Endodontic-Periodontal Lesions: Evidence-Based Multidisciplinary Clinical Management [1st ed.] 978-3-030-10724-6, 978-3-030-10725-3

Table of contents :
Front Matter ....Pages i-v
Lesions of Endodontic Periodontal Origin (Igor Tsesis, Carlos E. Nemcovsky, Joseph Nissan, Eyal Rosen)....Pages 1-6
Etiology and Classification of Endodontic-Periodontal Lesions (Eyal Rosen, Carlos E. Nemcovsky, Joseph Nissan, Igor Tsesis)....Pages 7-13
Endodontic Considerations in the Management of Endodontic-Periodontal Lesions (Kenneth J. Frick, Eyal Rosen, Igor Tsesis)....Pages 15-51
Prosthetic Considerations in the Management of Endodontic-Periodontal Lesions (Joseph Nissan, Roberto Sacco, Roni Kolerman)....Pages 53-57
Endodontic-Periodontal Lesions: Periodontal Aspects (Carlos E. Nemcovsky, José Luis Calvo Guirado, Ofer Moses)....Pages 59-85
Modern Clinical Procedures in Periodontal Reconstructive Treatment (Carlos E. Nemcovsky, Jose Nart)....Pages 87-123
VRF as an Endodontic Periodontal Lesion (Spyros Floratos, Aviad Tamse, Shlomo Elbahary)....Pages 125-140
Treatment Alternatives Following Extraction of Teeth with Periodontal-Endodontic Lesions (Carlos E. Nemcovsky, Massimo del Fabbro, Ilan Beitlitum, Silvio Taschieri)....Pages 141-194
Dental Implants Biological Complications: Tooth Preservation Reevaluated (Carlos E. Nemcovsky, Eyal Rosen)....Pages 195-214
Integration of Clinical Factors and Patient Values into Clinical Decision-Making in the Management of Endodontic-Periodontal Lesions (Igor Tsesis, Russell Paul, Eyal Rosen)....Pages 215-221

Citation preview

Endodontic-Periodontal Lesions Evidence-Based Multidisciplinary Clinical Management Igor Tsesis Carlos E. Nemcovsky Joseph Nissan Eyal Rosen Editors

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Endodontic-Periodontal Lesions

Igor Tsesis  •  Carlos E. Nemcovsky Joseph Nissan  •  Eyal Rosen Editors

Endodontic-Periodontal Lesions Evidence-Based Multidisciplinary Clinical Management

Editors Igor Tsesis Department of Endodontology School of Dental Medicine Tel Aviv University Tel Aviv Israel Joseph Nissan Department of Oral- Rehabilitation School of Dental Medicine Tel Aviv University Tel Aviv Israel

Carlos E. Nemcovsky Department of Periodontology and Implant Dentistry The Maurice and Gabriela Goldschleger School of Dental Medicine Tel Aviv University Tel Aviv Israel Eyal Rosen Department of Endodontology School of Dental Medicine Tel Aviv University Tel Aviv Israel

ISBN 978-3-030-10724-6    ISBN 978-3-030-10725-3 (eBook) https://doi.org/10.1007/978-3-030-10725-3 Library of Congress Control Number: 2019931053 © Springer Nature Switzerland AG 2019 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors, and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland

Contents

1 Lesions of Endodontic Periodontal Origin������������������������������������   1 Igor Tsesis, Carlos E. Nemcovsky, Joseph Nissan, and Eyal Rosen 2 Etiology and Classification of Endodontic-Periodontal Lesions����������������������������������������������������������������������������������������������   7 Eyal Rosen, Carlos E. Nemcovsky, Joseph Nissan, and Igor Tsesis 3 Endodontic Considerations in the Management of Endodontic-Periodontal Lesions����������������������������������������������������   15 Kenneth J. Frick, Eyal Rosen, and Igor Tsesis 4 Prosthetic Considerations in the Management of Endodontic-Periodontal Lesions����������������������������������������������������   53 Joseph Nissan, Roberto Sacco, and Roni Kolerman 5 Endodontic-Periodontal Lesions: Periodontal Aspects����������������   59 Carlos E. Nemcovsky, José Luis Calvo Guirado, and Ofer Moses 6 Modern Clinical Procedures in Periodontal Reconstructive Treatment ��������������������������������������������������������������   87 Carlos E. Nemcovsky and Jose Nart 7 VRF as an Endodontic Periodontal Lesion����������������������������������� 125 Spyros Floratos, Aviad Tamse, and Shlomo Elbahary 8 Treatment Alternatives Following Extraction of Teeth with Periodontal-Endodontic Lesions���������������������������������� 141 Carlos E. Nemcovsky, Massimo del Fabbro, Ilan Beitlitum, and Silvio Taschieri 9 Dental Implants Biological Complications: Tooth Preservation Reevaluated ���������������������������������������������������� 195 Carlos E. Nemcovsky and Eyal Rosen 10 Integration of Clinical Factors and Patient Values into Clinical Decision-Making in the Management of Endodontic-­Periodontal Lesions������������������������������������������������ 215 Igor Tsesis, Russell Paul, and Eyal Rosen v

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Lesions of Endodontic Periodontal Origin Igor Tsesis, Carlos E. Nemcovsky, Joseph Nissan, and Eyal Rosen

The association of the degenerative changes in the pulp tissues and periodontal disease presents a clinical and conceptual dilemma ever since it was first described in the beginning of the twentieth century by Cahn (1927) [1]. Multiple investigations on that topic were later on published. Being one of the earliest published by Simring and Goldberg in 1964 [2], claiming that pulpal and periodontal problems are responsible for more than 50% of tooth mortality [2, 3]. During the following years many possible etiologies, definitions, classifications, and management alternatives based on different paradigms have been proposed. As a consequence, the understanding of this clinical scenario is a matter for ongoing debate. Due to the close relationship between endodontic and periodontal diseases, Weine (1972)

I. Tsesis (*) · E. Rosen Department of Endodontology, School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel C. E. Nemcovsky Department of Periodontology and Implant Dentistry, The Maurice and Gabriela School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel e-mail: [email protected] J. Nissan Department of Oral Rehabilitation School of Dental-Medicine, Tel Aviv University, Tel Aviv, Israel

[4] suggested that endodontics is actually “periapical periodontics.” However, this term, like many others’ proposed definitions, has not been widely accepted. Regardless of the exact definition and selected characterization scheme, the etiology of these endodontic-periodontal lesions derives from the etiologies of the associated endodontic and periodontal diseases. The relative parts of the endodontic and of the periodontal associated diseases in the ensuing endodontic-periodontal lesion vary depending on the nature and pathogenesis of the endodontic-periodontal lesion. It ranges from solitary endodontic lesions, in which most, if not the entire etiology, is of endodontic origin, to solitary periodontal lesion, in which the etiology is of periodontal origin only. Root canal space infection is the main etiology of apical periodontitis [5]. The advance of the disease involves inflammatory reaction of the peri-radicular tissues and periodontal ligamental space [6]. Periodontal disease, on the other hand, involves marginal periodontium and results in the progressive loss of the supportive tissues [7]. While the etiology of both is bacterial, their clinical presentation is different [8–11]. Endodontic disease initiates with the involvement of dental pulp and clinical signs and symptoms may include sensitivity to thermal stimuli

Rabin Medical-Center, Belinson Hospital, Petah-Tikva, Israel © Springer Nature Switzerland AG 2019 I. Tsesis et al. (eds.), Endodontic-Periodontal Lesions, https://doi.org/10.1007/978-3-030-10725-3_1

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and radiographic presentation of damage to the hard tissue of the tooth such as carries, trauma, or extensive restoration. If not treated, the pulp becomes progressively contaminated and peri-­ radical bone resorption becomes evident radiographically (Fig. 1.1). This process may remain asymptomatic or result in purulent inflammation, chronic or acute [12]. Infection is the main etiology for periodontal disease [13, 14]. Perio-pathogenic bacterial plaque together with calculus accumulation on the external root surfaces progress apically leading to gingival marginal inflammation that may progress to deeper supporting periodontal structures. Endotoxins from bacterial plaque together

with inflammatory mediators lead to destruction of gingival connective tissue, periodontal ligament, and alveolar bone [15] (Fig. 1.2). The transition of an endodontic disease or of a periodontal disease into a combined endodontic-­ periodontal disease depends on the anatomical communications between the root canal space and of the marginal periodontium. There are multiple routes of communication between the root canal space and marginal periodontium [8, 11, 16–23]. The main root canal opening (apical foramen) is the main pathway between the infected pulp in periodontal tissues. In addition, open dentinal tubuli and lateral canals may contain bacteria and had been

Fig. 1.1  Second maxillary premolar—the patient presented with a sensitivity to percussion: preoperative radiograph—extensive coronal restoration and radiolucent

periapical area; radiograph immediately after root canal treatment, resolution of the periapical lesion at the 1 year follow-up

a

b

Fig. 1.2 (a) Anterior mandibular teeth with severe periodontal disease: gingival recession and deep periodontal pockets. (b) Following flap elevation, calculus on root surface with large loss of periodontal support is evident

1  Lesions of Endodontic Periodontal Origin

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Fig. 1.3  Central maxillary incisor with pulp necrosis and periapical lesion (a). Following root canal filling: lateral canals communicating between the main root canal and periapical lesion are clearly seen (b)

reported as possible communication routes for bacteria [8, 11, 16–23] (Fig.  1.3). In addition, various pathological conditions, such as root fractures, perforations, resorption, or anatomical anomalies, may present a pathway for the bacteria [24]. By these communications the bacteria from the root canal space may contaminate and infect the marginal periodontium and vice versa [2, 5, 10, 15, 25]. The unique etiology and pathogenesis of the endodontic-periodontal disease dictates the required management plan of these challenging clinical cases and the prognosis of the affected teeth. The management of the pulpal disease is almost exclusively based on the elimination of the bacteria from the infected root canal space and reinfection prevention [26]. Unlike in endodontic disease, in periodontally affected teeth, bacteria reside on the exposed root surfaces in the gingival sulcus and periodontal pockets [8, 9, 14, 15, 25]. Accordingly, the manage-

ment of the periodontal disease is different, consisting on plaque and calculus elimination to render the root surface biocompatible that may be combined with periodontal reconstructive procedures to enhance periodontal support [27] (Fig. 1.4). The diagnosis of endodontic-periodontal lesions may be intriguing, since both periodontal and endodontic diseases have similar clinical and radiographic symptoms and may mimic each other. Moreover, the simultaneous occurrence of the pulpal and periodontal pathology can complicate diagnosis and treatment and compromise the prognosis of the involved teeth. While in most cases the manifestation of the periodontal and endodontic diseases is clearly distinct, there are certain clinical scenarios when the signs and symptoms may be confusing, making the final diagnosis complicated and ­subsequently result in the wrong treatment choice [8, 23, 28, 29] (Fig. 1.5). Misdiagnosis and subsequent wrong treatment choice may ultimately result in tooth extraction

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a

b

Fig. 1.4 (a, b) Clinical and radiographic (respectively) aspect of lower anterior teeth shows generalized loss of periodontal support, especially on distal aspect of lateral left incisor. (c) Radiograph taken 1 year following reconstructive periodontal treatment with use of enamel matrix proteins derivative, enhanced periodontal support may be

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c

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appreciated in most involved teeth, note large bone fill on distal aspect of lateral left incisor. (d) Radiograph taken 3 years following periodontal surgical treatment, further enhancement of periodontal support may be appreciated in most involved teeth

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Fig. 1.5  First maxillary molar: the tooth was diagnosed as having a necrotic and infected pulp, chronic apical abscess with a sinus tract traced to the disto-buccal root

using a gutta-percha cone (a), peri-radicular bone resorption, and advanced periodontal disease (b)

[28, 30, 31]. Numerous reports in the literature have presented possible options for the diagnosis and treatment of this condition [32]. Following treatment of teeth with endodontic-­ periodontal lesions, appropriate restorative plan is crucial for the prognosis of the teeth. Endodontic as well as periodontal pathologies are closely related to the restorative aspects of dentistry. Any restorative procedure may cause some degree of pulp damage, and at the same time faulty restoration may result in periodontal

involvement [4]. Besides, all root canal treated teeth require some type of coronal restoration, and in cases of severe damage to the tooth hard tissues, there may be even needs for surgical treatment. In consequence, restoration of teeth with endo-perio lesion is challenging due to uncertain prognosis while tooth structure preservation and proper restorative materials and techniques are essential for long-term success. Permanent restoration, direct or indirect, should be placed as soon as possible after the completion

1  Lesions of Endodontic Periodontal Origin

of root canal therapy due to the fact that coronal leakage is considered as one of the important factors that influence tooth survival during and after endo-perio treatment. From the above mentioned it is clear that the topic of endodontic- periodontal lesion is ultimately relevant to all areas of dentistry. The comprehensive multidisciplinary approach is of outmost importance in the diagnosis and management of the endodontic-­ periodontal lesions in order to provide the best chance of providing an optimal treatment. A simple and clinically relevant classification and appropriate treatment alternatives and considerations together with biological perspectives of the endodontic periodontal lesions are presented in the following book chapters.

References 1. Cahn LR. The pathology of pulps found in pyorrhetic teeth. Dent Items Int. 1927;49:598–617. 2. Simring M, Goldberg M.  The pulpal pocket approach: retrograde periodontitis. J Periodontol. 1964;35:22–48. 3. Chen SY, Wang HL, Glickman GN. The influence of endodontic treatment upon periodontal wound healing. J Clin Periodontol. 1997;24(7):449–56. 4. Weine F.  Endodontic therapy. Saint Luis: Mosby; 1972. 5. Signoretti FG, Gomes BP, Montagner F, Jacinto RC. Investigation of cultivable bacteria isolated from longstanding retreatment-resistant lesions of teeth with apical periodontitis. J Endod. 2013;39(10):1240–4. 6. Jakovljevic A, Knezevic A, Karalic D, Soldatovic I, Popovic B, Milasin J, et  al. Pro-inflammatory cytokine levels in human apical periodontitis: correlation with clinical and histological findings. Aust Endod J. 2015;41(2):72–7. 7. Ferreira MC, Dias-Pereira AC, Branco-de-Almeida LS, Martins CC, Paiva SM.  Impact of periodontal disease on quality of life: a systematic review. J Periodontal Res. 2017;52(4):651–65. 8. Belk CE, Gutmann JL.  Perspectives, controversies and directives on pulpal-periodontal relationships. J Can Dent Assoc. 1990;56(11):1013–7. 9. Kerekes K, Olsen I. Similarities in the microfloras of root canals and deep periodontal pockets. Endod Dent Traumatol. 1990;6(1):1–5. 10. Rocas IN, Siqueira JF Jr, Santos KR, Coelho AM. “Red complex” (bacteroides forsythus, porphyromonas gingivalis, and treponema denticola) in endodontic

5 infections: a molecular approach. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2001;91(4):468–71. 11. Simon JH, Glick DH, Frank AL.  The relation ship of endodontic-periodontic lesions. J Endod. 2013;39(5):e41–6. 12. Zanini M, Meyer E, Simon S.  Pulp inflammation diagnosis from clinical to inflammatory mediators: a systematic review. J Endod. 2017;43(7):1033–51. 13. Genco RJ, Borgnakke WS. Risk factors for periodontal disease. Periodontol. 2013;62(1):59–94. 14. Haffajee AD, Socransky SS. Microbiology of periodontal diseases: introduction. Periodontol. 2005;38:9–12. 15. Loe H.  The role of bacteria in periodontal diseases. Bull World Health Organ. 1981;59(6):821–5. 16. Arambawatta K, Peiris R, Nanayakkara D.  Morphology of the cemento-enamel junction in premolar teeth. J Oral Sci. 2009;51(4):623–7. 17. Bender IB, Seltzer S.  The effect of periodontal disease on the pulp. Oral Surg Oral Med Oral Pathol. 1972;33(3):458–74. 18. Gautam S, Galgali SR, Sheethal HS, Priya NS. Pulpal changes associated with advanced periodontal disease: a histopathological study. J Oral Maxillofac Pathol. 2017;21(1):58–63. 19. Gutmann JL.  Prevalence, location, and patency of accessory canals in the furcation region of permanent molars. J Periodontol. 1978;49(1):21–6. 20. Komabayashi T, Nonomura G, Watanabe LG, Marshall GWJ, Marshall SJ.  Dentin tubule numerical density variations below the CEJ. J Dent. 2008;36(11):953–8. 21. Ricucci D, Siqueira JF Jr. Fate of the tissue in lateral canals and apical ramifications in response to pathologic conditions and treatment procedures. J Endod. 2010;36(1):1–15. 22. Simon JH, Glick DH, Frank AL.  The relationship of endodontic-periodontic lesions. J Periodontol. 1972;43(4):202–8. 23. Torabinejad M, Trope M. Endodontic and periodontal interrelationships. In: Walton RE, Torabinejad M, editors. Principles and Practice of Endodontics; 1996. 24. Tsesis I, Rosenberg E, Faivishevsky V, Kfir A, Katz M, Rosen E.  Prevalence and associated periodontal status of teeth with root perforation: a retrospective study of 2,002 patients’ medical records. J Endod. 2010;36(5):797–800. 25. Kurihara H, Kobayashi Y, Francisco IA, Isoshima O, Nagai A, Murayama Y. A microbiological and immunological study of endodontic-periodontic lesions. J Endod. 1995;21(12):617–21. 26. Ng YL, Mann V, Gulabivala K.  Tooth survival following non-surgical root canal treatment: a systematic review of the literature. Int Endod J. 2010;43(3):171–89. 27. Martin-Cabezas R, Davideau JL, Tenenbaum H, Huck O. Clinical efficacy of probiotics as an adjunctive therapy to non-surgical periodontal treatment of chronic periodontitis: a systematic review and meta-­ analysis. J Clin Periodontol. 2016;43(6):520–30.

6 28. Singh P.  Endo-perio dilemma: a brief review. Dent Res J. 2011;8(1):39–47. 29. Terlemez A, Alan R, Gezgin O.  Evaluation of the periodontal disease effect on pulp volume. J Endod. 2018;44(1):111–4. 30. Mileman PA, van den Hout WB. Evidence-based diagnosis and clinical decision making. Dentomaxillofac Radiol. 2009;38(1):1–10.

I. Tsesis et al. 31. Rosenberg W, Donald A.  Evidence based medi cine: an approach to clinical problem-solving. BMJ. 1995;310(6987):1122–6. 32. Schmidt JC, Walter C, Amato M, Weiger R. Treatment of periodontal-endodontic lesions--a systematic review. J Clin Periodontol. 2014;41(8):779–90.

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Etiology and Classification of Endodontic-Periodontal Lesions Eyal Rosen, Carlos E. Nemcovsky, Joseph Nissan, and Igor Tsesis

2.1

Introduction

The periodontium and the dental pulp are closely associated, sharing embryonic, functional, and anatomical interrelationships. A century ago, Turner and Drew [1] described for the first time the effect of periodontal diseases on the pulp tissue. Then, in 1964 Simiring and Goldberg [2] described a disease of the periodontium caused by a pulpal disease, termed “Retrograde periodontitis.” They stated that unlike marginal periodontitis, in which the disease proceeds from the gingival margin as the source of infection toward the tooth apex, in “retrograde periodontitis” the pulp is the source of the pathogens affecting the periodontium, potentially causing a periodontal disease, con-

E. Rosen · I. Tsesis (*) Department of Endodontology, School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel C. E. Nemcovsky Department of Periodontology and Implant Dentistry, The Maurice and Gabriela Goldschleger School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel e-mail: [email protected] J. Nissan Department of Oral-Rehabilitation School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel Rabin Medical-Center, Belinson Hospital, Petach-Tikva, Israel

tributing to a periodontal disease, or preventing healing of a periodontal disease [2]. Simiring and Goldberg [2] also explained that these two processes generally exist side by side, and may have the same signs and symptoms. Thus, they may be difficult to distinguish [2]. The traditional classifications of endodontic-­ periodontal lesions are usually based on the origin of the infection, i.e., primary endodontic lesions, primary periodontal lesions, and different combinations of the above. However, due to the interrelationships of these two entities it had been claimed that these classifications are too academic and theoretical and may not be clinically practical. This chapter will review the etiological factors of endodontic-periodontal lesions, the common classifications of these pathologies, and will suggest a novel and clinically practical classification for these intriguing clinical scenarios.

2.2

Pulpal-Periodontal Routes of Communication

Although it may seem that the dental pulp and the periodontium are two distinct tissues, there are many potential routs in which these tissues can communicate [3–7], such as the apical foramen [2, 8]; exposed dentinal tubules [3]; lateral and accessory canals [4]; certain anatomical

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variations [9, 10]; or pathological conditions such as root perforations and fractures [11, 12]. The apical foramen is the main route of communication between the pulp and the periodontal tissues. In case of pulp infection, the bacteria and their by-products may exit through the apical foramen causing periapical inflammation. In certain cases, the associated periapical tissue destruction can spread coronally and involve the marginal periodontium. On the other hand, in case of severe periodontal disease with deep periodontal pockets the vice versa may happen [2, 8]. Dentinal tubuli are another possible route for the communication between the root canal system and periodontium. Between 13,700 and 32,300 dentinal tubules per square millimeter may be present in the cervical dentin [5]. Therefore, periodontal disease and procedures such as scaling and root planning may lead to exposed dentin [3], and allow the pulp tissue to communicate with the external root surface and the periodontium. Lateral and accessory canals can be present along the root including the cervical areas of the tooth. Gutmann [4] studied the external root surface of molars to determine patent accessory canals, and reported that accessory canals were demonstrated in the furcation region in 28% of the teeth. The presence of such patent accessory canals is a potential pathway for the spread of bacteria and toxic substances resulting in inflammatory process in the periodontal tissues [6]. Anatomical variations such as palatogingival groove [9], a relatively common developmental anomaly in maxillary incisors, or the presence of gaps between the enamel and cementum with exposed dentin [10], may provide favorable conditions for communication between the periodontal and the pulpal tissues, for plaque retention, and for periodontal disease progression toward the apical areas of the root that may eventually involve the pulp [9, 10]. Treatment complications such as root perforations or root originated fractures open up a significant communication passage between the root canal system and the periodontal tissues. In case of infection, these complications can lead to the formation of endodontic-periodontal lesions [11, 12].

2.3

 he Etiology of Endodontic-­ T Periodontal Lesions

Both endodontic and periodontal diseases are multifactorial with many demographic [13, 14], anatomical [4, 5, 9, 10, 15], genetic [16, 17], systemic [18, 19], behavioral [20, 21], and other potential contributing factors. However, since both endodontic [22] and periodontal diseases [23] are primarily associated with infection, even in the presence of these contributing factors, a disease will develop mainly in the presence of infection [22, 23]. In 1965, Kakehashi et  al. [24] evaluated the pathological changes resulting from untreated experimental pulp exposures in germ-free rats as compared with conventional rats with normal oral flora. In the normal rats, pulp necrosis and abscess formation occurred in all specimens. In contrast, no devitalized pulps or abscesses were found in the germ-free animals, thus demonstrating that bacterial infection is necessary for the development of an endodontic periapical disease [24]. In accordance, numerous studies have demonstrated that the basic etiology of periodontal diseases is also a bacterial infection [25, 26]. However, even when the conditions developed allow the progression of an endodontic-­ periodontal disease, for example, following root perforation or development of root originated fracture, it may take time until bacteria colonize the pulpal-periodontal communication site, and additional time until an associated pathology develops [27]. Traditionally, one of the most intriguing questions has been how endodontic and periodontal microorganisms link together to form an endodontic-periodontal disease. Zehnder et  al. [28] claimed that although the periodontal pocket presents a greater variety of microorganisms than the infected pulp, when an endodontic infection is caused by severe periodontitis, all bacterial species found within the root canals are also present in the periodontal pocket. These similarities in the microflora of these two niches were also reported by Kerekes and Olsen [29], supporting the concept that infection may spread from one niche to the other.

2  Etiology and Classification of Endodontic-Periodontal Lesions

However, other reports suggested that there are fundamental differences between the microflora recovered from infected root canals and from periodontal pockets, perhaps because coccus and rods predominate within infected root canals while spirochetes and rods predominate within periodontal pockets [30, 31]. Rôças et  al. [32] assessed the occurrence of the so-called “red complex bacteria” (Porphyromonas gingivalis, Bacteroides forsythus, and Treponema denticola) that may be associated with severe periodontal diseases, in root canal infections. They found that at least one member of the red complex was found in 33 of 50 cases, and concluded that since the “red complex” bacteria are known oral pathogens, their manifestation in root canal infections suggests that they may play a role in the pathogenesis of periradicular diseases [32]. Nevertheless, in recent years as our understanding of the ecology of biofilms improved, these traditional controversies seem to become redundant. Despite the commonly held perception of oral bacteria as solitary surviving microorganisms, in the different oral niches, bacteria form complex biofilm communities. These biofilms are specialized ecological communities, where the bacteria use different mechanisms to align their activity within the community in order to adopt to the constantly changing environmental conditions. These adaptations include dynamic changes in the biofilm species compositions and proportions within the community [33–36]. Thus, exposure of a specific biofilm to a different ecological niche, like exposure of endodontic biofilm to the periodontium and vice versa, would initiate these adaptation processes, altering these two communities to align together and to spread from one niche to the other.

2.4

Traditional Classifications of Endodontic-Periodontal Lesions

Many classifications were suggested along the years to describe the versatility of these clinical scenarios. Each of these was based on dif-

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ferent characteristics of the pathological process, such as: classifications that were based on the diagnosis, prognosis, and treatment of these lesions [7]; classifications that were based on pathologic relationship [37]; or classifications that were based on treatment [38]. Simon et al. [7] were the first to suggest a classification of endodontic-periodontal lesions that was mainly based on diagnosis, prognosis, and treatment. This classification included primary endodontic lesions, primary periodontal lesions, primary endodontic lesions with secondary periodontal involvement, primary periodontal lesions with secondary endodontic involvement, and true combined lesions. According to Simon et  al. [7], Primary endodontic lesions clinically manifest with a possible drainage from the gingival sulcus, swelling in attached gingiva, and some discomfort. The necrotic pulp may be associated with a sinus tract extending from the root apex along the root surface, to exit at the cervical line. The radiographic examination would usually show bone loss, appearing as a radiolucency along the entire root length. Other clinical presentations are also possible such as in multi-rooted teeth, were the sinus tract may drain into the bifurcation area with an associated radiographic appearance of periodontal involvement [39]. After some time plaque accumulates at the gingival margin which could result in marginal periodontitis, and then this primary endodontic disease may become secondarily involved with periodontal destruction. Simon termed this condition as Primary endodontic lesions with secondary periodontal involvement [7, 39]. When this occurs, both endodontic and periodontal therapy are required and the tooth prognosis depends mainly on the success of the periodontal treatment, assuming that the endodontic procedures are usually more predictable [7, 39]. Simon et  al. [7, 39] classified Primary periodontal lesions as lesions that are caused by a periodontal disease that gradually progresses along the root surface toward the apical region. The diagnosis is based on common periodontal examinations such as probing depth m ­ easurement.

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Pulp vitality examination should confirm that the pulp is vital. Thus, since the pulp in still vital, the prognosis in this scenario primarily depends upon the efficacy of the periodontal treatment [7, 39]. According to Simon et al. [7, 39], as the periodontal pocket progresses toward the apical areas of the root, lateral canals and eventually the apical foramen may become exposed to the periodontal microflora which can lead to pulp necrosis. This condition was termed Primary periodontal lesions with secondary endodontic involvement [7, 39]. Simon et  al. pointed out that diagnostically, these lesions may cause a dilemma as they may be indistinguishable from primary endodontic lesions with secondary periodontic involvement. It should be noted that the exact association between the progression of a periodontal disease and its effect on the condition of the dental pulp is a matter of long-lasting debate [40, 41]. However, modern studies reveled that in the presence of a significant chronic periodontal disease, pulp inflammation and necrosis do occur [41]. According to Simon’s classification [39] True combined lesions may develop when an endodontic periapical lesion progresses in a tooth that is also periodontally involved, until these two pathologies merge along the root surface. Again, this condition may also pose a significant diagnostic dilemma as its clinical and radiographic presentations are indistinguishable from other previously mentioned lesion types. From the treatment and prognosis aspects, periapical healing is probable following endodontic treatment. However, the periodontal disease may or may not respond to periodontal treatment, depending on the severity of the periodontal disease [39]. Following the publication of Simon’s classification, in 1982 Guldener and Langeland [37] suggested a new classification that was based on the pathologic relationship: endodontic-­ periodontal lesion, periodontal-endodontic lesion, and combined lesions. In 1990 Belk and Gutmann [42] suggested to add to the previously presented Simons’s classification an additional classification, termed Concomitant pulpal-periodontal lesion. In this clinical scenario, both endodontic and periodontal diseases coexist in the same tooth, with no

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evidence that either disease has influenced the other [42]. Then in 1996 Torabinejad and Trope [38] suggested another classification that was based on the treatment point of view: endodontic origin, periodontal origin, combined endo-perio lesions, separate endodontic and periodontal lesions, lesions with communication, lesions with no communication. Most of these classifications agreed on the possible origins of these lesions as some of these are of endodontic origin, some are of periodontal origin, and some are different combinations of the above [7, 37, 38]. However, there are significant disagreements among the traditional classification schemes as to how these pathologies should be further subdivided into additional subgroups as the pathology progresses. Accurate diagnosis of the exact nature of the lesion is crucial for an effective treatment, and to assess the tooth prognosis [8, 43, 44]. Generally, when it is a lesion of purely endodontic origin, the treatment of choice would be endodontic, and the prognosis would mainly depend on the ability to endodontically treat the disease. When the lesion is purely of periodontal etiology, a periodontal treatment is the main treatment of choice and the feasibility of this periodontal treatment would determine the tooth prognosis. In all other cases, both endodontic and periodontal treatments are required and the ability to control and treat both diseases would determine the tooth prognosis [8, 43, 44]. In this context, the diagnosis of primary endodontic lesions without periodontal involvement and primary periodontal lesions without endodontic involvement is usually straightforward and feasible. In primary endodontic lesions, the pulp is non-vital and infected, and on the other hand, in a tooth with primary periodontal lesion, the pulp is vital. However, a combined disease such as primary endodontic lesion with secondary periodontal involvement, primary periodontal disease with secondary endodontic involvement, concomitant lesions, or true combined lesions may all radiographically and clinically look alike, especially in advanced stages of the disease [43, 44]. Thus, it seems that from the treatment

2  Etiology and Classification of Endodontic-Periodontal Lesions

and prognosis aspects it is not practical to use the traditional categorization schemes. Two major groups of endodontic-periodontal lesions may be identified according to the etiological origin: pathological endo-perio lesions—resulting from the disease of the pulp or periodontium—and iatrogenic endo-perio lesions—representing a complication of the treatment that results in an artificial communication between the root canal space and marginal periodontium. Classical example of iatrogenic endo-­ perio lesion can be iatrogenic root perforation or iatrogenic root fractures. Thus, we suggest to use a three-component categorization scheme of endodontic-periodontal lesions: 1. Purely endodontic lesion: when the pulp is necrotic and infected, and there is a draining sinus tract coronally through the periodontal ligament into the gingival sulcus. 2. Purely periodontal lesion: when a deep periodontal lesion involves most of the root surface, and the dental pulp is vital. 3. Endodontic-periodontal lesion: when the pulp is necrotic and infected, and there is a deep periodontal pocket. For lesions of purely endodontic origin, the clinical manifestation and the diagnosis is usually consistent with chronic or acute apical abscess. The proper management of the disease will include eradication of the bacterial infection by a root canal treatment, and the tooth prognosis will depend mainly on the efficacy of the endodontic treatment. Purely periodontal lesions are clinically consistent with severe periodontal disease, involving a great part of the root/s surface. The management of these lesions is by periodontal treatment and there is no need for endodontic treatment. Tooth prognosis mainly depends on the efficacy of the periodontal treatment. Endodontic-periodontal lesions are cases with long-standing severe infection that involves both the root canal space and the marginal periodontium. In these cases, although the prognosis depends primarily on the severity of the peri-

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odontal disease, it is usually impossible to initially assess the contribution of the endodontic infection to clinical manifestation of this combined disease. On the other hand, the endodontic treatment is considered more predictable than the periodontal. Thus, it is advised to initially perform a root canal treatment, and only initial, nonsurgical periodontal procedures such as scaling and root planing. Following, it is advised to control healing for 3–4 months to monitor resolution of the endodontic infection and its effect on the tooth periodontal status. Provided endodontic improvement, based on the more specific and accurate understanding of the periodontal status of the tooth, a comprehensive periodontal treatment strategy may be planned. In cases involving teeth with previous endodontic treatment, the diagnosis and classification can be challenging. In these cases, since pulp vitality tests cannot be performed, it is more difficult to clinically assess the condition of the pulp space and its involvement in the disease. Therefore, in case of a doubt, when it is suspected that the root canal treated pulp space is infected, the cases should be endodontically retreated.

2.5

Conclusions

• A close anatomical association between endodontic and periodontal tissues may lead to spread of the infection between the root canal and marginal periodontium. • Classification of the endodontic-periodontal lesions should be based on the primary etiological factor of the pathology and clinical presentation as purely endodontic, purely periodontal or endodontic-periodontal lesions.

References 1. Turner JG, Drew AH.  An experimental inquiry into the bacteriology of pyorrhoea. J R Soc Med. 1919;12:104–18. 2. Simring M, Goldberg M.  The pulpal pocket approach: retrograde periodontitis. J Periodontol. 1964;35(1):22–48.

12 3. Adriaens PA, De Boever JA, Loesche WJ.  Bacterial invasion in root cementum and radicular dentin of periodontally diseased teeth in humans. A reservoir of periodontopathic bacteria. J Periodontol. 1988;59(4):222–30. 4. Gutmann JL.  Prevalence, location, and patency of accessory canals in the furcation region of permanent molars. J Periodontol. 1978;49(1):21–6. 5. Komabayashi T, Nonomura G, Watanabe LG, Marshall GWJ, Marshall SJ.  Dentin tubule numerical density variations below the CEJ. J Dent. 2008;36(11):953–8. 6. Ricucci D, Siqueira JF Jr. Fate of the tissue in lateral canals and apical ramifications in response to pathologic conditions and treatment procedures. J Endod. 2010;36(1):1–15. 7. Simon JH, Glick DH, Frank AL.  The relationship of endodontic-periodontic lesions. J Periodontol. 1972;43(4):202–8. 8. Rotstein I, Simon JH.  Diagnosis, prognosis and decision-making in the treatment of combined periodontal-endodontic lesions. Periodontol 2000. 2004;34:165–203. 9. Naik M, de Ataide Ide N, Fernandes M, Lambor R.  Treatment of combined endodontic: periodontic lesion by sealing of palato-radicular groove using biodentine. J Conserv Dent. 2014;17(6):594–7. 10. Arambawatta K, Peiris R, Nanayakkara D.  Morphology of the cemento-enamel junction in premolar teeth. J Oral Sci. 2009;51(4):623–7. 11. Tsesis I, Rosen E, Tamse A, Taschieri S, Kfir A.  Diagnosis of vertical root fractures in endodontically treated teeth based on clinical and radiographic indices: a systematic review. J Endod. 2010;36(9):1455–8. 12. Tsesis I, Rosenberg E, Faivishevsky V, Kfir A, Katz M, Rosen E.  Prevalence and associated periodontal status of teeth with root perforation: a retrospective study of 2,002 patients’ medical records. J Endod. 2010;36(5):797–800. 13. Demirbuga S, Tuncay O, Cantekin K, Cayabatmaz M, Dincer AN, Kilinc HI, et  al. Frequency and distribution of early tooth loss and endodontic treatment needs of permanent first molars in a Turkish pediatric population. Eur J Dent. 2013;7(Suppl 1):S99–S104. 14. Yu HC, Su NY, Huang JY, Lee SS, Chang YC. Trends in the prevalence of periodontitis in Taiwan from 1997 to 2013: a nationwide population-based retrospective study. Medicine (Baltimore). 2017;96(45):e8585. 15. Hou GL, Tsai CC.  Clinical significance of tooth morphology correlated with periodontal disease­I. Kaohsiung J Med Sci. 1997;13(4):200–12. 16. da Silva MK, de Carvalho ACG, Alves EHP, da Silva FRP, Pessoa LDS, Vasconcelos DFP. Genetic factors and the risk of periodontitis development: findings from a systematic review composed of 13 studies of meta-analysis with 71,531 participants. Int J Dent. 2017;2017:1914073. 17. Morsani JM, Aminoshariae A, Han YW, Montagnese TA, Mickel A.  Genetic predisposition to persistent apical periodontitis. J Endod. 2011;37(4):455–9.

E. Rosen et al. 18. Aminoshariae A, Kulild JC, Mickel A, Fouad AF.  Association between systemic diseases and endodontic outcome: a systematic review. J Endod. 2017;43(4):514–9. 19. Genco RJ, Borgnakke WS. Risk factors for periodontal disease. Periodontol. 2013;62(1):59–94. 20. Patel RA, Wilson RF, Palmer RM.  The effect of smoking on periodontal bone regeneration: a systematic review and meta-analysis. J Periodontol. 2012;83(2):143–55. 21. Stein C, Santos NML, Hilgert JB, Hugo FN.  Effectiveness of oral health education on oral hygiene and dental caries in schoolchildren: systematic review and meta-analysis. Community Dent Oral Epidemiol. 2018;46(1):30–7. 22. Haapasalo M, Udnaes T, Endal U.  Persistent, recurrent, and acquired infection of the root canal system post-treatment. Endod Top. 2003;6:29–56. 23. Loe H.  The role of bacteria in periodontal diseases. Bull World Health Organ. 1981;59(6):821–5. 24. Kakehashi S, Stanley HR, Fitzgerald RJ. The effects of surgical exposures of dental pulps in germ-free and conventional laboratory rats. Oral Surg Oral Med Oral Pathol. 1965;20:340–9. 25. Haffajee AD, Socransky SS.  Microbiology of periodontal diseases: introduction. Periodontol 2000. 2005;38:9–12. 26. Socransky SS, Haffajee AD.  The bacterial etiology of destructive periodontal disease: current concepts. J Periodontol. 1992;63(4 Suppl):322–31. 27. Tamse A, Tsesis I, Rosen E. Introduction. In: Tamse A, Tsesis I, Rosen E, editors. Vertical root fractures in dentistry. Switzerland: Springer International Publishing; 2015. p. 1–5. 28. Zehnder M. Endodontic infection caused by localized aggressive periodontitis: a case report and bacteriologic evaluation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2001;92(4):440–5. 29. Kerekes K, Olsen I. Similarities in the microfloras of root canals and deep periodontal pockets. Endod Dent Traumatol. 1990;6(1):1–5. 30. Kurihara H, Kobayashi Y, Francisco IA, Isoshima O, Nagai A, Murayama Y.  A microbiological and immunological study of endodontic-periodontic ­ lesions. J Endod. 1995;21(12):617–21. 31. Trope M, Rosenberg E, Tronstad L.  Darkfield microscopic spirochete count in the differentiation of endodontic and periodontal abscesses. J Endod. 1992;18(2):82–6. 32. Rocas IN, Siqueira JF Jr, Santos KR, Coelho AM. “Red complex” (Bacteroides forsythus, Porphyromonas gingivalis, and Treponema denticola) in endodontic infections: a molecular approach. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2001;91(4):468–71. 33. Stoodley P, Sauer K, Davies DG, Costerton JW. Biofilms as complex differentiated communities. Annu Rev Microbiol. 2002;56:187–209. 34. Miller MB, Bassler BL. Quorum sensing in bacteria. Annu Rev Microbiol. 2001;55:165–99.

2  Etiology and Classification of Endodontic-Periodontal Lesions 35. Aguilar C, Vlamakis H, Losick R, Kolter R. Thinking about Bacillus subtilis as a multicellular organism. Curr Opin Microbiol. 2007;10(6):638–43. 36. Kolter R, Greenberg EP.  Microbial sciences: the superficial life of microbes. Nature. 2006;441(7091):300–2. 37. Guldener PHA.  Beziehung zwischen Pulpa-und Parodontaler krankungen. In: Guldener PHA, Langeland K, editors. Endodontologie. Stuttgart: Thieme; 1982. p. 368–78. 38. Torabinejad M, Trope M. Endodontic and periodontal interrelationships. In: Walton RE, Torabinejad M, editors. Principles and practice of endodontics; 1996. 39. Simon JH, Glick DH, Frank AL.  The relation ship of endodontic-periodontic lesions. J Endod. 2013;39(5):e41–6.

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40. Bender IB, Seltzer S.  The effect of periodontal disease on the pulp. Oral Surg Oral Med Oral Pathol. 1972;33(3):458–74. 41. Gautam S, Galgali SR, Sheethal HS, Priya NS. Pulpal changes associated with advanced periodontal disease: a histopathological study. J Oral Maxillofac Pathol. 2017;21(1):58–63. 42. Belk CE, Gutmann JL.  Perspectives, controversies and directives on pulpal-periodontal relationships. J Can Dent Assoc. 1990;56(11):1013–7. 43. Chang KM, Lin LM. Diagnosis of an advanced endodontic/periodontic lesion: report of a case. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1997;84(1):79–81. 44. Singh P.  Endo-perio dilemma: a brief review. Dent Res J. 2011;8(1):39–47.

3

Endodontic Considerations in the Management of EndodonticPeriodontal Lesions Kenneth J. Frick, Eyal Rosen, and Igor Tsesis

Objectives 1. Understand endodontic diagnosis and how it relates to periodontal lesions. 2. Understand the pulpodentinal complex and how its dynamics can influence the development of endo-perio lesions. 3. Become familiar with a variety of endo-perio related lesions and their clinical presentation.

3.1

Endodontic Diagnosis: Getting to the “Root” of the Problem

3.1.1 Medical and Dental History Medical History: The age of the patient and current medical conditions can influence both the diagnosis and course of treatment. Younger patients often present with good health and are taking few oral medications that may affect their teeth. However, older patients can present with

K. J. Frick (*) Department of Endodontics, University of Missouri, Kansas City, MO, USA e-mail: [email protected] E. Rosen · I. Tsesis Department of Endodontology, School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel

multiple health conditions that may influence their oral health, such as diabetes, cardiovascular disease, and cancer. Patients with diabetes mellitus have been associated with increased risk to periodontal disease and may also be at greater risk of developing apical periodontitis [1]. Recent evidence has also been presented suggesting patients with periodontal disease may have delayed healing after endodontic therapy [2]. The presence of cardiovascular disease, from a clinical study in Sweden, was found to increase the odds of having apical periodontitis by a factor of 3.8 [3]. Many patients being treated for cardiovascular disease also have hypercholesterolemia and are most likely taking a statin drug. As a result, they may be at risk of developing pulp canal obliteration over time [4], which may make the tooth more susceptible to developing apical periodontitis. Even cancer, such as lymphomas, may mimic periodontal and periapical conditions [5]. So it is important to be aware of these possibilities when assessing the patients’ medical history and any possible link to their current chief complaint. Dental History: The dental history as reported by the patient is a critical element. It is a detailed review of the history of the patient’s chief complaint and can be a key to the diagnosis, although it is a subjective history, and is influenced by the patient’s memory and current emotional status or stress level. At times patients are very poor historians of their oral health! Questions to the patient

© Springer Nature Switzerland AG 2019 I. Tsesis et al. (eds.), Endodontic-Periodontal Lesions, https://doi.org/10.1007/978-3-030-10725-3_3

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should include: How long has the condition been present? Does the area feel swollen? What is the pain like? What brings on the pain? Does the pain linger? What does not affect the pain? Has the condition prevented sleep? These questions are designed to determine the nature of the problem, as endodontic symptoms (history of spontaneous pain, lingering pain to cold, pain to biting) usually develop over a period of weeks or months, but periodontal related symptoms (sore gums, bleeding gums, foul odor) may linger for months to years. Another important question to consider pertains to the possibility of a history of trauma. Were there any events with the patient that may have led to this current condition? This last question may be important to ask of the younger patients (or their guardian). Dental trauma, although not the scope of this chapter, is another possible etiology of gingival and dental conditions. The reader is referred to the publications of the International Association of Dental Traumatology for further information regarding the topic of dental trauma [6]. Another important question to ask as part of the dental history involves previous endodontic treatments. Could the current condition be related to a recently completed root canal procedure? Or has the patient had root canal therapy years ago, but currently periodontal disease has flared up, and now an issue has developed around one of these previously treated root canals. In a retrospective cohort study, Ruiz et al. has shown that the risk of developing apical periodontitis in endodontically treated teeth is 5.19 times greater for patients with periodontal disease compared to patients without the disease [7].

3.1.2 Clinical Exam Radiographs: In order to determine an accurate diagnosis, three areas must be considered: the history of the problem, current radiographs (and historical ones if available), and a thorough clinical exam. The first part of this, the medical and dental history, was presented above. The next step is to obtain radiographs of the affected area and complete the clinical exam. Although this is a problem-focused exam, do not ignore the overall presentation of the patient’s mouth.

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What is the level of oral hygiene? Is there generalized gingivitis, perhaps even hyperplastic tissue? This may point to a periodontal verses endodontic assessment; consider the side effect of calcium channel blocking agents causing gingival hyperplasia [8]. Radiographs should include two periapical and one bitewing projection, as it has been shown that radiographs exposed from multiple angulations are more diagnostic [9]. It also may be prudent to consider a 3D CBCT scan. Depending on the results of the periapical radiographs, CBCT scans may be indicated, as they are more accurate in revealing apical pathologies and root morphological anomalies as compared to 2D periapical images [10, 11]. In reviewing the radiographs, special attention is given to cortical bone height and bone loss associated with the roots of the tooth in the area of interest pointed out by the patient, as well as the condition of the root canals. The clinician must be aware of possible indications of horizontal or vertical bone defects that may suggest periodontal disease and will need to be probed in the mouth. Other questions the clinician must consider regarding the radiographs are whether canals are visible in the roots, do the canals appear calcified, are there areas of resorption, and has the tooth had endodontic therapy, as well as, what is the condition and type of any present restorations. Lastly, what is the condition of the PDL space and is it traceable on the radiograph next to the lamina dura? These are all questions to be considered when viewing the radiographs. Extraoral Exam: The purpose of the extraoral exam is twofold. First, it should be done as an oral cancer screening, checking lymph nodes, thyroid gland, and muscles of mastication for signs of abnormalities and asymmetry; second, as a means to see any evidence of odontogenic swelling of the face. Depending on the information derived from the dental history, the clinician might suspect temporomandibular disease (TMD) as part of the differential diagnosis, especially if no direct soft tissue or endodontic lesion is found to explain the chief complaint. TMD has been shown to be one of the most common causes of non-odontogenic pain that is mistaken for toothache [12].

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Intraoral Exam: It is during this portion of the examination process that most causes of the chief complaint will be revealed. Periodontal probing, palpation, percussion, and sensibility testing (Cold test and Electric Pulp Test (EPT)) of the suspected area will all need to be carefully considered. Most likely the patient will direct you to the area of concern, but before exploring that area, the clinician must do an intraoral sweep of the mouth as part of the oral cancer screening process, and to gauge the overall periodontal health (and oral hygiene) of the patient. Then, a periodontal probing survey of the mouth can be done, ending in the suspected problem area. Periodontal Probing: With the completion of the periodontal probing in multiple areas of the mouth, the clinician should be aware of the general periodontal health of the patient. With this knowledge, careful probing of the affected tooth is completed, paying particular attention to the pattern of probing depths around the tooth. A gingival abscess of periodontal origin would commonly have wide areas of pocketing compared to those from an endodontic origin, which tend to be narrower. Harrington published a classic illustration of this in 1979 [13] and a similar illustration based on it is shown in Fig. 3.1. Palpation: Documentation of the sensitivity of the alveolar gingival tissues, both buccal and lingual, is an important part of the examination process. Areas of palpation sensitivity and or swelling should be noted and recorded. Percussion: This test often identifies the offending tooth, especially if there is an endodontic component responsible. However, complications to this test exist. It is important to discern whether the percussion sensitivity is coming from an inflamed periodontal ligament

(PDL), or is it from dentinal sensitivity due to caries or a cuspal fracture. Percussion sensitivity that is present no matter where the tooth is tapped (buccal, occlusal, or lingual) is most probably from an inflamed PDL and apical periodontitis. Isolated areas of percussion sensitivity on the same tooth suggest a dentinal issue, such as a fracture, caries, or possible occlusal trauma. Endodontic etiologies tend to be more percussion sensitive than periodontal ones [14, 15]. Sensibility Testing: Testing a tooth’s response to cold or heat has often been called vitality testing, but this is actually an inaccurate use of the term. Vitality testing measures the level of vascularity of a tissue, and is more of a histological term. Sensibility testing measures the neural response of a tissue, and how the subject responds. The level of the response can be defined as the sensitivity of the test. Thus, when a cold or heat test is conducted on a tooth, the sensibility is tested, with the level of response being the sensitivity [14]. Endodontically involved teeth that have not become necrotic will usually have an exaggerated and delayed and/or lingering response. The clinician should not be surprised by this response if the patient reported lingering and spontaneous pain as part of their dental history. A negative response to the thermal tests would indicate a necrotic pulp, especially if it also tested negative (no response, i.e., 80 reading) to an electric pulp test (EPT). The combination of these negative responses to both tests has a high sensitivity and specificity in providing an accurate diagnosis of pulpal necrosis [16, 17]. Regarding the concept of sensitivity and specificity, terms that are sometimes confusing to the average clinician, consider this simple illustration as an example. Figure 3.2 shows a photo of a

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Fig. 3.1 (a) The probing depths of a wide periodontal pocket. (b) The probing depths of a narrow periodontal pocket (Illustration courtesy of Molly S Kaz Frick, 2018)

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18 Fig. 3.2  Sign on door not intended to be used as an example of a specificity test

Fig. 3.3  Routes of endodontic infection through the apex or lateral canals of a tooth (Courtesy Dr. Riley, UMKC School of Dentistry)

doorway with two doors. One of the doors is marked with a sign that says, “use other door.” So in this example, if the presence of disease would be identified by going through the correct door, the sign on the door identifying where you should not go, i.e., no disease, would be the specificity test. If instead, however, a sign was on the door intended to be opened said “use this door,” that sign would be the sensitivity test. So sensitivity are tests that identify a condition, response, or disease, and specificity tests identify the lack of the presence of a condition, response, or disease. Results of sensibility tests are a critical element in determining whether the diseased condition of the tooth is periodontal or endodontic origin. An etiology of endodontic origin is easily

Primary endodontic lesions

ruled out if the offending tooth responds normally to those tests. Figure 3.3 presents an illustration of the typical routes of infection of endodontic lesion, such as from apical foramina or lateral and furcal canals.

3.1.3 E  ndodontic Only or Periodontic Only Lesions In this next section several cases representing either only endodontic or only periodontic lesions are shown. Figure 3.4 shows an example of a purely endodontic in orgin lesion. Figures 3.5, 3.6, and 3.7 show an example of a case that tested normal to pulp testing and was diagnosed as a

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

a

Fig. 3.4 (a) shows tooth #31, initially referred to a periodontist for treatment of a periodontal abscess. Deep pocketing (9 mm +) was found on the buccal furcation, but all other areas around the tooth had normal probings (3 mm or less). The patient was not in pain but had some minor buccal swelling of the gingival tissue near the furcation.

Fig. 3.5  Clinical photograph of symptomatic gingival abscess buccal to tooth #19. Note the swelling on the lower right side as indicated by the arrow. Gentle palpation of the swelling was sensitive and produced suppuration from a broad 6  mm pocket, mesial buccal and midbuccal areas of the tooth. Subgingival calculus was clinically detectable. Sensibility testing with cold was normal (responded, no lingering) on this and all control teeth (Image courtesy Dr. Rex Livingston, UMKC School of Dentistry)

periodontal abscess. Another case illustrating this is shown in Fig. 3.8, where the patient was initially referred for endodontic therapy on tooth #14 due to chewing pain and buccal swelling. Pulp sensibility tests indicated the tooth was vital, so periodontal therapy with osseous surgery and grafting was completed. Regarding sensibility testing, it is important to note, however, that the actual histological condi-

19

b

Sensibility testing revealed no responses from both cold and EPT. A diagnosis of pulpal necrosis and chronic apical abscess were made and the tooth was treated endodontically. (b) shows osseous healing 9 months after endodontic treatment and restoration with a crown (Radiographs courtesy Dr. Stephanie Mullins)

tion of the pulp is not always accurately predictable, as discussed in Seltzer and Bender’s classic paper [18]. The terminology used at the time of Seltzer’s paper included terms such hyperemia, acute serous pulpitis, and acute suppurative pulpitis, and it were these diagnostic terms that were not correlated to the histological status of the tooth in their paper. The study at the time called into question the accuracy of pulpal sensibility testing for diagnostic purposes. However, the validity of clinical sensibility testing has been more recently demonstrated. In an evaluation of 150 patients receiving endodontic therapy, Weisleder et al. compared the clinical ability of cold and electric pulp testing (EPT) to predict tooth vitality or necrosis via direct observation of the status of the pulp after initiation of endodontic therapy. Ninety-seven percent of the teeth responding positively to both cold and EPT were found to be vital, and 90 percent of the teeth responding negatively to both were found to be necrotic [17]. In another study, Ricucci et  al. evaluated 95 human extracted teeth and compared their clinical diagnosis to the histological presentation of the tooth. Using current American Board of Endodontics terminology of normal pulp, reversible pulpitis, and irreversible pulpitis,

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Fig. 3.6  Radiographs of tooth # 19. Note normal appearance of the apical region (Radiographs courtesy Dr. Rex Livingston)

Fig. 3.7  Tooth #19 was treated with periodontal flap surgery, scaling and root planning, and regenerative osseous techniques. Note broad osseous dehiscence exposing the mesial root (Photograph courtesy Dr. Rex Livingston, UMKC School of Dentistry)

the clinical tests were found to be in good agreement with histological ­ classification (96% for normal pulp and 84% for irreversible pulp) [19]. While it is reassuring to know that clinical testing can be accurate and of value in determining the status of the dental pulp, clinicians need to be aware of another consequence of sensibility testing that may affect the diagnosis. It is important to understand a patient’s interpretation of the sensations to these tests, as they are a function of their anxiety and ability to communicate, and be aware of the skill and ability of the clinician to interpret these responses. It is possible for an anxious patient, not clear about the instructions from the clinician, to overreact to a cold test. The sensation of cold, even on a dental

pontic of a bridge, may cause the patient to raise their hand and indicate “pain.” It needs to be clearly explained to the patient the difference between the sensation of cold verses the sensation of pain from cold on a tooth. Without this understanding, many false positive responses by the patient may be given. This is another reason for testing ­ multiple control teeth to gage the patient’s normal response. With the basic understanding of the importance of the medical/dental history and the clinical exam having been presented, the pulpodentinal complex can now be explored next to see how it may explain the clinical presentation of endo-­ perio lesions, from an endodontic perspective.

3.2

Pulpodentinal Complex

It is not unreasonable to understand why a younger patient with generalized good periodontal health that presents with a localize gingival swelling (abscess), has a corresponding narrow deep pocket, and responds negatively to cold and electric pulp testing, is likely suffering from an endodontic infection. But what is it about an endodontic infection that can cause this localized loss of bone that can mimic or cause a localized periodontal infection? Or conversely, how a periodontal pocket or abscess can be present without negatively affecting the vitality of the tooth. To answer these questions the clinician must understand the unique dynamics of pulpodentinal com-

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

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Fig. 3.8  Example of periodontal only lesion. Tooth #14 after regenerative osseous surgery. Note improved bone responded normally to all sensibility testing. (a, b) pre-­ height between tooth #13 and #14 (Courtesy Dr. Stephanie periodontal treatment, and (c) is 6 months posttreatment Mullins)

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Fig. 3.9  Pathways of Communication. Bacterial insult to the pulp can come from dentinal fractures in the crown (a), caries within the dentin and dental fillings (b), expo-

sure of lateral and apical accessory canals and foramina (c), or cemental agenesis at the cemento-enamel junction (d) (Illustration courtesy Molly S. Kaz Frick, 2018)

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plex. Figure  3.9 outlines the various locations around a tooth that can be the source of insult to a pulp, or, in some cases, be the portal of exit of infection from an already infected pulp. These routes include caries of the crown, fractures of the crown, exposure of lateral canals, cervical exposure of patent dentinal tubules, or exposure of the apical root structure and associated foramina. Figure  3.3 was an example of one of these portals of exit with infection of pulp draining through the apex of the tooth. When and how these areas may be involved in endo-perio types of infection requires an understanding of general root anatomy, the nature of dentin in both young and old patients, and the nature of permeability of dentin over time, which is closely related to the status of the pulp and its blood supply. A brief review follows. For a more detailed treatment of this topic, the reader is directed to a text on oral histology and anatomy by Ten Cate [20].

3.2.1 Dentin Permeability Dentin is formed by primary dentinogenesis by odontoblasts during tooth development. The odontoblasts line the outer perimeter of the dental pulp, and as the dentin is deposited, leaves a tubular space over the entire thickness of the dentin, part of which the odontoblastic process occu-

a

b

Fig. 3.10  Demonstration of the change in tubular density as the pulp is approached. The number of tubules per surface unit area increase from location (a) to (b) (Illustration courtesy Molly S. Kaz Frick, 2018)

pies. The diameter of these dentinal tubules increase in size as they approach the pulp and make up more of the surface area as compared to the area near the enamel or cementum. Figure 3.10 illustrates this. The permeability of dentin is primarily dependent upon the presence of intact enamel and cementum, but is also influenced by the thickness of the dentin, the dentinal tubular size, and the relative amount of intraluminal mineralization that is present [21]. As dentin and the pulp within the tooth age, the dentin becomes thicker through secondary dentinogenesis, and less permeable due to dentinal sclerosis, primarily due to intraluminal mineralization of the tubules. This aging process results in a reduced size of the pulp chamber and root canal diameters. In time, even the pulp tissue itself becomes more fibrous and less cellular, with calcified masses forming within the pulp, often around blood vessel and nerve connective sheaths, were there is a large concentration of collagen bundles [22]. Eventually, the entire pulp may become obliterated (calcified) and not visible on a radiograph. As a result, vital teeth over time can become more resistant to the insults of periodontal tissue breakdown. The pulps of younger individuals have the benefit of a healthy blood flow, with positive tissue pressure traveling outward in the patent dentinal tubules [23], thus protecting against the inward flow of exogenous substances, such as bacteria and their toxins, from reaching the pulp and causing infection [24]. Also, the vital pulp, through its vascular circulation, can remove contaminates that may yet penetrate the dentinal tubule, and be removed from the pulp [21]. Then, as the tooth ages, the effect of reduced dentinal permeability and secondary dentinogenesis also protects the tooth from this inward flow of exogenous substances. As a result, intact vital teeth are usually very resistant to pulpal degeneration in the presence of periodontal disease, and tend not to be affected by its progression [25]. Even with this resistance of vital pulps to the effects of periodontal disease, however, there may be a consequence. Langeland et  al. concluded that there is a cumulative effect on the pulp as a result of periodontal disease, resulting

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

in pulpal inflammation, calcification, and resorption. More recently, in an elegant clinical crossover study, teeth exposed to chronic periodontal disease have been shown to develop reduced pulp volumes as compared to contralateral control teeth in the same patient not exposed to periodontal disease [26]. Periodontally involved teeth typically have less alveolar bone support and may be at risk to more occlusal trauma and mechanical stress than healthy teeth, resulting in accelerated tertiary dentin formation within the pulp space. Evidence supporting this has been presented that identify mechanoreceptors such as TRPM7 on odontoblasts, which when activated, result in signaling molecules being released to initiate localized neurogenic inflammation, substance P release, and initiation of angiogenesis to begin the process of tertiary dentinogenesis as a defense mechanism [27, 28].

3.2.2 Tertiary Dentinogenesis Bacteria, as the cause of periodontal and pulpal disease, have been clearly implicated in this disease process [29–31]. The pulp, however, has the ability to produce tertiary dentin as a defense against this bacterial invasion. Depending on the severity and timing of the injury, two forms of tertiary dentinogenesis exist. Chronic insults to the tooth which are milder in nature result in the formation of reactionary tertiary dentin [32, 33], as previously introduced. This dentin is deposited by the existing odontoblasts in the area opposite the insult to the tooth. Acute injuries to the tooth, on the other hand, may damage or destroy the adjacent odontoblasts. If the insult can be limited by the pulps immunological response, a tertiary process called reparative dentinogenesis occurs, with the formation of new odontoblast like cells from local progenitor cells in the pulp [34]. The formation of this dentin is usually a tubular and irregular as compared to primary and secondary dentin, and is much less permeable [32]. Figure 3.11 provides a simple illustration of the differences between reactionary and reparative dentinogenesis.

a

23

b

Fig. 3.11  Illustration of the differences between reactionary dentinogenesis and reparative dentinogenesis. (a) Reactionary dentinogenesis proceeds with the original postmitotic odontoblasts, maintaining a continuity of the dentinal tubules. (b) Reparative dentinogenesis occurs with newly differentiated odontoblasts from pulpal progenitor cells, with dentinal tubule continuity not maintained (Illustration courtesy Molly S. Kaz Frick)

Fig. 3.12  Extracted multiple rooted tooth with methylene blue dye marking multiple apical foramen and accessory canals (Courtesy Dr. William Watson)

Up to this point, evidence for the resistance of the dental pulp to succumb to periodontal pathogens has been presented. However, there may eventually be those instances where chronic

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periodontal disease my eventually cause the demise of the dental pulp. Although this is rare, the cumulative effect of periodontal disease can eventually expose the apical regions of the tooth, where a higher incidence of accessory canals and multiple foramina may exist [35]. Figure  3.12 shows the presence of a number of apical foramina that can exist on a root apex. Disruption of these areas by periodontal disease can lead to infection of the pulp and loss of the pulp blood supply in some instances. Interestingly, the exposure of the furcation region of multi-rooted teeth by periodontal disease does not seem to cause pulpal disease and necrosis, despite the incidence of furcal accessory canals being present as much as 29% of the time [36]. Due to external stimuli, it is likely these small accessory canals become occluded due to the process of tertiary dentinogenesis and sclerosis [32]. Eventually, however, these defensive pulpal processes may not be enough, and the pulp of a tooth present as a unique end-organ with only a blood supply entering from a distant site (the apex), and being in a non-compliant environment of an incased rigid shell (the dentin and enamel), necrosis of the pulp may inevitably result. Figure 3.4, presented previously, was an example of a case of endodontic necrosis that produced localized apical and lateral bone loss that fully resolved with only endodontic therapy. Given our previous discussion, it is understandable what the etiology of this process was, but is this an example of an endo-perio lesion, or just an endo

Endo Lesion

Perio Lesion

Endo with Secondary Perio

Perio with Secondary Endo

True Combined Lesion

Fig. 3.13  Relationships of Endo-Perio lesions similar to that presented by Simon et al. [37]

Endo Lesion

Perio Lesion

Sinus Tract/Gingival Abcsess Resolved with Endo Therapy

Gingival Lesion/Abscess Resolved with Perio Therapy

Endo-Perio Lesion Resolved with Both Endo and Perio Therapy

Fig. 3.14  Modified Simon relationships as proposed by Harrington

lesion? These questions will be addressed in the next section of the chapter.

3.3

Endo-Perio Lesions

Simon classically represented the relationships of endo-perio lesions in his paper from 1972 and it is reinterpreted in Fig. 3.13 [37]. In it he showed the possible interrelationships of endodontic and periodontal infections. However, Harrington in 1979 suggested that only the true combined lesions should be classified as endo-perio lesions, and the others as simply endodontic or periodontal lesions. Examples of lesions of only endodontic (Fig.  3.4) or periodontal (Figs.  3.5, 3.6, and 3.7) origin have already been presented. Harrington proposed that true endo-perio lesions required both endodontic and periodontic intervention to be resolved, and thus are the only true endo-perio lesions. Figure 3.14 attempts to show this relationship. It follows, then, that any disruption in the attachment apparatus of the tooth, involving gingiva, periodontal ligament, cementum, and bone, is in essence periodontal disease in nature [38], and any endodontic pathology that also effects these structures can be classified as endo-perio; but from a clinical perspective, only those conditions requiring both endodontic and surgical periodontal intervention should be considered as true endo-perio lesions. Following are some cases clinically classified as endo-perio lesions, in that both modalities of treatment were required to resolve the condition.

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

3.3.1 Advanced Periodontal Disease Causing Pulp Necrosis In patients with advanced periodontal disease, advanced bone loss results in the exposure of root anatomy. Root planing and scaling may remove protective cementum, which may expose dentinal tubules and accessory canals to periodontal pathogens. However, the incidence of pulpal necrosis because of this is quite rare, as previously discussed, and as demonstrated in multiple histological studies of vital periodontally involved teeth [25, 31]. Periodontal disease is typically a condition of the older patient, with dentin permeability reduced through secondary and tertiary dentinogenesis, as previously described, thus protecting the pulp. However, instances of bone loss involving the entire apex of the tooth may result in exposure of the pulp to periodontal pathogens through the apical foramen or by compromising the blood supply to the pulp. Figure  3.15 diagrams an example of this process, and Fig. 3.16 shows a unique case of a younger patient possibly presenting with this kind of condition. Tooth #3, with a history of

Primary periodontic secondary endo

Fig. 3.15 Example diagram of advanced bone loss exposing the apex and lateral canal of a tooth resulting in necrosis of the pulp. Both endodontic and periodontic therapy would be required to treat the condition (Courtesy Dr. Ron Riley, UMKC School of Dentistry)

25

never having been restored, developed a history of symptomatic irreversible pulpitis that progressed to necrosis and apical periodontitis. The tooth was nonresponsive to cold and was percussion sensitive, and demonstrated a deep buccal furcation pocket. Management of the tooth involved both endodontic root canal therapy and periodontal surgery. The flap surgery revealed a deep enamel pearl (an abnormal extension of enamel onto the root surface) located in the furcation between the buccal roots. It was theorized that the enamel defect initiated a severe periodontal abscess that exposed the apical and lateral root structures to periodontal pathogens that lead to the pulp necrosis. The tooth was eventually extracted due to lack of healing of the periodontal defect. Teeth with advanced periodontal disease may also develop endodontic pathosis independently. As described previously, endodontic infections typically are the result of bacterial breaching the protective layers of enamel and dentin and compromising the pulp [29]. As it has been shown, the pulps of periodontally involved teeth may be more susceptible to this breach. However, endodontic pathosis may be due to coronal/restorative issues, forming an apical endodontic lesion that is independent of the periodontal defect. Over time, this apical endodontic lesion may eventually communicate with the periodontal defect, forming a true combined lesion, as defined by Simon (Fig. 3.17). There is a third scenario, also described by Simon, where a chronic endodontic abscess forms a periodontal pocket defect that becomes secondarily involved with calculus and becomes periodontally infected as well (Fig. 3.18). In its advanced stage, this scenario may be indistinguishable from the true combined lesion. Figure 3.19 shows the treatment of tooth #31 that presented with a necrotic pulp and a wide, conical deep pocket on the mesio-facial aspect of the tooth. Calculus was present in the pocket. Root canal therapy was completed, but little healing was noted at the 6-month recall, at which time periodontal flap therapy was completed to address the periodontal defect. Six months post periodontal treatment the radiographed showed complete resolution of the lesion.

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Fig. 3.16  Presentation of tooth #3 with large pulp chamber and furcal bone loss, and subsequent endodontic and periodontic therapies (Courtesy Dr. Ron Riley, UMKC School of Dentistry) True combined lesions (result of untreated concomitant lesions)

Fig. 3.17  Diagram of combined Endo-Perio lesion that originated from independent endodontic and periodontic processes (Courtesy Dr. Ron Riley, UMKC School of Dentistry)

a

b

Fig. 3.19 (a) Preoperative radiograph. (b) Six months post-endodontic treatment without resolution of periodontal pocket. (c) Six month post periodontal treatment and 1

Primary endo with secondary perio caries

Fig. 3.18  Diagram of chronic endodontic abscess resulting in secondary periodontal infection (Courtesy Dr. Ron Riley, UMKC School of Dentistry)

c

year post-endodontic treatment (Courtesy Dr. Ron Riley, UMKC School of Dentistry)

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

a

b

27

c

Fig. 3.20 (a, b) Preoperative radiographs of #30 with endo-perio lesion. The tooth had gingival swelling and a sinus tract on the previously treated endodontic tooth. Both endodontic retreatment and periodontal scaling and

root planning were necessary to treat the condition. (c) Post endo retreatment and perio scaling. One year followup films not available (Courtesy Dr. Stephanie ­ Mullins)

Combined endo-perio lesions can also occur with previously endodontic treated teeth. Apical, lateral, and accessory canals still contaminated with bacteria can eventually lead to apical and lateral periodontitis, destroying bone and forming an isolated periodontal pocket. Over time the pocket also gets periodontally infected with the formation of calculus deposits (Fig.  3.18), thus requiring both periodontal scaling and endodontic retreatment. Figure 3.20 is an example of just such a case. The patient presented with buccal gingival swelling of tooth #30. A patent sinus tract was present in addition to a wide furcation pocket with detectable calculus. Both endodontic retreatment and periodontal scaling and root planning were necessary to resolve the case.

3.4.1 Perforation

3.4

 ndodontic Conditions that E Often Involve Periodontal Surgical Intervention

Many endodontic conditions develop concurrent gingival and periodontal issues that are addressed at the time of the endodontic procedure, and require surgical intervention as part of their treatment. They often may involve many endodontic conditions not typically thought of as endo-perio. It is important to remember that for favorable outcomes, both appropriate endodontic and periodontal principles must be followed [38, 39]. The next section presents a variety of endodontic conditions that may require surgical, thus periodontal, intervention to treat.

Endodontic treatment of teeth may lead to unintended outcomes where canal anatomy is not followed, thus resulting in a perforation of the root during treatment. This can occur due to very complex anatomy or the inability to find the canal location during treatment, or just the lack of experience of the operator. Often, these iatrogenic misadventures, when identified immediately, can be repaired with good results, using modern materials such as calcium silicate cements [40, 41]. However, if they are not identified at the time of occurrence and the tooth is restored, a gingival infection and pocket most likely will occur. A sinus tract may or may not be present. As long as adequate tooth structure remains, these perforations can still be repaired during retreatment of the tooth, and surgical repaired, if necessary. An example of a case where a post was placed incorrectly and resulted in a lateral perforation that was not repairable is presented in Fig. 3.21. The patient had recurring pain and swelling next to a tooth that had post and crown placed 6 months previously. The patient presented with deep mesial pocketing of tooth #7 and moderate gingival swelling. Periapical radiographs confirmed a midroot perforation of a fiber post with extensive lateral bone loss. The tooth was diagnosed as non-restorable. An example of a case with a perforation occurring and repaired at the time of root canal treatment is presented in Fig. 3.22. Crowned premolar teeth with partially calcified canals needing endodontic therapy can be very challenging to remain

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centered in the long axis of the tooth when accessing. This can be further complicated by the presence of the rubber dam, which limits the tooth’s longitudinal visibility. Luckily, in this case, the error and perforation were identified and repaired immediately with Mineral Trioxide Aggregate (MTA) and the root canal completed and then restored with a fiber post and core resin build-up. The tooth was then treated by a periodontist for crown lengthening surgery to refine the exposed perforation site and material, prior to final crown placement.

3.4.2 Recurrent Endodontic Disease

Fig. 3.21  Radiograph of tooth #7 with fiber post placed outside the root canal space, resulting in a midroot perforation and severe lateral periodontal bone loss. The tooth was extracted (Courtesy Dr. Ron Riley, UMKC School of Dentistry)

Gingival lesions and swellings not only can occur as a result of a primary endodontic infection, but also as a result of recurring disease after root canal therapy as discussed above, or even after previous surgical endodontic therapy. Recurrent endodontic disease typically results from the lack of treatment or access to areas of the root infected with bacteria [42].

a

b

c

d

e

f

Fig. 3.22  Iatrogenic lateral perforation of tooth #4 during root canal treatment that was immediately repaired with MTA and restored with a fiber post and resin core build-up. (a) Pre-op radiograph #4. (b) Discovery of the perforation. (c) Completion of the root canal and repair of perforation with MTA and fiber post and core build-up.

(d) Three months post-crown cementation and periodontal crown lengthening surgery radiograph. (e) Occlusal view showing perforation relative to access. (f) Correct orientation of access that initially should have been followed

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

a

b

c

d

e

f

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Fig. 3.23 Example of resolution of apical/gingival abscess with tooth #20 that was resolved by performing a second endodontic surgery to address previously missed canal anatomy. (a) Presurgical. (b) Postsurgical. (c) 14 months postsurgical. (d) Preoperative gingival swell-

ing. (e) Yellow arrow shows incorrect oriention of previous retrograde filling. (f) Clinical image demonstrating healing of the gingival lesion (Courtesy Michiel de Cleen, DDS, Amsterdam)

An excellent example of a case surgically retreated to address an area of the root canal apex previously missed during the first surgery is shown in Fig. 3.23. A sinus tract and swelling were present, but no abnormal pocketing was found. The patient was initially advised by two restorative dentists to have the tooth extracted and replaced with an implant. The patient was subsequently referred to an endodontist for a second opinion, who was able to diagnose the etiology with the use of 3D CBCT scanner. The images clearly showed the primary canal was never properly addressed in the first surgery, and there was no evidence of bone loss consistent with a root fracture. Fourteen months after the second surgery, the tooth continued to become healthy and functional. The success of modern endodontic surgery has been shown to be very high (91–94%) as compared to traditional surgery (44–59%) [43, 44]. Re-surgery, as described in this case, has also been shown in the literature to have success rates as high as 92% [45], when modern techniques are used.

One of the possible causes of recurrent endodontic disease in maxillary molars is the lack of treatment of the mesial buccal two (MB2), or mesial lingual, canal of the mesial buccal root [46]. Symptoms ranging from pain and gingival swelling over the mesial buccal root with corresponding radiographic apical radiolucency to no pain, with a buccally positioned sinus tract, are possible clinical presentations of this [47]. The dental history of previous endodontic treatment and the obtaining of appropriate radiographic surveys to include 3D CBCT scans can easily rule out the possibility of a periodontal abscess and identify the etiology of the missed canal [48, 49]. However, endodontic retreatment is not always successful in  locating this canal, even though its incidence has been reported as high as 93–95.2% [50, 51], and thus surgical intervention is recommended as the next step. In treating such cases, the clinician needs to be aware of the possible periodontal consequences as these lesions get large, and how to treat them for both their periodontal and endodontic needs [52,

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a

b

c

d

Fig. 3.24 (a) Frontal view of CBCT slice through MB root showing missed MB2 canal, confirmed in (b) with the axial view. (c) Periapical radiograph with Gutta Percha

tracing sinus tract. (d) Mesial angled radiograph (Courtesy Dr. Jerad Divine, UMKC School of Dentistry)

53]. An example of the surgical treatment of a patient, after initial endodontic therapy was unable to locate the MB2 canal, resulting in the continuation of the chronic apical abscess, is presented in Figs. 3.24, 3.25, and 3.26. Several months after initial nonsurgical endodontic treatment of tooth #14 was completed, in which the MB2 canal could not be located, the patient presented to the endodontist for reevaluation of the tooth. The tooth was asymptomatic in that it was negative to percussion and palpation, but a 12 mm buccal periodontal probing was present over the MB root, as was a sinus tract in the buccal attached gingiva. The sinus tract was traced

with a Gutta Percha cone and periapical radiographs were exposed, and a 3D CBCT scan was consented to and exposed, as shown in Fig. 3.24. The radiographs showed a large radiolucency around the MB root with erosion of the buccal plate. With a diagnosis of previously treated root canal and chronic apical abscess of tooth #14, surgical endodontic/periodontal intervention was recommended. Due to the size pattern of the lesion with little bone around the root, a vertical root fracture was also a possibility to be considered. Often bone grafting and guided tissue regeneration (GTR) therapies are not necessary in endodontic surgery, where the osteotomy is small

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

a

b

d

e

31

c

f

Fig. 3.25 (a) Presurgical photo. (b, c) show apical defect exposed and root stained with methylene blue dye. (d) Micro mirror positioned to show MB1 canal and isthmus.

(e) Retro preparation and (f) radiographic confirmation of retro preparation (Courtesy Dr. Jerad Divine, UMKC School of Dentistry)

and the cervical buccal bone is intact over the root [54]. However, when the destruction of bone is great, resulting in a complete bony dehiscence, and the presence of a root fracture is ruled out, GTR is a valuable tool to aid in its repair [54]. This was the case as can be seen in the images in Fig. 3.25 from the surgery of tooth #14. The complete dehiscence of the MB root was explored and the granulation tissue removed to allow methylene blue staining [55] of the root to aid in detection of a fracture. With none found, the root end was resected apically 3 mm and retroprepped to a depth of 3 mm with ultrasonic instrumentation, locating the untreated MB2 canal and an isthmus connecting to the MB1 canal [56]. The retroprep was filled with Endosequence Fast Set Root Repair Material (Brasseler USA®). The crypt curetted and irrigated with sterile saline and 0.012% Chlorhexidine solution (Peridex Oral Rinse®). A mineralized bone allograft was prepared and mixed with calcium sulfate (75% allograft to 25% calcium sulfate) to aid in its placement

and retention [57]. Once the allograft was in position within the crypt and covering the root, a collagen resorbable membrane (BioMend®) was placed over the graft, and the flap repositioned and sutured (Fig.  3.26). Outcomes for these procedures have been reported to be 88% [58]. Although the specific outcome of this example is yet to be determined, it served as an example of the need to apply periodontal principles to the treatment of a primarily endodontic condition. Had the case presented in Figs. 3.24, 3.25, and 3.26 turned out to have a fractured MB root, however, the course of treatment would be more like what is presented in Fig. 3.27. Occasionally, sustained gingival swellings and nonhealing periodontal pocket formation of endodontically treated teeth may indicate a root fracture is present. The case in Fig. 3.27 was one where a vertical root fracture was diagnosed as the cause of the nonhealing gingival swelling and isolated deep pocketing. The root fracture was visible in the MB root upon reflection of the gingival flap

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a

b

c

d

Fig. 3.26 (a) Placement of the mineralized bone allograft with calcium sulfate. (b) Placement of the collagen membrane. (c) The flap closed. (d) Posttreatment radiograph

a

showing retro fill placement (Courtesy Dr. Jerad Divine, UMKC School of Dentistry)

b

Fig. 3.27  Pre (a) and post (b) radiographs of the removal of the mesial buccal root of tooth #14 after diagnosis of a vertical root fracture (Courtesy Dr. Jerad Divine, UMKC School of Dentistry)

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

and the decision was made to perform a root amputation of the root in order to maintain the tooth. A brief discussion of this topic continues next. Additional information on this topic can be found in Chap. 7.

3.4.3 S  plit Root and Vertical Root Fracture As is written in Chap. 7, vertical root fractures of endodontically treated teeth are a leading cause of their failure. Understanding this is an important area of concern in the dental literature. Historically it was the concern with the pressures of lateral condensation during obturation [59], but more currently it has been thought to be the effect of greater taper rotary instruments and the possible excessive removal of tooth structure in the coronal third of the root [60], and the excessive loading of endodontically treated teeth (even non-endodontically treated) next to implants [61]. The presence of a crown fracture or crack in the tooth is indeed one of the primary etiologies that teeth need endodontic therapy. Figure  3.28 provides an example of a fracture in a tooth that rendered it non-restorable. It is a mesial to distal fracture line that went through the pulp floor. This kind of fracture eventually leads to a split tooth. Mostly all teeth with this condition require extraction, with subsequent socket preservation periodontal graft surgery to preserve the bone for a future implant [62]. Endodontically treated teeth with vertical root fractures often present with some common attria

b

Fig. 3.28  Sequential access of molar tooth that presented with a mesial to distal fracture. (a) Enamel removed. (b) Pulpal roof removed. (c) Canals found and preflared. The

33

butes, as described in Chap. 7. These may include a deep narrow periodontal pocket, often on the mesial or distal of the offending root, and an associated sinus tract, often located coronally on the gingival tissues. However, the level of clinical evidence of this is still weak [63]. Figure 3.29 is a typical presentation of this phenomenon. Tooth #10 presented with a sinus tract close to the attached gingival margin and a single deep mesial lingual narrow periodontal pocket. A vertical root fracture was diagnosed and the tooth was extracted.

3.4.4 External Cervical Resorption External cervical resorption, also referred to as invasive cervical resorption, occurs more often in teeth than internal resorption [64], and may not always have an obvious clinical presentation. However, radiographically, it can be differentiated from internal resorption as being independent of the pulp [65], and may present clinically with localized gingival inflammation and a pinkish hue to the tooth, often on the facial surface [66]. Heithersay was the first to categorize the extent of this resorption, based on the radiographic presentation, as class 1 through 4 [67]. With the advent of 3D CBCT imaging, however, other classification systems are being suggested to better incorporate the three-dimensional nature of the condition [68]. Risk factors for the development of external resorption are not completely understood, but it is clear that teeth with a history of trauma and/or the presence of defects c

fracture was shown to be into the furcation across the pulpal floor, rendering tooth non-restorable

34

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a

continues within the tooth, but the pulp is protected from exposure by the presence of a predentin layer that osteoclastic cells cannot attach to [69]. Depending on the extent of the resorption, treatment may involve only a simple periodontal flap procedure, debridement of the defect, and placing a restoration with Heithersay Class 1 and 2 cases, without the need of endodontic therapy, to more extensive external root repair and crown lengthening surgery with root canal therapy in Class 3 cases. Class 4 cases are typically considered not treatable. Figures 3.30 and 3.31 present a case of external resorption categorized as a Class 3 defect. The resorption was found after the patient had complained of occasional pain in the lower right quadrant. At the endodontic exam the tooth was asymptomatic, testing normal to cold, and had no pain to percussion and palpation. However, buccal probing was sensitive with 4  mm depths. A cavitation defect was just partially probable at the gingival margin. A CBCT 3D scan was recommended and consented to, revealing a buccally positioned early Class 3 Heithersay resorptive lesion. Due to the proximity to the dental pulp, root canal therapy was initiated first, followed by periodontal flap surgery to expose the buccal resorptive defect. Localized crown lengthening osseous surgery was accomplished to fully expose the extent of the lesion, which was thoroughly debrided and treated with trichloro acetic acid, and then restored with Geristore® (Den Mat Holdings, LLC).

b

c

d

Fig. 3.29  Tooth #10 diagnosed with a vertical root fracture. (a) Buccal sinus tract near attached gingiva, (b) deep narrow pocket on lingual, (c) tracer GP point in lingual pocket, (d) extracted tooth with vertical root fracture visible (Courtesy UMKC School of Dentistry)

within their protective cemental covering are at higher risk of developing the condition [69]. It is thought that localized damage to the PDL cells results in inflammation and hypoxia, which can activate osteoclasts. Normally, osteoclasts cannot attach to precementum, but if a defect in the precementum or coverage of the cementum over the dentin exists, a portal of entry and initiation of resorption may occur. The process of resorption of dentin and apposition of bone-like tissue

3.4.5 L  arge PA Lesion Treated with Decompression Teeth that become necrotic and develop apical periodontitis may develop large apical lesions that may be cystic [39, 70]. These large lesions may not resolve after endodontic therapy and may require surgical enucleation to remove the cyst. However, this may be a risky procedure for the patient and result in devitalization of adjacent teeth and the possible formation of a surgical defect [71, 72]. Although not typically considered as a type of endo-perio procedure, decom-

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

a

b

d

Fig. 3.30 Radiographic history of treatment of the resorption defect of tooth #29. (a) Radiograph shows presence of resorptive defect. (b) Frontal CBCT slice with arrow pointing to resorptive defect. (c) The tooth endodontically treated and restored with a fiber post and core

a

35

c

e

BU. (d) Defect restored with filling after surgical flap reflection. (e) Two months post-crown cementation radiograph (Courtesy Dr. Jerad Divine, UMKC School of Dentistry)

b

Fig. 3.31 (a) The resorptive defect debrided. (b) Restoration with Geristore® (Courtesy Dr. Jerad Divine UMKC School of Dentistry)

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a

b

c

Fig. 3.32  Endodontic treatment of tooth #7. Note size of apical lesion. (a) Preoperative radiograph, (b) working length film, (c) posttreatment film (Courtesy Dr. Shane Clark, UMKC School of Dentistry)

pression can require minor surgical manipulation of the apical tissues with the placement of a tubular drain, which allows the patient to irrigate with a saline or chlorhexidine solution for a period of 8–12 weeks; with the drain removed after this time, significant healing of the apical defect can occur in the first 6 months [71]. Figures 3.32, 3.33, 3.34, and 3.35 show the progress of a decompression done over a period of 7 months of a large apical lesion associated with tooth #7. The patient initially presented to the clinic with pain in the UR premaxilla region. Tooth #7 responded negatively to cold and EPT and both tooth #6 and #8 responded positively to these. There was only slight pain to palpation and percussion associated with tooth #7. No sinus tract present and all periodontal probings were normal. A diagnosis of necrosis #7 and symptomatic apical periodontitis was made. The periapical radiographs showed a large radiolucency extending from the apex area of #6 to the midline area between #8 and #9. Root canal therapy was initiated in August and completed in October. Given the size and shape of the radiographic defect, decompression of the lesion was recommended to the patient, with risks, benefits, and other treatments discussed. With the patient’s consent, decompression was begun in November with the

placement of a drain made from IV tubing. The cortical bone covering facially over the defect was thicker than anticipated, and a surgical flap was necessary to expose the alveolar bone to allow a small osteotomy to be formed to fit the drain. The patient was very compliant, following irrigating instructions using a disposable luer lock syringe system and Peridex® Oral Rinse and returning for monthly follow-ups. During the follow-up visits, the drain was removed, cleaned, and shortened such that it would continue to fit flush with the gingival tissues. The drain was permanently removed in July after 7 months. A follow-­up radiograph at approximately 11  months after decompression treatment was begun showed nearly complete resolution of the apical defect.

3.4.6 Intentional Replantation Endodontic infections in previously treated teeth may not always be treatable with orthograde or surgical retrograde techniques, due to unique root anatomy or anatomical position considerations. Teeth close to anatomical structures such as the mental foramen or mandibular canal, or second molars with thick buccal cortical bone of the external oblique ridge, or teeth with unique C-shaped

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

a

b

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Fig. 3.33  Surgical procedure to raise flap to allow formation of osteotomy to receive custom drain tubing. (a) Presurgical clinical view. (b) Flap reflected and osteotomy access to apical lesion. (c) Surgical bur confirmed of oste-

otomy position. (d) Radiograph with drain in place (Courtesy Dr. Robert Edwards and Dr. Shane Clark, UMKC School of Dentistry)

root anatomy would often thusly be considered for extraction. However, a renewed interest in the treatment choice of intentional reimplantation has occurred in the dental literature [73, 74]. As defined by Grossman, it involves the deliberate extraction of a tooth, evaluation of its roots, endodontic manipulation which may include root-end resection and root-end filling, and then replacement of the tooth back into its socket [75]. In a systematic review survival rates in the range of

73–100% were reported, with an average survival of 89.1% over periods of up to 12 years [74]. Much of this success is due to a careful protocol: appropriate case selection, atraumatic extraction, protecting the periodontal ligament cells, limitation of extraoral time to 15 min, the use of the dental operating microscope, and placement of calcium silicate cement materials for sealing defects and retro ­preparations [76]. Figure 3.36 demonstrates a protocol as proposed by Grzanich et al. [76].

K. J. Frick et al.

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a

Fig. 3.34 (a) Image of drain made from IV tubing. The flange-shaped end was made by pressing the tubing against a hot metal surface to melt and shape it. The drain was then adjusted to length to fit to the back wall of the

a

b

defect. (b) Drain in place. The patient was given instructions on how to irrigate through the drain (Courtesy Dr. Robert Edwards and Dr. Shane Clark, UMKC School of Dentistry)

b

c

Fig. 3.35 (a) Image of drain clinically after 2 months in place. The two radiographic images are at 4 months (b) and 11  months (c), since the initiation of treatment

(Courtesy Dr. Robert Edwards and Dr. Shane Clark, UMKC School of Dentistry)

An example of a case treated with a similar protocol as described by Grzanich is considered next. A 13-year-old female patient presented to the clinic for an evaluation of a tooth that had root canal therapy completed by her dentist 2 years previously. The tooth was asymptomatic, and had a buccal sinus tract. Radiographically there was a large lesion present. The diagnosis of previously treated and chronic apical abscess was made. With the permission of the parent, nonsurgical root canal retreatment was completed (Fig. 3.37), but several months after treatment the sinus tract did not resolve. Given the age of the patient and the size of the lesion, intentional reimplantation was

discussed with the parent, and consent was given. Completion of the intentional reimplantation was accomplished with two operators with total extraoral time of 16 min. The root ends were resected and a 2–3 mm retro preparation was placed in each root end and filled with BC RRM-­Fast Set Putty® (Brasseler USA). Radiographs and images at the time of the replantation are shown in Fig.  3.38. Images of the tooth immediately after replacement, 2 months after surgery, and radiographs 2 months and 6 months post-­surgery are presented in Fig. 3.39. Significant healing was noted at the 6 month recall with complete resolution of the sinus tract and apical lesion radiographically.

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

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a

b

c

d

e

f

g

h

i

j

k

l

Fig. 3.36  Protocol for intentional reimplantation: After atraumatic extraction procedure, the tooth is immediately placed in Hank’s balanced salt solution (a, b); root and remaining periodontal ligament should not be touched. Root inspection and dye staining of the tooth (c); tooth held (crown only) with a wet gauze (Hank’s balance salt solution). All granulomatous/inflammatory tissue should be removed from the roots and submitted to microscopic

a

b

analysis (d); root-end resection (e); root-end preparation performed with ultrasonic tips and constant irrigation with saline solution (f, g). All procedures were performed under dental operating microscope visualization (h). Root-end filling material is disposed and condensed into prepared tooth (i–k); tooth is replanted into the socket (l) (Grzanich et al. 2017, with permission)

c

Fig. 3.37  Retreatment of tooth #19. The tooth was medicated with calcium hydroxide for 2 months prior to obturation. (a) and (b) preoperative, and (c) post-endodontic

retreatment radiographs (Courtesy Dr. Anthony Altomare and Dr. Stephen Harrison, UMKC School of Dentistry)

3.4.7 Palatal Radicular Groove

aly primarily affecting maxillary incisors, most typically the lateral incisor [77], although there has been a case report of a palatal groove in a second maxillary molar [78]. The etiology is thought to

The palatal radicular groove, also referred to as the palato-gingival groove, is a developmental anom-

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a

d

b

e

c

f

Fig. 3.38 (a) Clinical presentation of Tooth #19 preoperatively on day of reimplantation surgery. (b) Pretreatment radiograph. (c) Extraction of the tooth with forceps. (d) Inspection of the roots and removal of granu-

lation tissue. (e) Resection of the root ends. (f) Placement of the bioceramic retrofilling material (Courtesy Drs. Altomare and Harrison, UMKC School of Dentistry)

involve the limited in-folding of the enamel organ and Hertwig’s epithelial sheath during odontogenesis [79]. The groove begins at the junction of the cingulum and continues apically down the proximal surface of the root. The presence of the groove often leads to a deep periodontal defect that can become infected, and due to the altered root anatomy, a greater chance of the tooth becoming necrotic, leading to true combined endo-perio lesion [80]. The incidence has been reported in the range of 2.8–8.5%, but may be as high as 44.6% in some ethnic populations [81, 82]. Most case reports in the literature describe treating the tooth endodontically first with obturation of the root canal system, followed periodontal flap surgery and guided bone regeneration therapy. An example of this is shown in Figs. 3.40 and 3.41 from a case report published in 2006 [83]. The patient presented for the evaluation of a sinus tract facially and an apical radiolucency found on the radiograph. The patient was asymptomatic, but was aware of the bump on the gum under the lip being present for over a year. Clinical testing found tooth #10

to be nonresponsive to sensitivity tests, percussion and palpation were both negative, but an isolated 10 mm lingual periodontal pocket was found. The sinus tract was traced with a gutta percha point and found to connect to the apical region of the tooth radiographically (Fig. 3.40). A pulpal diagnosis of necrosis was made with chronic apical abscess and a periodontal abscess due to the presences of the palato-gingival groove. Endodontic treatment was initiated, and after several months due to the pocket on the lingual not resolving, periodontal flap surgery was performed to address the periodontal defect with odontoplasty and guided bone regeneration using freeze-dried bone allograft and enamel matrix derivative (Fig. 3.41). In another case series treating palatal radicular grooves [84], a different approach was presented. Rather than perform periodontal flap surgery after the endodontic treatment as Schwartz et al., Tan et al. completed intentional reimplantation of the teeth to address the unique anatomical defects. An example of one of the eight cases is shown in Figs. 3.42 and 3.43. Once orthograde root canal

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b

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Fig. 3.39 (a) Tooth #19 immediately after replacement. (b) 2 month posttreatment clinical photo. (c) 2 months and (d) 6 months posttreatment radiographs (Courtesy Drs. Altomare and Harrison, UMKC School of Dentistry)

Fig. 3.40 (a) Sinus tract traced with Gutta Percha point with (b) corresponding radiograph. The tooth had an isolated 10 mm periodontal pocket on the lingual. Note the unique multiple canal anatomy (Schwartz et al., 2006, with permission)

a

b

K. J. Frick et al.

42 Fig. 3.41 (a) Periodontal flap surgery to expose and treat the lingual groove defect with odontoplasty and guided bone regeneration procedures. (b) Six month post-­ surgery follow-up (Schwartz et al. 2006, with permission)

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a

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Fig. 3.42  Tooth #10 as one of the specimens presented by Tan et al. [84]. (a) shows the preoperative radiograph, (b, c) are clinical photos showing the buccal sinus tract

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b

and lingual deep probing periodontal pocket (Tan et  al., 2017, with Permission)

c

Fig. 3.43 (a) Extracted Tooth #10 from Fig.  3.42, showing groove and second root. (b) root ends resected, canals identified prior to retrofilling. (c) One year posttreatment radiograph (Courtesy Tan et al. 2017, with permission)

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

therapy was completed, the extraction of the tooth allowed for excellent access of the palatal groove defect to perform odontoplasty and to fill the deeper portions of the groove with calcium silicate cement, and to perform apicoectomy surgery and placement of a retrofilling, after inspection of the root ends. These treatments of the palatal radicular groove are excellent examples of the combined endodontic and periodontal therapies available to clinicians, and underscores the importance of having an understanding of the relationships of endo-perio lesions.

3.5

 ther Rare Endodontic O Conditions that may Involve Periodontal Structures

3.5.1 Pulse Granuloma Patients presenting with chronically broken down teeth may develop a more rare condition described by Simon et al. as a Pulse Granuloma [85]. A pulse is defined as edible seeds of leguminous crops, such as peas, beans, and lentils. A pulse granuloma is a condition where one of these seeds becomes imbedded in the tissue of the body, resulting in the infection. Traditionally they have been reported to occur in the lungs or gastrointestinal tract [86, 87]. If a tooth has had the pulp chamber exposed by Fig. 3.44 Preoperative (a) and postoperative (b) radiographs of tooth #10 (Courtesy Dr. Chris Lingard and UMKC School of Dentistry)

a

43

gross caries and loss of tooth structure and has become necrotic, or if it has had endodontic therapy initiated but never completed and has lost the temporary filling, then a condition may result that allows food to be forced down the canal system as a result of mastication. Just such a case occurred with tooth #10 (Fig. 3.44). The patient had come to the dental clinic complaining of a hole in her upper left lateral incisor and pain on her palate. The tooth was sensitive to percussion and palpation. The tooth had had previously initiated root canal therapy over 1 year ago and had lost its filling. A diagnosis of previously initiated treatment and acute apical abscess were made for tooth #10 and an incision and drainage procedure was completed on the upper left palate. Purulent exudate was expressed. A week later the tooth was endodontically treated and restored with a fiber post and core in preparation of a crown. The patient returned to the clinic 1 month later still with the complaint of palatal swelling with pain. At that appointment a second incision and drainage procedure was completed with irrigation of saline in the wound after expression of purulence. The saline rinse produced a foreign object from the wound that had an odd appearance (Fig. 3.45). The object was a 3 mm by 3  mm coiled crystalline mass. Processing for microscopic examination caused the object to dissolve, and the presence of filamentous bacteria consistent with actinomycosis were found. Four months after this last appointment and 5 months b

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a

b

c

Fig. 3.45 (a) Image of foreign body removed during the I&D procedure. (b) One millimeter scored periodontal probe (for scale) next to foreign body. (c) Four months

post I&D radiograph showing evidence of apical healing. Patient reported no symptoms at this time (Courtesy Dr. Chris Lingard, UMKC School of Dentistry)

after the root canal therapy, the palatal swelling and all symptoms where resolved. Upon questioning the patient, it was admitted that the tooth had food impaction for over a period of a year before coming to the clinic for treatment. It is logical that food matter and bacteria were forced out of the apex of the tooth, forming the coiled mass over time, as a dental “pulse” granuloma. Unfortunately, the patient was lost to recall, so demonstration of healing of the large periapical defect cannot be shown.

ficient periodontal breakdown that could compromise pulp vitality, thus leading to a true endo-perio lesion [90]. Often, however, the condition can be resolved with only periodontal intervention with removal of the cemental tear and repair of the defect with guided tissue regeneration [91, 92]. A detailed study on the phenomenon of cemental tears was completed by Lin et  al. in 2011 [90]. In what was called a Multicenter Cemental Tear Study, conducted between the years of 1987 and 2008 at four hospitals, data on 71 teeth with cemental tears was collected. Some of the predisposing factors analyzed included age, sex, tooth type, traumatic injury, and occlusal trauma. It was reported that the condition occurred more frequently in men aged 60 years and older, most often in incisor teeth, and least often in maxillary and mandibular molars. The presence of occlusal trauma was a significant risk factor as well. There was no correlation of the cemental tear to the tooth being vital or previously endodontically treated. An example of one of the cases described in the study is presented in Fig. 3.46. It is a maxillary first molar, previously treated with endododontic therapy and a post and core build-up. The tooth had gingival inflammation and a deep narrow periodontal pocket. Treatment involved reflecting a periodontal flap, removal of the cemental tear, root planing the root surface, and placement of a bone graft.

3.5.2 Cemental Tear The development of periodontal disease becomes a greater risk to a person as they age [38]. With the progression of periodontal disease there is reduced bone support for the teeth, which may result in increased stresses on root structures that can produce a condition known as a cemental tear [88]. A cemental tear is a complete or incomplete separation within the root surface along the cementodentinal interface. The clinical presentation may vary, but often includes an area of deep probing with gingival inflammation, possible sinus tract, and pain, which left untreated can lead to significant periodontal destruction [89, 90]. This condition is different from a vertical root fracture in that it does not involve the root canal space, but if left untreated may lead to suf-

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

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b

c

d

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Fig. 3.46 (a) A typical preoperative radiograph showing a cemental tear (arrow) on tooth #8 of a 46-year-old male patient. (b) A clinical picture of tooth #8 exhibiting gingival inflammation (arrowhead) and narrow deep pocket. (c)

The removed cemental tear fragment. (d) Histological picture of the cemental tear shown in C (original magnification, 200X) (Courtesy Lin et  al., 2011, with permission)

When evaluating a patient presenting with a gingival swelling, deep narrow pocket, and occlusal pain, having an understanding of the possible etiological processes that could be causing the condition is an important part of developing a differential diagnosis. Only then can the clinician know if they are dealing with an endodontic or periodontal condition, or both. Being aware of the existence of cemental tears and the potential similarity in their presentation compared to vertical root fractures

and endodontic apical abscess is an important part that process.

3.5.3 T  ransient Apical Breakdown and Periapical Cemento-­ Osseous Dysplasia The last conditions to be discussed are not typically considered as endo-perio lesions, but their existence and understanding are an important

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a

e

b

f

c

g

d

h

Fig. 3.47 (a) TAB in the form of persistent expansion of the apical periodontal ligament of fully formed roots after extrusive luxation of the maxillary right central and lateral incisors in a 19-year-old male patient. TAB as seen as apical radiolucency (b, c) is followed by apical blunting and

obliteration of the root canal in the lateral incisor (f, g) and apical blunting of the central incisor (g, h). Internal surface resorption can be seen in both teeth at 4 months (d) and 1 year (e) after trauma (arrows) (Courtesy Andreasen, 2015, with permission)

part of a differential diagnosis for patients presenting with teeth that may or may not be symptomatic but have evidence of radiographic apical pathology. Both transient apical breakdown and periapical cemento-osseous dysplasia are being considered together in that they may, at times, clinically appear similar, but are actually uniquely different entities. The knowledge and understanding of these conditions may lead to the avoidance of unnecessary endodontic therapy.

Transient apical breakdown (TAB) was originally described in 1986 by Francis Andreasen [93]. It was presented as one of the possible outcomes of traumatic luxation injuries to mature permanent anterior teeth where the pulp survives, but not after an intermediate period of altered pulp sensibility, color change, and apical radiographic root resorption and apical lucency [94] (Fig. 3.47). The condition reverses in time without intervention, but often results in root blunting

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions

and pulp canal obliteration. TAB has also been reported as a result of orthodontic treatment, with the tooth becoming nonresponsive to cold testing, sensitive to percussion, and having a gray discoloration [95]. Radiographically, a small area of radiolucency was present along with a widened periodontal ligament. After discontinuation of active orthodontic forces for 10  weeks, the tooth recovered, with normal sensibility testing and coloration having returned, and no evidence of apical pathology. Like TAB, periapical cemento-osseous dysplasia can present with a radiographic radiolucency, but they are typically larger and associated with more than one tooth, although often in the anterior jaw regions. They are typically asymptomatic and do not affect the vitality of the tooth (the teeth respond positively to tests). As in TAB, no treatment is indicated. Periapical cemento-­ osseous dysplasia and focal cemento-osseous dysplasia are similar terms referring to lesions in a single location in the jaws [96]. However, there is a form of the condition that affects multiple locations that is referred to as florid cemento-­ osseous dysplasia. Periapical cemental-osseous dysplasia is a mixed radiolucent and radiopaque lesion (Fig.  3.48) with lobular and irregular shapes associated with the apical regions of the teeth. In a systematic review of the literature it was found that 59% of the cases were in Black patients, 37% were in Asian patients, and 3% were in White patients [97]. Occasionally, the florid version seen in multiple locations (Figs. 3.49 and 3.50) in the jaws can become symptomatic and cause bony expansions and protrusions through the oral mucosa, resulting in secondary infections, which are difficult to treat [98]. The radiopaque lesions have been histologically described to consist of osteoid and cementum-like material, with fibroblasts being associated with the trabeculae of the calcified material [96, 99]. The presentation clinically of just such a patient may at first be confused for an endodontic or periodontal infection, but with the knowledge of these lesions and the

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Fig. 3.48  Periapical radiograph of patient referred to endodontist by her dentist for root canal therapy of the mandibular central incisors. The patient was a middle-­ aged black woman. Both central incisors were completely asymptomatic and responded normally to all sensibility testing

Fig. 3.49  Panoramic radiograph of patient with florid cemento-osseous dysplasia. Note Extensive mixed lesions in the mandibular premolar regions (Courtesy Tonioli et al., 2004, with permission)

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for those treating these conditions. Other pathological conditions exist that were not presented in this chapter that may cause oral lesions mimicking endodontic or periodontal lesions. It is the responsibility of the dentist to always rule out the endodontic etiology first before considering other odontogenic or non-odontogenic explanations.

3.6.1 Conclusions Various endodontic conditions and diseases may lead to periodontal involvement. Correct endodontic diagnosis based on dental history, clinical and radiographic evaluation plays important role in the following treatment plan and prognosis of the endodontic-periodontal lesions.

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26. Terlemez A, Alan R, Gezhin O.  Evaluation of the periodontal disease effect on pulp volume. J Endod. 2018;44:111–4. 27. Caviedes-Bucheli J, Gomez-Susa JF, et al. Angiogenic mechanisms of human dental pulp and their relationship with substance P expression in response to occlusal trauma. Int Endod J. 2017;50:339–51. 28. Won J, Vang H, Kim JH, Lee PR, Kang Y, Oh SB.  TRPM7 mediates mechanosensitivity in adult rat odontoblasts. J Dent Res. 2018; https://doi. org/10.1177/0022034518459947. 29. Kakehashi S, Stanley HR, Fitzgerald RJ. The effects of surgical exposures of dental pulps in germ-free and conventional laboratory rats. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1965;20:340–8. 30. Moller A, Fabricius L, Dahlen G, Ohman AE, Heyden G. Influence on periapical tissues of indigenous oral bacteria and necrotic pulp tissue in monkeys. Eur J Oral Sci. 1981;89:475–84. 31. Rubach WC, Mitchell D.  Periodontal disease, accessory canals and pulp pathosis. Periodontol. 1965;36:34–8. 32. Mjor I. Dentin permeability: the basis for understanding pulp reactions and adhesive technology. Braz Dent J. 2009;20(1):3–16. 33. Smith AJ, Cassidy N, Perry H, Begue-Kirn C, Ruch JV, Lesot H.  Reactionary dentinogenesis. Int J Dev Biol. 1995;39:273–80. 34. D'Souza RN, Bachman T, Baumgardner KR, Butler WT, Litz M.  Characterization of cellular responses involved in reparative dentinogenesis in rat molars. J Dent Res. 1995;74(2):702–9. 35. Langeland K, Rodrigues H, Dowden W. Periodontal disease, bacteria, and pulpal histopathology. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1974;37:257–70. 36. Gutmann JL.  Prevalence, location, and patency of accessory canals. J Periodontol. 1978;49(1):21–6. 37. Simon JHS, Glick D, Frank AL.  The relationship of endodontic-periodontic lesions. J Periodontol. 1972;43(4):202–8. 38. Glickman I.  Glickman's Clinical Periodontology. Philadelphia: WB Sounders Co; 1990. 39. Nair PNR, Sjögren U, Figdor D, Sundqvist G.  Persistent periapical radiolucencies of root-filled human teeth, failed endodontic treatments, and periapical scars. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1999;87:617–27. 40. Mente J, Hage N, Pfefferle T, Coch MJ, Geletneky B, Dreyhaupt J, Martin N, Staehle HJ. Treatment outcome of mineral trioxide aggregate: repair of root perforations. J Endod. 2010;36:208–13. 41. Torabinejad M, Parirokh M.  Mineral trioxide aggregate: a comprehensive literature review—part ii: leakage and biocompatibility investigations. J Endod. 2010;36(2):190–202. 42. Haapasalo M, Shen Y, Ricucci D. Reasons for persistent and emerging post-treatment endodontic disease. Endod Top. 2011;18(1):31–50.

50 43. Setzer FC, Shah S, Kohli MR, Karabucak B, Kim S. Outcome of endodontic surgery: a meta-analysis of the literature—part 1: comparison of traditional root-­ end surgery and endodontic microsurgery. J Endod. 2010;36:1157–765. 44. Tsesis I, Rosen E, Schwartz-Arad D, Fuss Z.  Retrospective evaluation of surgical endodontic treatment: traditional versus modern technique. J Endod. 2006;32:412–6. 45. Song M, Shin S, Kim E.  Outcomes of endodon tic micro-resurgery: a prospective clinical study. J Endod. 2011;37:316–20. 46. Ng YL, Mann V, Rahbaran S, Lewsey J, Gulabivala K. Outcome of primary root canal treatment systematic review of the literature part 2: influence of clinical factors. Int Endod J. 2008;41:6–31. 47. Nair P.  Pathogenesis of apical periodontitis and the causes of endodontic failures. Crit Rev Oral Biol Med. 2004;15:348–81. 48. Domark JD, Hatton JF, Benison RP, Hildebolt CF. An ex vivo comparison of digital radiography and cone-­ beam and micro computed tomography in the detection of the number of canals in the mesiobuccal roots of maxillary molars. J Endod. 2013;39(7):901–5. 49. Todd R.  Cone beam computed tomography updated technology for endodontic diagnosis. Dent Clin N Am. 2014;58:523–43. 50. Kulild JC, Peters D.  Incidence and configuration of canal systems in the mesiobuccal root of maxillary first and second molars. J Endod. 1990;16(7):311–7. 51. Stropko J.  Canal morphology of maxillary molars: clinical observations of canal configurations. J Endod. 1999;25(6):446–50. 52. Artzi Z, Wasersprung N, Weinreb M, Steigmann M, Prasad HS, Tsesis I. Effect of guided tissue regeneration on newly formed bone and cementum in periapical tissue healing after endodontic surgery: an in vivo study in the cat. J Endod. 2012;38:163–9. 53. Tsesis I, Rosen E, Tamse A, Taschieri S, Del Fabbro M.  Effect of guided tissue regeneration on the outcome of surgical endodontic treatment: a systematic review and meta-analysis. J Endod. 2011;37:1039–45. 54. von Arx T, Cochran D. Rationale for the application of the GTR principle using a barrier membrane in endodontic surgery: a proposal of classification and literature review. Int J of Periodontics Restorative Dent. 2001;21(2):127–39. 55. Cambruzzi JV, Marshall FJ, Pappin JB.  Methylene blue dye: an aid to endodontic surgery. J Endod. 1985;11(7):311–4. 56. Kim S, S K. Modern endodontic surgery concepts and practice: a review. J Endod. 2006;32(7):601–23. 57. Aichelmann-Reidy ME, Heath CD, Reynolds MA. Clinical evaluation of calcium sulfate in combination with demineralized freeze-dried bone allograft for the treatment of human intraosseous defects. J Periodontal. 2004;75:340–7. 58. Taschieri S, Del Fabbro M, Testori T, Saita M, Weinstein R. Efficacy of guided tissue regeneration in the management of through-and-through lesions fol-

K. J. Frick et al. lowing surgical endodontics: a preliminary study. Int J of Periodontics Restorative Dent. 2008;28(3):264–71. 59. Lertchirakarn V, Palamara J, Messer HH.  Load and strain during lateral condensation and vertical root fracture. J Endod. 1999;25:99–104. 60. Rundquist BD, Versluis A.  How does canal taper affect root stresses? Int Endod J. 2006;39:226–37. 61. Rosen E, Beitlitum I, Tamse A, Taschieri S, Tsesis I. Implant-associated vertical root fracture in adjacent endodontically treated teeth: a case series and systematic review. J Endod. 2016;42:948–52. 62. Fickl S, Zuhr O, Wachtel H, Bolz W, Huerzeler M. Tissue alterations after tooth extraction with and without surgical trauma: a volumetric study in the beagle dog. J Clin Periodontol. 2008;35:356–63. 63. Tsesis I, Rosen E, Tamse A, Taschieri S, Kfir A.  Diagnosis of vertical root fractures in endodontically treated teeth based on clinical and radiographic indices: a systematic review. J Endod. 2010;36:1455–8. 64. Haapasalo H, Endal U.  Internal inflammatory root resorption: the unknown resorption of the tooth. Endod Top. 2008;14:60–79. 65. Gartner AH, Mack T, Somerlott RG, Walsh LC.  Differential diagnosis of internal and external root resorption. J Endod. 1976;2:329–34. 66. Heithersay G.  Clinical, radiologic, and histopathologic features of invasive cervical resorption. Quintessence Int. 1999a;30:27–37. 67. Heithersay G. Invasive cervical resorption: an analysis of potential predisposing factors. Quintessence Int. 1999b;30:83–95. 68. Goodell KB, Mines P, Kersten DD. Impact of cone-­ beam computed tomography on treatment planning for external cervical resorption and a novel axial slice-­ based classification system. J Endod. 2018;44:239–44. 69. Mavridou AM, Hauben E, Wevers M, Schepers E, Bergmans L, Lambrechts P.  Understanding external cervical resorption in vital teeth. J Endod. 2016;42:1737–51. 70. Simon JHS, Glick D, Frank AL.  Incidence of periapical cysts in relation to the root canal. J Endod. 1980;6(11):845–8. 71. Freedland J.  Conservative reduction of large peri apical lesions. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1970;29:455–64. 72. Neaverth EJ, Burg H. Decompression of large periapical cystic lesions. J Endod. 1982;8(4):175–82. 73. Becker B. Intentional replantation techniques: a critical review. J Endod. 2018;44:14–21. 74. Mainkar A.  A Systematic review of the survival of teeth intentionally replanted with a modern technique and cost-effectiveness compared with single-tooth implants. J Endod. 2017;43:1963–8. 75. Grossman L.  Intentional replantation of teeth. J Am Dent Assoc. 1966;72:577–82. 76. Grzanich D, Rizzo G, Silva RM. Saving natural teeth: intentional replantation-protocol and case series. J Endod. 2017;43:2119–24. 77. Lee KW, Lee E, Poon KY.  Palato-gingival grooves in maxillary incisors: a possible predisposing fac-

3  Endodontic Considerations in the Management of Endodontic-Periodontal Lesions tor to localised periodontal disease. Br Dent J. 1968;124(1):14–8. 78. Benenati F.  Maxillary second molar with two palatal canals and a palatogingival groove. J Endod. 1985;11:308–10. 79. Simon JHS, Dogan H, Ceresa LM, Silver GK.  The radicular groove: its potential clinical significance. J Endod. 2000;26(5):295–6. 80. Lara VS, Consolaro A, Bruce RS.  Macroscopic and microscopic analysis of the palato-gingival groove. J Endod. 2000;26(6):345–50. 81. Everett FG, Kramer G.  The disto-lingual groove in the maxillary lateral incisor; a periodontal hazard. J Periodontal. 1972;43(6):352–61. 82. Goon WWY, Carpenter W, Brace NM, Ahlfeld RJ.  Complex facial radicular groove in a maxillary lateral incisor. J Endod. 1991;17(5):244–8. 83. Schwartz SA, Koch M, Eeas DE, Powell CA. Combined endodontic-periodontic treatment of a palatal groove: a case report. J Endod. 2006;32:573–8. 84. Tan X, Zhang L, Zhou W, Li Y, Ning J, Chen X, Song D, Zhou X, Huang D. Palatal radicular groove morphology of the maxillary incisors: a case series report. J Endod. 2017;43:827–33. 85. Simon JHS, Chimenti R, Mintz GA. Clinical significance of the pulse granuloma. J Endod. 1982;8:116–9. 86. Head M.  Foreign body reaction to the inhalation of lentil soup. Giant cell pneumonia. J Clin Pathol. 1956;9:295–9. 87. Sherman FE, Moran T.  Granulomas of the stom ach. Response to injury of muscle and fibrosis tissue of wall of human stomach. Am J Clin Pathol. 1954;24:415–21. 88. Ishikawa I, Oda S, Hayashi J, Arakawa S.  Cervical cemental tears in older patients with adult periodontitis: case reports. J Periodontal. 1996;67(1):15–20.

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89. Leknes KN, Lie T, Selvig KA. Cemental tear: a risk factor in periodontal attachment loss. J Periodontal. 1996;67(6):583–8. 90. Lin HJ, Chan C, Yang CY, et  al. Cemental tear: clinical characteristics and its predisposing factors. J Endod. 2011;37:611–8. 91. Harrel S.  Treatment of Periodontal Destruction Associated With a Cemental Tear Using Minimally Invasive Surgery. J Periodontal. 2000;71(11):1761–6. 92. Tulkki MJ, Baisden M, McClanahan SB.  Cemental tear: a case report of a rare root fracture. J Endod. 2006;32:1005–7. 93. Andreasen F. Transient apical breakdown and its relation to color and sensibility changes after luxation injuries to teeth. Dent Traumatol. 1986;2(1):9–19. 94. Andreasen FM, Kahler B. Pulpal response after acute dental injury in the permanent dentition: clinical implications-a review. J Endod. 2015;41:299–308. 95. Gonzalez O, Vera J, Orozco MS, Mancera JT, Gonzalez KV, Malagon GV.  Transient apical breakdown and its relationship with orthodontic forces: a case report. J Endod. 2014;40:1265–7. 96. Su L, Weathers D, Waldron CA.  Distinguishing features of focal cemento-osseous dysplasias and cemento-ossifying fibromas. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1997;84(3):301–9. 97. MacDonald-Jankowski D.  Florid cemento-osseous dysplasia: a systematic review. Dentomaxillofac Radiol. 2003;32(3):141–9. 98. Bencharit S, Schardt-Sacco D, Zuniga JR.  Surgical and prosthodontic rehabilitation for a patient with aggressive florid cemento-osseous dysplasia: a clinical report. J Prosthet Dent. 2003;90:220–4. 99. Tonioli MB, Schindler W.  Treatment of a maxillary molar in a patient presenting with florid cemento-­ osseous dysplasia. J Endod. 2004;30:665–7.

4

Prosthetic Considerations in the Management of EndodonticPeriodontal Lesions Joseph Nissan, Roberto Sacco, and Roni Kolerman

4.1

Introduction

Endodontic-periodontal lesions can provide dilemmas and clinical challenges. The interrelationship between periodontal and endodontic disease has always produced misunderstanding, questions, and clinical disagreement. Distinguishing between a periodontal and an endodontic pathology can be challenging. The nature of tooth pain is often the initial sign in determining the etiology of such a clinical dilemma, due to the fact that the influence of pulpal pathology may cause the periodontal involvement and vice versa [1, 2]. Deficiency of evidence among dentists about treatment options of endo-perio lesions is a main

reason of extracting those teeth. Simultaneous elimination of pathogens both from periodontal pocket and from root canal is a key factor for effective treatment due to infection elimination and regeneration of tooth-supported structures [1, 2]. The most common method to restore those endo-perio treated teeth is based on a combination of post, core, and crown, which should be able to resist mechanical and biological challenges in the oral cavity during functions [3]. Leading to the fact that remaining coronal and radicular tooth structure are important features for long-term survival. While perio-endo treatment has been widely studied, the restorative treatment planning, materials, and some other clinical features are still controversial.

4.2 J. Nissan (*) Department of Oral-Rehabilitation, School Dental-­ Medicine, Tel Aviv University, Tel Aviv, Israel Rabin Medical-Center, Belinson Hospital, Petah-Tikva, Israel R. Sacco Barts and The London School of Medicine and Dentistry, London, UK R. Kolerman Department of Periodontology and Dental Implantology, School Dental-Medicine, Tel Aviv University, Tel Aviv, Israel e-mail: [email protected]

 irect vs. Indirect D Restoration

Restoration of endo-perio treated teeth can be challenging due to their doubtful prognosis. Direct restoration (Fig.  4.1a, b) involves placement of a restorative material (amalgam or composite) into the tooth while Indirect restorations consist of cast metal or ceramic crowns (Fig. 4.2a, b) or indirect partial restorations (e.g., inlays and onlays, Fig.  4.3a–c). The comparative clinical performance of direct or indirect technique to restore those teeth is controversial. The choice

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a

b

Fig. 4.1 (a) Indirect restorations—molar without post insertion and premolar containing post. (b) Clinical view

a

b

Fig. 4.2 (a) Direct restoration—before restoration. (b) Final restoration using spherical “Ceram.X” composite

of restoration depends on the amount of remaining tooth, and may influence durability and cost. The decision to use a post and core in addition to the crown is clinician driven; usually the decision depends on the amount of remaining coronal tooth structure and the functional requirements [3, 4]. Loss of tooth structure greater than 50%, especially marginal ridges loss, would determine the use of root posts to retain a core. Posts should be used only for retention of a core within remaining tooth structure when there are no other alternatives, and not to strengthen the teeth. The preservation of sound root structure while using posts increases fracture resistance and decreases occurrence of periapical lesions of the restored endodo-perio treated teeth [5–13]. Posts with a reduced length in combination with compos-

ite resin cement are recommended in order to improve tooth survival [14]. Based on the evidence, root filled posterior teeth with limited coronal loss, where 50% or more coronal structure is preserved, can be restored without intraradicular retention, predominantly when indirect or indirect partial restorations are used [15, 16]. In most of these cases direct restorations are recommended, particularly when the marginal ridges are preserved, due to their conservative mode of treatment. Prospective and retrospective clinical studies of direct or indirect restorations with an observation period of at least 3 years showed a weak recommendation for indirect restorations to restore endodontically treated teeth, especially for teeth with extensive coronal damage.

4  Prosthetic Considerations in the Management of Endodontic-Periodontal Lesions

a

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b

c

Fig. 4.3 (a) Indirect partial restorations—before restoration. (b) Clinical view. (c) Radiologic appearance

Indirect restorations using mostly crowns have higher short-term (5-year) and medium-term (10-year) survival than do direct restorations using composite or amalgam, but no difference in short-term (≤5  years) restorative. There is a need for high-­quality clinical trials, especially well-designed RCTs [17, 18].

4.3

Restorations Scheduling and Features

Coronal leakage is considered a major factor that influences tooth survival during and after canal treatment due to bacteria and endotoxin penetration along the root canal filling [19–22]. It has been shown that endotoxins from mixed bacterial communities can penetrate the root canal system easily and more quickly than bacteria, leading to periapical lesions around endodontically treated teeth [23, 24]. Another clinical dilemma is whether to place a permanent restoration, immediately after-

ward the endodontic treatment or awaiting for resolution of the lesion. A higher success rate was found in treated teeth with permanent restorations vs. provisional restorations, the study recommended a proper and prompt permanent restoration after completion of endodontic treatment [25]. Cementing agents also contribute to protect from coronal leakage when post and direct restoration are performed. Rubber-dam isolation is recommended in all the clinical procedures (endo treatment and all kind of restorative treatments). Resin cements are recommended as efficient coronal sealers due to minimizing micro leakage potential for both posts and indirect restorations, by creating adhesion to the tooth substance. In contrast, Zinc Phosphate Cement relies on micromechanical retentive features only [26–28]. The “ferrule effect” is another important factor to the long-term indirect restoration success. A ferrule is a vertical strip of tooth structure at the gingival aspect of a crown preparation.

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It enhances some retention, but primarily provides resistance form and increases longevity. A ferrule with 1 mm of vertical height has been shown to double the resistance to fracture versus teeth restored without a ferrule [29]. Its maximum valuable effects range from a minimum of 2 mm of vertical height and 1  mm of dentin thickness leading to positive effect on fracture resistance of the treated teeth. Ferrule effect and maintaining cavity walls are the predominant factors with regard to tooth and indirect restoration survival of endodo-perio treated teeth [30].

term (10-year) survival than do direct restorations using composite or amalgam, but no difference in short-term (≤5 years) restorative. There is a need for high-quality clinical trials, especially well-designed RCTs.

References

1. Pico-Blanco A, Castelo-Baz P, Caneiro-Queija L, Liñares-González A, Martin-Lancharro P, Blanco-­ Carrión J.  Saving single-rooted teeth with combined endodontic-periodontal lesions. J Endod. 2016;42(12):1859–64. 2. Al-Fouzan KS.  A new classification of endodontic-­ 4.4 Conclusion and Clinical periodontal lesions. Int J Dent. 2014;2014:919173. 3. Pontius O, Hutter JH.  Survival rate and fracture Recommendations strength of incisors restored with different post and core systems and endodontically treated incisors Principles for achievement of long-term clinical without coronoradicular reinforcement. J Endod. success in restoration of endodo-perio treated 2002;28(10):710–5. 4. Schwartz RS, Robbins JW.  Post placement and resteeth are: toration of endodontically treated teeth: a literature review. J Endod. 2004;30(5):289–301. • Remaining tooth structure is the indicating 5. Kvist T, Rydin E, Reit C.  The relative frequency of factor for decision restoration type and techperiapical lesions in teeth with root canal-retained posts. J Endod. 1989;15:578–80. nique (Direct restoration, Indirect restorations 6. Pilo R, Tamse A.  Residual dentin thickness in manor indirect partial restorations). dibular premolars prepared with gates Glidden and • Permanent restoration, direct or indirect, parapost drills. J Prosthet Dent. 2000;83:617–23. should be placed as soon as possible after the 7. Sornkul E, Stannard JG. Strength of roots before and after endodontic treatment and restoration. J Endod. completion of root canal therapy. 1992;18:440–3. • Coronal leakage is considered as one of the 8. Tjan AHL, Whang S.  Resistance to root fracture of important factors that influence tooth survival dowel channels with various thickness of buccal denduring and after endo-perio treatment. tin walls. J Prosthet Dent. 1985;53:496–500. • Preservation of coronal and radicular tooth 9. Assif D, Bitenski A, Pilo R, Oren E.  Effect of post design on resistance to fracture of endodontically structure is major required affecting both treated teeth with complete crowns. J Prosthet Dent. direct and indirect restoration longevity. 1993;69:36–40. • Loss of tooth structure greater than 50% 10. Robbins JW.  Guidelines for the restoration of endodontically treated teeth. J Am Dent Assoc. would determine the use of root posts only for 1990;120:558–66. core retention, when there are no other alter 11. Trope M, Maltz DO, Tronstadt L. Resistance to fracnatives, and not to strengthen endodontically ture of restored endodontically treated teeth. Endod treated teeth. Dent Traumatol. 1988;4:190–6. • The cement combination proposing the great- 12. Assif D, Oren E, Marshak BL, Aviv I.  Photoelastic analysis of stress transfer by endodontically treated est coronal sealing is the resin cement for both teeth to the supporting structure using different restorposts and indirect restorations. ative technique. J Prosthet Dent. 1989;61:535–43. • A ferrule is highly desirable when indirect res- 13. Isidor F, Brondum K, Ravnholt J.  The influence of post length and crown ferrule length on the resistance toration is used. A suitable ferrule is considto cyclic loading of bovine teeth with prefabricated ered a minimum of 2  mm of vertical height titanium posts. Int J Prosthodont. 1999;12:78–82. and 1 mm of dentin thickness. 14. Nissan J, Dmitry Y, Assif D.  The use of reinforced • Indirect restorations using mostly crowns composite resin cement as compensation for reduced post length. J Prosthet Dent. 2001;86:3048. have higher short-term (5-year) and medium-­

4  Prosthetic Considerations in the Management of Endodontic-Periodontal Lesions 15. Faria AC, Rodrigues RC, de Almeida Antunes RP, de Mattos Mda G, Ribeiro RF.  Endodontically treated teeth: characteristics and considerations to restore them. J Prosthodont Res. 2011;55(2):69–74. 16. Aurélio IL, Fraga S, Rippe MP, Valandro LF. Are posts necessary for the restoration of root filled teeth with limited tissue loss? A structured review of laboratory and clinical studies. Int Endod J. 2015;49(9):827–35. 17. Sequeira-Byron P, Fedorowicz Z, Carter B, Nasser M, Alrowaili EF. Single crowns versus conventional fillings for the restoration of root-filled teeth. Cochrane Database Syst Rev. 2015;25(9):CD009109. 18. Shu X, Mai QQ, Blatz M, Price R, Wang XD, Zhao K. Direct and indirect restorations for endodontically treated teeth: a systematic review and meta-analysis, IAAD 2017 consensus conference paper. J Adhes Dent. 2018;20(3):183–94. 19. Trope M, Chow E, Nissan R. In vitro endotoxin penetration of coronally unsealed endodontically treated teeth. Endod Dent Traumatol. 1995;11:90–4. 20. Alves J, Walton R, Drake D. Coronal leakage: endotoxin penetration from mixed bacterial communities through obturated, post-prepared root canals. J Endod. 1998;24:587–91. 21. Torabinejad M, Ung B, Kettering JD. In vitro bacterial penetration of coronally unsealed endodontically treated teeth. J Endod. 1990;16:566–9. 22. Swanson K, Madison S.  An evaluation of coronal microleakage in endodontically treated teeth. Part I. time periods. J Endod. 1987;13:56–9.

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23. Magura ME, Kafrawy AH, Brown CE Jr, Newton CW.  Human saliva coronal microleakage in obturated root canals: an in  vitro study. J Endod. 1991;17:324–31. 24. Khayat A, Lee SJ, Torabinejad M. Human saliva penetration of coronally unsealed obturated root canals. J Endod. 1993;19:458–61. 25. Safavi KE, Dowden WE, Langeland K. Influence of delayed coronal permanent restoration on endodontic prognosis. Endod Dent Traumatol. 1987;3:187–91. 26. Gorodovsky S, Zidan O.  Retentive strength disin tegration and marginal quality of luting cements. J Prosthet Dent. 1992;68:269–74. 27. Mendoza DB, Eakle WS. Retention of posts cemented with various dentinal bonding cements. J Prosthet Dent. 1994;72:591–4. 28. Nissan J, Rosner O, Gross O, Pilo R, Lin S. Coronal leakage in endodontically treated teeth restored with posts and complete crowns using different luting agent combinations. Quintessence Int. 2011;42(4):317–22. 29. Sorensen JA, Engelman MJ.  Ferrule design and fracture resistance of endodontically treated teeth. J Prosthet Dent. 1990;63:529–36. 30. Naumann M, Schmitter M, Frankenberger R, Krastl G. “Ferrule comes first. Post is second!” fake news and alternative facts? A systematic review. J Endod. 2018;44(2):212–9.

5

Endodontic-Periodontal Lesions: Periodontal Aspects Carlos E. Nemcovsky, José Luis Calvo Guirado, and Ofer Moses

5.1

Introduction

Periodontal-endodontic lesions are the combination of pulp involvement and periodontal disease in the same tooth. Whenever both endo and perio lesions are present, diagnosis of this type of situation may become difficult; however, in those cases differential etiological consideration is indispensable for appropriate treatment. Etiologic factors such as bacteria, fungi, and viruses together with several contributing factors such as trauma, root resorptions, iatrogenic causes, and dental malformations play an important role in the development and progression of such lesions [1]. Endodontic and periodontal disease may be either the result or cause of the other or have origin from two different and independent processes, which, later on, may become associated [2, 3]. Dental pulp and periodontal tissues have embryonic, anatomic, and functional interrelationships. Both dental pulp and PDL cells originate

C. E. Nemcovsky (*) · O. Moses Department of Periodontology and Implant Dentistry, The Maurice and Gabriela Goldschleger School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel e-mail: [email protected]; [email protected] J. L. Calvo Guirado Faculty of Health Sciences, Department of Oral Surgery and Implant Dentistry, Universidad Católica San Antonio de Murcia (UCAM), Murcia, Spain e-mail: [email protected]

from ecto-mesenchymal layers that differentiate to form either the dental papilla or follicle. Although, later on separated by the formation of the tooth hard tissue, this embryonic common origin gives rise to anatomical connections also present in fully developed teeth. Accessory or lateral canals communicate the pulp and periodontium and may provide a gate by which pathological agents pass from one compartment to the other; however, the exact role of those tubules, in the etiology of perioendo lesions, is not clear. The majority of these accessory and lateral canals is found in the apical third of the root and the molar furcation regions. Dentin tubules number gradually increases from the cemento–dentinal junction towards the pulp [4–6]. Through these tubules, fluid and irritants may allow communication of both compartments; therefore, in the absence of an intact covering of enamel or cementum, the pulp may be considered as exposed to the oral environment via the periodontal pocket. While there have been a number of attempts to classify perio-endo lesions [7], the most quoted classification remains that of Simon et al. 1972 [8]. This classification is based on the observation that most perio-endo lesions originate either in the pulp or in the periodontium, classifying initial lesions as primary periodontal or primary endodontic lesions, respectively. A recent classification [9] differentiates between lesions with and without root damage, where root damage refers mainly to perforations, fractures, and cracking or external root resorption. Lesions without root damage may occur in periodontitis

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and non-­periodontitis patients. Within each group, subgroups were established according to the extent of the periodontal destruction around the affected teeth. Based on their etiology, lesions may be classified as: purely periodontal, purely endodontic and endodontic-periodonal combined lesions. 1. Purely periodontal lesion. Bacterial plaque accumulation on exposed root surfaces and subsequent periodontal disease may induce pathological changes in healthy pulp tissue along the same pathways, but in the opposite direction, that an endodontic infection can affect the periodontium. There is no consensus concerning pulpal reactions due to bacterial transfer from the infected periodontium. Clinical and radiographic signs of periodontal disease are usually present in several areas of the dentition, periodontal pockets are wide, and, in most cases, pulp remains vital. 2. Purely endodontic lesion. The pulp is necrotic and infected, and there is a draining sinus tract coronally through the periodontal ligament into the gingival sulcus. An untreated infected endodontic lesion may lead to marginal periodontal breakdown. Plaque forms at the gingival margin of the sinus tract and leads to periodontitis. Pathogens in necrotic root canals may stimulate epithelial down-growth along denuded dentin surfaces with marginal communication and thus enhance periodontal disease. Clinical and radiographic signs of periodontal disease may be present only in very few teeth, teeth with purely endodontic lesions present narrow periodontal pockets, and pulp does not respond positive to vitality tests, sometimes with periapical radiolucency. In purely endodontic lesions, conventional endodontic therapy alone will resolve the lesion; clinical and radiographic postoperative follow-up should show periodontal pocket healing and bony repair. 3. Endodontic-periodontal lesion—when the pulp is necrotic and infected, and there is a deep periodontal pocket. Root damage mainly caused by iatrogenic lesions such as perforations or root cracks or fissures, and root resorption defects may be included in this category.

In endodontic-periodontal lesions, disease entities mainly differ in their infection etiology, while periodontal disease is produced by bacterial biofilms in the dento-gingival region; endodontic lesions are caused by infectious elements released from the pulpal space organized in biofilms adhering to the inner walls of the root canal.

5.2

Purely Periodontal Lesion

Plaque and calculus accumulation on the external root surfaces progress apically leading to gingival marginal inflammation. Endotoxins from bacterial plaque together with inflammatory mediators lead to destruction of gingival connective tissue, periodontal ligament, and alveolar bone (Fig. 5.1). Bacterial plaque accumulation on exposed root surfaces and subsequent periodontal disease may induce pathological changes in healthy pulp tissue along the same pathways, but in the opposite direction, that an endodontic infection can affect the periodontium (Fig.  5.2). There is no consensus concerning pulpal reactions due to bacterial passage from infected periodontium. While certain studies suggest that periodontal disease has no effect on the pulp, unless the apex is involved, others have shown that periodontal disease has a degenerative effect of on the pulp

Fig. 5.1  Endodontic periodontal lesion of the first left lower molar. Note periapical lesion of the distal root and advanced periodontal involvement in other areas. Sub-­ gingival calculus is evident

5  Endodontic-Periodontal Lesions: Periodontal Aspects

Fig. 5.2  Endodontic periodontal lesion left lower molar. Reduced bone support is evident also in neighboring teeth

Fig. 5.3  Deep periodontal defect in the mesial aspect together with furcation involvement of the first lower right molar, a slight widening of the PDL space in the periapical area is also evident

including increased calcifications, fibrosis, and collagen resorption [3, 6, 10–17] (Figs. 5.3, 5.4, and 5.5). Pathological changes and pulp necrosis due to periodontal disease, especially when accessory canals are present [15, 18, 19], have been described. Caries-free teeth with different degrees of periodontitis [20] showed pathologic changes in the pulp; however, pulp remained vital as long as the main pulpal blood supply from the apical foramen was not involved. Large percentage of teeth with periodontal disease, but without caries or fillings, showed pathological alterations in the pulp [12, 21]. Pathogens from the oral cavity may colonize the lateral or

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Fig. 5.4  Purely periodontal lesion of the second premolar, the mesial intra-bony defect involves also the periapical area. Tooth positively responded to pulp vitality test. Note periodontal status of proximal teeth

Fig. 5.5  During periodontal surgical treatment, largely exposed root surface, without communication with the periapical area

accessory canals reaching the pulp and causing a chronic inflammatory reaction, which could lead to pulp necrosis [20–22]. Something similar may happen during scaling, curettage, or periodontal surgery, when accessory canals are severed and/ or opened to the oral environment. Plaque accumulation on root dentin exposed by periodontal treatment may cause hypersensitivity, however, does not threaten pulp vitality [23, 24]; localized inflammatory alterations usually occur adjacent to instrumented root surfaces, followed by tissue repair in the form of hard tissue depositions on the root canal walls [25]. The presence of an intact cementum layer is important for the

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protection of the pulp from pathogenic agents produced by the bacterial plaque (Figs. 5.6, 5.7, 5.8, 5.9, 5.10, 5.11, 5.12, 5.13, 5.14, and 5.15). The apical foramen is the principal route of communication between the pulp and the periodontium, total pulp disintegration will only occur when the bacterial plaque involves the

Fig. 5.8  Very deep probing pocket depth on the mesial aspect of central right incisor

Fig. 5.6  3-years postoperative radiograph shows large healing of the periodontal defect, no involvement of the periapical area

Fig. 5.9  Large periodontal defect on mesial side of central right incisor not involving the periapical area

Fig. 5.7  Large intra-bony periodontal defect reaching the periapical area. Tooth responded positive to cold pulp test

main apical foramina compromising the vascular supply. Inflammatory by-products from deep periodontal pockets may affect the pulp through the apex [15, 20, 26, 27]. Microbiological and immunological studies support the hypothesis that the source of endodontic infection in primary periodontal perio-endo lesions is the periodontal pocket bacteria. Microorganisms present in the

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Fig. 5.12  Clinical evaluation 1 year after the periodontal regenerative surgical procedure. Note that in spite of the splint, the right central incisor spontaneously slightly moved in a vestibular and mesial direction. Interdental papilla does not fill the embrasure Fig. 5.10  Periodontal defect did not involve the periapical area. Defect dimensions may be appreciated with a probe placed by the root surface

Fig. 5.13  Clinical evaluation 1 year after the periodontal regenerative surgical procedure. Probing pocket depth with a pressure-sensitive periodontal probe shows a 4 mm deep pocket Fig. 5.11 Aspect of the area after completing the procedure

root canals of caries-free teeth with advanced periodontitis are similar to those found in the adjacent periodontal pockets, suggesting their periodontal origin [28–32]. The organisms most often involved are probably bacteroides, fusobacteria, eubacteria, spirochetes, wolinellas, selenomonas, campylobacter, and peptostreptococci [30, 33–37]. Others have reported no definite relationship between periodontal disease and pulpal status [3,

14, 26, 28, 38, 39] (Figs. 5.3, 5.4, 5.5, and 5.6). Only 2% of accessory canals actually communicated deep periodontal pockets and the pulp [40]. Clinical and radiographic signs of periodontal disease are usually present in several areas of the dentition, periodontal pockets are wide, and, in most cases, pulp remains vital (Figs.  5.16, 5.17, 5.18, and 5.19). However, pulp vitality tests are not definitive; the probability of a sensitive reaction representing a vital pulp is 90% with the cold test and only 84% with the electric pulp test [41].

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Fig. 5.14  Radiographic evaluation during orthodontic treatment to realign the right central incisor in place. Radiographic defect fill on its mesial aspect is evident

Fig. 5.15  Clinical evaluation 2 years after the periodontal regenerative surgical procedure and after completion of orthodontic tooth movement to realign the right central incisor. Interdental papilla now fills the embrasure

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Fig. 5.16  Radiograph 2 years after the periodontal regenerative surgical procedure. Radiographic defect fill on the mesial aspect of right central incisor is evident

Fig. 5.17  Radiograph shows periodontal involvement on first upper right molar, furcation involvement and mesio-­ buccal root almost devoid of bone support

5  Endodontic-Periodontal Lesions: Periodontal Aspects

Fig. 5.18  Radiograph shows periodontal involvement on first upper right molar, furcation involvement, and defect around the mesio-buccal root beyond the apex. Tooth tested positive for cold pulp test

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Fig. 5.20  Radiograph shows periodontal loss of support in all teeth in the upper right quadrant, especially a deep intrabony defect on the distal aspect of second premolar, reaching the peri-apex with a slight radio-lucency in the area

Fig. 5.21  Clinical aspect during periodontal surgical treatment shows periodontal involvement on second premolar, however, without not involving the root apex

Fig. 5.19  Clinical aspect during periodontal surgical treatment shows periodontal involvement on first upper right molar, furcation involvement, and defect around the mesio-buccal clearly not involving the apex

With positive results to pulp vitality test, purely periodontal lesions are, in the first instance, treated by periodontal therapy, otherwise, endodontic treatment is mandatory (Figs. 5.20, 5.21, 5.22, 5.23, 5.24, 5.25, 5.26, 5.27, 5.28, 5.29, 5.30, 5.31, and 5.32).

Fig. 5.22  Probe placed by the root surface shows intra-­ bony pocket depth

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Fig. 5.23  Radiograph 2 years after periodontal regenerative surgery shows bone support in all teeth in the upper right quadrant, with bone fill especially in the intra-bony defect on the distal aspect of second premolar, no endodontic involvement, the tooth remained positive to cold pulp test

Fig. 5.25  Radiograph shows periodontal loos of support in all lower anterior teeth, especially a deep intra-bony defect on the left central incisor, reaching the periapical area. Tooth responded positive to cold pulp test

Fig. 5.24  Radiograph 3 years after periodontal regenerative surgery shows improved bone support in the upper right quadrant, especially in the intra-bony defect on the distal aspect of second premolar, no endodontic involvement, the tooth remained positive to cold pulp test

5.3

Purely Endodontic Lesion

An inflammatory process in the periodontal tissues resulting from noxious agents present in the root canal system of the tooth.

Fig. 5.26  During periodontal surgical treatment, a large intra-bony defect may be appreciated involving the lingual aspect of both central incisors. Note that teeth have been splinted to avoid luxation during treatment

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Fig. 5.27  During periodontal surgical treatment, loss of bone support is evident in all incisors, a fenestration with root surface exposure may be seen between central and lateral left incisors

Fig. 5.29  Follow-up radiograph taken 2 years after periodontal reconstructive treatment shows bone healing of the area. Tooth responded positive to cold pulp test

Fig. 5.28 During periodontal surgical treatment, periodontal probe allows for evaluation of loss of bone support. Periodontal defect deepest part is in the periapical area

An untreated infected purely endodontic lesion may secondarily induce marginal periodontal breakdown. Plaque accumulation at the gingival margin of the sinus tract of endodontic source may lead to periodontitis. Pathogens in necrotic root canals may stimulate epithelial down-growth along denuded dentin surfaces with marginal communication and thus enhance periodontal disease. Root canal infections could be the cause for an inflammatory response in the marginal periodontium [15, 42–46]. Teeth with periapical radiolucency were found to be significantly cor-

Fig. 5.30  Follow-up radiograph taken 3 years after periodontal reconstructive treatment shows bone healing of the area

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Fig. 5.31  Follow-up radiograph taken 4 years after periodontal reconstructive treatment shows bone healing of the area

Fig. 5.32  Clinical aspect of the area 4 years after periodontal reconstructive surgery. Note soft tissue aspect with no clinical signs of inflammation

related to deeper periodontal pockets [42–44, 46–49], more radiographic attachment loss, angular bony defects, more marginal bone loss, unfavorable response to treatment, and attachment loss in the furcation area of molars compared to teeth without endodontic infection. Dentinal tubules devoid of cementum layer covering represent possible pathways for bacteria

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that may lead to further periodontal breakdown [62]. In experimentally replanted infected monkey teeth, denuded dentin surfaces were associated with epithelial down-growth [50] and show significantly larger areas of resorption compared to noninfected roots. Endodontic infection has a negative influence on periodontal healing [29, 42, 46–49, 51, 52]. Periodontal defects in endodontically infected teeth were covered by more epithelium and presented less connective tissue formation [42, 46, 53]. Within the same periodontitis patient, more bone loss in teeth with than in those without periapical lesions [42, 46] was reported. The effect of root canal therapy and enhanced periodontal destruction is not clear [54, 55]. Accessory canals in the furcation area may increase the risk for periodontal involvement [56, 57]. Furcation involvement was more often diagnosed in molars with root canal therapy [58]. The survival of molars with periodontal and endodontic involvement carrying a prosthetic restoration over an observation period of 13.2 years was lower (67.4%) than the survival for molars in general (85%) [58]. However, teeth after root canal therapy may have restorations with margins that facilitate plaque acumulation. Molars with root canal treatment and periodontal involvement survive for over 10  years following treatment in 83% of the cases, and two-­ thirds of endodontically treated molars will still be present in the jaw 20 years during supportive periodontal therapy. In most cases, even molars with combination of periodontal and endodontic risk factors can be retained for more than 10  years and survival rates may be improved by a high standard of interdisciplinary treatment. Clinical and radiographic signs of periodontal disease may be present only in very few teeth, teeth with purely endodontic lesions present narrow periodontal pockets, and pulp does not respond positive to vitality tests, sometimes with periapical radiolucency. In purely endodontic lesions, conventional endodontic therapy alone will resolve the lesion; clinical and radiographic postoperative follow-up should show periodontal pocket healing and bony repair. However, in cases where lesions persist

5  Endodontic-Periodontal Lesions: Periodontal Aspects

Fig. 5.33  Radiograph shows large periapical radiolucency in second right premolar together with loss of periodontal support. Tooth did not respond positive to cold pulp test vitality. A purely endodontic lesion commanded a root canal treatment

Fig. 5.34  Radiograph 3  months after root canal treatment. No evident lesion reduction may be appreciated. Surgical combined periodontal-endodontic treatment was, therefore, indicated

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Fig. 5.35  During periodontal surgical treatment, dimensions of the bony defect may be clearly appreciated

Fig. 5.36  During periodontal surgical treatment, periodontal probe shows communication between periodontal and periapical lesions

despite proper endodontic treatment, they may have independent periodontal involvement, these types of lesions will not resolve with endodontic treatment alone [59] (Figs. 5.33, 5.34, 5.35, 5.36, and 5.37).

5.4

Endodontic-Periodontal Lesion

Both an endodontic and periodontal lesion developing independently and progressing concurrently meet and merge at a point along the root surface (Figs. 5.38, 5.39, 5.40, 5.41, 5.42, 5.43, 5.44, 5.45, 5.46, 5.47, and 5.48).

Fig. 5.37  Radiograph 6  months after periodontal and periapical surgery. Considerable radiographic lesion reduction may be appreciated

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Fig. 5.38  Periapical radiograph shows large periapical radiolucency together with periodontal involvement suggesting an endodontic-periodontal lesion in upper left cuspid. Tooth was negative to cold pulp test

Fig. 5.40  Clinical aspect, deep probing pocket depth (over 15 mm), clinical signs of inflammation with a suppurating fistula that did no heal after root canal therapy. Surgical periodontal reconstructive treatment was indicated

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Fig. 5.39  Periapical radiograph after root canal therapy, no clinical and radiographic resolution of the periapical radiolucency and severe periodontal involvement suggesting an endodontic-periodontal lesion

Fig. 5.41  Clinical aspect, with the 15 mm probe outside the pocket, illustrating probing pocket depth

5  Endodontic-Periodontal Lesions: Periodontal Aspects

Fig. 5.42  During periodontal surgical treatment, perio-­ endo lesion with a largely exposed root surface, bone defect beyond the root apex

In these cases, periodontal and endodontic diseases present independent pathophysiology. Endodontic-periodontal lesions are formed when a coronally progressing endodontic infection joins an apically progressing infected periodontal pocket. The radiographic appearance of combined endodontic/periodontal disease may be similar to that of a vertical root fractures. The ideal interval between the endodontic treatment and periodontal surgery has also been challenged, with times ranging from performing both treatments simultaneously to 6 months lapse between the endodontic and periodontal treatments [37, 43, 44, 47, 48, 51, 60–66, 60–66]. Delaying periodontal intervention for a certain time after root canal treatment completion has been suggested to be beneficial for three main reasons: the endodontic space may be sealed and disinfected, which is not possible with the periodontal space, thereby closing the communication pathways between the pulpal and periodontal systems [72]; root planning may

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Fig. 5.43  During periodontal surgical treatment, periodontal probe illustrates large extent of exposed root surface

Fig. 5.44  Follow-up radiograph taken 3 years after periodontal reconstructive treatment shows bone healing in the perio-endo lesion

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Fig. 5.45  Follow-up radiograph taken 4 years after periodontal regenerative treatment shows stable results with bone healing in the perio-endo lesion

Fig. 5.46  Clinical aspect of the area 4 years after periodontal reconstructive surgery. Gingival recession with root exposure is evident, however, no clinical signs of inflammation

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Fig. 5.47  A pressure-sensitive probe shows large reduction in probing pocket depth to approximately 4 mm

Fig. 5.48  A pressure-sensitive probe outside the pocket illustrates probing pocket depth of approximately 4 mm

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inadvertently remove healthy periodontal ligament fibers having the potential of reattachment after root canal treatment [64]; and irritants from the root canal may compromise periodontal healing if periodontal treatment is performed before endodontic treatment [73]. A negative effect of infection from endodontic origin on periodontal healing has been reported where endodontic therapy was performed after periodontal surgical treatment or even when both therapies were simultaneously performed [51, 52] (Figs.  5.49, 5.50, 5.51, 5.52, 5.53, 5.54, 5.55, 5.56, 5.57, 5.58, 5.59, 5.60, 5.61, 5.62, 5.63, and 5.64). Bacteria from the root canal space do not invade the periodontal space when a layer of the cementum is intact [74]; however, cementum removal during periodontal treatment has been correlated with increased patency of dentinal tubules [75]. On the other hand, it is nearly impossible to entirely remove the cementum from the middle and apical portions of the root [76]; rather, periodontal treatment and supportive therapy

only remove contaminated and necrotic cementum [77] reducing the amount of pathogens in the periodontal pocket [78]. Performing both treatments simultaneously has also been advocated; the treatment approach of performing definitive periodontal therapy 1–3  months after completion of endodontic treatment prolongs treatment duration and may lead to enhanced amounts of periodontal pathogens, leading to worsening of periodontitis [79]. Microflora associated with a periodontal pocket could reinvade dentinal tubules and may act as a reservoir for recolonization of the pocket after debridement, thus affecting periodontal treatment outcome [10, 11, 79]. No significant difference in periodontal healing between simultaneous and delayed periodontal treatment groups, of combined endodonticperiodontal lesions without communication has been reported [80], suggesting that an observation period may not be required after endodontic treatment and before definitive periodontal

Fig. 5.49  Preoperative radiograph shows extensive loss of periodontal support in most anterior lower teeth, especially in left central incisor and cuspid with no response to pulp vitality test

Fig. 5.50  Preoperative radiograph shows extensive loss of periodontal support in most anterior lower teeth, especially in left central incisor and cuspid with no response to pulp vitality test. An endodontic-periodontal lesion was evident

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Fig. 5.53  Periodontal probe in place during periodontal reconstructive surgery illustrates extent of bony defect around the lower left cuspid

Fig. 5.51  Radiograph after completion of root canal treatments in left central incisor and cuspid. Large loss of periodontal support is evident

Fig. 5.52 During periodontal reconstructive surgery, extent of the perio-endo lesions around left central incisor and cuspid is evident, in both teeth the defects involved the root apex

Fig. 5.54  1-year postoperative radiograph shows resolution of the endodontic lesion together with enhanced bone support, especially in left central incisor and cuspid

5  Endodontic-Periodontal Lesions: Periodontal Aspects

Fig. 5.55  2-years postoperative radiograph shows resolution of the endodontic lesion together with enhanced bone support, especially in left central incisor and cuspid

Fig. 5.57  Clinical aspect of the area 4 years after periodontal regenerative surgery. Gingival recession with root exposure is evident, however, no clinical signs of inflammation

therapy. Medicaments in the canal space may also be beneficial in promoting periodontal healing during postoperative periods when mechanical cleaning may be impaired. The local delivery of antimicrobials is a complementary approach

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Fig. 5.56  4-years postoperative radiograph shows resolution of the endodontic lesion together with enhanced bone support, especially in left central incisor and cuspid

Fig. 5.58 A pressure-sensitive probe shows probing pocket depth of approximately 3 mm on distal aspect of central incisor

to the treatment of periodontitis [81, 82] and has a synergistic effect in the healing of periodontal lesions [83, 84]. Intra-canal chlorhexidine application has been shown effective for promoting periodontal healing after surgical periodontal

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Fig. 5.59  Preoperative radiograph of lower anterior area, shows large perio-endo lesions in most front teeth. No response to vitality test commanded endodontic treatment in both cuspids and right central incisor

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Fig. 5.60  Postoperative radiograph of lower anterior area taken 2  years after periodontal reconstructive surgery shows resolution of endodontic lesions; however, periodontal support remained extremely reduced, especially in right central incisor

Fig. 5.62  Clinical aspect of the area 2 years after periodontal regenerative surgery. Gingival recession with root exposure is evident, however, no clinical signs of inflammation

Fig. 5.61  Postoperative radiograph of lower anterior area taken 3 years after periodontal regenerative surgery shows resolution of endodontic lesions with stable periodontal support

5  Endodontic-Periodontal Lesions: Periodontal Aspects

Fig. 5.63  A periodontal probe shows probing pocket depth of approximately 3 mm on distal aspect of lateral incisor

Fig. 5.64  Clinical aspect of the area 3 years after periodontal regenerative surgery. Gingival recession with root exposure is evident, however, no clinical signs of inflammation

Fig. 5.65  Radiograph of upper right quadrant. Second premolar and first molar after root canal treatment and prosthetic rehabilitation. Most teeth in the area show better bone support. Molar mesio-buccal root is almost devoid of

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therapy in concomitant endodontic-­periodontal lesions [31]. While a negative impact of endodontic treatment and obturation materials on periodontal healing has been reported [85], others have observed similar periodontal healing in adequately endodontically treated teeth and vital teeth [61, 86]. Cases with endodontic-periodontal lesions usually present with several clinical and radiological features, such as altered response to testing of pulp sensitivity, clinical signs of gingival inflammation, increased probing pocket depth, sinus tracts, pus secretion and different types of radiological bony defects, several areas of the dentition show periodontal involvement, all of which difficult the diagnosis of the primary cause [22, 87, 88]. Endodontic-periodontal lesions are treated initially as for primary endodontic lesions with secondary periodontal involvement; however, periodontal treatment must always follow, and this type of lesions will not heal with endodontic treatment alone. The long-term prognosis of endodontic-periodontal lesions may often not be clear [89, 90]; however, modern periodontal and endodontic treatment approaches may allow treatment and longtime preservation even of severely involved teeth (Figs. 5.65, 5.66, 5.67, 5.68, 5.69, 5.70, 5.71, 5.72, 5.73, 5.74, 5.75, and 5.76). Before a treatment plan is established, diagnosis and etiological factors of the disease as well as the prognosis of the remaining teeth should

bone support. Perio-endo iatrogenic lesion is due to endodontic complication following treatment, either root crack or fissure or perforation

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Fig. 5.66  Radiograph of lower right quadrant. All three posterior teeth after root canal treatment and prosthetic rehabilitation. Radiolucency around the second molar root, together with a deep and narrow mid-buccal probing depth, indicate that the perio-endo lesion is iatrogenic, due to a vertical root fissure.

Fig. 5.68  Radiograph after root canal treatment in lateral incisor, no endodontic treatment was performed in the cuspid. Periodontal treatment is indicated

Fig. 5.67  Radiograph shows periodontal involvement of lateral incisor and right upper cuspid, with certain radiolucency also in the peri-apical area. Lateral incisor, contrary to cuspid, did not respond to pulp vitality test. A combined perio-endo lesion is evident

be determined, while predicting the final functional and esthetic result. According to several patient and tooth related factors, tooth prognosis can artificially be classified into good, fair, poor, questionable, hopeless, and indicated for extrac-

Fig. 5.69  Clinical aspect during periodontal reconstructive surgical treatment. Largely exposed roots of lateral incisor and cuspid are evident. Other proximal teeth present different degrees of periodontal disease. The defect in the lateral, not in the cuspid, involved the peri-apical area

tion; however, borders are not always evident. Finally, the treating clinician will have to decide whether the tooth/teeth are treatable and maintainable or not [91]. In most periodontal involved dentitions, several difficult decisions must be taken

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Fig. 5.70  Periodontal probe placed near the cuspid root illustrates extent of periodontal defect

Fig. 5.72  Post-operative radiograph taken 1 year after periodontal reconstructive surgery. Note enhanced bone fill in the periodontal defects

Fig. 5.71  Post-operative radiograph taken 6 months after periodontal reconstructive surgery. Note bone fill in the periodontal defects

regarding the survival of a variable number of teeth. In cases with severe periodontal breakdown, it seems, however, difficult to establish a definite line and clearly decide which teeth will not respond to periodontal treatment and are, therefore, indicated for extraction [92, 93].

Fig. 5.73  Post-operative radiograph taken 2 years after periodontal reconstructive surgery. Note enhanced bone fill in the periodontal defects, also in the central incisors

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Fig. 5.76  Clinical aspect of the area 4 years after periodontal reconstructive surgery. Gingival recession with root exposure is evident mainly in the lateral incisor and the cuspid, however, with no clinical signs of inflammation

Fig. 5.74  Post-operative radiograph taken 3 years after periodontal reconstructive surgery. Note enhanced bone fill in the periodontal defects

Fig. 5.77 A pressure sensitive probe shows probing pocket depth of 4 mm on distal aspect of lateral incisor

Fig. 5.75  Post-operative radiograph taken 4 years after periodontal reconstructive surgery. Note enhanced bone fill in the periodontal defects

An accurate diagnosis and prognosis is most critical when periodontal therapy is combined with large oral prosthetic rehabilitation or with dental implants; in these complex cases, an accurate long-term prognosis of the involved teeth must be established at the time of treatment planning; teeth with root surface damage rarely respond to any type of treatment (Figs.  5.77 and 5.78). Oral implants do not surpass the long-term longevity of teeth, even if periodontal or endodontic problems are present [94]. Although one or several teeth might be lost, this does not detract from the possible

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Following extraction of teeth with large periodontal destruction, usually bone augmentation procedures are required to obtain adequate bone volume for dental implant reconstruction involving increased the costs and frequently enhanced patient morbidity, and are not exempt from future biological and/or mechanical complications [100–103]. Increased susceptibility for periodontitis may also translate to an increased susceptibility for implant loss, loss of supporting bone, and postoperative infection [104]. A retrospective study carried out encompassing all patients who had initial periodontal treatment followed by implant placement and maintenance therapy found that peri-­implantitis prevaFig. 5.78 A pressure sensitive probe shows probing lence was 53.5% at the patient level and 31.1% at the implant level. Further findings showed pocket depth of 3 mm on mesial aspect of cuspid that, although the mean number of disease-free years was statistically significantly similar for relative success of the treatment, provided the implants and teeth, the extra cost of maintaining dentition can be restored to good function with the implants was about five times higher than for good chances of long-term survival [91]. An teeth [105]. Peri-implant mucositis was found in ideal treatment plan should address the main 63.4% of the evaluated population and 30.7% complaints of the patient; provide the longest-­ of implants, and peri-implantitis in 18.8% of lasting, most cost-effective treatment; and meet participants and 9.6% of implants. A higher freor exceed the patient’s expectations whenever quency of peri-implant diseases occurrence was possible [95]. The definition of good has much recorded for smokers [100]. higher predictability than the one for a worse Age, furcation involvement, tooth prognoprognosis [96]. sis at the start of supportive periodontal therapy, In combined endodontic-periodontal lesions, and previous endodontic therapy have been sigteeth usually present severe destruction of sup- nificantly associated with the risk of tooth loss porting tissues beyond the apex, thus consid- [106]. In a retrospective evaluation, with up to ered as having a hopeless prognosis [97]. Teeth 10 years follow-up, the overall tooth survival rate with hopeless prognoses affected by com- was 97.4%; teeth were mainly lost due to late bined endodontic-periodontal lesions beyond endodontic problems with no association between the apex have been treated and maintained for the initial bone level and tooth survival [107]. On 5  years after surgical treatment that included a long-term basis, nonsurgical endodontic treatboth endodontic and regenerative periodontal ment represents a procedure that supports retentreatment [98] (Figs.  5.48, 5.49, 5.50, 5.51, tion of molars in periodontally compromised 5.52, 5.53, 5.54, 5.55, 5.56, 5.57, 5.58, 5.59, patients after active and during supportive peri5.60, 5.61, 5.62, 5.63, and 5.64). It is difficult odontal treatment. In most cases, even molars to clearly establish which teeth will not respond with combination of periodontal and endodontal to periodontal treatment and should, therefore, risk factors can be retained for more than 10 years be extracted [92, 99]. Treatment outcome in and survival rates may be improved by a high these cases is not predictable and patients must standard of interdisciplinary treatment. Only facbe willing to invest time, suffering, and costs in tors on tooth-level such as through-and-through spite of these unforeseeable results; it should furcation involvement and periapical involvement be emphasized that certain teeth may have to be significantly contributed to loss of molars with extracted even after treatment. root canal fillings in periodontitis patients [58].

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Combination of class II furcation and advanced periodontal breakdown represents a higher risk for molar long-term survival. Residual periodontal support assessed as vertical subclassification of furcation involvement seems to be a good predictor of survival of molar with class II horizontal furcation. Subclassification of class II furcation involvement in molars may be established considering the area with greater vertical attachment loss/bone loss: A  =  extending to the coronal third of the root; B = extending to the middle third of the root; C = extending to the apical third of the root. Ten-year survival of all molars with class II furcation involvement was 52.5%; however, when the different degrees were evaluated, the following survival rates were reported: 91% for subclass A, 67% for subclass B, and 23% for subclass C.  Mean years of survival were 9.5–10.1, 8.5–9.3, and 6–7.3 for subclasses A, B, and C, respectively. Hazard rates for tooth e­xtraction/ loss were 4.2 and 14.7 for subclasses B and C, respectively [108]. Modern endodontic techniques and advanced regenerative periodontal treatment make possible to improve prognosis and maintain the tooth/ teeth on a long-term basis [109].

5.5

Conclusions

An accurate prognosis is most critical when periodontal and endodontic therapy are combined with large oral prosthetic rehabilitation or with dental implants; in these complex cases, an accurate long-term prognosis of the involved teeth must be established at the time of treatment planning. In purely endodontic lesions, conventional endodontic therapy alone will resolve the lesion; however, in cases where lesions persist, they may have independent periodontal involvement; these types of lesions will not resolve with endodontic treatment alone. The long-term prognosis of endodontic-­ periodontal lesions may often not be clear, however modern periodontal and endodontic treatment approaches may allow treatment and longtime preservation even of severely involved teeth.

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5  Endodontic-Periodontal Lesions: Periodontal Aspects 85. Breault LG, Schuster GS, Billman MA, et  al. The effects of intracanal medicaments, filers and sealers on the attachment of human gingival fibroblasts to an exposed dentin surface free of a smear layer. J Periodontol. 1995;66:545–51. 86. Cortellini P, Tonetti MS. Evaluation of the effect of tooth vitality on regenerative outcomes in infrabony defects. J Clin Periodontol. 2001;28:672–9. 87. Harrington GW. The perio-endo question: differential diagnosis. Dent Clin N Am. 1979;23:673–90. 88. Abbott P.  Endodontic management of combined endodontic-­ periodontal lesions. J N Z Soc Periodontol. 1998;83:15–28. 89. Nirola A.  Pulpal perio relations: Interdisciplinary diagnostic approach I.  J Indian Soc Periodontol. 2011;15(1):80–2. 90. Tseng CC, Harn WM, Chen YH, Huang CC, Yuan K, Huang PH. A new approach to the treatment of True combined Endodontic-periodontic lesions by the guided tissue regeneration technique. J Endod. 1996;22:693–6. 91. Nemcovsky CE, Sculean A.  Evidence-based decision making in periodontal tooth prognosis and maintenance of the natural dentition. In: Rosen E, Nemcovsky CE, Tsesis I, editors. Evidence-based decision making in dentistry. Multidisciplinary management of the natural dentition. Switzerland: Springer International Publishing; 2017. p. 39–60. 92. Tonetti MS, Muller-Campanile V, Lang NP. Changes in the prevalence of residual pockets and tooth loss in treated periodontal patients during a supportive maintenance care program. J Clin Periodontol. 1998;25:1008–16. 93. Tonetti MS, Steffen P, Muller-Campanile V, Suvan J, Lang NP.  Initial extractions and tooth loss during supportive care in a periodontal population seeking comprehensive care. J Clin Periodontol. 2000;27:824–31. 94. Holm-Pedersen P, Lang NP, Müller F. What are the longevities of teeth and oral implants? Clin Oral Implants Res. 2007;18:5–9. 95. Torabinejad M, Goodacre CJ. Endodontic or dental implant therapy: the factors affecting treatment planning. J Am Dent Assoc. 2006;137(7):973–7. 96. Ioannou AL, Kotsakis GA, Hinrichs JE. Prognostic factors in periodontal therapy and their association with treatment outcomes. World J Clin Cases. 2014;2(12):822–7. 97. Cortellini P, Prato GP, Tonetti MS.  The modified papilla preservation technique. A new surgical approach for interproximal regenerative procedures. J Periodontol. 1995;6:261–6. 98. Cortellini P, Stalpers G, Mollo A, Tonetti MS. Periodontal regeneration versus extraction and prosthetic replacement of teeth severely compromised by attachment loss to the apex: 5-year results

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6

Modern Clinical Procedures in Periodontal Reconstructive Treatment Carlos E. Nemcovsky and Jose Nart

6.1

Introduction

Regenerative periodontal procedures improve tooth survival while reducing periodontitis progression and re-intervention needs providing long-term outcome stability [1]. The decision of tooth extraction for periodontal reasons in favor of a dental implant should be carefully considered. In compliant patients, high long-term natural dentition survival may be achieved even in cases with advanced loss of periodontal support. Although certain factors such as active smoking, furcation involvement, and degree III mobility may increase the risk for tooth loss up to fivefold, early tooth extraction is usually contraindicated [2]. Provided adequate periodontal treatment and maintenance, even when periodontal attachment level is reduced, natural dentition yields better long-term survival and marginal bone level changes compared with dental implants [3].

C. E. Nemcovsky (*) Department of Periodontology and Implant Dentistry, The Maurice and Gabriela Goldschleger School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel e-mail: [email protected] J. Nart Department of Periodontology, Universitat Internacional de Catalunya (UIC), Barcelona, Spain e-mail: [email protected]

6.2

Biologic Background for Periodontal Regeneration

Periodontal regeneration is a complex biological process that involves de novo formation of the lost tooth supporting structures, including alveolar bone, periodontal ligament, and cementum over a previously diseased root surface [4]. Tissue regeneration depends on the combined presence of progenitor cells, signaling molecules, blood supply, and scaffolds. The different tissues that conform the attachment apparatus must be reconstituted while, at the same time, maintaining their characteristics and normal anatomical distribution [5–7]. Cementum is a mineralized connective tissue, it does not resorb in normal situations, and only minimal amounts are deposited throughout lifetime. Periodontal ligament is a non-mineralized connective tissue that links between the root cementum and the alveolar bone, a calcified tissue that follows a normal process of resorption and apposition. However, periodontal treatment outcome is usually repair, where healing occurs with a long epithelial attachment lining most of the previously exposed root surface and where minimal amounts of new connective tissue attachment, new cementum and bone are limited only to the apical part of the defect. Reconstructive periodontal procedures have shown advantage over conventional surgical

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p­ rocedures in terms of better results in long-term stability, improved tooth survival, lesser periodontitis progression, and fewer needs for re-­ intervention over long periods [1]. Clinically, periodontal reconstruction may be achieved by application of barrier membranes, grafts, wound-healing modifiers, and their combinations. Guided tissue regeneration (GTR) is based on the application of a separating barrier membrane that mechanically isolates the defect, thus giving advantage to PDL and bone cells to repopulate it, while avoiding cells with a higher proliferation capacity like connective tissue and epithelial cells from the gingiva [8–13]. Although this mechanical/biological concept has been widely proven, in both preclinical and clinical studies, several shortcomings such as treatment of multiple proximal defects, complications due to membrane exposure [14, 15], and incomplete adaptation of the membrane around irregularly shaped roots limit their application in reconstructive periodontal surgical procedures. Currently, two preparations containing growth and/or differentiation factors are available for clinical application in periodontal reconstructive procedures: enamel matrix derivative and platelet-­derived growth factor mixed in a beta-­ tricalcium phosphate bone-replacement graft. Enamel matrix protein derivatives are, by far, the most largely evaluated in both preclinical [16] and clinical models. Enamel matrix proteins are secreted by ameloblasts and serve as important regulators of enamel mineralization [17]. Once the root crown is formed, during root formation, these proteins are secreted by epithelial cells and have profound biological roles during the formation of the periodontal supporting tissues, such as initiation of cementogenesis, induction of differentiation of dental follicle cells to cementoblasts [18], and the attachment of cementum to root dentin [19]. Enamel matrix protein derivative (EMD) is mainly composed of amelogenins, with smaller amounts of other non-amelogenin components such as tuftelin, ameloblastin, and enamel proteases [20]. EMD is a biologically active compound that once applied on a denuded root surface starts a cas-

C. E. Nemcovsky and J. Nart

cade of biologic events, such as enhanced attraction and migration of mesenchymal cells, their attachment to the root surface [21], and differentiation into cementoblasts, PDL fibroblasts, and osteoblasts. Enamel proteins enhance gene expression responsible for protein and mineralized tissue syntheses in PDL cells [22]. This process may finally lead to reconstitution of the periodontal apparatus. Due to the highly conserved structure and function of amelogenins, EMD, although of porcine origin, can be applied in other species, without triggering allergic or other immunologic reactions [23]. Histologic evidence of periodontal regeneration, including cementum formation, in humans following EMD has been extensively reported [24–34] (Figs. 6.1, 6.2, 6.3, 6.4, 6.5, and 6.6). There is preclinical and clinical evidence concerning the positive effect of recombinant human platelet-derived growth factor-BB combined with recombinant human insulin-like growth factor-1 on periodontal wound healing and regeneration [35–37]. Bone gain was usually reported; however, results for clinical attachment level gain were not homogeneous.

Fig. 6.1  Largely exposed root of upper second right premolar. Implants were placed mesially and distally to the tooth. Reconstructive periodontal surgical treatment with enamel matrix protein derivative in combination with a bone graft was performed in the proximal teeth. The premolar was scheduled to be extracted at second stage implant surgery and histologically evaluated

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Fig. 6.2  Occlusal view shows a 1-wall defect on the buccal aspect of the second upper right premolar

Fig. 6.4  Low magnification histologic aspect, Mallory’s tri-chrome staining. New connective tissue with inserting fibers may be appreciated. The root surface is lined by the old cementum layer (in red), and, lining most of it, new cementum has been formed (in blue) Fig. 6.3  Aspect at second stage implant surgery. Note healing with complete fill of the intrabony and partly of suprabony components of the defect. The tooth was extracted with the surrounding tissues and prepared for decalcified histological evaluation. Slices were performed bucco-lingually parallel to the tooth long axis

6.3

Clinical Outcome

Although periodontal regeneration can exclusively be assessed through histologic evaluation (Figs. 6.4, 6.5, and 6.6), in clinical practice, periodontal treatment results can solely be evaluated through clinical and radiographic follow-up. Application of EMD during regenerative periodontal surgical therapy enhanced outcome in

clinical attachment level (CAL) gain, probing pocket depth reduction, and new bone formation compared with open-flap debridement and/or modified Widman flap [14, 15, 27, 29, 33, 38– 50]. Moreover, EMD promotes a progressive increase of radiographic bone support and CAL gain [51]. Results can usually be appreciated only several months after treatment. New cementum-like, calcified tissue formation was appreciated along the scaled root surface in most defects treated with EMD, not related to the base of the periodontal defect or within the periodontal ligament [25]. During the first months after surgery, bone formation will start close to the treated root surface (Figs. 6.7, 6.8, 6.9, 6.10,

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Fig. 6.5 Higher magnification histologic aspect, new connective tissue with inserting fibers may be clearly appreciated. Old cementum layer (in red) lines most of the root surface, while the new cementum layer (in blue) covers almost all its extension

6.11, 6.12, 6.13, 6.14, and 6.15). Further organization of the newly formed tissues may continue for several months after surgery when new bone, induced by the previously formed cementum on the root surface, may be appreciated in the radiographic evaluation. Later on, a new functional attachment may be established, although the regenerative/reparative process may continue for a long time. A second EMD application might even enhance previously achieved results [52] (Fig. 6.15). Radiographic follow-up might reveal a similar healing pattern concerning defect bone fill (Figs. 6.16, 6.17, 6.18, 6.19, 6.20, 6.21, 6.22,

6.23, 6.24, 6.25, 6.26, and 6.27). EMD application without rising a periodontal flap enhanced soft tissue healing, however, did not lead to periodontal regeneration [53–55]. Similar results in CAL gain have been reported for treatment of single infrabony defects with both GTR and EMD [15, 33, 56–62]. GTR was more effective than EMD in terms of percentage of CAL gain in patients with a baseline clinical attachment loss of more than 9 mm; however, EMD appeared to be better than GTR in patients with smaller CAL levels [63] (Figs. 6.28, 6.29, 6.30, 6.31, 6.32, 6.33, 6.34, 6.35, 6.36,

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Fig. 6.6 Large magnification histologic aspect, new connective tissue with inserting fibers may be clearly appreciated. New cementum layer (in blue) covers the old cementum layer. New cementum is lined, mainly in the apical part, by cells, probably, cementoblasts

6.37, 6.38, and 6.39). Clinical and radiographic improvements can be maintained for long periods of time [64–72]. Following EMD treatment probing pocket depth was higher than with GTR, although gingival recession was smaller in the EMD cases [73] and thus CAL gains were similar for both treatment alternatives [58]. Due to a lesser gingival recession, EMD treatment seems indicated for esthetic regions. A combined procedure with the use of a barrier membrane and EMD application did not lead to enhanced results [33, 57, 62]; therefore, there seems to be no rational for this kind of combined procedure [74]. EMD

treatment presents less patient morbidity than GTR as membrane exposure occurs in the vast majority of cases treated with GTR (Figs. 6.28, 6.29, 6.30, 6.31, 6.32, 6.33, 6.34, 6.35, 6.36, 6.37, 6.38, and 6.39), while only few complications occur in EMD-treated sites. The possibility of treating multiple proximal defects with GTR is doubtful, due to the very difficult task of adapting a membrane around several teeth. Moreover, in these cases, the blood nourishment of the flap is extremely reduced and the possibility of extensive membrane exposure is evident. EMD is then a valuable treatment alternative also for these

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Fig. 6.9  Extent of the bone defect on right lateral incisor is illustrated by a periodontal probe, showing over 10 mm distance from most apical aspect of defect and the cemento-enamel junction. Periodontal reconstructive surgical treatment with use of enamel matrix proteins and a bone graft was performed

Fig. 6.7  Preoperative radiograph, note large defect on distal aspect of right lateral incisor

Fig. 6.8  Intraoperative aspect of 1-wall extensive bone defect on distal aspect of right lateral incisor, buccal root surface largely exposed

cases (Figs.  6.40, 6.41, 6.42, 6.43, 6.44, 6.45, 6.46, 6.47, 6.48, and 6.49). Periodontal regenerative surgery with GTR seems questionable in suprabony defects with horizontal bone loss [75, 76]; however, EMD application may enhance treatment outcome in these type of defects [50, 52, 77] (Figs. 6.50, 6.51, 6.52, 6.53, 6.54, 6.55, 6.56, and 6.57). Enhanced clinical wound heal-

Fig. 6.10  Two-months post-surgery radiograph

ing rate following EMD treatment may be appreciated. EMD improved oral mucosa incisional wound healing by promoting formation of blood vessels and collagen fibers in the connective tissue [78]. The increase in soft tissue density was faster following EMD application compared to the access flap [79].

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Fig. 6.11  Radiograph 6 months post-surgery, not formation of slightly radiopaque nodule in middle portion on the distal aspect of the lateral incisor, not related to the original bony defect

Fig. 6.13  Reentry of case, note healing of the defect on distal aspect of right lateral incisor and on the cuspid mesial aspect

EMD enhances gingival fibroblasts proliferation [80–85] and positively affects the inflammatory and healing responses by different cellular mechanisms [86, 87].

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Fig. 6.12  Radiograph 2  years post-surgery, note radiopaque tissue formation in distal aspect of lateral incisor combined with fill of the bony defect

Fig. 6.14  Periodontal probe on mesial aspect of upper right lateral incisor illustrates extent of hard tissue fill of the original defect, as compared to aspect in Fig. 6.9

Patient characteristics, defect configuration, surgical technique, follow-up, and maintenance will determine clinical success of periodontal regenerative procedures.

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Fig. 6.15  A second reconstructive periodontal procedure with use of enamel matrix protein derivative was performed at the reentry

Fig. 6.16  Preoperative X-ray showed an intrabony defect in the mesial aspect of the first lower right molar

Fig. 6.17 Following initial preparation a remaining 10 mm periodontal pocket was evident

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Fig. 6.18  Following full-thickness flap elevation, thorough debridement was performed. An intrabony defect was evident, the defect had a single bony wall on most of its extension, while 2- and 3-wall defect was present in the most apical areas. Ten-­millimeter distance from most apical aspect of bony defect to the cemento-enamel junction is illustrated with a periodontal probe

Fig. 6.19  Enamel matrix protein derivative was applied on the denuded root surface filling the defect

Fig. 6.20  Enamel matrix protein derivative gel fills the bony defect

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Fig. 6.21  Bone graft in place Fig. 6.24  Sequence of radiographs shows gradual bone fill of the defect. 6 months postoperative

Fig. 6.22  The area was sutured to achieve primary soft tissue closure

Fig. 6.25  Radiograph 3 years post-surgery

Fig. 6.23 Immediate postoperative radiograph shows bone graft in place

Fig. 6.26  Radiograph 7 years post-surgery

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Fig. 6.27  Radiograph 20 years post-surgery

Fig. 6.28  Preoperative radiograph shows extensive periodontal destruction around the first upper left molar. Mesial and distal loss of periodontal support together with radiographic furcation involvement

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Fig. 6.30  During periodontal surgical procedure, following debridement, large periodontal tissue destruction and mesial furcation involvement may be clearly appreciated

Fig. 6.31  Following bone grafting, a non-resorbable, an ePTFE membrane has been adapted and sutured to isolate the periodontal defect preventing soft tissue ingrowth

Fig. 6.32  Four weeks after the procedure, the membrane collar is slightly exposed, with no signs of infection Fig. 6.29  A periodontal probe illustrates clinical attachment loss of approximately 9 mm together with bleeding upon probing

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Fig. 6.33  Six weeks postoperatively, after the first intervention, a second surgical procedure for membrane retrieval is performed

Fig. 6.34 Following membrane retrieval, the newly formed tissue underneath may be appreciated

Fig. 6.35  Postoperative aspect of the area. Note slight gingival recession

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Fig. 6.36  Postoperative radiograph, 6  months after the initial procedure. Note radiographic bone fill, mainly on the mesial aspect

Fig. 6.37  Postoperative radiograph, 1 year following the initial procedure. Note radiographic bone fill, covering also the mesial furcation entrance

Fig. 6.38  Postoperative radiograph, 3  years following the initial procedure. Note radiographic bone fill, even covering the mesial furcation entrance

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Fig. 6.39  Different angulation postoperative radiograph, 3 years following the initial procedure shows considerable gain of bone support on the first upper left molar

Fig. 6.41  Intraoperative aspect of right front teeth. Note large root exposure, with horizontal (suprabony) loss of periodontal bone support. Enamel matrix protein derivative was applied on the denuded root surfaces and soft tissues sutured to achieve primary closure

Fig. 6.42  Intraoperative aspect of left front teeth. Note horizontal (suprabony) loss of periodontal bone support, however, less extensive compared to the right side. Enamel matrix protein derivative was applied on the denuded root surfaces and soft tissues sutured to achieve primary closure

Fig. 6.40  Preoperative radiograph. Note extensive periodontal destruction around the upper incisors with a definitive horizontal pattern

6.4

Clinical Aspects

6.4.1 Patient Characteristics Although, most studies have reported a detrimental effect of cigarette smoking on clinical attachment level gain [2, 42, 48, 51, 62, 88–91], others

could not find significant difference between smokers and nonsmokers [29, 92, 93]. Impaired healing in diabetic patients may jeopardize results of periodontal regenerative surgery [94, 95]. Personality traits appear to play a significant role in determining the therapeutic outcomes of periodontal therapy [96].

6.4.2 Defect Configuration Defect morphology plays a major role in healing following periodontal reconstructive treatment. Although all intrabony defects may present a similar relative improvement following

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Fig. 6.43  Two years postoperative radiograph shows certain degree of bone repair, in spite of the horizontal architecture of the lost bone support

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Fig. 6.45  Nine  years postoperative radiograph shows further bone repair

Fig. 6.46  Clinical aspect of the area at the 9-year follow­up. Note minimal recession and no signs of inflammation, in spite of the initial extent of bone loss and large root surface exposure at the time of surgical treatment (Figs. 6.41 and 6.42)

Fig. 6.44  Six years postoperative radiograph shows further bone repair, in spite of the initial, mostly horizontal, loss of bone support

therapy, the depth of the defect intrabony component positively influences clinical attachment and bone gain [61, 97, 98]. Following regenerative periodontal therapy with EMD, larger relative CAL gains can be expected where a higher preoperative loss of attachment is present [29, 39, 42, 45, 48, 61, 62, 88, 93, 99]. Narrow (1–2  mm, as measured between the tooth root and the osseous wall) defects responded more

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Fig. 6.47  A pressure-sensitive probe illustrates a shallow, 3 mm, probing pocket depth on the mid-buccal aspect of the right central incisor

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Fig. 6.50  Preoperative radiograph shows large periodontal destruction around both lower right premolars. Horizontal bone loss pattern is evident

Fig. 6.48  Clinical aspect of the area at the 18-year follow-­up. Note stable results throughout time Fig. 6.51 Deep periodontal probing pocket depth on the mesial aspect of second premolar may be appreciated

favorably to EMD application than the wider (4–6 mm) ones [100, 101]. In GTR procedures, a negative correlation between the radiographic defect angle width of the intrabony defects and the regenerated probing attachment level was found. This correlation was positive between the intrabony defect depth and the relative CAL gain and bone fill [98, 102–105]. A narrow (equal or less than 22°) baseline radiographic defect angle of the intrabony defects is associated with higher CAL gains after regenerative surgery with EMD [106]. The number of residual bony walls is also correlated with the outcomes of different periodontal regenerative treatments [107] especially Fig. 6.49  18 years postoperative radiograph shows stable situation

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Fig. 6.52  Deep pocket depth on the distal aspect of first premolar as measured with a periodontal probe

Fig. 6.53  Intraoperative aspect of the area. Note mostly horizontal suprabony defect, with minimal 1-wall defects in the apical part, involving roots of both premolars

Fig. 6.54  Following root conditioning with EDTA in a neutral pH, enamel matrix protein derivative was applied on the denuded root surfaces and combined with a bone grafting material

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Fig. 6.55  Radiograph taken 1  year after the procedure, note bone fill of the interproximal defect between both premolars

Fig. 6.56  Radiograph taken 3 years after the procedure, note enhanced bone support

Fig. 6.57  Radiograph taken 10 years after the procedure, in spite of the initial, mostly suprabony defect, enhanced bone support is evident

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when bioresorbable barriers and amelogenins are applied [48, 61, 103]. For the treatment of deep, non-contained intrabony defects, EMD application, without a bone graft, resulted in lower PD reduction and CAL gain [108], questioning the suitability EMD without a bone graft for the treatment of defects with a nonsupporting anatomy as wide defects with missing bony walls. Influence of defect anatomy appears to be reduced, if stable flap designs and supportive biomaterials are applied (Figs.  6.58, 6.59, 6.60, 6.61, 6.62, 6.63, 6.64, 6.65, 6.66, 6.67, 6.68, and 6.69). These aspects will be discussed in following sessions concerning surgical technique: soft tissue considerations and combination therapies.

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Fig. 6.59  Fourteen millimeters probing pocket depth on mesial aspect of left central incisor is illustrated with a 15 mm length probe in place

6.4.3 Tooth Mobility Teeth with increased mobility and largely reduced periodontal support should be provisionally splinted to avoid spontaneous avulsion during the

Fig. 6.60  Intraoperative aspect of extensive combined supra and infrabony bone defect on mesial aspect of left central incisor. In the coronal aspect, a 1-wall defect, while in the apical part, 2–3-wall defect were present

Fig. 6.58  Preoperative radiograph. Note vertical bony defect in mesial aspect of left central incisor

Fig. 6.61  Intraoperative aspect of bone defect on mesial aspect of left central incisor. Periodontal probe illustrates extent of bony defect, with 15 mm from the most apical extent of bony defect to cemento-enamel junction

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Fig. 6.62 Following EMD application the area was grafted with a composite bone graft of mineralized allogeneic bone and calcium sulfate mixed with enamel matrix protein derivative to achieve a putty consistency

Fig. 6.64  Three years postoperative radiograph. Note improved bone healing in vertical bony defect in mesial aspect of central left incisor compared to preoperative and 1-year postoperative radiographs

Fig. 6.63  One-year postoperative radiograph. Note bone fill in bony defect in mesial aspect of central left incisor

surgical procedure or immediately afterwards and/or discomfort to the patient during the immediate postsurgical period [52]. Tooth mobility has long been considered an important factor for periodontal regeneration [109]. Increased tooth mobility is negatively and dose-dependently

Fig. 6.65 Four years postoperative radiograph. Note continuous improved bone healing in vertical bony defect in mesial aspect of central left incisor

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Fig. 6.66  Clinical aspect at 4 years posttreatment, certain gingival recession is evident, no clinical signs of inflammation

Fig. 6.69  Clinical aspect during reentry of the area with probe. Note extensive bone fill, with 7  mm hard tissue gain compared to intraoperative situation (Fig. 6.61)

associated with the clinical outcomes of regeneration [110]. Teeth with baseline mobility of less than 1  mm horizontally may be successfully treated by periodontal regeneration. Severe, uncontrolled tooth mobility, especially vertical tooth mobility, negatively affects periodontal regeneration outcomes [111].

6.5

Surgical Technique

6.5.1 Soft Tissue Considerations Fig. 6.67 Pressure-sensitive probe illustrates shallow probing pocket depth on mesial aspect of tooth 21

Fig. 6.68  Clinical aspect during reentry of the area 4 years postoperatively. Note large healing of the defect compared to situation at treatment time

Soft tissue management is one of the most important factors for successful outcome of periodontal regenerative surgical treatments. Initially, flap designs were based in conventional periodontal procedures, later on, techniques evolved towards soft tissue preservation to achieve and maintain passive primary closure together with optimal wound stability over the reconstructive materials, which is critical especially during the initial healing stages [101, 112]. Papilla preservation, modified papilla preservation, simplified papilla preservation, entire papilla preservation, and the single-flap approach procedures have been suggested and evaluated for soft tissue management. The papilla preservation technique is based on an access flap created by an intrasulcular incision at buccal, palatal, and proximal sides; the inci-

6  Modern Clinical Procedures in Periodontal Reconstructive Treatment

sion on the palatal side includes a semicircular incision at the palatal base of the papilla. Soft tissue is then pushed with a blunt instrument through interdental space and lifted together with the buccal flap [113]. The modified papilla preservation technique is indicated only where the interdental space is at least 2 mm [48, 114–116] and is based on buccal and palatal intrasulcular incisions, the buccal flap is delineated with an horizontal incision with a slight internal bevel at the base of the buccal side of the papilla. The buccal full-thickness flap is elevated without the interproximal tissue, a buccal horizontal incision at the base of the interproximal supra crestal connective tissue detaches the interdental tissues that are lifted together with a full-thickness palatal flap. A buccal periosteal incision may be performed to increase buccal flap mobility, thus allowing tension-free primary soft tissue closure while, at the same time, increasing the space for regeneration mainly in the ­interdental area. Suturing is performed with a double-­layer technique following coronally flaps repositioning. The modified papilla preservation technique may be successfully applied in conjunction with barriers, biologically active materials, growth factors, and bone-replacement grafts [48, 115–118]. Due to reduced gingival recession, this type of procedure results in improved clinical outcomes compared to conventional flap approaches without interdental soft tissue preservation [89, 90]. The simplified papilla preservation is indicated where the interdental space, as measured at the level of the supracrestal portion of the papilla, is less than 2  mm. The access is performed by intrasulcular buccal and palatal incisions, in the interdental area, an oblique incision, beginning at the gingival margin of the line angle and reaching the midpoint of the proximal tooth just below the contact point, the blade is kept parallel to the long axis of the tooth. A buccal full-thickness flap elevated, leaving the papilla in site. A bucco-lingual horizontal incision at the base of the papilla close to the bone crest detaches this area and a palatal full-thickness flap including the papilla is elevated.

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The entire papilla preservation provides access through an intrasulcular incision and a bevelled vertical releasing incision in the buccal gingiva of the interdental space, following a buccal flap elevation; an interdental tunnel is prepared by undermining of the defect-associated papilla. After granulation tissue is removed and root surfaces are carefully debrided, bone substitutes and enamel matrix derivative may be applied. This surgical approach improves blood clot stabilization, therefore reducing the risk of wound failure, particularly in the early healing phases [119]. When a defect may be reached through a minimal buccal window access, the modified minimally invasive surgical technique can be applied [117, 118, 120]. The minimally invasive approach is suitable for single and multiple intrabony defects treatment in conjunction with biologically active agents that may be combined with grafting materials [121]. According to the dimensions of the interdental spaces, the access to the defect-associated interdental papilla may be achieved either with the simplified papilla preservation [114] or with the modified papilla preservation flap [89, 90]. After elevation of the interdental tissues, the buccal and the lingual incisions are slightly extended mesio-distally and reduced full-thickness flaps are elevated to expose only the coronal edges of the residual bony walls. No periosteal and/or vertical releasing incisions are performed and primary soft tissue closure is achieved with a single internal modified mattress suture, if necessary, additional sutures may be placed [117, 118]. The modified minimally invasive surgical technique [120] improves flap stability, access to the defect is gained through a reduced interdental buccal triangular flap, while the papilla is left in place; the granulomatous tissue is sharply dissected and removed from the papillary supracrestal connective tissue and from the bony walls and root surface is debrided. The reduced size of the wound and minimal flap elevation allows for preservation of most of the blood supply to the interdental tissue with enhanced wound healing. A single internal modified mattress suture repo-

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sitions the flap, while additional sutures may be applied, if necessary. The reduced buccal access does not allow for instrumentation of difficult to reach diseased root surfaces [120]. Microsurgery instruments as well as magnification tools are needed to develop these type of techniques. The minimally invasive surgical technique combined with bioactive materials has shown a very low rate of postoperative complications [121, 122]. The single-flap approach provides access to the surgical site by elevation of a single, either buccal or lingual/palatal (as assessed by preoperative bone sounding), full-thickness flap [123–128]. The interproximal supracrestal gingival tissues are left intact, allowing for an easy flap repositioning with stable primary wound closure. Increased post-surgery gingival recession usually occurs where deep intraosseous are associated with buccal dehiscence defects. The combination of a bioactive agent and a graft material together with a single-flap approach may limit postoperative gingival recession [123, 124, 126–128].

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In most defect types, application of bone grafting material together with EMD or human platelet-derived growth factor-BB led to additional clinical improvements in CAL gain and PD reduction compared with those obtained with the biologically active agent alone [129–131]. However, while the ­combination of EMD with some bone grafting materials favored periodontal regeneration, others showed no additional benefit when compared to EMD or even to the bone graft application alone [134–145]. The possibility that the bone graft could act as a reservoir and allow for a slow release of an inductive compound has been suggested [52, 146–148]. There is still no definite answer regarding the most appropriate filler to apply with EMD [49]. Periodontal regeneration is the full reconstitution of the lost periodontal support; therefore, application of non-resorbable biomaterials (such as most xenografts) will not lead to true periodontal regeneration. Several different bone grafting materials have been evaluated, such as autogenous bone [149, 150], bovine bone mineral [144, 151–155], bone allograft [156–158], bioactive glass [136, 159, 160], tri-calcium phosphate [151] 6.5.2 Combination Therapies and calcium sulfate [52, 161] (Figs.  6.58, 6.59, 6.60, 6.61, 6.62, 6.63, 6.64, 6.65, 6.66, 6.67, 6.68, Combination therapy refers to the simultaneous and 6.69) and bi-phase bone ceramic [162–164]. application of various periodontal reconstructive Results with bovine bone mineral have been contreatment alternatives to obtain an additive effect. troversial [137, 165–167]. Addition of bioactive This approach may lead to assemblage of differ- glass [92] and bi-phase bone ceramic [162–164] ent regenerative principles, such as conductivity to EMD did not enhance clinical results. Among and inductivity, space provision and wound stabil- all possibilities, the suitable bone graft for each ity, matrix development and cell differentiation. clinical situation should be chosen according to EMD alone, as single therapy, may be applied the dimension of the bone defect (e.g., large parmainly in narrow defects with a prevalent three-­ ticles are not convenient for small defects), histowall morphology or in well-supported two-wall logical (leading to true periodontal regeneration) defects, biomaterials provide soft tissue sup- and clinical evidence for success, and manipulaport, especially in non-self-contained defects tion characteristics. (Figs.  6.53 and 6.60). A large access flap may not provide proper wound stability, which may be achieved with barriers or fillers, combinations 6.5.3 Free Connective Tissue Grafts in Periodontal Regenerative of barriers and fillers, or combinations of ameloProcedures genins and fillers. The combination of a graft biomaterial with biological agents, including EMD, may reduce the post-surgery recession following Another type of combination therapy is the surgical treatment accessed with the single-flap application of autogenous connective tissue approach [125]. grafts during periodontal reconstructive treatment

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with EMD (Figs.  6.70, 6.71, 6.72, 6.73, 6.74, 6.75, 6.76, 6.77, 6.78, 6.79, 6.80, 6.81, 6.82, 6.83, 6.84, 6.85, 6.86, 6.87, 6.88, and 6.89) [168, 169]. Histological evaluation of combining a connective tissue graft with EMD in humans has shown varying results, including also formation of new cementum, new attachment, and new bone after treatment [170, 171]. EMD has an enhancing effect on gingival fibroblasts, by increasing up to two-fold both their proliferation and amount of matrix produced by these cells [80–85] and positively affecting the inflammatory and healing responses by different cellular mechanisms [86, 87]. Thus, besides the possible periodontal regeneration induction on the denuded root surface, EMD will also enhance the vitality of the free connective tissue graft. During periodontal reconstructive surgery, in cases with minimal amounts of keratinized tissue, a connective tissue can be applied after EMD application onto the denuded root surfaces [52]. This procedure is likely to reduce postoperative gingival recession and increase the keratinized tissue in the area (Figs. 6.70, 6.71, 6.72, 6.73, 6.74, 6.75, 6.76, 6.77, 6.78, 6.79, 6.80, 6.81, 6.82, 6.83, 6.84, 6.85, 6.86, 6.87, 6.88, and 6.89). The beneficial effect of CTG may partly reside in the increase in gingival thickness. Thick gingival tissues show greater resistance to recession due to surgical trauma and tissue remodeling following different surgical procedures, including reconstructive surgery. It may also be

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Fig. 6.71  Preoperative radiograph of lower anterior area showing reduced bone support, with mainly horizontal bone loss

Fig. 6.72  Intraoperative aspect, all four lower incisors present extensive root exposure due to advanced horizontal bone loss

Fig. 6.70  Preoperative aspect of lower incisors presenting thin gingival biotype, gingival recession, minimal attached and keratinizing gingiva width, muscle and frenum pull

speculated that the conversion from a thin to a thick phenotype may have a beneficial effect on the long-term stability of the gingival profile, since thick biotypes were shown less prone to develop gingival recessions [172, 173]. The single-flap approach may be combined with an autologous soft tissue graft [168, 172, 173]. Improved clinical outcomes in terms

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Fig. 6.73  EMD was applied onto denuded root surfaces

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Fig. 6.76  One year postoperative aspect of lower anterior area. Note gingival aspect, with minimal recession compared to preoperative aspect, increased attached and keratinizing gingival width, with no frenum and muscle pull

Fig. 6.74  Connective tissue graft secured on top of the denuded root surfaces, after EMD application

Fig. 6.75 Buccal flap was coronally advanced and sutured after the combination therapy procedure consisting of periodontal reconstructive treatment with a connective tissue graft

Fig. 6.77  Two years postoperative radiograph, in spite of horizontal preoperative bone defects, certain bone gain can be appreciated

of defect resolution, reduction of postoperative gingival recession (or even root coverage), and increase in gingival dimensions in addition to a substantial CAL gain especially at deep intraosseous lesions associated with buccal bone dehiscences, also at challenging

intraosseous defects associated with Miller’s class IV gingival recession have been reported [52, 168, 172, 173] (Figs.  6.70, 6.71, 6.72, 6.73, 6.74, 6.75, 6.76, 6.77, 6.78, 6.79, 6.80, 6.81, 6.82, 6.83, 6.84, 6.85, 6.86, 6.87, 6.88, and 6.89).

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Fig. 6.78  Two years postoperative aspect of lower anterior area. Note improved gingival aspect, certain degree of root coverage together with increased attached and keratinizing gingival width

Fig. 6.80  Preoperative radiograph of lower anterior area shows reduced bone support in all incisors, with a deep vertical defect on the mesial aspect of the central left incisor Fig. 6.79  Preoperative aspect of lower incisors presenting thin gingival biotype. Note left central incisor with advanced buccal gingival recession together with absence of attached and keratinizing gingiva

The adjunctive use of a CTG unavoidably results in a more technically demanding procedure and increases the intra- and postoperative morbidity due to the need for an additional surgical site for graft harvesting. The addition of connective tissue grafts to periodontal reconstructive surgical procedures seems to be particularly beneficial at defects with thin gingival tissues and severe buccal bone dehiscence, usually in the lower anterior area, however, of limited relevance in thick biotypes and shallow buccal dehiscences. The stability of the buccal gingival profile becomes more important particularly in estheti-

Fig. 6.81  Intraoperative aspect following elevation of a single buccal flap and debridement. Note largely exposed root surface of the left central incisor

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Fig. 6.82  EMD was applied on the denuded root surfaces and surrounding hard tissues

Fig. 6.85  One year postoperative radiograph, bone healing, mainly on the mesial aspect of the central left incisor can be appreciated

Fig. 6.83  Connective tissue graft secured on top of the denuded root surfaces of the central incisors, after EMD application

Fig. 6.86  One year postoperative aspect of lower anterior area. Note gingival aspect, with root coverage on central left incisor, enhanced attached and keratinized gingiva width

Fig. 6.84 Buccal flap was coronally advanced and sutured covering the connective tissue graft

cally sensitive areas [172] (Figs. 6.70, 6.71, 6.72, 6.73, 6.74, 6.75, 6.76, 6.77, 6.78, 6.79, 6.80, 6.81, 6.82, 6.83, 6.84, 6.85, 6.86, 6.87, 6.88, and 6.89).

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Fig. 6.89  Three years postoperative aspect of lower anterior area. Note gingival aspect, with root coverage on central left incisor, increased attached and keratinizing gingival width

6.6

Fig. 6.87  Two years postoperative radiograph, further bone healing, mainly on the mesial aspect of the central left incisor can be appreciated

Fig. 6.88  Three years postoperative radiograph, note further healing and improved bone support

Follow-Up and Maintenance

Clinical outcomes obtained with periodontal regeneration can be preserved on a long-term basis, provided supportive periodontal treatment is regularly performed (Figs.  6.16, 6.17, 6.18, 6.19, 6.20, 6.21, 6.22, 6.23, 6.24, 6.25, 6.26, and 6.27). Both GTR (Figs.  6.90, 6.91, 6.92, 6.93, 6.94, 6.95, 6.96, 6.97, 6.98, 6.99, 6.100, 6.101, 6.102, 6.103, and 6.104) and EMD (Figs.  6.40, 6.41, 6.42, 6.43, 6.44, 6.45, 6.46, 6.47, 6.48, and 6.49) result in outcomes that can be maintained over long periods [68, 174, 175, 176, 177]. Results from controlled clinical studies have shown that the stability of gained clinical attachment following conventional and reconstructive periodontal therapy is dependent upon stringent oral hygiene and compliance with a maintenance periodontal care program [72, 178]. Following regenerative periodontal treatment, it is imperative that the patient be monitored and kept on high standards of oral hygiene, with regular maintenance visits. Patients that suffer from severe periodontal disease are more prone to newly develop the disease than similar cohorts that never suffered from periodontitis [179], especially if maintenance is not adequate. Furthermore, since regions with advanced peri-

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odontal breakdown within a certain patient are those usually treated by reconstructive therapy, it seems that those sites will be most susceptible for relapse and new breakdown. This seems to be host dependent, since, in experimental periodontal lesions in laboratory animals, it was shown that the periodontal attachment apparatus regenerated is not more susceptible to periodontal breakdown than the original, pristine, periodontium.

6.7

Endodontic-Periodontal Lesions

Combined endodontic and periodontal lesions, with a primary periodontal etiology, will not heal with only endodontic therapy [180]. In these cases, even after proper intra-canal treatment has been successfully completed, little or no periodontal healing might result (Figs. 6.90, 6.91, 6.92, 6.93, 6.94, 6.95, 6.96, 6.97, 6.98, 6.99, 6.100, 6.101, 6.102, 6.103, and 6.104). After endodontic therapy is concluded, and in the presence of periodontal involvement, reconstructive periodontal therapy is indicated (Figs.  6.90, 6.91, 6.92, 6.93, 6.94, 6.95, 6.96, 6.97, 6.98, 6.99, 6.100, 6.101, 6.102, 6.103, and 6.104). In combined endodontic-periodontal lesions, teeth usually present severe destruction of supporting tissues beyond the apex, thus considered as having a hopeless prognosis [89, 90]. Several case series have shown that it is possible to change the prognosis of teeth affected by combined endodontic-­periodontal lesions, even if the periodontal support is destroyed beyond the apex. Teeth with hopeless prognoses affected by combined endodontic-periodontal lesions beyond the apex have been treated and maintained for over 5 years after surgical treatment that included both endodontic and regenerative periodontal treatment. Most of the treated teeth had a periodontal lesion exceeding the apex of the tooth and involving three to four sides of the root. The application of reconstructive therapy can change the prognosis of hopeless teeth into

Fig. 6.90  Preoperative radiograph. Note large periodontal-­endodontal bone defect in right cuspid. Lateral incisor presents largely reduced bone support

Fig. 6.91  Fifteen millimeters probing pocket depth were measured on distal aspect of the cuspid

maintainable units even in extreme conditions [181] (Figs.  6.90, 6.91, 6.92, 6.93, 6.94, 6.95, 6.96, 6.97, 6.98, 6.99, 6.100, 6.101, 6.102, 6.103, and 6.104). It is difficult to clearly estab-

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Fig. 6.94  Intraoperative occlusal view during periodontal reconstructive surgical treatment. Large periodontal destruction around the cuspid involves three (buccal, distal, and palatal) of the four root aspects

Fig. 6.92  Certain bone healing may be appreciated in the periapical radiograph after endodontal re-treatment

Fig. 6.95 Following bone grafting, non-resorbable e-PTFE barrier membranes were adapted and sutured around the cuspid and first molar

Fig. 6.93  Intraoperative buccal aspect following through debridement. Large periodontal destruction, especially on distal aspect of the cuspid is evident

lish which teeth will not respond to periodontal treatment and should, therefore, be extracted [104, 115, 116]. Treatment outcome in these cases is not predictable and patients shall be willing to invest time, suffering, treatment morbidity, and costs in spite of these unforeseeable

Fig. 6.96 Occlusal view shows the non-resorbable e-PTFE barrier membranes in place

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Fig. 6.99  Pressure-sensitive probe on distal aspect of cuspid shows a relatively shallow probing pocket depth as compared to the preoperative situation (Fig. 6.91)

Fig. 6.97  One year postoperative radiograph. Note healing of bony defect around the cuspid and improved bone support of lateral incisor

Fig. 6.100  Five years postoperative radiograph. Note further healing of bony defect around the cuspid and improved bone support of lateral incisor

Fig. 6.98  Five years clinical aspect. Prosthetic reconstruction was performed with supra-gingival margins. Lack of clinical signs of gingival inflammation is evident

results. It should be emphasized that certain teeth may have to be extracted even after ­treatment. Modern endodontic techniques and advanced reconstructive periodontal treatment

make possible to improve prognosis and maintain the tooth/teeth on a long-term basis [182]. Experts’ clinical opinion when handling theses perio-endo cases might indicate performing the surgical periodontal treatment immediately after completing the endodontic treatment, to avoid root canals reinfection from the periodontal pathogenic flora.

6  Modern Clinical Procedures in Periodontal Reconstructive Treatment

Fig. 6.101  Ten years postoperative radiograph. Note stable bone support around right cuspid, even improved throughout time

Fig. 6.102  Clinical aspect of the upper right area 10 years post-surgical procedure clinical. Gingival recession on buccal aspect of cuspid is evident, however, stable throughout time

6.8

Conclusions

This chapter reviews several aspects of reconstructive periodontal procedures. Even when periodontal attachment level is largely reduced,

115

Fig. 6.103  Fifteen years postoperative radiograph. Note stable bone support of cuspid and lateral incisor

Fig. 6.104  Clinical aspect of upper right area 15  years postsurgical procedure, proper maintenance and lack of clinical signs of gingival inflammation are key factors for long-term stability

natural dentition yields better long-term survival rate and marginal bone level changes compared with dental implants. Patient characteristics, surgical procedure, defect morphology, and soft tissue management are some of the most important factors for successful outcome of periodontal regenerative surgical treatments.

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C. E. Nemcovsky and J. Nart 113. Takei HH, Han TJ, Carranza FA Jr, Kenney EB, Lekovic V.  Flap technique for periodontal bone implants. Papilla preservation technique. J Periodontol. 1985;56(4):204–10. 114. Cortellini P, Pini-Prato G, Tonetti M. The simplified papilla preservation flap. A novel surgical approach for the management of soft tissues in regenerative procedures. Int J Periodontics Restorative Dent. 1999;19:589–99. 115. Tonetti MS, Cortellini P, Lang NP, Suvan JE, Adriaens P, Dubravec D, Fonzar A, Fourmousis I, Rasperini G, Rossi R, Silvestri M, Topoll H, Wallkamm B, Zybutz M. Clinical outcomes following treatment of human intrabony defects with GTR/ bone replacement material or access flap alone. A multicenter randomized controlled clinical trial. J Clin Periodontol. 2004;31:770–6. 116. Tonetti MS, Fourmousis I, Suvan J, Cortellini P, Bragger U, Lang NP, European Research Group on Periodontology (ERGOPERIO). Healing, post-­ operative morbidity and patient perception of outcomes following regenerative therapy of deep intrabony defects. J Clin Periodontol. 2004;31:1092–8. 117. Cortellini P, Tonetti MS.  A minimally invasive surgical technique (MIST) with enamel matrix derivate in the regenerative treatment of intrabony defects: a novel approach to limit morbidity. J Clin Periodontol. 2007;34:87–93. 118. Cortellini P, Tonetti MS. Minimally invasive surgical technique (M.I.S.T.) and enamel matrix derivative (EMD) in intrabony defects. (I) Clinical outcomes and intra-operative and post-operative morbidity. J Clin Periodontol. 2007;34:1082–8. 119. Aslan S, Buduneli N, Cortellini P.  Entire papilla preservation technique in the regenerative treatment of deep intrabony defects: 1-Year results. J Clin Periodontol. 2017;44(9):926–32. https://doi. org/10.1111/jcpe.12780. 120. Cortellini P, Tonetti MS.  Improved wound stability with a modified minimally invasive surgical technique in the regenerative treatment of isolated interdental intrabony defects. J Clin Periodontol. 2009;36:157–63. 121. Cortellini P, Nieri M, Pini Prato GP, Tonetti MS.  Single minimally invasive surgical technique (MIST) with enamel matrix derivative (EMD) to treat multiple adjacent intrabony defects. Clinical outcomes and patient morbidity. J Clin Periodontol. 2008;35:605–13. 122. Ribeiro FV, Casarin RC, Palma MA, Junior FH, Sallum EA, Casati MZ. Clinical and patient-centered outcomes after minimally invasive non-surgical or surgical approaches for the treatment of intrabony defects: a randomized clinical trial. J Periodontol. 2011;82:1256–66. 123. Farina R, Simonelli A, Minenna L, Rasperini G, Trombelli L. Approach in combination with enamel matrix derivative in the treatment of periodontal intraosseous defects. Int J Periodontics Restorative Dent. 2014;34:497–506.

6  Modern Clinical Procedures in Periodontal Reconstructive Treatment 124. Farina R, Simonelli A, Rizzi A, Pramstraller M, Cucchi A, Trombelli L.  Early postoperative healing following buccal single flap approach to access intraosseous periodontal defects. Clin Oral Investig. 2013;17:1573–83. 125. Farina R, Simonelli A, Minenna L, Rasperini G, Schincaglia GP, Tomasi C, Trombelli L.  Change in the gingival margin profile after the single flap approach in periodontal intraosseous defects. J Periodontol. 2015;86:1038–46. https://doi. org/10.1902/jop.2015.150040. 126. Schincaglia GP, Hebert E, Farina R, Simonelli A, Trombelli L.  Single versus double flap approach in periodontal regenerative procedures. J Clin Periodontol. 2015;42:557–66. 127. Trombelli L, Farina R, Franceschetti G, Calura G. Single-flap approach with buccal access in periodontal reconstructive procedures. J Periodontol. 2009;80:353–60. 128. Trombelli L, Simonelli A, Schincaglia GP, Cucchi A, Farina R. Single-flap approach for surgical debridement of deep intraosseous defects: a randomized controlled trial. J Periodontol. 2012;83:27–35. 129. Matarasso M, Iorio-Siciliano V, Blasi A, Ramaglia L, Salvi GE, Sculean A.  Enamel matrix derivative and bone grafts for periodontal regeneration of intrabony defects. A systematic review and meta-­ analysis. Clin Oral Investig. 2015;19(7):1581–93. https://doi.org/10.1007/s00784-015-1491-7. 130. Tu Y-K, Woolston A, Faggion CM Jr. Do bone grafts or barrier membranes provide additional treatment effects for infrabony lesions treated with enamel matrix derivatives? A network meta-analysis of randomizedcontrolled trials. J Clin Periodontol. 2010;37:59–79. 131. Tu YK, Needleman I, Chambrone L, Lu HK, Faggion CM Jr. A Bayesian network meta-analysis on comparisons of enamel matrix derivatives, guided tissue regeneration and their combination therapies. J Clin Periodontol. 2012;39(3):303–14. 132. Guida L, Annunziata M, Belardo S, Farina R, Scabbia A, Trombelli L.  Effect of autogenous cortical bone particulate in conjunction with enamel matrix derivative in the treatment of periodontal intraosseous defects. J Periodontol. 2007;78:231–8. https://doi.org/10.1902/jop.2007.060142. 133. Gurinsky BS, Mills MP, Mellonig JT. Clinical evaluation of demineralized freeze-dried bone allograft and enamel matrix derivative versus enamel matrix derivative alone for the treatment of periodontal osseous defects in humans. J Periodontol. 2004;75:1309– 18. https://doi.org/10.1902/jop.2004.75.10.1309. 134. Kuru B, Yilmaz S, Argin K, Noyan U.  Enamel matrix derivative alone or in combination with a bioactive glass in wide intrabony defects. Clin Oral Investig. 2006;10:227–34. https://doi.org/10.1007/ s00784-006-0052-5. 135. Lekovic V, Camargo PM, Weinlaender M, Nedic M, Aleksic Z, Kenney EB.  A comparison between enamel matrix proteins used alone or in combination with bovine porous bone mineral in the treat-

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122 bone formation in mouse hind leg muscles induced by native reindeer bone morphogenetic protein. Arch Orthop Trauma Surg. 2005;125(1):10–5. 146. Urist MR, Lietze A, Dawson E.  Beta-tricalcium phosphate delivery system for bone morphogenetic protein. Clin Orthop Relat Res. 1984;187:277–80. 147. Cochran DL, Jones A, Heijl L, Mellonig JT, Schoolfield J, King GN. Periodontal regeneration with a combination of enamel matrix proteins and autogenous bone grafting. J Periodontol. 2003;74(9):1269–81. 148. Trombelli L, Annunziata M, Belardo S, Farina R, Scabbia A, Guida L. Autogenous bone graft in conjunction with enamel matrix derivative in the treatment of deep periodontal intra-osseous defects: a report of 13 consecutively treated patients. J Clin Periodontol. 2006;33(1):69–75. 149. Döri F, Arweiler N, Gera I, Sculean A.  Clinical evaluation of an enamel matrix protein derivative combined with either a natural bone mineral or beta-tricalcium phosphate. J Periodontol. 2005;76(12):2236–43. 150. Lekovic V, Camargo PM, Weinlaender M, Kenney EB, Vasilic N.  Combination use of bovine porous bone mineral, enamel matrix proteins, and a bioabsorbable membrane in intrabony periodontal defects in humans. J Periodontol. 2001;72:583–9. 151. Lekovic V, Camargo PM, Weinlaender M, Vasilic N, Djordjevic M, Kenney EB.  The use of bovine porous bone mineral in combination with enamel matrix proteins or with an autologous fibrinogen/ fibronectin system in the treatment of intrabony periodontal defects in humans. J Periodontol. 2001;72:1157–63. 152. Pietruska MD.  A comparative study on the use of Bio-Oss and enamel matrix derivative (Emdogain) in the treatment of periodontal bone defects. Eur J Oral Sci. 2001;109:178–81. 153. Sculean A, Windisch P, Keglevich T, Chiantella GC, Gera I, Donos N. Clinical and histologic evaluation of human intrabony defects treated with an enamel matrix protein derivative combined with a bovine-derived xenograft. Int J Periodont Rest Dent. 2003;23:47–55. 154. Boyan BD, Ranly DM, Schwartz Z. Use of growth factors to modify osteconductivity of demineralized bone allografts: lessons for tissue engineering of bone. Dent Clin N Am. 2006;50(2):217–28. 155. Boyan BD, Weesner TC, Lohmann CH, Andreacchio D, Carnes DL, Dean DD, et al. Porcine fetal enamel matrix derivative enhances bone formation induced by demineralized freeze dried bone allograft in vivo. J Periodontol. 2000;71:1278–86. 156. Rosen PS, Reynolds MA. A retrospective case series comparing the use of demineralized freeze-dried bone allograft and freeze-dried bone allograft combined with enamel matrix derivative for the treatment of advanced osseous lesions. J Periodontol. 2002;73:942–9. 157. Hattar S, Asselin A, Greenspan D, Oboeuf M, Berdal A, Sautier JM.  Potential of biomimetic surfaces to

C. E. Nemcovsky and J. Nart promote in vitro osteoblast-like cell differentiation. Biomaterials. 2005;26(8):839–48. 158. Sculean A, Windisch P, Keglevich T, Gera I. Clinical and histologic evaluation of an enamel matrix protein derivative combined with a bioactive glass for the treatment of intrabony periodontal defects in humans. Int J Periodontics Restorative Dent. 2005;25(2):139–47. 159. Orsini M, Orsini G, Benlloch D, Aranda JJ, Sanz M.  Long-term clinical results on the use of bone-­ replacement grafts in the treatment of intrabony periodontal defects. Comparison of the use of autogenous bone graft plus calcium sulfate to autogenous bone graft covered with a bioabsorbable membrane. J Periodontol. 2008;79(9):1630–7. https://doi. org/10.1902/jop.2008.070282. 160. Hoffmann T, Al-Machot E, Meyle J, Jervøe-Storm PM, Jepsen S.  Three-year results following regenerative periodontal surgery of advanced intrabony defects with enamel matrix derivative alone or combined with a synthetic bone graft. Clin Oral Investig. 2016;20(2):357–64. https://doi.org/10.1007/ s00784-015-1522-4. 161. Losada M, González R, Garcia ÀP, Santos A, Nart J.  Treatment of non-contained infrabony defects with enamel matrix derivative alone or in combination with biphasic calcium phosphate bone graft: a 12-month randomized controlled clinical trial. J Periodontol. 2017;88(5):426–35. https://doi. org/10.1902/jop.2016.160459. 162. Pietruska M, Pietruski J, Nagy K, Brecx M, Arweiler NB, Sculean A.  Four-year results following treatment of intrabony periodontal defects with an enamel matrix derivative alone or combined with a biphasic calcium phosphate. Clin Oral Investig. 2012;16(4):1191–7. https://doi.org/10.1007/ s00784-011-0611-2. 163. Camargo PM, Lekovic V, Weinlaender M, Vasilic N, Kenney EB, Madzarevic M.  The effectiveness of enamel matrix proteins used in combination with bovine porous bone mineral in the treatment of intrabony defects in humans. J Clin Periodontol. 2001;28:1016–22. 164. Scheyer ET, Velasquez-Plata D, Brunsvold MA, Lasho DJ, Mellonig JT. A clinical comparison of a bovine-derived xenograft used alone and in combination with enamel matrix derivative for the treatment of periodontal osseous defects in humans. J Periodontol. 2002;73:423–32. 165. Sculean A, Chiantella GC, Windisch P, Gera I, Reich E.  Clinical evaluation of an enamel matrix protein derivative (Emdogain) combined with a bovine-­ derived xenograft (Bio-Oss) for the treatment of intrabony periodontal defects in humans. Int J Periodont Rest Dent. 2002;22:259–67. 166. Nemcovsky CE, Beitlitum I.  Combination therapy for reconstructive periodontal treatment in the lower anterior area: clinical evaluation of a case series. Dent J (Basel). 2018;6(4):E50. https://doi. org/10.3390/dj6040050.

6  Modern Clinical Procedures in Periodontal Reconstructive Treatment 167. Sato S, Yamada K, Takashi K, Kotaro H, Koichi I.  Treatment of Miller class III recessions with enamel matrix derivative (Emdogain) in combination with subepithelial connective tissue grafting. Int J Periodontics Restorative Dent. 2006;26:71–7. 168. Carnio J, Camargo PM, Kenney EB, Schenk RK. Histological evaluation of 4 cases of root coverage following a connective tissue graft combined with an enamel matrix derivative preparation. J Periodontol. 2002;73:1534–43. 169. Rasperini G, Silvestri M, Schenk RK, Nevins ML.  Clinical and histologic evaluation of human gingival recession treated with a subepithelial connective tissue graft and enamel matrix derivative (Emdogain): a case report. Int J Periodontics Restorative Dent. 2000;20:269–75. 170. Trombelli L, Simonelli A, Minenna L, Rasperini G, Farina R. Effect of a connective Tissue graft in combination with a single flap approach in the regenerative treatment of intraosseous defects. J Periodontol. 2017;88(4):348–56. https://doi.org/10.1902/ jop.2016.160471. 171. Zucchelli G, Mazzotti C, Tirone F, Mele M, Bellone P, Mounssif I. The connective tissue graft wall technique and enamel matrix derivative to improve root coverage and clinical attachment levels in Miller Class IV gingival recession. Int J Periodontics Restorative Dent. 2014;34:601–9. 172. Heden G, Wennström JL.  Five-year follow-up of regenerative periodontal therapy with enamel matrix derivative at sites with angular bone defects. J Periodontol. 2006;77(2):295–301. 173. McClain PK, Schallhorn RG.  Long-term assessment of combined osseous composite grafting, root conditioning, and guided tissue regeneration. Int J Periodont Rest Dent. 1993;13:9–27.

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7

VRF as an Endodontic Periodontal Lesion Spyros Floratos, Aviad Tamse, and Shlomo Elbahary

7.1

Introduction

Vertical root fracture (VRF) is a root canal treatment complication and probably the third reason for extraction of endodontically treated teeth [1]. The etiology of this complication is multifactorial, and the end result is always similar—an inflammatory process in the supporting tissues resulting in an endodontic-periodontal lesion and bone loss [2]. This complication of an endodontically treated tooth is often vexing and frustrating both for the dentist and for the patient alike, because often it is difficult to diagnose accurately and in most cases the tooth or the involved root has to be extracted [3]. These root fractures usually mimic other dental pathological conditions. Signs and symptoms, like dull pain or pain on mastication, mobility, presence of a sinus tract, deep probing defects, a periodontal-type abscess, and periapical radiolucencies, are often similar to those found in poor outcome of an endodontic treatment or mimic periodontal disease [3]. An inaccurate and/or delayed diagnosis can lead to inappropriate management and the perS. Floratos Department of Endodontics, University of Pennsylvania, Philadelphia, PA, USA A. Tamse (*) · S. Elbahary Department of Endodontology, Tel Aviv University, Tel Aviv, Israel e-mail: [email protected]

sistence of the endodontic periodontal lesion. Therefore, the need for meticulous clinical and radiographic examination coupled with the relevant information from the tooth history is quite important. According to the AAE consensus statement [4], the combination of sinus tract and deep isolated probing defect in the endodontically treated tooth is pathognomonic for this entity; however, these signs do not coexist in many cases. The difficulties in achieving an accurate and timely VRF diagnosis will be elaborated in this chapter. It was shown, in 2010 [3], that there is no substantive evidence-based data concerning the diagnostic accuracy as to the effectiveness of clinical and radiographic evaluation of VRF diagnosis. To date, most published information on this topic is lower level of evidence studies, such as case reports, case series, or case control studies. The aim of this chapter is to present the best available evidence and the most updated information regarding the vertically fractured tooth as an endodontic-periodontal lesion.

7.2

Categorization, Susceptible Teeth, and Clinical Presentation

Vertical root fracture (VRF) is a frustrating complication of root canal treatment that leads most of the time to extraction [5]. VRFs usually involve

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restored endodontically treated teeth [6]. It was also shown that VRFs can occur in patients of Chinese origin in non-endodontically treated teeth [7]. Vertical root fractures are chronic longitudinally oriented fractures, with an apico-­ coronal direction. Study regarding reasons for extraction of endodontically treated teeth showed that the vertically fractured teeth amount to 11% of the extracted teeth [8]. VRFs can originate at any level along the root [4, 9] although it appears that they usually initiate at the apical part. If they originate in the middle part of the root, they can propagate in either direction, apical or coronal. From the horizontal aspect, the fractures originate in the root canal wall and extend to the root surface over time, and may involve either one side—buccal or lingual (incomplete) or both sides (complete fracture). For the most part, both the incomplete and complete fractures have a bucco-lingual pattern. Rarely does a VRF have a mesio-distal orientation [10]. Vertical root fracture is a slow dynamic process, and after an incomplete fracture is exposed to masticatory forces for a long time, it may propagate to become a complete fracture [11]. In multi-rooted teeth the fracture occurs mostly in one root (mostly mesial buccal root of the maxillary molar), but a fracture on both roots of the mandibular molar or the two buccal roots of the maxillary molar can also be seen. Although VRFs for the most part are longitudinal (vertical), they a

Fig. 7.1  Vertical root fracture of a mesial root of an endodontically treated mandibular molar. (a) A periapical radiograph reveals the radiolucent lesion around the two

do not always follow the root axis and may progress diagonally based on the bulkiness of the root, its curvature and the impact of occlusal forces (Fig. 7.1). Patient’s signs and symptoms of VRFs are similar to those of periodontal disease or failing endodontic treatment. In addition, they are usually diagnosed years after the endodontic and prosthodontic procedures have been completed [6]. The periodontal destruction resulting from the communication of the root canal space with the periodontium and its contamination is a slow process. Thus it may take a long time for the signs and symptoms to be clinically evident [11]. These findings lead to frustration both for the patient and for the dentist. An isolated deep probing pocket, sometimes all the way to the root apex practically facing the fracture line, is considered typical clinical sign for the bone loss in the vertically fractured root. However, it is not easy to demonstrate or diagnose this entity in all instances, especially early on in the inflammatory process. This manifestation of the probing defect is usually different than in a periodontally involved tooth. In the “true” periodontal cases, the pocket is initiated most of the time in the interproximal areas and the bone resorption is initiated in the crestal area. When the isolated bony defect in the suspected VRF tooth does exists, it is not easy sometimes to probe the pocket and patient discomfort can also be an issue. Administering local infiltration in the area can be helpful and is sometimes necessary. To achieve the accurate VRF diagnosis,

b

roots, the periapical area and in the bifurcation. (b) A diagonal fracture in the mesial root seen not following the root axis

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the probing finding should be coupled with other signs such as a sinus tract [4]. In VRF cases, the sinus tract is usually highly located in the attached gingiva as compared to a chronic apical abscess from a failing endodontically treated tooth [12]. However, even if there are some signs and symptoms in the VRF tooth that can sometimes differentiate this entity from periodontal or endodontic disease [3], in many cases the similarity in signs and symptoms between VRF and periodontalendodontic lesion may lead to misdiagnosis and incorrect treatment (Figs. 7.2 and 7.3 exhibit two cases which could be easily misdiagnosed as VRF or Endo-Perio lesion). a

The teeth and roots most susceptible to VRF are those in which their mesio-distal diameter in cross section is narrow compared to the bucco-­ lingual dimension (oval, hourglass shaped, kidney shaped, ribbon shaped). Such teeth and roots are the maxillary and mandibular premolars, the mesial root of mandibular molars, the mandibular anterior teeth, and mesio-buccal roots of the maxillary molars. From the apical-coronal aspect, the fracture can be limited to the apical area only, limited to the coronal part, both coronal and middle parts, limited only to the middle part of the root, or involving both the middle and apical parts.

b

c

Fig. 7.2  A mandibular molar was endodontically treated and coronally restored. (a) 10  years post op, the patient complained with “soreness on biting for the last couple of months in my lower left molar.” Upon examination, an 8 mm probing defect was detected on the mesio lingual root. The radiographs (a, b) revealed well-condensed canals with gutta-percha a wide metal post in the distal root and amalgam dowels in the mesial roots. An apical and lateral radiolucent area can be seen adjacent to the apical third of the mesial and distal roots. The diagnosis

d

could either be a VRF (deep probing, halo radiolucency, and a susceptible root) or a failing root canal treatment. The patients were offered with either to extract the tooth (assuming the mesial root was vertically fractured) or to perform endodontic surgery (assuming the radiolucency resulting from failed endodontic treatment). Endodontic surgery was performed on both roots and no detection of VRF could be noticed during surgery under operating microscope (c). One year post op (d) revealed complete healing

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a

c

b

d

Fig. 7.3  A 24-year-old patient complained about “draining pus from the gum” in the upper jaw. Clinical examination revealed a PFM crown in the second premolar that was endodontically treated and restored 5 years earlier (a, b). A highly located sinus tract was noted (b), but the probing numbers were between normal limits. Root canal treatment appeared adequate in the radiographs (a, b), but a large radiolucent area can be seen apical and laterally in

the mesial aspect of the premolar tooth (b). Poor outcome of the endodontic treatment in the maxillary premolar (chronic apical abscess) led to the treatment plan of endodontic surgery. Endodontic surgery was performed in this tooth. A VRF was noted in the buccal aspect (c, d), but it was of the incomplete type since it was not seen in the palatal aspect (c, d) (see black arrow)

Often when a VRF diagnosis of an endodontically treated root is made, all three thirds of the root are involved, i.e., from the tip of the root to the cervical part of the crown. Often the fracture is complete from the buccal to the lingual side [10].

Occasionally a VRF is confined only to the middle part of the root and not involving either the coronal or apical parts. In this case there is no communication with the marginal periodontium and no endodontic-periodontal lesion is formed, except the lateral bone loss that can be

7  VRF as an Endodontic Periodontal Lesion

detected at times in the radiographs or the CBCT (Fig.  7.2a, b). An isolated lateral radiolucency can be also the result of a lateral canal that was not detected during the root canal treatment, and therefore the accurate VRF diagnosis is confusing at times. When a tooth with VRF is extracted and a full length fracture is present, i.e., from the apical part to the cemento-dentinal junction, it is difficult to speculate whether the fracture originated in the coronal part of the root or even from the crown itself (Crown Originated Fracture) [13] and progressed apically or was it initiated in the apical part, and progressed coronally to the cementoenamel junction [14] (Fig. 7.3c). The correlation, retrospectively between the fractured tooth, the signs and symptoms and the radiographic features cannot be done in most cases, thus making it difficult to understand the pathogenesis of the VRF in specific cases. The susceptibility of restored endodontically treated teeth to vertical fractures has been discussed in literature [6, 15, 16]. Current endodontic procedures, such as root canal treatment and retreatment, necessitate the removal of dentin to accomplish the treatment. Such loss of tooth structure probably reduces a tooth’s resistance to fracture even when normal functional pressure during occlusion is applied. Identifying and reducing the risk factors for the vertical root fractures is necessary knowledge for the clinician [17]. Indeed, many of the VRFs occur in root canal treated teeth where extensive amounts of dentin are removed from the root canal wall and the dentin in the crown. Canal preparation techniques that overenlarge the canal, and overly aggressive instruments, either nickel–titanium rotary files or hand files that are more tapered, change the fracture resistance of teeth and ability to create dentin defects [18–20]. There are claims [21–25] about the best system or technique that it may be less prone to create dentinal defects, but there is no consensus with respect to motion kinematics [22, 24], reciprocating motion compared with continuous rotation or different NiTi systems [24]. Some argue that there’s no causal relationship between dentinal micro crack formation and canal preparation procedures [21, 23, 25].

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7.3

Etiology

The etiology of vertical root fractures in endodontically treated teeth is complex and confusing at times due to its multifactorial nature. There is no single specific etiology that is pathognomonic for this endodontic complication that can be identified; thus, prevention of vertical root fractures in the endodontically treated tooth is quite difficult. There are predisposing etiological factors as well as contributing ones. The predisposing factors are practically non-controllable. These include the specific anatomy of the susceptible roots [26], biochemical changes in the root dentin of the endodontically treated tooth [27], preexisting cracks in the dentin [23], and loss of healthy tooth substance as a result of caries and trauma before beginning endodontic procedures. The contributing factors are attributed to the iatrogenic risk factors associated with dental procedures performed in the tooth. As described before, most susceptible roots to fracture are the maxillary and mandibular premolars, mesial roots of mandibular molars, mandibular incisors, and the mesio-buccal root of the maxillary molars [26, 28] (Figs.  7.1, 7.2, 7.3, 7.4, 7.5, 7.6, and 7.7). In a retrospective prevalence study of fractured roots among this group of teeth, Tamse et  al. [14] found that the most frequently fractured roots and teeth were those with this specific long bucco-lingual dimension (79%). To minimize the risk of VRF, familiarity with the root anatomy and morphology is essential for factors associated with various dental procedures performed on the tooth [29].

7.4

The Pathogenesis-­ Histopathology

The pathogenesis of the vertical root fracture is the most important issue leading to the endodontic-­periodontal inflammation in the vertical root fracture cases. When a longitudinal bucco-lingual fracture occurs in the root, even if the fracture parts are still attached and the fracture is incomplete (i.e., only buccal or lingual

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a

b

Fig. 7.4  A 55-year-old male patient was referred to the endodontic office for an evaluation of an asymptomatic maxillary right first molar. Clinical examination revealed a PFM crown in the maxillary molar and a coronally located sinus tract in the mesial aspect of tooth #16. The tooth was asymptomatic to percussion and palpation. 12  mm deep, isolated mesiobuccal probing pocket was

noticed. Radiographic examination revealed a previous endodontic treatment with a periradicular radiolucent area on the mesial side of the mesiobuccal root (a). After local anesthesia the gum margin was pushed apically alongside the deep pocket and the root surface was stained with 1% methylene blue (magnification 8×) (b). A VRF was revealed (magnification 16×) (b, white arrow)

aspect is fractured and the other side is intact), tissue remnants and bacteria that remained in the root canal even after the obturation tend to leave the root, formulate a biofilm, and reach the periodontal ligament [2]. This process is causing an inflammatory reaction in the soft tissue which increases as the fracture parts tend to separate. This usually occurs as a result of the continuous occlusal pressure. At the same time, due to the inflammation in the soft tissue, the cortical bone facing the fracture resorbs quickly and a dehiscence in most of the cases follows [30]. The most typical pattern of bone resorption seen in VRF cases is the “dehiscence” in the buccal plate, which is prone to rapid resorption. Initially, when the thin buccal plate is resorbed, a narrow bony cleft develops and resorbs in an apico-coronal rather than in a lateral direction, that is, propagates with the fracture to form an oblong triangle. At a later stage when the inflammatory process continues, it becomes wider in a diagonal direction and resorbs the interproximal areas. This is the usually typical feature seen after reflection of the

flap and cleaning the granulomatous soft tissue [30, 31] (Fig. 7.4b). Unfortunately, clinical final VRF diagnosis can be done only during flap procedure or extraction [31] (Figs. 7.1–7.5). The flap procedure has its pitfalls, since if the fracture is not complete (buccal-lingual) or even located in the lingual aspect only of the root, the chances to locate and diagnose it during surgery is very slim due to the very thick lingual bony plate [31]. On the lingual side, the bone which is much thicker compared to the buccal side resorbs backwards first and later propagates laterally, forming a shallow rounded U-shape resorption while the height of the plate is preserved [30] (Fig. 7.2a, b, Fig. 7.5a). The other pattern of bone resorption in VRF cases is the “fenestration” type. This type of bone loss occurs when the VRF is located somewhere along the root, usually on the buccal side but only in the middle part. In these cases, since the bone loss is opposite the fracture site, the bone in the other areas is intact. Clinically it is difficult to diagnose it. There is no probing pocket that could be detected before flap reflection. Usually, the

7  VRF as an Endodontic Periodontal Lesion

a

Fig. 7.5  A 63-year-old female patient was referred to the endodontic office for an evaluation of a symptomatic mandibular right canine. Clinical examination revealed hypersensitivity to percussion and palpation, intraoral swelling and a 12  mm isolated buccal probing on tooth #43. Radiographic examination revealed a previous end-

a

Fig. 7.6  A 43-year-old male patient was referred for an evaluation of a symptomatic bifurcated maxillary right second premolar. Clinical examination revealed tenderness to percussion and a 10 mm isolated probing on the mesiobuccal side of tooth #15. Radiographic examination

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b

odontic treatment with a halo-like radiolucent area, mainly along the distal aspect of the root (a). An exploratory surgery revealed a VRF on the distolingual side of the root visible upon inspection of the resected surface with a micromirror (b, see white arrow)

b

at two different angles, orthoradial (a) and distal angulation (b), revealed a previous endodontic treatment and a VRF on the mesial side of tooth #15. The VRF was clearly visible on the distal view (b, white arrow)

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a

b

Fig. 7.7  A 63-year-old female patient was referred for treatment of asymptomatic mandibular first right molar. Her chief complaint was a dull toothache when chewing food at the right side. She complained also of localized swelling in the same tooth. The symptoms lasted for approximately 1 year. Clinical examination revealed an amalgam restoration in the mesio-occlusal aspect. (a) The periodontal examination detected an 8 mm probing defect on the mid-buccal surface at the tooth. A sinus tract 3 mm apical from the free gingival margin, on the attached gingiva. The tooth was slightly sensitive to percussion and palpation. Grade 1 mobility was also noted. Radiographic

examination (a) revealed poor root canal filling and bone loss around the roots bilateral and in the furcation which is usually typical for a VRF.  Considering the clinical and radiographic findings a VRF was suspected. The following options were suggested, nonsurgical root canal retreatment or extraction. The patient was motivated to keep the tooth. A nonsurgical root canal retreatment was preformed and the tooth was restored without intracranial post and with temporary crown (b). Six months clinical and radiographic examination showed significant decrease in periapical radiolucency (b) and symptoms free. Full coronal coverage was performed (courtesy of Dr. Arnan Jabarin)

only clinical sign, as in the dehiscence type, is an acute or chronic abscess, similar to a dento-­ alveolar abscess [32] since infection may drain along the periodontium or via a sinus tract (fistula). This fact as explained previously is mimicking a failing endodontic treatment and causing difficulty to achieve accurate and timely VRF diagnosis (Figs. 7.2 and 7.3).

Segment separation with the large resorptive lesion indicates a long-standing inflammation, probably unnoticed by the patient (Fig. 7.6). The variety of bony radiolucent patterns often resembles other pathologic entities, such as periodontal or endodontic inflammatory disease [4]. It is important to note that a vertical root fracture may demonstrate no bone resorption at all in the periapical radiograph [14, 31, 35]. These findings highlight the point that it is sometimes very difficult not only to achieve the accurate diagnosis and in timely manner as well. In suspected VRF cases it is highly recommended to take two periapical radiographs from two different angulations [33] (Fig. 7.6). One of the most frequent bony radiolucencies seen around VRF teeth radiographic feature of VRF is the “halo” (“J shaped”) appearance. This is a combined periapical and lateral radiolucency along the side of the root, or a lateral radiolucency on one or both sides of the root [34]. Another typical bony radiolucency is the “angular” type. It is an angular radiolucency from the crestal bone terminating on the side of the root [33] (Fig. 7.5a).

7.5

Diagnosis

In VRF cases, periapical images show a variety of patterns of bone resorption surrounding the root or the tooth [33]. In only two instances the dentist can make a definitive diagnosis of a vertical root fracture from the periapical radiograph. The first one is, when the beam angulation is at the same plane as the fracture [34]. The other one when the two parts of the root are separated completely. Separated root segments are often visible on radiographs. This is usually accompanied by a large radiolucency between the roots, which is the inflammatory tissue separating the segments.

7  VRF as an Endodontic Periodontal Lesion

The “angular” radiolucency is more often typical in a case with a “true” periodontal disease, but as in the previous more “typical” bony radiolucencies of a VRF tooth, it is only the presence of the “pathognomonic combination” of clinical signs and symptoms that will confirm the diagnosis. The typical bony radiolucencies as seen in the periapical radiographs can only be suggestive and an adjunct for the clinical diagnosis of VRF [31]. In mandibular molars, a radiolucency in the bifurcation area is frequently found and is often coupled with other periapical/lateral changes [33, 36]. It occurs usually around the mesial root of this tooth combining its lateral side and the bifurcation. Lustig et al. [30] found that in most patients with other signs and symptoms (sinus tract, large osseous defect, mobility) or with acute exacerbations, greater interproximal bone loss was recorded than in patients in whom the VRF diagnosis was made at an early stage of the coronal third. Radiographic evaluation may demonstrate no radiographic changes [2, 14] in some VRF cases. A recent systematic review concluded that there is no substantial evidence regarding the accuracy of clinical and radiographic indices for the diagnosis of VRFs in endodontically treated teeth [3]. 3D radiography (CBCT) is currently not recommended as a reliable method of VRF detection in endodontically treated teeth [37–41]. Chavda [38] demonstrated poor diagnostic ability in detected VRF in both digital radiography and CBCT imaging. Another study [42] suggested digital subtraction radiography (PA digital radiography) as alternative tool for the investigation of VRF. Another study [40] mentioned that the imaging artifacts caused by the gutta-percha root filling within the root canal may cause overestimation of VRF with CBCT.  It is quite clear that vertical root fracture in an endodontically treated tooth is not clinically evident until infection occurs in the fracture site with ensuing of emergence of clinical signs and symptoms [11]. It may very well be that the narrow mesio-distal width of the root and the magnitude of the masticatory forces which is different in every individual can be suggested as the main risk factors affecting the appearance of the signs and symp-

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toms in the susceptible teeth and roots [43]. The inability to visualize vertical root fractures in endodontically treated teeth by conventional imaging techniques necessitated the development of alternative imaging modalities [44]. Using the new imaging modality, the Cone beam CT may be helpful at times to diagnose the fracture, and when it happens, it will be mostly in the axial slices [45]. However in the last consensus statement by the AAE [4] it was stated that in the majority of cases the indication of a VRF is often due to the specific pattern of bone loss and PDL space enlargement rather than direct visualization of the fracture (Figs. 7.1, 7.4, 7.5a).

7.6

Histopathology

As mentioned earlier, the most significant problem related to VRFs is the fact that they become extensively colonized by bacteria arranged in biofilms, their metabolites [46, 47], necrotic pulpal tissue [48], sealer components [49, 50], and food debris, all which forced into the fracture during mastication and may propagate and reach the periodontal ligament [51]. The bacteria may be seen in defects, secondary fractures, or dentinal tubules that communicate with the fracture [2, 51]. There are several potential sources for the bacteria seen in the fracture. One is anachoresis. However, this is unlikely, as bacteria could not be introduced into empty pulp spaces [52] or even into pulp canals containing necrotic tissue [47]. Another source may be directly from the oral cavity when the fracture communicates with the gingival sulcus. The most interesting possibility is from the canal space itself. Often bacteria are not totally removed during canal preparation [53, 54]. Following obturation, some of these microorganisms may survive in an inactive state. However, with a subsequent fracture, substrates may enter the pulp canal, allowing the microorganisms to proliferate and to produce virulent factors. It is readily accepted that bacteria are an important etiological factor for periapical inflammation [55]. The same principle should apply to the fracture, with the exception that a greater area of exposure is provided by the fracture.

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With the passage of time, exacerbated by the masticatory load, crack lines (dentinal cracks) may further propagate apically or laterally to reach the periodontium and result in bone resorption in response to bacteria colonizing the crack [2, 30, 56]. Dense bacterial colonization of the cracked dentin and tubules cause secretion of bacterial virulence factors, antigens, and bacterial by-products to the periodontium. Blomlöf et  al. [57] created defects on root surfaces of intentionally extracted monkey teeth with either open or mature apices. The canals were either infected or filled with calcium hydroxide and replanted back in their sockets. After 20 weeks, marginal epithelial downgrowth was found on the denuded dentin surface of the infected teeth. Jansson and Ehnevid [58] also investigated the effect of endodontic infection on periodontal probing depth and the presence of furcation involvement in mandibular molars. They found that endodontic infection in mandibular molars was associated with more attachment loss in the furcation area. These authors suggested that endodontic infection in molars associated with periodontal disease may enhance periodontitis progression by spreading pathogens through accessory canals and dentinal tubules. Another problem is that bacterial penetration may occur from the oral space to the dentin. A histopathologic and histobacteriologic study showed [51] that tooth cracks, regardless of their location, direction, and extent, were always colonized by bacterial biofilms. Cracks are bathed by saliva and are difficult or impossible to be cleaned during routine oral hygiene. Because cracks are retentive, food and bacteria accumulate to the point when the cracks become congested with a bacterial biofilm. In most cases, depending on the crack’s direction and extent, bacteria from the biofilm invade the tissues beneath the crack line. The response varies in intensity according to the depth of bacterial infection.

7.7

Microbiology

Although specific bacterial species have not been conclusively identified in the longitudinal fractured root, they are known to be present and

important both in initial and in failed root canal treatments [59, 60]. Biofilms tend to persist and are composed of mixed flora that includes pathogenic bacteria [61]. Gram staining showed the presence of gram-positive and gram-negative bacteria, with a predominance of gram positive [2]. Bacteria were seen in defects, secondary fractures, or dentinal tubules that communicated with the fracture [2, 51]. These microorganisms were pathogens associated strongly with periapical pathosis. Studies indicate that root canal systems cannot be completely cleaned and disinfected [62–64] and microbes may survive in the canal. Some publications [65, 66] showed that the apical portion of a root canal may stay infected even after instrumentation to larger sizes than typically used. Obturation of the radicular space is necessary to eliminate leakage. Obturation reduces coronal leakage and bacterial contamination, seals the apex from the periapical tissue fluids, and entombs the remaining irritants in the canal [67]. Intracanal bacteria were recovered in 45% of teeth that showed absence of an apical radiolucency after root canal treatment [68]. Similar findings were found by Engström [69], who isolated microorganisms in 24% of such cases. Hence, as long as there is no pathway to the periapex, a periapical tissue response will not develop. But in case a VRF occurs, an avenue is opened up to the periodontium, nutritional supply will increase, and an inflammatory reaction may be induced and could not be possibly sealed. Among the live pathogens encountered in a diseased pulp and periapical tissues are bacteria, fungi, and viruses. These pathogens and their by-­ products may affect the periodontium in a variety of ways and need to be eliminated during root canal treatment [70]. It is known that many of the periodontal pathogens are also endodontic pathogens, and that is why it is not surprising that combined endodontic-periodontal lesions pathogens and those found in VRFs present similar profile. Blomlöf et  al. [57] created defects on root surfaces and found marginal epithelial downgrowth on the denuded dentin surface of infected teeth. Jansson and Ehnevid [58] found that endodontic infection in mandibular molars was associated with more attachment loss in the furcation area.

7  VRF as an Endodontic Periodontal Lesion

Many bacteria share in both endodontic and periodontal infections. Proteolytic bacteria are predominant in the root canal flora, which changes over time to a more anaerobic microbiota [55, 71]. Rupf et al. [72] detected using PCR Actinobacillus actinomycetemcomitans, Tannerella forsythensis, Eikenella corrodens, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella intermedia, and Treponema denticola. These pathogens were found in all endodontic samples and the same pathogens were found in teeth with chronic apical periodontitis and chronic (adult) marginal periodontitis. Spirochetes are another type of microorganisms associated with both endodontic and periodontal diseases [73, 74]. Yeast colonization has been demonstrated in dentinal tubules [75, 76]. Studies reported prevalence of 3.7–33% in cases of previously treated canals [60, 68, 77, 78]. The majority of the recovered fungi were Candida albicans [78]. C. albicans also showed the ability to colonize canal walls and penetrate into dentinal tubules [79]. It has been found that approximately 20% of chronic periodontitis patients also harbor subgingival yeasts [80]. As in endodontic infections, C. albicans was also the most common species of fungi isolated [81]. Viruses also play role in both endodontic and periodontal diseases. In patients with periodontal disease, herpes simplex virus is frequently detected in gingival crevicular fluid and in gingival biopsies of periodontal lesions [82–84]. Human cytomegalovirus was found in about 65% of periodontal pocket samples and in about 85% of gingival tissue samples [82]. Epstein–Barr virus type I was detected in more than 40% of pocket samples and in about 80% of the gingival tissue samples [82]. Gingival herpesviruses were associated with increased occurrence of sub-gingival P. gingivalis, T. forsythensis, P. intermedia, Prevotella nigrescens, T. denticola, and A. actinomy-­cetemcomitans, suggesting that they may play a role in promoting overgrowth of pathogenic periodontal bacteria [83]. Combined endodontic-periodontal lesions include species of the general Eubacterium, Fusobacterium, Peptostreptococcus, Porphyromonas, Prevotella, and Streptococcus [85, 86]. However, other species such as Dialister invisus, D. pneumosintes, P. alactolyticus, R. mucilaginosa, T. forsythia, T. maltophilum, T.

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socranskii, and the phylotypes, among others, were found [86, 87]. Microbiological aspects of the fractures described earlier [2, 88]. A frequent finding in the fracture spaces [2] is bacteria both gram-positive and gram-negative, with a predominance of gram-positive, within the canals. The dentinal tubule diameter is usually compatible with the cell diameter of most oral bacterial species [89, 90]. In fact, several oral species have been shown to invade and colonize dentinal tubules in vitro [91–93]. Most oral bacteria are nonmotile, and, therefore, tubular invasion from the biofilm covering the cracked dentin possibly occurred after repeated cell division, which pushes cells into tubules. Bacterial cells may also be forced into tubules by hydrostatic pressures developed on dentin during mastication [94].

7.8

Management

Many studies indicated that extraction was the only predictable treatment for VRF especially in the posterior teeth [95–98]. Some authors attempted to conserve roots with vertical fracture by sealing the fracture gap [99–101]. Masaka [102] reported cases of fractured roots that were preserved for 10 years by 4-methacryloxyethyl trimellitate anhydride/methyl methacrylate-tri-n-­ butyl borane (4-META/MMA-TBB) resin bonding. In addition, Sugaya et  al. [103] carried out bonding using 4-META/MMA-TBB resin in 23 teeth with vertical root fracture, and of those, 18 teeth (78%) were conserved for an observation period of 6–74  months. Hayashi et  al. [104] extracted 26 teeth with vertical root fracture, bonded the fractured roots, and replanted them. They reported results over an observation period of 4–74 months, and longevity was found as high as 69.2% at 36  months after replantation. These reports indicate the possibility that bonding of roots may be an option for the treatment of vertical root fracture. Moreover, in many of the cases where vertical root fractures were bonded with resin, improvement in the inflammation of periodontal tissue and a reduction in periodontal probing depth were reported even without debridement of the root surface.

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Histopathologically, increased probing depth is indicative of two possible conditions. The first is the formation of a periodontal pocket by epithelial downgrowth and accumulation of bacteria in the periodontal pocket, so that the condition resembles marginal periodontitis. The second is periodontal inflammation caused by bacteria in the root canal and the fracture gap, and while there is no epithelial downgrowth, the periodontal probe penetrates the inflamed connective tissue [105–107]. If the probe only penetrates inflamed connective tissue and the bacteria are localized in the root canal and the fracture gap, it is likely that elimination of the bacteria and sealing of the fracture gap will resolve the inflammation and repair the resorbed bone. Results of latest studies [104] indicate the possibility that periodontal inflammation along the fracture line can be prevented and improved if the fracture gap is sealed with adhesive resin. However, in one study [108], the bonded roots were not subjected to occlusal load and is unclear whether the bonded roots exhibit resistance to refracture when involved in a mechanical action such as occlusal force. The use of enamel matrix derivative (EMD) when bonding and replanting tooth roots after a vertical fracture has been reported [109]. The author mentioned important EMD properties concerning VRF bonded replanted teeth; EMD inhibits inflammation [110], has an antibacterial effect [111], promoted the formation of cementum after surface resorption [108, 109], and reduces ankylosis [112]. Periodontal reattachment showed important biomechanical role in bonded and replanted vertically fractured teeth as well [113]. However it should be emphasized that studies mentioned above are case reports and case series with low level of evidence. Most of the time, the tooth or root that is involved with a vertical root fracture should be extracted, thus eliminating the inflammatory process and the bone loss. However, management is possible in some cases in multi-rooted teeth. A complete root amputation of the fractured root can be done or shaving some of the root to eliminate the fracture. This procedure may shorten one root but keeps the tooth [5, 114]. This procedure

not only eliminates the endodontic-­periodontal lesion but also achieves satisfactory functional and esthetic results.

7.9

Conclusions

This chapter focused on the clinical diagnosis and pathogenesis of vertical root fractures in the endodontically treated teeth as an endodontic-­ periodontal lesion. There are two typical signs and symptoms for definitive VRF diagnosis—the highly located sinus tract and the deep probing defect. When these two occur together in the endodontically treated tooth, the final and accurate diagnosis can be done in most cases. The typical bony radiolucencies around the susceptible teeth and roots were also described in the chapter. The difficulties to achieve the accurate VRF diagnosis are: (1) the fact that not all the VRF cases manifest themselves as with the “pathognomonic combination,” (2) the signs, symptoms, and radiographic manifestations are mimicking either periodontal disease or poor outcome of endodontic treatment, (3) no correlation can be found as to the location and extent of the root fracture and the signs, symptoms, and radiographic features, and (4) vertical root fracture in endodontically treated teeth is not clinically evident until infection occurs in the fracture site with ensuing emergence of signs and symptoms. A brief description of the nomenclature of chronic, longitudinal type of tooth fractures in endodontically treated teeth which is based on the initiation and propagation of the fracture was presented. This part was followed by a short summary of the complex etiology of these fractures. The typical pathogenesis of the vertical root fracture and the bacteria involved in the process are the most important issues to understand in the endodontic-periodontal involvement in these cases. When a longitudinal-bucco lingual fracture occurs in the root, even if the fracture parts are still attached, tissue remnants and bacteria tend to leave the root, formulate a biofilm, and reach the periodontal ligament. This scenario is causing an inflammatory process in the soft

7  VRF as an Endodontic Periodontal Lesion

tissue which increases as the fracture parts tend to separate. The separation of the root segments is the result of the continuous occlusal pressure. As a result, the cortical bone facing the fracture is resorbing. A dehiscence type occurs in most of the cases and in the buccal bone, and subsequently it deteriorates more quickly as originally the buccal plate is thin facing the susceptible teeth and roots to fracture.

References 1. Zadik Y, Sandler V, Bechor R, Salehrabi R. Analysis of factors related to extraction of endodontically treated teeth. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2008;106:e35. 2. Walton RE, Michelich RJ, Smith GN.  The histopathogenesis of vertical root fractures. J Endod. 1984;10:48–56. 3. Tsesis I, Rosen E, Tamse A, Taschieri S, Kfir A. Diagnosis of vertical root fractures in endodontically treated teeth based on clinical and radiographic indices: a systematic review. J Endod. 2010a;36:1455–8. 4. Rivera EM, Walton RE. Cracking the cracked tooth code: detection and treatment of various longitudinal tooth fractures. Am Assoc Endod Colleagues Excellence News Lett. 2008;2:1–19. 5. Taschieri S, Tamse A, Del Fabbro M, Rosano G, Tsesis I.  A new surgical technique for preservation of endodontically treated teeth with coronally located vertical root fractures: a prospective case series. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2010;110:e52. 6. Fuss Z, Lustig J, Katz A, Tamse A.  An evaluation of endodontically treated vertical root fractured teeth: impact of operative procedures. J Endod. 2001;27:46–8. 7. Yang S, Rivera EM, Walton RE. Vertical root fracture in nonendodontically treated teeth. J Endod. 1995;21:337–9. 8. Fuss Z, Lustig J, Tamse A.  Prevalence of vertical root fractures in extracted endodontically treated teeth. Int Endod J. 1999;32:283–6. 9. Rosen E, Beitlitum I, Tamse A, Taschieri S, Tsesis I.  Implant-associated vertical root fracture in adjacent endodontically treated teeth: a case series and systematic review. J Endod. 2016;42:948–52. 10. Bakland LK, Tamse A. Categorization of dental fractures. In: Anonymous vertical root fractures in dentistry. Berlin: Springer; 2015. p. 7–28. 11. Von Arx T, Bosshardt D.  Vertical root fractures of endodontically treated posterior teeth. Swiss Dent J. 2017;127(1):14–23. 12. Tamse A, Tsesis I, Rosen E. Vertical root fractures in dentistry. Berlin: Springer; 2015.

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7  VRF as an Endodontic Periodontal Lesion 61. Siqueira JF, Rôças IN.  Community as the unit of pathogenicity: an emerging concept as to the microbial pathogenesis of apical periodontitis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2009;107:870–8. 62. Heard F, Walton RE.  Scanning electron microscope study comparing four root canal preparation techniques in small curved canals. Int Endod J. 1997;30:323–31. 63. Siqueira JF, Silva CH, Md C, Lopes HP, Md U.  Effectiveness of four chemical solutions in eliminating Bacillus subtilis spores on gutta-percha cones. Endod Dent Traumatol. 1998;14:124–6. 64. Wu MK, Sluis L, Wesselink PR.  The capability of two hand instrumentation techniques to remove the inner layer of dentine in oval canals. Int Endod J. 2003;36:218–24. 65. Card SJ, Sigurdsson A, Ørstavik D, Trope M.  The effectiveness of increased apical enlargement in reducing intracanal bacteria. J Endod. 2002;28:779–83. 66. Wu M, Barkis D, Roris A, Wesselink PR.  Does the first file to bind correspond to the diameter of the canal in the apical region? Int Endod J. 2002;35:264–7. 67. Vakalis SV, Whitworth JM, Ellwood RP, Preshaw PM.  A pilot study of treatment of periodontal-­ endodontic lesions. Int Dent J. 2005;55:313–8. 68. Molander A, Reit C, Dahlen G, Kvist T.  Microbiological status of root-filled teeth with apical periodontitis. Int Endod J. 1998;31:1–7. 69. Engström B. The significance of enterococci in root canal treatment. Odontol Revy. 1964;15:87. 70. Rotstein I, Simon JH.  Diagnosis, prognosis and decision-making in the treatment of combined periodontal-endodontic lesions. Periodontol 2000. 2004;34:165–203. 71. Sundqvist G.  Ecology of the root canal flora. J Endod. 1992;18:427–30. 72. Rupf S, Kannengiesser S, Merte K, Pfister W, Sigusch B, Eschrich K. Comparison of profiles of key periodontal pathogens in periodontium and endodontium. Endod Dent Traumatol. 2000;16:269–75. 73. Choi BK, Paster BJ, Dewhirst FE, Göbel UB.  Diversity of cultivable and uncultivable oral spirochetes from a patient with severe destructive periodontitis. Infect Immun. 1994;62:1889–95. 74. Dewhirst FE, Tamer MA, Ericson RE, Lau CN, Levanos VA, Boches SK, Galvin JL, Paster BJ.  The diversity of periodontal spirochetes by 16S rRNA analysis. Oral Microbiol Immunol. 2000;15:196–202. 75. Siqueira JF, Sen BH. Fungi in endodontic infections. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004;97:632–41. 76. Waltimo TM, Haapasalo M, Zehnder M, Meyer J. Clinical aspects related to endodontic yeast infections. Endod Topics. 2004;9:66–78. 77. Jackson FL, Halder AR. Incidence of yeasts in root canals during therapy. Brit Dent J. 1963;115:459–60.

139 78. Waltimo T, Siren EK, Torkko H, Olsen I, Haapasalo M.  Fungi in therapy-resistant apical periodontitis. Int Endod J. 1997;30:96–101. 79. Peterson K, Söderström C, Kiani-Anaraki M, Levy G. Evaluation of the ability of thermal and electrical tests to register pulp vitality. Endod Dent Traumatol. 1999;15:127–31. 80. Dahlén G, Wikström M. Occurrence of enteric rods, staphylococci and Candida in subgingival samples. Oral Microbiol Immunol. 1995;10:42–6. 81. Hannula J, Saarela M, Alaluusua S, Slots J, Aslkainen S.  Phenotypic and genotypic characterization of oral yeasts from Finland and the United States. Oral Microbiol Immunol. 1997;12:358–65. 82. Contreras A, Nowzari H, Slots J.  Herpesviruses in periodontal pocket and gingival tissue specimens. Oral Microbiol Immunol. 2000;15:15–8. 83. Contreras A, Zadeh HH, Nowzari H, Slots J.  Herpesvirus infection of inflammatory cells in human periodontitis. Oral Microbiol Immunol. 1999;14:206–12. 84. Slots J, Contreras A.  Herpesviruses: a unifying causative factor in periodontitis? Oral Microbiol Immunol. 2000;15:277–80. 85. Kobayashi T, Hayashi A, Yoshikawa R, Ookuda K, Hara K.  The microbial flora from root canals and periodontal pockets of non-vital teeth associated with advanced periodontitis. Int Endod J. 1990;23:100–6. 86. Li H, Guan R, Sun J, Hou B.  Bacteria community study of combined periodontal-endodontic lesions using denaturing gradient gel electrophoresis and sequencing analysis. J Periodontol. 2014;85:1442–9. 87. Gomes BP, Berber VB, Kokaras AS, Chen T, Paster BJ. Microbiomes of endodontic-periodontal lesions before and after chemomechanical preparation. J Endod. 2015;41:1975–84. 88. Andreasen JO.  Intra-alveolar root fractures: radiographic and histologic study of 50 cases. J Oral Surg. 1967;25:414–26. 89. Garberoglio R, Brännström M.  Scanning electron microscopic investigation of human dentinal tubules. Arch Oral Biol. 1976;21:355–62. 90. Santos AL, Siqueira JF Jr, Rôças IN, Jesus EC, Rosado AS, Tiedje JM.  Comparing the bacterial diversity of acute and chronic dental root canal infections. PLoS One. 2011;6:e28088. 91. Berkiten M, Okar İ, Berkiten R. In vitro study of the penetration of Streptococcus sanguis and Prevotella intermedia strains into human dentinal tubules. J Endod. 2000;26:236–9. 92. Perez F, Calas P, De Falguerolles A, Maurette A.  Migration of a Streptococcus sanguis strain through the root dentinal tubules. J Endod. 1993;19:297–301. 93. Siqueira JF, De Uzeda M, Fonseca MEF. A scanning electron microscopic evaluation of in vitro dentinal tubules penetration by selected anaerobic bacteria. J Endod. 1996;22:308–10.

140 94. Michelich VJ, Schuster GS, Pashley DH.  Bacterial penetration of human dentin in  vitro. J Dent Res. 1980;59:1398–403. 95. Bhaskar U, Logani A, Shah N.  True vertical tooth root fracture: case report and review. Contemp Clin Dent. 2011;2:265. 96. Pitts DL, Natkin E. Diagnosis and treatment of vertical root fractures. J Endod. 1983;9:338–46. 97. Rivera EM, Walton RE.  Longitudinal tooth fractures. Endod Principles Pract. 2014;5:121. 98. Testori T, Badino M, Castagnola M.  Vertical root fractures in endodontically treated teeth: a clinical survey of 36 cases. J Endod. 1993;19:87–90. 99. Michanowicz AE, Perchersky JL, McKibben DH. A vertical fracture of the crown and root. ASDC J Dent Child. 1978;45:310–2. 100. Stewart GG. The detection and treatment of vertical root fractures. J Endod. 1988;14:47–53. 101. Trope M, Ray HL.  Resistance to fracture of endodontically treated roots. Oral Surg Oral Med Oral Pathol. 1992;73:99–102. 102. Masaka N.  Long-term observation of fractured tooth roots preserved by adhesion. Adhes Dent. 1995;13:156–70. 103. Sugaya T, Kawanami M, Noguchi H, Kato H, Masaka N. Periodontal healing after bonding treatment of vertical root fracture. Dent Traumatol. 2001;17:174–9. 104. Hayashi M, Kinomoto Y, Takeshige F, Ebisu S. Prognosis of intentional replantation of vertically fractured roots reconstructed with dentin-bonded resin. J Endod. 2004;30:145–8. 105. Armitage GC, Svanberc GK, Löe H.  Microscopic evaluation of clinical measurements of connective tissue attachment levels. J Clin Periodontol. 1977;4:173–90. 106. Listgarten MA.  Periodontal probing: what does it mean? J Clin Periodontol. 1980;7:165–76.

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8

Treatment Alternatives Following Extraction of Teeth with Periodontal-Endodontic Lesions Carlos E. Nemcovsky, Massimo del Fabbro, Ilan Beitlitum, and Silvio Taschieri

8.1

Introduction

One of the most common dilemmas in clinical dental practice is the choice on whether to maintain or extract compromised teeth. The decision becomes even more complex when combination of periodontal, endodontic, and reconstructive aspects must be considered. Implant-supported restoration seems to be the most widely accepted treatment alternative to replace missing teeth. However, implant therapy success is related to a number of factors such as the timing of surgery and surgical approach following tooth extraction, the residual bone volume, and the presence of residual infection [1]. Immediate implants placed in periodontally compromised maxillae show higher failure rate [2]. Extraction of teeth with severe alveolar bone damage, as in cases with untreatable periodontalendodontic lesions, results in different scenarios with varying levels of difficulty in their surgical management. Several treatment alternatives may C. E. Nemcovsky (*) · I. Beitlitum Department of Periodontology and Dental Implantology, Maurice and Gabriela Goldschleger School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel e-mail: [email protected]; [email protected] M. del Fabbro · S. Taschieri Department of Biomedical, Surgical and Dental Sciences, Università degli Studi di Milano, IRCCS Istituto Ortopedico Galeazzi, Dental Clinic, Milan, Italy e-mail: [email protected]

be available, such as immediate implant placement, primary soft tissue closure of the extraction site that may be followed by early implant placement, ridge preservation, and ridge augmentation. Immediate implant placement is a complex procedure and should be performed only under ideal anatomic conditions, which are not usually present following extraction of teeth affected by periodontal-endodontic lesions. When those ideal conditions are not met, and especially where bone augmentation procedures are indicated, early implant placement after 4–8 weeks of soft tissue healing should be preferred. In cases with insufficient bone volume to allow predictable implant placement, implants will be placed, usually after a few months, only after hard tissue augmentation is achieved and predictable implant placement granted [3]. Evidently, even after soft and hard tissue healing is advanced, certain cases will not allow proper implant placement, and bone augmentation procedures will have to be performed before implants may be inserted. Post-­extraction healing periods of 6  months or longer, without any intervention, carry a risk for significant ridge alterations or even advanced ridge atrophy. Late implant placement should only be used if there are patient- and/or site-specific therapeutic reasons. Post-extraction socket healing involves important alterations in its volume and shape, as the result of concomitant mechanisms of bone resorption and apposition [4, 5]. The cascade

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of biological events leading to alveolar healing, following tooth extraction, has been described [6, 7]. Briefly, immediately after tooth extraction a blood clot fills most of the fresh socket. Histologic analysis shows the beginning of the formation of a fibrin network. Already, during the first 48 h, neutrophilic granulocytes, monocytes, and fibroblasts begin to migrate within the fibrin network, enhancing tissue healing through an inflammatory response. After a couple of days, granulation tissue starts clot replacement. One week after extraction, the clot is already partly replaced with a provisional matrix while most of the socket is filled with granulation tissue, young connective tissue, and osteoid in its apical area. On the beginning of the second week, the socket tissue mainly comprises provisional matrix and woven bone, and on day 30, mineralized bone already occupies almost 90% of the socket volume [8]. Eight weeks after tooth extraction signs of ongoing hard tissue resorption on the outside and on the top of the buccal and lingual bone walls may be appreciated. Residual infection after tooth extraction could cause a slower and incomplete healing [9]. Tooth extraction causes major changes to residual alveolar bone [4, 8, 10, 11]. Following extraction, the height of the buccal wall tends to decrease and bundle bone disappears [4, 8, 11, 12]. Most changes occur during the first month, while minor additional decrease in the ridge continues over periods ranging between 10 and 20 weeks [6, 10]. Reduction of the residual alveolar ridge of up to 50% in width may occur during the first 3 months of healing [11]. Multiple adjacent extractions induce greater apico-coronal alterations than single extractions [10] (Figs. 8.1 and 8.2). During the first 3–6  months of healing, the alveolar ridge shows a mean horizontal reduction of 3.8 mm and a mean vertical reduction of 1.2 mm [13]. This biological healing process cannot be completely counteracted by any treatment alternative. This reduction in buccolingual width normally occurs after 4–6 months independent of the implant insertion [4, 14, 15]. Implants placed immediately into extraction sockets are unable to preserve the alveolar bony crest in its entire

C. E. Nemcovsky et al.

Fig. 8.1 Aspect immediately after atraumatic tooth extraction, flaps were not raised

Fig. 8.2  Aspect of the ridge a few weeks after tooth extraction, not large reduction of the buccolingual dimension of the residual alveolar ridge

outline [16–19]. Marginal defects at buccal and oral aspects of immediate implants will be filled by new bone formation from the internal aspect of the socket; however, marked bone resorption from the external side, mainly the buccal, of the alveolar ridge will occur [20, 21]. At extraction sites where proximal teeth have intact PDL support, reduction of crestal bone is usually limited to the buccal wall. Otherwise, marked apico-­ coronal resorption of all extraction site walls will occur (Figs. 8.3, 8.4, 8.5, 8.6, 8.7, 8.8, 8.9, 8.10, and 8.11). The fresh extraction site type defect has been considered favorable; however, an animal experiment showed impaired bone healing in these sites; after implant placement, most defects prepared in healed alveolar ridges were completely filled, whereas healing of fresh extraction sockets was incomplete [22].

8  Treatment Alternatives Following Extraction of Teeth with Periodontal-Endodontic Lesions

Fig. 8.3 Aspect immediately after atraumatic tooth extraction of second right premolar, flaps were not raised

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Fig. 8.6  The space between the implant and the facial bony wall was filled with a non-resorbable xenograft

Fig. 8.4  An implant was placed immediately after tooth extraction Fig. 8.7  Radiograph taken at the end of the surgical procedure. Note slight loss of bone support in the proximal teeth

Fig. 8.5  Implant was placed close to the palatal residual bony wall and good primary stabilization was achieved. A healing abutment was inserted for transmucosal healing. A space between the implant and the internal aspect of the buccal bony wall is evident

Classifications taking in consideration the remaining alveolar socket integrity following tooth extraction have been suggested to decide the appropriate treatment alternative for each clinical situation [23].

Fig. 8.8  A few months after tooth extraction and immediate implant placement, recession of the mucosal margin is evident, involving also the proximal teeth

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8.2

Treatment Alternatives

8.2.1 Immediate Implant Placement The immediate implant placement presents certain advantages, including patient satisfaction, low morbidity, early prosthetic loading with ­possibility for immediate restoration, and reduction of overall treatment time. The primary objective of implant therapy in the esthetic zone is an optimal esthetic treatment Fig. 8.9  Occlusal view illustrates reduction in the bucco-­ outcome with high predictability and a low risk palatal aspect of the alveolar ridge of complication. Esthetic restoration outcomes in sites with post-extraction implant placement must be evaluated after several months, since the stability of the facial hard and soft tissues in this type of procedure may be deceiving. Immediate implant placement is a complex procedure and should be performed only under ideal anatomic conditions. These include an intact facial bone wall with at least 1 mm thickness, thick gingival biotype, no acute infection at the extraction site, and a sufficient bone volume apical and palatal of the extraction site to allow primary implant stability, which are present only in a small percentage of cases, especially in the anterior maxilla. Thick wall phenotypes are rare Fig. 8.10  A posterior radiograph shows good bone appoin the anterior maxilla [24–26]. In central incisor sition and crestal bone level around the implant areas, only 4.6% have a thick wall phenotype, while this condition is present in 27.5% of the first premolar sites [24], 52% of sites will have dehiscence or fenestration defects of the facial bone [27]. Treatment of choice for each clinical case depends on the clinical and radiographic preoperative analysis assessing patients’ risk profile. The following anatomical landmarks should be carefully evaluated when considering immediate implant placement in the esthetic zone [3]: (a) facial bone wall, (b) palatal bone wall, (c) mesial and distal crest width, measured 3  mm apical to the CEJ of adjacent teeth, (d) alveolar ridge height and inclination, (e) periFig. 8.11  Final restoration in place, mucosal margin odontal bone support of adjacent teeth, (f) anatrecession is evident on facial aspect of implant and neighomy of the naso-palatal canal, (g) bone volume boring teeth available apically and palatally of the root, and (h) mesio-distal size of the resulting single tooth gap post extraction.

8  Treatment Alternatives Following Extraction of Teeth with Periodontal-Endodontic Lesions

Implants placed in fresh extraction sockets have survival rates comparable to implants placed in healed sites [28–31] with the majority of studies reporting above 95% survival [3]. On the other hand, a systematic review found that in single tooth implant-supported crowns and controlled studies, implants inserted in fresh extraction sockets present a higher risk ratio for failure of 1.58 [32]. However, this treatment approach is not devoid of complications. Mucosal vestibular recession is frequently observed on restored immediate implants, where 1 out of 3–4 cases shows over 1  mm soft tissue recession [33–39]. A systematic review reported that the bone dimensions of immediate implant sites showed approximately 0.5–1.0  mm reduction in vertical and horizontal aspects 4–12 months following surgery [40]. Risk factors for mucosal recession are thin tissue biotype, facial malposition of the implant, and thin or damaged facial bone wall at extraction [3]. Early implant placement, where the implant is placed a few weeks after tooth extraction, shows lower risks for mucosal margin recession [41–46]. In fresh extraction sites in the anterior maxilla, thin or damaged facial bone wall is frequently encountered [24–26, 47], vertical bone loss may frequently be observed mid-­facially in extraction sites in the anterior maxilla with less than 1 mm bony wall thickness [48]. A recent comparative clinical study between immediate and delayed implant placement ­questions the advantages of immediate implant procedures [49]. This study reported higher needs for bone augmentation at the time of immediate implant placement (72% vs. 43.9%); primary soft tissue closure was achieved in only 61.7% of the immediate implants sites while on 82.1% of the delayed. Wound healing complications were five times more frequent in the immediate implants group than in the delayed, one out of four (26.1%) immediate implants showed this type of complication. Deeper probing depths were noted around immediately placed implants compared with delayed implants at 1  year post-loading. Higher rates of suboptimal soft tissue esthetics and deeper implant placement were recorded in

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the immediate implant group. A trend for greater radiographic bone loss at 3  years after loading was observed in the immediate implant group as compared with implants placed following delayed approach. Accordingly, it seems difficult to recommend immediate implant placement at sites where esthetic result is important. Immediate implant placement may be performed with and without flap elevation, bone and soft tissue grafting, and immediate, early, or conventional loading protocols. Flapless extraction and implant placement combined with bone and connective tissue grafting together with an immediate provisional crown lead to predictable outcome in selected cases [50–53]. However this procedure of immediate tooth replacement should be performed only under strict clinical situations including intact alveolus bony walls, no bony defects (dehiscence/fenestration), at least 2  mm distance between implant and tooth, at least 3 mm distance between proximal implants, good primary stabilization, correct emergence profile (even gingival margins of the tooth before extraction), thick biotype, and no infection. Flapless implant placement has been shown to be associated with less recession of the mid-­ facial mucosa [54]; therefore, whenever possible, and, under ideal conditions, raising a buccal flap should be avoided at immediate implant procedures. Although it might seem to be a simple surgical procedure, a flapless approach for the placement of an implant into a fresh extraction socket is a complex surgical procedure due to impaired visual access during surgery and risk of unnoticed apical perforation of the facial bone if preparation axis is incorrect. Clinical studies have indicated that tissue alterations can be observed after many years post placement [55, 56]. Although single immediate implants present high survival rates, midfacial recession and mid-facial contour and alveolar process deficiency deterioration may be appreciated after 1  year [55], rendering an esthetic complication rate of almost 50% in well-selected patients who had been treated by experienced clinicians, accordingly, immediate

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implant placement may not be recommended for daily practice in the esthetic area. Facial malposition of the implant is an important risk factor for mucosal recession [36]. A gap of at least 2 mm between the implant and the internal surface of the facial bone wall should be maintained [47]. A gap of this dimension provides a space that can be grafted with an appropriate bone filler allowing the formation of a blood clot, which can subsequently reorganize into a provisional connective tissue matrix and support the formation of newly formed woven bone. The positioning of the implant within the extraction socket has been demonstrated to influence the final location and volume of the alveolar bony crest [57, 58]. The more lingual an implant is installed, the less supra-crestal exposure of the implant is expected to occur. However, such implant placement will not preserve the alveolar bony ridge. Implant macro geometry and its placement relative to the bone crest influence crestal bone loss and bone-to-­implant contact in immediate (post-extraction) implants. All immediate post-extraction implants undergo crestal bone loss, and BIC was largest in implants subcrestally placed with double-spiral thread and microrings on the collar [59]. Bone substitutes with a low substitution rate such as deproteinized bovine bone mineral (DBBM) may reduce the post-surgical oro-facial bone resorption [12, 33, 60–64] and contribute to the preservation of the alveolar ridge. However, there is no consensus concerning this issue, an augmentation procedure with use of bovine bone mineral and a collagen barrier membrane within the remaining buccal defects as well as on the outer contour of the buccal bony crest did not maintain the volume of the hard and soft tissues [65]. Autogenous, allogenic, or xenogeneic soft tissue grafting may be performed to thicken the buccal tissues and improve future restoration emergence profile. Vertically, the implant shoulder should be placed just apical to the mid-facial bone crest to compensate for approximately 0.5–1.0  mm of crestal bone resorption that may be anticipated following flapless tooth extraction [27].

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The effect of barrier membrane application to reduce alveolar bone changes after tooth extraction and immediate implant placement is not clear. Some studies have reported a more pronounced bone resorption in sites with both nonresorbable and resorbable membranes, compared with the control implants [66]. Wound healing at immediate implants placed into molar extraction sites with buccal self-contained defects in conjunction with bone augmentation resulted in less favorable outcomes compared with those around implants placed in healed alveolar ridges resulting in a lack of “complete” osseointegration [67]. On the other hand, guided bone regeneration (GBR) techniques were able to partially limit resorption of the alveolar crest after tooth extraction and implant placement [14]. Bone remodeling after tooth extraction and implant placement was observed both in the control (no GBR) and in test sites (GBR); however, the amount of bone remodeling in sites that received augmentation techniques was lower than in sites where regenerative procedures were not performed. The contour augmentation performed with DBBM particles and a collagen membrane at the buccal aspects of immediate implants placed was not able to maintain the tissue volume [65, 68]. Immediate implant placement does not counteract alveolar ridge modeling after tooth extraction. Furthermore, the currently available evidence does not allow for conclusive statements regarding the efficacy of a concomitant regenerative technique to prevent the amount of alveolar reduction [69]. In the esthetic zone, cases of tooth extraction due to vertical or horizontal root fracture, especially if one or both of the adjacent teeth are restored with a crown or an implant-­ supported restoration, may demand a different treatment plan. In these cases, delayed implant placement may lead to mucosal margin recession also in the papillary region. Thus, whenever possible immediate implant placement with a flapless approach should be considered. Loss of interproximal papilla between proximal implant-­ supported rehabilitations is common, although there are certain soft tissue management procedures that have been suggested for interproximal

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papilla augmentation [70], a minimal distance of at least 3 mm between the implants seems to be necessary [71] (Figs. 8.12, 8.13, 8.14, 8.15, 8.16, 8.17, and 8.18).

Fig. 8.12 Preoperative periapical X-ray shows an implant-supported restoration in the central left incisor area, a fissure was present on the palatal aspect of the lateral incisor, indicating its extraction

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8.2.1.1 Primary Soft Tissue Coverage on Immediate Implants Sites Second stage implant surgery for implant uncovering allows further soft tissue management, opposite to flapless transmucosal implant placement. Submerged implant protocols through primary soft tissue closure over the immediate implants could have advantages especially in cases with preoperative gingival recession, thin periodontium, and high esthetic risk. The soft tissue covering the occlusal aspect of the implant may be displaced at second stage surgery to create or enlarge the buccal keratinizing tissue, and/or augment the buccal and interproximal areas tissue volume [72–75]. However, raising and coronally advancing a buccal flap should be avoided, it may cause enhanced resorption of the thin buccal plate, and change the muco-gingival junction position while reducing the keratinized tissue width [34]. Primary wound closure is more difficult to obtain at immediate implant sites, and consecutive wound failure is more frequent in these cases [49]. Due to largely reduced blood supply, free gingival and connective tissue grafts applied over the implant cover screw have a low survival rate; these grafts sealing fresh extraction sites are mainly dependent on underlying tissue vascularization and have unpredictable outcome [76]; furthermore, they are usually indicated for single tooth cases. Rotated palatal flaps offer a valuable treatment alternative to achieve primary soft t­ issue closure without raising a buccal flap [72, 73, 77–83]. Rotated split palatal flap is a surgical approach

Fig. 8.13  Preoperative CT scan serial slices show a palatal bone defect with an intact, and thick facial bony plate on the lateral incisor

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Fig. 8.14  Preoperative clinical aspect shows correct gingival contour on the implant-supported restoration on the left central incisor with a shorter clinical crown on the lateral, indicated for extraction

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Fig. 8.17  After 3  months for soft tissue stabilization, a final implant-supported restoration was placed. Result shows minimal mucosal margin changes and even improvement in the papilla aspect between the two implants (compared to Fig. 8.14)

Fig. 8.15 After extraction of the lateral incisor, an implant was immediately placed close to the palatal wall, without raising a buccal flap in a single stage protocol

Fig. 8.16  A provisional restoration was adapted immediately after implant placement

Fig. 8.18  Postoperative periapical X-ray shows both implant-supported restorations; distance between implants is beyond 3 mm to avoid vertical bone resorption in the area, maintaining the papilla between the implants

(Figs.  8.19, 8.20, 8.21, 8.22, 8.23, 8.24, 8.25, 8.26, 8.27, and 8.28) based on a rotated splitthickness palatal flap (RSPF) containing periosteum and connective tissue, covering the implant and bone graft; if applied [79], however, the technique is sensitive and applicable only where the palatal tissues are thicker than 5  mm (Figs.  8.29, 8.30, 8.31, 8.32, 8.33, 8.34, 8.35, 8.36, and 8.37). Rotated palatal is applicable for

all types of palatal tissues and consists of a pediculate full thickness palatal flap that is labially rotated (Figs.  8.38, 8.39, 8.40, 8.41, 8.42, 8.43, 8.44, 8.45, 8.46, 8.47, 8.48, 8.49, 8.50, 8.51, 8.52, and 8.53); this procedure is easier to perform and presents lower patient morbidity [80] (Figs.  8.54, 8.55, 8.56, 8.57, 8.58, 8.59, 8.60, 8.61, 8.62, 8.63, 8.64, 8.65, 8.66, 8.67, and 8.68).

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Fig. 8.21  Empty socket immediately after tooth extraction, the buccal flap was slightly raised to illustrate thickness of buccal bone and not for treatment purpose

Fig. 8.19 Preoperative periapical radiograph shows upper central incisors, left incisor, rehabilitated with a full crown presents with a vertical root fissure, commanding its extraction

Fig. 8.20  Preoperative aspect of the area, slight gingival recession and thin soft tissue biotype is evident

Fig. 8.22  Implant placed close to the palatal bony wall leaving a void with the buccal bony plate

Fig. 8.23  Rotated split palatal flap procedure where the deeper layer covers the implant and grafted fresh alveolus. The deep part of the palatal tissues, containing connective tissue and periosteum is sutured to the buccal tissues

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Fig. 8.24  Occlusal aspect. The superficial layer of the split palatal flap, containing connective tissue and epithelium, has been repositioned partially covering the previously rotated deep layer. Connective tissue is left exposed to heal by secondary intention

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Fig. 8.27  Occlusal aspect without the restoration, the slight buccal concavity is no longer present

Fig. 8.25  Buccal aspect. No flap was raised on the facial side, interdental tissues are left untouched. Primary soft tissue closure is achieved only by the rotated split palatal flap

Fig. 8.28  Buccal aspect of the area shows adequate mucosa morphology, allowing proper restoration emergence profile

Fig. 8.26  Occlusal aspect of the area, following 4 months of healing, note soft tissue full coverage of the area. However, a certain concavity may be appreciated on the buccal aspect. Soft tissue management at the time of implant uncovering may be performed

Fig. 8.29  Upper right incisor presents with a fissure on the palatal aspect, commanding its extraction

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Fig. 8.30 Empty socket immediately after tooth extraction

Fig. 8.33  Final sutures achieving primary soft tissue closure with the rotated split palatal flap

Fig. 8.31  An implant has been placed and grafting with a biomaterial performed

Fig. 8.34  Buccal aspect of the area, no buccal flap has been raised; maximum of soft tissue is preserved and partially augmented

Fig. 8.32  A rotated split palatal flap procedure is performed for primary soft tissue closure. The deep layer has been sutured to the buccal tissues

Fig. 8.35  Buccal aspect of the area after healing for a few months, note soft tissue contour

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Fig. 8.36  Occlusal aspect shows a slight concavity indicating soft tissue management at the time of second stage implant surgery

Fig. 8.37  Final restoration in place

Fig. 8.38  Preoperative view of first right upper premolar, due to a buccal root fissure the tooth was indicated for extraction. Note gingival recession commanding a staged procedure for its treatment

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Fig. 8.39 Periapical preoperative radiograph shows radiolucency, proximal teeth have correct bone support

Fig. 8.40  The tooth has been extracted without raising a buccal flap

Fig. 8.41  Implant has been placed close to the palatal bony wall and buccal area grafted with a non-resorbable xenograft

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Fig. 8.42 After implant placement, a full thickness pediculate palatal flap is prepared and facially rotated to achieve primary soft tissue closure over the implant site. Incisions are beveled to avoid bone exposure

Fig. 8.43  Palatal aspect. Final sutures after the procedure completed. A small area in the palate, covered by connective tissue heals by secondary intention

Fig. 8.44  Occlusal aspect after completion of the procedure, enhanced soft tissue thickness is evident

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Fig. 8.45  Fixed interim partial denture bonded to proximal teeth. Especially in esthetic areas, a removable provisional restoration should be avoided

Fig. 8.46  Occlusal aspect of the alveolar ridge after retrieval of the provisional restoration, at second stage implant uncovering surgery. Note dimensions of the ridge, with no collapse on the facial aspect

Fig. 8.47  Buccal aspect at the time of implant uncovering, positive soft tissue architecture is clear

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Fig. 8.48  A U-shaped incision opening towards the buccal aspect has been performed. Soft tissue covering the implant has been buccally displaced and then split into two proximal mini-flaps to enhance soft tissue volume in buccal and proximal areas. According to [75]

Fig. 8.51  The soft tissue excess has been eliminated and the provisional restoration relined to allow proper soft tissue contouring. Correct implant positioning, 3 mm apical to the gingival margin of the proximal teeth allowed a simple soft tissue excisional procedure

Fig. 8.49  Occlusal aspect after completion of the second stage implant uncovering procedure. Primary soft tissue closure at the time of implant placement allows soft tissue management to enhance the buccal and interproximal areas performed at the time of second stage implant uncovering procedure

Fig. 8.52  Soft tissue aspect before impressions for final restoration. Note buccal contour at the implant site, similar to proximal teeth. The contouring has been achieved and evaluated with the provisional restoration, assuring the outcome of the definitive rehabilitation

Fig. 8.50  After initial healing a provisional restoration has been placed. Besides a diagnostic value, provisional restorations contour the soft tissues to achieve a correct emergence profile before impressions for the final restoration are taken. In this case, soft tissue excess is evident

Fig. 8.53  Final restoration in place

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Fig. 8.54  Preoperative aspect of upper front teeth. Root fracture in right incisor commanded its extraction

Fig. 8.55 Tooth has been extracted with a flapless approach, preserving buccal tissues attachment to underlying bone

Fig. 8.56  The site preparation for implant placement has been performed on the palatal aspect, and not following the empty socket

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Fig. 8.57  Implant has been placed in the prepared osteotomy. Note buccal space

Fig. 8.58  Voids between the implant and hard tissues have been filled with a non-resorbable xenograft for soft tissue support

Fig. 8.59  A full thickness pediculate palatal flap has been prepared. Beveled incisions are performed to avoid bone exposure after flap rotation

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Fig. 8.63  Buccal aspect of area shows acceptable soft tissue contour Fig. 8.60  Palatal aspect after completion of the procedure. The palatal flap has been rotated to cover the implant grafted site and achieve primary soft tissue closure. Tensionless primary soft tissue coverage has been achieved with the rotated palatal flap, a minimal area will heal by secondary intention. Augmented soft tissue thickness covering the grafted implant may be appreciated

Fig. 8.64  Implant uncovering procedure to enlarge the volume of buccal soft tissue was performed applying a modified roll technique. A pouch was created by undermining the buccal tissues and the deep part of the partial thickness palatal flap has been introduced underneath enlarging the volume of the area. The superficial layer of the partial thickness flap is replaced to achieve soft tissue closure of the area Fig. 8.61  Occlusal aspect of the area 5  days following implant placement. Advanced healing and vitality of the rotated tissues is evident

Fig. 8.62  Occlusal view of the area after a few months healing, note the slight concavity on the buccal aspect that can be solved by soft tissue management at the time of implant uncovering. Primary soft tissue coverage of the area has been preserved

Fig. 8.65  Aspect a few days after the uncovering procedure. Note enhanced buccal soft tissue contour

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Fig. 8.66  Provisional restoration fitted on the implant abutment. Provisional restoration contours the soft tissues and has an important diagnostic role

Fig. 8.67  Aspect of soft tissues before impressions for final restoration. Note buccal contour at the implant site, similar to proximal teeth. Provisional restoration provides soft tissue contouring, and once optimized, final restorations may be performed

Fig. 8.68  Final restoration in place, note adequate buccal and inter proximal soft tissue contour

8.2.2 Early Implant Placement Delaying implant placement for a few weeks after tooth extraction, especially in compromised sites, presents several advantages. Soft tissues

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spontaneous healing provides additional keratinized mucosa. Soft tissue thickening mainly in sites with a thin or a damaged facial bone wall [84] with enhanced vascularity improves its healing capacity, diminishing needs for soft tissue augmentation, and ameliorating flap manipulation. Early implant placement allows for resolution of local infection and increase in area and volume of soft tissue for flap adaptation [85]. New bone formation will take place at the apical portion of the socket enhancing implant primary stability. Radiographic 3D imaging shows the real situation after tooth extraction, and proximal to surgical intervention for implant placement or bone augmentation; thus, treatment planning is more precise. Procedures are simpler, tooth or teeth extraction is performed in a previous surgical intervention, and, after the short healing period, soft and/or hard tissue augmentation may be performed previous or at the time of implant placement [77, 85]. As previously discussed, a minimal width of 1–2 mm of buccal bone is necessary to maintain a stable vertical dimension of the alveolar crest. However, this is not likely to occur, especially in the anterior maxilla where 87% of the bony walls have less than 1  mm width and only 3% of the walls are 2 mm wide. In the posterior sites, the corresponding values were 59 and 9%, respectively. The mean width of the buccal and palatal bony walls is 1 and 1.2 mm, respectively. For the anterior maxillary sites, the mean width of the buccal bony wall is 0.8 mm, while it was 1.1 mm for the premolar sites [86]. Since a minimal buccal bone width of 2 mm is necessary to maintain a stable buccal bony wall, only a limited number of sites in the anterior maxilla display such situation, accordingly, in most cases, especially in the anterior areas, augmentation procedures are needed to achieve adequate bony contours. Following extraction of teeth with advanced bone loss, as is the case of those with periodontal-endodontic lesions, needs for bone augmentation is likely. Bone augmentation procedures are commonly based on the application of barrier membranes isolating the bone-grafted defect from soft tissue interference. The four corner stones for bone augmentation procedures are

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presence of bone forming cells, primary wound closure, space creation and maintenance and angiogenesis. Early spontaneous barrier membrane exposure in GBR procedures has a significant detrimental influence on bone augmentation ­outcome, both if performed as a separate procedure or together with implant placement [87, 88]. Sites without membrane exposure showed 74% more horizontal bone gain for alveolar ridge augmentation and 27% more defect reduction for peri-­implant dehiscence defects than the sites with exposure [89]. Spontaneous early barrier membrane exposure due to wound dehiscence is more frequent when augmentation procedures are performed immediately after tooth extraction, both with and without concomitant implant placement [49, 78, 81]; therefore, it should preferably be avoided immediately after tooth extraction and performed only after a few weeks, when soft tissue healing is advanced.

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Fig. 8.69  Upper right lateral incisor presented with serious esthetic problem due to advanced gingival recession and pathologic migration, large loss of periodontal support and increased mobility. Since no predictable treatment alternative was available, tooth extraction was scheduled

8.2.3 Primary Soft Tissue Closure Primary soft tissue closure to achieve healing by primary intention is always preferred due to a more rapid healing and earlier soft tissue tensile strength gain; however, following tooth extraction, due to lack of soft tissue coverage, secondary intention healing usually occurs. After tooth/ teeth extraction, primary soft tissue closure may be achieved by raising and coronally displacing a buccal flap; however, as previously mentioned, this type of procedure will cause a coronal shift in the muco-gingival junction and exposure of the remnant buccal bone, reducing even further its blood nourishment. In the maxilla, rotated palatal flaps can be used to achieve primary soft tissue at the time of tooth extraction to accelerate soft t­issue healing and gain keratinized tissue without involving the buccal area [78, 82]. After initial soft tissue healing, usually 4–6  weeks, a bone augmentation procedure may be performed previous or concomitant with implant placement, according to the defect dimensions (Figs.  8.69, 8.70, 8.71, 8.72, 8.73, 8.74, 8.75, 8.76, 8.77, 8.78, 8.79, 8.80, 8.81, 8.82, 8.83, and 8.84). This 2-stage surgical protocol allows

Fig. 8.70  Occlusal aspect shows pathologic tooth malposition in the arch

Fig. 8.71 Aspect immediately after tooth extraction. Note apical position of the soft tissue margin

implants placement in compromised sites, together with bone augmentation procedures, shortly post extraction with good clinical results [77]. In a study, where a rotated palatal flap was

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Fig. 8.72  Rotated palatal flap has been prepared to achieve primary soft tissue closure of the fresh extraction socket. Note beveled incisions to avoid bone exposure after flap rotation

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Fig. 8.75  Buccal aspect of the area 1  week post tooth extraction and primary soft tissue coverage. Tissue vitality is evident

Fig. 8.76  Buccal aspect a few weeks after the procedure, note soft tissue healing with considerable reduction of the buccal defect Fig. 8.73  Sutures following buccal rotation of the full thickness palatal flap achieving primary soft tissue closure. Small areas will heal by secondary intention

Fig. 8.74  Occlusal aspect, single interrupted resorbable sutures secure the rotated palatal flap to the buccal tissues to achieve primary soft tissue healing. Beveled incisions in the palate prevent bone exposure

Fig. 8.77  Implant in its final position showed vertical and lateral bone defects. Bone augmentation around the implant was performed to treat bony defects while at the same time achieving the best hard and soft tissue architecture for the future restoration. Combination of mineralized allograft and xenograft was applied

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Fig. 8.78  Bone graft has been covered by a double layer of a cross-linked collagen membrane

Fig. 8.81  Buccal aspect of the area after a few months healing, the vertical defect has been completely resolved

Fig. 8.79  Final sutures after completion of the surgical procedure. The buccal flap has been coronally displaced through periosteal releasing incisions and tensionless sutured to the palatal tissues

Fig. 8.82  Occlusal aspect, primary soft tissue closure has been maintained, allowing a good soft and hard tissue architecture

Fig. 8.80  Palatal aspect of the area after a few days, note primary soft tissue closure, no membrane exposure, assuring undisturbed healing

Fig. 8.83  A minimal U-shaped incision allows implant uncovering, note soft tissue thickness and bone graft particles in the coronal aspect of the implant

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Fig. 8.84  Buccal aspect of sutures immediately after the second stage implant uncovering. Note complete resolution of the vertical defect that was present at the time of tooth extraction (Fig. 8.69)

used to achieve primary soft tissue closure after extraction of maxillary teeth and implants were placed after a few weeks together with bone augmentation procedures, the mean percentage of defect reduction (clinical bone fill) was 97%, no wound dehiscence occurred, meaning that most defects were completely healed at second stage surgery for implant uncovering [77]. Implants placed immediately after tooth extraction together with bone augmentation procedures showed higher incidence of wound dehiscence and concomitant lower degrees of bone healing [78]. In a comparative study that evaluated bone reconstructive treatment outcome for buccal dehiscence defects around immediate, delayed, and late maxillary implants placed together with collagen membranes, the best results were obtained with early implantation and the worst for late implantation. Differences between groups were statistically significant. The mean percentage of the reduced defect height and area was significantly smaller in cases where wound dehiscence lead to spontaneous barrier membrane exposure [81]. A similar procedure may be performed when multiple proximal extractions are performed (Figs. 8.1, 8.2, 8.3, 8.4, and 8.5); however, in cases of teeth extraction on both sides of the middle line, a double RPF should be considered (Figs  8.85, 8.86, 8.87, 8.88, 8.89, 8.90, 8.91, 8.92, 8.93, 8.94, 8.95, 8.96, 8.97, 8.98, 8.99, 8.100, 8.101, 8.102, 8.103, 8.104, 8.105, 8.106, 8.107, 8.108, 8.109, 8.110, 8.111, 8.112, 8.113, 8.114, 8.115 and 8.116).

Fig. 8.85  Periapical radiograph of upper incisors, large reduction of bone support, together with clinical signs of inflammation, flaring and extremely increased mobility commanded all four incisors extraction. Implant-­ supported rehabilitation was considered the best treatment alternative

Fig. 8.86  Immediately after teeth extraction, empty alveoli were debrided. Epithelium lining the coronal part of the alveoli was eliminated

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Fig. 8.87  Two palatal full thickness pediculate flaps were prepared and buccally rotated, note that the pedicle receives nourishment from the distal area. Incisions are beveled to avoid bone exposure after flap rotation. Buccal tissues were not raised from the underlying bone

Fig. 8.90  Occlusal aspect of the area after few weeks healing, note soft tissue contour, as was achieved immediately after finalizing the procedure, no soft tissue sloughing occurred

Fig. 8.88  Simple interrupted sutures fixed the palatal flaps to the buccal tissues and the palatal incisions. Certain areas in the palate will heal by secondary intention

Fig. 8.91  Access incision for implant placement together with bone augmentation or bone augmentation alone is performed within the palatal tissues that were rotated

Fig. 8.89  Buccal aspect after few weeks healing, note advanced soft tissue healing, achieved by primary soft tissue closure

Fig. 8.92  Buccal flap was raised, allowing access to the residual alveolar ridge for implant placement or bone augmentation procedures, easy flap manipulation together with early achieved soft tissue tensile strength reduce risk for wound dehiscence

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Fig. 8.93  Upper anterior area presents with a failing restoration due to secondary caries, increased mobility and severe periodontal involvement

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Fig. 8.95  Empty alveoli immediately after extraction of the three incisors. A buccal flap was not raised. Following debridement, epithelial lining in the internal aspect of the empty sockets was retrieved

Fig. 8.96  Primary soft tissue closure was achieved with a double pediculate rotated palatal flap. Minimal areas with exposed connective tissue will heal by secondary intention

Fig. 8.94  Periapical radiograph shows left incisors with minimal remaining bone support

Fig. 8.97  Occlusal aspect a few weeks after teeth extraction shows advanced soft tissue healing

8.2.4 Ridge Preservation

pronounced than the vertical. Ridge preservation procedures are intended to preserve the ridge volume within the envelope existing at the time of extraction, preventing alveolar ridge atrophy to facilitate adequate implant placement; while ridge augmentation is performed to increase the

Tooth extraction results in a statistically significant horizontal and vertical resorption of the alveolar ridge, as part of the natural remodeling, the magnitude of the horizontal shrinkage is more

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Fig. 8.98  Two implants were placed, according to a surgical stent in the lateral incisors areas. In the esthetic area, whenever possible, proximal implants should be avoided, to allow future interproximal areas soft tissue contouring. Note extensive implant surface exposure, mainly on the buccal aspect of right side implant

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Fig. 8.101 Multilayered resorbable collagen cross-­ linked membrane applied to cover the bone graft

Fig. 8.102  Buccal flap was released, coronally advanced and sutured to achieve primary soft tissue closure over the augmented area Fig. 8.99  Enamel matrix proteins derivative (Emdogain®) being applied on denuded root surface proximal to implant site to enhance periodontal reconstruction

Fig. 8.100  Bone grafting on the buccal side of implants and the edentulous ridge

Fig. 8.103  Occlusal aspect, tensionless primary soft tissue closure has been achieved by coronally displacing the buccal flap, after sufficient release

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Fig. 8.104  Occlusal aspect shows advanced wound healing a few days after the procedure

Fig. 8.105  Occlusal aspect after a few months healing, no spontaneous membrane exposure occurred during this period, improving success of bone augmentation procedure

Fig. 8.106  Large lateral bone augmentation has been achieved, as compared with Fig.  8.98, at the time of implant placement. Crestal buccal bone thickness of over 2 mm allows stable long-term results

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Fig. 8.107  Soft tissue grafting on the buccal aspect of the implants is performed to further improve soft tissue quality

Fig. 8.108  Sutures after completion of second stage implant uncovering surgery

Fig. 8.109  A fix interim partial denture has been fitted on the implant abutments. The provisional restoration is used to achieve a proper soft tissue contour with the use of ovate pontics, applying pressure on the residual alveolar ridge and contouring the marginal mucosa at the implants sites. A similar procedure is performed every 2 weeks until desired soft tissue architecture is achieved

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Fig. 8.110  Buccal aspect of the area after 2 weeks shows initial formation of papilla like areas in the interproximal areas as well as mucosa “scalloping”

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Fig. 8.113  Occlusal aspect of the area after the second “soft tissue sculpturing” procedure, difference in ridge and interproximal soft tissue contour compared to the previous session may be appreciated

Fig. 8.111  Occlusal aspect of the area after 2  weeks shows indentations achieved with the ovate pontics, a similar procedure may again be performed, at this time, to further improve soft tissue architecture Fig. 8.114  Buccal aspect of the area after the third “soft tissue sculpturing” procedure, note enhanced papillae volume and scalloping compared to previous sessions

Fig. 8.112  Buccal aspect of the area after a second “soft tissue sculpturing” procedure, note enhanced papillae volume compared to the previous session Fig. 8.115  Occlusal aspect of the area after the third “soft tissue sculpturing” procedure, difference in ridge and interproximal soft tissue contour compared to previous sessions may be appreciated. After achieving the desirable soft tissue architecture, the final restoration may be prepared

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Fig. 8.116  Final restoration fitted in place

ridge volume beyond the skeletal envelope existing at the time of extraction [90]. Ridge augmentation, different from preservation procedures, are generally performed using biomaterials covered with barrier membranes, which commands flap raising to achieve primary soft tissue closure. As earlier discussed, early spontaneous barrier membrane exposure after GBR procedures has a significant detrimental influence on bone augmentation outcome [87, 88]. Sites without membrane exposure showed 74% more horizontal bone gain for alveolar ridge augmentation and 27% more defect reduction for peri-implant dehiscence defects than the sites with exposure [89]. Spontaneous early barrier membrane exposure due to wound dehiscence is more frequent when augmentation procedures are performed immediately after tooth extraction [49, 78, 81]; therefore, this type of procedure should preferably be avoided immediately after tooth extraction and performed only after a few weeks, once soft tissue healing is advanced. Placement of a biomaterial in the empty socket commands delaying implant placement for few months, according to the type of graft applied. Although alveolar ridge preservation results in reduction in the vertical bone dimensional change following tooth extraction when compared to unassisted socket healing, the reduction in horizontal alveolar bone dimensional change is not complete and most important, unpredictable, likely due to the influence of local and systemic factors that are not fully understood. The type of alveolar ridge preservation intervention does not affect bone dimensional preservation,

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bone formation, keratinized tissue dimensions, and/or patient complications [91, 92]. Difficult to predict is in which cases alveolar ridge preservation will result in the maintenance of sufficient bone volume to place an implant in an ideal restorative position without the need of further bone augmentation procedures [93]. There is limited evidence to support the clinical benefit of alveolar ridge preservation over unassisted socket healing in improving implant-­ related outcomes despite a decrease in the need for further ridge augmentation during implant placement. Similar implant placement feasibility, survival/success rates, and marginal bone loss should be anticipated following alveolar ridge preservation or unassisted socket healing. Currently, it is not clear which type of alveolar ridge preservation procedure has a superior impact on implant outcomes [19, 94]. Only limited evidence supports the clinical benefit of alveolar ridge preservation, namely the reduction of necessity of further augmentation in conjunction with implant placement. No evidence exists on comparison of the survival or success rate of implants, placed in sites after alveolar ridge preservation or in control sites. No evidence exists on cost-effectiveness, patient’s preference, or quality of life following alveolar ridge preservation. The case selection criteria for performing alveolar ridge preservation remain undetermined. The presence of intact socket walls and primary flap closure are often associated with favorable results [95]. Histology demonstrated a large proportion of residual graft material that may account for some of the differences in alveolar ridge dimensions at follow-up [96]. Insertion of a biomaterial into the fresh socket will ease cell repopulation by conductivity. Most biomaterials are not bone inductive, but conductive, the origin of the cells that will repopulate the defect will establish the type of tissue that will be formed in that specific area. In the absence of a buccal wall, as is the case of teeth with large loss of bone support, following extraction, the cells that will repopulate mainly the coronal area originate mainly from the gingival connective tissue. Therefore, connective tissue and not bone will be the main

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tissue formed in that area (Figs.  8.117, 8.118, 8.119, and 8.120). Non-­resorbable biomaterials, as most xenografts, will limit the amount of vital bone formed and available for osseointegration. Many of the grafted sites evaluated in most articles had remnants of the graft materials in histologic samples. If the grafting material resorbs too quickly, the site may exhibit increased vertical and/or horizontal collapse of the alveolar socket. If the grafting material resorbs too slowly, the site may exhibit reduced amounts of vital bone formation [97]. Although some bone substitutes may be able to limit the resorption of post-­extraction alveolar ridge up to a certain extent, the grafts remnants interfere with normal healing process; therefore, the quality of the new tissue in the socket may not have ideal biological properties to anchor the

Fig. 8.117  CT scan of the lower right posterior area. A ridge preservation procedure was performed at time of extraction of the first molar with use of bovine bone mineral, without a barrier membrane. Note the clear demarcation between the graft material and the pristine bone, by a radiolucent area surrounding the more radio opaque roots like areas

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future implant [95]. Alveolar ridge preservation does not appear to promote de novo hard tissue formation. Due to the broad variety of employed materials, techniques, defect morphologies, healing periods, as well as the relatively small sample sizes, meta-analysis or comparative assessment of alveolar ridge preservation cannot be made. Consequently, no material or method can be claimed to serve superior to another [95]. Following ridge preservation procedures, bone quality might not be suitable for implant support (Figs.  8.117, 8.118, 8.119, and 8.120). In a human histomorphometric study where biopsies were taken 9  months after ridge preservation procedures with use of bovine bone mineral without a barrier membrane, findings revealed that in the coronal area, tissue consisted mostly of connective tissue (52.4%) and xenograft particles with minimal amounts of bone tissue area (15.9%) [98]. Sockets grafted with autologous bone exhibit a healing pattern similar to non-grafted post-extraction sites [99]. After 3  months healing, autologous bone-grafted and non-grafted alveoli were filled with similar amounts of mineralized bone (mainly woven bone) and marrow, the autograft material failed to enhance healing and/or to stimulate hard tissue formation in the socket. In comparison with sockets that had been filled with autologous bone, the bovine bone mineral plus collagengrafted sites exhibited a delayed healing pattern. Thus, in xenograft-treated sites, there was less mineralized bone, a smaller proportion of bone marrow and a substantial amount of remaining provisional connective tissue [99]. However, no significant differences in clinical outcome

Fig. 8.118  Sagittal serial CT slices of the case clearly show that the graft material is not integrated with the surrounding bone; a radiolucent area separates the bone graft from the patient’s bone

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Fig. 8.119  Clinical aspect of the area at the time of reentry, seven months after tooth extraction, the graft material fills the area previously occupied by the roots. However, it had “wet sand” aspect and consistency, the graft particles were within connective tissue, a delayed healing pattern with no or minimal bone formation was evident [99]

Fig. 8.120  The soft material in the sockets was removed with hand instruments. The soft tissue encapsulated xenograft prevented bone healing

between the different materials may be established, except for the collagen plug alone, which revealed negative results [90]. Primary soft tissue closure may lead to enhanced results [90]. Although there is no scientific evidence based on comparative studies, primary wound closure may have advantages. As discussed in the section concerning soft tissue management in immediate implants procedures, several treatment approaches have been suggested to achieve primary closure. Buccal flaps should be avoided, to prevent resorption of the thin buccal plate, and change the mucogingival junction position and reducing the keratinized tissue width. Due to largely reduced blood supply, free gingival and connective tis-

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sue grafts applied over the non-nourishing graft have a low survival rate; these grafts sealing fresh extraction sites are mainly dependent on underlying tissue vascularization and have unpredictable outcome [76]. Rotated full and slit palatal flaps earlier described offer a valuable treatment alternative to achieve primary soft tissue closure without raising a buccal flap. A surgical procedure to preserve the alveolar ridge after extracting maxillary anterior teeth with advanced bone loss indicated for toothsupported fixed partial denture rehabilitation applying a non-resorbable graft material and a rotated pediculate split-thickness palatal flap showed predictable results with minimal postoperative ridge deformation [83]. A split-­ thickness palatal flap in which the pediculated deep portion is rotated to cover the grafted alveolus showed useful to predictably obtain primary closure in the maxilla prior to or during implant placement [72, 73]. Soft tissue preservation or augmentation with 6–8 weeks of healing after tooth extraction before ridge augmentation procedures with or without concomitant implant placement seems to be the treatment of choice for cases with advance bone loss [100]. In the maxilla, primary soft tissue closure with rotated palatal flaps, without application of a bone graft at the time of extraction, enhances soft tissue healing [82], allows easier flap manipulation at the time of bone augmentation either with or without implant placement performed after a few weeks (Figs. 8.93, 8.94, 8.95, 8.96, 8.97, 8.98, 8.99, 8.100, 8.101, 8.102, 8.103, 8.104, 8.105, 8.106, 8.107, 8.108, 8.109, 8.110, 8.111, 8.112, 8.113, 8.114, 8.115, and 8.116). In conclusion, most systematic reviews and meta-analyses evaluating ridge preservation have found this procedures clinically and histologically unpredictable (Figs  8.117, 8.118, 8.119 and 8.120). Therefore, indications for ridge preservation procedures seem to be very limited and reduced to cases where implant placement has to be delayed for long periods; the restoration will be performed by conventional, tooth-supported, prosthetic treatment

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Fig. 8.121  Clinical aspect of upper anterior left area. Due to advanced periodontal destruction and increased mobility, lateral incisor was indicated for extraction. A tooth-supported fixed partial denture was planned as future rehabilitation

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Fig. 8.123  After tooth extraction and alveolus debridement, the area was primary closed with a rotated palatal flap. Note palatal beveled incisions. Improved soft tissue thickness in the occlusal socket area is evident

Fig. 8.124  Aspect after a few days healing, note integrity of the soft tissue rotated to achieve primary closure

Fig. 8.122  Periapical radiograph shows minimal remaining bone support on the lateral incisor

(Figs.  8.121, 8.122, 8.123, 8.124, 8.125, and 8.126) and to reduce the needs for elevation of the sinus floor by a lateral approach [101] (Figs. 8.127, 8.128, 8.129, 8.130, 8.131, 8.132, 8.133, 8.134, 8.135, 8.136, 8.137, 8.138, and 8.139).

Fig. 8.125  Buccal aspect after a few weeks healing, note preservation of the crestal ridge contour achieved by the rotated palatal flap procedure

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Fig. 8.126  Occlusal aspect after a few weeks healing, note preservation of the crestal ridge contour achieved by the rotated palatal flap procedure. Pontic emergence profile has been achieved by the ovate pontic technique previously described in Figs. 8.109, 8.110, 8.111, 8.112, 8.113, 8.114, 8.115, and 8.116)

Fig. 8.127  Panoramic X-ray shows upper left first molar with large carious lesion. Roots apexes are close or even beyond the sinus floor. Tooth was indicated for extraction

Fig. 8.128  Sagittal serial slices of the CT scan show that root apexes are very close to the sinus floor. Tooth extraction might cause rapid sinus pneumatization, command-

ing afterwards an open, lateral window approach, sinus floor elevation for implant placement

8.2.5 Ridge Augmentation

bone volume and properly develop the implant site [102, 104]. The principles of GBR are creation and maintenance of a secluded space for the desired period achieved by the application of resorbable or non-resorbable barrier membranes, excluding epithelial and connective tissues, to enable bone progenitor cell proliferation and ­differentiation into the isolated area and bone-­ grafting materials [105–108]. Cell occlusion and

Advanced alveolar bone atrophy may prevent appropriate implant placement. Various alveolar bone augmentation approaches have been suggested to enlarge the bone volume before or at the time of implant placement [102, 103]. Guided bone regeneration (GBR) is a well-documented surgical procedure to increase a limited alveolar

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Fig. 8.129  Tooth was extracted and empty alveolus filled with mineralized bone allograft, minimally raising the sinus Schneiderian membrane. Picture illustrates primary soft tissue closure by a rotated palatal flap

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Fig. 8.132  Clinical aspect of the area after 3 months healing. Complete soft tissue healing may be appreciated

Fig. 8.133 Panoramic X-ray shows ridge height preservation Fig. 8.130  Aspect of the area after 2 weeks healing, note full soft tissue coverage

Fig. 8.131  Periapical radiograph shows empty alveolus and proximal apical sinus floor filled with the bone allograft

space provision are critical factors for alveolar bone regeneration [109]. Survival rates of dental implants placed in conjunction with GBR are similar to those placed in native bone [110, 111]. Treatment of large vertical and horizontal ridge deficiencies with use of non-resorbable barrier membranes and particulate bone grafts [88, 112–117] and titanium mesh [118, 119] has been widely reported; resorbable collagen membranes have shown equally effective, even for alveolar bone augmentation of large defects [87, 88, 112, 113, 120–123]. No differences were observed between resorbable and non-resorbable barriers for vertical ridge augmentation [124]. A meta-­ analysis that evaluated guided bone regeneration using collagen membranes and particulate grafting materials in alveolar bone reconstruction

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Fig. 8.134  Serial CT sagittal scan slices show above eight millimeters between the sinus floor and the bone crest. Allowing for implant placement, without need for an open, lateral window access, sinus floor elevation

Fig. 8.135  Implants placed at the second premolar and first molar positions. A close sinus floor elevation through the osteotomy was performed at the molar site. Bone graft particles may be noticed

Fig. 8.136  Immediate postoperative radiograph shows implants in place together with bone graft beyond the sinus floor, used to raise the Schneiderian sinus membrane apically to the molar site implant with a closed sinus floor augmentation

Fig. 8.137  Immediate postoperative radiograph shows distal implant in place together with bone graft beyond the sinus floor, applied for a crestal sinus floor elevation

Fig. 8.138 Aspect of the area a few months after implant placement together with crestal approach sinus floor elevation. Note acceptable convex facial contour on both implant sites with acceptable keratinized attached mucosa

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Fig. 8.139  Periapical radiograph taken a few months after the procedure, sinus floor augmentation on the apical area of the distal implant is evident

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Fig. 8.140  Preoperative aspect, thick frenum insertion close to the alveolar ridge crest, missing left central incisor planned to be replaced by an implant-supported prosthesis. Frenectomy was performed before bone augmentation procedure

Fig. 8.141  CT scan sagittal serial slices show large horizontal bone deficiency, commanding a bone augmentation procedure before implant placement

concluded that particulate graft materials covered with resorbable collagen membranes is an effective technique [125]. Alveolar bone defect resolution was around 90%, statistically similar with both resorbable and non-resorbable membranes. Although both treatment modalities were clinically effective in regenerating bone as demonstrated by a similar horizontal thickness and vertical defect fill at 6 months, bone augmented with non-resorbable membranes exhibited significantly less horizontal bone thickness reduction from baseline to follow-up [126]. Complete defect fill may be equally obtained with non-­ resorbable ePTFE membranes and resorbable collagen membranes [127].

Non-absorbable membranes, mostly made of polytetrafluoroethylene, require a second surgical procedure for their retrieval. Therefore, bio-­absorbable membranes [87, 88, 120, 128] have become suitable alternative in bone regeneration procedures (Figs.  8.140, 8.141, 8.142, 8.143, 8.144, 8.145, 8.146, 8.147, 8.148, 8.149, 8.150, 8.151, 8.152, 8.153, 8.154, 8.155, 8.156, 8.157, 8.158, 8.159, 8.160, 8.161, 8.162, 8.163, 8.164, 8.165, 8.166, 8.167, and 8.168). Spontaneous membrane exposure leads to significant decreased new bone formation [88, 129]. This event seems to be frequent in bone augmentation procedures [88, 112, 113]. Early exposure, of non-resorbable membranes, to the

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Fig. 8.142  Aspect of the upper incisor area, gingival recession in both proximal teeth, mainly in right central incisor. Horizontal bone deficiency is evident

Fig. 8.143  Occlusal aspect shows ridge concavity in the area of missing tooth

Fig. 8.144  Large horizontal bone deficiency evident in the area of missing tooth. Probe shows horizontal thickness of residual alveolar of approximately 2 mm

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Fig. 8.145  Buccal aspect after intra-marrow perforations to enhance bone graft integration

Fig. 8.146  Double-layered bone grafting, the bone close to the bone surface is a mineralized freeze-dried allograft, while, a xenograft has been placed on top of the deeper layer. Two layers of a cross-linked collagen barrier membrane cover the bone graft

Fig. 8.147  Final internal mattress sutures after bone augmentation procedure, tensionless primary soft tissue closure is indispensable and achieved by proper flap releasing

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Fig. 8.148  CT scan sagittal serial slices show adequate bone healing after the bone augmentation procedure, allowing proper implant placement. Compare with preoperative aspect in Fig. 8.141

Fig. 8.149  Buccal aspect, note coverage of roots of proximal teeth, together with adequate ridge dimensions. Keratinized attached mucosa band in the toothless area is relatively narrow

Fig. 8.151  After flap elevation, alveolar ridge augmentation is evident as compared to Fig. 8.144

Fig. 8.150  Occlusal aspect shows considerable increase in alveolar ridge width, however, a small depression in the crestal part compared to proximal teeth is evident

Fig. 8.152  Implant with cover screw in place, buccal aspect. Implant platform is situated 3  mm apical to the line linking the gingival margins of the proximal teeth

oral environment and subsequent contamination [129] commands their entire early removal [88]. Spontaneously exposed resorbable membranes disintegrate, losing their barrier function at the exposed site; however, part of the membrane remains functional within the tissues [128, 130, 131]. Successful regeneration is possible

provided cell exclusion and space maintenance are continued throughout the time needed. This can vary between 3 and 12  months, depending on the dimensions of the bony defect [132, 133] (Figs. 8.169, 8.170, 8.171, 8.172, 8.173, 8.174, 8.175, and 8.176). The main factor for success of bone augmentation procedures with use of bar-

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Fig. 8.153  Occlusal aspect of implant in place. Buccal bony wall thickness is over 2 mm

Fig. 8.154  Enamel matrix proteins derivative (Emdogain®) applied to denuded root surfaces proximal to implant site

Fig. 8.155 Occlusal aspect with connective tissue retrieved from the palate sutured in place. Purpose of the procedure is to enhance the soft tissue profile and further cover exposed root surfaces

rier membranes is avoiding spontaneous early membrane exposure [81, 88, 134, 135]. There is a large variation on the incidence of this event ranging from 15% to almost 50% of the cases,

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Fig. 8.156  Enamel matrix proteins derivative (Emdogain®) applied on the connective tissue graft to enhance gingival fibroblasts vitality and soft tissue healing

Fig. 8.157  Final sutures after completion of procedure of implant placement and soft tissue grafting. Connective tissue graft is exposed at the gingival margins of proximal teeth

depending on the type of membrane and treated defect [87, 88, 116, 136]. As already discussed, performing bone augmentation procedures immediately after tooth extraction, ­ especially when dealing with large defects, significantly enhances the risk for wound dehiscence, leading to decreased bone formation, and should, therefore, be avoided. A treatment alternative that allows for soft tissue healing before performing the bone augmentation procedure is advised. Resorbable barrier membranes may be applied in a selective double layer technique; the deeper layer completely covers the bone graft and underlying bone and the superficial layer covers mainly the defect area, for vertical deficiencies, the occlusal and for lateral, the buccal (Figs. 8.177, 8.178, 8.179, 8.180, 8.181, 8.182, 8.183, and 8.184). The rational for this application is that in case of small wound dehiscence and subsequent membrane exposure, the superfi-

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Fig. 8.160  Occlusal aspect of alveolar ridge with adequate buccal soft tissue contour

Fig. 8.158 Periapical radiograph taken shortly after implant placement Fig. 8.161  An access minimal incision is performed for implant uncovering and the soft tissue is buccally pushed. The healing abutment is inserted, appropriate soft tissue contour is evident

Fig. 8.159  Buccal aspect of the area at the time of second stage surgery for implant uncovering. Complete root coverage and enhanced keratinized mucosa band as compared to preoperative situation and before implant placement and soft tissue grafting (Figs. 8.142 and 8.149)

cial layer may resorb, while soft tissue may heal and cover the deeper layer [130]. Furthermore, the use of a double-layered membrane results in a barrier of increased collagen area and thickness, compared with application of a single layer [137]. Collagen membranes can reduce bone graft resorption; the double-layer technique has proven more effective than the single in experi-

Fig. 8.162  Occlusal aspect of area with healing abutment in place, note difference with situation before implant uncovering (Fig. 8.161)

mental bone augmentation procedures [138]. Remnants of the membranes could usually be appreciated, in cases with undisturbed healing (Figs. 8.185, 8.186, 8.187, 8.188, 8.189, 8.190, 8.191, 8.192, 8.193, 8.194, and 8.195); however,

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Fig. 8.163  Provisional restoration in place used for soft tissue contouring and diagnostic before preparation of the final restoration

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Fig. 8.166  Occlusal aspect of the implant site with no restoration, note proper contouring achieved with the provisional restoration

Fig. 8.167  Final restoration in place. Note even gingival margins in all proximal teeth after gingival recession correction in natural teeth

Fig. 8.164  Buccal soft tissue contour and emergence profile as evaluated with provisional restoration are adequate

Fig. 8.168  Periodontal probe illustrates ridge thickness of less than 2 mm in the crestal area, not allowing implant placement

Fig. 8.165  Buccal aspect of area with no provisional restoration, soft tissue contouring with the provisional restoration has been achieved

they were not always present where spontaneous exposure had occurred [130]. Membrane degradation starts shortly after implantation [139]. Membranes should be appropriate to the clinical

demands of each case, barriers with high degradation rates might have a shorter than desired effect [140]. The effect of collagen membrane coverage on bone graft volume maintenance is dependent on the membrane integrity and stability during healing [141]. Although the advantage of slowly resorbable collagen barrier membranes in healing of bone defects is still not clear [142] and no definite landmarks are available, it has

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Fig. 8.169  Intra-marrow perforations have been performed to enhance graft vascularization

Fig. 8.170  Bone graft in place, augmenting the lateral ridge dimension

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Fig. 8.172  Final sutures after the ridge augmentation procedure. Note eversion of the mucosal margins to achieve contact between the connective tissue layers of both buccal and lingual flaps, avoiding their invagination, leading to epithelial interposition

Fig. 8.173  Aspect of the area after 3  weeks healing, complete soft tissue coverage over the augmented area is preserved

Fig. 8.171  Two layers of a cross-linked collagen barrier membrane applied covering the bone graft. Since both buccal and lingual augmentation were performed, the membrane was placed completely covering the ridge as “horse saddle”

Fig. 8.174  Periodontal probe illustrates ridge thickness in the crestal area largely increased compared to the preoperative situation as seen in Fig. 8.168

been suggested that 1  month barrier function time for each millimeter of bone regeneration are needed; accordingly, 2–3-month barrier function time will be required for small dehiscence and fenestration defects; however, larger defects may require longer barrier function times

[143]. In small surgically created defects, boneto-implant contact and bone fill values increased over time in membrane covered defects; however, membrane exposure was associated with loss of supporting alveolar bone even occurring 10–12 weeks post implantation [135]. Collagen

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Fig. 8.175  Occlusal aspect of alveolar ridge after implant site preparation for 4  mm implant diameter, note aspect and quality of newly formed ridge

Fig. 8.176  Anteroposterior slice of left posterior mandible shows recent extraction site and a short distance between the inferior alveolar nerve canal and the ridge crest Fig. 8.177  CT scan sagittal serial slices of left posterior mandible show limited bone height above the inferior alveolar nerve canal

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membranes with a higher degree of cross-linking remain intact for longer periods [140, 144]. Angiogenesis pattern of native and cross-linked collagen membranes: an immunohistochemical study in the rat. This could enable improved healing of larger defects [145, 146], and therefore may offer advantages for treatment of large non-self-contained bone defects, where prolonged membrane barrier functions are desirable [131] (Figs.  8.185, 8.186, 8.187, 8.188, 8.189, 8.190, 8.191, 8.192, 8.193, 8.194, and 8.195).

Fig. 8.178  After intra-marrow perforations, the osteotomies were prepared for placement of two implants in the molar sites. Implants were only partially inserted into the existing bone, achieving excellent primary stability, while the coronal part was left exposed

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Fig. 8.179  Exposed implants surface and the surrounding alveolar ridge were grafted with a combination of allograft and xenograft

Fig. 8.180  Multiple layers of a cross-linked collagen barrier membrane were applied covering beyond the grafted area; first membrane layer is applied in a “horse riding saddle” form, covering both buccal and lingual aspects

Fig. 8.181  Sutures after finalization of the procedures, internal mattress sutures create mucosal margins eversion allowing close contact between the connective tissue layers of both buccal and lingual flaps

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Fig. 8.182  Aspect of the area 6 months after implant placement, note primary soft tissue closure with no wound dehiscence or spontaneous implant exposure

Fig. 8.183  Aspect of the area at the time of second stage implant uncovering surgery. Note healing around the implants as compared to initial situation as shown in Fig. 8.178

Fig. 8.184  Implant cover screws were retrieved, and a thin layer of non-mineralized tissue on the most coronal part of the implant connector was eliminated. The entire textured implant surface is embedded in newly formed bone

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Fig. 8.185  CT scan sagittal serial slices of right posterior mandible show very limited bone height above the inferior alveolar nerve canal, not allowing implant placement, especially in the distal areas

Fig. 8.186 After intra-marrow perforations, stainless steel tenting screws were placed. Tenting screws were only partially inserted into the existing bone, achieving primary stability, while most of their length was left exposed to serve as support for the vertical bone augmentation procedure

Fig. 8.187  Bone graft around and on top of the tenting screws and the underlying bone was performed

Fig. 8.188  Two layers of a cross-linked collagen barrier membrane applied cover the bone graft and underlying bone, supported by the tenting screws. Membranes were placed covering the ridge as “horse saddle”

Fig. 8.189  Sutures after finalization of the procedure, internal mattress sutures create mucosal margins eversion allowing close contact between buccal and lingual flaps connective tissue layers

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Fig. 8.190  Aspect of the lower left area 7 months after the bone augmentation procedure, primary soft tissue over the augmented area has been maintained throughout the entire healing period

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Fig. 8.194  Implants inserted in the augmented bone

Fig. 8.195  Panoramic X-ray post-implant placement on both sides of the jaw Fig. 8.191  Access incision shows remnants of the collagen barrier membranes still in place

Fig. 8.192  After flap raising, tenting screws are completely covered by newly formed tissue. Compared with Fig. 8.186, large degree of new tissue formation may be appreciated

Fig. 8.193  Occlusal aspect of the area shows the heads of the three tenting screws while the newly formed tissue covers their whole extent

Slow-resorption collagen membranes have the potential to promote vertical ridge augmentation [122]. However, certain cross-linked membranes present reduced tissue integration and vascularity [144, 147] and, in clinical trials, have shown a higher incidence of spontaneous exposure following their application in the oral cavity [88]. Large vertical and/or horizontal ridge deficiencies may be treated with cross-linked collagen barrier membranes with good clinical outcome (Figs. 8.185, 8.186, 8.187, 8.188, 8.189, 8.190, 8.191, 8.192, 8.193, 8.194, and 8.195). For cases with large defects, a staged procedure where bone augmentation procedure is performed a few months before implant placement is indicated, if necessary, another bone augmentation procedure may be performed at that time. Although bone augmentation simultaneously performed with implant placement and staged, performed as a separate previous procedure show similar osseointegration levels over time, the staged approach shows enhanced newly formed bone, higher osteoconduction around the grafted mineral, less crestal bone resorption, better implant stability,

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and smaller vertical bone defect over time compared with the combined approach [148, 149]. Vertical bone augmentation procedures simultaneously performed with implant placement (Figs. 8.176, 8.177, 8.178, 8.179, 8.180, 8.181, 8.182, 8.183, and 8.184) may show bone growth in height close to, or in direct contact with the membrane; however, this new bone, generally, is not in direct contact with the implants; usually, a zone of dense connective tissue is interposed between the implants and the newly formed bone [150]. Accordingly, the formation of considerable amounts of bone following vertical ridge augmentation with particulate bone grafts simultaneously with implants placement is not ­accompanied by predictable osseointegration of the implants [150] and, therefore, should not be performed in cases where over 3  mm of bone height gain are necessary. There is no consensus concerning the best bone graft for each clinical application. Several bone grafts are available, namely: autogenous from the same patient, both from intraoral and extra-oral origin; allografts, mainly mineralized, from human donors; xenografts, mainly bovine bone mineral and alloplasts, synthetic materials. Autogenous bone has been considered the gold standard due to its osseoinductive and conductive properties, however; several inconveniences such as fast resorption rate, limited available amount, and patient morbidity limit their application. The vitality of autografts is not evident, the majority of the osteocytes of monocortical bone grafts do not survive grafting, and non-vital bone is progressively remodeled into new vital bone 7  months after grafting [151]. Allografts, xenografts, and alloplastic materials are currently applied with successful clinical outcome. Bone substitutes may replace autogenous bone for sinus lift procedures even in extremely atrophic sinuses [103, 152]. Mineralized freezedried bone allograft (FDBA) both in particulate [153–156] and blocks shapes [157] have been applied in bone augmentation procedures with successful clinical and histological outcome. In a study that evaluated the clinical outcome of augmentation procedures in largely atrophic alveolar ridges with the use of particulate FDBA

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with or without the addition of autogenous bone, applied in a bi-­layered technique, in conjunction with a resorbable ribose cross-linked collagen membrane, there was no added clinical effect of the use of autogenous bone. New bone formation within the defect appears to be completed by 7 months [158]. Bone grafts effectively enhance space-­provision, and this appears to be the principal mechanism by which biomaterials actually support bone regeneration [159]. A bi-layered (sandwich) bone augmentation procedure, for treatment of dehiscence defects based on the application of mineralized human cancellous allograft (inner layer), mineralized human cortical allograft (outer layer), and coverage with barrier membrane [134, 160], has reported good clinical results. Histomorphometric analyses of sites augmented with FDBA have revealed predictable acceptable results, showing over 40% new bone formation [153, 161]. When resorbable materials such as autografts, allografts, and alloplasts are applied, their resorption rate should accompany bony formation, otherwise large loss of volume with connective tissue replacement will occur [162, 163]. On the contrary, non-­ resorbable materials, as most xenografts, do not present loss of volume [162–164], however, will become included within the newly formed tissue, meaning that the biological and bio-mechanical characteristics will not be the same as pristine natural bone. Biomechanics and the reaction of this type of tissue including xenograft particles to peri-implant infections is not clear. Treatment alternatives, using layered bone grafting of bovine bone mineral on other resorbable materials to maintain the volume [165], while avoiding augmentation of large defects with this type of material as the only graft, have been suggested [166] (Figs. 8.77 and 8.146). In vertical bone augmentation procedures, without simultaneous implant placement, with use of non-self-supporting barriers and particulate bone grafts, tenting screws or osteosynthesis microplates may be used to prevent membrane and biomaterial collapse and preserve the space where bone can grow [87, 121, 167–171] (Figs.  8.186, 8.187, 8.188, 8.189, 8.190, 8.191, 8.192, 8.193, 8.194, 8.195, and

C. E. Nemcovsky et al.

186

8.196). A review of the “tentpole technique” that evaluated its effectiveness to augment large vertical alveolar ridge defects for implant placement was found that this procedure offers predictable functional and esthetic reconstruction of large vertical alveolar defects [172]. In cases with a vertical ridge deficiency, where a 2-stage procedure is performed, supporting stainless steel screws may be inserted in the treatment area, leaving part of their extension exposed, thus serving as supporting tenting posts. The rehydrated bone allograft is then applied to achieve the desired volume. In cases where the supporting screw/s become spontaneously exposed, they are retrieved shortly before implants placement, to allow for complete soft tissue healing previous to the next surgical procedure. Bone graft is usually covered with a resorbable cross-linked collagen barrier membrane. Membranes may be fixed to the underlying bone [120] to avoid displacement of particulate bone grafts at the time of wound closure which could result in partial collapse of the collagen membrane in the coronal portion of the augmented site. The stability of the bone substitute and collagen membrane may be enhanced by the application of fixation pins and by the use of block bone substitutes instead of particulate ones. When collagen membranes and particulate grafts are applied, the primary challenge seems to be the correct positioning and fixation of the graft and membrane [173]. The importance of intra-marrow perforations in bone augmentation procedures is not completely clear [174, 175]. Fig. 8.196 Flowchart of treatment alternatives, after tooth/teeth extraction, taking in consideration the integrity of the buccal bony plate

8.2.5.1 Flow-Chart Treatment Alternatives After Tooth/Teeth Extraction (Fig. 8.196) Considering the integrity of the buccal bony plate, following tooth or teeth extraction, there are two possibilities, either the buccal bone is intact or it is damaged. When the buccal plate is intact and in presence of ideal conditions, as already discussed, an immediate implant may be placed. Transmucosal placement both with and without provisional restoration and primary soft tissue closure are options after immediate implant placement. Under nonideal conditions, an early implant placement protocol, after a few weeks, should be preferred. Delaying implant placement for a few weeks after tooth extraction presents several advantages mainly concerning soft tissues healing. In the upper jaw, primary soft tissue closure with rotated palatal flaps enhances soft tissue healing. Implants are placed after a few weeks, if indicated; bone augmentation procedures may be applied. In cases where the buccal plate is damaged, demanding bone augmentation procedures, immediate implant placement should be avoided. In these cases, initial soft tissue healing after a few weeks will allow for better flap manipulation. In the upper jaw, primary soft tissue closure through rotated palatal flaps presents advantages, enhancing soft tissue healing. After 4–8 weeks healing, and according to a CT scan, performed after tooth/teeth extraction, if fully predictable, when initial implant primary stability in an ideal position can be achieved, implant placement with bone

Buccal wall is intact

Immediate implant

Primary soft tissue closure

Early implant with or without ridge augmentation

Buccal wall is damaged

Primary soft tissue closure

Early implant with ridge augmentation

Ridge augmentation Late implant placement

8  Treatment Alternatives Following Extraction of Teeth with Periodontal-Endodontic Lesions

augmentation procedures may be performed. Otherwise, bone augmentation without implant placement is preferred, delaying implant installation for a few months, once sufficient bone volume for adequate implant placement has been achieved. If indicated, another bone augmentation procedure may be performed at the time of implant placement. In all cases where bone augmentation procedures are performed, primary soft tissue closure and maintenance throughout the entire healing period is mandatory.

8.3

Conclusions

Marked resorption of the residual alveolar bone is usually appreciated 3 months after tooth extraction. This process may impair implant-supported restoration outcome, especially in the upper jaw, where esthetics is a key factor. Different treatment alternatives are available at the time of tooth extraction, namely immediate implant placement, primary soft tissue closure of the extraction site that may be followed by early implant placement, ridge preservation, and ridge augmentation. For each clinical case, treatment possibilities should be considered and evaluated according to tooth location, esthetics, soft tissue characteristics, infection, number of implants simultaneously placed, available bone volume, bony defects, and treatment convenience. This chapter discusses the different treatment alternatives providing the scientific evidence for the different possibilities to enable the choice of the most appropriate treatment alternative for each clinical situation.

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8  Treatment Alternatives Following Extraction of Teeth with Periodontal-Endodontic Lesions 88. Moses O, Pitaru S, Artzi Z, Nemcovsky CE. Healing of dehiscence-type defects in implants placed together with different barrier membranes: a comparative clinical study. Clin Oral Implants Res. 2005;16(2):210–9. 89. Garcia J, Dodge A, Luepke P, Wang HL, Kapila Y, Lin GH.  Effect of membrane exposure on guided bone regeneration: a systematic review and meta-­ analysis. Clin Oral Implants Res. 2018;29(3):328– 38. https://doi.org/10.1111/clr.13121. 90. Hämmerle CH, Araújo MG, Simion M, Osteology Consensus Group 2011. Evidence-based knowledge on the biology and treatment of extraction sockets. Clin Oral Implants Res. 2012;23(Suppl 5):80–2. https://doi.org/10.1111/j.1600-0501.2011.02370.x.. Review. Erratum in: Clin Oral Implants Res. 2012 May;23(5):641 91. MacBeth N, Trullenque-Eriksson A, Donos N, Mardas N.  Hard and soft tissue changes following alveolar ridge preservation: a systematic review. Clin Oral Implants Res. 2017;28(8):982–1004. https://doi.org/10.1111/clr.12911. 92. Willenbacher M, Al-Nawas B, Berres M, Kämmerer PW, Schiegnitz E. The effects of alveolar ridge preservation: a meta-analysis. Clin Implant Dent Relat Res. 2016;18(6):1248–68. https://doi.org/10.1111/ cid.12364. 93. Avila-Ortiz G, Elangovan S, Kramer KW, Blanchette D, Dawson DV. Effect of alveolar ridge preservation after tooth extraction: a systematic review and meta-­ analysis. J Dent Res. 2014;93:950–8. 94. Mardas N, Trullenque-Eriksson A, MacBeth N, Petrie A, Donos N.  Does ridge preservation following tooth extraction improve implant treatment outcomes: a systematic review: Group 4: therapeutic concepts & methods. Clin Oral Implants Res. 2015;26(Suppl 11):180–201. https://doi. org/10.1111/clr.12639. 95. Horváth A, Mardas N, Mezzomo LA, Needleman IG, Donos N.  Alveolar ridge preservation. A systematic review. Clin Oral Investig. 2013;17(2):341–63. https://doi.org/10.1007/s00784012-0758-5. 96. Morjaria KR, Wilson R, Palmer RM. Bone Healing after Tooth Extraction with or without an Intervention: A Systematic Review of Randomized Controlled Trial. Clin Implant Dent Relat Res. 2014;16(1):1–20. https://doi.org/10.1111/j.1708-8208.2012.00450.x. 97. Horowitz R, Holtzclaw D, Rosen PS.  A review on alveolar ridge preservation following tooth extraction. J Evid Based Dent Pract. 2012;12(3 Suppl):149–60. https://doi.org/10.1016/S15323382(12)70029-5. 98. Artzi Z, Tal H, Dayan D. Porous bovine bone mineral in healing of human extraction sockets. Part 1: histomorphometric evaluations at 9 months. J Periodontol. 2000;71(6):1015–23. 99. Araújo MG, Lindhe J. Socket grafting with the use of autologous bone: an experimental study in the dog. Clin Oral Impl Res. 2011;22:9–13. https://doi. org/10.1111/j.1600-0501.2010.01937.x.

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192 deproteinized anorganic bovine bone (Bio Oss). Clin Oral Implants Res. 2007;18:620–9. 115. Simion M, Jovanovic SA, Trisi P, Scarano A, Piatelli A.  Vertical ridge augmentation around dental implants using a membrane technique and autogenous bone or allografts in humans. Int J ­ Periodontics Restorative Dent. 1998;18:8–23. 116. Tinti C, Parma Benfenati S. Vertical ridge augmentation: surgical protocol and retrospective evaluation of 48 consecutively inserted implants. Int J Periodontics Restorative Dent. 1998;18:434–43. 117. Tinti C, Parma Benfenati S.  Treatment of peri-­ implant defects with the vertical ridge augmentation procedure: a patient report. Int J Oral Maxillofac Implants. 2001;16:572–7. 118. Artzi Z, Dayan D, Alpern Y, Nemcovsky CE. Vertical ridge augmentation using xenogenic material supported by a configured titanium mesh: clinicohistopathologic and histochemical study. Int J Oral Maxillofac Implants. 2003;18:440–6. 119. Roccuzzo M, Ramieri G, Bunino M, Berrone S.  Autogenous bone graft alone or associated with titanium mesh for vertical alveolar ridge augmentation: a controlled clinical trial. Clin Oral Implants Res. 2007;18:286–94. 120. Beitlitum I, Sebaoun A, Nemcovsky CE, Slutzkey S. Lateral bone augmentation in narrow posterior mandibles, description of a novel approach, and analysis of results. Clin Implant Dent Relat Res. 2018;20(2):96– 101. https://doi.org/10.1111/cid.12580. 121. Le B, Rohrer MD, Prasad HS.  Screw "tent-pole" grafting technique for reconstruction of large vertical alveolar ridge defects using human mineralized allograft for implant site preparation. J Oral Maxillofac Surg. 2010;68(2):428–35. https://doi. org/10.1016/j.joms.2009.04.059.. Erratum in: J Oral Maxillofac Surg. 2010 Apr;68(4):953 122. Llambés F, Silvestre FJ, Caffesse R.  Vertical bone regeneration with bioabsorbable barriers. J Periodontol. 2007;78:2036–42. 123. Merli M, Bernardelli F, Esposito M. Horizontal and vertical ridge augmentation: a novel approach using osteosynthesis microplates, bone grafts, and resorbable barriers. Int J Periodontics Restorative Dent. 2006;26:581–7. 124. Merli M, Moscatelli M, Mariotti G, Rotundo R, Bernardelli F, Nieri M.  Bone level variation after vertical ridge augmentation: resorbable barriers versus titanium-reinforced barriers. A 6-year double-blind randomized clinical trial. Int J Oral Maxillofac Implants. 2014;29(4):905–13. https:// doi.org/10.11607/jomi.320. 125. Wessing B, Lettner S, Zechner W. Guided bone regeneration with collagen membranes and particulate graft materials: a systematic review and meta-analysis. Int J Oral Maxillofac Implants. 2018;33(1):87– 100. https://doi.org/10.11607/jomi.5461. 126. Naenni N, Schneider D, Jung RE, Hüsler J, Hämmerle CHF, Thoma DS.  Randomized clinical study assessing two membranes for guided bone regeneration of peri-implant bone defects: clinical

C. E. Nemcovsky et al. and histological outcomes at 6 months. Clin Oral Implants Res. 2017;28(10):1309–17. https://doi. org/10.1111/clr.12977. 127. Merli M, Merli I, Raffaelli E, Pagliaro U, Nastri L.  Nieri M.  Bone augmentation at implant dehiscences and fenestrations. A systematic review of randomised controlled trials. Eur J Oral Implantol. 2016;9(1):11–32. 128. Simion M, Masitano U, Salvato A.  Treatment of dehiscences and fenestration around dental implants using resorbable and non-resorbable membranes associated with bone autografts: a comparative clinical study. Int J Oral Maxillofac Implants. 1997;12:159–67. 129. Nowzari H, Matian F, Slots J. Periodontal pathogens on polytetrafluoroethylene membrane for guided tissue regeneration inhibit healing. J Clin Periodontol. 1995;22(6):469–74. 130. Tal H, Kozlovsky A, Artzi Z, Nemcovsky CE, Moses O.  Cross-linked and non-cross-linked collagen barrier membranes disintegrate following surgical exposure to the oral environment: a histological study in the cat. Clin Oral Implants Res. 2008;19:760–6. 131. Tal H, Kozlovsky A, Artzi Z, Nemcovsky CE, Moses O.  Long-term bio-degradation of cross-linked and non-cross-linked collagen barriers in human guided bone regeneration. Clin Oral Implants Res. 2008;19:295–302. 132. Hämmerle CH, Chiantella GC, Karring T, Lang NP.  The effect of deproteinized bovine bone mineral on bone regeneration around titanium dental implants. Clin Oral Implants Res. 1998;9:151–62. 133. Schlegel AK, Mohler H, Busch F, Mehl A.  Preclinical and clinical studies of a collagen membrane (BioGide). Biomaterials. 1997; 18:535–8. 134. Park S-H, Lee K-w, Oh T-J, Misch CE, Shotwell J, Wang H-L.  Effect of absorbable membranes on sandwich bone augmentation. Clin Oral Implants Res. 2008;19:32–41. 135. Schwarz F, Rothamel D, Herten M, Wűstefeld M, Sager M, Ferrari D, Becker J. Immunohistochemical characterization of guided bone regeneration at a dehiscence-type defect using different barrier membranes: an experimental study in dogs. Clin Oral Implants Res. 2008;19:402–15. 136. Merli M, Migani M, Bernardelli F, Esposito M. Vertical bone augmentation with dental implant placement: efficacy and complications associated with 2 different techniques. A retrospective cohort study. Int J Oral Maxillofac Implants. 2006;21:600–6. 137. Kozlovsky A, Aboodi G, Moses O, Tal H, Artzi Z, Weinreb M, Nemcovsky CE.  Bio-degradation of a resorbable collagen membrane (Bio-Gide®) applied in a double-layer technique in rats. Clin Oral Implants Res. 2009;20:1116–23. 138. Kim SH, Kim DY, Kim KH, Ku Y, Rhyu IC, Lee YM. The efficacy of a double-layer collagen membrane technique for overlaying block grafts in a

8  Treatment Alternatives Following Extraction of Teeth with Periodontal-Endodontic Lesions rabbit calvarium model. Clin Oral Implants Res. 2009;20:1124–32. 139. von Arx T, Broggini N, Storgärd Jensen S, Bornstein MM, Schenk RK, Buser D.  Membrane durability and tissue response of different bioresorbable barrier membranes: A histologic study in the rabbit calvarium. Int J Oral Maxillofac Implants. 2005;20:843–53. 140. Moses O, Vitrial D, Aboodi G, Sculean A, Tal H, Kozlovsky A, Artzi Z, Weinreb M, Nemcovsky CE. Biodegradation of three different collagen membranes in the rat calvarium: a comparative study. J Periodontol. 2008;79:905–11. 141. Adeyemo WL, Reuther T, Bloch W, Korkmaz Y, Fischer JH, Zöller JE, Kuebler AC.  Healing of onlay mandibular bone grafts covered with collagen membrane or bovine bone substitutes: a microscopical and immunohistochemical study in the sheep. Int J Oral Maxillofac Implants. 2008;37:651–9. 142. Bornstein MM, Heynen G, Bosshardt DD, Buser D.  Effect of two bioabsorbable barrier membranes on bone regeneration of standardized defects in calvarial bone: a comparative histomorphometric study in pigs. J Periodontol. 2009;80:1289–99. 143. Smiler D, Soltan M. The bone-grafting decision tree: a systematic methodology for achieving new bone. Implant Dent. 2006;15:122–8. 144. Rothamel D, Schwartz F, Sager M, Herten M, Sculean A, Becker J.  Biodegradation of differently cross-linked collagen membranes: an experimental study in the rat. Clin Oral Implants Res. 2005;16:369–78. 145. Bunyaratavej P, Wang HL.  Collagen membranes: a review. J Periodontol. 2001;72:215–29. 146. Brunel G, Piantoni P, Elharar F, Benque E, Marin P, Zahedi S.  Regeneration of rat calvarial defects using a bioabsorbable membrane technique: influence of collagen cross-linking. J Periodontol. 1996;67:1342–8. 147. Schwarz F, Rothamel D, Herten M, Sager M, Becker J. Angiogenesis pattern of native and crosslinked collagen membranes: an immunohistochemical study in the rat. Clin Oral Implants Res. 2006;17(4):403–9. 148. Artzi Z, Nemcovsky CE, Tal H, Kozlovsky A. Timing of implant placement and augmentation with bone replacement material: clinical assessment at 8 and 16 months. Clin Implant Dent Relat Res. 2013;15(1):121–9. https://doi. org/10.1111/j.1708-8208.2011.00421.x. 149. Artzi Z, Nemcovsky CE, Tal H, Weinberg E, Weinreb M, Prasad H, Rohrer MD, Kozlovsky A.  Simultaneous versus two-stage implant placement and guided bone regeneration in the canine: histomorphometry at 8 and 16 months. J Clin Periodontol. 2010;37(11):1029–38. https://doi. org/10.1111/j.1600-051X.2010.01621.x. 150. Simion M, Dahlin C, Rocchietta I, Stavropoulos A, Sanchez R, Karring T.  Vertical ridge augmentation with guided bone regeneration in association with

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9

Dental Implants Biological Complications: Tooth Preservation Reevaluated Carlos E. Nemcovsky and Eyal Rosen

9.1

Introduction

A common dilemma encountered by dental practitioners is the decision whether to extract a compromised natural tooth and replace it with a dental implant, or to attempt preservation of the natural tooth by endodontic periodontal and restorative treatments. This intriguing dilemma has been extensively debated over the years, shifting back and forth [1–3]. In the early stages of modern dental implant therapy, it was anticipated that implants would offer a reliable and complications-­free solution to most patients, furthermore, surpassing teeth survival. Thus, since the early days of implant dentistry their use gained significant popularity among dental practitioners and patients alike, and extraction of compromised teeth that required relatively complex periodontal, endodontic, and restorative procedures, and, sometimes, not extremely complex, became common [1–4]. On the other hand, keeping in mind that the original goal of dental implants was to replace missing, and not present, natural teeth, reasonable

C. E. Nemcovsky (*) Department of Periodontology and Implant Dentistry, Maurice and Gabriela Goldschleger School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel e-mail: [email protected] E. Rosen Department of Endodontology, School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel

efforts to maintain natural teeth [1, 5, 6] should be attempted. Accordingly, this complex dilemma requires the incorporation of many periodontal, endodontic, and restorative considerations into the clinical decision-making, capabilities offered by modern endodontic and restorative treatments to retain compromised natural teeth, the common biological complications of dental implants, and the expected post-treatment quality of life [3, 7–9] should be weighted. Even with state-of-the-art periodontal and endodontic treatment certain cases may pose significant clinical and practical challenges for natural dentition preservation. It has become more and more apparent that the long-term survival of endodontically treated teeth is equivalent or even higher than that of dental implants [10, 11]. A systematic review of the literature dealing with the long-term survival rates of teeth and implants [10] reported an overall long-term loss ranging between 3.6 and 13.4% and 0 and 33% for teeth and implants, respectively. They concluded that implant survival rates do not exceed those of compromised but adequately treated and maintained natural teeth [10]. In addition, in perspective of long-term complications, it has become evident that, compared to natural teeth, dental implants are more susceptible to complications and demand more meticulous postoperative treatments to be maintained [12, 13] to assess the outcome of dental implants compared to endodontically treated teeth. In a longitudinal study where 129 implants and 143

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endodontically treated teeth were followed up for an average of 36 and 22 months, respectively, it was reported that although the overall success rates of implants and endodontically treated teeth were identical, 12.4% of implants and only 1.3% of the endodontically treated teeth required additional posttreatment interventions, and that this difference was statistically significant [12]. Lately, more and more scientific evidence assessing implant-associated complications, especially concerning significance and extent of peri-implant diseases, have become available [14], thus stressing the risks and questioning the benefits of teeth extraction and their replacement with implants. Furthermore, in light of this emerging data the benefit to maintain even compromised teeth by additional endodontic and restorative treatments is nowadays evident [4–6, 15]. Recent evidence supports conservative treatment plans aimed to maintain the natural dentition by endodontic, periodontal, and restorative procedures while avoiding tooth extraction whenever possible [4, 15]. This chapter reviews the common biological complications of dental implants as compared to treatment alternatives offered by modern dentistry to retain natural teeth, and their subsequent effects on clinical decision-making.

9.2

 ental Implants Biological D Complications

Peri-implant diseases may affect both the surrounding hard and soft tissues. Peri-implant mucositis is a bacteria-induced, reversible inflammatory process of the peri-implant soft tissue with reddening, swelling, and bleeding on periodontal probing. Peri-implantitis is an inflammatory process of the peri-implant soft and hard tissues associated with clinically significant progressive crestal bone loss after the adaptive phase following prosthetic loading [16]. Peri-implant diseases are typically described as the result of an imbalance between host response and bacterial load, supported by gram-negative anaerobic microflora. Peri-implant mucositis may not result in peri-implantitis; how-

ever, apparently, all peri-­implantitis cases had preexisting mucositis [17–21]. In recent years it became apparent that these serious peri-implant biological complications are extremely frequent, the incidence of mucositis has been reported to be around 80% and that of peri-implantitis between 28 and 56% [22]. After 10 years in function, 10–50% of the dental implants showed signs of peri-implantitis [23]. A recent meta-analysis reported that periimplant mucositis is present in 43% (range: 32–54%) of patients, while peri-implantitis in 22% (range: 14–30%) of patients [24]. Another recent long-­ term, cross-sectional analysis has shown 91.6% dental implant survival rate; however, peri-­implant mucositis was found in 33% of the implants and 48% of the patients at the same time while peri-implantitis was detected in 16% of the implants and 26% of the patients. Which means that, after 11 years, one out of four patients and one in six implants will suffer from peri-­implantitis [25]. However, although bacterial infection due to plaque accumulation is the main etiologic factor [24], this is not the only cause for the disease, and patient-, surgical-, and prosthetic-related factors contribute to its development and severity [26–28]. Risk factors are environmental, behavioral, or biological factors that if present directly increase the disease probability, and if absent or removed that probability is reduced. Single factors may not be sufficient to produce disease; therefore, several factors are usually present. Risk factors may be classified as local and general [20, 29]. Local factors influence bacterial composition and load while the general are related to the individual and may influence the patient’s susceptibility to infection. Subject-level and implant-level risk factors have been identified [30]. Among the general risk factors, present and past periodontal disease, faulty oral hygiene, parafunction, genetic predisposition, history of one or more implant failures, smoking habits, diabetes, immunosuppression, cardiovascular diseases, and an inadequate maintenance ­program have been reported. While among the local risk factors, inaccessibility for oral hygiene, deep peri-implant pockets, implant supra-

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structure connexion, soft tissue characteristics 48% of implants presenting peri-implantitis had (keratinized tissue), iatrogenic causes (cement no accessibility and/or capability for proper oral remnants, implant mal-position, surgical proce- hygiene [24, 45]. dure), implant surface roughness, bone augmenSmokers have been proven to present impaired tation procedures, and full arch rehabilitations humoral immune response. Nicotine may impair have shown effect on disease development. wound healing, especially considering that nicoSuccessful periodontal treatment prior to tine concentrations in gingival crevice fluid are implant placement lowers the risk for peri-­ approximately X300 than in plasma. Although implantitis. Residual pockets (PPD >5 mm) at the gingival blood and gingival crevice fluid flow end of active periodontal therapy represent a sig- increase already 3–5  days after smoking cesnificant risk for peri-implantitis and implant loss. sation, the enhanced susceptibility of smoking Periodontal patients showed increased suscepti- patients is reflected by a highly increased risk for bility to peri-implantitis (4.1 OR) [31]. Patients peri-implantitis, bone loss and implant failure, experiencing recurrent periodontitis had a signifi- especially in maxilla [20, 46–56]. Clinical and cantly greater risk for peri-implantitis and implant radiographic peri-implant parameters were worse loss [32–34]. Several studies have suggested and levels of advanced glycation end products that in partially edentulous patients, periodontal in peri-implant sulcular fluid were increased in pathogens may be transmitted from periodontally individuals with prediabetes and type 2 diabetic compromised teeth to newly installed implants [57, 58]. implying that periodontal niches may serve as Implants placed too close together, too deeply reservoirs for bacterial colonization [35–41]. The or buccal may result in bone loss, higher ORs importance of treating existing periodontitis prior were observed for implants in the mandible (OR, to the placement of dental implants has been 2.0) and for a distance from the prosthetic margin widely reported [40–42]. to crestal bone at baseline of 1.5 mm or less (OR, A positive relationship between peri-­2.3) [31]. The proficiency of the clinician perimplantitis and history of periodontal dis- forming the oral rehabilitation has been shown ease was found in several clinical evaluations. to influence the odds ratio for peri-implantitis by Although microorganisms initiate the infection, 4.3 [31]. Cement excess seems to be an important tissue breakdown is mainly caused by the host risk factor; 81% of implants with cement remresponse. Individuals genetically predisposed to nants had peri-implant disease, and in the same overproduce pro-inflammatory cytokines may patients, no excess cement was found in any of have increased tissue destruction. Patients that the healthy implants. In 74% of the implants, previously suffered from periodontitis (especially removal of excess cement lead to absence of peri-­ aggressive periodontitis) [43] are at higher risk implant disease. All implants with cement remto develop peri-implantitis and implant loss [20, nants in patients with a history of periodontitis 32, 44]. Long-term survival and success rates are developed peri-implantitis [20, 59–62]. lower in patients with a history of periodontal Patients with four or more implants had an disease, even adhering to maintenance [34]. increased risk for peri-implantitis (OR, 15.1) As plaque is the main etiological factor, [31]. Implants from certain brands and surface there is, evidently, a close association between treatment seem to be more prone to disease than peri-­implant bone loss and poor oral hygiene. others [31]. In patients with a history of severe Indeed, patients with poor oral hygiene or with periodontitis, minimally rough implants showed no or even limited access for proper oral hygiene more favorable clinical parameters after 5 years have been shown to be up to 14 times at greater of loading, when compared to moderately rough odds of developing peri-implantitis [22]. In a implants [63]. cohort of 23 patients with 109 implants, only Autogenous soft tissue grafting leading to 4% of the implants in patients with optimal oral keratinized tissue gain results in improved gingihygiene presented with peri-implantitis, while val health as represented by bleeding and gingi-

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val indexes, with lower probing depth values and plaque index score, together with higher marginal bone levels. However, soft tissue grafting procedures for gain of mucosal thickness did not result in bleeding indices improvements, but lead to less marginal bone loss over time [64]. Enrollment in regular maintenance program including anti-infective preventive measures usually leads to higher long-term survival and success rates of dental implants and their restorations. Therapy of peri-implant mucositis should be considered as a preventive measure for the onset of peri-implantitis. The simple fact of including patients in a regular maintenance program may reduce the risk of peri-implantitis from 43.9 to 18% at patient level [65, 66]. Patient compliance to these programs may represent a fundamental factor for peri-implantitis prevention [67].

9.3

Measures to Prevent Implant-Associated Periodontal Complications

Due to the lack of long-term efficacy and evidence-­based guidelines for the treatment of peri-implantitis, prevention strategies are extremely important. Prevention of peri-implant disease starts with a thorough evaluation of individual risk factors, establishment of optimal soft and hard tissue conditions, the choice of the correct implant design followed by a maximally atraumatic approach, and regular clinical examinations and maintenance [29]. Patients must be made aware that implants are more susceptible to plaque-related diseases than natural teeth [8, 33]. Implant therapy must not be limited to the placement and restoration of dental implants but to the implementation of peri-­implant maintenance therapy to potentially prevent biologic complications and hence to heighten the long-term success rate. Mean periimplant preventive maintenance therapy interval was demonstrated to influence the incidence of peri-­ implantitis. The maintenance program must be tailored to a patient’s risk profiling, with a minimum recall interval of 5–6  months [68]. However, it must be stressed that even

with regular preventive maintenance, biologic complications might occur [69]. Professional mechanical plaque removal as the sole element of professional preventive care is inappropriate since education and behavior change are fundamental to sustained improvements in health status. The use of adjunctive chemical approaches to biofilm control in support of mechanical plaque removal protocols in high-risk patients should be considered.

9.4

Treatment Alternatives for Peri-Implant Diseases

Long-term results of peri-implantitis treatments have been proven unpredictable, with advanced lesions usually commanding implants retrieval. Furthermore, most treatment protocols involve a surgical intervention, which leads to considerable gingival recession accompanied by esthetic and functional impairment. There is no reliable evidence suggesting which could be the most effective interventions for treating peri-implantitis. In the long-term evaluation, systematic reviews have found no evidence that the more complex and expensive therapies were more beneficial than the nonsurgical therapies [70], which basically consisted of simple subgingival mechanical debridement combined or not with some type of anti-infective treatment. Follow-up longer than 1 year suggested recurrence of peri-implantitis in up to 100% of the treated cases for some of the tested interventions, making re-treatment necessary. Larger well-designed RCTs with follow-ups longer than 1 year are still needed [71]. Different preventive/treatment protocols have been suggested. One of the first ones was the Cumulative Interceptive Supportive Therapy (CIST) described by Lang et  al. in 2000 [72]. CIST is cumulative in nature and includes four steps which should not be used as single procedures, but rather as a sequence of therapeutic procedures with increasing antibacterial potential depending on the severity and extent of the lesion. Diagnosis, therefore, represents a key characteristic of this maintenance care program.

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Evidence posterior to the Lang’s et al. publica- [81]; therefore, preferably, this type of treatment tion in 2000 [72] has revealed that chlorhexidine should be considered only in cases where nonsurwas not more effective than placebo for treat- gical therapy was not effective. ment of peri-implant mucositis, locally applied Nonsurgical therapy is of limited value in chlorhexidine, as rinses and gels, have limited advanced cases, where a surgical approach may antimicrobial effects in peri-implant lesions provide access to effectively remove the inflamed [73–76], with no statistically significant differ- tissues and decontaminate or modify the implant ences found between test and control groups. surface. However, these procedures, per-se do not Recent clinical evaluations have shown limited solve the problem and stringent regular mainteevidence that systemic antibiotics are helpful nance is essential [70]. [22]. However, application of local slow-release If clinical signs of infection may not be conantibacterial devices that remain at the site for at trolled by any means, or if a previously osseoleast 7–10 days in a concentration high enough to integrated oral implant has lost most of its bone penetrate the submucosal biofilm have proven to support or becomes clinically mobile, explantabe an effective treatment approach. tion is mandatory [72]. The first prerogative in treatment is successful infection control. Only once achieved, treatment approaches to restore the implant bone support 9.4.1 Conservative Treatment Alternatives by regenerative techniques or to reshape the peri-­ implant soft tissues and/or bony architecture by means of resective procedures, depending on Since the primary objective of peri-implantitis esthetic considerations and morphological char- treatment is debridement and decontamination of the implant surface which may lead to resoluacteristics of the lesion may be considered. However, even if bone fill of peri-implant tion of the inflammatory lesion, and due to the defects may be achieved [77, 78], re-­ side effects of surgical interventions, whenever osseointegration of a previously contaminated feasible, nonsurgical treatment alternatives are implant surface into newly regenerated bone does preferable [22]. Most authors recommend surginot seem to be the usual outcome [79]. Although cal interventions only when nonsurgical therapy new bone, and/or the bone graft, may fill the has failed. However, the patient must be fully osseous defects, as documented by an increase aware that due to gingival recession, surgical in radiographic bone density, in most cases, it procedures will compromise the esthetic result is apparently a simple healing process, where of the restoration and lead to functional impairthis radiopaque material is not really connected ment [80]. Accordingly, the actual trend is to try to the implant surface. Deep circumferential to deal with early, and sometimes moderate, and intrabony defects may be treated thorough peri-implant lesions by nonsurgical treatment debridement, implant-surface decontamination, alternatives (Figs. 9.1, 9.2, 9.3, 9.4, 9.5, 9.6, 9.7, and defect reconstruction while defects without 9.8, and 9.9). Adjunctive subgingival administration of clear bony walls or predominantly supra-bony by thorough debridement and apical repositioning minocycline following nonsurgical periodontal of the marginal mucosa [80]. A recent meta-anal- treatment has shown a significantly better and ysis has shown that despite clinically important prolonged effect compared to scaling/root planimprovements, a complete disease resolution ing alone on the reduction of probing depth, may not be expected by any of the treatment pro- clinical attachment loss, gingival index, and tocols investigated [81]. Furthermore, the major interleukin-1-beta content [82], together with a drawback of surgical therapy for peri-implant greater reduction in the proportions and numbers disease seems to be that healing usually leads of red complex bacteria [83]. Subgingival debridement plus use of locally to marked gingival recession compromising the esthetic and functional result of the restoration applied antibiotics as a slow-release device has

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Fig. 9.1  Preoperative periapical X-ray shows initial loss of bone support in the crestal area of the implant in the upper first right premolar

Fig. 9.4  After initial debridement with ultrasonic scaler and hand curettes, mainly to gain access to the submucosal area around the implant, the implant surface is cleaned with a chitosan brush mounted on a low-speed micromotor with saline irrigation. During this process, the submucosal area is copiously rinsed with 3% hydrogen peroxide

Fig. 9.2  Marked clinical signs of inflammation on facial aspect on the first upper right premolar are evident

Fig. 9.5  The chitosan brush is soaked in saline for at least 2 min before its use

Fig. 9.3  Probe in place illustrates deep probing pocket depth and bleeding upon probing

Fig. 9.6  At the end of the procedure, minocycline microspheres in a slow-release device are applied submucosal. One or two vials per implant are usually applied

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Fig. 9.7  Aspect of the area after 4 months, note largely diminished clinical signs of inflammation

Fig. 9.8  Four months postoperative, pressure-sensitive probe in place shows shallow probing pocket depth and no bleeding on probing

Fig. 9.9  Six months postoperatively, no signs of inflammation, shallow probing pocket depth, and no bleeding on probing

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also been proven effective for peri-implantitis treatment [7]. Clinical results after application of minocycline microspheres as an adjunct to mechanical treatment of incipient peri-implant infections compared to adjunctive treatment employing 1% chlorhexidine gel application have been evaluated. The combined mechanical/antimicrobial treatment for the chlorhexidine group did not result in any reduction in probing depth and only limited reduction of bleeding scores. The adjunctive use of minocycline microspheres (ARESTIN®, Valeant Pharmaceuticals North America LLC, USA), on the other hand, resulted in improvements in both probing depths and bleeding scores [76, 84–86]. Among the nonsurgical treatments evaluated, especially in initial/moderate peri-implantitis, debridement in conjunction with local minocycline microspheres in a slow-release device (SRD) application (Arestin®) achieved the greatest additional reduction in probing pocket depth, number of bleeding upon probing positive sites and counts of Porphyromonas gingivalis and Tannerella forsythia [76, 84, 86, 87]. A recent meta-analysis has shown that local minocycline microspheres in a slow-release device was more effective than slow-release chips containing chlorhexidine for peri-implant inflammation treatment [88]. Besides its antibacterial effect, minocycline microspheres, as all tetracycline family, also has an important anti-inflammatory action. Its application locally reduces cytokine levels (i.e., interleukin 1b), combined with debridement, results in serum reductions of cholesterol, C-reactive protein, and interleukin 1 level [82, 89, 90]. However, the effect of adjunctive therapy diminishes with time, being the most positive effect is within 1–2  months. The risk for reinfection favors repeated SRD application in peri-implant areas. Accordingly, although in certain cases and under good oral hygiene measures a single treatment may have a long-term effect, based on the presence of clinical signs of inflammation, this anti-­ infective/anti-inflammatory may have to be periodically repeated (Figs.  9.10, 9.11, 9.12, 9.13, 9.14, 9.15, and 9.16) [76, 84, 86, 91].

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Fig. 9.10  Preoperative periapical X-ray shows initial loss of bone support in the crestal area of the implant in the upper second right premolar

Fig. 9.11 Marked clinical signs of inflammation on facial aspect of the second upper right premolar implant supported restoration are evident

Fig. 9.12  After initial debridement with ultrasonic scaler and hand curettes, mainly to gain access to the submucosal area, the implant surface is cleaned with a chitosan brush mounted on a low-speed micromotor with saline irrigation. During this process, the submucosal area is repeatedly rinsed with 3% hydrogen peroxide

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Fig. 9.13  Minocycline microspheres in a slow-release device are applied underneath the peri-implant mucosa

Fig. 9.14  Six months postoperatively, signs of inflammation resolved

Fig. 9.15  Six months postoperatively, periodontal probe in place illustrates shallow probing pocket depth and no bleeding on probing

9  Dental Implants Biological Complications: Tooth Preservation Reevaluated

Fig. 9.16  Clinical aspect 2  years after the procedure, adequate oral hygiene and maintenance, although a single treatment procedure was performed, the area shows no relapse and no need for re-treatment

Prevention is always the best treatment alternative. Based on the individual risk assessment for each patient, presence of clinical signs of inflammation, and loss of implant bone support, a maintenance and treatment protocol based on three combined actions may be suggested: Debridement, Decontamination, Anti-infective/ Anti-inflammatory therapy (DDA). Debridement is usually performed with ultrasonic scalers and hand curettes, where the therapeutic action is mainly cleaning and rinsing of the submucosal area and allow access for the decontamination devices. Calculus does not strongly adhere to titanium surfaces; therefore, only light contact with the metal surfaces of the abutment and/or implant is recommended. Release of titanium particles into the soft tissue, due to scaling of the implant surface, may cause a foreign body inflammatory reaction and even bone resorption [92]. Decontamination may be performed with a combined application of a sodium hypochlorite gel and an activating vehicle [93, 94]; however, copious irrigation and decontamination with hydrogen peroxide 3% [95, 96] together with submucosal cleaning with a chitosan brush (LABRIDA- BioClean®, AS OSLO Norway) has also led to good clinical outcomes. Chitosan is a fully resorbable bio-material, made from shell of marine crustaceans such as shrimp

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shell and crab shell however chemically modified, it is nonallergenic and may present certain anti-­ inflammatory properties. Once bleeding stops, the third step is the submucosal application of minocycline microspheres. However, since minocycline microspheres effect is largely reduced after the first 3 months after application, in cases where a certain relapse is observed, mainly reflected by intensification of the clinical signs of inflammation, this procedure may have to be repeated (Figs. 9.17, 9.18, 9.19, 9.20, 9.21, 9.22, 9.23, and 9.24).

Fig. 9.17  Preoperative periapical X-ray shows initial loss of bone support in the crestal area of the implant in the upper left cuspid

Fig. 9.18  Marked clinical signs of inflammation are evident around the implant supported restoration in the cuspid area

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Fig. 9.19  Periodontal probe illustrates a 10  mm deep pocket with bleeding and suppuration upon probing

Fig. 9.21  The submucosal area around the implant is further cleaned with the help of a chitosan brush mounted in a low-speed micromotor with copious saline irrigation using a 300 rpm speed together with hydrogen peroxide 3% irrigation performed with a syringe with a blunt needle

Fig. 9.20  The submucosal peri-implant area is debrided with ultrasonic and hand instruments, gaining access to the exposed abutment and implant surfaces

9.4.2 T  he Significance of Peri-­ Implant Diseases and Its Effect on the Clinical Decision-Making

Fig. 9.22 At the end of the procedure, minocycline microspheres in a slow-release device are applied underneath the peri-implant mucosa

The introduction of dental implants into dentistry significantly extended treatment alternatives available to practitioners, enabling esthetic and functional solutions that did not exist in the past [97, 98]. However, in recent years it has become clear that peri-implant diseases are more common than what was previously estimated, and that their prevention and management is complex and, according to present evidence, unpredictable [14]. Furthermore, their considerable extent may pose

considerable risks for patients’ quality of life following treatment [1, 12, 99]. As the scientific reports regarding implant-­ associated complications accumulated [14], the willingness of many clinicians to simply extract natural teeth and replace them with implants without careful consideration has decreased. Furthermore, it appears that after several decades of tendency towards implant-based treatment

9  Dental Implants Biological Complications: Tooth Preservation Reevaluated

Fig. 9.23  Aspect of the area 6  months postoperatively shows largely reduced clinical signs of inflammation

Fig. 9.24  Periodontal probe in place, 6 months postoperatively, illustrates considerable reduction in probing pocket depth compared to the preoperative situation as seen in Fig. 9.19, with no bleeding or suppuration upon probing

plans, in the past few years the pendulum swings back towards adopting more conservative treatment plans that include significant attempts to maintain even compromised teeth by additional endodontic, periodontal, and restorative treatments [3]. In high-risk patients, tooth extraction and implant placement does not always provide a real definitive solution and it might be that we are just replacing one problem with another. In a large amount of cases with peri-implant disease, clinical signs of infection may not be controlled by any means, and implants lose most of the

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bone support commanding their retrieval. This usually leaves large bony defects that are difficult to treat, where extensive bone augmentation procedures before new implant placement must be performed (Figs. 9.25, 9.26, 9.27, 9.28, 9.29, 9.30, 9.31, 9.32, 9.33, 9.34, 9.35, 9.36, 9.37, 9.38, 9.39, 9.40, and 9.41). With the recent understanding of the nature of dental diseases and its mechanisms, minimally invasive procedures are gaining popularity in modern dentistry, shifting the treatment planning viewpoint to a more conservative approach [100, 101]. Minimally invasive dentistry can be defined as “the application of a systematic respect for the original tissue,” and is based on a recognition that replacements are of less biological value than the original healthy tissue [102]. Chapter 6 reviews Modern clinical procedures in periodontal reconstructive treatment. The improved scientific understanding of the endodontic diseases and modern technological advances, such as the use of surgical operation microscopes [103], electronic apex locators [104], modern imaging systems [105], and ultrasonic instruments [104, 106], have led to a new era in endodontics and to the ability and the capability to predictably treat and maintain teeth that were previously considered untreatable [4]. Moreover, modern endodontics offers a range of nonsurgical and surgical treatment modalities

Fig. 9.25  Periapical radiograph shows extensive loss of bone support around the two distal implants on the left lower jaw

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Fig. 9.26  Panoramic view of CT scanning. Implants have been retrieved leaving a large bone defect, apically extending to the close proximities of the inferior alveolar

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nerve. In addition, the second premolar has been extracted and replaced by an implant supported restoration

Fig. 9.27  CT scan serial slices after implants retrieval show vertical bone deficiency preventing implant placement. A vertical bone augmentation procedure was mandatory to place new implants

Fig. 9.28  Four tenting screws have been placed, the coronal part is left exposed to serve as support for the vertical bone augmentation procedure

Fig. 9.29  Aspect of the tenting screws in place. Only part of the screws’ length is within the pristine bone

9  Dental Implants Biological Complications: Tooth Preservation Reevaluated

Fig. 9.30  Particulate bone graft is applied supported and covering the tenting screws

Fig. 9.32  Final sutures after the procedure, tensionless primary soft tissue closure has been procured by flap releasing and internal mattress sutures

Fig. 9.34  CT scan serial slices 7 months after bone augmentation procedure show extensive vertical hard tissue healing, as compared to Fig.  9.27, covering almost the

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Fig. 9.31  Cross-linked collagen barrier membrane is applied in a selective two-layer procedure, the second layer covers mainly the occlusal area

Fig. 9.33  Aspect of the surgical area after 2 weeks, note primary soft tissue closure with advanced soft tissue healing

entire extent of the tenting screws, making implant placement possible

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Fig. 9.35  Clinical aspect of the alveolar ridge at the time of implant placement shows that primary soft tissue closure over the augmented area has been preserved throughout the complete healing period

Fig. 9.36  After flap elevation, tenting screws are completely covered by newly formed hard tissue. Compare to situation at the time of the bone augmentation procedure in Figs. 9.28 and 9.29

Fig. 9.37  Three of the tenting screws have been retrieved, the fourth is completely embedded in newly formed hard tissue even covering the screw head

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Fig. 9.38  Tenting screws removed and implant recipient sites prepared. Note quality of newly formed hard tissue

Fig. 9.39  Implants in place

Fig. 9.40  Periapical X-ray 3 months after implant placement shows good implant integration with surrounding tissue

9  Dental Implants Biological Complications: Tooth Preservation Reevaluated

Fig. 9.41  Periapical X-ray 1-year post implant supported reconstruction shows stable situation

that enable the management of complications such as retained separated instruments [107], root perforations [5, 6], root resorptions [108], and tooth fractures [109]. Some of these modern endodontic modalities adopted the “minimally invasive dentistry” concept. As an example, recent studies have suggested treatment of mature permanent teeth with carious pulp exposure by direct pulp capping using modern endodontic bioceramic materials and not by conventional root canal treatment [110]. Another modern trend in endodontics, termed “Regenerative endodontics,” is aimed to provide an alternative for the management of immature permanent teeth with pulpal necrosis. This approach is based on the assumption that regenerating functional pulpal tissue will eventually enable the replacement of damaged structures, and continued development of the tooth tissues including dentin and root structures [111]. However, although these modern “minimally invasive” endodontic modalities seem promising, their scientific basis is lacking and they are mainly based on case reports and small cases series evaluation. Recent systematic literature reviews have revealed that there is still no consensus concerning the most appropriate clinical protocol for regenerative endodontic therapy [112]. Significant knowledge gaps still exist within the available evidence being unable to provide definitive conclusions on the predictability of regenerative endodontic treatment outcomes [113].

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Clinical decision-making should be based on solid scientific data, and new treatment modalities, such as regenerative endodontic treatments, should be researched and carefully reviewed before implemented in the daily practice [4]. Nevertheless, many modern endodontic treatment modalities such as surgical endodontic treatment of cases where the traditional root canal treatment is impractical are already scientifically well established [114], and may provide predictable results even for compromised teeth and complex cases. Moreover, to date most of the teeth that are endodontically treated and adequately restored are expected to survive and function for many years, and those which are finally lost are usually extracted due to non-­endodontic-­related complications, such as periodontal or prosthetic causes [4, 115, 116]. Nowadays it is clear that when the treatment plan is appropriate and well performed, both endodontically treated teeth and dental implants exhibit similar survival rates [11]. However, since a tooth extraction is irreversible, and since there is no guarantee for either a natural tooth or a dental implant, during the clinical decision-making, both modalities should be considered as complementing, rather than competing treatment alternatives [4, 11].

9.5

Conclusions

The main goal of dentistry is to provide patients long-term dental functioning and quality of life [4–6, 15]. The alternative to maintain even compromised natural teeth by additional treatments should be carefully considered before an irreversible decision to extract the natural teeth and their replacement with an implant is made [4, 11]. Modern endodontic, periodontal, and rehabilitation treatment strategies offer outstanding conservative treatments, that have proven predictable outcomes even in the management of compromised natural dentitions [4–6]. Moreover, in most cases, and in light of the significance and magnitude of peri-implant diseases and complications, the choice to replace natural teeth with implants should be made only after all conservative treatments have been considered and discarded or

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failed, and teeth present with a hopeless or irrational to treat clinical prognosis [3–6, 15]. Hopefully, this emerging shift towards conservative dentistry and the preservation of natural teeth will even gain more momentum in the future, ensuing benefits for both the dental practitioners and the patient are expected. The practitioners will encounter less unnecessary implant-related medical complication and medico-­legal consequences, and the long-term satisfaction and quality of life of the patients will improve.

References 1. Iqbal MK, Kim S.  A review of factors influencing treatment planning decisions of single-tooth implants versus preserving natural teeth with nonsurgical endodontic therapy. J Endod. 2008;34(5):519–29. 2. Lundgren D, Rylander H, Laurell L.  To save or to extract, that is the question. Natural teeth or dental implants in periodontitis-susceptible patients: clinical decision-making and treatment strategies exemplified with patient case presentations. Periodontol. 2008;47:27–50. 3. Nemcovsky CE, Rosen E. Biological complications in implant-supported oral rehabilitation: as the pendulum swings back towards endodontics and tooth preservation. Evid Based Endod. 2017;2(4):1–8. 4. Rosen E, Nemcovsky CE, Tsesis I. Evidence-based decision making in dentistry. Switzerland: Springer; 2017. 5. Tsesis I, Nemkowsky CE, Tamse E, Rosen E. Preserving the natural tooth versus extraction and implant placement: making a rational clinical decision. Refuat Hapeh Vehashinayim. 2010;27(1):37– 46, 75. 6. Tsesis I, Rosenberg E, Faivishevsky V, Kfir A, Katz M, Rosen E. Prevalence and associated periodontal status of teeth with root perforation: a retrospective study of 2,002 patients' medical records. J Endod. 2010;36(5):797–800. 7. Faggion CM Jr, Schmitter M. Using the best available evidence to support clinical decisions in implant dentistry. Int J Oral Maxillofac Implants. 2010;25(5):960–9. 8. Fardal O, Grytten J.  A comparison of teeth and implants during maintenance therapy in terms of the number of disease-free years and costs -- an in  vivo internal control study. J Clin Periodontol. 2013;40(6):645–51. 9. Topcu AO, Yamalik N, Guncu GN, Tozum TF, El H, Uysal S, Hersek N. Implant-site related and patient-­ based factors with the potential to impact patients' satisfaction, quality of life measures and percep-

C. E. Nemcovsky and E. Rosen tions toward dental implant treatment. Implant Dent. 2017;26(4):581–91. 10. Levin L, Halperin-Sternfeld M.  Tooth preservation or implant placement: a systematic review of long-­ term tooth and implant survival rates. J Am Dent Assoc. 2013;144(10):1119–33. 11. Setzer FC, Kim S. Comparison of long-term survival of implants and endodontically treated teeth. J Dent Res. 2014;93(1):19–26. 12. Hannahan JP, Eleazer PD.  Comparison of success of implants versus endodontically treated teeth. J Endod. 2008;34(11):1302–5. 13. Tsesis I. Complications in endodontic surgery: prevention, identification and management. Berlin: Springer; 2014. 14. Derks J, Tomasi C. Peri-implant health and disease. A systematic review of current epidemiology. J Clin Periodontol. 2015;42(Suppl 16):S158–71. 15. Setzer F, Kim S.  Preserving the natural tooth versus extraction and implant placement: an evidence-­ based approach. In: Rosen E, Nemcovsky CE, Tsesis I, editors. Evidence-based decision making in dentistry. Berlin: Springer International Publishing; 2017. p. 73–95. 16. Canullo L, Schlee M, Wagner W, Covani U. Montegrotto Group for the Study of P ­ eri-­implant disease. International brainstorming meeting on etiologic and risk factors of Peri-implantitis, Montegrotto (Padua, Italy), August 2014. Int J Oral Maxillofac Implants. 2015;30(5):1093–104. 17. Ericsson I, Berglundh T, Marinello C, Liljenberg B, Lindhe J.  Long-standing plaque and gingivitis at implants and teeth in the dog. Clin Oral Implants Res. 1992;3(3):99–103. 18. Leonhardt A, Adolfsson B, Lekholm U, Wikstrom M, Dahlen G.  A longitudinal microbiological study on osseointegrated titanium implants in partially edentulous patients. Clin Oral Implants Res. 1993;4(3):113–20. 19. Pontoriero R, Tonelli MP, Carnevale G, Mombelli A, Nyman SR, Lang NP. Experimentally induced peri-­ implant mucositis. A clinical study in humans. Clin Oral Implants Res. 1994;5(4):254–9. 20. Renvert S, Quirynen M.  Risk indicators for peri-­ implantitis. A narrative review. Clin Oral Implants Res. 2015;26(Suppl 11):15–44. 21. Salvi GE, Aglietta M, Eick S, Sculean A, Lang NP, Ramseier CA.  Reversibility of experimental peri-implant mucositis compared with experimental gingivitis in humans. Clin Oral Implants Res. 2012;23(2):182–90. 22. Lindhe J, Meyle J, D. o. E.  W. o. P.  Group. Peri-­ implant diseases: consensus report of the sixth European workshop on periodontology. J Clin Periodontol. 2008;35(8 Suppl):282–5. 23. Roos-Jansaker AM, Renvert H, Lindahl C, Renvert S.  Surgical treatment of peri-implantitis using a bone substitute with or without a resorbable membrane: a prospective cohort study. J Clin Periodontol. 2007;34(7):625–32.

9  Dental Implants Biological Complications: Tooth Preservation Reevaluated 24. Jepsen S, Berglundh T, Genco R, Aass AM, Demirel K, Derks J, Figuero E, Giovannoli JL, Goldstein M, Lambert F, Ortiz-Vigon A, Polyzois I, Salvi GE, Schwarz F, Serino G, Tomasi C, Zitzmann NU.  Primary prevention of peri-implantitis: managing peri-implant mucositis. J Clin Periodontol. 2015;42(Suppl 16):S152–7. 25. Daubert DM, Weinstein BF, Bordin S, Leroux BG, Flemming TF. Prevalence and predictive factors for peri-implant disease and implant failure: a cross-­ sectional analysis. J Periodontol. 2015;86(3):337–47. 26. Albrektsson T, Buser D, Chen ST, Cochran D, DeBruyn H, Jemt T, Koka S, Nevins M, Sennerby L, Simion M, Taylor TD, Wennerberg A. Statements from the Estepona consensus meeting on peri-­ implantitis, February 2-4, 2012. Clin Implant Dent Relat Res. 2012;14(6):781–2. 27. Carcuac O, Berglundh T.  Composition of human peri-implantitis and periodontitis lesions. J Dent Res. 2014;93(11):1083–8. 28. Konstantinidis IK, Kotsakis GA, Gerdes S, Walter MH.  Cross-sectional study on the prevalence and risk indicators of peri-implant diseases. Eur J Oral Implantol. 2015;8(1):75–88. 29. Smeets R, Henningsen A, Jung O, Heiland M, Hammacher C, Stein JM.  Definition, etiology, prevention and treatment of peri-implantitis--a review. Head Face Med. 2014;10:34. 30. Kumar PS, Dabdoub SM, Hegde R, Ranganathan N, Mariotti A.  Site-level risk predictors of peri-­ implantitis: a retrospective analysis. J Clin Periodontol. 2018;45(5):597–604. https://doi. org/10.1111/jcpe.12892. 31. Derks J, Schaller D, Hakansson J, Wennstrom JL, Tomasi C, Berglundh T.  Effectiveness of implant therapy analyzed in a Swedish population: prevalence of peri-implantitis. J Dent Res. 2016;95(1):43–9. 32. Ong CT, Ivanovski S, Needleman IG, Retzepi M, Moles DR, Tonetti MS, Donos N. Systematic review of implant outcomes in treated periodontitis subjects. J Clin Periodontol. 2008;35(5):438–62. 33. Pjetursson BE, Helbling C, Weber HP, Matuliene G, Salvi GE, Bragger U, Schmidlin K, Zwahlen M, Lang NP. Peri-implantitis susceptibility as it relates to periodontal therapy and supportive care. Clin Oral Implants Res. 2012;23(7):888–94. 34. Salvi GE, Zitzmann NU.  The effects of anti-­ infective preventive measures on the occurrence of biologic implant complications and implant loss: a systematic review. Int J Oral Maxillofac Implants. 2014;29(Suppl):292–307. 35. Apse P, Ellen RP, Overall CM, Zarb GA. Microbiota and crevicular fluid collagenase activity in the osseointegrated dental implant sulcus: a comparison of sites in edentulous and partially edentulous patients. J Periodontal Res. 1989;24(2):96–105. 36. Bragger U, Burgin WB, Hammerle CH, Lang NP.  Associations between clinical parameters assessed around implants and teeth. Clin Oral Implants Res. 1997;8(5):412–21.

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212 51. Morozumi T, Kubota T, Sato T, Okuda K, Yoshie H. Smoking cessation increases gingival blood flow and gingival crevicular fluid. J Clin Periodontol. 2004;31(4):267–72. 52. Ryder MI, Fujitaki R, Lebus S, Mahboub M, Faia B, Muhaimin D, Hamada M, Hyun W.  Alterations of neutrophil L-selectin and CD18 expression by tobacco smoke: implications for periodontal diseases. J Periodontal Res. 1998;33(6):359–68. 53. Tanur E, McQuade MJ, McPherson JC, Al-Hashimi IH, Rivera-Hidalgo F.  Effects of nicotine on the strength of attachment of gingival fibroblasts to glass and non-diseased human root surfaces. J Periodontol. 2000;71(5):717–22. 54. Tipton DA, Dabbous MK.  Effects of nicotine on proliferation and extracellular matrix production of human gingival fibroblasts in  vitro. J Periodontol. 1995;66(12):1056–64. 55. Tran DT, Gay IC, Diaz-Rodriguez J, Parthasarathy K, Weltman R, Friedman L.  Survival of dental implants placed in grafted and nongrafted bone: a retrospective study in a university setting. Int J Oral Maxillofac Implants. 2016;31(2):310–7. 56. Veitz-Keenan A.  Marginal bone loss and dental implant failure may be increased in smokers. Evid Based Dent. 2016;17(1):6–7. 57. Alrabiah M, Al-Aali KA, Al-Sowygh ZH, Binmahfooz AM, Mokeem SA, Abduljabbar T.  Association of advanced glycation end products with periimplant inflammation in pre-diabetes and type 2 diabetes mellitus patients. Clin Implant Dent Relat Res. 2018;20(4):535–40. https://doi. org/10.1111/cid.12607. 58. Al-Sowygh ZH, Ghani SMA, Sergis K, Vohra F, Akram Z.  Peri-implant conditions and levels of advanced glycation end products among patients with different glycemic control. Clin Implant Dent Relat Res. 2018;20(3):345–51. https://doi. org/10.1111/cid.12584. 59. Korsch M, Robra BP, Walther W. Cement-associated signs of inflammation: retrospective analysis of the effect of excess cement on peri-implant tissue. Int J Prosthodont. 2015;28(1):11–8. 60. Linkevicius T, Puisys A, Vindasiute E, Linkeviciene L, Apse P.  Does residual cement around implant-­ supported restorations cause peri-implant disease? A retrospective case analysis. Clin Oral Implants Res. 2013;24(11):1179–84. 61. Linkevicius T, Vindasiute E, Puisys A, Linkeviciene L, Maslova N, Puriene A.  The influence of the cementation margin position on the amount of undetected cement. A prospective clinical study. Clin Oral Implants Res. 2013;24(1):71–6. 62. Wilson TG Jr. The positive relationship between excess cement and peri-implant disease: a prospective clinical endoscopic study. J Periodontol. 2009;80(9):1388–92. 63. Raes M, D'hondt R, Teughels W, Coucke W, Quirynen M.  A 5-year randomized clinical trial

C. E. Nemcovsky and E. Rosen comparing minimally with moderately rough implants in patients with severe periodontitis. J Clin Periodontol. 2018;45(6):711–20. https://doi. org/10.1111/jcpe.12901. 64. Thoma DS, Naenni N, Figuero E, Hämmerle CHF, Schwarz F, Jung RE, Sanz-Sánchez I.  Effects of soft tissue augmentation procedures on peri-implant health or disease: a systematic review and meta-­ analysis. Clin Oral Implants Res. 2018;29(Suppl 15):32–49. https://doi.org/10.1111/clr.13114. 65. Aguirre-Zorzano LA, Estefania-Fresco R, Telletxea O, Bravo M. Prevalence of peri-implant inflammatory disease in patients with a history of periodontal disease who receive supportive periodontal therapy. Clin Oral Implants Res. 2015;26(11):1338–44. 66. Costa FO, Takenaka-Martinez S, Cota LO, Ferreira SD, Silva GL, Costa JE.  Peri-implant disease in subjects with and without preventive maintenance: a 5-year follow-up. J Clin Periodontol. 2012;39(2):173–81. 67. Frisch E, Ziebolz D, Vach K, Ratka-Kruger P. Supportive post-implant therapy: patient compliance rates and impacting factors: 3-year follow-up. J Clin Periodontol. 2014;41(10):1007–14. 68. Tonetti MS, Chapple IL, Jepsen S, Sanz M. Primary and secondary prevention of periodontal and peri-­ implant diseases: introduction to, and objectives of the 11th European workshop on periodontology consensus conference. J Clin Periodontol. 2015;42(Suppl 16):S1–4. 69. Monje A, Aranda L, Diaz KT, Alarcon MA, Bagramian RA, Wang HL, Catena A.  Impact of maintenance therapy for the prevention of peri-­ implant diseases: a systematic review and meta-­ analysis. J Dent Res. 2016;95(4):372–9. 70. Renvert S, Polyzois I. Treatment of pathologic peri-­ implant pockets. Periodontol. 2018;76(1):180–90. https://doi.org/10.1111/prd.12149. 71. Esposito M, Grusovin MG, Worthington HV.  Treatment of peri-implantitis: what interventions are effective? A Cochrane systematic review. Eur J Oral Implantol. 2012;5:S21–41. 72. Lang NP, Wilson TG, Corbet EF.  Biological complications with dental implants: their prevention, diagnosis and treatment. Clin Oral Implants Res. 2000;11(Suppl 1):146–55. 73. Carcuac O, Abrahamsson I, Charalampakis G, Berglundh T.  The effect of the local use of chlorhexidine in surgical treatment of experimental peri-implantitis in dogs. J Clin Periodontol. 2015;42(2):196–203. 74. Menezes KM, Fernandes-Costa AN, Silva-Neto RD, Calderon PS, Gurgel BC.  Efficacy of 0.12% Chlorhexidine Gluconate for non-surgical treatment of Peri-implant Mucositis. J Periodontol. 2016;87(11):1305–13. 75. Porras R, Anderson GB, Caffesse R, Narendran S, Trejo PM.  Clinical response to 2 different thera-

9  Dental Implants Biological Complications: Tooth Preservation Reevaluated peutic regimens to treat peri-implant mucositis. J Periodontol. 2002;73(10):1118–25. 76. Renvert S, Lessem J, Dahlen G, Lindahl C, Svensson M.  Topical minocycline microspheres versus topical chlorhexidine gel as an adjunct to mechanical debridement of incipient peri-implant infections: a randomized clinical trial. J Clin Periodontol. 2006;33(5):362–9. 77. Hammerle CH, Fourmousis I, Winkler JR, Weigel C, Bragger U, Lang NP.  Successful bone fill in late peri-implant defects using guided tissue regeneration. A short communication. J Periodontol. 1995;66(4):303–8. 78. Persson LG, Ericsson I, Berglundh T, Lindhe J. Guided bone regeneration in the treatment of periimplantitis. Clin Oral Implants Res. 1996;7(4):366–72. 79. Wetzel AC, Vlassis J, Caffesse RG, Hammerle CH, Lang NP. Attempts to obtain re-osseointegration following experimental peri-implantitis in dogs. Clin Oral Implants Res. 1999;10(2):111–9. 80. Figuero E, Graziani F, Sanz I, Herrera D, Sanz M. Management of peri-implant mucositis and peri-­ implantitis. Periodontol. 2014;66(1):255–73. 81. Schwarz F, Becker K, Sager M.  Efficacy of professionally administered plaque removal with or without adjunctive measures for the treatment of peri-implant mucositis. A systematic review and meta-analysis. J Clin Periodontol. 2015;42(Suppl 16):S202–13. 82. Lu HK, Chei CJ. Efficacy of subgingivally applied minocycline in the treatment of chronic periodontitis. J Periodontal Res. 2005;40(1):20–7. 83. Bland PS, Goodson JM, Gunsolley JC, Grossi SG, Otomo-Corgel J, Doherty F, Comiskey JL.  Association of antimicrobial and clinical efficacy: periodontitis therapy with minocycline microspheres. J Int Acad Periodontol. 2010;12(1):11–9. 84. Bassetti M, Schar D, Wicki B, Eick S, Ramseier CA, Arweiler NB, Sculean A, Salvi GE.  Anti-infective therapy of peri-implantitis with adjunctive local drug delivery or photodynamic therapy: 12-month outcomes of a randomized controlled clinical trial. Clin Oral Implants Res. 2014;25(3):279–87. 85. Renvert S, Lessem J, Lindahl C, Svensson M.  Treatment of incipient peri-implant infections using topical minocycline microspheres versus topical chlorhexidine gel as an adjunct to mechanical debridement. J Int Acad Periodontol. 2004;6(4 Suppl):154–9. 86. Salvi GE, Persson GR, Heitz-Mayfield LJ, Frei M, Lang NP.  Adjunctive local antibiotic therapy in the treatment of peri-implantitis II: clinical and radiographic outcomes. Clin Oral Implants Res. 2007;18(3):281–5. 87. Schar D, Ramseier CA, Eick S, Arweiler NB, Sculean A, Salvi GE.  Anti-infective therapy of peri-implantitis with adjunctive local drug delivery or photodynamic therapy: six-month outcomes of

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Integration of Clinical Factors and Patient Values into Clinical Decision-Making in the Management of Endodontic-­ Periodontal Lesions

10

Igor Tsesis, Russell Paul, and Eyal Rosen

10.1 Introduction

is “common” for all the patients. This assumption doesn’t necessarily direct the practitioner as to Since the introduction of evidence-based medi- what is best and preferred for the specific patient. cine in the early 1990s, the medical community It seems that although it is generally accepted has developed a practice that incorporates the that it is important to treat the patient and not just best available scientific evidence to support the his disease [2, 3], in practice there is a lack of clinical decision-making process [1]. Various sci- clinical decision-making mechanisms available entific groups and specialty committees have to practitioners to aid the incorporation of the worked ever since to improve the quality and the preferences and values of individual patients [4]. global use of clinical decision-making in To translate evidence into clinical practice, clinihealthcare. cians need to judge how to apply the evidence to The clinical decision-making in the manage- individual patients [5]. ment of endodontic-periodontal lesions is comAn extensive, broad dental treatment that plex and presents significant clinical challenges to includes tooth extractions, and large prosthetic practitioners as far as diagnosis, treatment plan- restorations, while sometimes is a “correct” treatning, and prognosis assessment. Appropriately, ment plan, may be not suitable for a specific in this era of evidence-based decision-­making, patient with a specific clinical problem (Fig. 10.1). practitioners usually tend to utilize scientific eviKeeping in mind that preservation of the natdence to guide them in these complex clinical ural teeth is an ultimate goal, in some clinical cases. scenarios extraction may be the best treatment However, the scientific evidence usually choice. On the other hand, the decision-making guides the practitioner in his clinical decision-­ process regarding endodontic treatment should making based on the assumption that the disease be guided by the strategic importance of the tooth. Certain conditions may present a contraindication for endodontic treatment, such as poor compliance, patients with Parkinson’s disease, I. Tsesis (*) · R. Paul · E. Rosen tremors, or dementia. The appropriateness of preDepartment of Endodontology, School of Dental serving the tooth should be considered [6]. Medicine, Tel Aviv University, Tel Aviv, Israel

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a

b

c

Fig. 10.1  The patient is an elderly female who complains of pain and swelling in the buccal vestibule of the maxilla. She is satisfied with the fixed prosthetic restoration which has been present for many years. Her only concern relates to pain elimination. In the radiograph, the maxillary first premolar has a necrotic pulp, a periapical lesion, and an osseous periodontal defect on the distal aspect of the root. The treatment decision was made following a discussion

with the patient to perform endodontic surgery, thus preserving the existing restoration. (a) Pretreatment radiograph. (b) Immediate posttreatment radiograph. (c) At the 1  year follow-up appointment, there is complete resolution of the apical disease. While there is still a periodontal lesion, the patient is symptom-free and satisfied with the treatment outcome

Although there is wide agreement as to the immense value of the practice of evidencebased medicine in the art and science of clinical decision-­ making, its clinical usefulness could be enhanced if clinicians understood the gaps that exist between the research evidence and the care of the individual patient, and dealt with them accordingly [7]. Data collected from carefully conducted and controlled studies may not be directly applicable to an individual patient. Applying average results derived from groups of

patients to a unique patient is bound to be problematic [7, 8]. In addition, the patients themselves vary significantly in their willingness to take part in the decision-making process, ranging from “traditional patients” that grant all responsibilities and decision to the practitioner, to more involved patients that prefer the modern shared decision-­ making approach in which the practitioner and the patient work collaboratively to assess and chose the preferred treatment alternative [9].

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Fig. 10.2  The patient presented with discomfort relating to the maxillary first molar. Upon examination, the tooth had a necrotic pulp with an apical periodontitis accompanied by advanced periodontal disease. While the prognosis in such cases is not favorable and extraction may be a good treatment choice, in this case the patient refused extracting the tooth and was willing to accept the financial risk including any costs relating to the treatment. Following a discussion with the patient, the decision was

made to treat the tooth endodontically in order to make an effort to retain it as long as possible. (a) Preoperative radiograph—a carious lesion with extensive bone loss in the periradicular area. (b) Immediate postoperative radiograph. (c) A 2 year follow-up of the treatment. While the long-term prognosis remains questionable, the treatment results are in agreement with the patient’s expectations

In clinical decision-making, it is not only important to empirically estimate the probability of the possible outcomes with each treatment alternative. The patient preferences and value judgments associated with these outcomes must also be recognized and incorporated into the process to guide individual patient decision-making [4, 9, 10]. A patient’s own wishes and preferences may determine how evidence is applied to them (Fig. 10.2). There are delicate but crucial differences between the terms “patient preferences” and “patient values.” Patient preferences can be defined as “the relative importance that patients place on various health outcomes.” On the other hand, patient values can be defined as “a person’s beliefs, desires, and expectations of what is right or wrong.” Values are not specific to a certain context [11]. The patient’s autonomy, rights, and point of view should be respected and taken into consideration [7]. It is a generally accepted idea that patients should have a say in treatment decision-­making [12]. Treatment options should be clearly and objectively communicated to the patient and the patient should be fully informed

regarding the disease. Subjectivity and personal values may then influence the decision-making process [13]. While patient autonomy in decision-making is desired, if the information presented by the dentist or dental specialist is biased, it could influence the patient toward one treatment option over another, clinicians’ decision-making style may affect patients’ preferences [14] (Fig. 10.3). In this study [14], first-year dental students simulated the role of patients. All students were given the same scenario of a tooth with failed endodontic therapy and asked to select from between two treatment options. Biased presentations significantly influenced the treatment selection by the students. Thus, if treatment options are presented in a biased manner toward one option, the patient is more likely to select that treatment option. It is important for dentists to recognize that the preferences of patients can differ from their own [15]. While there is a general impression that patients themselves are in the best position to evaluate the trade-offs between the benefits and risks of alternative treatments [16, 17], patient

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Fig. 10.3  A patient with an extensive restoration in the anterior mandibular area presented with a draining sinus tract and periodontal pockets in the labial area of the mandibular lateral incisor. While the prognosis of the tooth is questionable, after discussing the possible treatment choices with the patient, which included an obvious option of extraction of the lateral incisor, a conservative

approach of surgical endodontic treatment was chosen. (a) Preoperative radiograph showing an extensive bone loss in the mesial area of the mandibular lateral incisor with an endo-perio communication. (b) Immediate postoperative radiograph. (c) Complete healing in the periapical area and bone regeneration 1 year following the treatment

autonomy in itself is not a rationale for treatment and does not give the patient the right to choose inappropriate treatment [18]. Psychological or emotional considerations appear to influence a seemingly irrational treatment choice by the patient. Sometimes the patient’s request for certain type of treatment is based not on rational considerations, but instead on fear or some other psychological condition [18]. Patients’ preferences are influenced by: demographic variables (with younger, better educated patients and women being quite consistently found to prefer a more active role in decision-­ making), their experience of illness and medical care, their diagnosis and health status, the type of decision they need to make, the amount of knowledge they have acquired about their condition, their attitude toward involvement, and the interactions and relationships they experience with health professionals [17]. Patients’ impressions of dentists’ examination styles, personali-

ties, and ability to relate to them as individuals seem to mediate both treatment acceptance and willingness to participate in the decision-making process [19]. When patient values and dentist perceptions were examined, the dentists’ perceptions were not closely matched to patient values [20]. While research has shown that doctors underestimate the amount of information that patients want, it is less clear how much patients actually want to be involved in making decisions about their treatment and what influences their preference for involvement [17, 21]. Thus, patients and health professionals often have different views on and preferences for treatment because they look at treatment from different standpoints. The direction and magnitude of these preference differences do not appear to be consistent and may vary with the clinical condition of interest [22]. Regardless of how involved with the decision-making the

10  Integration of Clinical Factors and Patient Values into Clinical Decision-Making in the Management

patient wants to be, it is essential for the clinician to explore the patient’s values about the treatment and its potential risks and benefits in order to incorporate them into decision-making process [5]. Patient expectations about their role in choice and decision-making have been influenced by living in a consumer society [16]. One of the most important aspects of patient values and preferences is the cost of dental treatment. It has been suggested that in many cases cost outcomes are just as important as clinical and humanistic outcomes, and should be discussed with patients who would actively participate in making their treatment decisions [23, 24]. Illness-related costs consist of three components: direct, indirect, and intangible costs. Direct illness-related costs relate to financial expenses that must be incurred in order to treat a disease. It comprises monetary payments, travel expenses to visit the doctor, and nonmedical costs (i.e., costs for nonmedical services that are results of illness or disease such as transportation or travel costs) [23]. Indirect cost—measured as loss of productive time (loss of productivity), lost leisure time, and absences from work. Every hour not worked due to illness is regarded as a loss of productivity [25]. Finally there is the cost type that is termed intangible cost. Intangible cost refers to patients’ psychological pain and discomfort [26]. It is a cost in the form of pain and suffering, or generally a lowered quality of life, and these are borne by patients, relatives, and those close to the patient [27]. Thus, the cost of treatment and patients’ financial ability to afford more expensive treatments may affect their decision-making potential.

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Higher annual family income was associated with a higher rate of participants’ preferring endodontic therapy to retain a posterior tooth [15]. Differences related to the population (genetic, cultural, environmental, healthcare facilities) and individual differences (age, comorbidity, past or current treatments, nonbiological variables) may affect the translation of evidence from a study sample to an individual patient [7, 8]. More recently, there is an increase in the life expectancy of the world population, and consequently a growing number of elderly individuals. Various surveys indicate that increasing numbers of adults are retaining teeth into old age [28]. It is widely accepted that root canal treatment is as predictable in the old as the young, provided that pulp canal infection can be properly managed. The response of teeth in older healthy adults to high-quality endodontic procedures is as good as it would be in younger adults [29]. However, technical challenges to proper infection control may be encountered in damaged, biologically old teeth [6]. The teeth of elderly patients present various alterations of pulp tissue [30], pulp tissue fibrosis, and decrease in vascularization [31], making it difficult to perform endodontic treatment [28, 32]. In conclusion, dentists’ preferences notwithstanding, the important ethical principle of patient autonomy is that patients’ values should play a very substantial role in clinical decisions [15] (Fig. 10.4). In this person-centered approach, the patient is dynamic, context-aware, and cooperates with the health professional in order to achieve the most satisfactory treatment decision for him/herself, creating a balance between the preferences of the former and the expertise of the latter [33].

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Fig. 10.4  Preoperative radiograph of the mandibular second molar. There was a deep caries lesion, the pulp was necrotic with an apical periodontitis coupled with periodontal involvement of the furcation. (a) Preoperative radiograph. (b) Immediate postoperative radiograph. (c) One year following the treatment. The tooth was asymptomatic; radiographically a partial resolution of the apical

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