The principles of endodontics [Third ed.] 9780198812074, 0198812078

Table of contents :
Cover
The Principles of Endodontics
Copyright
Dedication
Contents
About the editors
About the contributors
Abbreviations
1 Introduction
2 Life of a tooth
3 Diagnosis, treatment planning, and patient management
4 Preserving pulp vitality
5 Root canal preparation
6 Root canal filling
7 Restoration of the endodontically treated tooth
8 Treatment outcomes
9 Dealing with post-​treatment disease
10 Dento-​legal aspects of endodontics
Index

Citation preview

The Principles of Endodontics

The Principles of Endodontics THIRD EDITION

Edited by

Shanon Patel Justin J. Barnes

1

3 Great Clarendon Street, Oxford, OX2 6DP, United Kingdom Oxford University Press is a department of the University of Oxford. It furthers the University’s objective of excellence in research, scholarship, and education by publishing worldwide. Oxford is a registered trade mark of Oxford University Press in the UK and in certain other countries © Oxford Unviersity Press 2020 The moral rights of the authors have been asserted First Edition published in 2005 Second Edition published in 2013 Third Edition published in 2020 Impression: 1 All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, without the prior permission in writing of Oxford University Press, or as expressly permitted by law, by licence or under terms agreed with the appropriate reprographics rights organization. Enquiries concerning reproduction outside the scope of the above should be sent to the Rights Department, Oxford University Press, at the address above You must not circulate this work in any other form and you must impose this same condition on any acquirer Published in the United States of America by Oxford University Press 198 Madison Avenue, New York, NY 10016, United States of America British Library Cataloguing in Publication Data Data available Library of Congress Control Number: 2019943848 ISBN 978–​0–​19–​881207–​4 Printed and bound in India by Replika Press Pvt. Ltd. Oxford University Press makes no representation, express or implied, that the drug dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up-​to-​date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publishers do not accept responsibility or legal liability for any errors in the text or for the misuse or misapplication of material in this work. Except where otherwise stated, drug dosages and recommendations are for the non-​pregnant adult who is not breast-​feeding Links to third party websites are provided by Oxford in good faith and for information only. Oxford disclaims any responsibility for the materials contained in any third party website referenced in this work.

This book is dedicated to: Almas, Genie, and Zarina Shanon Patel Kathleen and Colm Justin J. Barnes

Preface to the Third Edition The aim of this third edition is to provide a contemporary comprehensive guide to endodontics. This edition covers the many advances in endodontic knowledge, techniques, materials, and equipment since the second edition was published. The intended readership remains undergraduate dental students who wish to develop an understanding of ‘why’ and ‘how’ safe, predictable, and effective endodontic treatment is carried out. The book will also benefit recent graduates who want to refresh their knowledge and the established clinicians who are continuing their professional development. The fantastic feedback we have had on the simple and user-​friendly style remains in this new edition. Respected academics, as well as up-​and-​coming clinicians and academics, have kindly contributed to the book. There are several changes since the second edition. Existing chapters have been significantly revised and updated with new figures and illustrations. New features include troubleshooting and self-​assessment sections. There has been continued effort to ensure consistency of terminology throughout the book. References are kept to a minimum, with readers being invited to explore an updated suggested further reading at the end of each chapter. We really hope that this third edition will continue to help your understanding of the principles of endodontics so that you can achieve satisfying results and goals in your clinical practice. Shanon Patel Justin J. Barnes

Acknowledgements The editors are grateful to Professors Michael Manogue and Richard Walker who were instrumental in developing the first edition of this novel book. We appreciate all of the contributors for their help in producing this third edition of the book; without them this new edition would not have been possible. We acknowledge our colleagues and other publishers who kindly gave permission to reproduce their outstanding illustrative material. We thank the companies who kindly sent materials and equipment for photographing. We express thanks to the staff at Oxford University Press, especially Geraldine Jeffers, Senior Commissioning Editor, for their advice and patience, and their hard work in assembling the final product. Finally, we are indebted to our families who have been pillars of support throughout the editing of the third edition. Figures 2.1 and 2.4  courtesy of Dr José Freitas Siqueira Jr. Figure  4.5 adapted from Patel S and Vincer L (2017) Case report:  single visit indirect pulp cap using biodentine. Dental Update 44, 141–​5. Printed with permission from Dental Update. Figure 4.9  adapted from Patel S and Duncan H (2011) Pitt Ford’s Problem-​Based Learning in Endodontology. Printed with permission from Wiley-​Blackwell. Figure 5.38  courtesy of and printed with permission from Dr Bhavin Bhuva. Figures  7.3 and 7.24 adapted from Patel S and Duncan H (2011) Pitt Ford’s Problem-​Based Learning in Endodontology. Printed with permission from Wiley-​Blackwell. Figures 7.14, 7.18, and 7.20  adapted from Mannocci F, Cavalli G, and Gagliani M (2008) Adhesive Restoration of Endodontically Treated Teeth. Printed with permission from Quintessence Publishing. Figure 7.21  courtesy of Dr Edward Sammut. Figure 9.24  courtesy of Dr I. Zainal Abidin. Table 10.1  adapted from patient information leaflet and consent form designed by Dr Melissa Good. Figure 10.5  courtesy of Dr Steve Williams. Adapted from Patel S and Duncan H (2011) Pitt Ford’s Problem-​ Based Learning in Endodontology. Printed with permission from Wiley-​Blackwell.

Contents About the editors

xiii

About the contributors

xv

Abbreviations

xvii

1 Introduction Shanon Patel and Justin J. Barnes

1

2 Life of a tooth Federico Foschi, Sadia Ambreen Niazi, and Moya Meredith Smith

7

3 Diagnosis, treatment planning, and patient management Justin J. Barnes and Shanon Patel

21

4 Preserving pulp vitality Avijit Banerjee and Shanon Patel

51

5 Root canal preparation Edward Brady and Conor Durack

63

6 Root canal filling Conor Durack and Edward Brady

99

7 Restoration of the endodontically treated tooth Bhavin Bhuva, Francesco Mannocci, and Shanon Patel

121

8 Treatment outcomes Justin J. Barnes and Shanon Patel

141

9 Dealing with post-​treatment disease Shanon Patel and Shalini Kanagasingam

153

10 Dento-​legal aspects of endodontics Len D’Cruz

177

Index

189

About the editors Shanon Patel  BDS, MSc, MClinDent, MRD RCS(Edin), PhD, FDS RCS (Edin), FHEA Shanon divides his time between working in multi-disciplinary specialist practice in central London, and teaching future Specialists in Endodontics in the Postgraduate Unit at King’s College London Dental Institute. His PhD thesis assessed the use of CBCT in the management of Endodontic problems, and he continues to be actively involved in research and has (co-)supervised over 45 Masters and PhD students. Shanon has published over 80 papers and has been lead author of 3 European guidelines in dental imaging and root resorption. Shanon have co-edited/authored several textbooks: The Principles of Endodontics is considered essential reading for undergraduates in the UK and the commonwealth; Pitt Ford’s Problem Based Learning in Endodontics was the first PBL book published in Endodontics; Endodontology at a Glance is a revision guide; and CBCT in Endodontics is considered essential reading for Endodontists using CBCT and has been translated into Mandarin, Japanese and Portuguese.

Justin J. Barnes  BDS, BSc, MFDS RCPS(Glasg), MClinDent, MRD RCS(Edin) Justin offers a specialist endodontic service in Northern Ireland. Justin has published several papers in peer-​reviewed journals, co-​edited and contributed to The Principles of Endodontics, second edition, and has contributed to Manual of Clinical Procedures in Dentistry. Justin regularly delivers endodontic educational courses.

About the contributors Avijit Banerjee  BDS, MSc, PhD (Lond), FDS (Rest Dent), FDS RCS (Eng), FHEA Specialist in Prosthodontics, Periodontics and Restorative Dentistry Professor of Cariology & Operative Dentistry Head of Department, Conservative & MI Dentistry Honorary Consultant & Clinical Lead, Restorative Dentistry Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, UK

Bhavin Bhuva  BDS, MFDS RCS (Eng), MClinDent, MRD RCS (Edin), FHEA Specialist in Endodontics, Hertfordshire and London, UK Consultant in Endodontics, Endodontic Postgraduate Unit, Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, UK

Edward Brady  BChD, MJDF RCS (Eng), MClinDent, MEndo RCS (Edin) Consultant in Endodontics Department of Restorative Dentistry and Traumatology, King’s College Hospital, London, UK

Len D’Cruz  BDS, LDS RCS (Eng), Dip FOd, MFGDP (UK), LLM, PgCert Med Ed General Dental Practitioner, London, UK Senior Dento-legal Advisor, British Dental Association, London, UK

Conor Durack  BDS NUI, MFD RCSI, MClinDent, MEndo RCS (Edin) Specialist in Endodontics, Riverpoint Specialist Dental Clinic, Limerick, Republic of Ireland

Federico Foschi  BDS, MSc, PhD, FHEA, FDS RCS (Eng) Consultant in Endodontics/​Honorary Senior Lecturer, Programme Director MSc in Endodontics Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, UK

Shalini Kanagasingam  BDS (Mal), MClinDent, MFDS RCS (Eng), MRD RCS (Edin), MFDS RCPS(Glasg), M (RestDent) RCPS(Glasg), FHEA Senior Clinical Lecturer, Course Lead MSc Endodontology School of Dentistry, Faculty of Clinical and Biomedical Sciences, University of Central Lancashire, UK

Francesco Mannocci  MD, DDS, PhD, FHEA Specialist in Endodontics and Restorative Dentistry, Professor and Head of Endodontology/​Honorary Consultant, Postgraduate Endodontic Unit, Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, UK

Sadia Ambreen Niazi  BDS, MSc, PhD, FHEA Academic Clinical Fellow in Endodontics, Postgraduate Endodontics Unit, Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, UK

Moya Meredith Smith  BSc, PhD, DSc Professor of Evolutionary Dento-Skeletal Biology, Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, UK Scientific Associate at the Natural History Museum London, UK

Abbreviations BC RRM

bioceramic root repair material

BMPS

bone morphogenic proteins

CAD

computer-​aided  design

CAM

computer-​aided manufacture

CBCT

cone beam computed tomography

CCD

charge-​coupled devices

CEJ

cemento-​enamel junction

CMOS

complementary metal oxide semiconductors

DPI

Dental Practicality Index

DPO

data protection officer

EAL

electronic apex locator

EBV

Epstein-​Barr  virus

EDJ

enamel-​dentine junction

EDTA

ethylenediaminetetraacetic acid

DGGE

denaturing gradient gel electrophoresis

FRS

file removal system

GDC

General Dental Council

GDPR

General Data Protection Regulation

GIC

glass-ionomer cement

GP

gutta-​percha

HCMV

human cytomegalovirus

ICO

Information Commissioners Office

IGF

insulin-​like growth factor

IP

Internet protocol

ISO

International Organization for Standardization

LPS lipopolysaccharide MALDI-​TOF MS

matrix assisted laser desorption/​ionization-​time of flight mass spectrometry

MAF

master apical file

MI

minimally invasive

MMPS

matrix-​metalloproteinases

MTA

mineral trioxide aggregate

NICE

National Institute for Health and Clinical Excellence

NITI

nickel titanium

xviii

Abbreviations

NSAID

non-​steroidal anti-​inflammatory  drugs

PDGF

platelet-​derived growth factor

PMN

polymorphonuclear neutrophils

PUI

passive ultrasonic irrigation

RT-​PCR

Real-​time Polymerase Chain Reaction

TGF-​β

transforming growth factor beta

VZV

varicella-​zoster  virus

1

Introduction Shanon Patel and Justin J. Barnes

Chapter contents What is endodontics?

2

Which clinical conditions require endodontic management?

2

What are the aims and scope of endodontics?

4

What does it take to be competent?

4

How has endodontics developed?

5

What is the purpose of this textbook?

5

Suggested further reading

6

2

Introduction

What is endodontics? Endodontics means the science of the inside of the tooth. The term has its origins from the Greek ‘endo’ meaning ‘within’ and ‘odont’ meaning ‘tooth’. The suffix ‘-​ics’ means ‘area of work and study’. Teeth and their supporting tissues may become involved in dental infections that are caused by microbes from the oral microflora. These microbes, primarily bacteria, may cause disease around teeth (periodontal disease) and/​or inside teeth (endodontic disease). Endodontic disease affects the enamel, dentine, pulp, and periapical tissues. It is characterized by loss of the integrity of the enamel and dentine; in advanced cases the pulp and the periapical tissues may also become (in)directly involved. Endodontology is the branch of dental science concerned with the form, function, health, injuries to, and diseases of, the dentine, dental pulp, and periapical tissues. Endodontics is the branch of clinical dentistry concerned with the prevention, diagnosis, and treatment of endodontic disease. Essentially, endodontics involves all procedures required for the maintenance of healthy teeth and, where teeth have become diseased, treatments required to return teeth to a healthy status. Understanding

endodontics requires knowledge of the biological processes affecting teeth and their supporting tissue (Chapter 2), and knowledge of the related basic science subjects, including: • Embryology, in particular, the development of teeth and their supporting tissues. • Anatomy, in particular, the structures of teeth and their supporting tissues. • Histology, in particular, the microscopic structures of enamel, dentine, and pulp. • Physiology, in particular, the normal functions of the pulp. • Pathology, in particular, the cause and effects of disease of the pulp and periapical tissues. • Microbiology, in particular, oral microbes and infections. • Pharmacology, in particular, drugs used in general dentistry and endodontics. • Dental materials science, in particular, the instruments and materials used in endodontics.

Which clinical conditions require endodontic management? Patients with endodontic disease may present in a variety of ways, ranging from being completely symptom-​free, to presenting with severe orofacial pain and swelling. The clinical conditions that may require endodontic treatment are: • Dental caries (Figure 1.1).

• Tooth surface loss (Figure 1.4). • Cracked teeth (Figure 1.5). • Pulpitis (Figure 1.6). • Periapical periodontitis: acute, suppurative, and chronic (Figure 1.7).

• Traumatized teeth (Figure 1.3).

It is only with a thorough understanding of the subject that the clinician will be able to effectively examine the patient and arrive at a correct diagnosis (Chapter 3).

Figure 1.1  Dental caries in close proximity to the pulp chamber and an emerging periapical radiolucency associated with a mandibular premolar.

Figure 1.2  Internal root resorption associated with a maxillary central incisor.

• Root resorption (Figure 1.2).

Which clinical conditions require endodontic management?

3

Figure 1.3  Dental trauma: complicated crown fracture of a maxillary central incisor. There has been a fracture involving enamel and dentine, and the pulp has been exposed.

Figure 1.5  Cracked tooth: a crack is visible on the floor of the cavity of this mandibular molar.

Figure 1.4  Tooth surface loss: erosion and attrition of the incisal edges, and cervical abrasion of the mandibular anterior teeth.

Figure 1.6  Pulpitis: intraoperative bleeding from an inflamed pulp associated with a mandibular first molar.

(a)

(b)

(c)

(d)

Figure 1.7  Periapical periodontitis: (a) acute facial swelling associated with an acute periapical abscess; (b) labial sinus associated with suppurative periapical periodontitis; (c) purulent intracanal discharge associated with suppurative periapical periodontitis; and (d) periapical radiolucency associated with chronic periapical periodontitis.

4

Introduction

What are the aims and scope of endodontics? The aim of endodontic treatment is to prevent or cure periapical periodontitis by controlling infection. Essential components to achieving this aim are:

a much wider role in the general dental care of patients. The scope of endodontics includes:

• Disinfection of teeth to reduce microbial load. This ranges from removing caries-​affected dentine (Chapter 4) to a disinfection of the entire root canal system (Chapter 5).

• Vital pulp therapies (Chapter 4).

• Sealing of teeth to prevent reinfection. This ranges from placement of a root canal filling (Chapter 6) to providing a well-​fitting definitive coronal restoration (Chapters 4 and 7). It is important to appreciate that endodontics is not simply concerned with root canals and root canal treatment. The discipline plays

• Diagnosis of orofacial pain (Chapter 3). • Root canal treatment (Chapters 5 and 6). • Dental whitening of endodontically treated teeth. • Restoration of endodontically treated teeth (Chapter 7). • Advanced endodontic procedures:  root canal retreatment and surgical endodontics (Chapter 9). • Management of dental trauma.

What does it take to be competent? All dentists should be able to carry out safe and effective endodontic treatment. As per guidance published by the General Dental Council in the UK, you must only carry out a type of treatment if you are appropriately trained, competent, confident, and indemnified. Competence is attained through sound theoretical knowledge together with appropriate clinical experience and skills. During your undergraduate dental training, it is imperative that: • You attend teaching sessions and carry out self-​directed learning. • You gain experience using simulated and extracted teeth before embarking on treating patients. • You reflect on your pre-​clinical laboratory and clinical performance, and the feedback given by your supervisors. Reflection should be documented in a logbook. After your undergraduate training, it is important that you continue to maintain and develop your professional knowledge, skills,

and competence. This can be achieved through various learning, training, and developmental activities, such as private study, reading journals, carrying out clinical audit, and attending lectures and courses. Continuing professional development will allow you to keep up to date with advances in endodontics. It is also important that you continue to reflect on your work as a qualified clinician. You need to be aware of your limitations and recognize when referral to a specialist is necessary for more advanced endodontic procedures (Chapter 9). You also need to recognize when things go wrong, how to manage these situations and prevent them from occurring again (Chapter 10). Competency in endodontics requires the use of rubber dam (Figure 1.8). It is of paramount importance that you continue to use rubber dam throughout your professional career. Box 1.1 summarizes the benefits of using rubber dam for all non-​surgical endodontic procedures.

Box 1.1  Benefits of using rubber dam for non-​surgical endodontic procedures Tooth • Prevents contamination of root canal system by saliva and microbes. • Controls moisture to ensure optimal conditions for restoration. Patient • Protects the patient’s oropharynx from instruments, debris, and irrigants. • Improves patient comfort. Clinician • Encourages the clinician to use acceptable irrigants. • Improves access and vision by retracting the soft tissues, for example buccal mucosa and tongue, and preventing fogging of the dental mirror by the patient’s breath. Figure 1.8  Rubber dam isolation during endodontic treatment.

• Increases clinician efficiency.   

What is the purpose of this textbook?

5

How has endodontics developed? Endodontic disease and its management have been well chronicled. Ancient civilizations believed that toothache and dental disease was caused by a tooth worm. Historical management of endodontic disease has included primitive dental drills, herbal remedies, cauterizing the pulp, placement of arsenic into the root canal, and extraction. It was not until the nineteenth century that microbes became associated with endodontic disease. Miller (1894) was the first to demonstrate the presence of bacteria in samples retrieved from the pulp. Other developments in the 1800s included the invention of the reclining dental chair, introduction of the rubber dam, and discovery of X-​rays. The development of endodontics was hampered in the early twentieth century by the theory that dental infection was a source for systemic disease (Focal Infection Theory). This led to extraction becoming the treatment of choice for endodontic disease. Since the 1950s, the Focal Infection Theory has largely been dispelled and there have been many developments in endodontics. Investigations in the 1960s confirmed that infection within the tooth is essential for periapical periodontitis to occur. Kakehashi et al. (1965) revealed that when pulps were exposed to oral microbes, endodontic disease developed in normal rats; whilst, in germ-​free rats, the pulps and periapical tissues remained healthy. The 1970s and 1980s increased our understanding of the microbiology of infected root canals and the ways in which irrigants, agitation of irrigants, and medicaments can disinfect root canals. Since the 1990s our knowledge of the nature of endodontic disease has significantly improved, including microbial biofilms, the causes of post-​treatment persistent disease, and the factors which influence the outcome of endodontic treatment. There have also

been advancements in materials, equipment, and techniques, including: bioactive endodontic cements, cone beam computed tomography (CBCT), improved design features of nickel titanium (NiTi) files, and newer generations of electronic apex locators and magnification devices. These developments have improved the diagnosis, consistency, safety, and efficiency in endodontics, as well as improving patient comfort. Bioactive pulp capping and root canal filling materials as well as endodontic microsurgery have resulted in improved patient outcomes. For teeth that are already missing or have a hopeless prognosis, dental implants can be an excellent replacement option. Indeed, until the early 2000s there was a belief with some of the dental profession that the need for endodontics was on the decline as dental implants were considered to be a superior and predictable treatment option. However, this belief has now changed, as studies show that the survival rate of endodontically treated teeth is similar, if not better, than that of dental implants. Therefore, if a tooth is deemed to be restorable and treatable, the patient should be offered the option of endodontic treatment so that the tooth can be retained for as long as possible. There are numerous advantages to preventing and treating endodontic disease so that teeth can be retained in a healthy state. These include: • Cost-​effective and predictable treatment. • Expedient treatment. • Retention of the periodontal ligament. The future of endodontics is exciting, with prospects of revascularization of root canals, regeneration of the diseased pulp and dentine, and predictable pulp protection procedures resulting in the maintenance of pulp vitality.

What is the purpose of this textbook? The purpose of this textbook is to provide a contemporary comprehensive guide to endodontics. The intended readership is undergraduate dental students who wish to develop an understanding of ‘why’ and ‘how’ safe, predictable, and effective endodontics may be carried out. This book covers the essential theory of ‘why’ endodontic treatment is performed, and provides a step-​by-​step guide to the clinical

practicalities of ‘how’ endodontic treatment is performed. Apart from being an adjunct to undergraduate dental teaching, this book acts as a refresher to recently qualified dentists and as an update to the established clinician who is continuing their professional development.

Summary points

• Endodontics is a branch of clinical dentistry concerned with

the prevention, diagnosis, and treatment of diseases of the dentine-pulp complex, and periapical tissues. There are a wide range of clinical conditions which require endodontic management. The aim of endodontics is to prevent or cure periapical periodontitis so that a tooth can be retained in a healthy state.



• Endodontics involves the diagnosis of orofacial pain, pulp

preservation procedures, root canal treatment, restoration

of the endodontically treated tooth, and advanced endodontic procedures such as root canal retreatment and surgical endodontics.

• You must be competent to carry out endodontic treatment. It is of paramount importance that you use rubber dam for all non-​surgical endodontic procedures.



• Endodontics continues to develop, and it is important that you keep up to date with these developments.

6

Introduction

Suggested further reading De Moor R, Hülsmann M, Kirkevang LL, Tanalp J, and Whitworth J (2013) Undergraduate curriculum guidelines for endodontology. International Endodontic Journal 46, 1105–​14.

General Dental Council (2017) Scope of Practice. London: GDC.

European Society of Endodontology (2006) Quality guidelines for endodontic treatment: consensus report of the European Society of Endodontology. International Endodontic Journal 39, 921–​30.

Kakehashi S, Stanley HR, and Fitzgerald RJ (1965) The effects of surgical exposures of dental pulps in germ-​free and conventional laboratory rats. Oral Surgery, Oral Medicine, and Oral Pathology 20, 340–​49.

General Dental Council (2013) Standards for the Dental Team. London: GDC.

Miller W (1894) An introduction in the study of the bacteriopathology of the dental pulp. Dental Cosmos 36, 505.

General Dental Council (2017) Enhanced CPD Guidance for Dental Professionals. London: GDC.

2

Life of a tooth Federico Foschi, Sadia Ambreen Niazi, and Moya Meredith Smith

Chapter contents Introduction

8

Tooth embryogenesis and dentine-pulp complex formation

8

Dentine

9

Pulp

10

Dentine-pulp response to caries

12

Endodontic infections

15

Self-assessment

19

Suggested further reading

20

Self-assessment answers

20

8

Life of a tooth

Introduction The life of a tooth is dynamic, with several phases: • Firstly, during embryogenesis the main components of the tooth are formed (i.e. enamel, cementum, pulp, and dentine). • Eruption of the tooth leads to the development of root(s) and root canal systems (i.e. main root canal(s), lateral root canals, branches, and deltas). • After eruption, the tooth is still a dynamic entity with physiological changes:  a continuous secondary dentine formation leads to progressive dentinal sclerosis. • In the event of pathological processes, such as caries and tooth surface loss, or operative procedures, (self-)defensive mechanisms arise. The dentine-pulp complex mounts an immune response and increases dentine deposition in the form of tertiary dentine. The

presence of mesenchymal stem cells in the pulp allows a dynamic response to external insults. • If the integrity of enamel or cementum is breached or absent, the dentine-pulp complex represents an ideal environment for colonization by specific pathogens. The endodontic microbiota differs significantly between primary and persistent infections, and also with or without presence of oral communication (i.e. sinus tracts). Understanding the life of a tooth and its associated biological processes allows a deeper understanding of the clinical signs associated with the development and progression of endodontic disease from the early stages of reversible pulpitis through to irreversible pulpitis, pulpal necrosis, periapical periodontitis, and possibly post-treatment persistent endodontic infections.

Tooth embryogenesis and dentine-pulp complex formation Teeth have two main embryological contributors: the ectoderm, which forms the enamel, and the neural crest-derived ectomesenchyme, which forms the dentine-pulp complex. Development begins in the sixth week of embryonic life, from a thickening of the oral ectoderm that creates the dental lamina. Teeth in the primary and permanent dentition form in essentially the same way at different times. The three main stages of the tooth development are:

invagination and will lead to the formation of the dentine-pulp complex. The two cell layers facing each other have different fates: the cells of the inner layer of the enamel organ will differentiate into ameloblasts, whereas the cells of the outer layer of the dental papilla will differentiate into odontoblasts and initiate the dentine deposition.

• Bud stage. The developing tooth assumes the shape of a ‘bud’, from the invagination of the epithelium from the dental lamina proliferating into the ectomesenchyme (Figure 2.1a).

• Bell stage. The developing tooth assumes the shape of a ‘bell’, where the invagination deepens. The dental papilla is contained within this

Subsequently the cells of the inner and outer enamel epithelium merge to form the cervical loop, with a toroid/donut shape, and the root starts to form at the cemento-enamel junction. This process is induced and controlled by the Hertwig’s epithelial sheath, which guides and initiates root formation by providing signals for the differentiation of odontoblasts and cementoblasts. Further differentiation leads to the formation of the periodontal support structure, with the cementum attached through the Sharpey’s fibres, and the outer layer of the dental sac allowing the bone to be anchored to the periodontal fibres.

(a)

(b)

• Cap stage. The developing tooth assumes the shape of a ‘cap’, where further epithelial proliferation gives rise to the enamel organ (Figure 2.1b).

Figure 2.1  Initial stages of tooth development: (a) bud stage and (b) cap stage. Courtesy of Dr José Freitas Siqueira Jr.

Dentine

9

Dentine Composition Dentine, together with the pulp, can be considered embryologically and functionally as a single entity, known as the dentine-pulp complex. Structurally they are very different, with dentine consisting of 70%, by weight, of mineralized (hydroxyapatite). The non-mineralized components are 20% organic matrix (mostly collagen) and 10% water. The major organic component is type I collagen, with type V being a minor component. Several growth factors and enzymes are also present; transforming growth factor (TGF)-β, platelet-derived growth factor (PDGF), insulin-like growth factor (IGF), bone morphogenic proteins (BMPs), and matrix-metalloproteinases (MMPs). These growth factors and enzymes are embedded in the dentine during the dentinogenesis, but can be released during demineralizing processes (e.g. caries, erosion, and etching). The releasing of these factors triggers dentinal reparative events, including stimulation of tertiary dentine formation.

Types of dentine There are three main types of dentine (Figure 2.2): 1. Primary dentine is deposited by odontoblasts at a rate of 4 μm per day. Primary dentine constitutes the largest part of the tooth structure. Primary dentine can be sub-categorized into:

(a) Mantle dentine is the first layer of dentine to be formed. It is located closest to enamel or cementum.



(b) Predentine is a 10–40 μm layer of dentine undergoing completion of its mineralization. This dynamic region is located

Cementum

Predentine

between the odontoblast layer and the mineralized dentine, moving centripetally during the secondary dentine deposition. 2. Secondary dentine is deposited by odontoblasts after root formation is complete and throughout the life of a tooth at a lower rate of less than 0.4 μm per day. This leads to the progressive reduction of the root canal space. 3. Tertiary dentine is formed in reaction to external stimuli (e.g. bacterial toxins, trauma, attrition, dental operative procedures). It is deposited in proximity to the site of injury. Tertiary dentine can be sub-categorized as:

(a) Reactionary dentine is formed when the insult to the odontoblast is not severe and the odontoblastic layer survives. Morphologically tertiary reactionary dentine is similar to the primary and secondary dentine, with the dentinal tubule structure remaining continuous.



(b) Reparative dentine is formed when the insult is more severe, with excessive damage to the odontoblastic layer. Pulpal stem cells are recruited and differentiate into odontoblast-like cells. Dentinal tubules are usually not present or not continuous with those from secondary or reactionary dentine.

Sclerotic dentine may also occur as a physiological process or in response to external insult. It is characterized by an enhanced mineralization of the intratubular (or peritubular) dentine. Both sclerotic and tertiary dentine are important to protect the pulp from external potentially harmful stimuli.

Dentinal tubules During primary and secondary dentinogenesis, the odontoblast mineralization front moves in a centripetal direction. The odontoblast is a columnar cell with a polarized process that leaves an imprint in the newly formed dentine (Figure 2.3). The odontoblast processes may extend up to half way into the dentine.

Secondary dentine

Primary dentine

Mantle dentine Pulp

Tertiary dentine Carious lesion

Enamel

Figure 2.2  Types of dentine.

Figure 2.3  Photomicrograph showing the surface of the root canal wall, devoided of the organic component, with the dentinal tubules and the globular structure of the calcospherites at the front of mineralization.

10

Life of a tooth

The inner part of the dentinal tubules is intratubular (peritubular) dentine. The dentine located between the intratubular dentine is intertubular dentine, and makes up most of the dentinal structure. Intratubular dentine is more calcified compared with intertubular. During the sclerosis process the intratubular dentine is calcified further within the tubules cavity. Dentinal tubule has a diameter of 2.5 μm nearest the pulp and narrows to 1 μm at the enamel or cementum. The tubular density is higher (65,000 tubules/mm2) nearer the pulp, compared with the cementum or enamel junction (15,000 tubules/mm2). Dentinal tubules contain dentinal fluid, the odontoblastic processes, nerve fibres, type I collagen, and the ground substance (glycosaminoglycans, proteoglycans, glycoproteins).

Cold Sweets Air blasts

Heat

Dentinal permeability and sensitivity The tubular structure provides dentine with two important properties:  permeability and sensitivity. Dentinal permeability has been studied in depth; there is good evidence to confirm that operative procedures localized on the outer surface of dentine can still affect the pulp. Similarly, pathological processes, such as caries and tubular infection, can lead to pulpal damage. The dentine permeability varies in different areas, increasing progressively towards the pulp chamber. Dentinal sclerosis reduces the permeability of the dentinal tubules. Furthermore, operative procedures can create a smear layer that occludes the tubules. The pathophysiological mechanism of dentinal sensitivity and hypersensitivity has been extensively studied. The ‘hydrodynamic theory’ is considered the main mechanism (Figure 2.4). The rapid displacement

Figure 2.4  Hydrodynamic theory for dentine sensitivity. External stimuli can cause movement of the dentinal fluid, leading to distortion of the odontoblastic process and the coupled nerve fibres will feedback the potentially nociceptive signals to the central nervous system. Printed with permission from Dr José Freitas Siqueira Jr.

of the dentinal fluid within the dentinal tubules induces deformation of the odontoblastic processes and activates the A-δ fibres, leading to the transmission of the nociceptive signal. Many factors can trigger this dentinal fluid movement: temperature (e.g. cold and hot substances), osmolarity (e.g. sweet substances), and mechanical pressure (e.g. chewing and probing).

Pulp Functions

Composition

The main functions of the pulp are:

The pulp is a connective tissue composed of different type of cells, extracellular connective matrix (fibres and ground substance), blood vessels, and nerves. The main cell lineages present in the pulp are odontoblasts, mesenchymal stem cells, fibroblasts, Schwann cells, and defence cells (antigen presenting cells, macrophages, lymphocytes). Odontoblasts are post-mitotic cells with a columnar shape within the crown and more cuboid within the root. They are organized into a single layer of cells (odontoblastic layer) facing the predentine. The odontoblast is polarized: the nuclei are localized towards the pulp; a mitochondria-rich area is closer to the predentine and localized at the formative end before the cytoplasmic projection (odontoblastic process), which is contained within the dentinal tubules. The pulpal stem cells are interspersed in the pulp, but mostly localized in the cell-rich area. The fibroblasts are the most abundant cell lineage. The fibroblast produces the extracellular matrix (glycosaminoglycan, proteoglycans, and glycoprotein), representing the medium for the diffusion

• Formative: the pulp produces dentine, forming the coronal and radicular structure during the odontogenesis. • Sensitivity and proprioception:  the pulp can sense potentially harmful stimuli (nociception) and to a certain extent it can sense its own position (proprioception) related to pressure, thus providing a warning mechanism signalling potential tissue damage. • Defence:  the pulp is immunocompetent and can induce sclerotic and tertiary dentine formation. It is now known that periapical periodontitis can still develop in the presence of a vital pulp. The inflammatory cascade elicited during the pulp defence can trigger the cytokine cascade that leads to apical bone resorption. The pulp defence prevents systemic dissemination of dental infection by inducing a foreign body reaction.

Pulp

(a)

11

(b)

Figure 2.5  (a) Histological zones of the pulp (haematoxylin and eosin stain). The odontoblast layer is the outermost zone in the pulp, lining the predentine and forming it. The cell free zone called the zone of Weil contains the blood capillaries and network of nerve fibres (Rashkow’s nervous Plexus). The cell rich zone (sub-odontoblasts) is formed of fibroblasts, undifferentiated stem cells, and immune cells. The pulp proper is the central mass of the pulp tissue and contains the larger blood vessels, nerves, fibroblasts, and other cells. (b) Dentine (D); calcospherites (CS), mineralizing front; predentine (PD); odontoblastic layer (OL); cell free zone (CFZ); cell rich zone (CRZ); blood vessels (BV).

of signals and nutritive substance. Collagen types I and III are the most diffuse type of fibres. Different histological zones are present within the pulp (Figure 2.5).

Pulp vascularization The pulp blood supply is provided by vessels entering from the main apical foramen and the lateral canals. The arterioles entering the root canal follow the long axis of the root, with capillaries branching

off towards the odontoblastic layer, which represents the vascular zone adjacent to the cell-rich zone (Figure 2.6). Venules are present towards the centre of the pulp. Arteriovenous and venous-venous shunts are also present, and these control the microcirculation. The pulpal blood flow (20–60 ml/min × 100 g tissue) is relatively high compared to other cranial tissues. This characteristic may favour a washout effect of irritants. The presence of a hard encasing surrounding the pulp led to the formulation of a self-strangulation theory, where the low compliance, in case of inflammation, can promptly lead to pulpal hypoxia.

Innervation

Figure 2.6  Blood vessel in the pulp: blood capillary (BC), fibroblast (F), stacked erythrocytes (*). (Haematoxylin and eosin stain.)

The pulp is innervated from the mandibular and maxillary branches of the trigeminal nerve. An autonomic component is also present. Among the nerve fibres reaching the pulp, 80% are unmyelinated C fibres, and the remaining 20% consist of myelinated A fibres. The nerves are in close proximity to the blood vessels. The nerve fibres create a rich network (Rashkow’s nervous plexus). The three types of sensory nerve fibres present in the pulp (A-β, A-δ, and C fibres) evoke different responses due to their difference in conductivity. A-β fibres are myelinated with a very fast conduction speed (30–37 m/sec). A-δ are also myelinated with a fast conduction (6–30 m/ sec). The A fibres induce the sharp, short pain associated with dentinal hypersensitivity. After leaving the Rashkow’s nervous plexus the A fibres lose their outer Schwann cells layer and enter the dentinal tubules for the first 100 μm, in close conjunction with the odontoblastic processes. The C fibres have a slower conduction speed of the signal, being unmyelinated. The nociceptive signal conducted by these fibres is typically of a dull

12

Life of a tooth

non-localized pain associated with the advanced stages of irreversible pulpitis. Autonomic sympathetic fibres are also present in the pulp and closely associated with the pulp vessels; these fibres are involved in the homeostasis of the pulpal circulation. Vasodilation of the of the blood vessels is directly elicited in presence of pain stimuli, increasing the blood flow in situations of reversible/irreversible pulpitis.

Dentine-pulp response to caries The most common cause of pulpal inflammation is caries. Loss of enamel results in exposure of the underlying dentine. The permeability of the dentine is dependent on the location of the dentinal tubules and their proximity to the pulp chamber. The pulp has several self-defence mechanisms including reduction of the dentine permeability by progressive sclerosis, formation of tertiary dentine, and pulpal immune response. Depending on the intensity and extension of the caries, the self-defence processes can have a rapid or slower response.

Reduction in dentine permeability In healthy dentine, an outward movement of dentinal fluid and the presence of the odontoblastic processes reduce bacterial infection. The intrapulpal pressure increases in the presence of prolonged and/ or strong irritating stimulus, which increases the outward movement of dentinal fluid. Host defence system, including antibodies and cytokines are present in the dentinal fluid of vital teeth and protect it from bacterial invasion of the pulp. In the presence of constant low-grade irritation, the dentinal permeability is reduced by progressive mineralization of the intratubular dentine. The dentinal tubules lumen is restricted in the event of dentinal sclerosis. The progression of the endotoxins and bacteria within sclerosed dentine is greatly hindered. Dentine sclerosis reduces permeability and it is localized underneath carious lesions. In cases of rapid insults there is no host response and adaptation of the pulp, the dentinal sclerosis process is interrupted and the odontoblast process coagulates within the tubules forming the dead tracts (Figure 2.7). Pulp stones may also form in the presence caries (Figure 2.8a–b).

The tertiary dentine self-defence mechanism Tertiary dentine is formed to further protect the pulp from an ongoing potential bacterial infection. Tertiary dentine may be subclassified as reactionary or reparative. Tertiary dentine is formed in response to external stimuli (i.e. dental caries). Reactionary dentine is characterized by persistence of the tubular structure and by an increased speed of deposition of the dentine, still with a more irregular structure (Figure 2.9). Reparative dentine is formed beneath the area of irritation and is characterized by dead tracts where the odontoblastic layer has been eradicated. The structure of reparative dentine

Figure 2.7  Ground section of the tooth showing dead tract.

is atubular (Figure 2.10), and is formed from mesenchymal stem cells which differentiate into odontoblast-like cells. The balance between reactionary and reparative dentine formation is determined by the presence of a low-grade progressive stimulus (e.g. slow attrition) versus a strong and rapid one (e.g. deep decay), respectively (Figure 2.11).

Pulp immunity The pulp is an immunocompetent connective tissue that is able to respond to the bacterial insult by activating the usual host immune system cascades. The inflammatory process is triggered at the early stages of caries, that is, once the enamel or cementum is breached. The permeability of the dentinal tubules can allow the passage of bacterial by-products before an actual dentinal infection occurs. The decay process results in the release of enzymes and other proteases interspersed within the collage matrix of the dentine. In addition, the passage of bacterial by-products in the dentinal tubules can trigger the odontoblasts to release pro-inflammatory cytokines. The A-fibres associated with odontoblastic processes within the dentinal tubules can trigger a nociceptive signal, which feeds back to the autonomous system, increasing the pulpal blood flow; this mechanism will increase the dentinal fluid extravasation. Once the inflammatory cytokine cascade is triggered, the defence cells are recruited (e.g. dendritic cells, polymorph nucleates, and macrophages). Tubular invasion by bacteria can also trigger the release of pro-inflammatory molecules directly by the odontoblasts, which

Dentine-pulp response to caries

13

(a)

(b)

Figure 2.9  Decalcified section of dentine showing odontoblastic processes with the lateral branches in the dentine proper and irregular structure of the tertiary dentine. (Picrothionin stain.)

Figure 2.8  (a) Tertiary reactionary dentine (RD) in the ageing pulp and pulp stones (arrows). (Haematoxylin and eosin stain.) (b) Pulp stones (PS) atubular in nature. (Haematoxylin and eosin stain.)

are affected by the tubular content through their odontoblastic process. Caries progression leading to demineralization of dentine structure and increase in dentinal permeability can enhance the pulpal inflammatory response, leading to clinical symptoms. Pulp innervation plays an important role in the regulation of blood flow. Vasodilation is triggered to improve the clearance of bacterial by-products and increase the immune response. The clinical signs of reversible/irreversible pulpitis can be vague and undefined, leading to an unclear diagnosis in the early stages of inflammation. Dentinal hypersensitivity is not dissimilar to the signs of early stages of pulpitis.

Figure 2.10  A carious lesion (CL) has stimulated formation of reparative dentine (RD) which has protected the pulp (P). (Hematoxylin and eosin stain.)

With the progression of the inflammation the diagnosis may become clearer with the specific symptoms of irreversible pulpitis (i.e. lingering and spontaneous pain).

14

Life of a tooth

Strong stimulus

Dentine

Reparative dentine

Mesenchymal stem cells

Mild stimulus

Reactionary dentine

Pulp

Odontoblasts

Figure 2.11  The two faces of the tertiary dentine coin: reparative and reactionary dentine formation are the two ways the pulp protects itself from external stimuli. A strong stimulus causes death of odontoblasts and stimulates reparative dentine formation by mesenchymal stem cells. A mild stimulus stimulates reactionary dentine formation by odontoblasts.

Irreversible pulpitis, pulpal necrosis, and periapical periodontitis If the aetiological factor(s) are not adequately managed pulpal inflammation increases, reaching a level defined as irreversible. Beyond this point, the pulp is unable to recover spontaneously and will result in cellular apoptosis and the development of micro-abscesses. The borderline between reversible and irreversible pulpitis is less clear than historically thought, and several misconceptions may affect endodontic diagnosis. In particular, the presence of periapical radiolucency has been incorrectly associated with complete pulpal necrosis. It is now apparent that the cytokines cascade can trigger periapical breakdown in the early stages of the pulp inflammation. Studies using cone beam computed tomography (CBCT) have revealed the presence of small periapical radiolucencies in cases diagnosed with reversible pulpitis. If bacterial invasion (e.g. caries, dental trauma) of the dentinal tubules and pulp chamber carry on, the pulpitis will progress from the reversible to the irreversible stage. This may then advance to pulp necrosis. Within a tooth the infection front moves apically. The symptoms associated with irreversible pulpitis usually cease when pulpal necrosis develops. In response to the bacterial ingress in the pulp chamber, an acute inflammation occurs. The typical characteristics of inflammation follow, in particular vasodilation with increased pulpal blood flow and extravasation due to increased vascular permeability. The intrapulpal pressure is a controversial topic, as many authors attribute this phenomenon to the self-strangulation of the pulp due to the low compliance of the surrounding tissue (i.e. dentine). Pulpal oedema leads to blood stasis and reduces the clearance of waste products. This leads to an increased nociceptive signalling of cellular apoptosis and tissue necrosis. Cellular apoptosis and bacterial by-products result in micro-abscess formation within the affected area of the pulp. The progression

of the infection may be delayed by the pulp’s immune response. For this reason, partial or complete pulpotomy may be successful in preserving the vitality of the remaining pulp tissue (Chapter  4). Nevertheless, further tertiary dentine deposition may occur in the presence of bioactive endodontic cement, leading to calcification of the root canal. The periapical lesion is the endpoint of the endodontic disease. The development of external inflammatory resorption adjacent to the main portal(s) of exit of the root canal system (lateral canals and main apical foramina) is the manifestation of the ongoing infection of the root canal system. Occasionally occlusal trauma can mimic the formation of periapical lesion; however, the presence of a vital pulp tissue is the main discriminating factor. Ultimately, the presence of a necrotic pulp associated with a periapical lesion is pathognomonic of endodontic infection. Biologically the periapical lesion is an immune response following the pattern of a foreign body reaction, where the host response is attempting to prevent the infection spreading systemically. Several hypotheses have been formulated regarding the kinetics of periapical lesion progression. In particular, the direct effect of bacterial proteolytic enzymes on the initiation of the periapical breakdown. Extensive research with knockout genes murine models clarified the immunological pathways of protective and destructive cytokines. The bacterial by-products (i.e. lipopolysaccharides (LPS) and endotoxins) trigger the cytokine cascades that signal via RANK-ligand the differentiation of osteoclasts that induce an enhanced periapical bone resorption. Within the periapical resorption an immunologic response will actively limit bacterial dissemination via polymorphonuclear neutrophils (PMNs) and macrophage activity. Acute periapical periodontitis may be an early stage of apical inflammation with associated acute symptoms; however, a subclinical immune response may develop into a chronic periapical periodontitis that may be often diagnosed as an incidental radiological finding. An acute exacerbation of chronic periapical periodontitis can occur, with

Endodontic infections

15

development of an abscess with associated symptoms. A  dynamic interplay between the host immune system and the bacteria colonizing the root canal system can tip the balance of the clinical presentation. Effective endodontic treatment reduces the bacterial load and therefore interrupts the immune reaction and osteoclast activation, ultimately leading to healing of the periapical lesion.

(a)

(b)

Leaking restoration Tooth surface loss or enamel-dentime fracture

Operative dental procedure

Superficial caries

Deep caries

Tooth surface loss or enamel-dentinepulp fracture

Naturally absent cementum External cervical resorption

Loss of cementum following root planing

Periodontal disease (subgingival biofilm)

Figure 2.12  Routes that microorganisms may take to invade the pulp (a) via dentinal tubules and (b) directly into pulp.

Deep crack

16

Life of a tooth

Figure 2.13  Confocal Laser Scanning Microscopy images of an in vitro Propionibacterium acnes biofilm.

Figure 2.14  Confocal Laser Scanning Microscopy image of an in vitro stressed multi-species biofilm grown on the root, half stained with the LIVE/DEAD stain: live bacteria (green); dead bacteria (red).

Endodontic infections

(a)

17

(b)

Figure 2.15  Scanning electron microscope image of an in vivo biofilm in the root canal acquired at: (a) magnification ×300 and (b) ×1.5k.

Endodontic infections Routes of pulpal invasion More than 700 bacterial species are known to inhabit the healthy human mouth. Enamel and cementum help to isolate the dentinepulp complex from the oral microbiota, keeping the dentine-pulp complex sterile under normal conditions. Bacteria can take several pathways to invade and infect the dentine and pulp. The major routes of pulpal invasion are exposed dentinal tubules, direct pulp exposure and periodontium (Figure 2.12).

Dentinal tubules If enamel or cementum is missing due to hereditary/developmental absence, caries, tooth surface loss, trauma, root resorption, or iatrogenic removal, bacteria may invade the dentine and, eventually, the pulp through exposed dentinal tubules. Dentinal tubules extend from the pulp to the enamo-dentinal and cemento-dentinal junctions. They are approximately 2.5 μm in diameter near the pulp, and 1 μm near the enamel and cementum. Large numbers of these dentinal tubules (approximately 15,000 per square millimetre) are present near the enamel and cementum. Therefore, due to the size and numbers of dentinal tubules, bacteria can enter, multiply, and invade numerous exposed tubules. Although, a number of studies have demonstrated bacteria within the exposed dentinal tubules of vital teeth, bacterial penetration into dentinal tubules has been shown to be greater in non-vital teeth. This might be due to the presence of natural resistance factors in the dentine-pulp complex, reduced tubule permeability by the presence of dentinal fluid, the living odontoblastic processes, and the formation of sclerotic and/or tertiary dentin. Bacterial metabolites and toxic products diffuse along the dentinal tubules, cause breakdown of the odontoblasts, and usually result in inflammatory responses in pulp. Removal of these advancing bacteria through biological selective carious tissue removal can result in healing

(Chapter 4). If left untreated, bacteria will reach the pulp via the dentinal tubules.

Direct pulp exposure Bacteria may enter the pulp through a direct pulp exposure caused by caries, restorative procedures, or traumatic injury that fractures, cracks, or displaces the tooth. There is clinical evidence that bacteria may enter the pulp in cases of cracked-tooth syndrome and even minor cracks in enamel and dentine following trauma. However, the susceptibility to bacterial invasion depends on the virulence of the bacteria, pulp status (i.e. its health) and host resistance. A vital pulp is

Figure 2.16  Scanning electron microscope image of an in vitro biofilm model grown on the sectional root canal using Enterococcus faecalis strain OMGS 3202 (acquired at ×1.5k). The bacteria can be seen growing with in the dentinal tubules.

18

Life of a tooth

Table 2.1  Representatives species of bacterial phyla in endodontic infections Phyla

Common representative species/ phylotypes

Firmicutes

Dialister spp., Filifactor alocis, Parvimonas micra, Pseudoramibacter alactolyticus, Enterococcus faecalis, Eubacterium spp., Mogibacterium spp., Streptococcus spp., Lachnospiraceae spp., Veillonella parvula, Lactobacillus spp., Catonella morbi, Gemella morbillorum, Selenomonas spp., Peptostreptococcus spp.

Actinobacteria

Olsenella uli, Actinomyces spp., Propionibacterium acnes, Propionibacterium propionicum, Slackia exigua

Synergistes

Clone BA121, clone W090

Spirochaetes

Treponema denticola, Treponema socranskii, Treponema maltophilum, Treponema parvum

Fusobacteria

Fusobacterium nucleatum

Proteobacteria

Eikenella corrodens, Campylobacter rectus, Campylobacter gracilis

TM7

Clone I025

SR1

Clone X112

Bacteroidetes

Tannerella forsythia, Porphyromonas endodontalis, Porphyromonas gingivalis, Prevotella spp., clone X083

quite resistant to bacterial invasion. Based on these factors, the pulp tissue may stay inflamed for an extended period or it may rather rapidly undergo necrosis.

Periodontium Loss of periodontal attachment, resulting in increased probing depths, can provide possible routes of invasion into the dentine-pulp complex by the subgingival microflora and their by-products. Subgingival periodontal pockets comprise predominantly of anaerobic microflora, including different Gram-negative rods, spirochetes, and various Grampositive rods and cocci, which are also well suited for growth in a necrotic root canal system. This similarity in endodontic and periodontal microflora suggests bacteria from periodontal pockets can invade nonvital non-carious teeth. Routes of entry from periodontal pockets include accessory, lateral, and furcation root canals, the apical foramen, and dentinal tubules exposed due to root caries, root resorption, gaps in cementum formation in the cervical area, or by removal of the cementum during root planning. If the pulp is vital, the bacteria will be eliminated, followed by healing of the dentine-pulp complex. Therefore, impaired status of the pulp is a prerequisite for such infections.

Anachoresis Another possible source of pulpal infection is anachoresis. This is a phenomenon by which blood-borne bacteria are attracted to inflamed

or necrotic tissue during bacteraemia, where they establish infection. Transient bacteraemia is a quite well-established phenomenon in humans. Bacteria from dental plaque or infected root canals have been retrieved from venous blood after dental extraction, endodontic treatment, non-surgical and surgical periodontal treatment, tooth brushing, and even chewing. Bacteraemia can attract either oral or non-oral circulating bacteria to localize in inflamed pulp or necrotic root canal systems.

Endodontic biofilm Bacteria within the root canal system exist in the form of a biofilm. Biofilms are sessile microbial communities composed of cells attached to a substratum or interface or to each other, embedded in a matrix of extracellular polymeric substances that they have produced, and exhibit an altered phenotype with respect to growth rate and gene transcription. Biofilms form mushroom-shaped sessile micro-colonies with interspersed open water channels that provide an effective means of exchanging nutrients and metabolites with the bulk aqueous phase of the root canal system (Figures 2.13 and 2.14). The nature of biofilm structure and the physiological attributes of its microorganisms confer an inherent resistance to antimicrobial agents. Biofilms are capable of persisting in the presence of 1000-fold higher concentration of antimicrobials than those necessary to eradicate a planktonic population. Various survival strategies could be responsible for biofilm tolerance and resistance including: • Delayed penetration of the antimicrobial agent through the biofilm matrix acting as a physical barrier. • Nutritional starvation and slower growth rate of biofilm organisms than their planktonic counterparts, making them less vulnerable to antimicrobial agents. • Physiological changes due to the biofilm mode of growth altering the environment and making it less favourable for antimicrobial agents to exert their desired effects. Therefore, the endodontic biofilm constitutes a protected mode of growth that allows bacterial survival in the hostile environment of the root canal, and may result in the subsequent development of persistent endodontic infections. Environmental factors such as oxygen and nutrient availability, pH, and residual antibacterial effects of endodontic medications create a selective habitat for the establishment of the biofilm. Survival of bacteria in their respective niches depends on how well the biofilm adapts for growth to these restricted environmental factors. Root canal walls represent an ideal substratum for the adherence of biofilms (Figure 2.15), together with the honeycomb structures represented by the dentinal tubules (Figure 2.16).

Methods for identification of bacteria in endodontic infections Understanding the composition and diversity of pathogenic microflora associated with different forms of endodontic disease is pivotal in the development of strategies for effective endodontics. Traditionally, endodontic infections have been studied using culture techniques. Since 50% of oral microflora may be uncultivable, culture

Endodontic infections

techniques can cause underestimation of the bacterial diversity within the root canal system. Further advances in microbiological research led to the introduction of molecular approaches, such as: • Species or genus specific polymerase chain reaction on cultivable bacteria. • Polymerase chain reaction amplification of 16S rRNA gene, followed by cloning and sequencing of polymerase chain reaction product. • Genetic finger printing using denaturing gradient gel electrophoresis (DGGE). • DNA hybridization assay and real-time polymerase chain reaction (RT-PCR). • Matrix assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS). • Next-generation sequencing. Uncultivated phylotypes that were previously unrecognized and overlooked bacteria have been revealed with these molecular approaches. They may play a role in the pathogenesis of different forms of periapical periodontitis.

Representative of bacterial phyla commonly found in endodontic infections Bacterial taxa recovered from endodontic infections have been found to belong to nine phyla:  Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria, Fusobacteria, Spirochaetes, Synergistes, TM7, and SR1. Culture-dependent and culture-independent molecular studies have revealed a range of microbiota from endodontic infections. The common representative species detected are shown in Table 2.1. It is important to understand that inter-individual variation in the bacterial community profile exists and not all of them are present in the same individual at the same time.

Microbiota of endodontic infections The microflora of endodontic infections is extremely diverse. The composition of the microbiota in primary (untreated) lesions is significantly different from that of persistent endodontic infections. Periapical abscesses are caused by the microbial invasion of the periapical tissues that eventually leads to purulent inflammation.

Microbiota of primary endodontic infections Primary intraradicular infections are caused by bacteria that initially invaded and colonized the necrotic root canal system as a result of caries, trauma, or periodontal disease. The infection is caused by a mixed microbiota conspicuously dominated by Gram-negative anaerobic rods. An infected root canal can harbour about 10–20 bacterial species, reaching a density of about 103–108 bacteria. Teeth with either sinus tract or large periapical radiolucency can be heavily infected, containing over 50 species. Although collectively culture and molecular methods have identified a vast variety of bacteria, including fungi and viruses, the microbial communities vary from person to person. Each

19

individual harbours a unique endodontic microbiota, indicating that primary periapical periodontitis has a varied aetiology. Therefore, no single bacteria can be considered as the main endodontic pathogen, and combination of bacterial taxa play a role in causing the disease.

Microbiota of persistent endodontic infections Microorganisms that were either members of primary infections or were introduced into the root canal afterwards cause persistent endodontic infections. These organisms somehow resisted intracanal antimicrobial procedures and endured periods of nutrient stress in root-filled canals. Persistent endodontic infections are one of the major challenges faced by the dentists. According to some studies the microbiota of persistent lesions is composed of few bacterial species, generally Gram-positive bacteria. Gram-negative bacteria which are normally found in primary lesions are mostly eliminated after root canal treatment procedure. The prevalent microbiota of persistent lesions include Propionibacterium species (P. acnes and P. propionicum), streptococci (S. mitis, S. gordonii, S. anginosus, S. sanguinis, and S. oralis), P. micra, Actinomyces species, lactobacilli (L. paracasei and L. acidophilus), E. faecalis, Olsenella species, Bifidobacterium species, and staphylococci.

Microbiota of endodontic infections with periapical abscesses Periapical abscesses are caused by the microbial invasion of the periapical tissues that eventually leads to purulent inflammation. Formation of periapical abscess is dictated by interaction between the endodontic microbial community and the host defences. The pathogenic microbiota is mixed and dominated by anaerobic bacteria. The persistent endodontic lesions with periapical abscesses have a higher bacterial load and are more diverse microbiota as compared to persistent endodontic lesions without periapical abscesses. Niazi et  al. (2010) found that the mean number of taxa from lesions with periapical abscesses was significantly higher, almost double compared to the ones without periapical abscesses. Therefore, the root canals of teeth without abscesses exhibit a decreased diversity compared with those with abscesses. There is existence of mutual interactive processes between the habitat and its microbiota in different endodontic diseases. As abscesses are enclosed lesions within the alveolar bone at the tip of root apex containing pus, the availability of various nutrients such as the influx of the serum proteins and tissue constituents help support the proliferation of the Gram-negative proteolytic anaerobic bacteria within such lesions.

Other microorganisms in endodontic infections Bacteria are the most common microorganisms detected in endodontic infections. Several studies have confirmed the presence of other microorganisms, including fungi, viruses, and archaea, in endodontic infections. Bacteria are the essential cause of periapical periodontitis; further studies are necessary to confirm whether other microorganisms have a functional role in the pathogenesis of periapical periodontitis. Fungi are occasionally identified in primary endodontic infections, but they are more frequently detected in persistent endodontic infections.

20

Life of a tooth

Detection frequencies for Candida species range from 3% to 18% of cases. Candida albicans is the most commonly isolated Candida species from persistent endodontic infections. Among the viruses, human cytomegalovirus (HCMV), Epstein-Barr virus (EBV), and varicellazoster virus (VZV) have been detected in periapical periodontitis where viable host cells remain.

Iatrogenic endodontic infections Skin commensals, such as Propionibacterium acnes and Staphylococcus epidermidis, are opportunistic pathogens that have been identified in endodontic infections. They may be introduced into root canals intraoperatively and may cause iatrogenic or nosocomial endodontic infections. Possible transmission routes may be via unsterilized materials (e.g. gutta-percha points and certain paper points), some endodontic instruments, and contaminated gloves. The practice of dentistry, including endodontics, requires that Standard Precautions apply to all patient care regardless of suspected

or confirmed infection status. Ways to prevent transmission of infectious agents include, but are not limited to: • Hand hygiene, that is, use soap and water or alcohol-based hand rub. • Use of personal protective equipment. Examples include safety glasses, face shields, masks, gowns, gloves. It is strongly advisable that gloves are changed frequently throughout endodontic procedures i.e. after taking intra-operative radiographs. • Sterilization and disinfection of instruments, devices, and equipment. Examples include the use of pre-sterilized and packaged endodontic files and paper points, and disinfection of gutta-percha (GP) points. • Clean and disinfected environmental surfaces. It is advisable that once a rubber dam has been placed, the tooth surface and surrounding rubber dam sheet are disinfected using sodium hypochlorite or other suitable disinfectant. • Use of high-speed vacuums/suction to minimize droplets and splatter.

Summary points • Understanding the life of a tooth and its associated biological processes allows a deeper understanding of the progression and management of endodontic disease.



• There are several types of dentine. Primary dentine is deposited by odontoblasts and forms the bulk of the tooth. Secondary dentine is continuously laid down after root formation is complete and throughout the life of a tooth. Tertiary dentine is formed in response to external stimuli and may be reactionary (laid down by odontoblast) or reparative (formed by newly recruited mesenchymal stem cells).



• Endodontic



• Endodontic infections are primarily caused by bacteria which

• The pulp is a connective tissue composed of different cells, an extracellular matrix, blood vessels, and nerves. The main functions of the pulp are dentine formation, sensitivity, nociception, and defence.

• The dentine-pulp complex is usually sterile; however, there

are several potential routes by which bacteria, and other microorganisms, can invade. infection initially results in pulpitis and can progress to pulpal necrosis and finally periapical periodontitis. Periapical periodontitis can develop at early stages of pulpitis, following activation of the cytokine cascade. grow as a biofilm. Endodontic infections may be primary, persistent with or without periapical abscess, or iatrogenic.



• It

is important to prevent iatrogenic or nosocomial endo­ dontic infections by using Standard Precautions.   

3

Diagnosis, treatment planning, and patient management Justin J. Barnes and Shanon Patel

Chapter contents What is diagnosis?

22

What are the aims of history taking?

23

What are the aims of the extraoral examination?

24

What are the aims of the intraoral examination?

24

What are the aims of special investigations?

24

How do you arrive at a diagnosis?

28

How do you take a history?

29

How do you carry out an extraoral examination?

30

How do you carry out an intraoral examination?

31

How do you carry out special investigations?

35

What are the common errors in diagnosis?

39

Treatment planning

41

Patient management

44

Self-​assessment

49

Suggested further reading

50

Self-​assessment answers

50

22

Diagnosis, treatment planning, and patient management

What is diagnosis? This section will introduce the rationale for diagnosis. It is important that you read the whole chapter to appreciate how the theory and practice of diagnosis are related. Diagnosis is the process in which a disease, abnormality, or complaint is identified by collecting and analysing information on the presenting symptoms, clinical signs, and the results of specific investigations or tests. An accurate diagnosis is the key to successful treatment. The importance of the process cannot be overemphasized. A  correct diagnosis serves not only to confirm but also exclude other causative factors. The treatment options available and the planned management of the patient are dependent on a correct diagnosis. It is not uncommon for a patient to have self-​ diagnosed their problem as being of dental origin and to expect immediate and effective treatment. However, the clinician should always maintain an open mind when considering a patient’s complaint. The possibility of other (including non-​dental) causes, should always be borne in mind (Table 3.1). The question: ‘Is this a dental problem or not?’ should always be asked when making a diagnosis. In general, endodontic diagnosis involves identifying the state of pulpal and periapical health, in order to arrive at a suitable treatment plan. It should always take into account the patient as an individual, the potential technical difficulties associated with treatment that may be encountered, and the clinician’s competence. Some of the initial questions that the clinician should ask themselves include:

Table 3.1  Examples of non-​dental causes of orofacial pain Source

Examples

Extraoral

• Salivary gland disease

• Is the complaint related to a dental cause? • Are the symptoms pulpal and/​or periodontal in origin? • Is the presentation suggestive of a healthy pulp or not? • Is it possible to manage and treat this patient successfully? If a complaint of pain does not appear to be associated with teeth, that is, non-​odontogenic, it is necessary to consider other causes of orofacial pain (Table 3.1). If a definitive diagnosis cannot be established, or if the patient’s complaint is not dental in origin, referral to an appropriate specialist may be indicated. Irreversible treatment should be avoided until a definitive diagnosis can be reached. A sound diagnosis can only be reached when information is collected from the patient in a systematic and meticulous manner (Table 3.2). The information can then be interpreted and acted upon accordingly. Each step of the diagnostic process is aimed at: • Gaining the relevant and the maximum information regarding the complaint. • Providing help and guidance towards additional tests or further investigations. • Corroborating the information collected as to the likely cause(s) of the complaint. When the information from one aspect of the diagnostic procedure does not tally with the results from another aspect of the diagnostic procedure(s), it may mean that further investigations are required, and/​or the information collected so far maybe incorrect and/​or insufficient. Diagnostic errors usually arise when the process is not performed in a systematic and methodical manner or some of the steps have been missed. For example, if the clinical examination is only cursory, this may lead to the clinician choosing the wrong investigations and, more crucially, the formulation of an incorrect treatment plan.

• Angioedema • Lymphadenitis Musculoskeletal

• Temporomandibular joint dysfunction • Masticatory muscle disorders • Myocardial infarction (referred pain)

Neuropathic

Neurovascular

Patient history

• Presenting complaint

• Trigeminal neuralgia

• History of the presenting complaint

• Atypical odontalgia

• Dental history

• Post-​herpetic neuralgia

• Medical history

• Tension-​type headaches • Migraine • Cluster headaches

Psychogenic

Table 3.2  The stages involved in reaching a diagnosis

• Major depressive disorders • Anxiety disorders

• Personal history Examination of the patient

• Extraoral

Special investigations

• Sensibility testing

• Intraoral • Radiographic examination

What are the aims of history taking?

23

What are the aims of history taking? The primary aim of history taking is to gain as much relevant information as possible from the patient to arrive at an initial provisional diagnosis. It is, therefore, important to ask appropriate questions and listen carefully to what the patient has to say. History taking also aims to:

Oral hygiene and dietary habits

• Guide the clinician in deciding what to concentrate on during examination and what special investigations will be necessary to confirm a diagnosis.

The patient’s oral hygiene and dietary habits should be noted. The level of sugar consumption and the acidic components in their diet should also be determined. Key questions may help in elucidating causal factors related to the patient’s complaint. For example, a patient with a ‘sweet tooth’ will be more susceptible to caries, which may, eventually, lead to pulpal involvement.

• Establish a rapport and trust with the patient.

Previous trauma

• Gain insight into the patient’s motivation and assess the patient’s expectations from dental treatment. • Reveal any potential complications that may dictate the need to modify the treatment plan. The amount of useful information gleaned from the patient will vary and is dependent on several factors. These include the patient’s ability to convey or describe the symptoms experienced and its accuracy; the severity of the distress, discomfort, or pain; and the impact of the symptoms on the patient. At times, a patient may present with more than one complaint. In these situations, it is prudent to concentrate on each complaint separately according to their seriousness or urgency. Other factors include the clinician’s experience, chairside manner, and rapport with the patient. This section will focus on aspects of history taking that are of direct relevance to endodontics.

Presenting complaint

It may be pertinent to ask the patient if there is a history of dental trauma related to the tooth in question. Dental trauma more frequently involves anterior rather than posterior teeth. For example, pulpal necrosis or discolouration of an unrestored anterior tooth may have been caused by previous traumatic injury such as a sports-​related accident or alleged assault.

Recent dental treatment In some cases, the patient’s presenting symptoms may be associated with recent dental treatment. For example, tenderness to biting (and percussion) associated with a recently restored tooth may be due to a high spot on the restoration. A poorly contoured restoration with no or a poor contact may result in gingival irritation due to food packing, which may present as a toothache.

Medical history

The diagnostic process starts with asking the patient why they are seeking dental care. The opening question should be simple and to the point, for example: ‘How can I help you?’ The patient’s presenting complaint should be in their own words. Endodontic problems commonly include pain/​discomfort, swelling, discharge, bad taste, and/​or tooth discolouration. The history of the presenting complaint should then be explored to find out how long the patient has been suffering, and if or how the symptoms have changed with time.

The aim of the medical history is to ascertain if there are any medical conditions that may directly or indirectly influence patient management. It is, therefore, essential that the medical history is thorough and up to date. If there are any uncertainties or queries about the general health of the patient, or if it is likely to have an impact on treatment, it is advisable to liaise with the patient’s general medical practitioner or their medical consultant. Although there are no medical conditions which strictly contraindicate endodontic treatment, there are some conditions that may modify the endodontic management. Common medical problems that may influence or require modification of the treatment plan include:

Dental history

• Blood dyscrasias or anticoagulation therapy.

The aim of the dental history is to gain an insight into what previous dental treatment has been carried out, as well as the patient’s attitude towards dental treatment and their own teeth.

Attendance It is useful to know about the past dental history to establish whether the patient is a regular attender or only attends when in pain. A patient in the latter category may be less motivated. If pain is the reason for seeking a second opinion, it is worthwhile establishing whether the presenting complaint may be related to recent dental treatment with another dentist. The patient should be asked for details about any recent dental treatment.

• Recent history of myocardial infarction. • Immunocompromised patients. • Steroid treatment or recent history of steroid treatment. • Bisphosphonate treatment or history of bisphosphonate treatment. • Poorly controlled diabetes. • History of depression or psychiatric illness. • Pregnancy. • Allergies. Often, the patient’s medical history may only be an issue depending on the type of treatment required. For example,

24

Diagnosis, treatment planning, and patient management

non-​surgical endodontic treatment of a patient on anticoagulant therapy rarely presents problems. However, if the patient requires surgical endodontics then the anticoagulant therapy may have to be altered. A patient who is on or has been on bisphosphonates is another example; in these cases, extraction, even of a very compromised tooth, may be inadvisable and endodontic treatment may be the treatment of choice. Before prescribing any type of medication as part of dental treatment, it is essential that checks are made on possible interactions with any medication the patient may be taking. A  note should also be made of any antibiotics (including dosage, frequency, and duration) the patient may have taken recently, as this may influence the prescription of further antibiotics that may become necessary. Specific questions regarding allergy to latex, household bleach, and iodine compounds, for example, should be asked as these materials and chemicals are commonly used in endodontic treatment. Previously, patients considered at risk of infective endocarditis undergoing interventional procedures were given antibiotic prophylaxis. As a result, patients with a wide range of cardiac conditions, including a history of rheumatic fever, were prescribed this preventative measure. However, the current medical consensus is that there is

little evidence to support this empirical practice. Antibiotic prophylaxis has not been proven to be effective and there is no clear association between episodes of infective endocarditis and interventional procedures. In addition, any benefits from prophylaxis need to be weighed against the risks of adverse effects for the patient and of antibiotic resistance developing. Following newer guidelines issued by the National Institute for Health and Clinical Excellence (NICE), antibiotic prophylaxis should no longer be routinely offered for defined interventional procedures. It is advisable to liaise with the patient’s general medical practitioner or their cardiologist if clarification on the need for antibiotic prophylaxis is required.

Personal history It is useful to obtain an insight into the patient’s personal and professional lifestyles as there may be clues to possible contributory or aetiological factors that may have a bearing on the presenting complaint. A classic example is pain from temporomandibular dysfunction, initiated or aggravated by episodes of stress in a patient’s personal or professional life, which may be mistaken for an endodontic problem. Patients should also be asked if they think or know that they clench their teeth during the day and/​or while they sleep.

What are the aims of the extraoral examination? In the dental/​endodontic context, the aims of the extraoral examination are to assess the head and neck region whilst looking for signs that may be related to pulpal or periapical diseases, for example a

facial swelling. The muscles of mastication, lymph glands, and temporomandibular joints may also be assessed.

What are the aims of the intraoral examination? The aims of the intraoral examination are to gain a general view of the mouth, and then a specific view of the area(s) of the main complaint. The intraoral examination should be sufficiently detailed to detect

signs of non-​endodontic and endodontic disease. It is also important to assess the patient’s tolerance of dentistry.

What are the aims of special investigations? Special investigations or tests are needed to corroborate or exclude initial findings and to obtain further information of relevance. They may also be used to identify or confirm the provisional diagnosis by reproducing the reported symptoms, for example cold sensibility testing. The commonest special investigations carried out are sensibility testing and radiographic examination.

Sensibility testing The aim of sensibility testing (traditionally referred to as vitality testing), is to attempt to assess the health of the pulp. As it is reliant on the responsiveness of the nerve supply to the applied stimulus (electric or thermal), sensibility testing equipment can only provide an indication but not an absolute confirmation of pulpal health. Sensibility

testing assumes that the status of the nerve supply of the tooth is a reflection of the status of the blood supply. It is important to be aware that sensibility testing may provide false positive, as well as false negative results. A positive response is usually due to stimulation of Aδ nerve fibres by the electric stimulus or contraction/​expansion of the fluid within the dentinal tubules by thermal stimulus. If the sensation disappears quickly following removal of the stimulus, this is considered to indicate that the pulp-​dentine complex is healthy. When a lingering dull ache persists following the removal of the stimulus, suggesting that there has been stimulation of the C fibres, this is considered indicative of irreversible pulpal inflammation. No response from pulp testing indicates that the tooth is non-​vital, that is, the pulp is necrotic, or the tooth has already been endodontically treated.

What are the aims of special investigations? Radiographic examination Preoperative periapical radiographs should always be taken as part of the diagnostic process. Periapical radiographs are usually the most valuable radiographic views of the teeth and their surrounding periapical structures. Periapical radiographs may reveal clues about the status of the pulp. There may be obvious signs of pulpal involvement:  for example, a periapical radiolucency (Figure 3.1), evidence of caries (Figure 3.2), or resorption (Figure 3.3). However, more subtle signs of pulpal involvement include the presence of tertiary dentine (Figure 3.4), calcified root canals (Figure 3.5), and widening of the periodontal ligament space. Periapical radiographs may also reveal signs indicative of a vertical root fracture such as the unique circumferential pattern of bone loss (Figure 3.6) or visible separation of the fractured fragments (Figure 3.7). It must be remembered that the absence of a periapical radiolucency does not rule out the possibility of a chronic inflammatory process occurring apically. Bone loss as a consequence of an infected root canal system is detected on a radiograph only after there has been significant demineralization of the alveolar bone, usually perforation of the cortical plate, adjacent to the apices of the affected tooth. A periapical radiopacity may also be indicative of an underlying pathological process. Low-​grade chronic inflammation due to an endodontic problem may cause condensing osteitis, that is, the formation of dense, sclerotic bone around the tooth apex. It may be necessary to take additional ‘angled’ views by changing the horizontal plane of the X-​ray tube head by 10–​15º in a distal direction to separate otherwise superimposed roots, thus allowing them to be assessed more accurately. The ‘parallax principle’ or ‘buccal object rule’ may be used to locate the relative positions, in the bucco-​lingual plane, of two objects to each other, which may appear superimposed on one another. The radiographic position of the two objects will (a)

25

alter when the angle, either horizontal or vertical, of the X-​ray tube, and therefore, the X-​ray beam is changed. The more buccally located object will move in the opposite direction to which the X-​ray tube is moved. Lingually or palatally located objects will move in the same direction as that of the X-​ray tube. This is useful when roots overlie each other in the radiographic plane: for example, maxillary first premolars, or to distinguish between the mesial roots of a mandibular first molar. Bitewing radiographs are a useful adjunct in those cases where the presence of proximal caries in relation to the pulp chamber anatomy needs to be confirmed. In some cases, a dental panoramic radiograph may also be indicated. Occlusal radiographs should be avoided as the image produced is distorted and therefore does not convey the true nature of the underlying hard tissue problem. One of the very few indications for the use of bisecting angled radiographs is the detection of a possible horizontal root fracture. The fracture line will only be revealed if the X-​ ray beam passes within 15º of the plane of the fracture. Therefore, if there is a possibility of a horizontal root fracture, bisecting radiographs should be taken at two or three different horizontal angles in the same vertical plane. Digital radiography is now becoming more common in dentistry. Two types of direct digital image receptors are available: solid state or photostimulable phosphor storage plates. The photostimulable phosphor storage plates are placed in a special processor and scanned by a laser, resulting in a digital image. The solid state sensors may be charge-​coupled devices (CCD) or complementary metal oxide semiconductors (CMOS); the X-​ray energy is detected, and when transferred to a computer, it is processed into a digital image. Conventional radiographic images captured on X-​ ray films or via digital sensors are two-​ dimensional ‘shadowgraphs’ with inherent problems of geometric distortions and anatomical noise. Over the past two decades, cone beam computed tomography (CBCT) has been introduced into dentistry. Cone beam computed

(b)

Figure 3.1  Periapical radiographs showing periapical radiolucencies associated with (a) a mandibular incisor and (b) a mandibular molar.

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Diagnosis, treatment planning, and patient management

Figure 3.2  Periapical radiograph showing caries associated with a mandibular premolar.

Figure 3.3  Periapical radiograph showing external cervical resorption associated with a mandibular second molar.

Figure 3.4  Periapical radiograph showing partial calcification of the pulp chamber associated with the mandibular first molar.

Figure 3.5  Periapical radiograph showing partial calcification of the root canal associated with the maxillary central incisor.

Figure 3.6  Periapical radiograph showing circumferential radiolucency, in keeping with a vertical root fracture, associated with the mesial root of an endodontically treated mandibular first molar.

Figure 3.7  Periapical radiograph showing a visible vertical root fracture associated with the distal root of an endodontically treated mandibular first molar.

What are the aims of special investigations?

27

Box 3.1  Benefits of cone beam computed tomography over conventional radiography • Three-​dimensional images are produced. • Accurate reproduction of structures with no geometric distortion. • Elimination of anatomical noise which may mask the area of interest.   

tomography is an extraoral imaging system, which can produce three-​ dimensional scans of the maxillofacial skeleton with an effective dose, which is comparable to conventional radiographs. It offers many benefits over, and can be used as an adjunct to, conventional radiography (Box 3.1). The volumetric data set obtained from the CBCT scanner (Figure 3.8) is reconstructed using sophisticated computer software to allow viewing of the image in three orthogonal planes: axial, sagittal, and coronal simultaneously (Figures 3.9 and 3.10). An area can be assessed by selecting and moving the cursor on a chosen image, which simultaneously alters the other reconstructed slices. In endodontics, CBCT with limited field of view is suitable as it captures small volumes of data that can include just 3–​4 individual teeth, and thus limits the area being irradiated to the area of interest. The radiation dose is equivalent to 2–​4 periapical radiographs. For example, the 3D Accuitomo (J Morita Corporation, Osaka, Japan) captures a 40 mm (height) by 40 mm (diameter) volume of data, which is similar in overall height and width to a periapical radiograph. Due to its increased sensitivity, CBCT can detect endodontic lesions which are not visible on conventional radiographs. Box 3.2 gives the situations where CBCT with limited field of view may be considered. It should be emphasized that the use of CBCT should be limited to complex cases that should be assessed and treated by a specialist in endodontics.

(a)

(b)

Figure 3.8  Cone beam computer tomography scanner (3D Accuitomo 170 CBCT scanner, [Morita, Japan] at the Dawood & Tanner specialist dental practice).

(c)

(d)

Figure 3.9  Dens-​in-​dente: (a) conventional radiograph, and cone beam computed tomography images; (b) axial; (c) sagittal; and (d) coronal planes.

28 (a)

Diagnosis, treatment planning, and patient management

(b)

(c)

(d)

Figure 3.10  External cervical resorption: (a) conventional radiograph, and cone beam computed tomography images; (b) axial; (c) sagittal; and (d) coronal planes.

Box 3.2  Cone beam computed tomography with limited field of view may be considered in the following situations in endodontics • Diagnosis of radiographic signs of periapical pathosis when there are contradictory (non-​specific) signs and/​or symptoms. • Assessment and/​ or management of complex dento-​ alveolar trauma, which may not be readily evaluated with conventional radiographic views. • Appreciation of extremely complex root canal systems prior to endodontic management (e.g. class III & IV dens invaginatus). • Assessment of extremely complex root canal anatomy in teeth treatment planned for nonsurgical endodontic re-​treatment. • Assessment of endodontic treatment complications (e.g. perforations) for treatment planning purposes when existing conventional radiographic views have yielded insufficient information. • Assessment and/​or management of root resorption, which clinically appears to be potentially amenable to treatment. • Pre-​surgical assessment prior to complex periradicular surgery (e.g. posterior teeth).   

Adapted from the European Society of Endodontology position statement: the use of CBCT in endodontics (2014).

How do you arrive at a diagnosis? This section covers some of the basics on how to arrive at a diagnosis and the common errors in diagnosis. The process involves collecting, assessing, and processing the information in order to arrive at a diagnosis. It is not a skill that can be learned just by reading textbooks; it requires practice, experience, and reflection. There are many, often conflicting, pieces of information that must be assessed and prioritized. The synthesis of clinical data, higher-​order thinking, critical reasoning, and problem-​solving will lead to decision-​making and a diagnosis, all of which takes time to learn. Crucial to endodontic diagnosis is the relationship between symptoms, signs, and the histopathological state of the pulp.

Unfortunately, these relationships are not easy to elucidate; they are not always clearly defined or reproducible. The differential diagnosis of the pulpal and periapical conditions is dependent on the presenting symptoms, and clinical and radiographic signs (Table 3.3). As it is impossible to accurately diagnose the status of the pulp from clinical signs and symptoms, it has been suggested that the terms:  ‘acute’ or ‘chronic’ may not be appropriate. Instead, the terms ‘symptomatic’ and ‘asymptomatic’ may be preferable. The terms ‘apical’, ‘periapical’, and ‘periradicular’ have also been used interchangeably.

How do you take a history?

29

Table 3.3  Pulpal and periapical conditions Condition

Characteristics

Healthy pulp

• Symptom-​free • Positive response to sensibility testing

Reversible pulpitis

• Sharp, transient pain • Does not linger when stimulus removed • Often poorly localized • No tenderness to percussion • No obvious radiographic changes

Irreversible pulpitis

• Dull, throbbing pain, may be spontaneous • Lingers when stimulus removed • May be kept awake at nights • Usually no tenderness to percussion

Pulp necrosis

• May or may not be painful • No response from sensibility testing or partial response in multi-​rooted  tooth • Usually no obvious radiographic changes

Healthy periapical tissues

• No tenderness to percussion or palpation • Lamina dura intact and uniform periodontal ligament space

Acute periapical periodontitis

• Pain on biting and percussion or palpation • Slightly widened periodontal ligament space • Thinning of the lamina dura • Periapical radiolucency may be present

Acute periapical abscess

• Rapid onset, spontaneous pain • Tooth tender to any pressure and may be mobile • Swelling present

Chronic periapical periodontitis

• Often symptom-​free or only very mild symptoms • Widened periodontal ligament space • Periapical radiolucency present

Chronic periapical abscess

• Usually symptom-​free • Sinus tract present • Periapical radiolucency present

Condensing osteitis

• Usually symptom-​free • No radiolucency, instead a periapical radiopacity

How do you take a history? It is essential that the clinician is attentive, sympathetic, and interested in the patient’s presenting complaint. This will result in the patient being more inclined to provide a full and accurate account of their complaint. It is advisable to always ask open-​ended, non-​leading questions instead of those that only require a ‘yes’ or ‘no’ answer. The questions asked should also be easy to understand and unbiased. By doing this, it allows the patient to explain and describe their complaint

in their own words. If necessary, further questions for the purpose of clarification should be asked.

Presenting complaint It is useful to have a mental checklist of the type of questions that should be asked that will cover the various aspects of the presenting

30

Diagnosis, treatment planning, and patient management

complaint. As many endodontic complaints are related to pain, the questions asked are often directed at obtaining a pain history and covering the following features: • Character • Duration or onset • Frequency • Severity • Site • Radiation • Provoking or relieving factors • Associated factors Therefore, the following are examples of questions that may be asked as part of endodontic history taking: • How may I help? What is the problem? • When did you first notice the problem? How long have you had pain?

Dental history Examples of questions that should be asked during dental history taking include: • Are you anxious about having dental treatment? • Have you had any previous bad dental experiences? • When was your last visit to a dentist or dental professional? • How often do you attend your dentist? • How often do you clean your teeth? • What dental cleaning products do you use? • Do you have a sweet tooth? • Do you recall any trauma or knocks to your teeth? • Have you had orthodontic treatment? • Have you had recent dental treatment? (if so, what, where, when, and from whom?)

• What does the pain feel like? How would you describe the pain?

Medical history

• Has the pain coincided with any recent dental treatment?

A medical history questionnaire should be used to provide a comprehensive record so that no items of importance are missed. There are many examples of pro forma questionnaires, which are available from commercial sources, dental associations, or specialist societies. It is useful to ask the patient to complete the medical history questionnaire in advance; this can then be discussed during the consultation. Questions should include current and previous medications, allergies, serious illnesses, and, when appropriate, pregnancy status.

• What brings on the pain? • Where is the pain located? • How long does the pain last? • When does it hurt most? • What makes the pain better? • What makes the pain worse? • Is there anything else associated with the pain? • Is the pain sharp or dull in nature?

How do you carry out an extraoral examination? An extraoral examination commences as soon as you meet the patient. It should be carried out by viewing the patient from the front and above while they are in a reclined position in the dental chair. The extraoral examination should include assessment of: • Patient anxiety. • Patient cooperation: can the patient tolerate treatment in a supine position? • Facial asymmetry. • Extraoral swelling, including size, location, consistency. • Extraoral sinus tracts (Figure 3.11). • Trauma to the orofacial region. • Head and neck lymph nodes for lymphadenopathy. • Temporomandibular joint dysfunction, for example tenderness to palpation of the muscles of mastication, clicking or crepitus of the temporomandibular joint.

Figure 3.11  Extraoral sinus tract.

How do you carry out an intraoral examination?

31

How do you carry out an intraoral examination? Magnification devices, for example dental loupes or dental operating microscope (Figure 3.12), with co-​axial illumination are helpful for carrying out an intraoral examination. The intraoral examination should include assessment of: • Patient’s tolerance of dentistry. • General examination of the mouth. • Specific examination of the area(s) of main complaint.

Patient’s tolerance of dentistry Patient’s tolerance of dentistry should be assessed, including: • Mouth opening. Does the patient have adequate mouth opening to access the tooth? Can the patient open their mouth adequately and comfortably for a long period of time? • Gag reflex. Can the patient tolerate radiographs and rubber  dam?

It may be challenging or impossible to perform endodontic treatment if the patient has restricted mouth opening or a pronounced gag reflex.

General examination of the mouth The general state of the oral cavity should be surveyed before homing in on the area of interest related to the main complaint. The general examination should include checking for the following: • Abnormal appearance of the oral mucosa, for example sinus tract, ulceration or erythema. • Frictional keratosis (Figure 3.13) or scalloping of the tongue (common signs of parafunction). • Presence, location, tenderness, consistency, and size of any soft tissue abnormalities and swellings. • Missing or unopposed teeth. • Oral hygiene status (Figure 3.14) and basic periodontal examination. • Food traps and plaque retentive factors. • Tooth discolouration (Figure 3.15). • Tooth surface loss (Figure 3.16). • Caries (Figure 3.17). • Quality and quantity of the existing dental treatment or restorations (Figure 3.18). • Signs of marginal leakage. • Fractured teeth or restorations (Figure 3.19). All of this information should then be correlated to the patient’s past dental history.

Specific examination of the area(s) of main complaint Figure 3.12  Dental operating microscope (Global Surgical, St Louis, MO, USA).

Figure 3.13  Buccal linear keratosis.

The area(s) in question should be assessed visually in the first instance. The location, size, and consistency, for example rubbery, firm, or

Figure 3.14  Poor oral hygiene: plaque accumulation and gingivitis of a 10 year old who has traumatised their maxillary anterior teeth.

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Diagnosis, treatment planning, and patient management

(a)

(b)

Figure 3.15  Discolouration: (a) dark discolouration of a maxillary central incisor, (b) pink discolouration (white arrow) at gingival margin of a maxillary central incisor, also note the translucency and wear of the incisal edges-this patient also had acid reflux and parafunctional habits.

fluctuant, and localized or diffused, of any soft or hard tissue swellings should be noted (Figure 3.20). Similarly, any abnormal appearance of the mucosa overlying the area in question, for example the presence of a sinus tract should be noted. Where appropriate, diagrams and photographs of the relevant findings may be used to supplement note taking.

Palpation The mucosa on either side of the area related to the main complaint should be palpated gently using finger pressure (Figure 3.21). A note should be made of any tenderness, the extent and severity; the contralateral and adjacent quadrant should also be palpated for comparison. Tenderness or swelling of the overlying mucosa usually indicates that infection or inflammation has extended beyond the apex and into the overlying soft tissues. Figure 3.16  Marked tooth surface loss may affect the integrity of the pulp.

Figure 3.17  Caries: distal cavitation and occlusal staining.

Figure 3.18  Unsatisfactory restoration with no contact point, resulting in food packing and gingival irritation.

Figure 3.19  Fractured teeth and restorations.

How do you carry out an intraoral examination?

33

Mobility Tooth mobility should be noted and graded according to the extent. Excessive mobility may be due to loss of attachment as a result of chronic periodontal disease or an acutely inflamed periodontal ligament resulting from pulpitis or occlusal trauma. Other common causes of excessive mobility include a vertical or horizontal root fracture or a decemented post. With fingers or the end of two mirror handles placed on opposing sides of the tooth, pressure is applied in both vertical and horizontal directions. The extent of any mobility is graded accordingly: • Grade I: just perceptible, slightly more than normal movement. • Grade II: >1 mm in any horizontal direction. • Grade III: >1 mm in any horizontal or vertical directions.

Periodontal probing

Figure 3.20  Intraoral swelling (yellow arrow) related to a maxillary posterior tooth.

A detailed periodontal examination should be carried out on the tooth under investigation. Attachment loss may be due to periodontal disease, vertical root fracture, or iatrogenically-​induced perforation. When carrying out periodontal probing (Figure 3.23a), the periodontal probe should be ‘walked’ around the whole circumference of the tooth. Otherwise, it is not uncommon to miss an isolated, deep periodontal pocket, which may be indicative of a vertical root fracture (Figure 3.23b).

Occlusal examination Occlusal examination comprises:

Percussion The tooth or teeth should, initially, be gently pressed with a finger to see if there is any tenderness. If necessary, greater force may be applied using the end of a mirror handle (Figure 3.22). However, the end of a mirror handle should never be used with unnecessary force when carrying out this test. With a posterior tooth, it is important to tap each cusp and therefore, each root, as only one root may be tender to percussion. Tenderness to percussion indicates that infection or inflammation has involved the periodontal ligament. However, a common non-​endodontic cause is occlusal trauma from bruxism, and/​ or occlusal interferences (e.g. high restorations).

Figure 3.21  Tenderness to palpation assessed by gently pressing the mucosa, also note the wear of the incisal edges/tips of the maxillary left lateral incisor and canine teeth.

• Assessing for signs of excess occlusal loading and/​or parafunctional habits (clenching and/​or grinding), for example loss of canine guidance, faceting, chipped incisal edges (Figures 3.21, 3.24). • Assessing the occlusion in retruded contact and intercuspal positions, and then lateral excursions. Articulating paper may be used to identify points of premature contact. • Occlusal factors may cause:

• Temporomandibular

joint or related muscle pain, which may present as symptoms similar to pulpal or periapical disease. • Propagation of cracks in teeth, which may then give rise to endodontic problems, such as ‘cracked tooth syndrome’ or, by acting as an entry route for microbes leading to pulpal inflammation, necrosis and infection.

Figure 3.22  Gentle percussion of a tooth with a mirror handle.

34

Diagnosis, treatment planning, and patient management

Assessment of teeth The strategic nature of the tooth or teeth under investigation should be assessed as this may well have a bearing on the final treatment plan. For example, an unopposed and non-​functional tooth may be better extracted. A note should be made of any breach of tooth structure, as this may initiate and perpetuate pulpal and periapical diseases. Magnification in the form of dental loupes or operating microscope is of tremendous help. It is important to look out for: • Infractions, crazing, and fracture lines in the enamel (Figure 3.25). Detection may be aided by transillumination, special dyes, or a tooth sleuth (Figure 3.26). • Primary and recurrent secondary caries (Figure 3.17). • Restorations with signs of microleakage or macroleakage (Figures 3.18 and 3.19), for example ditching, poorly adapted restorations, and discoloured margins, which causes plaque retention, may lead to pulpal involvement, or food packing, which may mimic pulpal symptoms.

(a)

• Exposed dentine may give rise to thermal hypersensitivity or pulpal changes. • Exposed pulpal tissues, for example a complete crown fracture following trauma, or gross caries. An assessment should be made as to the likely amount of sound coronal tooth tissue that would remain after removal of caries and the previous restorations as this will provide guidance as to the restorability of the tooth. Endodontic treatment is futile when carried out on a tooth that is clearly unrestorable. It is also pertinent to consider the type of post-​endodontic restoration the tooth may require as part of treatment planning. Any colour differences should be noted (Figure 3.15) as these may be a sign of pulpal haemorrhage, pulpal necrosis, microleakage, or staining from the root canal filling material. The following should be recorded: • Intrinsic or extrinsic discolouration. • Degree of discolouration. • Uniformity of the discolouration. • Extent of the discolouration (partial or total). (b)

Figure 3.23  Vertical root fracture of a maxillary central incisor restored with a post-​retained crown. (a) ‘Walking’ the periodontal probe around the gingival sulcus reveals a deep, isolated, and narrow periodontal pocket adjacent to the fracture line. (b) Fractured tooth fragments following extraction. (a)

Figure 3.24  (a) and (b) Chipped and worn incisal edges.

(b)

How do you carry out special investigations?

Figure 3.25  Enamel infraction lines associated with maxillary incisor teeth.

35

Figure 3.26  A ‘tooth sleuth’ over a selected cusp and then asking the patient to close down firmly. If a crack is present, then the wedging forces will provoke a painful response.

How do you carry out special investigations? Sensibility testing

• Repeat the test if necessary.

The following are essential for predictable and accurate sensibility testing:

• Record all the findings.

• Be aware of false positive or false negative test results.

• Explain the nature of the test to the patient.

Electric testing

• Request that the patient indicates, for example by raising a hand, when the stimulus is felt.

An electric current from a battery-​ operated device (Figure 3.27) is used as the stimulus in this test. A  small clip is hooked onto the patient’s lip and the probe is placed on the coronal half, usually the labial/​buccal surface (Figure 3.28), of the tooth in question to complete the circuit. Alternatively, the patient is allowed to hold the handle of the test probe, which is in contact with the tooth, and this completes the circuit. A  conducting medium such as toothpaste or prophylaxis paste is essential to improve the conduction of the electrical current from the probe to the tooth. The patient is asked to indicate by, for example raising a hand, or letting go if they are holding the handle of

• Dry the tooth to be tested with gauze or cotton wool pledgets. • Isolate the tooth with cotton wool rolls. • As a control, test a healthy tooth first. • Test the questionable tooth next. • Test an adjacent and a contralateral tooth to gain a more objective comparison. • Test both the buccal and lingual/​palatal aspects of multirooted  teeth.

Figure 3.27  An electric pulp tester: Digitest (Parkell, Edgewood, NY, USA).

Figure 3.28  An electric pulp tester in use. The probe of the electric pulp tester is placed on the buccal surface of the tooth. Prophylaxis paste has been used as a conducting medium.

36

Diagnosis, treatment planning, and patient management

the test probe, when they feel warmth or tingling on the tooth being tested. With some electric pulp testers on the market, the electric current passing through the tooth will increase automatically the longer the probe is in contact with the tooth; the rate at which the current increases may also be adjusted. If a tooth has a full coronal coverage restoration, for example a crown, there is no natural tooth surface for probe placement to carry out electric pulp testing. With some electric pulp testers, a finer probe is available, and it may just be possible to place this fine probe on uncovered tooth tissue near the crown margins.

Cold testing Cold tests can be performed using a variety of materials and equipment: • Ice. • Ice cold water while the tooth is isolated under rubber dam. • Ice crystals formed on foam pellets or cotton wool pledgets using refrigerant sprays. • Dry ice sticks (CO2 snow).

It is generally accepted that the colder the stimulus, the more reliable the test. Ice and ethyl chloride are not cold enough to be sufficiently discriminatory and may give rise to false negative results; the authors do not recommend either of these. Refrigerant spray is recommended as it is easy to use and readily available (Figure 3.29). This is applied to a foam pellet or cotton wool pledget. Sufficient time should be allowed for ice crystals to form prior to application on the tooth surface (Figure 3.30).

Heat testing Heat tests can be performed using a variety of materials and equipment: • Warm gutta-​percha (GP) point/​pellet/​stick (Figure 3.31). The point of application on the tooth should first be coated with a separating medium, such as petroleum jelly, to prevent the warm GP from sticking to the tooth. • Warm, not hot or boiling, water while the tooth is isolated under rubber dam (Figure 3.32). • Heated probe, for example Elements Obturation Unit (Kerr Endodontics, Orange, CA, USA). • A rotating prophy cup to create frictional heat.

Figure 3.29  Examples of refrigerant sprays: (left) Endo Cold Spray (Henry Schein UK Holdings Ltd, Gillingham, UK), (right) Endo-​Frost (Coltene/​Whaledent AG, Alstatten, Switzerland).

Figure 3.30  Cold testing being carried out; ice crystals have formed on the foam pellet following application of a refrigerant spray.

Figure 3.31  Heat testing being carried out using a warm GP point.

Figure 3.32  Heat testing being carried out by syringing warm water on to a tooth isolated with rubber dam.

How do you carry out special investigations?

(a)

37

(b)

Figure 3.33  Beam-​aiming paralleling devices: (a) for anterior teeth and (b) for posterior teeth.

Test cavity preparation As a last resort, a small test cavity may be prepared in the tooth but without local anaesthetic. The patient is advised to signal if any pain is felt. It is prudent to be aware that with some patients, especially if they are nervous, a false positive result may be obtained. It must be emphasized that indiscriminate test cavity preparation purely for the purpose of ascertaining pulpal health is inadvisable.

Radiographic examination Every aspect of endodontics is heavily reliant upon information gained from radiography. Radiographs are usually needed preoperatively, intraoperatively, postoperatively, and at reviews.

Periapical radiographs Radiographs (film-​based or digital) should be taken using a beam-​ aiming, paralleling device to ensure undistorted and reproducible (a)

images (Figure 3.33). These devices are designed for use with both anterior and posterior teeth. The radiograph should show the whole tooth together with at least 3–​4  mm of surrounding bone (Figure 3.34). When examining a periapical radiograph, start initially with an overview of the teeth and structures visible. Next, focus on the area of interest and then the tooth or teeth concerned. The features to note and to assess when viewing a periapical radiograph are covered in Table 3.4. If there is an intraoral or extraoral sinus, the source of the infection may be traced by inserting a GP point into the sinus tract(s) and taking a periapical radiograph (Figure 3.35).

Parallax This involves taking two periapical radiographs at slightly different horizontal angles of about 10–​15º. A horizontal shift of the X-​ray tube may produce more relevant information about the tooth under investigation (Figure 3.36).

(b)

Figure 3.34  Periapical radiographs taken using a beam-​aiming paralleling device showing (a) anterior teeth and (b) posterior teeth.

38

Diagnosis, treatment planning, and patient management

Table 3.4  The features to note and assess when interpreting a periapical radiograph General overview

Tooth and area of interest

• Caries status

• Quality of any root canal fillings

• Periodontal health

• Abnormalities/​pathosis

• Quality of existing restorations

• Relationship to vital structures, e.g. maxillary sinus, inferior dental bundle

Crown of tooth

• Caries • Quality of existing restoration: overhangs, marginal fit, contact points • Amount of tooth structure

Periodontal and periapical tissues

• Level and quality of crestal bone • Vertical/​horizontal/​furcation bone  loss • Continuity and width of the periodontal ligament space • Integrity and thickness of the lamina dura • Presence of any radiolucent or radiopaque areas • Relationship to adjacent anatomy (e.g. inferior dental nerve)

Roots and root canal system

• Number, length, form, and shape of roots • Outline and curvature of the root canal(s) • Calcifications of the root canal or pulp chamber • Root resorption • Root fracture • Quality and type of any root canal fillings present • Iatrogenic problems, for example separated file, root perforation

(a)

(b)

Figure 3.35  Two GP points have been used to ‘track’ the sinus tracts: (a) clinical view and (b) periapical radiograph.

What are the common errors in diagnosis?

(a)

(b)

(c)

(d)

39

Figure 3.36  Parallax radiography: two periapical radiographs are taken (a) straight on and (b) with a horizontal shift of 10º to the distal. Parallax views of an endodontically treated mandibular molar provide a better appreciation of the quality of the root canal fillings in both the mesial and distal roots: (c) normal view and (d) distal view.

What are the common errors in diagnosis? Endodontic diseases usually manifest clinically in the form of pain, swelling, and/​ or a periapical radiolucency. However, the clinician should always be aware that there are also non-​endodontic causes, which may mimic endodontic problems; detailed explanations on the subject are provided in standard texts on oral medicine and oral pathology and they should be consulted.

Limitations of radiographs In certain situations, an incidental radiographic finding of a periapical radiolucency may be the only sign of endodontic disease in an otherwise symptom-​free tooth (Figure 3.37). However, it must be remembered that not all radiolucencies are indicative of pathosis. It is well established that in some cases, conventional radiographs reveal

40

Diagnosis, treatment planning, and patient management

Figure 3.37  Large periapical radiolucency associated with symptom-​free  teeth.

Figure 3.38  Radiographic appearance of the mental foramen (yellow arrow) may be mistaken for the presence of periapical pathosis.

limited information of the dento-​alveolar anatomy because of their two-​ dimensional nature, geometic distortion, and anatomic noise. An example of ‘noise’ is the radiographic appearance of the mental foramen or incisive foramen which may be mistaken for a lesion (Figure 3.38). The dental anatomy can only be assessed in the mesio-​ distal plane; the bucco-​lingual plane is compressed and cannot be assessed. Finally, geometric distortion in the radiographic image is inevitable as it is impossible to align the image sensor parallel to the long axis of the tooth and perfectly perpendicular to the X-​ray beam; this distortion is worse in the maxilla than in the mandible. Alternatively, radiographic examination may reveal signs of endodontic or periodontal disease which are not related to the patient’s perceived problems but in the region of the reported problem area; this may be attributed wrongly to the symptoms or clinical findings. It may result in misdiagnosis and, possibly, incorrect treatment being carried out. A differential diagnosis of radiographic lesions is dependent on the location, size, shape, radiodensity, outline, and effect on neighbouring structures. A summary is shown in Box 3.3. and revision on the subject by consulting the relevant books is recommended. Examples of errors that occur when over-​reliance is placed on radiographic findings alone include the following:

will help confirm that these ‘radiolucencies’ are anatomical landmarks. Additional existing radiographs, for example panoramic views, showing the contralateral side may also help confirm the position of the mental foramen, which should be in a symmetrically similar location. Widening of the periodontal ligament space and apparent radiolucencies may

Anatomical landmarks The radiolucent shadows of the mental and incisive foramina may be mistaken for lesions associated with periapical diseases. Sensibility testing

Box 3.3  Differential diagnosis of radiolucent lesions Normal anatomy • Mandible, for example mental foramen, inferior dental canal. • Maxilla, for example maxillary sinus, incisive foramen. Artefact • Processing errors. Pathological* • Infection, for example periapical periodontitis. • Trauma, for example extrusion injury, alveolar fracture. • Odontogenic cysts, for example radicular cyst, dentigerous cyst, odontogenic keratocyst, nasopalatine duct cyst. • Odontogenic tumours, for example odontoma, ameloblastoma, ameloblastic carcinoma. • Bone tumours and related lesions, for example giant cell lesion, fibro-​cemento-​osseous dysplasia.   

Adapted from WHO Classification of Head and Neck Tumours, 4th edition (2017).

*

Treatment planning

also be due to superimposition of root apices over the maxillary sinuses and the inferior dental canal. Sparse bony trabeculation and varying bone density may also be mistaken for pathosis.

Periapical osseous dysplasia This condition, also known as periapical fibro-​cemento-​osseous dysplasia, is where bone is replaced by fibrous tissue, which is then replaced with bone or mineralized tissue to varying degrees. The lesions are usually associated with the apices of mandibular incisor teeth and may be mistaken for periapical lesions. Sensibility testing and even

41

follow-​up radiographs will help confirm that there is no pathosis and therefore no treatment is required.

Non-​inflammatory swellings Although non-​ inflammatory swellings have unique presenting features, in reality the range of presenting features do not preclude their occasional and passing resemblance to those of periapical origin. It is important to be familiar with the characteristics and able to differentiate between them. Details of such diseases are covered comprehensively in more appropriate texts.

Treatment planning Once a diagnosis has been reached, the patient should be informed of the various treatment options available. For each treatment option, the patient should be informed of the following:

be indicated, and it would be necessary to discuss other treatment options for the resultant space.

• Advantages and disadvantages. • Prognosis of each treatment outcome.

Where does endodontic treatment fit in treatment planning?

• Duration and number of appointments needed.

Initial phase

• Cost implications (if applicable).

The initial phase is usually to relieve pain by, for example, pulp extirpation or incision and drainage. These are discussed later in this chapter.

• Risks and possible complications. The patient can only make an informed decision on the most suitable treatment once each option has been discussed (Chapter 10). The principle of informed consent requires that the patient is advised on the most appropriate treatment option after all options have been explained.

What is a treatment plan?

Definitive phase The definitive phase is disease stabilization. The aim is to treat existing dental disease and prevent its recurrence, for example caries removal (Chapter 4) or root canal treatment (Chapters 5 and 6) and replacement of deficient restorations with well-​adapted definitive restoration (Chapter 7).

A treatment plan is a list of procedures, a timetable, individually tailored for each patient, based on their unique dental problem(s) and needs. The treatment plan aims to address patient care in an ordered, systematic, and logical fashion. It can be broken down into different phases: • Pain relief. • Disease stabilization, including oral hygiene instruction and dietary advice. • Maintaining or restoring function. • Maintaining or restoring aesthetics. • Review or maintenance. A treatment plan may be relatively simple if there is only a single, solitary problem in need of attention. In other cases, it may be more complicated, requiring a multidisciplinary approach that needs to be broken down into phases of implementation such as those mentioned above. The initial treatment plan may also have to be modified, to allow for unplanned or unforeseen circumstances. An example of this is where root canal treatment has been planned, but upon accessing the tooth or removing the existing restoration, a vertical fracture is detected (Figure 3.39). If the fracture runs through the pulp chamber, mesiodistally, the tooth is split and untreatable. The treatment plan would obviously need to be modified, as extraction would

Figure 3.39  Fracture running mesio-​distally through a maxillary first molar.

42

Diagnosis, treatment planning, and patient management

Maintenance and review

• Importance and strategic nature of the tooth.

It is important to assess the outcome of endodontic treatment (Chapter  8). Follow-​up may reveal that treatment has an unfavourable outcome and this may mean that further endodontic treatment (Chapter 9) or extraction may be indicated.

• Restorability.

• Size of the pulp chamber and presence of any calcifications.

Record keeping It is imperative to keep contemporaneous and comprehensive records, including noting down all discussions about treatment options and plans. Dentolegally, it should be remembered that ‘no records equals no defence’ should there be any potential misunderstanding or future litigation (Chapter 10). In addition, before starting any treatment, consent must be obtained and this must be recorded.

What are the factors that influence treatment planning? Patient-​related factors These factors include the patient’s medical and dental history, expectations, motivation, attitude, and compliance with treatment. Occasionally, a patient’s expectations may be unrealistic; unless the patient is cooperative it would be challenging to carry out the treatment plan.

Dental-​related factors As mentioned previously, the dental factors that may influence treatment planning include: • Access. • Oral hygiene standard. • Periodontal support.

Figure 3.40  Calcified root canal associated with a maxillary left central incisor.

In terms of dental anatomy, endodontic management may be influenced by: • Number of root canals and their relative size and degree of any calcification (Figure 3.40). • Complexity of root canal contour and curvature (Figure 3.41). • If a tooth has already been endodontically treated, the quality of the root canal filling (Figure 3.42), and the presence of foreign objects such as a separated instrument.

Clinician-​related factors Knowledge, experience, and the skill of the clinician are all important considerations in treatment planning. These factors will influence the treatment options the clinician is able to offer to the patient and will impact on the decision-​making process. Access to equipment (e.g. dental operating microscope) and secondary dental care (e.g. specialist in endodontics) may also influence the treatment approach adopted. Complex problems and challenging cases are often best managed by specialists in endodontics. Regulatory bodies and dentolegal defence organizations have also advised that, where necessary, patients should be referred for further advice or treatment, or if requested by the patient.

What does decision-​making involve? Decision-​ making involves analysis of all the elicited information, prioritizing, and ‘weighing up’ all the pieces of information, and giving balanced consideration to the various factors involved. Clinicians

Figure 3.41  Acute curvature associated with a maxillary central incisor.

Figure 3.42  An underextended and poorly compacted root canal filling associated with a maxillary central incisor.

Treatment planning

are challenged by the need for accountability. Fundamental to accountability are the concepts of risk assessment and evidence-​based practice. Risk assessment is the formal procedure of evaluating the significance of risks in order to facilitate the decision-​making process. Several case assessment forms are available to aid assessing restorability. The Dental Practicality Index (DPI; Table 3.5) is intended to assist clinicians with treatment planning. The DPI assesses the tooth’s periodontal, endodontic, and overall restorative status, as well as the context, that is, the practicality of restoring the tooth in context of the ‘bigger picture’. Each of the restorative categories:  structural integrity, periodontal state, and endodontic state are assessed and weighted according to their current state and the complexity of potential treatment. These levels are inevitably somewhat arbitrary

43

and therefore will vary between clinicians depending upon their own skillset, training, and experience. The context of treatment is also considered and scored in relation to the local and general factors. An overall score >6 suggest that treatment would not be practical to carry out. Evidence-​based practice requires the conscientious, explicit, and judicious use of current best evidence for the care of individual patients. With growing knowledge, confidence, and experience, the process of decision-​making and the formulation of treatment plans will gradually become easier and more routine. Whilst a novice may find the decision-​ making process slow and frustrating, a step-​ by-​ step approach is essential to the development of competence and, ultimately, expertise.

Table 3.5  The categories that the tooth should be assessed in; Endodontic (treatment need), Periodontal (treatment need), (structural) Integrity as well as Context (EPIC) are summarised in the grey shaded coumns. Each row shows examples of different levels (0,1,2,6) of complexity for each category. An overall DPI score of >6 indicates that treatment may be impractical, this is reduced to 4 if the tooth to be treated is to be used as a bridge abutment Weighting

Endodontic

Periodontal

Integrity

Context

0 No treatment required

Vital pulp Previously successfully treated endodontic disease

Probing 5.5 mm (BPE 4) Compromised support (e.g. short root, crown lengthening required, grade 2 mobility) Grade 2–​3 furcation involvement

Minimal residual sound tooth structure (e.g. subgingival margins, post-​core restoration required etc.)

Local: Prosthodontic treatment planned of multiple, including adjacent teeth

6 Impractical to treat

Untreatable root canal system

Untreatable periodontal disease

Inadequate structure for ferrule

Local: Retention of the tooth being assessed would constrain and/or compromise an otherwise simple and predicable treatment plan (for example extensive bridge work)

General: Replacing of a strategic tooth may be excessively complex histroy of IV bisphosphonates, head & neck radiotherapy Local: Prosthodontic treatment planned of neighbouring teeth which may influence treatment plan for tooth being assessed Tooth to be used as a bridge abutment General: Radiotherapy of head and neck region planned Immunocrompromised patient

General: High caries rate Poor oral hygiene Parafunctional habits, extensive tooth surface loss Active periodontal disease

General: Potentially life threatening medical conditions which should be managed in tertiary care Adapted from Dawood A and Patel S (2017) The Dental Practicality Index—​assessing the restorability of teeth. British Dental Journal 222, 755–​8. Printed with permission from Springer Nature.

44

Diagnosis, treatment planning, and patient management

Patient management The remainder of this chapter is a summary of the issues that may be pertinent to patient management if endodontic treatment is provided. It is not meant to be comprehensive but based on commonly encountered clinical scenarios.

methods of administration; there are also factors that may modulate their effectiveness. Reasons for ineffective anaesthesia may include:

Local anaesthesia and analgesics

• Variation in patient’s anatomy.

Effective pulpal and periapical anaesthesia is essential for endodontic treatment, to ensure the patient is comfortable, and to maintain the patient’s confidence and trust. A significant number of patients are very nervous of dental treatment due to previous painful treatment experiences in the past or may already be in considerable pain. The fear of pain itself may often be the reason why some patients defer or do not seek treatment. The following points will help to ensure effective anaesthesia is achieved: • Decide on the appropriate local anaesthetic technique using a sound knowledge of the associated anatomy. • Decide on the appropriate type of local anaesthetic solution. • Inform the patient what you are going to do and how the anaesthetized area will feel. • Apply topical anaesthetic to the injection site and allow time for this to anaesthetize the surface of the mucosa. • Administer injections slowly using a self-​aspirating syringe. • Ensure that an adequate volume of local anaesthetic is administered. • Before starting treatment, confirm effective soft tissue anaesthesia has been achieved by, for example, gently probing the mucosa in the area. • Before starting treatment, confirm effective pulpal anaesthesia has been achieved by, for example, carrying out a sensibility test. • Advise patient to indicate, for example raising a hand, if they feel any pain or discomfort.

• Poor technique. • Inadequate amounts of local anaesthetic administered. • Very inflamed pulpal and periapical tissues. • Variation in absorption, metabolism, and excretion of local anaesthetic drug. • Psychological factors. In rare circumstances, it may not be possible to achieve effective anaesthesia. In some cases, oral, inhalation or intravenous sedation may have to be considered. For further information, textbooks on local anaesthesia and sedation in dentistry should be consulted. Patients may still be in some discomfort after treatment has been completed, especially if they have been experiencing pain beforehand. They should be given reassurance and advised that it is normal to be in some discomfort for several days after treatment. Patients should be given pain relief advice, including continuing with any analgesics they may have been taking. A courtesy telephone call one or two days later to enquire about a patient’s wellbeing is also recommended, as it is of tremendous psychological benefit. Non-​steroidal anti-​inflammatory drugs (NSAID), such as ibuprofen, are the first choice for postoperative pain. These may be supplemented with paracetamol (acetoaminophen) or codeine phosphate/​ paracetamol preparations. Whichever analgesic is chosen, it is imperative to ensure that it is tolerated by the patient and does not interfere with any medication the patient may be taking. Very rarely, a stronger opioid-​based analgesic may have to be prescribed if pain relief from over-​the-​counter analgesics is insufficient or ineffective.

• Inform the patient that it is normal to feel some pressure and vibration.

Vital pulp extirpation

For maxillary posterior teeth, effective anaesthesia is usually achieved by administering an infiltration technique into the buccal mucosa adjacent to the roots of the tooth to be treated. In some cases, it is advisable to consider supplementing the customary buccal infiltration with a palatal infiltration. For mandibular posterior teeth, effective anaesthesia is rarely achieved by infiltration techniques on their own, due to the thickness of the cortical bone. It is advisable to use an inferior dental nerve block, which may be supplemented with a long buccal infiltration. If effective anaesthesia has not been achieved, additional or supplementary anaesthetic techniques may be required including:

Extirpation is indicated when the pulp is irreversibly inflamed. Effective pulpal anaesthesia is required for successful extirpation. Unfortunately, it can be difficult to achieve effective pulpal anaesthesia with a ‘hot tooth’ due to the extent of the inflammation. Supplemental anaesthetic techniques may be required and it is essential to inform patients, especially if they are nervous, that they may feel some discomfort or pain during the procedure.

• Regional nerve blocks, for example for maxillary teeth. • Intraligamental. • Intraosseous. • Intrapulpal. • Alternative techniques, for example Gow-​Gates or Akinosi for the inferior dental nerve. Many factors may influence the effectiveness of local anaesthesia, including the choice of anaesthetic drug, its mechanism of action, the

Incision and drainage A localized swelling, either intraoral or extraoral, must be treated as a matter of urgency. In extreme cases the swelling may result in life-​ threatening conditions, for example Ludwig’s angina or septicaemia. An attempt must be made to incise and drain the swelling, especially if it is fluctuant. Adequate drainage will result in immediate pain relief and a reduction in the size of the swelling. Administration of local anaesthetic directly into the affected area is often contraindicated in these situations as it may help spread the infection along the fascial planes and the anaesthetic solution may not be very effective because of the acute inflammation. Where possible, regional or nerve block type anaesthetics are more appropriate.

Patient management

45

Otherwise, limited surface anaesthesia may be achieved using a topical anaesthetic or ethyl chloride. The practical steps required to incise and drain an intraoral swelling include:

Leaving a tooth on open drainage is not advisable. If left opened, over time it will allow the entry of oral microbes, foreign objects, and food debris into the root canal system further complicating endodontic management.

• Explain the nature of the incision and drainage procedure to the patient.

Antibiotics

• Palpate the swelling gently to confirm that it is fluctuant. • Lance the area, in one quick stroke, with the tip of scalpel blade. • Gently massage either side of swelling with fingers to express as much pus as possible. • Aspirate the discharge and wait for the exudation to cease. • Prescribe antibiotics if there are signs of systemic involvement. • Give supportive care advice, for example analgesics, plenty of fluids, and a soft diet.

Antibiotics should not be prescribed as the first line of treatment for dento-​alveolar abscesses. If prescribed, antibiotics are only an adjunct to treatment. They do not actually treat abscesses or their cause(s); they are used to limit swelling and to prevent spread of the infection. The overzealous use of antibiotics as a ‘quick fix’ is to be discouraged as it is not a long-​term solution and it may also result in microbes developing increased resistance to antibiotics. The majority of dento-​alveolar abscesses can be treated without antibiotics but there are situations where they are indicated:

In addition to incision and drainage of any intraoral fluctuant swelling, drainage via the root canal system (Figure 3.43) should also be attempted. The practical steps required to achieve drainage via the root canal system include:

• If a patient presents with a diffused swelling that cannot be adequately drained via the root canal system or by incision and drainage.

• Explain the nature of the proposed procedure to the patient.

• If there is cervical lymphadenopathy and a raised temperature, usually in association with malaise, which are indications of systemic spread of infection.

• Support the tooth with, for example, a finger to reduce the vibration from the handpiece. • Gain access into the root canal(s). • If necessary, explore the root canal(s) with a fine file to facilitate drainage. • Gently massage the associated swelling with fingers to express as much pus/​tissue fluid/​blood as possible though the root canal(s). • Once drainage from the root canal(s) has stopped, irrigate the pulp space copiously. • Medicate the tooth and place a temporary filling. • If extruded from the socket, adjust the tooth so that it is out of occlusion. • Prescribe antibiotics if there are signs of systemic involvement. • Give supportive care advice, for example analgesics, plenty of fluids, and soft diet.

• If the infection is spreading, invading the fascial spaces below the mandible or the orbital area.

When prescribing a course of antibiotics, the following should be considered: • Signs of systemic involvement. • Antibiotics would not interfere with other medications or existing medical conditions. • The most suitable antibiotic, an adequate dose, duration, and suitable route of administration. • The patient is informed of any possible interactions or side effects. Commonly suggested antibiotics and regimes are shown in Table 3.6.

Table 3.6  Type, dosages, and duration of antibiotics prescribed in endodontics Drug of choice

Loading dose

Maintenance dose

Duration

Penicillin VKa

1000mg

500mg q4–​6h

3–​7 days

Amoxicillin or co-​amoxiclav

1000mg

500 mg q8h or 875 mg q12h

3–​7 days

Clindamycinb

600mg

300mg q6h

3–​7 days

Metronidazole

1000mg

500mg q6h

3–​7 days

If penicillin VK alone is not effective after 48–​72 hours, metronidazole can be used in combination with penicillin VK, or penicillin VK is switched to amoxicillin or co-​amoxiclav or clindamycin. a

If the patient is allergic to penicillin. Alternatives to clindamycin may include clarithromycin or azithromycin. b

Figure 3.43  Drainage of pus obtained through the root canal. A caulking agent was necessary to seal the margins of the rubber dam.

Adapted from the European Society of Endodontology position statement: the use of antibiotics in endodontics (2017).

46

Diagnosis, treatment planning, and patient management

(a)

(b)

(c)

Figure 3.44  Rubber dam kit: (a) a selection of rubber dam clamps; (b) punch, forceps, frame, and dental floss; (c) selection of rubber dam sheets.

Patient management

(a)

(b)

(c)

(d)

47

Figure 3.45  One-​step rubber dam technique: (a) open the clamp and rubber dam assembly using forceps; (b) rubber dam and clamp in place; (c) flick the rubber dam off the clamp wings using a flat plastic instrument; (d) rubber dam secured in position.

Preparatory treatment of an extensively restored and/​or carious tooth prior to endodontic treatment It may be challenging to achieve effective rubber dam isolation for an extensively restored or grossly carious tooth. The disassembly of a complex defective restoration may also mean that there is limited coronal tooth structure to provide rubber dam retention. In these cases, it is advisable to build up a provisional core or temporary restoration prior to starting endodontic treatment. The practical steps required to prepare an extensively restored and/​or carious tooth include: • Remove all the existing restorative material and caries. • Place a well-​adapted matrix band. • Place PTFE tape or a cotton pledget directly over the entrances of the root canals to prevent their blockage with restorative material. • Place a provisional restoration. • Prepare the access cavity through the newly provided provisional restoration and remove the PTFE tape or cotton pledget.

Rubber dam Rubber or dental dam isolation is mandatory for endodontic treatment. The main reasons and benefits for using rubber dam are listed in Table 1.1. The essential components to a rubber dam kit are shown in Figure 3.44. Rubber dam may be used to isolate a single tooth or multiple teeth. The rubber dam sheet is usually secured in place using a rubber dam clamp. Alternatively, it may be secured by wedging the proximal contact points with tiny strips of rubber dam, rubber or silicone cords, or wooden wedges. If there are any signs of suboptimal seal (e.g. saliva leakage) once the rubber dam is in place, then a caulking/​sealing agent may be used (Figure 3.43). To improve patient comfort, a paper napkin or tissue may be placed between the rubber dam sheet and patient’s skin.

Isolation of a single tooth using the one-​step technique The practical steps required to isolate a single tooth using the one-​step technique (Figure 3.45) include: • Punch a clean hole through the centre of the rubber dam sheet. • Floss through adjacent contact points.

48

Diagnosis, treatment planning, and patient management

(a)

(b)

(c)

Figure 3.46  Two-​step rubber dam technique: (a) secure the wingless clamp to the tooth using forceps and ensuring a good four-​point contact; (b) stretch the rubber dam over the clamp; (c) rubber dam secured in position.

• Select and try in a winged clamp to ensure four-​point contact around the cervical region of the tooth (floss may be tied around the clamp, as a precaution, to aid retrieval of the clamp should it fracture). • Apply gentle pressure with a forefinger on the bow of the clamp to confirm stability. • Remove the clamp. • Place the clamp on top of the rubber dam sheet and push the wings underneath the punched hole. • Apply the rubber dam and clamp assembly with the forceps onto the tooth. • Slip the rubber dam sheet under the wings of the clamp with an instrument, for example a flat plastic. • Attach the frame (or this can be attached before applying to the tooth).

(a)

Isolation of a single tooth using the two-​step technique The practical steps required to isolate a single tooth using the two-​step technique (Figure 3.46) include: • Punch a clean hole through the centre of the rubber dam sheet. • Floss through adjacent contact points. • Select and try in a winged or wingless clamp to ensure four-​point contact around the base of the tooth (floss may be tied around the clamp, as a precaution, to aid retrieval of the clamp should it fracture). • Apply gentle pressure with a forefinger on the bow of the clamp to confirm stability. • Stretch the rubber dam sheet over the clamp and the tooth. • Attach the frame (or this can be attached before applying to the tooth).

(b)

Figure 3.47  (a) Isolation of a broken down maxillary lateral incisor using the split dam technique. (b) Isolation of multiple teeth using two rubber dam clamps.

Patient management

49

Isolation of multiple teeth

• Floss through adjacent contact points.

The practical steps required to isolate multiple teeth include (Figure 3.47):

• Select and try in a winged or wingless clamp(s) that gives four-​point contact around the gingival margins of the neighbouring tooth/​ teeth (floss may be tied around the clamp, as a precaution, to aid retrieval of the clamp should it fracture).

• Punch multiple clean holes through the rubber dam sheet 5–​7 mm apart, depending on the number and the size of the teeth to be isolated. • Link the two punched holes by cutting the sheet with scissors if using a ‘split dam’ technique.

• Apply gentle pressure with a forefinger on the bow of the clamp(s) to confirm stability. • Stretch the rubber dam over the clamp and the teeth. • Apply the frame.

Summary points





• An accurate diagnosis is the key to successful treatment. The



• History taking should involve open-​ended, non-​leading questions in order to obtain a full and accurate account of the patient’s complaint; give an insight into the patient’s motivation for, and expectation of, treatment; and identify any conditions which may dictate the need to modify treatment.



• Common



• If

• Special

investigations may involve sensibility testing or radiographs. The former may include electric, cold, and

• Once a diagnosis has been reached, a treatment plan can be

formulated. This is a list of timetabled procedures individually tailored for the patient. It may be necessary to modify the treatment plan as treatment progresses.

• The examination comprises extraoral and intraoral assessment. It should be thorough and systematic in order to identify any non-​endodontic and endodontic disease.



heat tests; the latter may include conventional radiographs and CBCT.

diagnostic process involves history taking, examination, and special investigations. Endodontic diagnosis involves identifying the status of pulpal and periapical tissues.

errors in endodontic diagnosis include misinterpretation of signs and symptoms which may appear to be endodontic in origin. It is important to rule out non-​ endodontic and even non-​odontogenic causes. a diagnosis cannot be reached, treatment should be delayed, and consideration should be given to referring the patient to a specialist.

Self-​assessment Select the single best answer (SBA). Answers are provided after suggested further reading. SBA 3.1  A patient is complaining of a lingering throbbing pain aggravated by cold substances which they feel is coming from the maxillary right posterior teeth. To localize the source tooth, the following is advisable: a. Tap each tooth with the end of a mirror handle. b. Test the teeth using compressed air from the 3-​in-​1. c. Carry out cold sensibility testing using ethyl chlorite. d. Carry out cold sensibility testing using a refrigerant spray and consider also using an electric pulp tester. e. Take and assess a conventional intraoral periapical radiograph.

SBA 3.2  The most appropriate initial management of a patient with an acute apical abscess associated with a carious mandibular molar with fluctuant extra-​oral swelling and signs of systemic involvement is: a. Prescribe a course of antibiotics and review in 2–​3 days. b. Provision of a temporary filling. c. Draining via the root canal system leaving the tooth on open drainage for a week. d. Draining via incision and/​or the root canal system in conjunction with a course of antibiotics and analgesics. e. Extraction.

50

Diagnosis, treatment planning, and patient management

Suggested further reading Barnes JJ and Patel S (2011) Contemporary endodontics—​part 1. British Dental Journal 211, 463–​68. Bhuva B, Chong BS, and Patel S (2008) Rubber dam in clinical practice. Endodontic Practice Today 2, 131–​41.

European Society of Endodontology, Patel S, Durack C, Abella F, Roig M, Shemesh H, Lambrechts P, et al. (2014) European Society of Endodontology position statement: the use of CBCT in endodontics. International Endodontic Journal 47, 502–​04.

Dawood A and Patel S (2017) The Dental Practicality Index-​assessing the restorability of teeth. British Dental Journal 222, 755–​58.

Pitt Ford TR and Patel S (2004) Technical equipment for assessment of dental pulp status. Endodontic Topics 7,  2–​13.

European Society of Endodontology (2006) Quality guidelines for endodontic treatment: consensus report of the European Society of Endodontology. International Endodontic Journal 39, 921–​30.

Segura-​Egea JJ, Gould K, Şen BH, Jonasson P, Cotti E, Mazzoni A, et al. (2018) European Society of Endodontology position statement: the use of antibiotics in endodontics. International Endodontic Journal 51,  20–​25.

Self-​assessment answers SBA 3.1  Answer is d. The presenting complaint is aggravated by cold substances, and so it is appropriate to carry out cold sensibility testing to localize the source tooth. The colder the test, the more accurate the result.

SBA 3.2  Answer is d. It is not sufficient to solely prescribe antibiotics or provide a temporary filling. Open draining is no longer advisable due to re-​ infection of the root canal system. Extraction could be considered as definitive management once the acute phase of the disease process has been managed.

4

Preserving pulp vitality Avijit Banerjee and Shanon Patel

Chapter contents Introduction

52

Why is vital pulp preservation important?

52

Minimally invasive dentistry

52

What procedures are available to preserve pulp vitality?

53

Foundations of clinical practice

56

How do you carry out biological selective (minimally invasive) carious tissue removal?

56

How do you carry out direct pulp protection (capping)?

57

How do you carry out a pulpotomy?

58

How do you monitor the outcome of vital pulp therapies?

59

Prognosis

60

Summary

60

Self-​assessment

61

Suggested further reading

61

Self-​assessment answers

62

52

Preserving pulp vitality

Introduction This chapter will introduce the underlying theory of preserving pulp vitality, before exploring how this transfers to clinical practice. It is

important that you read the whole chapter to understand how the theory and practice of preserving pulp vitality are related.

Why is vital pulp preservation important? Endodontics includes the study and clinical practice of preserving the vitality of the pulp; it is not just limited to root canal treatment. The preservation of pulp vitality underpins the successful practice of endodontics. The benefits of preserving pulp vitality are described in Chapter 2 and summarized in Box 4.1. The vitality of the pulp may be challenged by microbes which may enter via caries, dental trauma, operative procedures, stress cracks in teeth, and/​or periodontal disease. There are steps a clinician can take to conservatively manage these situations with the aim of preserving a healthy pulp and avoiding the need for root canal treatment. If it is not possible to preserve pulp vitality (e.g. irreversible pulpitis) or the pulp has already become infected-​necrotic (e.g. periapical periodontitis), then root canal treatment is indicated.

Box 4.1  Benefits of preserving the pulp • To allow root development to continue in immature teeth (primary dentine formation). • To maintain lifelong tooth development (secondary dentine formation). • To preserve tooth structure. • To maintain sensory function-​nociception. • To maintain a defensive/​protective role against caries, trauma, tooth surface loss.   

Minimally invasive dentistry Minimally invasive (MI) dentistry is a term used to describe the management philosophy for carious lesions, based upon the selective, biological approach to caries removal as opposed to a purely mechanistic, surgical approach taught for many years when dental amalgam was the material of choice for the majority of resulting restorations. The improved understanding of the progressive histopathology of the caries process (Table 4.1) along with the development of adhesive materials with the ability to form a clinically acceptable sealed restoration, means that some residual caries-​affected (demineralized) dentine may be retained within the depths of a deep cavity during

operative procedures. It is essential that, wherever clinically possible, a peripheral border of sound enamel and/​or sound or, in some cases, caries-​affected dentine, can be achieved. This, coupled with suitable operative parameters (i.e. rubber dam isolation, magnification, competent clinician skills, appropriate instruments/​materials), will result in the sealed-​in residual caries-​affected dentine arresting as the dentine-​pulp complex defends against the disease process and is able to repair/​remineralize the retained tooth structure. The methods by which the dentine-​pulp complex can achieve this are outlined in Chapter 2.

Table 4.1  Summary of the histological features of the zones of carious dentine Caries-​infected (contaminated) dentine*

Caries-​affected (demineralized) dentine*

Location

Subjacent to enamel dentine junction

Deeper, towards the pulp

Consistency to a sharp probe

Soft, wet, sticky

Slightly sticky

Bacterial load

Highly infected, necrotic bacterial biomass

Reduced compared to infected dentine

Demineralization

Gross

Progressively less than infected dentine

Collagen

Denatured

Partially damaged due to proteolysis, but potentially repairable

Dentine tubular structure

Lost

More evident as lesion progresses towards sound dentine

Quality of substrate to bond/​seal/​ support the final restoration

Poor

More potential

* Note that these zones are separated for description only and that they blend histologically in continuity from one to another without distinct, definable boundaries.

What procedures are available to preserve pulp vitality?

53

When the active carious lesion is in close proximity to the vital pulp (the shadow of the pulp may be seen through the remaining thin dentine cavity floor after caries removal) or may have breached the pulp (an exposure), vital pulp therapies can be considered in an attempt to protect the remaining pulp tissue from further histological damage and encourage healing, thus preserving the vitality of the pulp. However, for these measures to be effective certain important criteria must be met:

Achieving a favourable outcome following vital pulp therapies is dependent upon:

• There are no pre-​existing symptoms in keeping with irreversible pulpitis.

• Deposition of reactionary or reparative tertiary dentine at the pulp-​ dentine interface.

• There is a positive response to sensibility testing (Chapter 3). • There are no signs of periapical periodontitis (e.g. widening of the periodontal ligament or periapical radiolucency).

• Gross removal of noxious stimuli. • Stimulation of specific dentinogenic responses. • Deposition of translucent dentine at the advancing front of the lesion.

• Release of immunoglobulins and cytokines in dentine fluid. • Prevention of future microleakage using an overlying sealed adhesive restoration which is maintained by the patient.

What procedures are available to preserve pulp vitality? Biological selective (minimally invasive) carious tissue removal Minimally invasive operative caries management dictates the complete removal of the soft, wet, necrotic caries-​infected (contaminated) dentine where possible without detriment to a vital pulp (Table 4.2). Caries-​infected dentine has a high bacterial load and is not a suitable substrate for achieving a seal to or for physically supporting a restoration under masticatory load. Removal of caries-​infected dentine can be accomplished using hand excavators, rotary burs, and/​ or chemomechanical gel systems, for example Carisolv System (RLS Global AB, Mölndal, Sweden; Figure 4.1). The tactile quality rather than the colour (usually dark brown) determines the amount of caries which should be removed. Caries-​infected dentine is soft and sticky whereas the deeper caries-​ affected (demineralized) dentine has a scratchy-​tacky texture to a sharp dental explorer/​probe. Removal of the caries should start at the periphery of the cavity in order to: • Delineate the extent of the lesion and to allow the clinical assessment of the remaining extent of viable tooth structure (thus ascertaining the overall restorability of the tooth).

• To estimate the histological depth of the lesion (i.e. to assess the depth of infected and affected dentine). • To reveal suitable dental substrate on which to achieve a peripheral adhesive seal. Once the peripheral caries has been removed, the caries overlying the pulp can be carefully removed, again leaving caries-​affected dentine only when the above listed criteria regarding the pathological signs/​symptoms have been fulfilled. Finally, assuming suitable conditions exist for instrument access and moisture control, a sealed adhesive restoration must be placed and reviewed for any symptoms within 4–​6 weeks. It is essential that rubber dam and a magnification device are used (Figure 4.2). Evidence exists that if there are no adverse signs or symptoms during this period, it can be assumed that the dentine-​ pulp complex is winning its battle against the caries process, lesion progress has arrested, and the remineralization process may have begun. No radiographic changes will be evident at this stage. The procedure known as stepwise excavation (where the caries-​infected dentine is removed superficially and a therapeutic lining plus provisional restoration are placed and then removed approximately

Table 4.2  Summary of procedures to preserve pulp vitality Procedure

Pulp exposed

Amount of pulp removed

Material used to protect the pulp

Biological selective carious tissue removal

No

None

Adhesive restoration (glass-ionomer cement or resin composite) or bioactive endodontic cement If amalgam is chosen as the definitive restoration, then consider the placing a thin layer of glass-ionomer cement

Indirect pulp protection

No, but close to an exposure

None

Same as for biological selective carious tissue removal

Direct pulp protection

Yes

None

Bioactive endodontic cement followed by an adhesive restoration

Partial coronal pulpotomy

Yes

Part of coronal pulp removed

Bioactive endodontic cement followed by an adhesive restoration

Coronal pulpotomy

Yes

All of coronal pulp

Bioactive endodontic cement followed by an adhesive restoration

54

Preserving pulp vitality

surface may be veneered with resin composite, as and when it is clinically necessary, so including it as part of the definitive restoration.

Cavity lining or pulp protection

Figure 4.1  Carisolv gel (RLS Global AB, Mölndal, Sweden).

4–​6 months later so that further removal of arrested caries and definitive restoration can be provided) has now become superfluous. Clinical research has shown that if the original restoration has sealed the residual caries, with adequate patient maintenance there is no benefit gained by re-​entering for further cavity preparation. If a glass-ionomer cement has been used for this initial, provisional restoration, its occlusal

The concept of placing a separate therapeutic cavity lining material to protect the pulp originated because dental amalgam, the restorative material of choice for many years, does not seal or interact chemically with the remaining cavity walls. Setting calcium hydroxide and zinc oxide-​eugenol based cements have been used for many years as separate cavity liners; however, neither of these types of materials fulfil many of the ideal properties required in contemporary MI operative dentistry. The ideal properties of a dental material used to protect the pulp are listed in Box 4.2. Modern adhesive restorative materials, along with the procedural steps used to achieve their adherent seal, often negate the need for a separate therapeutic lining material as they intrinsically exhibit many of the ideal properties listed in Box 4.2. This assumes that the adhesive materials are handled optimally and placed with the appropriate, rigorous clinical technique. Therefore, the term ‘cavity lining’ should now be considered historical and the term ‘pulp protection’ better used when required.

Box 4.2  Ideal properties of a dental material used to protect the pulp Protects the underlying pulp from: • Bacterial invasion (bacteriocidal). • Thermal/​ electrical stimuli (only relevant for overlying amalgam/​metal-​based restorations). Stimulates the underlying pulp to produce: • Tertiary (reparative) dentine. • Tertiary (reactionary) dentine to form a dentine bridge over an exposure. • Anti-​inflammatory chemical mediators. Prevents further long-​term pulpal assault by: • Creating an adherent seal over the pulp, so preventing microleakage. • Reinforcing the remaining dentine by physico-​ chemical infiltration. • Providing a physical support and barrier between the overlying restoration and the pulp. Other ideal properties: • Biocompatible. • Non-​toxic and non-​mutagenic. • Inexpensive. • Long shelf-​life. • Easy to prepare and place. • Radiopaque. • Dimensionally stable on setting.

Figure 4.2  The use of magnification devices, for example, dental loupes is essential when carrying out minimally invasive dentistry.

• Non-​staining of tooth substance.   

What procedures are available to preserve pulp vitality?

Indirect pulp protection (capping) Indirect pulp protection is a procedure when residual caries-​affected dentine in close proximity to the vital pulp is retained, therefore preventing the pulp from being exposed. The entire cavity is then definitively restored with an adhesive restoration (resin composite or glass-ionomer cement), or bioactive endodontic cement, for example Biodentine (Septodont, Saint-​Maurdes Fosses, France). If non-​ adherent amalgam is used as the definitive restoration, a thin layer of glass-ionomer cement can be placed as the ‘indirect pulp-​capping’ material of choice over the cavity floor closest to the pulp. The pulp status can be assessed at review appointments via symptoms, clinical signs, and sensibility testing. If an irreversible pulpitis develops, then root canal treatment will be indicated. The patient must be advised of the possibility of root canal treatment before commencing treatment. The advantage of indirect pulp protection is that it gives the dentine-​ pulp complex a chance to recover from the caries process, heal, and remineralize the remaining dentine, whilst preserving the medium-​to long-​term vitality of the pulp and retaining as much sound tooth structure as possible. Clinical evidence shows that in the majority of cases managed in this minimally invasive way, pulps and the tooth-​restoration complexes survive long-term. Those cases that fail in the short-term are usually due to inaccurate diagnosis of the original pulp status, where root canal treatment should, in hindsight, have been the original treatment of choice.

Direct pulp protection (capping) Direct pulp protection involves managing the exposed surface of the still vital pulp using a suitable ‘direct pulp-​capping’ material to stimulate

55

dentine bridge formation to repair the exposure and to stimulate the regenerative potential of the dentine-​pulp complex. Causes of pulp exposure include: • Caries process (leading to an infected pulp). • Dental trauma (pulp may or may not be infected). • Iatrogenic (caused inadvertently by the clinician during cavity preparation—​pulp often not infected). The factors to be considered when deciding whether direct pulp protection would have a good prognosis include: • The level of microbial infection the pulp has sustained. • The length of time the pulp has been affected. • The histological status of the pulp (extrapolated from sensibility testing and dependent on the above two bullet points). • The size of the breach (if greater than 2–​3 mm, the prognosis is likely to deteriorate in a carious exposure). • Achievable haemostasis (persistent haemorrhage is a clinical indicator of an irreversibly damaged pulp). There are several materials available for direct pulp protection. Historically, setting calcium hydroxide cements have been the material of choice. These have now been superseded by mineral trioxide aggregate (MTA) and other bioactive endodontic cements (Figure 4.3). In the past it was thought that pulp-​capping materials mildly irritated and inflamed the exposed pulp surface, so stimulating the differentiation of mesenchymal cells into odontoblasts, resulting in the rapid production

Figure 4.3  Examples of mineral trioxide aggregate and other bioactive endodontic cements: (left to right) ProRoot Mineral Trioxide Aggregate (MTA) (Dentsply Sirona, Tulsa, OK, USA); MTA-​Angelus (Angelus, Londrina-​PR, Brazil); Biodentine (Septodont, Saint-​Maurdes Fossés, France).

56

Preserving pulp vitality

of reparative tertiary dentine. However, there is now evidence that indicates that bioactive molecules, including transforming growth factors and bone morphogenic proteins, released from the dentine organic matrix by the action of the pulp-​capping materials, are responsible for the differentiation and upregulation of the odontoblasts.

coronal portion of the pulp until more healthy pulp tissue is exposed and haemostasis is readily achieved. A suitable direct pulp-​capping material is placed over the exposed pulp, and the tooth is restored with a well-​adapted adhesive restoration. There are different pulpotomy procedures, dependent upon the amount of pulp tissue removed:

Pulpotomy

• A partial coronal (Cvek) pulpotomy is removal of part of the coronal pulp.

Pulpotomy is a relatively more invasive procedure with similar aims to direct pulp protection. It involves removal of part or all of the inflamed

• A coronal pulpotomy is removal of all of the coronal pulp.

Foundations of clinical practice The remainder of this chapter will cover the clinical MI operative aspects to carrying out vital pulp therapies. It will also discuss how to monitor the outcome of vital pulp therapies.

How do you carry out biological selective (minimally invasive) carious tissue removal? The practical steps required to carry out biological selective carious tissue removal (Figures 4.4 and 4.5) include: • Check the occlusion preoperatively with articulating paper in inter­ cuspal position and excursions. • Obtain a suitable shade match for the final tooth-​coloured restoration. • Administer local anaesthetic. • Isolate the tooth with rubber dam. • Gain access to the carious dentine through the enamel. • Commence caries removal at the enamel-​ dentine junction (EDJ) using rose-​head burs in a slow speed handpiece or hand excavators. Carious, demineralized, unsupported enamel should be removed, along with the soft, wet, and sticky caries-​infected dentine. Ideally, sound dentine should be exposed at the periphery of the lesion, along with sound enamel borders where possible. There are instances

when, if significant amounts of sound enamel are present, some caries-​affected dentine might even be retained even at the periphery (e.g. in occlusal cavities). • Move towards the caries overlying the pulp and carefully remove this with hand excavators. Chemomechanical gels may be used to selectively remove the infected, rather than affected, dentine. • Gently wash and dry the final cavity. • Restore the cavity with a suitable restorative material (e.g. resin composite). • If Biodentine is the restorative material of choice, restore its surface with resin composite. This may be done after the initial setting time (twelve minutes) or within six months after placement of Biodentine. • If amalgam is the restorative material of choice, place a thin layer of glass-ionomer cement over the cavity floor closest to the pulp.

Caries-infected dentine to be removed

Adhesive restoration

Caries-affected dentine to be retained

Caries-affected dentine retained

Pulp

Pulp

Figure 4.4  Biological selective carious tissue removal. Caries-​infected dentine is removed. Caries-​affected dentine overlying the pulp is not removed. An adhesive restoration is placed over the caries-​affected dentine without the need for a lining material.

How do you carry out direct pulp protection (capping)?

(a)

(b)

(c)

(d)

(e)

(f)

57

Figure 4.5  Biological selective carious tissue removal with indirect pulp protection: (a) periapical radiograph of mandibular molar tooth with caries; (b) access is gained to caries-​infected dentine; (c) caries-​infected dentine is removed and caries-​affected dentine in close proximity to pulp is retained; (d) Biodentine is placed and allowed to set; (e) adhesive restoration is placed; (f) one-​year review periapical radiograph. Adapted from Patel S and Vincer L (2017) Case report: single visit indirect pulp cap using biodentine. Dental Update 44, 141–​5. Printed with permission from Dental Update.

How do you carry out direct pulp protection (capping)? The practical steps required to carry out direct pulp protection (Figures 4.6 and 4.7) include: • Check the occlusion preoperatively with articulating paper in intercuspal position and excursions. • Obtain a suitable shade match for the final tooth-​coloured restoration. • Administer local anaesthesia.

• Isolate the tooth with rubber dam. • If required, commence biological selective carious tissue removal as described in the previous section. Clear all caries-​infected and caries-​affected dentine over the pulp, whilst trying to keep the size of the carious pulpal exposure as small as possible. This step is not applicable in the case of dental trauma.

Adhesive restoration Carious pulp exposure Pulp

Direct pulp cap Pulp

Figure 4.6  Direct pulp protection. Carious exposure of pulp. A bioactive endodontic cemented is placed over pulpal exposure following removal of caries. The tooth is restored with an adhesive restoration.

58

Preserving pulp vitality

(a)

(b)

(c)

(d)

(e)

(f)

Figure 4.7  Direct pulp protection: (a) periapical radiograph of mandibular molar showing extent of carious lesion; (b) access is gained to caries-​ infected dentine; (c) pulpal exposure following caries removal; (d) direct pulp cap using bioactive endodontic cement; (e) review periapical radiograph at 12 months; (f) review periapical radiograph at 36 months showing healthy periapical tissues.

• Rinse the exposed pulp with 0.5% sodium hypochlorite solution and then rinse with sterile, isotonic saline. • Pulp haemorrhage should stop after 2–​3 minutes. It may be necessary to blot the pulp gently with a moist sterile cotton wool pledget to achieve haemostasis. Remove the blood clot. • Place a direct pulp-​capping material over the pulpal exposure. • If using MTA as the direct pulp cap, place a thin layer of glass-ionomer cement over the MTA, and restore the cavity with resin composite.

• If using Biodentine as the direct pulp cap, restore its surface with resin composite. This may be done after the initial setting time (twelve minutes) or within six months after placement of Biodentine. Persistent or extremes of bleeding (too much or too little) are usually a sign that the pulp is irreversibly damaged. In these cases, a pulpotomy or root canal treatment will be indicated. The prognosis of this procedure is affected adversely if the blood clot is not removed prior to application of the direct pulp-​capping material.

How do you carry out a pulpotomy? The practical steps required to carry out a pulpotomy (Figures 4.8 and 4.9) include: • Check the occlusion preoperatively with articulating paper in intercuspal position and excursions. • Obtain a suitable shade match for the final tooth-​coloured restoration.

(a)

(b)

Pulp

• Administer local anaesthesia. • Isolate the tooth with rubber dam. • If required, commence biological selective carious tissue removal as described in the previous section. Clear all the caries-​infected and caries-​affected dentine over the pulp. This step is not applicable in the case of dental trauma. • Rinse the exposed pulp with 0.5% sodium hypochlorite solution and then rinse with sterile, isotonic saline. • Remove the pulp in 1–​2  mm increments using a diamond bur in a high-​speed rotary handpiece with copious sterile water coolant

Direct pulp cap Pulpal exposure Adhesive restoration Figure 4.8  Pulpotomy. (a) Pulpal exposure. A bioactive endodontic cement is placed after removal of pulp tissue within pulp chamber. (b) The tooth is restored with an adhesive restoration.

How do you monitor the outcome of vital pulp therapies?

(a)

(b)

(c)

(d)

59

(e)

Figure 4.9  Pulpotomy of a previously traumatized maxillary incisor tooth: (a) preoperative radiograph; (b) immediately post-​treatment; (c) 6 months; (d) 12 months; (e) 24 months. Adapted from Patel Sand Duncan H (2011) Pitt Ford’s Problem-​Based Learning in Endodontology. Printed with permission from Wiley-​Blackwell.

until excessive bleeding stops. Blood is removed with gentle irrigation with sterile saline and haemostasis achieved by blotting the pulp surface with moist sterile cotton wool pledgets. • Place a suitable direct pulp-​capping material. • If using MTA as the direct pulp cap, place a thin layer of glassionomer cement over the MTA, and restore the cavity with resin composite.

• If using Biodentine as the direct pulp cap, restore its surface with resin composite. This may be done after the initial setting time (twelve minutes) or within six months after placement of Biodentine. To prevent tearing and additional trauma to the already distressed pulp tissues, manual excavation or the use of steel burs in a slow-​speed handpiece are contraindicated. For the same reason, dry cotton wool pledgets must never be used.

How do you monitor the outcome of vital pulp therapies? It is important to review the vital pulp therapy within 6–​12 months of treatment, and then annually thereafter for three years. The review should include patient’s symptoms (if any), assessment of the pulpal and periapical status of the tooth, and the coronal seal of the overlying restoration. If a provisional restoration has been placed, this must be replaced with a definitive adhesive restoration as soon as possible to minimize the chances of marginal microleakage. Adhesive systems must be used carefully, always appreciating the vital interplay between the tooth substrate, the chemistry of the material, and the clinical handling procedures of both. Marginal integrity can be examined carefully using dental explorers, ensuring no deficiencies develop and that the patient’s oral hygiene procedures are adequate at removing the plaque biofilm from the restoration-​tooth surface.

Criteria for a favourable outcome following vital pulp therapy Clinical examination • The patient should not suffer ongoing symptoms of pulpitis or periapical periodontitis. • The tooth and surrounding tissues should appear healthy. • Within a few weeks, there should be a positive response to sensibility testing.

Radiographic examination • Immature teeth should show signs of further root development (compare to adjacent and contralateral teeth). • The presence of a dentine bridge between the pulp and capping material (the absence of a bridge does not necessarily indicate an unfavourable outcome). • Healthy periapical tissues, that is, intact lamina dura and periodontal ligament.

Criteria for an unfavourable outcome following vital pulp therapy Clinical examination • No improvement, or worsening symptoms. • Coronal discolouration. • Negative response to sensibility testing. • Further periapical involvement may be indicated by tenderness to palpation on the alveolar mucosa overlying the root apex, tenderness to percussion, presence of a sinus, or tooth mobility (periodontal alveolar bone levels should have been assessed preoperatively).

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Radiographic examination

• Loss of lamina dura.

• Further widening of the periodontal ligament space.

• A developing periapical radiolucency.

Prognosis Ultimately, the critical factors to be considered for a favourable prognosis of all vital pulp therapies include: • Using an aseptic technique. Rubber dam isolation and sterile solutions ensure the exposed pulp is not contaminated with microbes.

• Controlling pulp haemorrhage. Once haemostasis is achieved the blood clot must be removed carefully to permit the biochemical interaction between the pulp-​capping material and the vital pulp tissue. • Achieving a coronal seal. This is imperative to prevent microleakage.

Summary The preservation of pulp vitality is dependent upon numerous factors. If dental disease (caries) is prevented or controlled, the dentine-​pulp complex will not be significantly affected, and it will remain healthy. However, it is also important to note that most invasive operative procedures (including cavity or crown preparation) can render the dentine-​pulp complex at risk of irreversible damage from microbial microleakage along freshly exposed dentine tubules and/​or heat conduction from the operative procedure. It is therefore necessary for the clinician to appreciate the histology and materials being used to reduce the overall risk to the pulp. Regular insults to the pulp reduce its recuperative powers and may lead to irreversible damage. Therefore, full consideration should be given to the removal of causative factors, whilst bearing in mind the possible consequences of the operative procedures that may lead to future complications as a result of microleakage and the reduced remaining dentine thickness overlying the pulp. After pulp therapy is complete, a coronal seal must be achieved with an adhesive restoration, so preventing subsequent infection, which could go undetected until the pulp status is irreversibly compromised.

Failure to achieve haemostasis is a clinical sign that the pulp may be irreversibly inflamed and/​or infected, as indeed is very little or no haemorrhage. In these cases, complete extirpation of the pulp (pulpectomy) will be necessary. It is always wise to monitor the outcome of pulp preservation procedures on a periodic basis. In addition to checking signs/​symptoms, sensibility testing should be carried out and an annual radiographic periapical examination may show signs of dentine bridge formation as well as no periapical changes. In immature teeth, the vitality of the pulp should be preserved, when possible, to allow for further root development. In fully mature teeth, root canal treatment is usually the treatment of choice if there is any doubt of the vitality of the pulp and/​or there has been a large carious pulpal exposure. This is especially relevant when the tooth is to be restored with an extensive restoration (e.g. a multi-​surface class 2 composite restoration or a cuspal coverage restoration). There is evidence to suggest that the incidence of loss of vitality is higher in these teeth when compared to teeth restored with less extensive restorations.

Summary points • Clinicians should take a biological approach to caries removal and pulp protection. • Clinicians should consider vital pulp therapies when possible, especially in vital immature teeth, to allow for further root development. • Vital pulp therapies are contraindicated in teeth with irreversible pulpitis or teeth with large carious pulpal exposures.



• Procedures



• Contemporary

available to preserve pulp vitality include:  biological selective carious tissue removal, direct pulp protection, and pulpotomy. pulp protection materials include bioactive endodontic cements and adhesive restorative materials.

Summary

61

Self-​assessment Select the single best answer (SBA). Answers are provided after suggested further reading. SBA 4.1  Which of the following is the best way to minimize the risk of microbial contamination of the pulp when treating a mandibular first molar which has a deep carious lesion and a clinically healthy pulp? a. Carrying out a direct pulp protection procedure. b. Carrying out biological selective carious tissue removal utilizing rubber dam isolation. c. Getting the patient to preoperatively rinse with chlorhexidine solution. d. Applying of ozone therapy to the affected tooth. e. Prescribing a course of antibiotics.

b. Progressively less demineralization than caries-​infected dentine. c. Collagen partially damaged due to proteolysis, but potentially repairable. d. Tubular structure becoming more evident as lesion progresses towards deeper sound dentine. e. The potential to seal and support an overlying adhesive restoration. SBA 4.4 The factors to be considered when deciding whether direct pulp protection would have a good prognosis would not include: a. The level of bacterial infection the pulp has sustained. b. The length of time the pulp has been affected. c. The histological status of the pulp. d. The size of the pulpal exposure.

SBA 4.2 Which of the following characteristics is not found in caries-​infected (contaminated) dentine?

e. The size of the cavity created after caries removal.

a. Highly infected, necrotic bacterial biomass.

SBA 4.5 Which of the following criteria describe a favourable outcome following vital pulp therapy?

b. Soft, wet, sticky consistency due to gross demineralization. c. Denatured collagen.

a. Developing tenderness to palpation on the alveolar mucosa overlying the root apex of the affected tooth.

d. A regular dentine tubular structure.

b. Coronal discolouration and/​or a negative response to sensibility testing.

e. Poor quality substrate to bond, seal, and support the final restoration.

c. Developing tenderness to percussion, presence of a sinus, or tooth mobility.

SBA 4.3 Which of the following characteristics is not found in caries-​affected (demineralized) dentine?

d. Reduced widening of the periodontal ligament space radiographically.

a. The bacterial load is the same as that in caries-​infected dentine.

e. A developing periapical radiolucency.

Suggested further reading Ainehchi M, Eslami B, Ghanbariha M, and Saffar AS (2003) Mineral trioxide aggregate (MTA) and calcium hydroxide as pulp-​capping agents in human teeth: a preliminary report. International Endodontic Journal 36, 225–​31.

Cox CF, Bergenholtz G, Heys DR, Syed SA, Fitzgerald M, and Heys RJ (1985) Pulp capping of dental pulp mechanically exposed to oral microflora: a 1–​2 year observation of wound healing in the monkey. Journal of Oral Pathology 14, 156–​68.

Banerjee A and Watson TF (2015) Pickard’s Guide to Minimally Invasive Operative Dentistry, 10th edn. Oxford, UK: Oxford University Press.

Hashem D, Mannocci F, Patel S, Andiappan M, Brown JE, Watson TF, et al. (2015) Efficacy of calcium silicate indirect pulp capping; a randomized controlled clinical trial. Journal of Dental Research 94,  562–​8.

Banerjee A, Frencken JE, Schwendicke F, and Innes NPT (2017) Contemporary operative caries management: consensus recommendations on minimally invasive caries removal. British Dental Journal 223, 215–​22. Bjørndal L, Reit C, Bruun G, Markvart M, Kjaeldgaard M, Nasman P, et al. (2010) Treatment of deep carious lesions in adults: randomized clinical trials comparing stepwise vs. direct complete excavation, and direct vs. partial pulpotomy. European Journal of Oral Sciences 118, 290–​97. Cox CF, Bergenholtz G, Fitzgerald M, Heys DR, Heys RJ, Avery JK, and Baker JA (1982) Capping of the dental pulp mechanically exposed to the oral microflora—​a 5 week observation of wound healing in the monkey. Journal of Oral Pathology 11, 327–​39.

Nair PN, Duncan HF, Pitt Ford TR, and Luder HU (2008) Histological, ultrastructural, and quantitative investigations on the response of healthy human pulps to experimental capping with mineral trioxide aggregate: a randomized controlled trial. International Endodontic Journal 41, 128–​50. Smith AJ, Murray PE and Lumley PJ (2002) Preserving the vital pulp in operative dentistry: 1. A biological approach. Dental Update 29,  64–​9. Swift EJ, Trope M, and Ritter AV (2003) Vital pulp therapy for the mature tooth—​can it work? Endodontic Topics 5,  49–​56.

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Self-​assessment answers SBA 4.1  Answer is b. This is the recommended operative procedure that will minimize contamination of the pulp. Contemporary understanding of the caries process now appreciates that complete removal of bacteria in carious tissues is unachievable and unnecessary to halt caries progression. SBA 4.2  Answer is d. The regular tubular structure of dentine is deranged in the carious lesion. In caries-​infected (contaminated) dentine, the tissue destruction is extensive, with denaturation of collagen and demineralization leading to disruption of the regular dentine structure. SBA 4.3  Answer is a. Towards the advancing front of the progressing lesion, the bacterial load will diminish. It is not necessary to remove these

bacterial contaminants, but to ensure they are sealed from nutrients, to arrest the caries process. SBA 4.4  Answer is e. The size of the cavity after caries tissue removal has no relevance to the success of direct pulp protection. Using the selective biological carious tissue removal approach, deeper layers of carious tissue do not need to be removed and as such the incidence of pulp exposure will reduce. SBA 4.5  Answer is d. The other responses all indicate progressive pathosis leading to full pulp tissue necrosis. Reduced widening of the periodontal ligament seen on radiographs taken annually after the procedure, indicates a healing of the periapical tissues.

5

Root canal preparation Edward Brady and Conor Durack

Chapter contents Introduction What is root canal treatment and why do it? What are the aims of root canal preparation? What challenges are encountered during root canal preparation? What are the stages in mechanical preparation? What equipment and instruments are used for root canal preparation? What does chemical preparation involve? Why is a good temporary restoration required? Foundations of clinical practice How do you carry out preparation of the tooth for root canal treatment? How do you prepare an access cavity? How do you locate the entrances to root canals? How do you create straight-​line access? How do you carry out initial negotiation? How do you use hand files? How do you carry out coronal flaring? How do you carry out apical negotiation? How do you determine working length? How do you carry out apical preparation? How do you prevent procedural errors? How do you carry out chemical preparation? How do you temporarily restore the tooth?

64

Self-​assessment

96

Suggested further reading

96

Self-​assessment answers

97

64 64 65 67 70 77 81 81 81 83 84 85 85 85 86 87 87 89 91 93 95

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Root canal preparation

Introduction This chapter will introduce the rationale for root canal preparation before exploring how this translates to clinical practice. It is essential

that you read the whole chapter to understand how the theory and practice of root canal preparation are related.

What is root canal treatment and why do it? Root canal treatment is carried out to remove inflamed and/​or infected pulpal tissue, and control infection within the root canal system. The disinfected root canal system is then filled to prevent subsequent (re-​)entry and proliferation of microbes. The ultimate objective is to restore and maintain periapical health, enabling the tooth to be preserved as a healthy, functional unit within the dental arch. The indications for root canal treatment are: • Irreversible inflammation of the pulp. • Pulpal necrosis (e.g. after a traumatic injury to the tooth). • Pulpal necrosis and infection (usually with evidence of periapical periodontitis or abscess). • Elective root canal treatment is sometimes indicated as part of a restorative treatment plan, usually where the root canal space is required for the retention of a coronal restoration, for example a post-​retained  crown.

Root canal treatment is contraindicated in the following situations: • Tooth is unrestorable (e.g. extensive caries extending into the furcal region, subgingival fracture with no ferrule of dentine). • Tooth cannot be made functional. • Tooth with insufficient periodontal support. • Tooth with poor prognosis. • Patients who are uncooperative or who have poor oral condition that cannot be improved. Root canal treatment is carried out in two stages: • Root canal preparation (this chapter). • Root canal filling (Chapter 6).

What are the aims of root canal preparation? Root canal preparation involves simultaneous mechanical and chemical (chemo-​ mechanical) preparation, sometimes referred to as ‘shaping’ and ‘cleaning’.

Mechanical preparation

Chemical preparation Effective root canal treatment is dependent upon the elimination (as far as possible) of infection from the root canal system. This is achieved by chemical preparation using antimicrobial

Mechanical preparation is carried out using a variety of instruments to primarily shape the root canal system, and second, to create access for irrigants (irrigating solutions) and medicaments. The ideal prepared shape should be a smooth and continuously tapering cone, which is narrowest apically and widest at the root canal entrance. The taper should ideally be centred along the original axis of the root canal and maintain the original contour (Figure 5.1). The aims of mechanical preparation are to: • Remove pulpal debris and microbes. • Facilitate chemical preparation. • Create the optimal shape and resistance form for root canal filling. Mechanical preparation is generally carried out using a ‘crown-​ down’ approach:  the coronal portion of the root canal is initially instrumented and enlarged before instrumenting the apical portion of the root canal.

Figure 5.1  An endodontically treated maxillary molar: note the uniform taper of the root canal fillings and how they follow the root outline.

What challenges are encountered during root canal preparation?

irrigants and, in certain situations, also using interappointment medicaments. The aims of chemical preparation are to: • Flush out remnants of pulpal tissue and debris created during mechanical instrumentation. • Dissolve residual pulpal tissue. • Kill microbes and remove biofilm. • Disinfect parts of the root canal system which are inaccessible to mechanical preparation.

65

• Act as a lubricant to facilitate instrumentation. • Remove the smear layer. The root canal system should be frequently and copiously irrigated with antimicrobial solutions during and after mechanical preparation. This is essential if adequate cleaning and disinfection are to be achieved. Medicaments are used to dress the root canal system between visits to further reduce the levels of microbes. Although modern preparation techniques may enable mechanical preparation to be carried out quickly and efficiently, the importance of effective chemical preparation must not be overlooked.

What challenges are encountered during root canal preparation? The anatomy of the root canal system is frequently very complex. Several factors may present a challenge to safe and effective mechanical preparation:

• Teeth often have a greater number of root canals than anticipated, for example the mesio-​buccal roots of maxillary molars usually have two root canals (Figure 5.5).

• In addition to the main root canal(s), there are often accessory canals, lateral canals, fins, anastomoses, isthmi (Figure 5.2), and apical deltas, all of which are inaccessible to mechanical instrumentation.

• Deposition of secondary and tertiary dentine can result in partially or completely calcified root canals. Pulp stones and dystrophic calcifications may also be encountered (Figure 5.6).

• Root canals may have severe or double (S-​shaped) curvatures, which may not be readily detectable on radiographs. These present a challenge to instrumentation, as most instruments used for root canal preparation are straight and can be inflexible (Figure 5.3). • The cross section of root canals is frequently oval or ribbon shaped; some molar teeth have C-​shaped canals (Figure 5.4). • Most instruments are uniform in cross-​section and are unable to fully contact all surfaces of the root canals.

Figure 5.2  An endodontically treated mandibular molar: note that the isthmus between the root canals has been filled.

• Patient factors, such as restricted mouth opening, may preclude endodontic treatment of posterior teeth. A  pronounced gag reflex can complicate the placement and positioning of radiograph holders. • The position and angulation of the tooth may affect the feasibility of endodontic treatment. • Existing restorations may mask the true orientation of the tooth and lead to procedural errors when attempting to locate the root canals.

Figure 5.3  An endodontically treated maxillary molar: note the severe curvature of mesio-​buccal root canals.

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(a)

(b)

Figure 5.4  C-​shaped root canal in a mandibular molar: (a) intraoperative clinical appearance, (b) postoperative radiographic appearance. (a)

(b)

Figure 5.5  Second mesio-​buccal root canal in a maxillary molar: (a) initial instrumentation of root canal; (b) clinical appearance after root canal preparation. (a)

Figure 5.6  Calcifications: (a) partially calcified root canals, (b) pulp stones.

(b)

What are the stages in mechanical preparation?

67

What are the stages in mechanical preparation? Mechanical preparation can be divided into several stages (Figure 5.7):

Preparation of the tooth for root canal treatment

Once the entrances to the root canals have been located, straight-​ line access (Figure 5.9) to the root canals must be established. It is important to achieve straight-​line access for the following reasons: • It provides a clear path of insertion for instruments.

Before embarking on treatment, a thorough clinical and radiographic assessment needs to be made to determine the restorability and treatability of the tooth, and to predict any difficulties that may be encountered during treatment. Caries and defective restorations must be removed, and if there is any doubt regarding the restorability of the tooth, all restorative material should be removed to allow a full assessment to be made. It is frequently necessary to place a provisional restoration or to provide support for undermined cusps prior to embarking on treatment. Time spent on this stage of the procedure will save much time and stress later on.

• It helps to reduce the incidence of procedural errors.

Access cavity preparation, location of root canals, and creating straight-​line access

• Removal of obstructions and straightening of the coronal section of the root canal to enable unrestricted access to the apical portion of the root canal.

This stage is often the most difficult aspect of root canal treatment but if carried out proficiently, it will allow the subsequent procedure to progress much more smoothly. It is important to be familiar with usual tooth morphology (Figure 5.8). Awareness of the usual position of the pulp chamber, the number of root canals, and the location of root canal entrances will help to reduce the risk of excessive removal of tooth substance and the possibility that any root canals will be missed.

Preparation of the tooth for root canal treatment Access cavity preparation Location of root canal entrances Creating straight-line access Initial negotitaion Coronal flaring Apical negotiation Working length determination Apical preparation Figure 5.7  Stages of mechanical preparation of the root canal.

• It reduces stress on instruments, thereby reducing the probability of instrument separation.

Initial negotiation and coronal flaring The coronal half to two-​thirds of the root canal is initially negotiated and then enlarged to achieve a tapered preparation, which is widest at the root canal entrances (Figure 5.10). In some cases, minimal or no coronal flaring is required as the coronal portion of the root canals are already wide. Coronal flaring has the following benefits:

• Improved tactile feedback for apical preparation. • Removal of the bulk of infected pulpal tissue and debris to avoid it being pushed apically. • Provides a reservoir for irrigant coronally. • Minimizes the risk of creating apical blockages. • Maintenance of working length during subsequent preparation.

Apical negotiation and working length determination After coronal flaring has been completed, the apical portion of the root canal is negotiated and the working length is determined.

What is the working length and how is it determined? The working length is the length of the root canal preparation, measured from a suitable coronal reference point (e.g. cusp tip or incisal edge), to the estimated position of the apical constriction. Straightening of the coronal portion of the root canal during coronal flaring often causes a slight reduction in the working length, therefore it should be determined after coronal flaring. There are two main techniques for working length determination: • Radiograph technique. The working length is first estimated from a preoperative radiograph. A file is placed into the root canal at the estimated length, and a periapical radiograph using a beam aiming device is taken to estimate the distance of the file tip from the radiographic apex. • Electronic apex locator (EAL) technique. The EAL is attached to a file inserted into the root canal, which is gradually moved apically until the file reaches the apical foramen. This is indicated visually and audially on the EAL and is referred to as the ‘zero reading’.

1

23

1

2

22

1

3

26

1

4

21

1–5% 2–90% (B, P) 3–5% (MB, DB, P) 1–75% 2–25% (B, P)

6

22

P longer than MB and DB

7

20

21

3

Access cavity

Mesial Palatal

1

2

4

3

5

6

7

Access cavity

21

2

Distal

Buccal

Features

1

• Access starting at cingulum and extend towards incisal edge • Triangular shape to encompass pulp horns • Lateral insisor-apical 3–4 mm has palatal curvature which should always be borne in mind when instrumenting • Canine-rounder access cavity then incisors-no need to flare access cavity as there is only 1 pulp horn • Initial point of access should be centre of occlusal central groove • Widen access bucco-palatally to locate root canal entrance under respective cusp tips (P and B) • Second premolars if only one root canal then should be centred and oval in shape (bucco-palatally) to encompass pulp horns • Second premolars root canal entrance more centred, if not centred look for second entrance under other cusp tip • Separate root canals join apically commonly

• Rhomboid access cavity outline • Distal apect of access cavity is on the mesial aspect of transverse ridge 3–40% (MB, DB, P) 4–60% (MB1, MB2, DB, P) • Palatal root canal entrance is usually the largest and therefore easiest to locate • Disto-buccal and palatal root canal entrances usually rounder • Mesio-buccal root canal entrance usually more ovoid, reflecting ribbon shape of the mesio-buccal root • MB2 located between MB1 and palatal root canal • Troughing this area with fine burs or ultrasonic tips should P longer than MB and DB eventually reveal an opening of a root canal entrance • Lower incidence of MB2 in second molars 3–60% (MB, DB, P) 4–40% (MB1, MB2, DB, P) • DB root canal closer to centre of tooth in second and third molars • Increased likelihood of fusion of root canals in second and third molars (1 buccal and 1 palatal)

Number of canals

Root length

21

Mandibular teeth

5

Buccal

Features

Number of canals

Root canal preparation

Root length

Maxillary teeth

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Distal

Mesial Lingual

1–60% 2–40% (B, L)

• Starts at the base of the cingulum • Access cavity should be extented nearly to incisal edge to confirm the presence/absence of the second (lingual) root canal

24

1–90% 2–10% (B, L)

• Starts at the base of the cingulum

4

22

1–75% 2–25% (B, L)

• Starts in central occlusal groove • Access is oval bucco-lingually in shape

4

5

5

22

1–90% 2–10% (B, L)

6

21

3–65% (ML, MB, D) 4–35% (ML, MB, DL, DB)

6

7

7

20

3–90% (MB, ML, D) 2–10% (M, D)

• Mesial root canal entrances are found below respective cusp tips • Larger distal root canal entrance is more centred • If distal root canal entrance is not centred then there is an increased likelihood of a second root canal • Increased incidence of fused root canals with second and third molars

1

2

3

B, buccal; P, palatal; MB, mesio-buccal; DB, disto-buccal; MB1, first mesio-buccal; MB2, second mesio-buccal; L, ligual; ML, mesio-ligual; D, distal; DL, distol-lingual.

Figure 5.8  Root canal features, average lengths, and access cavities in various teeth.

What are the stages in mechanical preparation?

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Apical constriction

Apical foramen

Radiographic apex

Figure 5.11  Relationship between the apical constriction, apical foramen, and radiographic apex of the root. Figure 5.9  Refinement of access cavity to obtain straight-​line access to mesial root canals of a mandibular molar. Overhanging dentine (red arrow) prevents straight-​line access into the root canal.

Electronic apex locators are exceptionally useful for quick determination of the working length and are reliable and accurate, but a working length radiograph provides additional information, such as root canal curvature, that cannot be obtained using an EAL alone. For optimal accuracy, it is recommended that a combination of both methods be employed. Other techniques for working length determination include the use of tactile feedback to feel for the apical constriction, and the insertion of a paper point into the root canal beyond the apex to pick up moisture/​blood. The length of the dry section of the paper point gives some indication of the working length. These techniques are insufficiently reliable to be used exclusively, but can be useful in conjunction with the other methods.

(Figure 5.11). Once the distance to the apical foramen has been determined (i.e. the zero reading given by an EAL), 0.5–​1.0 mm is subtracted to give a working length that should terminate close to the apical constriction. The apical foramen is not always located at the radiographic apex of the root and may in some instances be located up to 3 mm from the radiographic apex.

Apical preparation After working length determination, apical preparation may be completed. The aim is to enlarge and shape the apical portion of the root canal so that it tapers smoothly into the coronal section (Figure 5.12). This creates an optimal shape for effective irrigation and root canal filling. When using stainless steel hand files, apical preparation involves two stages:

What is the terminus for the root canal preparation?

• Apical enlargement.

The root canal preparation and filling should end at the apical constriction (the narrowest part of the root canal). On average, the apical constriction is approximately 0.5–​1.0 mm short of the apical foramen

When using nickel-​titanium (NiTi) files the apical size and taper are created by the finishing file specific to the chosen system.

Figure 5.10  Diagram showing coronal flaring.

• Creation of apical taper.

Figure 5.12  Diagram showing transition from coronally flared root canal to apically prepared root canal.

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Root canal preparation

What should the size of the apical preparation be?

What is patency filing?

The size of the apical preparation is determined by the initial (pretreatment) size of the root canal. Stainless steel files are sequentially inserted passively into the root canal to the working length to determine the apical diameter of the root canal. This process is known as ‘gauging’. In situations where the root canal is initially very narrow, a decision has to be made regarding how large the apical preparation should be. Generally, the accepted minimum size of apical preparation is ISO (International Organization for Standardization) size 25, but larger sizes are often advocated. Root canal curvature often dictates the maximum acceptable size, especially if more rigid stainless steel files are used. The proposed advantages of larger sized apical preparations are:

Patency filing refers to the passive placement of a small K-​type file (ISO size 10 or smaller) 0.5–​1.0 mm through the apical constriction during root canal preparation. The file should not be inserted any further through the constriction than 0.5–​1.0  mm to avoid pushing infected debris into the periapical tissues or potentially damaging any nearby important anatomical structures. Patency filing has the following benefits:

• Greater removal of infected dentine in the apical portion of the root canal. • Improved irrigant exchange and access for medicaments. • Easier insertion of gutta-​percha (GP) points to the working length, and creation of an apical ‘stop’. The potential disadvantages of larger sized apical preparations are: • Increased risk of procedural errors especially in severely curved root canals. • Extrusion of irrigant or root canal filling materials. • Increased risk of vertical root fracture.

• Ensures negotiation of the root canal is smooth, reproducible, and predictable. • Allows accurate determination of working length, in particular when using an EAL. • Ensures sequentially larger sized files will ‘glide’ to the working length (i.e. ‘glide path’ is established and maintained). • Prevents procedural errors occurring. • Disrupts biofilm within the apical portion of the root canal. • Disrupts dentine debris created during instrumentation. A potential disadvantage of patency filing is the extrusion of infected debris into the periapical tissues, which may result in a postoperative flare-​up. Great care should be taken if the apex of the root(s) appears to be in close proximity to important anatomical structures, for example the inferior dental or mental nerves.

What equipment and instruments are used for root canal preparation? General equipment and instruments Rubber dam The use of rubber dam during root canal treatment is mandatory. The benefits and application of rubber dam are covered in detail in Chapters 1 and 3.

Magnification and illumination Good visibility is essential when carrying out root canal treatment. The use of dental loupes equipped with a light (Figure 5.13) or a dental operating microscope (Figure 5.14) greatly assists in the location of the entrances of root canals, and in the visualization of cracks and perforations.

Electric motor and speed reducing handpiece Endodontic electric motors and speed reducing handpieces (Figure 5.15) are used in conjunction with rotary or reciprocating NiTi files. Rotary electric motors are usually operated at 150–​500 rpm and allow the torque to be controlled to reduce the risk of file separation. Some motors also have an auto-​reverse setting that reverses the file out of the root canal if the pre-​set torque setting is reached. Speed reducing handpieces that operate on a standard slow-​speed motor are also available but generally do not allow such precise control over speed and torque and therefore are not recommended.

Figure 5.13  Dental loupes (SurgiTel, Ann Arbor, MI, USA).

Ultrasonic units and tips Piezo-​electric ultrasonic units (Figure 5.16) may be used in conjunction with dedicated endodontic tips (Figure 5.17) for the removal of controlled amounts of dentine, usually when locating the entrances to root canals. They may also be used with an ultrasonic file attached (Figure 5.18) to agitate irrigant in the root canal (passive ultrasonic irrigation).

What equipment and instruments are used for root canal preparation?

71

Figure 5.14  Dental operating microscope with observer scope for dental assistant (Global Surgical, St Louis, MO, USA).

Electronic apex locator Electronic apex locators are used to determine working length (Figure 5.19). They work by setting up a local electric current between the patient’s oral mucosa and the periodontal ligament at the end of the root canal. It is assumed that the electrical resistance of the periodontal ligament is the same as the oral mucosa. The EAL has two terminals: a hook, which rests on the patient’s lip, and a clip or probe, which connects to the file in the root canal. The EAL measures the resistance between the file in the root canal and the oral mucosa. When the file makes initial contact with the periodontal ligament, the display will give a ‘zero’ reading, which is used to decide where the apical preparation will end.

Figure 5.16  Ultrasonic device: P5 Newtron XS (SATELEC ACTEON, Merignac, France).

Endodontic radiograph holders Taking radiographs during endodontic treatment with rubber dam in place can be challenging. Specialized film or sensor holders (Figure 5.20)

Figure 5.15  Endodontic motor: X-​smart Plus (Dentsply Sirona, Ballaigues, Switzerland).

Figure 5.17  Start-​X ultrasonic tips (Dentsply Sirona, Ballaigues, Switzerland).

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Root canal preparation

have a beam-​aiming device and a basket to accommodate instruments, GP cones, and rubber dam clamps.

Front-​surface  mirror Standard mirrors produce a double image (Figure 5.21a). Front-​surface mirrors (Figure 5.21b) produce a clearer image than standard mirrors, as the reflective surface is at the front of the glass.

Endodontic explorer The endodontic explorer is a double-​ended probe with long, sharp tips (Figure 5.22). It is invaluable when exploring for root canal entrances.

Locking tweezers Locking tweezers are ideal for gripping paper and GP points, and for passing these between the dental nurse and clinician. Figure 5.18  Ultrasonic file for passive ultrasonic irrigation.

Long shank excavator A long shank excavator is used to remove pulp stones and debris from the floor of the pulp chamber.

Measuring device Various measuring devices are available for measurement of files, irrigating needles, and GP points (Figure 5.23). Some devices can be worn on the finger and hold a sponge to clean debris from the flutes of instruments.

Burs for access cavity preparation Tungsten carbide or diamond burs may be used for initial access cavity preparation. Tungsten carbide burs are more efficient for cutting through metallic restorations, but diamond burs should be used for cutting through ceramic. Safe-​ended burs (e.g. Endo-​Z bur; Dentsply Sirona, Ballaigues, Switzerland) allow lateral extension of the access cavity outline after initial penetration without damaging the floor of the pulp chamber. Long shank burs may be used to remove tertiary dentine when attempting to locate root canal entrances (Figure 5.24). Figure 5.19  Electronic apex locator: Root ZX Mini (J. Morita, Osaka, Japan).

Instruments used for mechanical preparation Gates Glidden drills Gates Glidden drills are side cutting stainless steel instruments with non-​ cutting tips, which may be used to flare the coronal portion of the root canal (Figure 5.25 and Table 5.1). They are manufactured in six sizes, indicated by the number of bands on the shank of the instrument. Due to their inflexibility, they must only be used in the straight part of the root canal. They have a long shank that is designed to separate at the neck, so that if they break they are usually retrievable (although this is not always the case). Gates Glidden drills have a very aggressive cutting action and if not used judiciously, are liable to remove excessive amounts of dentine, especially sizes four and above. This can result in strip perforations, especially in narrow roots, such as the mesial roots of mandibular molars.

Stainless steel files

Figure 5.20  Endodontic film holder: EndoRay (Dentsply RinnSirona, Elgin, IL, USA).

Traditionally, endodontic files have been manufactured from stainless steel (Figure 5.26). Stainless steel is flexible at smaller sizes (ISO size