difficu lt t o lo ca lize , in t e rm it t e n t p a in

3. Types o Abscesses o the Periodontium. Authors generally describe three types o periodontal abscesses: (1) the gingival abscess, (2) the periodontal abscess, and (3) the pericoronal abscess, but there is considerable overlap in this very loose classi cation system. A. Gingival Abscess. The gingival abscess re ers to an abscess o the periodontium that is primarily limited to the gingival margin or to the interdental papilla without involvement o the deeper structures o the periodontium. 1. The gingival abscess can occur in a previously periodontally healthy mouth when some oreign object is orced into a healthy gingival sulcus. An abscess o the periodontium that is limited to the gingival margin area can ollow this traumatic event. 2. Figure 28-4 illustrates a typical gingival abscess where the swelling is limited to the marginal gingiva o a single tooth. B. Periodontal Abscess. The true periodontal abscess re ers to an abscess o the periodontium that a ects the deeper structures o the periodontium as well as the gingival tissues.

Chapte 28

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517

1. The periodontal abscess usually occurs in a site with pre-existing periodontal disease including pre-existing periodontal pockets. 2. The periodontal abscess usually a ects the deeper structures o the periodontium and is not limited to the gingiva only. C. Pericoronal Abscess. The pericoronal abscess re ers to an abscess o the periodontium that involves tissues around the crown o a partially erupted tooth. The pericoronal abscess is also re erred to as pericoronitis. 1. This type o abscess is seen in teeth where some o the so t tissues surrounding the teeth actually cover part o the occlusal sur ace o the teeth. Figure 28-5 illustrates a patient with a pericoronal abscess under a so t tissue f ap partially covering a third molar tooth.

Fig u e 28-4. Ging ival Absce ss. Note that this abscess is limited to the gingival margin on the acial sur ace o this maxillary canine. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

Fig u e 28-5. Pe ico o nal Absce ss Invo lving a Mandibula Thi d Mo la To o th. The clinical photograph shows the typical clinical appearance o a mandibular third molar tooth with a pericoronal abscess. Note the swelling o the tissue that is partially covering the crown o the third molar. The radiograph o the site illustrated the position o the third molar in close relationship to the mandibular ramus. (Courtesy o Dr. Richard Foster, Guil ord Technical Community College, Jamestown, NC.)

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Bo x 28-3. Sig ns and S mpto ms o f a Pe ico o nal Absce ss • Pa in a t t h e sit e • Sw e llin g o f o p e rcu lu m • Po ssib le t rism u s (lim it e d m o u t h o p e n in g )

• Po ssib le e le va t e d b o d y t e m p e ra t u re • Po ssib le lym p h a d e n o p a t h y

2. The pericoronal abscess (or pericoronitis) is most requently seen around mandibular third molar teeth. Since many third molar teeth do not have space to erupt ully, these teeth can have a f ap o tissue covering part o the occlusal sur ace. 3. The f ap o gingival tissue that covers a portion o the crown o a partially erupted tooth can become in ected, and it is this type o in ection under this f ap o tissue that is re erred to as a pericoronal abscess. The f ap o so t tissue is called an operculum, and some authors also re er to the pericoronal abscess as an operculitis. 4. Streptococci m illeri group bacteria, well-known or their ability to cause suppurative in ections, are most likely involved in the pathogenesis o acute severe pericoronitis o the lower third molar (8). 5. The signs and symptoms o the pericoronal abscess are discussed below and outlined in Box 28-3. 6. Pain is common with the pericoronal abscess. The pain can arise rom the tissue swelling itsel , but pain can also arise when an opposing tooth occludes with the in ected, swollen operculum. 7. So t tissue swelling (edema) and redness (erythema) also usually accompany the pericoronal abscess. 8. As damage to tissue covering the partially erupted tooth progresses and the tissue swelling increases, the opposing tooth can requently be seen to impinge (press) on the swollen tissue, creating additional tissue damage and additional patient discom ort. 9. Limited mouth opening is also seen in some cases o advanced pericoronal abscess; limited mouth opening is re erred to as trismus. 10. Elevated body temperature ( ever) and swollen lymph nodes (lymphadenopathy) also can be seen in advanced cases o pericoronitis. 4. Management o Patients with Abscesses o the Periodontium A. Treatment o a Gingival or Periodontal Abscess. The treatment o a patient with either a gingival or a periodontal abscess is similar. 1. Fundamental treatment steps include (1) establishment o a path o drainage or the pus, (2) thorough periodontal debridement o the adjacent tooth sur aces in the area o the abscess, and (3) relie o pain. 2. Steps commonly ollowed in treatment o patients with a gingival or a periodontal abscess are discussed below and are outlined in Box 28-4. a. It is normally necessary to anesthetize the site to be treated, since manipulation o the tissues involved by an abscess can be quite uncom ortable. b. Drainage o the pus rom the abscess is critical. The abscess can be drained either through the pocket itsel or by per orming periodontal surgery (as discussed in Chapter 27). When drainage is established through the pocket, the toe o a sterile curet is used to puncture the so t tissue wall o the pocket to allow the drainage.

Chapte 28

Periodontal Emergencies

In some cases, drainage can be accomplished by incising through the sur ace tissues. c. Thorough periodontal instrumentation o the tooth sur aces in the site o the abscess is important in bringing this type o abscess under control. d. Some adjustment o the tooth occlusion is usually also indicated, since inf ammation resulting rom the abscess can orce a tooth to extrude slightly rom its socket, leading to trauma rom occlusion and pain when masticating. e. In more advanced cases o abscesses, antibiotics may also be needed, as with any other serious oral in ection. . Some clinicians recommend using warm saline (salt water) rinses several times each day to help keep the abscess draining until it has healed completely. g. A prescription or pain medication should always be considered, but overthe-counter pain medications can be adequate in many patients once the abscess has been drained. h. Following emergency treatment o a patient with any abscess o the periodontium, the dental team should appoint the patient or a thorough periodontal assessment, since the abscess o the periodontium requently occurs in a patient with existing untreated periodontal disease, and routine periodontal therapy may be needed. B. Treatment o a Pericoronal Abscess. Treatment o patients with pericoronal abscess di ers slightly rom treatment o patients with other types o abscesses o the periodontium because o the di erence in the anatomical location o these abscesses. 1. Fundamental treatment steps or a patient with pericoronitis include (1) establishment o a path o drainage or the pus, (2) irrigation o the undersur ace o the operculum, (3) thorough periodontal debridement o the tooth sur aces in the area o the abscess, and (4) relie o pain (9). 2. Steps commonly ollowed in treatment o patients with a pericoronal abscess are discussed below and outlined in Box 28-5. a. It is normally necessary to anesthetize the site to be treated, since manipulation o the tissues involved by an abscess can be quite uncom ortable. b. Drainage o the pus rom the abscess is critical. The abscess can be drained either through the pocket itsel or by per orming periodontal surgery (as discussed in Chapter 27). When drainage is established through the pocket, the toe o a sterile curet is used to puncture the so t tissue wall o the pocket to allow drainage. Abscesses around the crown o a partially erupted third molar tooth may be di cult to drain because o the anatomy o the region. c. Thorough periodontal instrumentation o the tooth sur aces in the site o the abscess is important in bringing this type o abscess under control. d. The area under the operculum that partially covers the tooth crown should be irrigated thoroughly. This irrigation can be done with sterile saline. e. In more advanced cases o abscesses antibiotics may be needed, as with any other serious oral in ection. . Some clinicians recommend using warm saline (salt water) rinses several times each day to help keep the abscess draining until it has healed completely. g. A prescription or pain medication should always be considered, but overthe-counter pain medications can be adequate in many patients once the abscess is drained.

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h. Following emergency treatment o a patient with any abscess o the periodontium, the dental team should appoint the patient or a thorough periodontal assessment, since the abscess o the periodontium requently occurs in a patient with existing untreated periodontal disease. i. In some cases ollowing resolution o the abscess, it is wise to excise the operculum that was involved in the pericoronal abscess. This removal can prevent recurrence o the abscess. In some cases ollowing resolution o the abscess, the dentist may recommend extraction o malposed third molar teeth i there is inadequate jaw space or the third molar teeth to ully erupt.

Bo x 28-4. Ste ps in T e atme nt o f a Ging ival o Pe io do ntal Absce ss • • • • • • • •

Ad m in ist e r lo ca l a n e st h e sia Dra in p u s Th o ro u g h p e rio d o n t a l in st ru m e n t a t io n Ad ju st o cclu sio n if n e e d e d Pre scrib e a n t ib io t ics if n e e d e d Re co m m e n d w a rm sa lin e rin se s Pre scrib e p a in m e d ica t io n s if n e e d e d Fo llo w u p a p p o in t m e n t s

Bo x 28-5. Co mmo n Ste ps in T e atme nt o f Patie nt w ith Pe ico o nal Absce ss • • • • • • • • •

Ad m in ist e r lo ca l a n e st h e sia Dra in p u s Th o ro u g h p e rio d o n t a l in st ru m e n t a t io n Irrig a t e u n d e r o p e rcu lu m Pre scrib e a n t ib io t ics if n e e d e d Re co m m e n d w a rm sa lin e rin se s Pre scrib e p a in m e d ica t io n s if n e e d e d Eva lu a t e t h e n e e d fo r t h ird m o la r e xt ra ct io n s Est a b lish fo llo w -u p a p p o in t m e n t s

Chapte 28

Periodontal Emergencies

Se ct io n 3

Ne c o tizing Pe io do ntal Dise ase s N ecrotizing periodontal diseases include necrotizing ulcerative gingivitis (o ten re erred to as N UG) and necrotizing ulcerative periodontitis (o ten re erred to as N UP) (10). N UG and N UP also are discussed in Chapter 9. Both o these diseases are acute in ections o the periodontium that can bring patients to the dental o ce or emergency treatment. N UG is an acute in ection a ecting the gingival tissues only. N UP is an acute in ection that mimics N UG but can also a ect the deeper structures o the periodontium such as the alveolar bone. Both conditions have been reported to occur in patients with compromised immune systems who there ore may have limited host de ense mechanisms. 1. N ecrotizing Ulcerative Gingivitis A. Overview o N ecrotizing Ulcerative Gingivitis (N UG) 1. N ecrotizing ulcerative gingivitis or N UG is an acute in ection o the periodontium that is limited to gingival tissues (11–13). O ther names or this condition are Vincent in ection, trench mouth, ulceromembranous gingivitis, and acute necrotizing ulcerative gingivitis (AN UG). As the name necrotizing ulcerative gingivitis implies, patients with N UG exhibit necrosis and ulceration o the gingiva. a. The term necrosis re ers to cell death, in this instance re erring to the death o the cells comprising the gingival epithelium. b. The term ulceration re ers to the loss o the epithelium normally covering underlying connective tissue. In N UG, ulceration results rom death o the epithelial cells and the subsequent loss o the epithelium that normally covers the underlying gingival connective tissue. 2. An impaired host response appears to be associated with the development o N UG in many patients (14). This impaired response may be related to any o several actors such as poor nutrition, atigue, psychosocial actors, systemic disease, alcohol abuse, or drug abuse. It should be noted that N UG also may be associated with the immunosuppression seen in H IV in ection. 3. It is not known i bacteria are the primary cause o N UG, but studies indicate that certain bacteria including spirochetal organisms and usi orm bacilli are always associated with the disease. O ther organisms have also been reported to be present in N UG. 4. N UG occurs in patients o all ages, but the highest incidence o N UG is seen in patients between 20 and 30 years o age (15). In the United States, N UG in children is not common, but it has been reported in children in underdeveloped countries. 5. There are several clinical signs that distinguish N UG rom other orms o gingivitis. a. O ne o those clinical signs is the presence o punched-out papillae (Fig. 28-6). In N UG, the necrosis associated with this condition can destroy the papillae between the teeth, resulting in the clinical appearance that the papillae are missing or “ punched out.” The term punched-out papillae is used to underscore the crater-like appearance le t by the absence o the papillae. b. Another clinical sign is the ormation o a pseudomembrane. The necrotic areas o gingiva are covered with a gray-white layer sometimes re erred to as a pseudomembrane. 1. This pseudomembrane actually consists o dead cells, bacteria, and oral debris; underlying this pseudomembrane is raw connective tissue.

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2. Patients with N UG usually exhibit bleeding with the slightest manipulation o the gingival tissues. This bleeding results rom breakage o some o the tiny blood vessels in the connective tissues exposed under the pseudomembrane.

Fig u e 28-6. Ne c o tizing Ulce ative Ging ivitis. Note that the necrotic areas have extended rom the papillae onto the acial sur aces. The necrotic areas o the gingiva are covered with gray-white layer called the pseudomembrane. The necrosis has destroyed the papillae leading to what is called punched-out papillae that can be hidden by the pseudomembrane.

Bo x 28-6. Cha acte istics o f NUG • • • • • • • •

Ora l p a in Ne cro t ic o r p u n ch e d -o u t g in g iva l p a p illa e Gin g iva l b le e d in g w it h e ve n slig h t m a n ip u la t io n o f t h e g in g iva l t issu e s Pre se n ce o f p se u d o m e m b ra n e o n a ffe ct e d sit e s Sw o lle n lym p h n o d e s (lym p h a d e n o p a t h y) Va g u e fe e lin g o f d isco m fo rt (m a la ise ) Ele va t e d b o d y t e m p e ra t u re Ext re m e h a lit o sis (fe t id b re a t h )

B. Characteristics o N ecrotizing Ulcerative Gingivitis. The characteristics o N UG are described below and outlined in Box 28-6. 1. Patients with N UG experience oral pain and requently seek emergency care or that oral pain; the ulceration associated with the in ection results in exposure o connective tissue, which can be quite uncom ortable or the patients. Because o the exposure o connective tissue, bleeding rom the area can appear to be spontaneous. 2. The tissue necrosis can lead to destruction o the interdental papillae resulting in punched-out papillae; areas are normally covered with a collection o dead tissue cells and debris called a pseudomembrane. 3. Patients with N UG can display swollen lymph nodes (lymphadenopathy), a vague eeling o discom ort (malaise), and an elevated body temperature. 4. Because o the necrosis or death o cells involved with this disease, there is usually noticeable halitosis or bad breath in N UG patients. Some authors have described this halitosis as a etid breath. 5. Certain associated behaviors or conditions are requently present in patients who develop N UG; these include a history o smoking, a history o poor nutrition, and a history o severe stress.

Chapte 28

Periodontal Emergencies

6. It has also been reported that some patients who develop N UG have a human immunode ciency virus (H IV)-positive status. N UG has also been reported to occur in some patients with H IV in ection. C. Typical Treatment Steps or N UG. The treatment o patients with N UG is summarized below and outlined in Box 28-7. 1. At the rst appointment. a. The pseudomembrane should be removed care ully with irrigation and moist cotton. b. Supragingival periodontal instrumentation is per ormed. Instrumentation is limited because o the discom ort elicited by tissue manipulation. c. The patient is instructed regarding a gentle sel -care regimen. Toothbrushing may need to be restricted to removal o debris with so t brushes. d. Patients may need to use standard regimens o twice daily rinses o chlorhexidine. Some authors have suggested using 3% hydrogen peroxide with equal parts o warm water every 2 to 3 hours. 2. At the rst ollow-up appointment 2 days a ter initial visit. a. Subgingival periodontal instrumentation usually can be begun at this appointment. b. Further instruction in sel -care should be included at this visit. 3. At the second ollow-up appointment approximately 5 days a ter initial visit, subgingival instrumentation usually can be completed. 4. In more advanced cases o N UG, antibiotics may be needed as in any other severe oral in ection. 5. Following the resolution o the in ection. The patient should be appointed or a comprehensive clinical assessment to identi y any underlying chronic periodontal disease. Figure 28-7 illustrates be ore and a ter treatment photographs o a typical patient with early stages o N UG. Following complete resolution o the in ection, some N UG patients require periodontal surgery to re-establish natural gingival contours.

Bo x 28-7. T pical T e atme nt Ste ps fo a Patie nt w ith Ne c o tizing Ulce ative Ging ivitis 1. At t h e rst a p p o in t m e n t . • Th e p se u d o m e m b ra n e sh o u ld b e re m o ve d ca re fu lly. • Su p ra g in g iva l p e rio d o n t a l in st ru m e n t a t io n is p e rfo rm e d . In st ru m e n t a t io n is lim it e d b e ca u se o f t h e d isco m fo rt e licit e d b y t issu e m a n ip u la t io n . • Th e p a t ie n t is in st ru ct e d re g a rd in g a g e n t le se lf-ca re re g im e n . 2. At t h e rst fo llo w -u p a p p o in t m e n t 2 d a ys a ft e r in it ia l visit . • Su b g in g iva l p e rio d o n t a l in st ru m e n t a t io n u su a lly ca n b e b e g u n a t t h is a p p o in t m e n t . • Fu rt h e r in st ru ct io n in se lf-ca re sh o u ld b e in clu d e d a t t h is visit . 3. At t h e se co n d fo llo w -u p a p p o in t m e n t a p p ro xim a t e ly 5 d a ys a ft e r in it ia l visit . • Su b g in g iva l in st ru m e n t a t io n u su a lly ca n b e co m p le t e d . 4. Fo llo w in g t h e re so lu t io n o f t h e in fe ct io n , t h e p a t ie n t sh o u ld b e a p p o in t e d fo r a co m p re h e n sive clin ica l a sse ssm e n t t o id e n t ify a n y u n d e rlyin g ch ro n ic p e rio d o n t a l d ise a se o r t h e p o ssib le n e e d fo r su rg ica l re sh a p in g o f t h e g in g iva .

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Fig u e 28-7. Ne c o tizing Ulce ative Ging ivitis: Be fo e and Afte T e atme nt. A: Necrotizing ulcerative gingivitis be ore treatment. B: The same patient a ter treatment. (Courtesy o Dr. Don Rol s, Periodontal Foundations, Wenatchee, WA.)

2. N ecrotizing Ulcerative Periodontitis A. Overview o N ecrotizing Ulcerative Periodontitis (N UP) 1. Symptoms o necrotizing ulcerative periodontitis or N UP can be similar to those o N UG but necrotizing ulcerative periodontitis also a ects the deeper structures o the periodontium such as the alveolar bone (10,16,17). N ecrotizing ulcerative periodontitis can occur in patients with N UG who go untreated. 2. O ne unusual nding in N UP is that it can be accompanied by the ormation o bone sequestra. A sequestrum is a ragment o necrotic (dead) bone. Sequestration is the process o orming a sequestrum. 3. Figure 28-8 illustrates a patient with N UP. B. Typical Treatment o N ecrotizing Ulcerative Periodontitis. Treatment o patients with N UP is complex and may require medical consultation, since the patients who develop this condition can have serious underlying medical compromising conditions that must be managed simultaneously with dental therapy (18–20). When patients with N UP are encountered in a general dental o ce, immediate re erral to a periodontist is indicated.

Fig u e 28-8. Ne c o tizing Ulce ative Pe io do ntitis. A: A patient with NUP. B: Close-up o the mandibular arch showing bone sequestration. (Courtesy o Dr. Don Rol s, Periodontal Foundations, Wenatchee, WA.)

Chapte 28

Se ct io n 4

P ima

Periodontal Emergencies

525

He pe tic Ging ivo sto matitis

1. Overview o Primary Herpetic Gingivostomatitis. A. Etiology o Primary Herpetic Gingivostomatitis. Primary herpetic gingivostomatitis is actually a medical condition resulting rom a viral in ection. It is listed here as a periodontal emergency condition, since patients with this condition can rst seek care in a dental o ce because o the nature o the oral symptoms that may develop in some cases. B. Characteristics o Primary Herpetic Gingivostomatitis 1. Primary herpetic gingivostomatitis is a pain ul oral condition that can result rom the initial in ection with the herpes simplex virus (H SV) (21–23). a. There are two types o herpes simplex virus, oral herpes virus (H SVI) and genital herpes virus (H SVII) (24). Primary herpetic gingivostomatitis is usually caused by initial in ection with H SVI but can also be caused by initial in ection with H SVII. b. In the majority o patients, the initial in ection with these viruses produces no noticeable clinical signs and can go undetected clinically. In other patients, however, the oral symptoms resulting rom this initial in ection can be quite severe, and it is these severe oral symptoms that are known as primary herpetic gingivostomatitis (Fig. 28-9).

Fig u e 28-9. P ima O al Infe ctio n w ith He pe s Simple x Vi us. These three children demonstrate the spectrum o primary oral in ection with the herpes simplex virus, which ranges rom nearly asymptomatic to severe. A: The irst patient has a single vesicle on his tongue.

B: The second patient mani ests widespread labial and gingival lesions. The parent’s ingers are shown in the photograph; however, touching the in ected area with bare ingers is not recommended. The dental hygienist should advise parents that contact with open sores or saliva can spread the virus.

C: The third patient shows a severe in ection with lesions on the ace. (From Fleisher GR, Ludwig W, Baskin MN. Atlas of Pediatric Emergency Medicine. Philadelphia, PA: Lippincott Williams & Wilkins; 2004.)

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Fig u e 28-10. P ima He pe s Simple x Vi us Infe ctio n in Infanc . Finger sucking likely caused the spread o the in ection rom the mouth to the hand o this in ant. The parent’s ingers are shown in the photograph; however, touching the in ected area with bare ingers is not recommended. (From Goodheart HP. Goodheart's Photoguide of Common Skin Disorders. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2003.)

2. Prim ary herpetic gingivostom atitis is contagious and requires careful attention to prevent its spread. a. In ections caused by H SV are contagious during the vesicular stage when the virus is contained in the clear f uid in the vesicles. b. H SV1 is primarily spread by direct contact through kissing and contact with open sores or by contact with in ected saliva. c. H SV1 can also spread rom one part o the body to another, such as rom saliva to the ngers, then to the eye. Touching the eye can result in a pain ul and dangerous herpetic in ection o the cornea (herpes keratitis). 3. The initial in ection with H SVI usually occurs in children or in young adults, but it can occur at any age (25). 4. O nce a patient is in ected with this virus, the in ection can recur periodically throughout the li e o the patient in the orm o herpes labialis ( ever blisters or cold sores). 2. Clinical Signs and Treatment o Primary Herpetic Gingivostomatitis A. Clinical Signs. As already mentioned, the clinical signs o primary herpetic gingivostomatitis can range rom subclinical (no noticeable signs at all) to rather severe; the severe clinical signs are discussed below and outlined in Box 28-8. 1. Severe oral pain can be associated with primary herpetic gingivostomatitis, and this discom ort results in di culty in eating and drinking. 2. The gingival tissues appear swollen (edematous), red (erythematous), and bleed quite easily when disturbed. 3. Primary herpetic gingivostomatitis is accompanied by pain ul oral ulcers. Care ul inspection o the gingival tissue can reveal small clusters o blisters (vesicles) on the tissues that burst, leaving numerous, pain ul oral ulcers. The ulcers are surrounded by a red halo. a. The ulcers can occur on lips, palate, and tongue as well as the gingival tissue. b. Pain caused by these ulcers can be such a major problem that eating and drinking can be impaired. Restricting f uids can even lead to dehydration, and dehydration in a child can be a serious medical emergency. 4. In the more severe clinical mani estation, this in ection is associated with signs and symptoms such as elevated body temperature, a vague eeling o discom ort (malaise), headache, and swollen lymph nodes (lymphadenopathy). B. Treatment. Treatment o patients with primary herpetic gingivostomatitis is primarily supportive (i.e., designed to keep the patient as com ortable as possible until the viral in ection runs its course). Typical steps in the management o a patient with primary herpetic gingivostomatitis are discussed below and outlined in Box 28-9.

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1. The dental hygienist should keep in mind that primary herpetic gingivostomatitis is contagious, and any plan or periodontal debridement o the teeth should be postponed until the initial in ection regresses (26,27). 2. In young children, herpes simplex virus is transmitted primarily by contact with in ected saliva. Precautions should be taken to protect others in the home, daycare center, or other environment in which the patient may encounter other children. Contact should be avoided with the child’s mouth, as a pain ul crossin ection can occur on the ngers or nail cuticle i in ected oral membranes are touched (Fig. 28-10). Dental assistants and hygienists must maintain universal precautions or in ection control, and parents or guardians should be in ormed as well. 3. Primary herpetic gingivostomatitis usually regresses spontaneously (goes away without treatment) in approximately 2 weeks. Controlling discom ort and ensuring f uid intake are the main ocus or supportive treatment. 4. Topical oral anesthetics can be used to control oral discom ort temporarily to allow the patient to eat or drink f uids. Examples o topical anesthetics that can be used are (1) 2% Lidocaine viscous and (2) O rabase with benzocaine (28,29). 5. In some patients, treatment will include antiviral medications (acyclovir), medications to reduce ever (antipyretics), and systemic medications to control pain (analgesics) (30,31). 6. In 2007, over 20,000 patients had hospital emergency department visits with a diagnosis o herpetic gingivostomatitis. Physicians should be trained to diagnose, manage, and re er patients. Improving access to dental care is crucial to managing this problem (32).

Bo x 28-8. Clinical Sig ns o f P ima

He pe tic Ging ivo sto matitis

• • • •

Ora l p a in w it h d if cu lt y in e a t in g a n d d rin kin g Ed e m a t o u s g in g iva l t issu e s (sw o lle n g in g iva l t issu e ) Ble e d in g fro m g in g iva l t issu e Ve sicle s (b list e rs) a n d u lce ra t io n o f t h e g in g iva l t issu e a n d so m e t im e s t h e lip s, t o n g u e , a n d p a la t e ; u lce ra t io n s su rro u n d e d b y re d h a lo • Ele va t e d b o d y t e m p e ra t u re • Ma la ise (va g u e fe e lin g o f d isco m fo rt ) • Sw o lle n lym p h n o d e s

Bo x 28-9. T pical Ste ps in Manag e me nt o f P ima Ging ivo sto matitis

He pe tic

1. Ke e p in m in d t h a t t h is d ise a se is h ig h ly co n t a g io u s. 2. Prim a ry h e rp e t ic g in g ivo st o m a t it is re g re sse s sp o n t a n e o u sly in a b o u t 2 w e e ks. 3. Co n t ro l o ra l d isco m fo rt . To p ica l o ra l a n e st h e t ics ca n b e u se d fo r t e m p o ra ry re lie f o f o ra l d isco m fo rt , so t h a t t h e p a t ie n t ca n e a t a n d d rin k u id s. 4. Re co m m e n d fre q u e n t u id in t a ke t o a vo id d e h yd ra t io n . 5. Re fe r t h e p a t ie n t t o a p h ysicia n if syst e m ic sym p t o m s a re se ve re o r if t h e p a t ie n t is u n a b le t o t o le ra t e u id in t a ke .

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Chapte Summa

State me nt

This chapter discussed some acute periodontal conditions that can bring patients to the o ce or an emergency visit. All members o the dental team should be on alert or these conditions. The dental hygienist may encounter some o these conditions in their earliest stages during routine treatment visits. Acute periodontal conditions include abscesses o the periodontium, necrotizing periodontal diseases, and primary herpetic gingivostomatitis.

Se ct io n 5

Fo cus o n Patie nts Clinical Patie nt Ca e CA S E 1 During a routine patient visit or periodontal maintenance, you note that there is swelling in the interdental papilla between a patient’s two central incisors. The swelling is quite localized to the area between the incisors. As you manipulate the tissues, you note pus coming rom the sulcus o one o the central incisors. You also note some mobility o one o the incisor teeth. When questioned, the patient in orms you that she is aware that these tissues are swollen and that she has been f ossing more in hope that the swelling would go down. In view o these clinical ndings, how should you proceed at this maintenance visit?

CA S E 2 A patient with necrotizing ulcerative gingivitis (N UG) is re erred to you by the dentist or calculus removal. Your examination o the patient reveals ulceration o most interdental papillae with the typical punched-out papillae o ten seen with this disease. The necrotic tissue pseudomembrane is present covering the ulcerations, and heavy calculus deposits are evident. The patient is quite uncom ortable. H ow should you proceed with the calculus removal?

Evide nce in Actio n A concerned mother, who is one o your maintenance patients, brings her 3-year-old daughter to the o ce. An examination reveals that the child has primary herpetic gingivostomatitis. H er mouth is very pain ul to the touch and she has an elevated temperature. What patient education would you provide to the child’s mother? What treatment recommendations should the dental team make?

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Ethical Dile mma You are in your last semester o dental hygiene school, and the clinic has booked your morning appointment. Your patient is Josh K, a 21-year-old senior premed student who attends your university. As you review Josh’s health history, he tells you that he is extremely stressed, as he has been studying or his M CATS, or entrance to medical school, as well as completing all o his papers and projects that are due be ore he graduates. H e admits to eating poorly, due to his busy schedule, as well as eeling very atigued. H e is getting very little sleep, only about 3 hours per night, just trying to keep up and get everything done. H e has scheduled his appointment today as his gums have become very sore and are bleeding. H e tells you that he is just very uncom ortable. Your clinical examination reveals that Josh’s interdental papilla seem to have a “ punchedout” appearance. There also appears to be a gray-white layer covering his gingival tissue. During your examination, even the slightest manipulation o his gingival tissues causes bleeding. Josh also presents with swollen lymph nodes, an elevated temperature, and extreme halitosis. Although the clinical dentist is on vacation this week and did not examine Josh, you remember rom your Periodontology class that these classic symptoms and appearance o his tissue appear to be consistent with a necrotizing periodontal disease. You excitedly tell Josh your diagnosis, and once you have nished his assessments, reappoint him or treatment next week. You meet your roommate M aeve, who is also a dental hygiene student, or dinner in the ca eteria a ter clinic. You tell her all about Josh, and his classic textbook case o N UG. You decide to become “ Poster Presentation” partners, and N UG will be your topic. You plan to take be ore and a ter photographs o Josh’s gingiva or your poster. 1. H ow would you explain necrotizing periodontal disease to Josh? 2. What are the typical treatment steps or a patient with N ecrotizing Ulcerative Gingivitis? 3. Are there ethical principles are in conf ict in this dilemma?

r e fe e nce s 1. Elangovan S, N alliah R, Allareddy V, et al. O utcomes in patients visiting hospital emergency departments in the United States because o periodontal conditions. J Periodontol. 2011;82(6):809–819. doi:10.1902/jop.2010.100228. 2. Parameter on acute periodontal diseases. American Academy o Periodontology. J Periodontol. 2000;71(5 suppl):863–866. doi:10.1902/jop.2000.71.5-S.863. 3. Ahl DR, H ilgeman JL, Snyder JD. Periodontal emergencies. D ent Clin N orth A m . 1986;30(3):459–472. 4. Silva GL, Soares RV, Z enobio EG. Periodontal abscess during supportive periodontal therapy: a review o the literature. J Contem p D ent Pract. 2008;9(6):82–91. 5. H errera D, Roldan S, Sanz M . The periodontal abscess: a review. J Clin Periodontol. 2000;27(6):377–386. 6. Valyi P, Gorzo I. [Periodontal abscess: etiology, diagnosis and treatment]. Fogorv Sz. 2004;97(4):151–155. 7. Antonelli JR. Acute dental pain, Part II: diagnosis and emergency treatment. Com pendium . 1990;11(9):526, 528, 530–533. 8. Peltroche-Llacsahuanga H , Reichhart E, Schmitt W, et al. Investigation o in ectious organisms causing pericoronitis o the mandibular third molar. J O ral M ax illofac Surg. 2000;58(6):611–616. 9. Blakey GH , White RP Jr, O enbacher S, et al. Clinical/biological outcomes o treatment or pericoronitis. J O ral M ax illofac Surg. 1996;54(10):1150–1160. 10. Wade DN , Kerns DG. Acute necrotizing ulcerative gingivitis-periodontitis: a literature review. M il M ed. 1998;163(5):337– 342. 11. Campbell CM , Stout BM , Deas DE. N ecrotizing ulcerative gingivitis: a discussion o our dissimilar presentations. Tex D ent J. 2011;128(10):1041–1051. 12. H orning GM , Cohen M E. N ecrotizing ulcerative gingivitis, periodontitis, and stomatitis: clinical staging and predisposing actors. J Periodontol. 1995;66(11):990–998.doi:10.1902/jop.1995.66.11.990. 13. Rowland RW. N ecrotizing ulcerative gingivitis. A nn Periodontol. 1999;4(1):65–73; discussion 78. doi:10.1902/ annals.1999.4.1.65. 14. H ooper PA, Seymour GJ. The histopathogenesis o acute ulcerative gingivitis. J Periodontol. 1979;50(8):419–423. doi:10.1902/jop.1979.50.8.419.

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15. Kumar A, M asamatti SS, Virdi M S. Periodontal diseases in children and adolescents: a clinician’s perspective part 2. D ent Update. 2012;39(9):639–642, 645–646, 49–52. 16. Berres F, M arinello CP. [N ecrotizing ulcerative periodontitis. Diagnosis, treatment and ollow-up–a case report]. Schw eiz M onatsschr Z ahnm ed. 2004;114(5):479–495. 17. N ovak M J. N ecrotizing ulcerative periodontitis. A nn Periodontol. 1999;4(1):74–78. doi:10.1902/annals.1999.4.1.74. 18. Barr CE, Robbins M R. Clinical and radiographic presentations o H IV-1 necrotizing ulcerative periodontitis. Spec Care D entist. 1996;16(6):237–241. 19. Feller L, Lemmer J, Wood N H , et al. N ecrotizing gingivitis o Kaposi sarcoma a ected gingivae. SA D J. 2006;61(7):314–317. 20. Gowdey G, Alijanian A. N ecrotizing ulcerative periodontitis in an H IV patient. J Calif D ent A ssoc. 1995;23(1):57–59. 21. Kolokotronis A, Doumas S. H erpes simplex virus in ection, with particular re erence to the progression and complications o primary herpetic gingivostomatitis. Clin M icrobiol Infect. 2006;12(3):202–211. doi:10.1111/j.1469–0691.2005.01336.x. 22. M ohan RP, Verma S, Singh U, et al. Acute primary herpetic gingivostomatitis. BM J Case R ep. 2013;2013. doi:10.1136/bcr2013-200074. 23. Tovaru S, Parlatescu I, Tovaru M , et al. Primary herpetic gingivostomatitis in children and adults. Q uintessence Int. 2009;40(2):119–124. 24. Usatine RP, Tinitigan R. N ongenital herpes simplex virus. A m Fam Physician. 2010;82(9):1075–1082. 25. Chauvin PJ, Ajar AH . Acute herpetic gingivostomatitis in adults: a review o 13 cases, including diagnosis and management. J Can D ent A ssoc. 2002;68(4):247–251. 26. Browning WD, M cCarthy JP. A case series: herpes simplex virus as an occupational hazard. J Esthet R estor D ent. 2012;24(1):61–66. doi:10.1111/j.1708–8240.2011.00469.x. 27. Lewis M A. H erpes simplex virus: an occupational hazard in dentistry. Int D ent J. 2004;54(2):103–111. 28. Faden H . M anagement o primary herpetic gingivostomatitis in young children. Pediatr Em erg Care. 2006;22(4):268–269. doi:10.1097/01.pec.0000218982.46225. 5. 29. Stoopler ET, Balasubramaniam R. Topical and systemic therapies or oral and perioral herpes simplex virus in ections. J Calif D ent A ssoc. 2013;41(4):259–262. 30. Blevins JY. Primary herpetic gingivostomatitis in young children. Pediatr N urs. 2003;29(3):199–202. 31. N asser M , Fedorowicz Z , Khoshnevisan M H , Shahiri Tabarestani M . Acyclovir or treating primary herpetic gingivostomatitis. Cochrane D atabase Syst R ev. 2008;(4):CD006700. doi:10.1002/14651858.CD006700.pub2. 32. Elangovan S, Karimbux N Y, Srinivasan S, et al. H ospital-based emergency department visits with herpetic gingivostomatitis in the United States. O ral Surg O ral M ed O ral Pathol O ral R adiol. 2012;113(4):505–511. doi:10.1016/j.oooo.2011.09.014.

STUDENT ANCILLAr y r ESOUr CES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

r e t p a h C

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Usi g Mo tivatio al I te rvie w i g to E ha ce Patie t Be havio r Cha g e 1

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Co mpo e ts o f Mo tivatio al I te rvie w i g

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Core Skills o Motivational Interviewing Four Processes o Motivational Interviewing

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Motivational Interviewing: Example 1 Motivational Interviewing: Example 2 Motivational Interviewing: Example 3

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Fo cus o

Patie ts

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Clinical Patient Care Ethical Dilemma

Cli ical Applicatio .

Behaviors such as e ective plaque biof lm removal, adherence to regular pro essional periodontal maintenance visits, periodontal risk actor reduction, and healthy li estyle habits are crucial issues or dental hygienists to address in their patient encounters. E ective management o the periodontal patient requires both knowledge o the disease process and understanding o human behavior and motivation to oster healthy oral sel -care practices in patients. Motivational interviewing as discussed in this chapter can be a use ul tool or hygienists to employ when attempting to enhance behavior change in patients.

Le ar i g Obje ctive s • Recognize the role o ambivalence in patient behavior change and explain the goal o motivational interviewing with respect to ambivalence. • Describe the primary di erence between how hygienists o ten approach patient education and the motivational interviewing approach. • Be able to identi y the our key elements o the motivational interviewing philosophy, the f ve core skills and the our overlapping processes. • Give examples o specif c motivational interviewing methods and how they are used to enhance patient motivation or change.

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Ke Te rms Motivational interviewing Patient-centered Guiding style Ambivalence Partnership Acceptance Compassion

Evocation Open-ended questions Re lective listening A irm Summarize Elicit, Provide, Elicit Engaging

Focusing Evoking Planning Change talk Sustain talk Developing discrepancy

Chapte r 29

Se ct io

1

I tro ductio

Using Motivational Interviewing to Enhance Patient Behavior Change

to Huma Be havio r Cha g e

Patients with periodontal disease o ten are advised to change certain behaviors—use tu t-end toothbrushes or stop smoking—in order to promote periodontal health. The dynamics o behavior change are among the most rewarding and most challenging encounters or dental hygienists. Chronic periodontitis is largely preventable, but prevention o ten requires that the patient becomes actively involved in making and maintaining changes in his or her li estyle habits. It is very common or the dental hygienist to encounter periodontal patients who do not use e ective oral sel -care measures or adhere to recommendations or pro essional periodontal maintenance. In order to persuade patients to improve, the dental hygienist o ten attempts to educate patients regarding the importance o these recommendations. Un ortunately the provision o education and expert advice alone are rarely su cient to activate the patient and bring about the desired patient behavior change. All too o ten a dynamic develops in which the dental hygienist takes on the role o “ the persuader” arguing or change while the patient takes on the role o “ the resistor,” shooting down all suggestions, and providing a long list o reasons why he or she can’t ollow the recommendations. Patients may also resist passively by not engaging and simply ignoring the attempt to persuade them. In the end, patients may become more resistant while dental hygienists may become rustrated and even convinced that addressing behavior change is utile (Fig. 29-1). Although it is tempting to blame the patient or being resistant, a wealth o research suggests the explanation or why patients struggle with health behavior change is ar more complex. Patients’ motivation is a unction o numerous actors ranging rom past li e experiences (e.g., attitudes, belie s, and habits developed over time); to current situational constraints (e.g., lack o time, nancial resources, health literacy and knowledge); to a lack o con dence and skills to make the necessary behavior change (1,2). Furthermore, the interpersonal communication style o a healthcare provider can play an important role in ostering or undermining patient motivation (3,4). Dental hygienists typically approach patient education in a persuasive, directive manner o ering acts about oral disease and unsolicited advice on prescriptive strategies to encourage oral health behavior change. The dental hygienist is the “ expert” and the patient is the “ recipient” o the expertise. When patients are not ready or behavior change, this directive, persuasive style can o ten induce eelings o embarrassment, guilt, or even shame, i they are not willing or able to make the change being recommended. N ot surprisingly the patient response is o ten de ensive (Fig. 29-2) and he/she may tune out the hygienist’s recommendations, or delay return or pro essional therapy (5–8). Studies have shown that approximately 30% to 60% o health in ormation provided in the clinician/patient encounter is orgotten within an hour and that patients and providers di er signi cantly in their recall about dental advice given and agreed upon actions or the uture (9,10). N ot surprisingly 50% o health recommendations provided by clinicians are not ollowed (10). For patients lacking in readiness or motivation, alternatives to the expert-oriented, directive, educational approach are needed. O ne empirically supported alternative is motivational interviewing (6).

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Fig ure 29-1. The Se lf-Care Strug g le . Patients o ten struggle with pro essional recommendations or sel -care—such as lossing—leading to rustration or even resistance to oral sel -care routines.

Dental hygienists typically approach patient education in a persuasive, directive manner o ering acts about oral disease and unsolicited advice on prescriptive strategies to encourage oral health behavior change. The dental hygienist is the “ expert” and the patient is the “ recipient” o the expertise. When patients are not ready or behavior change, this directive, persuasive style can o ten induce eelings o embarrassment, guilt, or even shame, i they are not willing or able to make the change being recommended. N ot surprisingly the patient response is o ten de ensive (Fig. 29-2) and he/she may tune out the hygienist’s recommendations, or delay return or pro essional therapy (5–8). Studies have shown that approximately 30% to 60% o health in ormation provided in the clinician/patient encounter is orgotten within an hour and that patients and providers di er signi cantly in their recall about dental advice given and agreed upon actions or the uture (9,10). N ot surprisingly 50% o health recommendations provided by clinicians are not ollowed (9). For patients lacking in readiness or motivation, alternatives to the expert-oriented, directive, educational approach are needed. O ne empirically supported alternative is motivational interviewing (5).

Fig ure 29-2. De fe sive Patie t Re spo se . Health education advice alone usually creates de ensiveness in the patient.

Chapte r 29

Using Motivational Interviewing to Enhance Patient Behavior Change

Wh a t is M o t iv a t io n a l in t e r v ie Win g ? Motivational interviewing (M I) is de ned as “ a patient-centered counseling style or addressing the common problem o ambivalence about change” (6). At its core, the motivational interviewing (M I) approach to counseling is “ patient-centered,” which means that the consideration o behavior change is viewed rom the patient’s perspective rather than the clinician’s perspective. For example, the clinician may wish that a patient did not smoke, as smoking is a major risk actor or periodontitis. The patient, on the other hand, might like to have healthier gums but enjoys smoking too much to quit. The clinician’s reasons why the patient should make a change—though they may be excellent—are considered ar less important than the reasons the patient sees or and against change. The clinician’s goal is to develop a clear understanding o the patient’s perspective on the possibility o change. Although the approach is patient-centered, M I is not “ nondirective” because the clinician DO ES attempt to inf uence or encourage the patient toward healthy behavior change. O ne might think o this patient-centered approach as being somewhere along a continuum between “ ollowing,” where the clinician mainly listens to the patient, and “ directing,” where the clinician tells or prescribes what the patient should do di erently (11). In M I, a guiding style is used to explore the ambivalence or pros and cons o change that the patient sees. Patients o ten eel ambivalent about behavior change—that is, they have mixed eelings and attitudes toward behavior change. Speci c methods are used to oster the patient’s intrinsic or “ internal” motivation. Fostering the patient’s internal motivation increases the likelihood that his or her ambivalence about changing will be resolved in the direction o change. O ne o the underlying assumptions o M I is that ambivalence is typical in AN Y change process (e.g., how do you eel about the need to eat at least ve servings o ruit and vegetables every day, or exercise or 40 minutes 5 to 7 days a week?). It also assumes in M I that, when possible, patients tend to move naturally toward health. In other words the assumption is that most people WAN T to be healthy, though they may not always eel motivated enough or capable enough o achieving it at any particular point in time. In M I the clinician attempts to tap into and enhance any natural internal desire or healthy change in patients.

e M p ir ic a l s u p p o r t f o r M o t iv a t io n a l in t e r v ie Win g M eta-analyses indicate that M I is e ective or a range o behavioral outcomes including various health promoting behaviors, smoking cessation, and treatment engagement (12,13). Recent studies have addressed M I related to oral care behavior change. O ne o the rst studies published compared M I to traditional health education among mothers o young children at high risk or dental caries. This study ound a signi cant reduction in early childhood caries among those receiving M I counseling at 1 year; however, at the 2-year evaluation, results were not signi cantly di erent despite a trend in caries rate di erence o 35% or M I compared to 52% or traditional education (14,15).

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Evidence or M I e ectiveness with periodontal patients has been largely positive. Almomani et al. (16) examined the e cacy o M I or improving oral sel -care in a sample o individuals with severe mental illness. Results revealed that at a single M I session prior to an oral health education session signi cantly enhanced motivation or regular brushing, increased oral health knowledge, and reduced plaque scores compared to oral health education alone. Similar e ects were achieved in two studies o chronic periodontal patients. In a proo -o -concept, case study design over time, two patients, with bleeding on probing values o 68% and 83% , respectively, were provided with an M I intervention that included oral care practice in multiple sessions. Results showed statistically signi cant reductions in plaque and gingival index scores or both patients, with changes being maintained over a 24-month period (17). These authors used a similar M I intervention in an evaluator blind, randomized clinical trial with 113 subjects compared to usual care. Results at 1 year showed that gingival index and plaque index scores or the M I intervention group were signi cantly improved compared to a usual care control (18). In contrast, two separate randomized clinical trials, both o which used a single M I session with periodontal patients, ailed to show superiority o M I adjunctive to oral health education compared to oral health education, alone (19,20). In both o these studies, participants showed an improvement in periodontal measures, irrespective o group assignment. The reason hypothesized or the lack o superiority o M I adjunctive to health education was two old. First the periodontal patients who were re erred or specialty periodontal care and success ully ollowed up had already demonstrated motivation to improve their oral health; additionally, or some patients, multiple sessions may be needed to induce sustainable behavior change. A recent meta-analysis that examined the e ect o M I across multiple health behaviors concluded that there does appear to be a dose–response e ect to M I, with increased M I sessions or increased treatment time related to improved outcomes (13). Given that hygienists o ten see periodontal patients or multiple appointments during the active treatment phase, and then again at regular intervals or periodontal maintenance, implementing multiple sessions o M I may be ideally suited to periodontal care. O ne concern o many health practitioners is whether M I can be e ective in a healthcare setting where clinicians are not trained counselors and time is short. Teaching M I skills to dental hygiene students as an integral part o the curriculum is increasing in the United States and abroad. A recent report on the experience o implementing a new curriculum that teaches M I or behavior change showed that teaching M I skills is viewed as positive by aculty and students alike. M ore critically, standardized patient assessment o the students’ ability to activate patients was signi cantly greater or students who received M I training compared to those that had traditional health education training (21). A meta-analysis also indicates that noncounselors can be e ective when using M I with a signi cant e ect in 80% o studies where M I was delivered by physicians (22). With respect to time, as little as 15 minutes has been shown to be e ective in the majority o studies (12,22).

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2

Co mpo e ts o f Mo tivatio al I te rvie w i g The philosophy or “ spirit” o M I is captured in our key elements. The rst element is partnership between the patient and clinician. In the M I approach, the clinician actively attempts to diminish his or her expert role. It is necessary to collaborate because the patient, not the clinician, is viewed as the expert on his or her li e and the challenges o the behavior change in question. The second element is deep acceptance o the patient and their behavioral choices. Acceptance includes avoiding judgment, supporting the patient’s autonomy, understanding the patient’s perspective, and a rming their strengths and e orts. Third, M I is used only or the wel are o patients, which is re erred to as compassion. The ourth element is evocation, in which the clinician encourages the patient to disclose their perspective and internal motivation rather than attempting to persuade or instill motivation “ rom the outside.” Although it is sometimes easy or a healthcare provider to eel responsible or a patient’s decisions, it is ultimately not the clinician’s choice or li e. Patients are ar more likely to choose and succeed with behavior change when they have voiced their own reasons or change and made their own decision to commit. In MI, the ocus o the clinician is not on the desired healthcare outcome but on acilitating a meaning ul conversation that provides the greatest opportunity or a patient to consider change. The nal decision or change rests with the patient. The clinician may communicate respect or the patient’s autonomy directly such as “So how would you like to proceed?” or indirectly such as at the beginning o the visit by asking permission to talk about oral sel -care (Fig. 29-3). “Can we t alk a lit t le bit about your daily oral care ?”

Fig ure 29-3. Aski g Pe rmissio . Starting with asking the patient’s permission can help oster a collaborative partnership.

c o r e s k il l s o f M o t iv a t io n a l in t e r v ie Win g M I requires skill in a set o core communication skills that are used in strategic ways throughout the conversation.

Ope -E de d Que stio s Open-ended questions (questions that are ramed to avoid a simple yes/no response) are pre erred in MI. For example, “How do you eel about using dental oss?” “How does brushing and ossing f t into your routine” rather than “Do you use dental oss?” or “Do you brush twice a day?” The open-ended style o questioning encourages patients to elaborate and provides much more in ormation to the clinician regarding the patient’s perspective (Fig. 29-4).

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“How do you f e e l about quit t ing smoking at t his st age in your lif e ?”

Fig ure 29-4. Use o f Ope -E de d Que stio s. Open-ended questions—that cannot be answered with a simple “ yes” or “ no” response—encourage the patient to provide additional in ormation.

“S o, it sounds like you want he alt hie r gums, but worry t hat you don’t have t he t ime t o do more . ”

Fig ure 29-5. Re fle cti g Liste i g . By paraphrasing the patient’s remarks, the clinician can double check i she understands the meaning o the patient’s comments correctly.

Re fle ctive Liste i g Re ective listening is the process in which the healthcare provider listens to the patient’s remarks and then paraphrases what the clinician heard the patient say. This allows the clinician to check with the patient that he or she is “ getting the patient’s message right,” ensuring that the clinician is developing a good picture o the patient’s perspective (Fig. 29-5). Ref ective listening has the e ect o validating the patient, expressing understanding (or empathy), and typically encourages the patient to elaborate, so that the clinician can learn more. Through the process o open-ended questioning and ref ective listening, the clinician can begin to shi t rom a clinician-centered approach to oral health education to a patientcentered view o oral health education. Research has shown that the average healthcare provider interrupts patient disclosures a ter 18 seconds (10). When this occurs, it sends a clear message that the patient’s input is not respected nor seen as relevant. A rming the patient’s e orts and interest or willingness to seek care increases the patient’s sense o trust. O nce trust is established the patient can honestly express him/hersel and begin to openly resolve ambivalence (mixed eelings) about change.

Affirm In M I, the patient’s strengths and e orts should be a f rmed (acknowledged) to communicate support to the patient or discussing something di cult (i.e., a change about which they may eel embarrassment, guilt, and ambivalence). Expressing appreciation or the patient taking the time to be there, or being willing to discuss their smoking, or taking some small steps toward change can enhance the therapeutic relationship and encourage the patient to engage urther in the counseling process.

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Summarize Brie summaries are used in M I to link and rein orce what has been discussed and provide an opportunity or the clinician to demonstrate empathy (e.g., “ So I think I now have a airly good picture o how you view your sm ok ing . . . .” ). Summaries can be used to move the conversation in a new direction (e.g., the summary can lead to a statement like “So given w hat we’ve talked about so ar, w hat are your thoughts about the nex t step… ?” or tie di erent elements o the conversation together (e.g., a ter summarizing the patient’s perspective on the di culties o brushing regularly, the clinician might link to an earlier part o the conversation on the patient’s dislike o the pain that he is experiencing: “ So it sounds like it’s a real challenge to get a good brushing routine but at the sam e tim e you are really unhappy w ith the pain you are ex periencing . . . .” ).

Pro vidi g I fo rmatio

a d Advice

Although the provision o in ormation and advice should be done with caution—to avoid taking the expert role and to avoid the pit all o pressing or change—there are nevertheless occasions when providing in ormation is appropriate. For example, providing in ormation may be necessary when the patient asks or in ormation, or when motivation might be enhanced by new in ormation that might help in overcoming obstacles to change. To avoid “taking on the expert role,” the clinician can ask permission rst: “Would you be interested in hearing som e m ore in ormation about the benef ts o quitting sm ok ing or your oral health?” (Fig. 29-6). The clinician avoids the “ expert role” by re erring to other sources or the in ormation such as “M any patients tell m e . . . .” or “ Research seem s to indicate . . .” rather than saying “ I have ound . . .” or “ I would recom m end . . .” A three-step process known as “Elicit, Provide, Elicit” is also a use ul method or delivering in ormation and advice in an M I consistent manner. The rst step (Elicit) involves enquiring what the patient already knows. For example, “W hat have you heard about the benef ts o ossing on a daily basis?” The second step (Provide) involves providing relevant in ormation and advice: “ Yes you are right, those are som e good reasons to oss daily. T here are also som e other reasons dental hygienists encourage ossing or cases like yours, such as . . . .” The nal step (Elicit) involves checking back with the patient to see what they have taken rom the in ormation or advice provided. For example, “So I’m wondering w hat you think about that research and how it applies to you?”

“The re are se ve ral ne w opt ions t hat have re ally he lpe d ot he rs quit . Would you like t o he ar about t he m?”

Fig ure 29-6. Pro vidi g i fo rmatio o r advice . In this example the clinician supports the patient’s autonomy by asking permission be ore providing in ormation.

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f o u r p r o c e s s e s o f M o t iv a t io n a l in t e r v ie Win g The method o M I involves our overlapping processes. The method begins with engaging in which a help ul rapport is established that serves as the oundation or everything that ollows. Engaging leads to the process o ocusing or establishing a direction or goal or behavior change. With the goal in mind the process o evoking is used to elicit the patient’s motivation or change. When patients become su ciently interested in making change the process o planning can begin involving the ostering o commitment and developing a speci c plan o action or change. The processes are not a rigid sequential roadmap. Any o the processes can be engaged in throughout the conversation as needed.

E g ag i g Patient engagement can be encouraged or discouraged depending on the clinician approach. For example, asking a series o speci c questions that the patient is obliged to answer discourages their involvement in a collaborative dialog. In M I the clinician is encouraged to ocus on eliciting and listening to the patient’s perspective. An open-ended question can be used to initiate the discussion (e.g., “W hat k inds o problem s have you been having w ith your teeth lately?”). Ref ective listening can then be used to encourage the patient to elaborate while at the same time communicating empathy and acceptance (e.g., “ You’ve noticed that your gum s are bleeding a lot.”). During the listening process the clinician pays attention to any opportunities to a rm the patient or any strengths or e orts (e.g., “You’ve really been m ak ing an e ort to try to brush m ore regularly.”). Summaries can be used to tie the conversation together highlighting the most relevant parts o the patient’s story.

Fo cusi g To employ M I e ectively, it is essential to have the behavior change goal or goals in mind. Focusing is the process o clari ying, in collaboration with the patient, what direction the conversation should take. A guiding style can be used to explore the patients’ pre erences, concerns, and priorities while considering the clinicians’ concerns and priorities. For example, taking into account both patient and clinician perspectives the clinician may o er a range o alternative options or discussion (e.g., “Based on w hat you have told m e it sounds like we should decide w hat is m ost im portant to ocus on today. W e could talk about som e o the challenges you’re having w ith your brushing and ossing routine, we could discuss how to go about changing som e o your eating habits to protect your teeth and gum s, or we could talk about your sm ok ing and how I could perhaps be o som e help.”). During ocusing it can also be necessary to provide in ormation to the patient that can in orm the direction that should be taken. The clinician can use the “ elicit, provide, elicit” method to accomplish this in an M I consistent style.

Evo ki g The assumption in M I is that most patients are ambivalent about change and the role o the clinician is to elicit or evoke their internal motivation as well as their con dence or making a change. Integral to this process is the encouragement or evoking o statements in the direction o change, re erred to as change talk (e.g., “I k now sm ok ing is bad or m e; I would like to do a better job w ith tak ing care o my teeth.”). Research

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indicates that change talk is predictive o actual behavior change (6,23). As indicated above, the assumption is that most individuals have mixed eelings about change. Those patients having mixed eelings (pros and cons) about change implies that they do have some reasons or desire or change. The task o the clinician is to evoke, acilitate, and strengthen this desire or change. Change talk can be elicited with simple open-ended questions such as “ W hat advantages do you see o cutting back on sugary oods?” Another approach is to use the “ motivation” or “ importance ruler” in which the clinician asks “ O n a scale o 0 to 10 with 10 being most important, how important is to you to improve your oral sel -care habits?” (Fig. 29-7).

No t at all 0

Fig ure 29-7. A Mo tivatio

Ve ry muc h 10

Rule r. A motivation ruler is a method or acilitating change talk.

O nce the patient identi es the sel -rated importance o change, the clinician elicits change talk by asking, “ W hat m ade you pick three rather than zero?” Rather than asking why the patient is N OT at 10, this open-ended question encourages the patient to express any importance that he or she DO ES place on improving oral sel -care behaviors. A ter eliciting and ref ecting change talk, barriers to change can also be explored by asking, “ W hat would it take or you to increase the im portance two or three additional levels?” This approach can also be used to evoke con dence (or sel -e cacy) in engaging in a new behavior, which is also o ten a key contributor to an individual’s motivation to change. In general, once the clinician has elicited change talk the goal is to encourage even more change talk. Ref ective listening is very e ective means o achieving this goal and the skilled M I clinician can encourage elaboration o a particular aspect o change talk by ending the ref ective statement on that topic. For example, a ref ection that ends with the change talk such as “ O n the one hand you really love sugary oods, but on the other hand you really want to set a good ex am ple to your children.” encourages elaboration by the patient o the desire to set a good example rather than the love o sugary oods because the change talk is ref ected at the end o the ref ective statement. This example highlights another element o M I, which is how to respond to the opposite o change talk or “ sustain talk” (e.g., “I don’t have enough tim e to oss every day.”). These statements are o ten thought o as “ resistance” but rom an M I perspective they are merely an indication o the ambivalence that is assumed to be a normal part o behavior change. When the patient expresses reasons not to change, this is an ideal opportunity to listen well and explore the patient’s perspective rather than attempting to persuade or provide counter arguments. This can be accomplished in various ways but most simply by using ref ective listening (Fig. 29-8). Typically patients who have been validated a ter expressing their reasons or not changing are then much more ready to talk about reasons why they might want to change. Evoking con dence is also essential or encouraging behavior change because individuals do not make e orts to change unless they believe they can succeed (2). Con dence can be evoked in various ways including brainstorming possible solutions, providing in ormation and advice, or reviewing past successes. Evoking may also involve “developing discrepancy” in which inconsistencies between a patient’s values and goals and their current behavior is explored to enhance motivation

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or change. For example, most patients want to be healthy even though they may have chronic periodontitis and poor oral sel -care. Similarly, they may want to avoid pain ul or unpleasant visits or dental care yet have poor oral sel -care habits. The discrepancy between what would be ideal (e.g., be healthy or have no pain) and the status quo (poor sel -care that results in periodontitis or pain and unpleasant visits or dental care) represents internal motivation or change that can be elicited or highlighted through open-ended questions and ref ective listening (Fig. 29-9). For example, the hygienist might highlight the discrepancy with this ref ection: “It sounds like you f nd it hard to stick with the thorough brushing and ossing each day, but you would really like to have healthy gums.” “You f ound t he cle aning painf ul and don’t want t o go t hrough t hat again?”

Fig ure 29-8. Re fle cti g Sustai Talk. When a patient expresses hesitation about change, the clinician should listen well and explore the patient’s point o view rather than attempting to persuade the patient that change is needed.

Pla

“On one hand, you want an implant but , on t he ot he r hand you re ally like s moking. ”

Fig ure 29-9. De ve lo p Discre pa c . Open-ended questions and re lective listening can highlight discrepancies between what would be ideal (e.g., improved periodontal health) and the status quo (continuing to smoke).

i g

The process o planning or change can begin when there are signs o patient readiness such as increased change talk, less sustain talk, small steps taken toward change, and questions about change. With sensitivity to any renewed patient ambivalence that might call or a return to one o the earlier processes, the clinician guides the patient to consider whether they want to make a change and how that change will occur. E ective planning involves discussing with the patient the precise “ how?” and “when?” o making the change. For example, rather than simply agreeing with the patient that they will “ try to do a better job o brushing” the clinician might help the patient to work out a speci c plan that will increase the likelihood o brushing (e.g., to brush right a ter eating dinner rather than waiting until just be ore going to bed when they eel too tired to do even one more thing). Once the plan is developed the clinician will attempt to strengthen commitment to the plan by evoking intention and commitment rom the patient (e.g., “W hat do you think o that strategy? or “D oes it sound like something you want to try?”).

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3

Implicatio s fo r De tal H g ie e Practice M oving rom the clinician-centered perspective o oral health education to the patientcentered view o behavior change can enhance the patient’s internal motivation or healthy behavior change. I the hygienist judges, lectures, and directs, the patient ceases to engage in dialog and be part o the solution. Ironically, this can result in yet more directive advice giving rom the clinician. Using M I, the hygienist can engage in a more productive interaction in which he or she no longer eels responsible (and rustrated!) about the patient’s decisions. Instead, the hygienist ocuses on encouraging the patient to examine his or her attitudes about periodontal disease or the periodontal maintenance schedule.

M o t iv a t io n a l in t e r v ie Win g : e x a M p l e 1 M rs. J. is a 50-year-old attorney who has been re erred to your periodontal dental o ce or evaluation and treatment. M rs. J. has type 2 diabetes, a glycosylated hemoglobin value (H bA1c) o 8, and moderately severe chronic periodontitis. M rs. J. has been sporadic in visiting her regular dentist and the letter rom the re erring dentist states that a ter a 1-year absence M rs. J. presented recently with increased bleeding on probing and evidence o increasing attachment loss. The general dentist is concerned that without periodontal therapy, M rs. J. will likely lose several teeth. Hygienist: I see that your general dentist has re erred you here or periodontal treatment. Can you tell me a little about your past dental care and why you are here today? Mrs. J.: Yes, Dr. Smith thinks that i I don’t get specialty treatment I’m going to lose some o my back teeth. I take care o my teeth and I think he’s overreacting to my gums bleeding a bit more than usual. Hygienist: I am very happy you ollowed up with Dr. Smith and came in to see us (A rmation). So i it’s okay with you, I’d like to spend a little time talking about the health o your gums (Getting permission). Mrs. J.: That’s ne with me. Hygienist: Good. So, i you would, can you tell me what is a typical day like or you and how taking care o your teeth ts into your normal day? (O pen-ended question.) Mrs. J.: Sure. M ost days I need to be at my o ce by 8:30, so I generally get up around 7, shower, have some co ee and toast, check emails, brush my teeth, and drive my 20-minute commute to the o ce. O nce I’m at my o ce, my schedule is really ull. I’m currently working on three really di cult cases that take up most o my time. I’m pretty stressed out! I don’t eat a regular lunch but will usually snack on a granola bar to hold me over to dinner. I’m usually home around 6:30, have dinner, and then catch up on reading documents or the next day. Sometimes I brush my teeth be ore bed, but mostly I’m just too exhausted to care at night. I do try, but don’t always succeed. The dental hygienist at Dr. Smith’s is always on my case about not brushing enough, not f ossing enough, and not coming in every 3 months. Hygienist: It sounds like you have a really busy schedule that makes it di cult or you to keep up with recommendations given by Dr. Smith’s hygienist. I I

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understand you, though, you do make a concerted e ort to brush at least every morning (Ref ective listening). Mrs. J.: Yes, I am very good about brushing in the morning. Hygienist: That’s great. It’s important to have a routine that works well or you (A rmation). You mentioned that the hygienist at Dr. Smith’s o ce is concerned about your not f ossing enough or coming in every 3 months. Tell me about that (O pen-ended questioning). Mrs. J.: Shelley, that’s her name, says that i I don’t f oss every day and come in to have my teeth scraped every 3 months that I’ll end up losing my teeth. She lectures me every time I go in, and I really dread going to see her. I don’t think she understands how busy my schedule is. The only reason I agreed to come here was that Dr. Smith thought you might be able to do something to get rid o my pockets. Hygienist: So, it sounds like you are interested in improving your gum health but don’t like being lectured when you go to the dentist (Ref ective listening). Mrs. J.: That’s right. I also read in a magazine that diabetes might make my gum disease worse, so I gured it’s worth nding out. Is that true? Can my diabetes make my gums worse? Can you get rid o my pockets, so this gum disease will stop? Hygienist: There is quite a bit o new in ormation about diabetes and periodontal disease, and there are some things that we can do at our o ce to reduce pockets. Research has shown that controlling gum disease, especially in diabetics, requires pro essional care but also requires patients to be actively involved in helping control the disease on a day-to-day basis. We have had many patients who have had very good success using this approach. Would you like to know more about it? (Providing in ormation that was requested/Supporting autonomy.) Mrs. J.: I would like to know more, but I’m skeptical that it’s going to be more o the same that I hear rom Shelley-–“ brush, f oss, come to see me; brush, f oss, come to see me.” Hygienist: Right… you want help but worry that it will still involve more e ort on your part than you really have time or (Ref ect). Mrs. J.: Exactly! Hygienist: Well, I want to emphasize that how we move orward is up to you. The time and e ort you put in brushing and f ossing is something you will need to determine based on what’s most important to you (Support autonomy). I it’s ok with you (Support autonomy/Ask permission), I’d like to try to go slowly, try to work with your busy schedule, and help you keep your teeth. A ter I conduct my exam, I’d also like to give you some in ormation on diabetes and gum disease that you can read be ore your next visit and then we can talk more about how that might be contributing to your gum disease. Are you interested in that? (Support autonomy/Ask permission.) Mrs. J.: That sounds good-–the magazine article didn’t give much detail, but it did say that diabetes can make gum disease worse. I’ll make it a point o adding it to my evening reading tonight. Hygienist: Excellent! I think you might nd the in ormation help ul as we work toward getting your gum disease under control.

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M o t iv a t io n a l in t e r v ie Win g : e x a M p l e 2 M r. A. is a 58-year old banker who has come to the dental o ce wanting an implant or a rst molar that was lost to periodontal disease last year. At the time, he was not interested in discussing a replacement but has made an appointment today, as he wants to get an implant or replacement. Although he contends that he brushes and f osses regularly, his oral sel -care has only been air or many years, he has a 30-year tobacco habit, and is currently smoking about 1½ pack o cigarettes a day. Hygienist: Good morning M r. A. What brings you in today? (O pen-ended questioning.) Mr. A.: Well, you know, I have this missing tooth here and when I chew it really bothers me. You know, ood gets stuck up in there and on top o that it just doesn’t look good when I smile. A buddy at work told me about implants and I’m seriously interested in getting one. Hygienist: So where that tooth is missing is causing you some problems and you aren’t happy with the appearance o that gap (Ref ective listening). Mr. A.: Yeah, every time I eat I get ood caught. It doesn’t hurt, but it’s gotten really irritating. I know we talked about it when you took the tooth out, but I don’t want a partial. I really want the implant. You mentioned then that my smoking might be a problem with getting an implant. Hygienist: Your riend told you about dental implants and you think it’s the right choice or replacing that tooth (Ref ective listening). Mr. A.: That’s right. I know when I was here be ore you said that my smoking might be a problem with getting an implant. Hygienist: Yes, smoking is a major barrier or using implants because it makes it much harder or healing to occur and then maintain the health o tissues around the implant. But it sounds like you are really interested in getting an implant (Providing in ormation in response to an implied question/Ref ective listening). Mr. A.: I am! Hygienist: Well, can we spend a ew minutes talking about your smoking, and what your thoughts and eelings about smoking are? (Asking permission.) Mr. A.: Sure, I’m a smoker and not ashamed o it. Hygienist: O kay, let me put it another way. O n the one hand you want an implant but on the other hand you really like smoking? (Developing discrepancy.) Mr. A.: Well I’ve tried to quit be ore and it wasn’t any un. I’m not sure I could quit i I wanted to. Hygienist: O kay. You have tried to stop be ore without any luck, so you have the sense that even i you wanted to try to quit again, you don’t think you could. It’s something that is very hard or you (Ref ective listening). Mr. A.: I went through that agony be ore and it didn’t work. I don’t want to put mysel through that again. Hygienist: Trying to quit would be too pain ul and it’s not important enough to you to stop right now (Rolling with resistance). Mr. A.: Yes, I enjoy it and haven’t had any ill e ects rom smoking. I’m pretty happy to continue as I am. Hygienist: Well, other than the possible disadvantage that smoking has to getting this implant, are there any other disadvantages that you see to smoking? (Evoking change talk.) Mr. A.: Taxes keep going up, and it’s an expensive habit, but I’m willing to pay the price. It’s one o my luxuries in li e.

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Hygienist: Anything else? (Evoking change talk.) Mr. A.: O nly one thing-–my kids really want me to quit. They are a raid I’m going to end up with something bad, but I haven’t had any ill e ects rom smoking. Hygienist: So, it sounds like the cost o smoking bothers you, but not too much, but you really haven’t had any health problems. Your amily worries though (Ref ective listening to evoke more change talk). Mr. A.: Yes, that’s right. Hygienist: I have the sense that you’re not ready to quit right now, but I’d like to learn more regarding your thoughts about smoking i that’s ok with you. Where would you put yoursel on a scale o 0 to 10 where 0 is “ no motivation at all to quit” and 10 is “ very motivated” ? I know you aren’t a 10, but where would you be? (Evoking change talk using the motivation ruler.) Mr. A.: H mmmm. I’d probably put mysel at a 2 or 3, somewhere in there. Hygienist: So you have some small amount o motivation to quit-–what gives you that level o motivation? (Evoking change talk using the motivation ruler.) Mr. A.: Well I know that smoking isn’t good or me, I’m not dumb. And like I said be ore, my amily really wants me to quit. It would be a nice gesture to do that or my amily. They really do have my best interests in mind. Hygienist: You mentioned that you know smoking isn’t good or you and your amily worries about health e ect. Can you tell me what ill health e ects worry you? (Evoking change talk.) Mr. A.: Sure-–cancer and lung disease. Hygienist: So, there are some disadvantages besides the implant that you’ve thought about, but you still aren’t su ciently motivated to quit. Earlier, though, you mentioned that you weren’t sure that you would be able to quit even i you wanted to (Ref ective listening to explore inf uence o con dence on motivation). H ow motivated would you be i you were more con dent that you could quit? Mr. A.: I guess i I knew I could succeed with quitting I’d be more motivated. Hygienist: I we could help you with improving your con dence in quitting, would you nd that help ul? (Evoking change talk/Assess interest be ore providing in ormation or advice to support autonomy.) Mr. A.: Yes, it might. Hygienist: There are several options that we could work on to improve your con dence to quit smoking. We could ocus on doing that while also discussing the easibility o the implant. Do you think you might be interested in pursuing this? (Evoke commitment/change talk while supporting autonomy.) Mr. A.: Sure. I guess I don’t have anything to lose.

M o t iv a t io n a l in t e r v ie Win g : e x a M p l e 3 Ms. S. is a 35-year-old administrative assistant at the local community college. She has come to the dental o ce as a new patient and desires tooth whitening or her “yellowed teeth.” During the routine dental evaluation no caries are ound; however, there is generalized moderate gingival inf ammation with slight bone loss in the interproximal posterior regions. The patient reports that she had a partial “deep cleaning” 2 years ago at her previous dentist but had really sensitive teeth and didn’t return or completing treatment. Hygienist: H ello M s. S. What brings you to our o ce? (O pen-ended questioning) Ms. S.: M y riend recently came to see you to have his teeth whitened and they look terri c. I haven’t been happy with the color o my teeth or a long time, so I thought you could make my smile whiter too.

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Hygienist: O kay. Can we rst spend a ew minutes talking about your mouth and oral health? (Getting permission.) Ms. S.: Sure, that’s ne. Hygienist: Good. Can you tell me a little about problems you have had and how taking care o your teeth ts into your regular day’s events? (O pen-ended questioning) Ms. S.: I have really healthy teeth and have never had any cavities. I’m really not happy with the yellow color o my teeth and want to do something about that. Hygienist: Anything else? Ms. S.: Well, the last dentist I went to said I had some gum disease. My gums have always bled when I brush, but they made a big deal out o it. I had to see the hygienist or a deep cleaning, but my teeth got so sensitive a terward, I didn’t go back. Hygienist: Tell me a little more about your gum treatment (O pen-ended questioning). Ms. S.: The dentist and hygienist told me I had to have that deep cleaning or I could lose my teeth. Everyone in my amily has gum disease and they still have most o their teeth. I must have inherited it. I’m really only interested in tooth whitening. I don’t want any more deep cleanings. Hygienist: It sounds like the deep cleaning you had was unpleasant and your gum disease is not very important to you (Ref ective listening). Ms. S.: I didn’t say it wasn’t important-–I just want my teeth to look better. M y teeth were so sensitive a ter having hal o my mouth deep cleaned, I could barely drink anything with ice in it. I that is what it takes to have healthy gums, I’m happy just as I am. Hygienist: The e ects o the deep cleaning treatment were so bad that you don’t want to go through it again even i it means not having healthy gums (Responding to sustain talk with ref ective listening). Ms. S.: It’s not that it isn’t important. I don’t want to lose my teeth, but I also don’t want all o that sensitivity. I was thinking that getting my teeth whitened will make me look better and wouldn’t hurt as much. Hygienist: Avoiding pain is really important to you (Responding to sustain talk with ref ective listening). Ms. S.: Yeah, I guess I sound pretty wimpy. M y teeth are important but i I have to be in pain or a long time a terward it’s not worth it to me. Hygienist: You want healthy teeth and i you could get your teeth whitened and gum disease treated without a lot o pain a terward, it might be worth doing (Ref ective listening). Ms. S.: I I knew that I could get my gums healthy and not have to go through what I did be ore, I might be willing to discuss gum treatments. Is that possible? Hygienist: There are several things that have worked or others to reduce the temperature sensitivity a ter deep cleaning. Are you interested in learning a little bit more? (Ask permission be ore providing in ormation.) Ms. S.: I might be. Hygienist: All right, let me give you some in ormation and we can talk about strategies or controlling the sensitivity a ter treatment. We can also talk about a plan or whitening your teeth once we get the gum disease under control. H ow would that meet your need or appearance and health? (Support autonomy.)

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Chapte r Summar State me t A key challenge or dental hygiene practitioners is working with patients to oster behavior change to improve oral sel -care. M I provides an empirically supported approach to the challenges o counseling patients or health behavior change. It rests on a oundation o partnership, acceptance, and compassion and uses speci c methods such as open-ended questions and ref ective listening to evoke patients’ own reasons or change. Use o this patient-centered approach to behavior change can enhance the quality o encounters between hygienists and their patients by ostering greater patient motivation or change, and strengthening the patient–provider relationship.

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Patie ts

Cli ical Patie t Care CA S E 1 Re er to the case o M rs. J. the 50-year-old attorney to answer the ollowing questions: 1. Why does the hygienist begin with the question “ Can you tell me a little about… why you are here today?” 2. Describe M rs. J’s ambivalence regarding behavior change (i.e., what cons AN D pros or change does SH E see?). 3. What examples o “ change talk” can you identi y in the dialog?

CA S E 2 Re er to the case o M r. A. the 58-year-old banker to answer the ollowing questions: 1. When the conversation rst turns to smoking the hygienist asks M r. A. “A re you su f ciently m otivated about the im plant to consider stopping sm ok ing?” This is labeled as an example o “ developing discrepancy.” What discrepancy does this re er to and how is this meant to oster motivation or change? 2. What is M r. A’s ambivalence regarding behavior change (i.e., what cons AN D pros or change does H E see?) 3. M r. A. provided lots o change talk in the dialog but what turns out to be the key barrier or change that, i the hygienist can help address, will signi cantly increase his motivation?

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CA S E 3 Using the in ormation in the case o M s. S., the 35-year-old administrative assistant, try the ollowing: 1. With a classmate take turns assuming the role o M s. S. and the hygienist. Practice asking an open-ended question to begin the visit ollowed by a ref ection o M s. S’s response. 2. M s. S. could bene t rom in ormation on how to get her gums healthy while reducing sensitivity. With a classmate practice using the three step “ Elicit, Provide, Elicit” process to give her some relevant in ormation.

Ethical Dile mma Dr. Jasper Greene hired Eden—a recent dental hygiene graduate—to work 4 days a week in his busy dental practice. Dr. Greene employs three other hygienists on a ull-time basis, as well as three other dentists. Dr. Greene was very pleased, as the patients really liked Eden, and he thought that she had excellent clinical skills, especially or a new graduate. Eden was quite happy too and enjoyed the o ce sta as well as the variety o patients she was treating. She was particularly excited to utilize the method o motivational interviewing, as a means to enhance patient behavior change, speci cally as it related to patient sel -care. While a student, Eden was praised by her clinical aculty or her exceptional mastery o this technique. Approximately 3 months later, Dr. Greene had a cancellation and was walking by Eden’s operatory while she was using motivational interviewing, and he stopped to listen to the conversation. Eden was working with a new patient, who was scheduled or periodontal instrumentation o deep periodontal pockets, but had a ear o needles, and re used anesthesia. She spent a signi cant amount o time counseling in a patient-centered manner. Dr. Greene was not amiliar with this approach, and quite rankly, disagreed with the patient “ calling the shots.” Later that day, Dr. Greene asked Eden to come to his o ce. H e told her that she was to stop all this “ mumbo jumbo,” and tell each patient what was best or him/her, as she was the expert. H e urther told her that none o the other hygienists or dentists in the o ce utilizes this technique, and he requires continuity among his o ce sta . Eden was very upset and did not know what to do. O n the one hand she loved working or Dr. Greene, but on the other hand, she realized that she was not com ortable compromising her belie o patient-centered counseling and moving her patients naturally toward health. 1. Are there advantages to motivational interviewing? 2. Are there ethical principles in conf ict in this dilemma? 3. What is the best way or Eden to handle this ethical dilemma?

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Re fe re ce s 1. Bandura A. Sel -E f cacy: the Exercise o Control. N ew York: W.H . Freeman; 1997. ix: 604. 2. Fishbein M . Factors inf uencing behavior and behavior change. In: Baum A, Revenson T, Singer J, eds. H andbook o H ealth Psychology. M ahwah, N J: Lawrence Erlbaum Associates; 2001: xx, 961. 3. Ryan RM , Deci EL. Sel -determination theory and the acilitation o intrinsic motivation, social development, and well-being. A m Psychol. 2000;55(1):68–78. 4. Williams GC, M cGregor H A, Z eldman A, et al. Testing a sel -determination theory process model or promoting glycemic control through diabetes sel -management. H ealth Psychol. 2004;23(1):58–66. 5. Freeman R. The psychology o dental patient care. 10. Strategies or motivating the non-compliant patient. Br D ent J. 1999;187(6):307–312. 6. M iller WR, Rollnick S; M yiLibrary. M otivational Interview ing H elping People Change. N ew York: Guil ord Press; 2013. Available rom: http://libproxy.temple.edu/login?url = http://lib.myilibrary.com/detail.asp?id = 394471 Connect to M yiLibrary resource. 7. Resnicow K, DiIorio C, Soet JE, et al. M otivational interviewing in health promotion: it sounds like something is changing. H ealth Psychol. 2002;21(5):444–451. 8. Shinitzky H E, Kub J. The art o motivating behavior change: the use o motivational interviewing to promote health. Public H ealth N urs. 2001;18(3):178–185. 9. M isra S, Daly B, Dunne S, et al. Dentist-patient communication: what do patients and dentists remember ollowing a consultation? Implications or patient compliance. Patient Pre er A dherence. 2013;7:543–549. 10. Prounis C. Doctor-patient communication. Pharm aceutical Executive [Internet]. 2005. Available rom: http://www.pharmexec.com. Accessed April 3, 2015. 11. Rollnick S, M iller WR, Butler C. M otivational Interview ing in H ealth Care: H elping Patients Change Behavior. N ew York: Guil ord Press; 2008: xiv, 210. 12. Lundahl B, M oleni T, Burke BL, et al. M otivational interviewing in medical care settings: a systematic review and metaanalysis o randomized controlled trials. Patient Educ Couns. 2013;93(2):157–168. 13. Lundahl W, Kunz C, Brownell C, et al. A meta-analysis o motivational interviewing: twenty- ve years o empirical studies. R es Social Work Prac. 2010;20(2):137–160. 14. Weinstein P, H arrison R, Benton T. M otivating parents to prevent caries in their young children: one-year ndings. J A m D ent A ssoc. 2004;135(6):731–738. 15. Weinstein P, H arrison R, Benton T. M otivating mothers to prevent caries: con rming the bene cial e ect o counseling. J A m D ent A ssoc. 2006;137(6):789–793. 16. Almomani F, Williams K, Catley D, et al. E ects o an oral health promotion program in people with mental illness. J D ent R es. 2009;88(7):648–652. 17. Jonsson B, O hrn K, O scarson N , et al. An individually tailored treatment programme or improved oral hygiene: introduction o a new course o action in health education or patients with periodontitis. Int J D ent H yg. 2009;7(3):166–175. 18. Jonsson B, O hrn K, O scarson N , et al. The e ectiveness o an individually tailored oral health educational programme on oral hygiene behaviour in patients with periodontal disease: a blinded randomized-controlled clinical trial (one-year ollowup). J Clin Periodontol. 2009;36(12):1025–1034. 19. Brand VS, Bray KK, M acN eill S, et al. Impact o single-session motivational interviewing on clinical outcomes ollowing periodontal maintenance therapy. Int J D ent H yg. 2013;11(2):134–141. 20. Stenman J, Lundgren J, Wennstrom JL, et al. A single session o motivational interviewing as an additive means to improve adherence in periodontal in ection control: a randomized controlled trial. J Clin Periodontol. 2012;39(10):947–954. 21. Bray KK, Catley D, Voelker M A, et al. M otivational interviewing in dental hygiene education: curriculum modi cation and evaluation. J D ent Educ. 2013;77(12):1662–1669. 22. Rubak S, Sandbaek A, Lauritzen T, et al. M otivational interviewing: a systematic review and meta-analysis. Br J G en Pract. 2005;55(513):305–312. 23. Amrhein PC, M iller WR, Yahne CE, et al. Client commitment language during motivational interviewing predicts drug use outcomes. J Consult Clin Psychol. 2003;71(5):862–878.

STUDEn T An CILLARy RESOURCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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Periodontal maintenance is generally thought to be one o the most important phases o therapy that can be provided or patients with periodontal disease, yet patient cooperation with this aspect o periodontal therapy is not good. Since the dental hygienist o ten plays a major role in periodontal maintenance, this topic is o critical importance to the dental hygienist as well as other members o the dental team. This chapter outlines some o the undamental aspects o periodontal maintenance or all members o the dental team to consider during patient care.

Le ar i g Obje ctive s • Explain the term periodontal maintenance. • List three objectives o periodontal maintenance. • Describe how periodontal maintenance relates to other phases o periodontal treatment. • List the usual procedures per ormed during an appointment or periodontal maintenance. • Explain the term baseline data. • Describe guidelines or determining whether the general practice o ce or the periodontal o ce should provide periodontal maintenance. • Describe how to establish an appropriate interval between maintenance appointments. • De ne the term recurrence o periodontitis. • List clinical signs o recurrence o periodontitis. • List reasons or recurrence o periodontitis. • Explain the term compliance. • De ne the terms compliant patient and noncompliant patient. • List reasons or noncompliance with periodontal maintenance recommendations.

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• Explain some strategies that can be used to improve patient compliance. • Explain the term root caries. • List recommendations or use o f uorides in the prevention o root caries.

Ke Te rms Periodontal maintenance Baseline data Periodontal disease recurrence

Re ractory periodontitis Compliance Compliant patient Noncompliant patient

Root caries Caries management by risk assessment (CAMBRA)

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1. Description o Periodontal Maintenance. Periodontal maintenance is a term that re ers to the continuing patient care provided by members o the dental team to help a patient maintain periodontal health ollowing the completion o nonsurgical or surgical periodontal therapy (1–5). A. Periodontal therapy is per ormed at selected intervals to assist the patient in maintaining oral health; the precise intervals are selected to meet the needs o the individual patient. B. O nce begun, periodontal maintenance is normally continued or li e o the natural dentition (or the li e o the dental implants). C. Periodontal maintenance can be discontinued temporarily i surgical or nonsurgical therapy must be reinstituted because o recurrent periodontal disease. D. Periodontal maintenance is per ormed on both natural teeth and dental implants. E. Though periodontal maintenance is the pre erred term, other terms that have been used or periodontal maintenance are supportive periodontal therapy (SPT) and periodontal recall. F. It is important to realize that periodontal maintenance is not synonymous with a dental prophylaxis. 2. Importance o Periodontal Maintenance A. Periodontal maintenance is one o the most important phases o periodontal treatment. 1. With good periodontal maintenance, most periodontitis patients can retain their teeth or implants in unction and com ort throughout their lives (3,5). 2. In the absence o periodontal maintenance, patients requently exhibit a recurrence o periodontal disease (6–10). 3. Periodontal maintenance can be success ul regardless o the speci c type o periodontal treatment (surgical or nonsurgical) needed by the patient. 4. The success o periodontal maintenance in reducing tooth loss is well documented in the literature (9,11,12). Figure 30-1 illustrates some o the outcomes possible with periodontal maintenance. With m a inte na nc e

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Fig re 30-1. Attachme t Lo ss With a d Witho t Mai te a ce . A study by Axelsson and Lindhe assessed the e icacy o a periodontal maintenance care program to prevent the recurrence o disease in patients treated or advanced periodontitis. Patients who were not in a periodontal maintenance program had progressive attachment loss over a 6-year period. Similar patients in the study who were placed on maintenance care every 2 to 3 months over the 6-year period exhibited some attachment gain. (Data rom Axelsson P, Lindhe J. The signi icance o maintenance care in the treatment o periodontal disease. J Clin Periodontol. 1981;8:281–294.)

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3. Goals o Periodontal Maintenance. There are several overlapping goals o periodontal maintenance; these goals are discussed below and are summarized in Box 30-1. A. To Minimize the Recurrence and Progression o Periodontal Disease. There are several reasons that periodontal disease tends to recur. 1. O course, the primary risk actor or inf ammatory periodontal disease is bacterial plaque bio lm. a. In spite o a patient’s best sel -care e orts, it is common or plaque bio lms to orm at some sites and or some calculus to re orm at some sites. Periodic pro essional bio lm and calculus removal is an important part o periodontal maintenance. b. It is common or a patient’s sel -care e orts to become less e ective over time. Rein orcement or improvement o sel -care techniques is also an important part o periodontal maintenance. 2. Secondary risk actors or inf ammatory periodontal diseases include plaqueretentive areas (such as restorations with overhangs), smoking, and certain systemic actors. a. Whereas these secondary risk actors should always be addressed as part o nonsurgical periodontal therapy, the condition o most patients changes over time. For example, restorative dental procedures can alter plaqueretentive sites or a patient’s systemic condition can change. b. Continuing reassessment o the impact o secondary risk actors is also an important part o periodontal maintenance (11,13–15). B. To Reduce the Incidence o Tooth Loss. O ne o the primary overall goals o all phases o periodontal therapy (including periodontal maintenance) or most patients is to reduce the incidence o tooth loss (or reduce the incidence o implant loss). 1. In a study by Wilson et al. (16), o tooth loss in maintenance patients in a private periodontal practice, tooth loss was shown to be inversely proportional to the requency o periodontal maintenance. 2. O ther studies have also shown that patients who maintain regular periodontal maintenance lose ewer teeth than patients who receive less periodontal maintenance (11,17). C. To Increase the Probability o Detecting and Treating Other Oral Conditions 1. As members o the healthcare community, members o the dental team need to be vigilant or the development o any oral condition that can a ect patient wel are. 2. Periodontal maintenance o ers an ideal opportunity or ongoing monitoring o the overall oral health o a patient.

Bo x 30-1. Go als o f Pe rio do tal Mai te a ce • Min im ize t h e re cu rre n ce a n d p ro g re ssio n o f p e rio d o n t a l d ise a se • Re d u ce t h e in cid e n ce o f t o o t h lo ss • In cre a se t h e p ro b a b ilit y o f d e t e ct in g a n d t re a t in g o t h e r o ra l co n d it io n s

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4. Patient/ Clinician Roles in Periodontal Maintenance A. Periodontal maintenance is a team e ort that requires commitment rom everyone involved. The periodontal maintenance team includes the members o the dental team plus the patient and occasionally other healthcare providers such as the patient’s physician. B. Periodontal maintenance requires considerable e ort rom the patient in sustaining meticulous sel -care and cooperating with regular ongoing pro essional periodontal maintenance care. Patients must be made aware o the need or this ongoing e ort even be ore receiving nonsurgical periodontal therapy. C. In addition, periodontal maintenance requires considerable e ort on the part o the dental health team or pro essional care at regular intervals, renewal o patient motivation, instruction in sel -care techniques, and elimination or reduction o primary and secondary risk actors. 5. Relationship o Periodontal Maintenance to Other Phases o Therapy. It is important or a clinician to understand how periodontal maintenance or a patient who has been treated or periodontal disease relates to other phases o comprehensive periodontal therapy; this relationship is summarized in Figure 30-2.

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Fig re 30-2. Phase s o f Pe rio do tal The rap . This lowchart illustrates how periodontal maintenance relates to other phases o periodontal therapy that are requently provided or patients with periodontal disease.

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1. When to Implement Periodontal Maintenance. Following nonsurgical periodontal therapy, a reevaluation o the patient’s periodontal status is per ormed with a particular emphasis on the results obtained rom nonsurgical therapy. A. Based upon the ndings o this reevaluation, additional therapy such as periodontal surgery might be recommended. B. At the reevaluation, the dental team must also decide what periodontal maintenance care will be needed. C. For most patients periodontal maintenance will begin ollowing this reevaluation, since or many patients no urther active therapy is needed at least in selected sites in the dentition. D. Even though periodontal surgery may be recommended in some sites, the maintenance phase begins ollowing nonsurgical therapy at least or those sites where no urther active periodontal therapy is indicated. 2. Procedures or Pro essional Biof lm Removal A. Traditionally, hand and/or ultrasonic instrumentation has been used or pro essional bio lm removal. 1. In the hands o a well-trained clinician, both these techniques are e ective in bio lm removal. 2. The subgingival bio lm removal process using either hand and/or ultrasonic instrumentation, however, is a technically demanding and time-consuming procedure or the clinician and uncom ortable or many patients (18,19). Unpleasant eelings toward dental procedures may have a negative e ect on patient compliance. B. Bio lm ormation occurs rapidly in periodontal pockets ollowing instrumentation. Pro essional bio lm removal must be per ormed requently at regular intervals or subgingival bio lm management. C. A Recent Innovation in Biof lm Management: Subgingival Air Polishing 1. Air polishing technology uses a combination o an abrasive powder with water and compressed air delivered to the tooth sur ace through an air polishing nozzle. Recently an air polishing device – H u-Friedy M anu acturing’s A irFlow Perio – has been introduced in the United States and Canada that uses a specially designed subgingival nozzle and low-abrasive glycine-based powder to remove subgingival bio lms. 2. The main objective o subgingival air polishing is to maintain the health o the periodontium by decreasing inf ammation caused by the host response to plaque bio lms in the periodontal pocket. 3. The unique technology or subgingival air polishing a. Subgingival air polishing devices use a specially designed disposable nozzle to deliver a low-abrasive powder to the subgingival environment. 1. By using the newly designed nozzle, the jet spray has a lower f ow and pressure than nozzles designed or supragingival polishing. 2. The subgingival nozzle directs the powder and air mainly toward the root sur ace while the water exits at the tip o the nozzle. b. Subgingival air polishing uses a glycine-based powder that is biocompatible and gentle on the so t tissues o the oral cavity, subgingival epithelium, and cementum (20–22). c. Before using this new technology, clinicians require special training in the proper use of the subgingival air polishing device. Explaining the

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techniques or use o subgingival glycine powder air polishing is beyond the scope o this chapter, but clinicians should be aware o this emerging technology and seek ormal training in its use. 4. Clinical evidence or subgingival air polishing with glycine-based powders a. Subgingival air polishing or the removal o bio lm rom root sur aces is a relatively new technology with clinical research supporting its sa ety and e cacy or use in nonsurgical periodontal therapy and treatment o periimplant disease. 1. Although subgingival air polishing is an emerging technology in the United States and Canada, this technology has been used and researched or several years in Europe. 2. In June 2012, during the EuroPerio 7 Conference in Vienna (23), a consensus con erence on mechanical bio lm management took place to review the current evidence rom the literature on the clinical relevance o subgingival use o air polishing and to make practical recommendations or the clinician. b. Box 30-2 summarizes these recommendations, as well as, additional current evidence rom the literature on subgingival bio lm management.

Bo x 30-2. S mmar o f C rre t Evide ce o Air Po lishi g

S bg i g ival

• In d ica t io n s fo r t h e u se o f a ir p o lish in g d e vice s h a ve b e e n e xp a n d e d fro m su p ra g in g iva l t o su b g in g iva l a ir p o lish in g in t h e p a st fe w ye a rs. In p a rt icu la r, t h e d e ve lo p m e n t o f n e w lo w -a b ra sive g lycin e -b a se d p o w d e rs a n d d e vice s w it h su b g in g iva l n o zzle s p ro vid e s b e t t e r a cce ss t o su b g in g iva l a n d in t e rd e n t a l a re a s (23). • In p e rio d o n t a l p o cke t s 5 m m o r g re a t e r in d e p t h , su b g in g iva lly a p p lie d lo w -a b ra sive p o w d e rs—u sin g a su b g in g iva l n o zzle —re m o ve su b g in g iva l b io lm sig n i ca n t ly m o re e f ca cio u sly t h a n cu re t s (21,24). • Clin ica l a n d m icro b io lo g ic o u t co m e s u p t o 2 m o n t h s w e re n o t sig n i ca n t ly d iffe re n t fo llo w in g su b g in g iva lly a p p lie d g lycin e p o w d e r a ir p o lish in g , u lt ra so n ic in st ru m e n t a t io n , o r in st ru m e n t a t io n w it h cu re t s (25,26). • Fu ll-m o u t h g lycin e p o w d e r a ir p o lish in g re su lt s in a sig n i ca n t ly d e cre a se d lo a d o f Po rp h yro m o n as g in g ivalis in t h e o ra l ca vit y (24). • Usin g su b g in g iva lly a p p lie d g lycin e p o w d e r a ir p o lish in g , su b g in g iva l b io lm re m o va l ca n b e a ch ie ve d in a co n sid e ra b ly sh o rt e r p e rio d o f t im e co m p a re d t o su b g in g iva l in st ru m e n t a t io n u sin g h a n d a n d /o r u lt ra so n ic in st ru m e n t a t io n (25,26). • Pa t ie n t s g e n e ra lly p e rce ive g lycin e -b a se d a ir p o lish in g a s m o re co m fo rt a b le t h a n h a n d a n d /o r p o w e r-d rive n in st ru m e n t a t io n (20,21,25–28). • Air p o lish in g d o e s NOT re m o ve ca lcu lu s d e p o sit s. Fo r ca lcu lu s re m o va l, h a n d o r u lt ra so n ic in st ru m e n t s a re st ill n e e d e d (27). • Glycin e -b a se d p o w d e rs re su lt in n o n crit ica l lo ss o f ce m e n t a l su b st a n ce (22,29). • Glycin e p o w d e r p o lish in g ca u se s le ss g in g iva l e ro sio n t h a n h a n d in st ru m e n t a t io n (20). • Glycin e p o w d e r p o lish in g is sa fe a n d e ffe ct ive o n t it a n iu m su rfa ce s o f d e n t a l im p la n t s (30,31). • Glycin e p o w d e r is sa fe o n a va rie t y o f re st o ra t ive m a t e ria ls a n d o rt h o d o n t ic b ra cke t s. • Clin ica l, m icro b io lo g ic, a n d h ist o lo g ic st u d ie s h a ve co n rm e d su b g in g iva l g lycin e p o w d e r a ir p o lish in g is sa fe , e f cie n t , a n d co m fo rt a b le w h e n u se d a s re co m m e n d e d b y a t ra in e d p ro fe ssio n a l (21,23–25,27,28,32).

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Bo x 30-3. Ove rvie w o f Pro ce d re s Pe rfo rme d D ri g a Pe rio do tal Mai te a ce Appo i tme t • • • • • • • •

Up d a t e m e d ica l st a t u s Pa t ie n t in t e rvie w Clin ica l a sse ssm e n t Eva lu a t io n o f e ffe ct ive n e ss o f p a t ie n t se lf-ca re Id e n t i ca t io n o f t re a t m e n t n e e d s Pe rio d o n t a l in st ru m e n t a t io n Pa t ie n t co u n se lin g Ap p lica t io n o f u o rid e s

3. Procedures Per ormed During Periodontal Maintenance. Success ul periodontal maintenance requires the active participation o the patient as well as all members o the dental team. In most dental o ces the dental hygienist plays a major role in procedures per ormed during periodontal maintenance. A typical patient o ce visit or periodontal maintenance includes procedures discussed below and outlined in Box 30-3 (33–35). A. Update o Medical Status. An update o a patient’s medical status is always the rst step in any clinical appointment. B. Patient Interview 1. A patient interview is part o a periodontal maintenance appointment; during the interview, changes in the social or dental status o the patient should be explored and documented. 2. Examples o social status issues that should be explored would be changes in li estyle, bereavement, and work status. 3. The patient interview should also include a review o dental care provided by other clinicians since the previous maintenance visit. 4. In addition, the patient interview should clari y the patient’s perception o his/her oral status including the patient’s thoughts about problems encountered during sel -care e orts. C. Clinical Assessment 1. Following the patient interview, a thorough clinical assessment should be per ormed. Results o the clinical assessment should then be compared with previous baseline data. The term baseline data re ers to clinical data gathered at the beginning o the periodontal treatment that is subsequently used or comparison. 2. The actual clinical assessment usually includes steps such as those listed below. a. Extraoral and Intraoral Examination b. Dental Examination c. Radiographic Examination i indicated d. Periodontal Examination including the ollowing eatures: 1. Probing depths a. Probing depths should be recorded with the same attention to detail that was employed during the initial examination. b. Disease progression (continuing attachment loss) should be suspected when a 2-mm increase in probing depth is noted at a site.

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2. Bleeding on probing a. When present, bleeding on probing is generally visible within a ew seconds a ter gentle periodontal probing. b. Research suggests that a ter a ew years o maintenance, a high requency o bleeding on probing is a predictor o increased risk or progressive attachment loss (36). c. Bleeding sites should be charted because these sites may need more attention during periodontal instrumentation. 3. Attachment level a. Attachment levels should be recorded at critical sites in the dentition. b. The most reliable way to evaluate periodontal disease control is by sequential comparison o clinical attachment level measurements. c. Disease progression is thought to be indicated by a 2-mm increase in clinical attachment loss at a speci c site as m easured w ith a m anual periodontal probe. 4. Tooth mobility a. In the assessment o tooth mobility, mobility can be stable or increasing. Increasing mobility over time is one o the important clinical eatures to note. b. The more severe the mobility measured in a tooth, the greater the risk o eventual tooth loss. 5. Furcation involvement a. Periodontal disease control is more di cult in areas o urcation involvement. b. The more advanced the urcation involvement, the greater the risk o tooth loss over time. 6. Mucogingival involvement 7. Levels o plaque biof lm and calculus D. Evaluation o E ectiveness o Sel -Care 1. Patients o ten spend considerable time on sel -care and justi ably expect to be in ormed about the e ectiveness o their e orts. a. Plaque scores recorded a ter using a disclosing solution are good indications o the patient’s level o sel -care compliance, and disclosing solution can be used to allow patients to see bio lm accumulation. b. Plaque scores may reveal that the patient is in need o renewed instruction in sel -care methods. 2. Bio lm accumulation can be related to many actors; examples o these actors are listed below. a. Patients may lack the manual dexterity needed to carry out the sel -care regimen that was recommended previously. When manual dexterity is a problem, alternative sel -care techniques should be considered. O lder patients can loose skills that they were per ectly capable o per orming at a previous maintenance visit. b. Un ortunately it is common or patients to discontinue the use o one or more o the sel -care methods recommended previously. c. Gingival recession or shrinkage may have occurred ollowing periodontal surgery; introduction o new interdental aids may be indicated or plaque bio lm removal on proximal root sur aces.

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E. Identif cation o Treatment N eeds 1. It is a routine part o periodontal maintenance to per orm thorough periodontal instrumentation to remove bio lm and calculus, but other treatment needs can also be identi ed. 2. Examples o other treatment needs can include local delivery o antimicrobials, restoration o dental caries, and reinstitution o active periodontal therapy. 3. Selective tooth polishing may be indicated or removal o tooth stains that are visible when the patient smiles. F. Biof lm Removal 1. Bio lms are resistant to topical chemical control; there ore, requent pro essional removal o plaque bio lm is an essential component o success ul nonsurgical periodontal therapy. 2. Pro essional bio lm may be accomplished by hand and/or ultrasonic instrumentation or subgingival glycine powder air polishing. G. Periodontal Instrumentation 1. The goal o periodontal instrumentation is to create an environment that is biologically acceptable to the tissues o the periodontium. 2. Thorough removal o all calculus deposits should be accomplished using hand/ and or ultrasonic instrumentation. 3. The main adverse e ect o requent mechanical instrumentation o the root sur ace is disturbance o the epithelial attachment and cumulative, irreversible root substance removal (37–42) and gingival recession (43,44). a. H ard tissue loss is one o the major causes o dentin sensitivity to hot and cold stimuli, as well as sensitivity to toothbrushing (45–48). b. Because periodontal instrumentation is a routine part o nonsurgical periodontal therapy, it is important that removal is accomplished in an e cient manner with minimal hard tissue damage (25). 1. Following periodontal therapy, some patients will present or periodontal maintenance with little or no subgingival calculus deposits. In these patients, rm stroke pressure with the instrument against the tooth is not necessary and should be avoided. 2. Ultrasonic instrumentation with a precision-thin tip has been shown to remove less root substance than hand instrumentation and o ers the added bene t o the antimicrobial e ect created by the vibrating ultrasonic tip (49–51). 3. Plastic curets (such as those used to debride dental implants) can be e ective or deplaquing root sur aces and minimize trauma to the root during maintenance care when no calculus is present or when implants are involved. H. Patient Counseling 1. As already discussed, maintenance patients should always be counseled related to the e ectiveness o sel -care e orts since bio lm control by the patient is a critical element in preventing recurrence o periodontitis. a. Failure to provide this in ormation may give a patient the impression that the dental team is not truly interested in the patient’s dental health status. b. M ost patients will need some rein orcement o motivation or bio lm control in addition to retraining in the complex skills involved. 2. It is also wise to include counseling that explains the need or compliance with the periodontal maintenance regimen, since compliance with the periodontal maintenance regimen will always remain a problem or some patients.

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Maintenance or the Periodontal Patient

3. O ther counseling may be indicated or speci c patients. Examples o counseling that may be needed are caries prevention counseling, smoking cessation, or dietary changes. I. Application o Fluorides 1. Pro essional application o f uoride treatments during periodontal maintenance care is normally indicated to promote remineralization o tooth sur aces, aid in the prevention o root caries, and aid in the control o dentinal hypersensitivity. 2. Research studies suggest that high concentrations o topical f uorides may also have some antimicrobial properties and may be o some bene t in decreasing plaque bio lm accumulation. 3. The use o f uorides is discussed in detail in Section 5 o this chapter. 4. Decisions Related to Periodontal Maintenance A. O f ce Guidelines or Provision o Periodontal Maintenance. For patients treated in a periodontal o ce, the general dental team should discuss guidelines or how periodontal maintenance should be provided (i.e., either in the general dental practice o ce or in the periodontal practice). This decision is o course dependent in part on the experience and com ort levels o the members o the dental team, but some general guidelines are outlined below. 1. Patients who have been treated or mild chronic periodontitis can usually receive periodontal maintenance in a general dental practice. 2. Patients who have been treated or moderate chronic periodontitis can usually be managed by alternating periodontal maintenance visits between the general dental practice and the periodontal practice. 3. Patients with severe chronic periodontitis should receive periodontal maintenance in a periodontal practice. In addition, annual or semiannual visits should be scheduled with a general dentist who will provide restorative and other general dental care. 4. Patients who have been treated or aggressive periodontitis should receive all phases o periodontal therapy including periodontal maintenance in a periodontal practice. In addition, annual or semiannual visits should be scheduled with a general dentist who will provide restorative and other general dental care. B. Establishing Appropriate Periodontal Maintenance Intervals 1. Establishing a periodontal maintenance interval that is appropriate or the patient can be challenging. The requency o periodontal maintenance visits must be determined on an individual basis (52). Some actors to consider in determining the interval between maintenance visits include the ollowing: a. Severity o periodontitis. In general the more severe the periodontitis, the shorter the intervals should be between periodontal maintenance visits. b. Adequacy o patient sel -care. In general the more e ective the patient’s sel care, the less requently the patient needs to be seen. For patients with less than optimal sel -care the intervals between maintenance visits should be shorter. c. Host response. Systemic or genetic actors may negatively a ect the host response. For example, a patient who continues to smoke or one with poorly controlled diabetes should be seen at shorter intervals (11,13). 2. An important guide or determining the requency o maintenance care is based on the time interval or the repopulation o periodontal pathogens ollowing thorough periodontal instrumentation. a. Studies indicate that ollowing periodontal instrumentation the subgingival pathogens return to preinstrumentation levels in approximately 9 to 11 weeks in most patients, though times can vary (53).

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b. Research evidence shows that periodontal maintenance should be per ormed at least every 3 months or less or the removal and disruption o subgingival periodontal pathogens. T his 3-m onth interval is the one m ost frequently recom m ended, though this interval m ay need to be adjusted based on clinical observation (52). c. Patients who receive requent periodontal maintenance will experience less attachment loss and tooth loss than patients who have less requent maintenance care.

Se ct io

3

Pe rio do tal Dise ase Re c rre ce 1. Understanding Periodontal Disease Recurrence A. Periodontal Disease Recurrence Def ned 1. The term periodontal disease recurrence re ers to the return o the disease in a patient w ho has been previously, successfully treated for periodontitis. 2. The term disease recurrence implies that the periodontitis was indeed brought under control during nonsurgical periodontal therapy (or nonsurgical periodontal therapy plus periodontal surgery), but that at some later time the periodontitis is once again resulting in progressive attachment loss. 3. It should be noted that in spite o having received excellent treatment, patients who have been treated or periodontitis are at risk or recurrence o periodontitis or as long as teeth (or implants) are present. 4. Recurrence o periodontitis can occur at speci c sites only (not necessarily throughout the dentition). For example, it would be possible or a patient treated or periodontitis to experience disease recurrence on the mesial sur ace o a single premolar tooth and or all other teeth in the dentition to continue to show good disease control. It is also possible or disease recurrence to be noted throughout the dentition. B. Clinical Recognition o Recurrence o Periodontitis. At present the most e ective way to identi y sites o recurrence o periodontitis (i.e., sites o progressive attachment loss) is through thorough periodic clinical assessments. The usual clinical signs o recurrence o periodontitis are listed in Box 30-4.

Bo x 30-4. Cli ical Sig s o f Re c rre ce • Pro g re ssive clin ica l a t t a ch m e n t lo ss • Po cke t s t h a t g e t d e e p e r o ve r t im e • Po cke t s t h a t b le e d u p o n p ro b in g

• Po cke t s t h a t e xh ib it e xu d a t e • Ra d io g ra p h ic e vid e n ce o f p ro g re ssin g b o n e lo ss • In cre a sin g t o o t h m o b ilit y

C. Reasons or Disease Recurrence. Periodontitis recurs in patients or a variety o reasons, and the members o the dental team should be aware that it is not always possible to determine a speci c reason or disease recurrence. H owever, the most common reasons or recurrence o periodontitis are the ollowing: 1. Inadequate sel -care by the patient

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Maintenance or the Periodontal Patient

2. Incomplete pro essional treatment a. Incomplete periodontal instrumentation b. Failure to control all local risk actors 3. Failure to control systemic actors 4. Inadequate control o occlusal contributing actors 5. Improper periodontal surgical technique 6. Attempting to treat teeth with a poor prognosis D. Re ractory Disease Di erentiated From Recurrent Disease. Re ractory periodontal disease should be di erentiated rom recurrent periodontal disease. Un ortunately periodontitis in certain patients is di cult or impossible to control even with all the modern therapies currently available and in spite o the e orts o the most skilled clinicians. 1. As already discussed, the term recurrence o periodontal disease re ers to the return of the disease in a patient w ho has been previously, successfully treated for periodontitis. 2. The term re ractory periodontitis, however, re ers to periodontitis that is resistant to treatment rom the outset o therapy even with what appears to be appropriate periodontal therapy. 3. Re erral to a periodontal practice is usually indicated when re ractory periodontitis is suspected in a patient. 2. Options or Management o Patients With Disease Recurrence. The members o the dental team should be alert or the need or retreatment that may be identi ed at any time during periodontal maintenance. When periodontal disease recurrence is identi ed, planning o the needed retreatment can usually include several options: A. I inadequate patient sel -care appears to be the undamental cause o the disease recurrence, then nonsurgical therapy should be reinstituted ollowed by a reevaluation o the patient’s periodontal status a ter an appropriate healing time. B. I ailure to comply with the schedule o periodontal maintenance appears to be the undamental cause o the disease recurrence, then nonsurgical therapy should be reinstituted along with urther patient education about the need or maintenance ollowed by a reevaluation o the patient’s periodontal status a ter an appropriate healing time. C. I there appears to be disease recurrence in limited individual sites in the presence o adequate patient sel -care, treatment options can include localized periodontal instrumentation, local delivery o antimicrobial agents, or localized surgical therapy. D. I there appears to be disease recurrence in multiple sites in the presence o adequate patient sel -care, periodontal surgical therapy is requently indicated. E. I generalized attachment loss has recurred, the systemic condition o the patient should be reassessed with emphasis on the possible need or periodontal surgical intervention, or possible microbial analysis, or or possible local or systemic antimicrobial therapy. Patients o this type should be managed by a specialist in periodontics.

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4

Patie t Co mplia ce w ith Pe rio do tal Mai te a ce 1. Overview o Patient Compliance. The term compliance is de ned as the extent to which a person’s behavior coincides with medical or health advice. Compliance has also called adherence or therapeutic alliance, but compliance is the most common term used in the literature. A. A patient is sometimes described as being a compliant patient i he/she ollows recommendations or healthcare advice. Examples o compliant patients would be a patient who aith ully takes antihypertensive medications as prescribed by a physician or a patient who cooperates in meeting regularly scheduled periodontal maintenance appointments as recommended by the dental team. B. A patient is sometimes described as being a noncompliant patient i he/she does not ollow recommendations or healthcare advice. Examples o noncompliant patients would be a patient who does not take prescribed medications daily to control diabetes or a patient who does not per orm adequate daily sel -care that has been recommended as part o a maintenance program. 2. Patient Compliance During Periodontal Maintenance. Patient compliance with a program o periodontal maintenance is not easy to achieve. It would require that a patient aith ully adhere to a strict program o recall appointments several times each year and ollow very speci c recommendations or meticulous daily sel -care. A. O verall, patient compliance with most medical advice is poor, and it should not be surprising that patient compliance with periodontal maintenance is also poor. B. Studies o compliance exhibited by periodontal maintenance patients indicate that only 16% to 30% o the patients are ully compliant with periodontal maintenance (54–56). C. Reasons or noncompliance with periodontal maintenance are complex, and those reasons can be di erent or each patient and even or the same patient at di erent times (17,57–61). D. Examples o some reasons that have been suggested or noncompliance with recommended programs o periodontal maintenance include the ollowing: 1. Patient ear o receiving dental treatment 2. The expense o the dental treatment involved 3. The low priority or dental care or some patients in the ace o competing demands or time 4. Denial on the part o some patients related to the periodontal challenges they ace 5. Failure or some patients to understand the implications o noncompliance 6. Perceived indi erence on the part o the dental healthcare providers 3. Strategies or Improving Compliance. The thought ul dental team will investigate and adopt strategies or improving patient compliance with periodontal maintenance (57). Some strategies or improving compliance are discussed below and outlined in Figure 30-3. A. Give a patient printed sel -care instructions, and make sure to supply the instructions written in the patient’s native language. B. Simpli y sel -care recommendations as much as possible or each patient. 1. Patients o ten perceive sel -care instructions as being di cult to ollow and as too time-consuming in their busy lives. 2. Sel -care instructions should be as clear and as simple as possible while addressing the speci c needs o the patient.

Chapte r 30

C.

D.

E. F.

G. H.

Maintenance or the Periodontal Patient

565

3. Caution should be exercised when recommending multiple types o sel -care aids. Patients are less likely to comply with sel -care when they are instructed to use multiple aids on a daily basis. 4. When possible, alternatives to traditional dental f oss should be considered, since compliance with f ossing is generally poor. Vary the o ce approach to patient education and sel -care instructions rom appointment to appointment. Patients o ten complain about having to listen to the “ same old lecture” rom the dental hygienist at each periodontal maintenance appointment. Seek out patient concerns and provide opportunities or communication by asking patients open-ended questions. Examples o open-ended questions appear below. 1. “ What are your concerns about this suggestion or treatment?” 2. “ H ow do you think you will t this sel -care recommendation into your daily schedule?” 3. “ H ow would you compare using this powered f ossing device to using traditional dental f oss?” Accommodate the individual patient’s needs whenever possible. A satis ed patient is more likely to comply with sel -care and maintenance appointments. Keep patients ully in ormed about their periodontal condition. 1. At each visit counsel the patients about their periodontal health status. 2. Explain the bene ts o having regularly scheduled periodontal maintenance visits and the risks o in requent pro essional care. M onitor compliance with the maintenance appointments and contact patients promptly when compliance seems to become a problem. Provide positive eedback to patients as requently as possible. Positive rein orcement can help improve compliance. 1. Areas o improvement should be pointed out to the patient (e.g., less bio lm accumulation, ewer bleeding sites, or less inf amed tissue). 2. Positive rein orcement should be used to convey a motivational message rather than criticism.

Co ns id e r a lte rn a tive s to flo s s

P rinte d s e lf-c a re in s tru c tio n s

S im p lify s e lf-c a re

Lim it nu m b e r o f a id s

Co m p lim e nt p a tie nt

Co nta c t re g a rd ing m is s e d a p p o in tm e n ts Va ry yo u r a p p ro a c h Ap p o intm e nt re m ind e rs

S trate g ie s fo r im pro ving c o m plia nc e

P o s itive fe e d b a c k

S e e k o ut p a tie nt c o nc e rns

Op e n -e n d e d q ue s tio ns

Fig re 30-3. S g g e stio s fo r Impro vi g Patie t Co mplia ce . An idea map o various strategies or improving patient compliance with recommendations or periodontal maintenance.

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5

Health Maintenance in Treated Periodontal Patients

Ro o t Carie s as a Co mplicatio

D ri g Mai te a ce

1. Introduction to Root Caries A. Occurrence o Root Caries in Patients With Periodontitis 1. Whereas dental caries requently occurs on enamel sur aces, the term root caries re ers to tooth decay that occurs on the root sur aces o the teeth. 2. According to the 1999–2004 N ational H ealth and N utrition Ex am ination Survey, a. root caries is a signi cant problem or adults: 21.6% o adults aged 50 to 64 years and 31% o adults aged 65 to 74 years had unrestored or restored root caries. b. the percentage o adults with root caries increases to 42.3% at age 75 (62). 3. The N orthwest Practice-based Research Collaborative in Evidence-based Dentistry research network recently reported a. a total o 19.6% o adults had root caries. b. the actors associated with increased prevalence o root caries in middleaged adults are being o the male sex, dry mouth, root sur aces exposed to the oral environment, and increased requency o eating or drinking between meals (63). 4. A 2004 systematic review on root caries incidence ound that 23.7% o older adults develop at least one new lesion annually (64). 5. Root caries occurs only i the root sur ace is exposed to the oral environment due to loss o attachment (65). a. In health, the root sur ace is protected by the periodontal attachment apparatus and is not exposed to the oral environment. b. The root may be exposed to the oral environment due to gingival recession or within a periodontal pocket. B. Clinical Appearance o Root Caries 1. Active root caries lesions, usually, look yellowish to light brown and may be covered with bio lm. Inactive lesions appear dark brown or black (65,66). Figure 30-4 shows a typical clinical appearance o root caries. 2. Root caries usually begins at or is slightly coronal to the ree gingival margin. The carious lesions can spread laterally and can even extend circum erentially around the root sur ace (67).

Fig re 30-4. Ro o t Carie s. Root caries on the mandibular incisors o an individual with periodontitis. (Courtesy o Dr. Richard J. Foster, Guil ord Technical Community College, Jamestown, NC.)

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Maintenance or the Periodontal Patient

C. Etiology o Root Caries 1. N o speci c microorganisms have been proven to cause root caries. Root caries is most likely the result o a mixed in ection or a succession o bacterial populations, such as Streptococcus m utans and L actobacillus. Recent studies, with ew exceptions, ail to nd association between A ctinomyces and root caries (68). 2. Like enamel caries, root caries requires a susceptible tooth sur ace, plaque bio lm, and time to initiate and progress. H owever, root caries di ers rom enamel caries in some aspects: a. Root sur aces are more vulnerable to demineralization than enamel sur aces. Root sur aces demineralize at a pH o 6.2 to 6.7 (69). b. M ineral loss or the root sur ace during the process o demineralization is up to 2.5 times greater than enamel (70). 3. Risk actors or the development o root caries include attachment loss, inadequate patient sel -care, a cariogenic diet, in requent dental visits, past caries experience, inadequate salivary f ow, lack o f uoride exposure, and removable partial dentures. 4. In addition, individuals who have coronal caries are 2 to 3.5 times more likely to develop root caries (71). 2. General Recommendations or the Prevention o Root Caries. Root caries is a common problem in patients with periodontitis. M anaging root caries rom a restorative standpoint can be quite di cult, and the best strategy or managing root caries is to prevent the root caries rom orming. A. Prevention o Periodontitis. The prevention o periodontitis and its associated attachment loss is the most e ective way to prevent root caries. In patients with existing periodontal disease, prevention o urther attachment loss will reduce the sur ace area susceptible to decay. B. Fluoride or the Prevention o Root Caries 1. Root lesions can be arrested by remineralization. A 2007 systematic review o f uoride interventions or root caries concluded that f uoride appears to be a preventive and therapeutic treatment or root caries (72,73). 2. A variety o f uoride products can be help ul in preventing root caries. Figure 30-5 depicts some o these products. A 2011 systematic review recommended 1.1% N aF pastes/gels and f uoride varnishes as the most e ective modalities or root caries remineralization (74). a. Fluoridated Drinking Water. Several studies have demonstrated that the presence o f uoridated drinking water throughout the li etime o an individual reduces the development o root sur ace caries (75). b. Fluoride Toothpaste 1. The use o an 1,100 ppm sodium f uoride (N aF) denti rice results in a signi cant decrease in root sur ace caries o 67% (76). 2. A recent randomized clinical trial demonstrates that prescription strength f uoride toothpaste, containing 5,000 ppm N aF, is e ective in reversing root caries (77). 3. Patients using f uoride toothpastes should avoid rinsing with large volumes o water a ter the use o f uoride toothpaste (78). c. Fluoride Mouthrinses. Fluoride mouthrinses containing 0.05% N aF have been shown to signi cantly reduce root caries incidence (79).

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Fig re 30-5. Fl o ride Pro d cts. There are a variety o luoride products or pro essional or home use that are help ul in the control o root caries. These include toothpastes, gels, oams, rinses, and varnishes. (Courtesy o Colgate-Palmolive company.)

d. Pro essional Application o Fluoride 1. A large long-term clinical study showed that semiannual applications o 1.23% APF gel signi cantly reduced the ormation o new root caries. The number o remineralized lesions was signi cantly increased by daily rinsing with a 0.05% N aF rinse (80). 2. Fluoride varnish applied every 3 months has been shown to reduce new root caries ormation by over 50% (81). e. N ew Fluoride Agents. N ew f uoride agents, such as silver diamine f uoride are available in some countries and show promise as root caries preventive agents. C. Antimicrobial and Supplemental Remineralization Therapies 1. A recent systematic review ound no bene t rom the use o chlorhexidine varnish in reducing root caries (82). There is limited evidence o bene t rom the use o a chlorhexidine mouthrinse (83). H igh and extreme caries risk adults should rinse with 10 mL o 0.12% chlorhexidine once daily or 1 wk/mo. 2. Xylitol-containing gums and mints are recommended or high and extreme caries risk patients. a. The therapeutic dose o xylitol is 6 to 10 g spread throughout the day. b. A recent randomized clinical trial ound 40% ewer root caries lesions in the xylitol group compared to placebo. The xylitol group received ve lozenges containing 1 g o xylitol. The lozenges were consumed across the day (84). 3. Casein phosphopeptide (CPP)-amorphous calcium phosphate (ACP) pastes are recommended or extreme caries risk patients. a. The paste can be applied with a ngertip on a daily basis. b. M ost research on CPP-ACP is laboratory based rather than in vivo. H owever, CPP-ACP may promote remineralization in patients with low salivary f ow. c. A 2008 systematic review concluded that there is insu cient evidence to make conclusions regarding the e ectiveness o CPP-ACP in preventing caries (85). 4. In a clinical practice guideline rom the American Dental Association, application o a 1:1 mixture o chlorhexidine and thymol varnish (Cervitec Gel), every 3 months was recommended to reduce the incidence o root caries (86). 3. Caries Management by Risk Assessment (CAMBRA) A. Caries Risk Assessment 1. Recent research clearly demonstrates that assigning caries risk assessment levels acilitates the e ective management o patients or dental caries (87).

Chapte r 30

Maintenance or the Periodontal Patient

2. Subsequent to this research, protocols or clinical management o caries risk actor level were developed and employed at a number o dental schools (88). While complete consensus on these protocols continues to develop, there is strong agreement about treating patients or dental caries based on risk level (88). 3. These protocols or clinical management o caries risk are known as “ Caries Management by Risk Assessment (CAMBRA)” (76,87). 4. The CAM BRA protocols seek to provide practical clinical guidelines or managing dental caries based upon risk group assessment. The protocols are based upon the best evidence at this time and can be used in planning e ective caries management or any patient (87,89). B. CAMBRA Treatment Recommendations 1. A caries risk assessment orm a. In 2002, a group o experts rom across the United States produced a caries risk assessment orm (89). b. In 2006, outcomes research based upon the use o the orm in a large cohort o patients was published, validating the orm (90). The results rom this study are the basis or the current version o the caries risk assessment orm shown in Figure 30-6. 2. Caries risk determination. Assigning a “ caries risk level” to a patient is the rst step in managing the disease process. Table 30-1 presents the our risk levels groups (low, moderate, high, and extreme) and the recommendations or caries management procedures or each level. a. Low or moderate caries risk is assigned based on clinical judgment ollowing an evaluation o the risk actors and protective actors o the patient. b. H igh caries risk is signi ed by the presence o any one o the ollowing: visible cavities or radiographic penetration o the dentin, radiographic interproximal enamel lesions, white spots on smooth sur aces, or restorations in the last 3 years. c. Extreme caries risk is high caries risk and severe salivary gland hypo unction (salivary f ow rate o less than 0.5 mL/min). 3. Evidence-based treatment plan. Following caries risk determination, the next step is to develop an evidence-based treatment plan based upon the patient’s risk level. a. Low-risk patients should use f uoride toothpaste twice daily and pro essional topical f uoride applications are optional. Bacterial and salivary tests are not necessary. M ost periodontal maintenance patients are not considered low risk because exposed roots are a primary risk actor or root caries. b. M oderate caries risk patients should use f uoride toothpaste twice daily, rinse with a 0.05% sodium f uoride mouthrinse, and receive f uoride varnish applications at maintenance appointments. Bacterial and salivary test are optional. c. H igh caries risk patients should use a prescription o 1.1% sodium f uoride toothpaste twice daily and receive one to three f uoride varnish applications during initial therapy. Fluoride varnish should be applied at 3-month intervals. Bacterial and salivary tests are recommended. d. Extreme caries risk patients receive the same CAM BRA therapies as high risk. In addition baking soda rinses, 0.5% sodium f uoride rinses and calcium/phosphate pastes may be recommended.

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Carie s Ris k As s e s s me nt Fo rm - Childre n Ag e 6 and Ove r/Adults Patient Name: As s e s s me nt Date : Is this (ple as e c irc le ) bas e line

Chart #: or

Date:

re c all

Dis e as e Indic ato rs (Any o ne “YES” s ig nifie s like ly “Hig h Ris k” and to do a bac te ria te s t**)

YES = CIRCLE

Vis ible cavities or radiographic penetration of the dentin

YES

Radiographic approximal enamel les ions (not in dentin)

YES

White s pots on s mooth s urfaces

YES

Res torations las t 3 years

YES

YES = CIRCLE

YES = CIRCLE

Ris k Fac to rs (Bio lo g ic al o r pre dis po s ing fac to rs )

MS and LB both medium or high (by culture**)

YES

Vis ible heavy plaque on teeth

YES

Frequent s nack (>3x daily between meals )

YES

Deep pits and s s ures

YES

Recreational drug us e Inadequate s aliva ow by obs ervation or meas urement (***If meas ured, note the ow rate below)

YES

Saliva reducing factors (medications /radiation/s ys temic)

YES

Expos ed roots

YES

Orthodontic appliances

YES

YES

Pro te c tive Fac to rs

Lives /work/s chool ouridated community

YES

Fluoride toothpas te at leas t once daily

YES

Fluoride toothpas te at leas t 2x daily

YES

Fluoride mouthrins e (0.05% NaF) daily

YES

5,000 ppm F uoride toothpas te daily

YES

Flouride varnis h in las t 6 months

YES

Of ce F topical in las t 6 months

YES

Chlorhexidine pres cribed/us ed one week each of las t 6 months

YES

Xylitol gum/lozenges 4x daily las t 6 months

YES

Calcium and phos phate pas te during las t 6 months

YES

Adequate s aliva ow (>1 mL/min s timulated)

YES

**Bac te ria/Saliva Te s t Re s ults : MS: LB: Flo w Rate : mL/min. Date :

VISUALIZE CARIES BALANCE (Us e circled indicators /factors above) (EXTREME RISK = HIGH RISK + SEVERE SALIVARY GLAND HYPOFUNCTION) CARIES RISK ASSESSMENT (CIRCLE): EXTREME HIGH MODERATE LOW

Signature:

Date:

Fig re 30-6. Carie s Risk Asse ssme t Fo rm. (Used with permission rom Featherstone JD, DomejeanOrliaguet S, Jenson L, et al. Caries risk assessment in practice or age 6 through adult. J Calif Dent Assoc. 2007;35(10):703–707, 710–713, Table 1.)

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Part 6

Health Maintenance in Treated Periodontal Patients

Chapte r S mmar State me t Periodontal maintenance re ers to continuing patient care provided by the dental team to help the periodontitis patient maintain periodontal health ollowing complete nonsurgical or surgical periodontal therapy. In most dental o ces the dental hygienist plays a major role in procedures per ormed during periodontal maintenance visits. Procedures in a typical o ce visit or periodontal maintenance include patient interview, clinical assessment, evaluation o e ectiveness o sel -care, identi cation o treatment needs, periodontal instrumentation, patient counseling, and application o f uorides. Currently the most requently recommended interval or periodontal maintenance is every 3 months. Recurrence o periodontitis in treated patients with the need or additional active periodontal treatment is always a possibility. Patient compliance with periodontal maintenance recommendations is poor, but strategies can be employed to improve compliance. Root caries is a complication in many treated periodontitis patients.

Se ct io

6

Fo c s o

Patie ts

Cli ical Patie t Care CA S E 1 Your dental team has just completed a reevaluation o the results o nonsurgical therapy or a patient with generalized slight chronic periodontitis. The ndings o the reevaluation reveal that the periodontitis appears to be under control and that periodontal maintenance is the next logical step. When should the rst maintenance appointment be scheduled and what actors should be considered when assigning this maintenance interval?

CA S E 2 O ne o your dental team’s chronic periodontitis patients has recently undergone periodontal surgery and now has several sites o gingival recession exposing tooth roots. Un ortunately, this patient has had a high incidence o both coronal and root caries over the past ew years. What measures might your team take to minimize the risk o urther root caries in this patient?

CA S E 3 A patient who has been treated or chronic periodontitis by your team has been ollowed or periodontal maintenance or more than 3 years. During each maintenance visit, there have been no indications o recurrence o the periodontitis. The patient calls you be ore her next maintenance visit to in orm you that she has just been diagnosed with diabetes mellitus. She looked up diabetes on the Internet and now wants to know i this will a ect her periodontal condition. H ow should your dental team respond to the patient’s concern?

Chapte r 30

Maintenance or the Periodontal Patient

Re fe re ce s 1. Allen E, Z iada H , Irwin C, et al. Periodontics: 10. M aintenance in periodontal therapy. D ent Update. 2008;35(3):150–152, 154–156. 2. Ram jord SP. M aintenance care and supportive periodontal therapy. Q uintessence Int. 1993;24(7):465–471. 3. Shumaker N D, M etcal BT, Toscano N T, et al. Periodontal and periimplant maintenance: a critical actor in long-term treatment success. Com pend Contin Educ D ent. 2009;30(7):388–390, 392, 394 passim; quiz 407, 418. 4. Tan AE. Periodontal maintenance. A ust D ent J. 2009;54(suppl 1):S110–S117. 5. Wilson TG Jr, Valderrama P, Rodrigues DB. The case or routine maintenance o dental implants. J Periodontol. 2014;85(5):657–660. 6. Bostanci H S, Arpak M N . Long-term evaluation o surgical periodontal treatment with and without maintenance care. J N ihon Univ Sch D ent. 1991;33(3):152–159. 7. Costa FO, Cota LO, Lages EJ, et al. Periodontal risk assessment model in a sample o regular and irregular compliers under maintenance therapy: a 3-year prospective study. J Periodontol. 2012;83(3):292–300. 8. Jansson L, Lagervall M . Periodontitis progression in patients subjected to supportive maintenance care. Swed D ent J. 2008;32(3):105–114. 9. Lorentz TC, Cota LO, Cortelli JR, et al. Tooth loss in individuals under periodontal maintenance therapy: prospective study. Braz O ral R es. 2010;24(2):231–237. 10. Soolari A. Compliance and its role in success ul treatment o an advanced periodontal case: review o the literature and a case report. Q uintessence Int. 2002;33(5):389–396. 11. Costa FO, M iranda Cota LO, Pereira Lages EJ, et al. Progression o periodontitis and tooth loss associated with glycemic control in individuals undergoing periodontal maintenance therapy: a 5-year ollow-up study. J Periodontol. 2013;84(5):595– 605. 12. N ibali L, Farias BC, Vajgel A, et al. Tooth loss in aggressive periodontitis: a systematic review. J D ent R es. 2013;92(10):868– 875. 13. Chambrone L, Chambrone D, Lima LA, et al. Predictors o tooth loss during long-term periodontal maintenance: a systematic review o observational studies. J Clin Periodontol. 2010;37(7):675–684. 14. Costa FO, Lages EJ, Cota LO, et al. Tooth loss in individuals under periodontal maintenance therapy: 5-year prospective study. J Periodontal R es. 2014;49(1):121–128. 15. Ravald N , Johansson CS. Tooth loss in periodontally treated patients: a long-term study o periodontal disease and root caries. J Clin Periodontol. 2012;39(1):73–79. 16. Wilson TG Jr, Glover M E, M alik AK, et al. Tooth loss in maintenance patients in a private periodontal practice. J Periodontol. 1987;58(4):231–235. 17. Lorentz TC, Cota LO, Cortelli JR, et al. Prospective study o complier individuals under periodontal maintenance therapy: analysis o clinical periodontal parameters, risk predictors and the progression o periodontitis. J Clin Periodontol. 2009;36(1):58–67. 18. Axtelius B, Soder eldt B, Edwardsson S, et al. Therapy-resistant periodontitis (II). Compliance and general and dental health experiences. J Clin Periodontol. 1997;24(9 Pt 1):646–653. 19. Cro t LK, N unn M E, Craw ord LC, et al. Patient pre erence or ultrasonic or hand instruments in periodontal maintenance. Int J Periodontics R estorative D ent. 2003;23(6):567–573. 20. Petersilka G, Faggion CM Jr, Stratmann U, et al. E ect o glycine powder air-polishing on the gingiva. J Clin Periodontol. 2008;35(4):324–332. 21. Petersilka GJ, Tunkel J, Barakos K, et al. Subgingival plaque removal at interdental sites using a low-abrasive air polishing powder. J Periodontol. 2003;74(3):307–311. 22. Sahrmann P, Ronay V, Schmidlin PR, et al. Three-dimensional de ect evaluation o air polishing on extracted human roots. J Periodontol. 2014;85(8):1107–1114. 23. Sculean A, Bastendor KD, Becker C, et al. A paradigm shi t in mechanical bio lm management? Subgingival air polishing: a new way to improve mechanical bio lm management in the dental practice. Q uintessence Int. 2013;44(7):475–477. 24. Flemmig TF, Arushanov D, Daubert D, et al. Randomized controlled trial assessing e cacy and sa ety o glycine powder air polishing in moderate-to-deep periodontal pockets. J Periodontol. 2012;83(4):444–452. 25. M oene R, Decaillet F, Andersen E, et al. Subgingival plaque removal using a new air-polishing device. J Periodontol. 2010;81(1):79–88. 26. Wennstrom JL, Dahlen G, Ramberg P. Subgingival debridement o periodontal pockets by air polishing in comparison with ultrasonic instrumentation during maintenance therapy. J Clin Periodontol. 2011;38(9):820–827. 27. Petersilka GJ. Subgingival air-polishing in the treatment o periodontal bio lm in ections. Periodontol 2000. 2011;55(1):124– 142. 28. Petersilka GJ, Steinmann D, H aberlein I, et al. Subgingival plaque removal in buccal and lingual sites using a novel low abrasive air-polishing powder. J Clin Periodontol. 2003;30(4):328–333. 29. Petersilka GJ, Bell M , H aberlein I, et al. In vitro evaluation o novel low abrasive air polishing powders. J Clin Periodontol. 2003;30(1):9–13. 30. Sahrmann P, Ronay V, Sener B, et al. Cleaning potential o glycine air-f ow application in an in vitro peri-implantitis model. Clin O ral Im plants R es. 2013;24(6):666–670. 31. Schwarz F, Ferrari D, Popovski K, et al. Inf uence o di erent air-abrasive powders on cell viability at biologically contaminated titanium dental implants sur aces. J Biom ed M ater R es B A ppl Biom ater. 2009;88(1):83–91. 32. Graumann SJ, Sensat M L, Stoltenberg JL. Air polishing: a review o current literature. J D ent H yg. 2013;87(4):173–180. 33. Parameters o Care. American Academy o Periodontology. J Periodontol. 2000;71(5 suppl):i–ii, 847–883. 34. American Academy o Periodontology. Comprehensive periodontal therapy: a statement by the American Academy o Periodontology *. J Periodontol. 2011;82(7):943–949. 35. Cohen RE; Research, Science and Therapy Committee, American Academy o Periodontology. Position paper: periodontal maintenance. J Periodontol. 2003;74(9):1395–1401. 36. Lang N P, Joss A, Tonetti M S. M onitoring disease during supportive periodontal treatment by bleeding on probing. Periodontol 2000. 1996;12:44–48.

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37. Flemmig TF, Petersilka GJ, M ehl A, et al. Working parameters o a magnetostrictive ultrasonic scaler inf uencing root substance removal in vitro. J Periodontol. 1998;69(5):547–553. 38. Flemmig TF, Petersilka GJ, M ehl A, et al. The e ect o working parameters on root substance removal using a piezoelectric ultrasonic scaler in vitro. J Clin Periodontol. 1998;25(2):158–163. 39. Flemmig TF, Petersilka GJ, M ehl A, et al. Working parameters o a sonic scaler inf uencing root substance removal in vitro. Clin O ral Investig. 1997;1(2):55–60. 40. Kocher T, Fanghanel J, Sawa H , et al. Substance loss caused by scaling with di erent sonic scaler inserts–an in vitro study. J Clin Periodontol. 2001;28(1):9–15. 41. Ritz L, H e ti AF, Rateitschak KH . An in vitro investigation on the loss o root substance in scaling with various instruments. J Clin Periodontol. 1991;18(9):643–647. 42. Schmidlin PR, Beuchat M , Busslinger A, et al. Tooth substance loss resulting rom mechanical, sonic and ultrasonic root instrumentation assessed by liquid scintillation. J Clin Periodontol. 2001;28(11):1058–1066. 43. Badersten A, N ilveus R, Egelberg J. E ect o nonsurgical periodontal therapy. I. M oderately advanced periodontitis. J Clin Periodontol. 1981;8(1):57–72. 44. Badersten A, N ilveus R, Egelberg J. E ect o nonsurgical periodontal therapy. II. Severely advanced periodontitis. J Clin Periodontol. 1984;11(1):63–76. 45. Chabanski M B, Gillam DG. Aetiology, prevalence and clinical eatures o cervical dentine sensitivity. J O ral R ehabil. 1997;24(1):15–19. 46. Fischer C, Wennberg A, Fischer RG, et al. Clinical evaluation o pulp and dentine sensitivity a ter supragingival and subgingival scaling. Endod D ent Traum atol. 1991;7(6):259–265. 47. Tammaro S, Wennstrom JL, Bergenholtz G. Root-dentin sensitivity ollowing non-surgical periodontal treatment. J Clin Periodontol. 2000;27(9):690–697. 48. von Troil B, N eedleman I, Sanz M . A systematic review o the prevalence o root sensitivity ollowing periodontal therapy. J Clin Periodontol. 2002;29 Suppl 3:173–177; discussion 195–196. 49. Dragoo M R. A clinical evaluation o hand and ultrasonic instruments on subgingival debridement. 1. With unmodi ed and modi ed ultrasonic inserts. Int J Periodontics R estorative D ent. 1992;12(4):310–323. 50. Jacobson L, Blomlo J, Lindskog S. Root sur ace texture a ter di erent scaling modalities. Scand J D ent R es. 1994;102(3):156–160. 51. M ishra M K, Prakash S. A comparative scanning electron microscopy study between hand instrument, ultrasonic scaling and erbium doped: Yttirum aluminum garnet laser on root sur ace: a morphological and thermal analysis. Contem p Clin D ent. 2013;4(2):198–205. 52. Darcey J, Ashley M . See you in three months! The rationale or the three monthly periodontal recall interval: a risk based approach. Br D ent J. 2011;211(8):379–385. 53. Shiloah J, Patters M R. Repopulation o periodontal pockets by microbial pathogens in the absence o supportive therapy. J Periodontol. 1996;67(2):130–139. 54. Famili P, Short E. Compliance with periodontal maintenance at the University o Pittsburgh: retrospective analysis o 315 cases. G en D ent. 2010;58(1):e42–e47. 55. O jima M , H anioka T, Shizukuishi S. Survival analysis or degree o compliance with supportive periodontal therapy. J Clin Periodontol. 2001;28(12):1091–1095. 56. Wilson TG Jr. Compliance. A review o the literature with possible applications to periodontics. J Periodontol. 1987;58(10):706–714. 57. de Carvalho VF, O kuda O S, Bernardo CC, et al. Compliance improvement in periodontal maintenance. J A ppl O ral Sci. 2010;18(3):215–219. 58. M endoza AR, N ewcomb GM , N ixon KC. Compliance with supportive periodontal therapy. J Periodontol. 1991;62(12):731– 736. 59. N ovaes AB Jr, N ovaes AB. Compliance with supportive periodontal therapy. Part 1. Risk o non-compliance in the rst 5-year period. J Periodontol. 1999;70(6):679–682. 60. N ovaes AB Jr, N ovaes AB. Compliance with supportive periodontal therapy. Part II: risk o non-compliance in a 10-year period. Braz D ent J. 2001;12(1):47–50. 61. Umaki TM , Umaki M R, Cobb CM . The psychology o patient compliance: a ocused review o the literature. J Periodontol. 2012;83(4):395–400. 62. Dye BA, Tan S, Smith V, et al. Trends in oral health status: United States, 1988–1994 and 1999–2004. Vital H ealth Stat. 2007;(248):1–92. 63. Chi DL, Berg JH , Kim AS, et al., N orthwest Practice-based RCiE-bD. Correlates o root caries experience in middle-aged and older adults in the N orthwest Practice-based REsearch Collaborative in Evidence-based DEN Tistry research network. J A m D ent A ssoc. 2013;144(5):507–516. 64. Gri n SO, Gri n PM , Swann JL, et al. Estimating rates o new root caries in older adults. J D ent R es. 2004;83(8):634–638. 65. Pitts N B, Ekstrand KR, ICDAS Foundation. International Caries Detection and Assessment System (ICDAS) and its International Caries Classi cation and M anagement System (ICCM S) - methods or staging o the caries process and enabling dentists to manage caries. Com m unity D ent O ral Epidem iol. 2013;41(1):e41–e52. 66. Shivakumar K, Prasad S, Chandu G. International Caries Detection and Assessment System: a new paradigm in detection o dental caries. J Conserv D ent. 2009;12(1):10–16. 67. Berry TG, Summitt JB, Si t EJ Jr. Root caries. O per D ent. 2004;29(6):601–607. 68. Z ambon JJ, Kasprzak SA. The microbiology and histopathology o human root caries. A m J D ent. 1995;8(6):323–328. 69. Atkinson JC, Wu AJ. Salivary gland dys unction: causes, symptoms, treatment. J A m D ent A ssoc. 1994;125(4):409–416. 70. O gaard B, Arends J, Rolla G. Action o f uoride on initiation o early root sur ace caries in vivo. Caries R es. 1990;24(2): 142–144. 71. Papas A, Joshi A, Giunta J. Prevalence and intraoral distribution o coronal and root caries in middle-aged and older adults. Caries R es. 1992;26(6):459–465. 72. Gri n SO, Regnier E, Gri n PM , et al. E ectiveness o f uoride in preventing caries in adults. J D ent R es. 2007;86(5): 410–415.

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73. H eijnsbroek M , Paraskevas S, Van der Weijden GA. Fluoride interventions or root caries: a review. O ral H ealth Prev D ent. 2007;5(2):145–152. 74. Gibson G, Jurasic M M , Wehler CJ, et al. Supplemental f uoride use or moderate and high caries risk adults: a systematic review. J Public H ealth D ent. 2011;71(3):171–184. 75. Brustman BA. Impact o exposure to f uoride-adequate water on root sur ace caries in elderly. G erodontics. 1986;2(6):203– 207. 76. Jensen M E, Kohout F. The e ect o a f uoridated denti rice on root and coronal caries in an older adult population. J A m D ent A ssoc. 1988;117(7):829–832. 77. Ekstrand KR, Poulsen JE, H ede B, et al. A randomized clinical trial o the anti-caries e cacy o 5,000 compared to 1,450 ppm f uoridated toothpaste on root caries lesions in elderly disabled nursing home residents. Caries R es. 2013;47(5):391–398. 78. Sjogren K, Birkhed D. Factors related to f uoride retention a ter toothbrushing and possible connection to caries activity. Caries R es. 1993;27(6):474–477. 79. Ripa LW, Leske GS, Forte F, et al. E ect o a 0.05% neutral N aF mouthrinse on coronal and root caries o adults. G erodontology. 1987;6(4):131–136. 80. Wallace M C, Retie DH , Bradley EL. The 48-month increment o root caries in an urban population o older adults participating in a preventive dental program. J Public H ealth D ent. 1993;53(3):133–137. 81. Schaeken M J, Keltjens H M , Van Der H oeven JS. E ects o f uoride and chlorhexidine on the microf ora o dental root sur aces and progression o root-sur ace caries. J D ent R es. 1991;70(2):150–153. 82. Slot DE, Vaandrager N C, Van Loveren C, et al. The e ect o chlorhexidine varnish on root caries: a systematic review. Caries R es. 2011;45(2):162–173. 83. Featherstone JD, White JM , H oover CI, et al. A randomized clinical trial o anticaries therapies targeted according to risk assessment (caries management by risk assessment). Caries R es. 2012;46(2):118–129. 84. Ritter AV, Bader JD, Leo M C, et al. Tooth-sur ace-speci c e ects o xylitol: randomized trial results. J D ent R es. 2013;92(6):512–517. 85. Azarpazhooh A, Limeback H . Clinical e cacy o casein derivatives: a systematic review o the literature. J A m D ent A ssoc. 2008;139(7):915–924. 86. Rethman M P, Beltran-Aguilar ED, Billings RJ, et al. N onf uoride caries-preventive agents: executive summary o evidencebased clinical recommendations. J A m D ent A ssoc. 2011;142(9):1065–1071. 87. Featherstone JD, Domejean-O rliaguet S, Jenson L, et al. Caries risk assessment in practice or age 6 through adult. J Calif D ent A ssoc. 2007;35(10):703–707, 710–713. 88. Young DA, Featherstone JD, Roth JR. Curing the silent epidemic: caries management in the 21st century and beyond. J Calif D ent A ssoc. 2007;35(10):681–685. 89. Featherstone JD, Adair SM , Anderson M H , et al. Caries management by risk assessment: consensus statement, April 2002. J Calif D ent A ssoc. 2003;31(3):257–269. 90. Domejean-O rliaguet S, Gansky SA, Featherstone JD. Caries risk assessment in an educational environment. J D ent Educ. 2006;70(12):1346–1354.

STu DEn T An CILLARy RESOu RCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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Se ctio n 1

Anato m o f the De ntal Implant

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Se ctio n 2

Failin Implants: Pe ri-implant Dise ase

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Se ctio n 3

Clinical Mo nito rin o f Pe ri-implant Dise ase

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Se ctio n 4

Mainte nance The rap fo r De ntal Implants

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Se ctio n 5

Fo c s o n Patie nts

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Clinical Patient Care

Clinical Applicatio n.

All dental healthcare providers will encounter patients with dental implants, and dental hygienists are at the ore ront o providing maintenance care or patients with dental implants. This chapter provides an overview o dental implants and guidance or establishing appropriate maintenance to insure periodontal health o implants.

Le arnin Obje ctive s • Describe the components o a typical dental implant and restoration. • Compare and contrast the periodontium o a natural tooth with the peri-implant tissues that surround a dental implant. • Def ne the terms osseointegration and biomechanical orces as they apply to dental implants. • Compare and contrast the terms peri-implant mucositis and peri-implantitis. • Discuss the special considerations or periodontal instrumentation o a dental implant. • Describe an appropriate maintenance interval or a patient with dental implants. • In the clinical setting, select appropriate sel -care aids or a patient with dental implants.

Ke Te rms Dental implant Implant body Implant abutment Biocompatible

Peri-implant tissues Biological seal Osseointegration Peri-implant mucositis

Peri-implantitis Biomechanical orces

Chapte r 31

Periodontal Maintenance o Dental Implants

577

Se ct io n 1

Anato m o f the De ntal Implant A dental implant is a nonbiologic (arti cial) device surgically inserted into the jawbone to (1) replace a missing tooth or (2) provide support or a prosthetic denture. O ver the past 30 years, research has validated the success o implant placement as a easible option to replace missing teeth in partially or ully edentulous patients (1–7). The dental hygienist plays an important role in patient education and pro essional maintenance o the dental implant. Understanding the basic concepts o implantology and the anatomy o the peri-implant tissues is a prerequisite to understanding the maintenance o dental implants. 1. The Dental Implant System A. Introduction to Dental Implant Systems. Dental implant systems are used to replace individual teeth or support a xed bridge or removable denture (Fig. 31-1). The components o a dental implant system are the (1) implant body, (2) the abutment, and (3) a prosthetic crown or prosthesis (Fig. 31-2). B. The Implant Body 1. An implant body is the portion o the implant system that is surgically placed into the living alveolar bone (Fig. 31-3–31-5). This is sometimes re erred to as the implant xture or implant. 2. The implant body acts as the “ root” o the implant restoration. The implant body usually is threaded like a screw. These threads provide a greater sur ace area or contact with the alveolar bone. a. The metal used or dental implants is titanium or titanium alloy. Titanium is an ideal material or dental implants because it is a bone- riendly metal that is biocompatible and because it is a poor conductor o heat and electricity. b. The major disadvantage o titanium is that it is so ter than other dental restorative metals and thus it scratches easily. C. The Abutment 1. The implant abutment is a titanium post that attaches to the implant body and protrudes partially or completely through the gingival tissue into the mouth (Fig. 31-4). 2. The abutment supports the restorative prosthesis (crown or denture). 3. The titanium abutment is extremely biocompatible (not rejected by the body) and allows tissue healing around the abutment.

A

B

Fi re 31-1. Re place me nt o f Missin Te e th. A: Extracted teeth replaced by a traditional removable partial denture. B: Missing teeth replaced by three individual dental implants.

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C ro w n

Ab u t m e n t p o s t

Im p la n t b o d y

Fi re 31-2. The De ntal Implant S ste m. The components o a dental implant system are the implant body and the abutment post. The implant body is placed into living alveolar bone. The abutment post extends into or through living gingival tissue into the mouth. A crown or other prosthesis is connected to the abutment either by a screw or by dental cement.

Fi re 31-3. Implants and Co mpo ne nts. Examples o screw-shaped titanium implant bodies and abutment posts.

A

B

C

Fi re 31-4. Ab tme nts. This photograph shows the healing abutments or our implants.

D

E

F

Fi re 31-5. S r ical Place me nt o f De ntal Implants. A: Edentulous alveolar ridge. B: Initial osteotomy site established. C, D: Drills o increasing diameters used to prepare osteotomy to the size o the planned implant. E: Implant body seated in the osteotomy. The top o the implant body may be placed slightly above, level with, or slightly below the crest o the bone. F: Implant body seated in bone with cover screw attached. At the end o placement surgery, the implant can be covered with gingiva or le t exposed to the oral cavity, as shown here. A healing time o several weeks to months is allowed, so that osseointegration can occur.

Chapte r 31

Periodontal Maintenance o Dental Implants

2. The Peri-implant Tissues. The peri-implant tissues are the tissues that surround the dental implant (Fig. 31-6). The peri-implant tissues are similar in many ways to the periodontium o a natural tooth, but there are some important di erences (Table 31-1). A. Implant-to-Epithelial Tissue Inter ace 1. The epithelium adapts to the titanium abutment post, or to the implant itsel , creating a biological seal. The union o the epithelial cells to the abutment or implant sur ace is very similar to that o the epithelial cells to the natural tooth sur ace. 2. The biological seal unctions as a barrier between the implant and the oral cavity. 3. As with a natural tooth, a sulcus lined by sulcular epithelium and junctional epithelium surrounds the abutment or in some cases, the top o the implant body. B. Implant-to-Connective Tissue Inter ace 1. The implant-to-connective tissue inter ace is signif cantly di erent rom that o connective tissue o a natural tooth. 2. The implant sur ace lacks cementum, so the gingival bers and the periodontal ligament cannot insert into the titanium sur ace as they do into the cementum o a natural tooth. a. O n a natural tooth: 1. The supragingival bers brace the gingival margin against the tooth and strengthen the attachment o the junctional epithelium to the tooth. The supragingival bers insert into the cementum. 2. The periodontal ligament suspends and maintains the tooth in its socket. 3. The periodontal ligament bers also serve as a physical barrier to bacterial invasion. b. O n an implant: 1. The connective tissue ber bundles support the healthy gingiva against the abutment. The connective tissue ber bundles in the gingiva around an implant have been shown to be either (1) oriented parallel to the implant sur ace or (2) encircling the implant abutment (8). The bers do not attach to the dental implant. 2. There are no periodontal ligament bers to provide protection or the dental implant. T here ore, periodontal pathogens can create in am m ation and destroy bone m uch m ore rapidly along a dental im plant than along a natural tooth w ith its protective barrier o periodontal ligam ent f bers (9–12). 3. Since there are no gingival or periodontal ligament bers inserting into the titanium sur aces, a periodontal probe will pass more easily through the tissues to the alveolar bone surrounding the implant. 3. Keratinized gingival tissue may or may not be present around the dental implant. C. Implant-to-Bone Inter ace 1. Osseointegration is the direct contact o the living bone with the sur ace o the implant body (with no intervening periodontal ligament). O sseointegration is the major requirement or implant success. 2. Clinically, osseointegration is regarded as success ul i there is a. an absence o clinical mobility o the implant b. no discom ort or pain when the implant is in unction c. no increased bone loss or radiolucency surrounding the dental implant on a radiograph d. less than 0.2 mm o bone loss annually a ter the rst year in unction (13).

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S u lc u s

S u lc u s Ab u t m e n t c o n n e c t io n

J unc tiona l e p ithe lium

AC

BW

B io lo g ic w id t h

J unc tiona l e p ithe lium

Sup ra gingiva l fib e r b und le s

Sup ra gingiva l fib e r b und le s

Muc ogingiva l J unc tion

Muc ogingiva l J unc tion

Bone

Bone

P e riod onta l liga me nt

Os s e ointe gra tion

Fi re 31-6. Co mpariso n o f Pe rio do nti m Inte rface w ith a Nat ral To o th Ve rs s a De ntal Implant. The implant lacks the periodontal ligament connection to the alveolar bone and the gingival ibers do not insert into the titanium.

TABLE 3 1 -1 . TISSu ES Su RROu NDINg A DENTAL IMPLANT Tiss e s

Pe ri-implant Tiss e s

Ju n c io n l

i

liu m

Co n n c iv

issu

ib

p io d o n

l lig m n

a s

r un No

c

s o

ll l o o io d o n

C m n um

No c m n u m

a lv o l

In d i c co n

bon

im l n su n ci cl

c o

b u m n su

im l n

c (b io lo g ic l s

n d b u m n su

c

l lig m n

c wi

im l n su

c (o ss o in

g

io n )

l)

Chapte r 31

Periodontal Maintenance o Dental Implants

581

Se ct io n 2

Failin Implants: Pe ri-implant Dise ase 1. Pathologic Changes in Implant Tissues A. Peri-implant Tissue In ammation 1. Plaque bio lm can accumulate on the sur aces o teeth, restorations, oral appliances, and also on implants and abutments. 2. The continuous presence o bacterial deposits can result in inf ammation o the so t tissues around the implant. 3. When the disease process progresses urther, partial or total loss o osseointegration can occur. B. Peri-implant Disease. Pathologic changes o the peri-implant tissues can be re erred to as peri-implant disease (Fig. 31-7). Peri-implant disease presents in two orms— peri-implant mucositis and peri-implantitis. 1. Peri-implant mucositis (also called peri-implant gingivitis) is plaque-induced inf ammation o the so t tissues—with no loss o supporting bone—that is localized in the mucosal tissues surrounding a dental implant. a. Peri-implant mucositis is reversible i the etiologic actors are removed (14). Peri-implant mucositis m ay progress to peri-implantitis. b. Peri-implant mucositis has been reported to occur in about 80% o subjects and 50% o implant sites, while peri-implantitis has been reported to occur in 28% to 56% o subjects and 12% to 43% o sites (15). H owever, the reported prevalence varies widely and change as implant designs evolve. 2. Peri-implantitis is essentially chronic periodontitis a ecting the so t and hard tissues surrounding a unctioning osseointegrated dental implant, resulting in loss o supporting alveolar bone (8). a. Peri-implantitis begins at the coronal portion o the implant while the apical portion continues to be osseointegrated. b. An advanced peri-implantitis lesion can be diagnosed by the detection o radiographic bone loss around the implant (Fig. 31-8). 1. The implant does not become mobile until the nal stages o periimplantitis. 2. Implants that show mobility and signs o loss o osseointegration should be removed (16,17). c. Di erences in the prevalence o peri-implantitis have been reported by a number o research studies. The prevalence reported in these studies ranges rom 6.61% to 47% (18–21).

Fi re 31-7. Pe ri-implant Dise ase . In lammatory enlargement o peri-implant tissue resulting rom poor daily sel -care o the abutments and implant supported removable denture.

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Fi re 31-8. Pe ri-implantitis. This radiograph shows a titanium implant supporting a single crown. Note the residual cement near the crown margin. This has become a contributing actor or peri-implantitis since bone loss is evident on the radiograph.

2. Etiology o Peri-implant Disease. The major etiological actors associated with periimplant disease are bacterial in ection and biomechanical actors. Smoking is an additional actor that has been implicated in implant ailure. A. Bacterial In ection 1. Peri-implantitis—like periodontitis—occurs primarily as a result o an overwhelming bacterial in ection and the subsequent host immune response (22). 2. It appears that periodontal disease in both the peri-implant tissues and periodontium in natural teeth progresses in a similar ashion. The rate o tissue destruction, however, tends to be more rapid in peri-implant tissues than in periodontal tissues. 3. H uman cross-sectional studies ound that peri-implantitis is associated with similar bacterial species to those associated with periodontitis (23–28). a. It is theorized that the natural teeth in a partially edentulous mouth act as a reservoir o periodontal pathogens that colonize the implants. b. This nding makes meticulous sel -care o dental implants even more critical or the partially edentulous patient than or the ully edentulous patient. B. Risk Factors. The risk actors identi ed or each patient are essential in the estimation o the prognosis or the implants and these actors should be included in the determination o the appropriate maintenance interval. As in the treatment o periodontal disease, each patient must be assessed or the presence o risk actors that may help lead to peri-implant disease or its progression. Risk actors that should be considered include previous history o periodontal disease, ine ective sel -care, residual cement, smoking, and biomechanical overload (22). 1. History o Previous Periodontal Disease. Several systematic reviews indicated that peri-implantitis is a more requent nding in patients with a history o periodontitis (29–32). 2. Poor Plaque Biof lm Control (22) 3. Smoking. Four systematic reviews concluded that there is an increased risk or peri-implantitis in smokers (30,33–35). 4. Residual Cement. Implant-supported crowns are commonly held in place with cement. Residual cement (Fig. 31-9) may be le t behind because o implant positioning that may hamper access to the subgingival space (36). Residual cement may induce inf ammation due to its rough sur ace topography providing an environment or bacterial attachment (37). 5. Biomechanical Overload a. Collectively, the orces placed on an implant have been called “ biomechanical orces” to underscore the importance o both “ biological” and “ mechanical” aspects o controlling those orces to achieve long-term success with implants.

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Fi re 31-9. Re sid al Ce me nt. The gap between the implant body and the crown exposes cement. Cement deposits typically are located subgingivally and are challenging to detect, especially i the cement is not visible radiographically. (Courtesy o Natalie A. Frost, DDS, MS, Omaha, NE.)

b. Biomechanical orces on implants are inf uenced by a variety o actors that must be assessed by the clinician. Factors that inf uence the biomechanical orces include how much the occlusion is placed on the implant(s), the position o the implant, the number o implants supporting a prosthesis, and the distribution o the occlusal orces among the implants and remaining teeth. c. Since dental implants do not have a periodontal ligament, orces placed on an implant are transmitted directly to the alveolar bone (38,39). It is critical to minimize orces placed on an implant to avoid damage to the surrounding alveolar bone. 1. Around a natural tooth the periodontal ligament helps absorb some o the orces placed on the tooth. These orces placed on natural teeth can arise rom chewing ood, supporting a dental appliance, or perhaps rom habits such as bruxing. 2. Dental implants lack the protective structure o the periodontal ligament that is ound on natural teeth. I osseointegrated, the dental implant is in direct contact with the alveolar bone that completely supports it. d. Both bacterial plaque-related causes and excess biomechanical orces can contribute to the development o peri-implant disease. Both should be assessed and managed during implant maintenance appointments. 3. Detection o a Failing Implant A. Clinical Signs o a Failing Implant 1. So t Tissue Indictors. Clinical signs o a ailing implant include the presence o a peri-implant pocket, bleeding a ter gentle probing, and/or suppuration rom the pocket. The surrounding gingival tissue may or may not be swollen. Pain is usually not present. 2. Implant Mobility. Absence o mobility is a very important clinical criterion or dental implants. The presence o mobility presently is the best indicator or diagnosis o implant ailure (12). a. Implants should not move i osseointegrated and healthy (40,41). 1. Implant mobility may indicate a lack o osseointegration. 2. In some instances, mobility o an implant restoration may indicate the presence o a loose abutment or the rupture o the cement seal on cemented restorations. M obility also can result rom a loosening o the internal screw that attaches the abutment to the implant or the restoration and thus is not the result o peri-implant disease (Fig. 31-10). 3. Severe mobility accompanied with discom ort also might indicate racture o the implant itsel .

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4. Long-term mobility or mis t between the prosthetic components (e.g., screws between the crown and the implant) may lead to persistent inf ammation, bone loss and the eventual complete ailure o the implant. b. The technique or assessing mobility o a dental implant is similar to that used to assess a natural tooth. Two instrument handles are used to grasp the im plant restoration and apply orce back and orth in the acial and lingual direction. Remember that the implant restoration can be mobile, while the implant itsel is healthy and not mobile. The use o two instruments with plastic handles is recommended i the implant itsel must be touched. c. Radiographic evaluation is recommended when any mobility is noted. Loose internal screws or components will o ten be seen as a gap between the implant components on a radiograph. B. Radiographic Signs o a Failing Implant 1. Radiographic signs o peri-implantitis include vertical destruction o the crestal bone around the implant—which assumes the shape o a saucer—while the bottom portion o the implant remains osseointegrated (42). 2. Another radiographic indicator o peri-implantitis are wedge-shaped de ects along the implant (42). 3. A peri-implant radiolucency usually indicates advanced bone loss adjacent to the implant (Fig. 31-11). 4. Treatment Modalities or Failing Implants A. There are various methods available or the treatment o peri-implantitis including nonsurgical periodontal instrumentation, the use o antiseptics, local and/or systemic antibiotics, and access f ap surgery (42). 1. All these treatment modalities have been used with varying degrees o success, but at this time, there is no standard protocol or the treatment o periimplantitis (42). 2. Surgical treatment in which the lost bone is reestablished through bone gra ting shows promising results (42,43). B. N onsurgical periodontal instrumentation o peri-implantitis lesions with adjunctive local delivery o microencapsulated minocycline, as well as periodontal instrumentation supplemented with chlorhexidine can be bene cial to patients with peri-implantitis (24,44–47). C. The available evidence suggests that subgingival glycine powder air polishing or bio lm removal may reduce clinical signs o peri-implant mucosal inf ammation to a greater extent than periodontal instrumentation with plastic curets combined with adjunctive irrigation with chlorhexidine (48).

Fi re 31-10. Lo o se Inte rnal Scre w . (Courtesy o Natalie A. Frost, DDS, MS, Omaha, NE.)

Fi re 31-11. Pe ri-implant Radio l ce nc . A peri-implant radiolucency with advanced bone loss adjacent to the implant. (Courtesy o Natalie A. Frost, DDS, MS, Omaha, NE.)

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Se ct io n 3

Clinical Mo nito rin o f Pe ri-implant Dise ase Routine monitoring o dental implants—as a part o a comprehensive periodontal examination and maintenance—is essential to the e ective management o peri-implant disease. 1. Probing A. Initial probing o the implant should be done once the nal restoration has been installed (22,49). 1. In the past, routine periodontal probing o dental implants was not recommended by some authors. M ore recent literature, however, suggests that routine probing should be part o implant maintenance (22,49). Changes in probing depths can be used to detect changes in tissue/attachment health. Probing around osseointegrated implants does not appear to have detrimental e ects on the so t tissue seal and, hence, does not seem to jeopardize the longevity o oral implants (50). 2. Some implant surgeons recommend that probing should be avoided until postoperative healing is complete, approximately 3 months a ter abutment connection. 3. A probing technique with light orce (0.25 N , tip diameter 0.45) should be used since the biological seal is weakly adherent to the titanium sur ace (50). H eavy probing orce will be invasive since the probe easily can penetrate through the biological seal and introduce bacteria into the peri-implant environment (9,51,52). The depth o penetration o the probe tip also is dependent on the health (or inf ammatory stage o the peri-implant tissues) and thickness o the tissue around the abutment. 4. Commercially available plastic probes have long been used when investigating the depth o the peri-implant sulcus (12). Recent literature recommends the use o conventional metal periodontal probes i probing pressures are kept light (53). Light lateral orces on the probe will protect against damaging titanium sur aces. H owever, plastic probes are more f exible and sometimes advantageous in probing excessive contours and angles ound in implant restorations. B. Clinical attachment levels can be used to monitor peri-implant health. 1. To interpret probe readings, the clinician must have baseline data recording previous probing levels o attachment, and a xed re erence point or repeatable probing comparisons. a. Initial probing o the implant should be done once the nal restoration has been installed. Probing depth should be recorded and de ned as the depth o probe penetration rom the base o the implant sulcus to the crest o the mucosa. Similar to assessing natural teeth, the level o the crestal so t tissue can be measured using a xed re erence point on the restoration and should be noted as the clinical attachment level. b. Changes in probing attachment levels over time may be more important than the initial f ndings as implants may have deeper so t tissue probing depths. Due to variation in the depth o surgical placement, the tissue thickness at the site, as well as di erent lengths o the abutments and the connective tissue inter ace with the abutment, probing depths may be deeper than the 1- to 3-mm depths that are considered normal with natural teeth. c. A healthy peri-implant sulcus has been reported to range rom 1.3 to 3.8 mm (54). 2. The depth o penetration o the probe tip also is dependent on the health (or inf ammatory stage o the peri-implant tissues) and thickness o the tissue around the abutment.

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2. Bleeding and Suppuration A. Bleeding on probing is a good indicator o current tissue inf ammation and should be recorded. 1. L ack o bleeding on gentle probing is use ul in predicting continuing tissue health around implants. 2. Elimination o the bleeding on probing in peri-implant mucositis is important and should be accomplished with improved bio lm removal by the clinician and the patient. 3. Increasing probing depth and bleeding are indicators or the need to per orm an additional radiographic examination (15,55). B. Any suppuration should also be recorded at speci c sites. Suppuration may be detected by probing, or by gently compressing the tissue over the implant with a gloved nger and observing or pus being expressed rom the opening o the sulcus or pocket. 3. Radiographs A. M aintenance o bone levels around dental implants is an important criterion or determining treatment success. Radiographic evaluation o bone height and topography is necessary or the longitudinal monitoring o peri-implant stability (9,12,51,52). 1. Vertical bone loss o less than 0.2 mm annually ollowing the implant’s rst year o unction is a criterion utilized to determine treatment success. 2. Baseline radiographs should include the day o surgical implant placement, the day o nal prosthesis insertion and periodically during implant maintenance (22). Bone remodeling during the rst year a ter the nal prosthesis insertion is expected, and then there should be less than 0.2 mm o bone loss annually therea ter. 3. The shape and amount o bone remodeling ollowing the nal prosthesis insertion is di erent or di erent implant systems and con gurations. 4. I prior radiographs are not available, use 2 mm o bone loss rom the expected bone level or the implant at that time point as the “ decision point” or the diagnosis o peri-implantitis (53). 5. Radiographs made on the day o the nal prosthesis insertion (or re-cementation) should be reviewed or the presence o remaining excess cement. Cements that are visible radiographically should be used or implant restorations, especially i the margins and probable location o excess cements are subgingival. 6. Radiographs also allow or the evaluation o the t o the prosthesis and the integrity and adaptation o the di erent implant components. B. Dental implants should be evaluated radiographically at least once a year and should be checked more o ten in patients in whom periodontal breakdown around an implant was noted at a previous visit.

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Se ct io n 4

Mainte nance The rap fo r De ntal Implants O ne o the most important actors in the long-term success o dental implants is the maintenance o the health o the peri-implant tissues. Success ul maintenance requires the active participation o the patient and the dental team. 1. Considerations or Implant Maintenance A. Goals o Maintenance Therapy or Dental Implants 1. Maintenance o Alveolar Bone Support a. Alveolar bone support is evaluated by use o good-quality radiographs taken with a long-cone paralleling technique at speci c time intervals. b. The bone height and density around the implants is compared with previous radiographs o the site. 2. Control o In ammation a. Patient and pro essional bio lm control is important or proper gingival health. b. Patient sel -care must be reevaluated and, i necessary, rein orced each time the patient is seen or maintenance. The better the patient sel -care, the better the possibilities o maintaining stable results. 3. Maintenance o a Healthy and Functional Implant a. Implant components should be checked or prosthesis integrity (such as mobility, loose screws, cement washout, material wear), implant, screw, or abutment racture; unseating o attachments and proper adaptation o all components. b. Any mobility o an implant or its restorative components requires immediate consultation with a dentist or specialist. B. Patient Provided In ormation. Be ore beginning an examination, it is very important to obtain in ormation rom the patient related to implant-supported restorations or prostheses. The patient can o ten identi y problems or clinicians that are otherwise di cult to nd. Implant patients should be encouraged to share their perceptions o any changes in the t, tightness, or eel o the implant restoration including the occlusion. H elp ul questions to ask the patient include the ollowing: 1. Questions About Daily Sel -care o Implant-supported Restorations/ Prosthesis a. Are you able to clean around the neck portions o your implants easily? b. Do you still have enough cleaning aids to per orm daily oral sel -care? 2. Questions Concerning Patient Satis action. General questions regarding the patient’s satis action with the implant-supported restorations/prosthesis are part o a quality management concept or maintenance. a. Are you satis ed with the way your implants unction? b. Are you satis ed with the appearance o your implants? 3. Questions Regarding Patient-perceived Changes Since Last Appointment a. Do you think any part o the implant is loose? b. Do the gums around your implants bleed? c. Do you notice a bad taste coming rom your implants? d. H ave you noticed any changes in your implants? C. The Dental Implant Maintenance Visit 1. M odern dental implants may be di cult to recognize intraorally since their restorations o ten have the same appearance as the crowns and xed bridges used to restore natural teeth (Fig. 31-12). For this reason, dental implants should be clearly noted in the chart, so that all dental team members are

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alerted to the act that this is a dental implant patient. Also, the patient’s radiographs should be reviewed be ore the start o periodontal instrumentation. 2. The ollowing may be included in a maintenance visit; however, each maintenance visit should be individualized based on previous examinations, history, and judgment o the clinician: evaluation o peri-implant tissue health, examination o prosthesis/abutment components, evaluation o implant stability, occlusal examination, assessment o patient’s sel -care, radiographic examination, and treatment (e.g., periodontal instrumentation). D. Maintenance Frequency 1. M aintenance intervals should be determined on an individual basis because there is a lack o data detailing precise intervals (4). a. A 3-month maintenance interval is usually appropriate or the rst year ollowing restoration o the implant (12). The clinician, however, must determine the best interval or each speci c case. b. A ter the initial 12-month period, a 3- to 6-month maintenance interval may be used (56). Periodontal maintenance appointments should be scheduled as requently as necessary to keep the periodontium and periimplant tissues healthy. c. The risk actors identi ed or each patient are essential in the estimation o the prognosis or the implants and these actors should be included in the determination o the appropriate maintenance interval. 2. The ollowing are indications or more requent maintenance intervals. a. Reduced Bone Support Around Implants. Reduced bone support indicates that close monitoring o bone support is needed or the dental implant might be lost. b. Inf ammation. A patient who has signs o inf ammation around implants, even in the presence o good plaque control, needs more requent maintenance visits. c. H ost Response. Systemic conditions or diseases, such as diabetes, may a ect the host-bacterial interaction. A shorter maintenance interval is needed or these patients.

Fi re 31-12. Fixe d Pro sthe tic Cro w n. The irst premolar in this photo is a prosthetic crown supported by a dental implant. During an intraoral examination, it would be di icult to distinguish between a crown that is supported by a natural tooth and a crown supported by a dental implant.

2. Procedures or Pro essional Biof lm Removal A. Plastic Curets or Biof lm Removal. Traditionally, plastic curets have been used or pro essional bio lm removal rom dental implants. B. A Recent Innovation in Biof lm Management: Subgingival Air Polishing 1. Air polishing technology uses a combination o an abrasive powder with water and compressed air delivered to a tooth or implant sur ace through an air polishing nozzle. Recently an air polishing device—H u-Friedy M anu acturing’s

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A ir-Flow Perio—has been introduced in the United States and Canada that utilizes a specially designed subgingival nozzle and low-abrasive glycine-based powder or subgingival bio lm removal. 2. The Unique Technology or Subgingival Air Polishing a. Subgingival air polishing devices use a specially designed disposable nozzle to deliver a low-abrasive powder to the subgingival environment. b. Subgingival air polishing uses a glycine-based powder that is biocompatible and gentle on the so t tissues o the oral cavity and subgingival epithelium (57–59). c. Prior to using this new technology, clinicians require special training in the proper use o the subgingival air polishing device. Explaining the techniques or use o subgingival glycine powder air polishing is beyond the scope o this chapter, but clinicians should be aware o this emerging technology and seek ormal training in its use. 3. Clinical Evidence or Subgingival Air Polishing with Glycine Air Polishing o Dental Implants a. Subgingival air polishing or the removal o bio lm rom titanium sur aces is a relatively new technology with clinical research supporting its sa ety and e cacy or use in the treatment o peri-implant disease. 1. Although subgingival air polishing is an emerging technology in the United States and Canada, this technology has been used and researched or several years in Europe. 2. It is important to note, that subgingival air polishing will not remove calculus deposits. 3. In June 2012, during the Euro-Perio 7 Con erence in Vienna (59), a consensus con erence on mechanical bio lm management took place to review the current evidence rom the literature on the clinical relevance o subgingival use o air polishing and to make practical recommendations or the clinician. b. Box 31-1 summarizes these recommendations, as well as, additional current evidence rom the literature on subgingival bio lm management.

Bo x 31-1. S mmar o f C rre nt Evide nce o n S b in ival Air Po lishin o f Titani m S rface s • Glycin owd o lis in g is s nd c iv o n i n iu m su c s o d n l im l n s (60,61). owd i o lis in g is m o c iv n d l ss in v siv n l s ic cu s o • Glycin m in n n c o i-im l n so issu s (62,63). • Su b g in g iv l g lycin owd i o lis in g m y d u c clin ic l sig n s o i-im l n i is ( io d o n l d s u c io n o u n d d n l im l n ) o g x n l iv o in s u m n io n u sin g cu s w i d ju n c iv i ig io n w i c lo xid in (48,64). • Glycin owd i o lis in g s o n ly m in u c on su c o o g yo d n im l n s (65). • Clin ic l, m ic o b io lo g ic l, n d is o lo g ic l s u d i s v co n f m d su b g in g iv l g lycin owd i o lis in g is s , f ci n , n d co m o b l w n u s d s co m m n d d b y in d o ssio n l (57,59,66–68).

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3. Periodontal Instrumentation o Dental Implants A. Special Considerations in Instrumentation Selection 1. The use o traditional metal curets is contraindicated around titanium implant components (56,69–72). Implant components are made o titanium, a so t metal, or titanium alloy that can be permanently damaged (grooved, scratched) i treated with metal instruments (Fig. 31-13). a. There is an increased likelihood o plaque retention and peri-implantitis i the titanium is scratched. b. M etal instruments can also disturb the sur ace coating o the implant, reducing the biocompatibility with the peri-implant tissues. c. The use o ultrasonic or sonic devices with standard metal tips is also contraindicated on titanium sur aces. Several manu acturers, however, o er specialized ultrasonic tips or use on titanium sur aces. 2. Instruments used or assessment and periodontal instrumentation o implants and other titanium sur aces should be made o a material that is so ter than the implant. Plastic instruments are commonly used (Fig. 31-14). a. Plastic instruments are sa e or use on all types o implants, abutments, and components and will not cause damage to the sur ace. b. Standard dental restorative materials; or example, gold and porcelain; can be cleaned with conventional periodontal instruments. Care must be taken, however, not to use these instruments apical to the margin o the prosthetic crown where titanium might be in contact. c. Usually calculus deposits are removed readily rom smooth titanium sur aces because there is no interlocking or penetration o the deposit with the sur ace. Light lateral pressure with a plastic instrument is recommended. Some calculus deposits, however, are densely calci ed and tenaciously attached to the titanium sur ace and require more vigorous removal attempts. In such cases, powered instrumentation with specially designed ultrasonic tips may be help ul.

Fi re 31-13. S rface Dama e fro m Impro pe r Instr me ntatio n. Metal instruments can scratch the sur ace o the implant. (Courtesy o Drs. Mota and Baumhammers, University o Pittsburgh School o Dental Medicine, Pittsburg, PA.)

Fi re 31-14. Plastic C re t. Plastic instruments are sa e or use on dental implants.

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3. Residual dental cement is a requent nding when restorations have been cemented to abutments. These residual deposits are a de nite contributor to periimplant disease (36,37). Cement deposits are typically located subgingivally and are challenging to detect, especially i the cement is not visible radiographically. In addition, some o the advanced cement ormulations used today are extremely strong and removal is very di cult. I removal e orts are not success ul in a short time period, surgical access should be accomplished. 4. Some sur aces in implant systems are intended and manu actured to be rough. Rough sur aces are very common on portions or all o the implant body. These sur aces are usually intended to be adjacent to bone and not exposed to the oral environment. I an intentionally rough sur ace becomes exposed to the oral cavity, it will need to be cleaned and deplaqued as part o implant maintenance. N onmetal instruments and air abrasives are the appropriate choices or instrumentation o such sur aces (71). B. Special Considerations or Polishing 1. Implants, abutments, and components do not require routine polishing. a. When indicated, polishing o the implant restoration can be accomplished with rubber cups and nonabrasive polishing paste or by supragingival air polishing (12,56,71,73–78). b. Polishing has been shown to improve titanium sur aces that have previously been roughened or scratched. H owever, i no sur ace alterations are noted, the titanium sur aces should not be polished. c. A systematic review by Louropoulou o 34 papers indicates that or rough implant sur aces, air abrasives are the instruments o choice i sur ace integrity needs to be maintained (71). Air polishing with glycine powder may be considered as a better method to remove plaque bio lm rom dental implants because glycine is less aggressive than sodium bicarbonate powder (74). 4. Patient Sel -care o Dental Implants A. Considerations 1. M eticulous sel -care is o the utmost importance in preventing peri-implant disease. An individualized sel -care routine should be developed or each patient. 2. Some patients undergoing implant therapy may have had a long history o dental neglect and/or poor plaque bio lm control. 3. The dental hygienist can assist the patient in maintaining dental implants by providing sel -care education appropriate or implants and home care devices that are e ective and simple to use. B. Care o Fixed Prosthetic Restorations 1. A xed prosthetic crown is an arti cial tooth that ts over the abutment. These are made rom a variety o routinely encountered restorative materials. 2. Sel -care Challenges a. The single tooth prosthesis (crown) can present a challenge or bio lm control in that the patient may quickly begin to regard it to be just the same as a natural tooth. 1. In act, these restorations o ten have di erent designs and unusual contours that require ocused sel -care attention. The better the patient understands the design and contours, etc. that must be cleaned, the better the oral hygiene e ectiveness will be. 2. Sel -care practices must be modi ed to include aids that can e ectively clean the altered morphology o the peri-implant region.

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Fi re 31-15. Implant Se lf-care . Dental loss is used to clean a single implant with a prosthetic crown. The “ bulky” contours o the crown may contact the tissue and then “ dip in” to meet the abutment at or below the gingival margin.

b. The crown covering the implant abutment is larger in circum erence than the abutment and will have contours added to it to make it look and unction like a natural tooth. 1. The “ bulky” contours o the crown may contact the tissue and then “ dip in” to meet the abutment at or below the gingival margin. 2. Dental f oss or tu ted dental f oss should be adapted along the margin o the crown and then pulled gently back and orth to direct it into the sulcus and around the abutment (Fig. 31-15). c. In some cases, the restoration may be similar to a xed bridge (e.g., a pontic supported by two dental implants). Tu ted dental f oss, specially designed interdental brushes, and water f ossers are e ective cleaning devices or deplaquing the large embrasure spaces and into the sulci o these xed bridge-type restorations. d. Restoration o multiple tooth replacement situations can involve complex, denture-like prostheses, which are attached to multiple implants and which are not removable by the patient. 1. These prostheses are removable by the dentist or specialist at which time cleaning access is optimal. 2. Daily care by the patient requires an individualized plan and a combination o devices to overcome the limited access o ten encountered. 3. Techniques and Devices a. Standard multitu ted, so t nylon bristle, manual toothbrushes can be used e ectively by patients having su cient dexterity and understanding o the task. b. Powered toothbrushes are sa e or titanium sur aces and these devices are particularly help ul or implant patients in general. c. Interdental brushes can be e ective in bio lm removal and may e ectively clean the peri-implant sulcus (78). 1. Note that interdental brushes used to clean implants and components should have a so t protective coating on the twisted wire that secures the bristles. 2. The use a standard interdental brush (that does not have a plastic or nylon coating on the twisted wire) should be avoided since the exposed wire could scratch titanium.

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d. Dental f oss can be used with dental implants. Patients must be instructed as to the gentle use o dental f oss in sometimes deep subgingival areas. Flosses with expanded spongy or f u y sections along with a sti er, f oss threader section (tu ted f oss) are particularly help ul. e. O ral irrigators may be sa ely used to deplaque dental implants. 1. In a study, M agnuson et al. compared the e cacy o a manual toothbrush paired with either traditional dental f oss or a water f osser. The study results demonstrate that the water f ossing group had statistically signi cantly greater reduction in bleeding than the dental f oss group. The authors conclude that water f ossing may be a use ul adjunct to implant maintenance (79). 2. Patients should be instructed to use the lowest setting and direct the f ow through the interdental contacts or perpendicular to the implants rather than directly into the implant sulcus (78). . Daily use o an antimicrobial mouth rinse is bene cial or many patients (80,81). The entire mouth can be rinsed twice daily a ter brushing. O r, i that is not acceptable to the patient, the mouth rinse can be applied topically to each implant area twice daily with a cotton-tipped applicator or with gauze. C. Care o a Removable Prosthesis 1. An implant supported removable prosthesis is similar to a traditional ull denture except that in the case o implants, it is attached to the abutments by devices such as o-rings, magnets, or clips (Fig. 31-16). a. This type o prosthesis can also be designed as an implant and tissue supported prosthesis or as an overdenture. b. The patient can remove the prosthesis to clean it, the attachment devices, the abutments, and the remainder o the mouth. 2. Techniques and Tools a. Selection o cleaning devices or the abutments that support a removable prosthesis should be based on the knowledge that implant components are made rom titanium, which is a relatively so t metal. b. Cleaning devices must be selected or ease o use by each individual patient, and the recommendation o ewer, rather than more, devices is best. The cleaning aids that are recommended should be demonstrated or the patient and then evaluated by the hygienist to veri y their e ective use by the patient. c. In some cases, a metal bar connects the abutments and is used to attach the prosthetic denture in the mouth. Tu ted dental f oss or an un olded 2 × 2 gauze square can be use ul in cleaning underneath the metal bar and around the abutments (Fig. 31-17). d. Patients who have limited ability or poor success with mechanical plaque removal will bene t rom the daily use o an antimicrobial mouth rinse (80,81). The entire mouth can be rinsed twice daily a ter brushing. M outh rinses can be applied topically to the implant abutments or implants with cotton tipped applicators or other recommended cleaning devices i the patient cannot tolerate rinsing the entire mouth.

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O-rin g s Ab u tm e nt p o s ts

Fi re 31-16. Implant S ppo rte d Re mo vable Pro sthe sis. A: Abutment posts on the mandibular arch. B: An implant supported removable prosthesis is attached to the abutment posts by o-rings, magnets, or clips.

Fi re 31-17. Ab tme nts Jo ine d b Me tal Bar. Tu ted dental loss is use ul in cleaning the implant abutments and underneath the connecting metal bar.

Chapte r S mmar State me nt As dental implant therapy becomes more common, dental hygienists will care or increasing numbers o patients needing implant maintenance. A signi cantly higher incidence o peri-implantitis is ound in patients with a history o periodontitis. The primary goals o treatment or peri-implantitis are to stop disease progression and maintain the implant in unction with healthy peri-implant tissues. Frequent pro essional maintenance is the most important step in the avoidance o peri-implantitis. An important role o the dental hygienist is the education o patients on the importance o meticulous sel -care and requent maintenance visits. Implant restorations necessitate customized sel -care instructions and devices. Implant maintenance appointments should include monitoring o plaque bio lm levels, examination o so t tissues, assessment o the restorative integrity, rein orcement o patient sel -care measures, periodontal instrumentation o implant abutments and prostheses, and radiographic examination.

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Se ct io n 5

Fo c s o n Patie nts Clinical Patie nt Care CA S E 1 While you are per orming nonsurgical therapy on a chronic periodontitis patient, the patient tells you that he is thinking about having all o his teeth removed since they are not healthy anyway, and just having some implants placed. H e tells you that this would be easier since he would not have to worry about the implants like he does his teeth. H ow should you respond?

CA S E 2 You are scheduled to record the in ormation needed to make a periodontal diagnosis or a patient new to your dental team. Radiographs have not yet been ordered or the patient. As you begin your probing, the patient in orms you that she has two dental implants. Visual examination o the patient’s dentition does not immediately reveal which teeth are replaced by the implants. H ow should you proceed?

CA S E 3 At a maintenance visit or one o your team’s patients you note obvious mobility o a crown supported by an implant. H ow should you (the dental hygienist) proceed?

Re fe re nce s 1. Albrektsson T, Dahl E, Enbom L, et al. O sseointegrated oral implants. A Swedish multicenter study o 8139 consecutively inserted N obelpharma implants. J Periodontol. 1988;59(5):287–296. 2. Cochran DL, N ummikoski PV, School eld JD, et al. A prospective multicenter 5-year radiographic evaluation o crestal bone levels over time in 596 dental implants placed in 192 patients. J Periodontol. 2009;80(5):725–733. 3. Fugazzotto PA, Gulbransen H J, Wheeler SL, et al. The use o IM Z osseointegrated implants in partially and completely edentulous patients: success and ailure rates o 2,023 implant cylinders up to 60+ months in unction. Int J O ral M ax illo ac Im plants. 1993;8(6):617–621. 4. Iacono VJ, Committee on Research, Science and Therapy, the American Academy o Periodontology. Dental implants in periodontal therapy. J Periodontol. 2000;71(12):1934–1942. 5. Patrick D, Z osky J, Lubar R, et al. Longitudinal clinical e cacy o Core-Vent dental implants: a ve-year report. J O ral Im plantol. 1989;15(2):95–103. 6. Sbordone L, Barone A, Ciaglia RN , et al. Longitudinal study o dental implants in a periodontally compromised population. J Periodontol. 1999;70(11):1322–1329. 7. Spiekermann H , Jansen VK, Richter EJ. A 10-year ollow-up study o IM Z and TPS implants in the edentulous mandible using bar-retained overdentures. Int J O ral M ax illo ac Im plants. 1995;10(2):231–243. 8. Lang N P, Karring T, British Society o Periodontology. Proceedings o the 1st European W ork shop on Periodontology, Charter H ouse at Ittingen, T hurgau, Sw itzerland, February 1–4, 1993. London: Q uintessence Publishing Co Inc.; 1994:478. 9. Bader H . Implant maintenance: a chairside test or real-time monitoring. D ent Econ. 1995;85(6):66–67. 10. Lang N P, Karring T, Lindhe J, European Federation o Periodontology, European Association o O sseointegration, Swiss Society o Periodontology. Proceedings o the 3rd European W ork shop on Periodontology: im plant dentistry: Charter H ouse at Ittingen, T hurgau, Sw itzerland, January 30–February 3, 1999. Berlin: Q uintessence Publishing Co Inc.; 1999:615. 11. N evins M , Langer B. The success ul use o osseointegrated implants or the treatment o the recalcitrant periodontal patient. J Periodontol. 1995;66(2):150–157. 12. Silverstein L, Garg A, Callan D, et al. The key to success: maintaining the long-term health o implants. D ent Today. 1998;17(2):104, 106, 108–111. 13. Albrektsson T, Z arb G, Worthington P, et al. The long-term e cacy o currently used dental implants: a review and proposed criteria o success. Int J O ral M ax illo ac Im plants. 1986;1(1):11–25. 14. Salvi GE, Aglietta M , Eick S, et al. Reversibility o experimental peri-implant mucositis compared with experimental gingivitis in humans. Clin O ral Im plants R es. 2012;23(2):182–190.

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15. Lang N P, Berglundh T, Working Group 4 o Seventh European Workshop on Periodontology. Periimplant diseases: where are we now?–Consensus o the Seventh European Workshop on Periodontology. J Clin Periodontol. 2011;38(suppl 11):178–181. 16. M ahesh L, Kurtzman GM , Shukla S. M icrobiology o peri-implant in ections. Sm ile D ent J. 2011;6:54–57. 17. Pye AD, Lockhart DE, Dawson M P, et al. A review o dental implants and in ection. J H osp In ect. 2009;72(2):104–110. 18. Atieh M A, Alsabeeha N H , Faggion CM Jr., et al. The requency o peri-implant diseases: a systematic review and metaanalysis. J Periodontol. 2013;84(11):1586–1598. 19. Koldsland O C, Scheie AA, Aass AM . Prevalence o peri-implantitis related to severity o the disease with di erent degrees o bone loss. J Periodontol. 2010;81(2):231–238. 20. M arrone A, Lasserre J, Bercy P, et al. Prevalence and risk actors or peri-implant disease in Belgian adults. Clin O ral Im plants R es. 2013;24(8):934–940. 21. Roos-Jansaker AM , Lindahl C, Renvert H , et al. N ine- to ourteen-year ollow-up o implant treatment. Part II: presence o peri-implant lesions. J Clin Periodontol. 2006;33(4):290–295. 22. Rosen P, Clem D, Cochran D, et al. Peri-implant mucositis and peri-implantitis: a current understanding o their diagnoses and clinical implications. J Periodontol. 2013;84(4):436–443. 23. H eitz-M ay eld LJ, Lang N P. Comparative biology o chronic and aggressive periodontitis vs. peri-implantitis. Periodontol 2000. 2010;53:167–181. 24. M ombelli A, Lang N P. Antimicrobial treatment o peri-implant in ections. Clin O ral Im plants R es. 1992;3(4):162–168. 25. Q uirynen M , De Soete M , van Steenberghe D. In ectious risks or oral implants: a review o the literature. Clin O ral Im plants R es. 2002;13(1):1–19. 26. Renvert S, Roos-Jansaker AM , Lindahl C, et al. In ection at titanium implants with or without a clinical diagnosis o inf ammation. Clin O ral Im plants R es. 2007;18(4):509–516. 27. Shibli JA, M artins M C, Lotu o RF, et al. M icrobiologic and radiographic analysis o ligature-induced peri-implantitis with di erent dental implant sur aces. Int J O ral M ax illo ac Im plants. 2003;18(3):383–390. 28. Shibli JA, M elo L, Ferrari DS, et al. Composition o supra- and subgingival bio lm o subjects with healthy and diseased implants. Clin O ral Im plants R es. 2008;19(10):975–982. 29. Karoussis IK, Kotsovilis S, Fourmousis I. A comprehensive and critical review o dental implant prognosis in periodontally compromised partially edentulous patients. Clin O ral Im plants R es. 2007;18(6):669–679. 30. Klokkevold PR, H an TJ. H ow do smoking, diabetes, and periodontitis a ect outcomes o implant treatment? Int J O ral M ax illo ac Im plants. 2007;22(suppl):173–202. 31. Schou S, H olmstrup P, Worthington H V, et al. O utcome o implant therapy in patients with previous tooth loss due to periodontitis. Clin O ral Im plants R es. 2006;17(suppl 2):104–123. 32. Van der Weijden GA, van Bemmel KM , Renvert S. Implant therapy in partially edentulous, periodontally compromised patients: a review. J Clin Periodontol. 2005;32(5):506–511. 33. H eitz-M ay eld LJ, H uynh-Ba G. H istory o treated periodontitis and smoking as risks or implant therapy. Int J O ral M ax illo ac Im plants. 2009;24(suppl):39–68. 34. H inode D, Tanabe S, Yokoyama M , et al. Inf uence o smoking on osseointegrated implant ailure: a meta-analysis. Clin O ral Im plants R es. 2006;17(4):473–478. 35. Strietzel FP, Reichart PA, Kale A, et al. Smoking inter eres with the prognosis o dental implant treatment: a systematic review and meta-analysis. J Clin Periodontol. 2007;34(6):523–544. 36. Linkevicius T, Puisys A, Vindasiute E, et al. Does residual cement around implant-supported restorations cause peri-implant disease? A retrospective case analysis. Clin O ral Implants Res. 2013;24(11):1179–1184. doi:10.1111/j.1600-0501.2012.02570.x. 37. Wilson TG Jr. The positive relationship between excess cement and peri-implant disease: a prospective clinical endoscopic study. J Periodontol. 2009;80(9):1388–1392. 38. H udieb M I, Wakabayashi N , Kasugai S. M agnitude and direction o mechanical stress at the osseointegrated inter ace o the microthread implant. J Periodontol. 2011;82(7):1061–1070. 39. Rungsiyakull C, Rungsiyakull P, Li Q, et al. E ects o occlusal inclination and loading on mandibular bone remodeling: a nite element study. Int J O ral M ax illo ac Im plants. 2011;26(3):527–537. 40. Ericsson I, Lindhe J. Probing depth at implants and teeth. An experimental study in the dog. J Clin Periodontol. 1993;20(9):623–627. 41. Lang N P, Wetzel AC, Stich H , et al. H istologic probe penetration in healthy and inf amed peri-implant tissues. Clin O ral Im plants R es. 1994;5(4):191–201. 42. M ahesh L, Kurtzman GM , Bali P, et al. Treatment o peri-implantitis. Inside D entistry. 2013;9(3):84–90. 43. Kammerer PW, Lehmann KL, Karbach J, et al. Prevalence o peri-implant disease associated with a rough-sur ace dental implant system: 9 years a ter insertion. Int J O ral Im plantol Clin R es. 2011;2(3):135–139. 44. Porras R, Anderson GB, Ca esse R, et al. Clinical response to 2 di erent therapeutic regimens to treat peri-implant mucositis. J Periodontol. 2002;73(10):1118–1125. 45. Renvert S, Lessem J, Lindahl C, et al. Treatment o incipient peri-implant in ections using topical minocycline microspheres versus topical chlorhexidine gel as an adjunct to mechanical debridement. J Int A cad Periodontol. 2004;6(4 suppl):154–159. 46. Renvert S, Polyzois I, Persson GR. Treatment modalities or peri-implant mucositis and peri-implantitis. A m J D ent. 2013;26(6):313–318. 47. Schar D, Ramseier CA, Eick S, et al. Anti-in ective therapy o peri-implantitis with adjunctive local drug delivery or photodynamic therapy: six-month outcomes o a prospective randomized clinical trial. Clin O ral Implants Res. 2013;24(1):104–110. 48. M uthukuru M , Z ainvi A, Esplugues EO, et al. N on-surgical therapy or the management o peri-implantitis: a systematic review. Clin O ral Im plants R es. 2012;23(suppl 6):77–83. 49. H eitz-M ay eld LJ, N eedleman I, Salvi GE, et al. Consensus statements and clinical recommendations or prevention and management o biologic and technical implant complications. Int J O ral M ax illo ac Im plants. 2014;29(suppl):346–350. 50. Etter TH , H akanson I, Lang N P, et al. H ealing a ter standardized clinical probing o the periimplant so t tissue seal: a histomorphometric study in dogs. Clin O ral Im plants R es. 2002;13(6):571–580. 51. Cochran D. Implant therapy I. A nn Periodontol. 1996;1(1):707–791. 52. Papaioannou W, Q uirynen M , N ys M , et al. The e ect o periodontal parameters on the subgingival microbiota around implants. Clin O ral Im plants R es. 1995;6(4):197–204. 53. Sanz M , Chapple IL, Working Group 4 o the VIII European Workshop on Periodontology. Clinical research on peri-implant diseases: consensus report o Working Group 4. J Clin Periodontol. 2012;39(suppl 12):202–206.

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54. van Steenberghe D, Klinge B, Linden U, et al. Periodontal indices around natural and titanium abutments: a longitudinal multicenter study. J Periodontol. 1993;64(6):538–541. 55. Lindhe J, M eyle J, Group D o European Workshop on Periodontology. Peri-implant diseases: consensus report o the sixth European workshop on periodontology. J Clin Periodontol. 2008;35(8 suppl):282–285. 56. Eskow RN , Smith VS. Preventive periimplant protocol. Com pend Contin Educ D ent. 1999;20(2):137–142, 144, 146 passim; quiz 54. 57. Petersilka GJ, Tunkel J, Barakos K, et al. Subgingival plaque removal at interdental sites using a low-abrasive air polishing powder. J Periodontol. 2003;74(3):307–311. 58. Sahrmann P, Ronay V, Schmidlin PR, et al. Three-dimensional de ect evaluation o air polishing on extracted human roots. J Periodontol. 2014;85(8):1107–1114. 59. Sculean A, Bastendor KD, Becker C, et al. A paradigm shi t in mechanical bio lm management? Subgingival air polishing: a new way to improve mechanical bio lm management in the dental practice. Q uintessence Int. 2013;44(7):475–477. 60. Sahrmann P, Ronay V, Sener B, et al. Cleaning potential o glycine air-f ow application in an in vitro peri-implantitis model. Clin O ral Im plants R es. 2013;24(6):666–670. 61. Schwarz F, Ferrari D, Popovski K, et al. Inf uence o di erent air-abrasive powders on cell viability at biologically contaminated titanium dental implants sur aces. J Biom ed M ater R es B A ppl Biom ater. 2009;88(1):83–91. 62. M ussano F, Rovasio S, Schierano G, et al. The e ect o glycine-powder airf ow and hand instrumentation on peri-implant so t tissues: a split-mouth pilot study. Inter J Prosthodont. 2013;26(1):42–44. 63. Schmage P, Kahili F, N ergiz I, et al. Cleaning e ectiveness o implant prophylaxis instruments. Int J O ral M ax illo ac Im plants. 2014;29(2):331–337. 64. Sahm N , Becker J, Santel T, et al. N on-surgical treatment o peri-implantitis using an air-abrasive device or mechanical debridement and local application o chlorhexidine: a prospective, randomized, controlled clinical study. J Clin Periodontol. 2011;38(9):872–878. 65. Sahrmann P, Ronay V, H o er D, et al. In vitro cleaning potential o three di erent implant debridement methods. Clin O ral Im plants R es. 2013. doi:10.1111/clr.12322. 66. Graumann SJ, Sensat M L, Stoltenberg JL. Air polishing: a review o current literature. J D ent H yg. 2013;87(4):173–180. 67. Petersilka GJ. Subgingival air-polishing in the treatment o periodontal bio lm in ections. Periodontol 2000. 2011;55(1):124– 142. doi:10.1111/j.1600-0757.2010.00342.x. 68. Petersilka GJ, Steinmann D, H aberlein I, et al. Subgingival plaque removal in buccal and lingual sites using a novel low abrasive air-polishing powder. J Clin Periodontol. 2003;30(4):328–333. 69. Guidelines or periodontal therapy. The American Academy o Periodontology. J Periodontol. 1998;69(3):405–408. 70. Supportive periodontal therapy (SPT). J Periodontol. 1998;69(4):502–506. 71. Louropoulou A, Slot DE, Van der Weijden FA. Titanium sur ace alterations ollowing the use o di erent mechanical instruments: a systematic review. Clin O ral Im plants R es. 2012;23(6):643–658. 72. Speelman JA, Collaert B, Klinge B. Evaluation o di erent methods to clean titanium abutments. A scanning electron microscopic study. Clin O ral Im plants R es. 1992;3(3):120–127. 73. Chairay JP, Boulekbache H , Jean A, et al. Scanning electron microscopic evaluation o the e ects o an air-abrasive system on dental implants: a comparative in vitro study between machined and plasma-sprayed titanium sur aces. J Periodontol. 1997;68(12):1215–1222. 74. Cochis A, Fini M , Carrassi A, et al. E ect o air polishing with glycine powder on titanium abutment sur aces. Clin O ral Im plants R es. 2013;24(8):904–909. 75. H uband M L. Problems associated with implant maintenance. Va D ent J. 1996;73(2):8–11. 76. Jovanovic SA. Peri-implant tissue response to pathological insults. A dv D ent R es. 1999;13:82–86. 77. M atarasso S, Q uaremba G, Coraggio F, et al. M aintenance o implants: an in vitro study o titanium implant sur ace modi cations subsequent to the application o di erent prophylaxis procedures. Clin O ral Im plants R es. 1996;7(1):64–72. 78. M engel R, Buns CE, M engel C, et al. An in vitro study o the treatment o implant sur aces with di erent instruments. Int J O ral M ax illo ac Im plants. 1998;13(1):91–96. 79. M agnuson B, H arsono M , Stark PC, et al. Comparison o the e ect o two interdental cleaning devices around implants on the reduction o bleeding: a 30-day randomized clinical trial. Com pend Contin Educ D ent. 2013;34(Spec N o 8):2–7. 80. Balshi TJ. H ygiene maintenance procedures or patients treated with the tissue integrated prosthesis (osseointegration). Q uintessence Int. 1986;17(2):95–102. 81. Ciancio SG, Lauciello F, Shibly O, et al. The e ect o an antiseptic mouthrinse on implant maintenance: plaque and periimplant gingival tissues. J Periodontol. 1995;66(11):962–965.

STu DENT ANCILLARy RESOu RCES A wide variety o resources to enhance your learning and understanding o this chapter are available on . • Visit thePoint to access: • Audio Glossary • Animations • Suggested Readings • Answers to Review Q uestions • Case Studies

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This chapter reviews current literature f ndings concerning periodontitis as a potential contributing actor to the severity o certain systemic diseases. The possibility o an association between periodontal disease and systemic disease suggests that periodontal therapy may play a role in decreasing the incidence and severity o certain systemic diseases. Interpro essional relationships between dental team members and other healthcare providers should be established early to provide the highest standard o care or patients with systemic disease.

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• Contrast the terms “ association” and “ cause” between a given actor (A) and a systemic disease (B). • Educate patients at risk or cardiovascular diseases about the possible impact o periodontal in ection on cardiovascular health and encourage oral disease prevention and treatment services. • Educate pregnant women and those planning pregnancy regarding the possible impact o periodontal in ection on pregnancy outcomes and encourage preventive oral care and treatment services. • Educate patients with diabetes about the probable bidirectional association between periodontal disease and diabetes; encourage oral disease prevention and treatment services. • Educate amily members and caregivers about the association between periodontal disease and pneumonia in health-compromised seniors in hospitals and long-term care. • Establish collaborative relationships with other healthcare providers to insure the highest standard o care or periodontal patients with systemic diseases and conditions.

K

Tr s

Atherosclerosis Atheroma C-reactive protein Dyslipidemia Lipoprotein

Low–birth-weight in ants Preeclampsia Glycemic control HbA1C

Community-acquired pneumonia Hospital-acquired pneumonia Ventilator-associated pneumonia

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t S st

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Current research suggests that there may be a bidirectional relationship between oral health and systemic health (1). O n one hand, as discussed in Chapter 15, the presence o systemic disease may increase the likelihood o periodontal disease initiation or increase the severity o existing periodontitis. O n the other hand, the presence o a chronic oral in ection (periodontitis) may have an adverse e ect on an individual’s systemic health. Published evidence supports a modest association between periodontitis and some systemic conditions. Dental pro essionals should be aware that currently there is limited evidence to support or re ute an association between periodontitis and systemic disease (2). 1. Association versus Causality A. Association. A large body o evidence documents an association o periodontitis with several systemic conditions including cardiovascular/cerebrovascular problems, diabetes mellitus, preterm labor, low–birth-weight delivery, and pneumonia (3). Current data indicates that the relationship between periodontitis and systemic diseases is a complex one. B. Causation. An association between a given actor (A) and a health e ect (B) does not mean that the actor (A) caused the speci c disease (B). 1. For example, a cohort study nds that eating red meat is associated with a higher risk o heart disease. a. A reader o this study might incorrectly conclude that eating red meat causes heart disease. b. The study, however, showed that those who ate red meat actually had the lowest cholesterol levels (4). Instead this study demonstrates that a whole variety o unhealthy li estyle actors (smoking, no exercise, alcohol consumption, diet) are all associated with a higher risk o heart disease. There ore, the reader must be very cautious in leaping to the assumption that an association between actors A and B means that A causes B. 2. Based on available research it is not possible to prove causality between periodontitis and systemic disease (2,3–5). It is possible that the association is the result o common risk actors and not causality. 2. Possible Mechanisms or Impact on Systemic Disease. Three mechanisms have been postulated as to how periodontitis may modi y some aspect o certain systemic diseases to make those diseases more severe: (a) in ection, (b) inf ammation, and (c) immune response (6). All three o these mechanisms have the potential to impact the systemic inf ammatory/immune response that in turn may mediate a range o systemic diseases. A. In ection 1. A periodontal in ection is not limited to the periodontium or even the oral cavity (7,8). The everyday acts o chewing and tooth brushing disseminate whole bacteria and their products to other nonadjacent organs or body parts (7). 2. O ral bacteria rom periodontal lesions and the DN A o periodontal pathogens can survive in the blood stream and adhere to nonoral body sites causing in ections such as endocarditis, lung in ections, abscesses o the brain or liver, and atty deposits in the carotid arteries (9–11).

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B. Inf ammation 1. In ection o the periodontal pocket can disseminate inf ammatory mediators to the blood stream triggering signi cant systemic inf ammation (12,13). 2. Proinf ammatory mediators—such as IL-1β, IL-6, TN F-α , and PGE2 —produced locally in the inf amed periodontal tissues disseminate into the blood stream and have a systemic impact (12,13). C. Immune Response 1. In chronic periodontitis, bacterial antigens are processed and presented to body’s immune system and recognized by lymphocytes (T-lymphocytes and B-lymphocytes). In response to a microbial challenge, host immune cells secrete proinf ammatory mediators. As discussed in Chapter 14, it is clear that the body’s immune response plays a signi cant role in inf ammation and tissue destruction. 2. Systemic inf ammation, de ned by increased circulating TN F-α , is associated with obesity and periodontitis and has been proposed as a mechanism or the connection between these two conditions (14,15). Understanding o the mechanism in many inf ammatory systemic conditions, such as obesity, diabetes, rheumatoid arthritis, and cardiovascular disease is incomplete.

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c D s as

1. Periodontitis and Atherosclerotic Cardiovascular Diseases A. Atherosclerotic Cardiovascular Diseases 1. Atherosclerotic cardiovascular disease (ACVD) is a group o heart or vascular diseases including angina, myocardial in arction, stroke, transient ischemic attack (TIA), and peripheral artery disease. 2. Atherosclerosis, a major component o cardiovascular disease, is a process characterized by a thickening o artery walls. Complications that arise rom atherosclerosis cause deaths rom heart attack or stroke and have been reported to account or nearly three- ourths o all deaths rom cardiovascular disease. 3. An atheroma is a atty deposit in the inner lining o an artery; also called arterial plaque. B. Summary o Research Studies 1. A large body o evidence exists relevant to the association o periodontitis with cardiovascular disease (3). Severe periodontal disease has been linked to cardiovascular disease in cross-sectional and cohort studies (3,16–18). 2. It is important to note, however, insu f cient evidence exists to show that the treatment o periodontal disease can reduce the risk or cardiovascular disease. The impact o treatment or periodontitis on the cardiovascular disease is an area or ongoing research. C. Possible Biologic Explanations. How is Periodontitis Related to Cardiovascular Disease? Four biologic pathways have been proposed to explain the possible link between inf ammation due to periodontitis and cardiovascular disease (19). These proposed biologic mechanisms are summarized in Figure 32-1. 1. Inf ammatory Mediators From Periodontal Lesions may Heighten Systemic Inf ammation a. In this rst proposed pathway, periodontal in ections may contribute to atherosclerosis by repeatedly challenging the blood vessel walls and arterial walls with proinf ammatory mediators. b. Subgingival plaque bio lm provides a large and persistent source o periodontal pathogens and proinf ammatory mediators that can enter into the systemic blood stream. These bacteria activate the host inf ammatory response by multiple mechanisms (20). The host immune response acilitates atheroma ormation and exacerbation (19,21). c. Bacteria or proinf ammatory mediators rom periodontal lesions may stimulate inf ammatory responses in tissues and organs distant rom the oral cavity (22–24). Thus, the evidence suggests an association between periodontal in ections and a heightened state o systemic inf ammation (25). 1. C-reactive protein (CRP) is a special type o plasma protein—produced by macrophages, endothelial cells, and smooth muscle—that is present during episodes o acute inf ammation or in ection (3,26). CRP is an important cardiovascular risk predictor (27–30). Elevations in serum CRP are well-accepted risk actors or cardiovascular disease (29,30). 2. O ne hypothesis is that periodontitis is the source o the inf ammation that triggers the production o CRP (30). Serum CRP levels are elevated

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in individuals with periodontitis when compared to individuals without periodontitis (31–33). d. Evidence rom clinical and epidemiological studies suggests that inf ammation is important in atherosclerosis and cardiovascular disease. Bacteria or their products could promote inf ammatory changes that contribute to the development o atheromatous lesions ( atty deposits in the inner lining o an artery) (25). 2. Periodontitis may Initiate the Host Immune Response: Antibody CrossReactivity a. In this second proposed biologic pathway, periodontal in ections may contribute to atherosclerosis by inducing a local immune response. Patients with periodontitis have elevated systemic antibody responses to a variety o periodontal microorganisms and are able to induce antibody cross-reactivity (19). b. Cross-reactivity occurs when an antibody reacts with an antigen other than the one that induced its production. In this proposed pathway, the antibody reacts with the endothelial cells o the blood vessel walls instead o the periodontal pathogens (19). c. This pathway suggests that periodontal pathogens induce the body’s immune response to mistakenly target cells in blood vessels leading to vascular inf ammation and atherosclerosis.

P e riod ontitis

Ba c te re mia a nd p roin a mma tory me d ia tors

Ind ivid ua lize d hos t re s p ons e

1. In a mma tory me d ia tors from p e riod onta l le s ions e nte r the b lood s tre a m a nd he ighte n s ys te mic in a mma tion; p romoting thic ke ning of the a rte rie s

2. P e riod ontitis s timula te s the hos t immune s ys te m (a ntib od y c ros s -re a c tivity); le a d ing to va s c ula r in a mma tion a nd thic ke ning of the a rte rie s

3. P e riod ontitis e le va te s le ve ls of b rinoge n inc re a s ing va s c ula r in a mma tion; p la ying a role in thic ke ning of the a rte rie s a nd c lot forma tion

4. Periodontitis elevates levels of serum cholesterol and lipoproteins; accelerating thickening of the arteries

S ome or a ll of the a b ove p roc e s s e s ma y oc c ur in the p e riod ontitis p a tie nt

Inc re a s e d p o te ntia l fo r p la q ue fo rm a tio n in the inne r lining o f the a rte rie s o r e xa c e rb a tio n o f thic ke ning a nd ha rd e ning o f the a rte ry wa lls re s ulting in inc re a s e d ris k o f a the ro s c le ro tic c a rd io va s ula r d is e a s e s

F g r 32-1. Pro po s d B o lo g c Pat a s. A schematic representation showing the our biologic pathways that have been proposed to explain the possible link between in lammation due to periodontitis and cardiovascular disease.

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Periodontal—Systemic Associations

3. Periodontitis Elevates Levels o Fibrinogen: Increased Vascular Inf ammation a. In this third proposed biologic pathway periodontal in ections may contribute to atherosclerosis by increasing circulating levels o brinogen in the blood stream and playing a role in vascular inf ammation. b. Under normal circumstances, blood coagulation (blood clotting) is a protective process that slows and stops blood loss. For example, an individual cuts her nger and it starts to bleed. Immediately the platelets in the blood stream stimulate the production o thrombin. Thrombin, in turn, converts f brinogen into brin, a protein substance that orms a network o threadlike structures and causes the blood plasma to gel. The blood cells and plasma enmesh in the network o brils to orm a clot, stopping the f ow o blood to the cut in the nger. c. A hypercoagulable state is a medical term or an abnormally increased tendency toward coagulation. In ACVD, blood coagulation can have an adverse e ect when a blood clot orms in a coronary artery, obstructing blood f ow to the heart. d. The coagulation and brinolytic systems play important roles in the thickening o the arteries and clot ormation (34,35). Elevated f brinogen is a risk actor or atherosclerosis. e. The association o periodontitis with blood clotting actors has been reported by a number o investigators. 1. In an early study, Kweider reported that patients with periodontitis have higher plasma brinogen levels than age-matched control subjects (36). 2. Recent studies note increased brinogen levels in patients with periodontitis (37–40) and an association between the number o periodontal pockets and brinogen levels (41). 4. Periodontitis may Result in Dyslipidemia a. In this orth proposed pathway, periodontal in ections may contribute to atherosclerosis by elevating levels o serum cholesterol, as well as lowdensity lipoproteins (LDLs), triglycerides, and very low-density lipoproteins (vLDLs) (19). b. Dyslipidemia (dys·lip·id·e·mia) re ers to abnormal amounts o lipids (“ ats” ) and lipoproteins in the blood. A lipoprotein is a molecule that is a combination o lipid ( at) and protein. Lipoproteins are the orm in which lipids are transported in the blood. c. Several studies indicate that blood serum concentrations o inf ammatory lipids, including cholesterol, LDLs, triglycerides, and vLDLs are elevated in periodontitis patients. These inf ammatory lipids may more easily enter the blood vessel wall and there ore are more likely to be incorporated into the atherosclerotic lesion (thickening o the vessel wall). This would accelerate development o the local lesions (42–46). D. Implications or Dental Hygiene Practice 1. Dental healthcare providers should be aware o the emerging evidence that periodontitis is a risk actor or developing ACVD. Dental hygienists should educate patients at risk or cardiovascular diseases about the possible impact o periodontal in ection on cardiovascular health (47,48). 2. There is evidence suggesting that periodontal therapy reduces systemic inf ammation, but limited evidence on its e ects on cardiovascular health in the long term (49). Well-designed research studies are needed to clari y associations o poor periodontal health on ACVD (50).

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Part 7 Other Aspects o the Management o Patients with Periodontal Diseases

3. Comprehensive periodontal therapy should include patient education and advice on modi able li estyle risk actors such as smoking, diet, and exercise. Collaboration with appropriate specialists may acilitate the patient’s e orts in making li estyle modi cations (47,48). 4. Periodontitis patients—with other risk actors or ACVD, such as smoking, hypertension, obesity, etc.—who have not been seen by a physician within the last year should be re erred or a physical examination (47,48). 5. The American Journal o Cardiology and Journal o Periodontology published clinical recommendations or care o individuals with periodontitis (Table 32-1) (47).

TABLe 3 2 -1 . CLin iCAL Re COm m e n DATiOn S: PATie n TS w iTh Pe RiODOn TiTiS Co d t o Mo d

os v

CVD R sk Facto rs

R co

No n

In fo m

os v

io d o n i is

On kn o w n isk f c o

r co m m n d

(sm o kin g , f m ily is o y o f

if

CVD, ig Mild , m o d s v

i n

fo CVD sso ci

io d o n i is Mo d

dat o s

,o io d o n i is

t wo o mo f co s

c ol s

/s

s no

m yb d wi i n s

n in c

s d isk

io d o n i is k

d o n in

m d ic l v lu

io n

l s 12 m o

o l)

kn o w n isk

r f no

i n fo d o n in

m d ic l v lu

io n if

l s 12 m o

2. Periodontitis and Adverse Pregnancy Outcomes A. Introduction to Periodontitis and Adverse Pregnancy Outcomes 1. Adverse pregnancy outcomes that have been associated with periodontitis include preterm birth, low–birth-weight, and preeclampsia. The strength o this association, however, is modest (51). a. Preterm delivery o low–birth-weight in ants is a leading cause o neonatal death and o long-term neurodevelopmental disturbances and health problems in children. b. Preeclampsia is a serious complication o pregnancy characterized by an abrupt rise in blood pressure, large amounts o the protein albumin in the urine and swelling o the hands, eet, and ace. Preeclampsia occurs in the third trimester (the last third) o pregnancy. 2. Adverse pregnancy outcomes most likely involve additional shared risk actors with periodontitis, such as tobacco use, alcohol use, obesity, and diabetes. B. Two Possible Biologic Explanations. How is Periodontitis Related to Adverse Pregnancy Outcomes? Research demonstrates a modest association between periodontal disease and adverse pregnancy outcomes; however exact mechanisms remain unclear. Two major pathways have been proposed (52–54). Figure 32-2 shows these proposed biologic pathways. 1. Pregnant women with severe periodontitis may develop bacteremia more requently than those with healthy periodontium, exposing the etus to aggressive periodontal pathogens.

/s

s

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Periodontal—Systemic Associations

605

Periodontal dis eas e or infection Maternal age, weight, stature, smoking, ethnicity, stress, genetics

Maternal expos ure to periodontal pathogens and products In ammation triggers (TNF-α , IL-1)

Premature rupture of membranes , preterm birth, low–birth-weight, preeclamps ia, intrauterine fetal growth res triction

Fetal expos ure to periodontal pathogens

a fo r Asso c at o B t P r o do tal D s as a d Adv rs F g r 32-2. Pro po s d B o lo g c Pat Pr g a c O tco s. Reservoirs o gram-negative organisms, such as those ound in periodontitis, may have a negative impact on pregnancy outcome.

2. Proinf ammatory mediators produced within diseased periodontal tissues may enter the bloodstream and trigger systemic inf ammation, thus leading to adverse pregnancy outcomes. C. Implications or Dental Hygiene Practice 1. Several research studies show a signi cant association between chronic periodontitis and preterm delivery and low birth weight. Dental healthcare providers should be knowledgeable on the extent o these associations and their possible implications or health care. 2. The American Academy o Periodontology issued a statement in 2004, recommending, “ Women who are pregnant or planning pregnancy undergo periodontal examinations. Appropriate preventive or therapeutic services, i indicated, should be provided. Preventive oral care services should be provided as early in pregnancy as possible. H owever, women should be encouraged to achieve a high level o oral hygiene be ore becoming pregnant and throughout their pregnancies.” (55) 3. The European Federation o Periodontology and American Academy o Periodontology published clinical recommendations or care o emales o childbearing age with periodontitis (51). A dental healthcare pro essional assessing a emale patient o childbearing age should inquire whether she is currently pregnant or trying to become pregnant. I the patient responds a rmatively, the dental healthcare pro essional should always consider this pregnancy status in planning periodontal therapy. a. H ealth promotion in ormation should be provided including education about preventing and treating periodontal diseases or the oral health o the patient and uture oral health o her children. Dental hygienists should educate patients about the association between adverse pregnancy outcomes and periodontal in ection and provide early oral hygiene services or pregnant women and those considering pregnancy.

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b. The patient should be educated about periodontal events usually occurring during pregnancy such as increased tissue response to bio lm, increase in vascularity, and possibility o increased bleeding or gingival enlargement. c. The dental team should provide education on sel -care or bio lm control; with special emphasis on interdental cleaning. d. Periodontitis should be treated with nonsurgical periodontal therapy with the goal o reducing subgingival bio lm and the signs o periodontal inf ammation. Emphasize that all preventive, diagnostic, and periodontal therapeutic procedures are sa e throughout pregnancy. Elective procedures should be avoided in the rst trimester. e. The patient should be scheduled or periodontal maintenance at a later stage during pregnancy. . Interpro essional collaboration between the dental hygienist and other health pro essionals involved with pregnancy care are encouraged. 3. Periodontitis and Diabetes Mellitus A. Introduction to Periodontitis and Diabetes Complications. To date, research studies suggest that there is a two-way relationship between diabetes and periodontal disease (3,56–59). 1. First, it is clear that diabetes increases the risk or and severity o periodontal diseases (58,60). The American Diabetes Association’s Standard o M edical Care 2008 includes taking a history o past and current dental in ections as part o the physician’s examination (61,62). 2. Second, periodontal disease may exacerbate diabetes mellitus by signi cantly worsening glycemic control over time (62,63). B. Overview o Glycemic Control in Diabetes 1. O verview o Glycemic Control a. Glycemic control is a medical term re erring to the typical blood glucose levels in those with diabetes mellitus. 1. O ptimal management o diabetes involves patients measuring and recording their own blood glucose levels. 2. I le t unchecked and untreated, prolonged and elevated levels o glucose in the blood will result in serious health complications, even death. b. Blood glucose level is measured by means o a glucose meter, with the result either in mg/dL (milligrams per deciliter in the United States) or mmol/L (millimoles per liter in Canada and Europe) o blood. 1. The average person should have a blood glucose level o around 4.5 to 7.0 mmol/L (80 to 125 mg/dL). 2. In the patient with diabetes, a be ore-meal level o