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(BQ) Part 1 book Textbook of endodontology has contents: Introduction to endodontology, introduction to endodontology, clinical pulp diagnosis and decision making, apical periodontitis, treatment of vital pulp conditions, microbiology of the inlamed and necrotic pulp,... and other contents.
Textbook of Endodontology Textbook of Endodontology Third Edition Edited by Lars Bjørndal Associate Professor, Section of Cariology and Endodontics Department of Odontology, Faculty of Health and Medical Sciences University of Copenhagen, Copenhagen, Denmark Lise-Lotte Kirkevang Associate Professor, Department of Dentistry and Oral Health Aarhus University, Aarhus, Denmark Professor of Endodontics, Institute of Clinical Dentistry, Faculty of Dentistry University of Oslo, Oslo, Norway John Whitworth Professor of Endodontology/Consultant in Restorative Dentistry School of Dental Sciences, Newcastle University/Newcastle Hospitals NHS Foundation Trust Newcastle, UK This edition first published 2018 © 2018 John Wiley & Sons Ltd Edition History Blackwell Munksgaard (1e, 2003); Blackwell Publishing Ltd (2e, 2010) All rights reserved No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by law Advice on how to obtain permission to reuse material from this title is available at http://www.wiley.com/go/permissions The right of Lars Bjørndal, Lise-Lotte Kirkevang and John Whitworth to be identified as the authors of the editorial material in this work has been asserted in accordance with law Registered Offices John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, USA John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK Editorial Office 9600 Garsington Road, Oxford, OX4 2DQ, UK For details of our global editorial offices, customer services, and more information about Wiley products visit us at www.wiley.com Wiley also publishes its books in a variety of electronic formats and by print-on-demand Some content that appears in standard print versions of this book may not be available in other formats Limit of Liability/Disclaimer of Warranty While the publisher and authors have used their best efforts in preparing this work, they make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of merchantability or fitness for a particular purpose No warranty may be created or extended by sales representatives, written sales materials or promotional statements for this work The fact that an organization, website, or product is referred to in this work as a citation and/or potential source of further information does not mean that the publisher and authors endorse the information or services the organization, website, or product may provide or recommendations it may make This work is sold with the understanding that the publisher is not engaged in rendering professional services The advice and strategies contained herein may not be suitable for your situation You should consult with a specialist where appropriate Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages Library of Congress Cataloging-in-Publication Data Names: Bjørndal, Lars, 1963- editor | Kirkevang, Lise-Lotte, 1970- editor | Whitworth, John M., editor Title: Textbook of endodontology / edited by Lars Bjørndal, Lise-Lotte Kirkevang, John Whitworth Other titles: Textbook of endodontology (Bergenholtz) Description: Third edition | Hoboken, NJ : Wiley, 2018 | Preceded by Textbook of endodontology / edited by Gunnar Bergenholtz, Preben Hørsted-Bindslev, Claes Reit 2nd ed 2010 | Includes bibliographical references and index | Identifiers: LCCN 2018000530 (print) | LCCN 2018001339 (ebook) | ISBN 9781119057321 (pdf) | ISBN 9781119057369 (epub) | ISBN 9781119057314 (hardback) Subjects: | MESH: Dental Pulp Diseases–therapy | Periapical Diseases–therapy Classification: LCC RK351 (ebook) | LCC RK351 (print) | NLM WU 230 | DDC 617.6/342–dc23 LC record available at https://lccn.loc.gov/2018000530 Cover images: © Lars Bjørndal Cover design by Wiley Set in 9.5/12pt PalatinoLTStd by Aptara Inc., New Delhi, India 10 Contents List of contributors Foreword Preface About the companion website Introduction to endodontology John Whitworth, Lise-Lotte Kirkevang, and Lars Bjørndal Endodontology The objective of endodontic treatment Clinical problems and solutions The diagnostic dilemma The outcome dilemma The tools of treatment References 2 6 Part The Vital Pulp The dentin–pulp complex: structure, functions, threats, and response to external injury Lars Bjørndal and Alastair J Sloan Introduction The odontoblast and the dentin–pulp complex The dental pulp Immune responses in the dentin–pulp complex Responses of the healthy dentin–pulp complex to nondestructive stimuli The dentin–pulp complex and responses to external injuries Summary References Dentinal and pulpal pain Inge Fristad and Matti Năarhi Introduction Classification of nerve fibers Morphology of intradental sensory innervation Function of intradental sensory nerves Sensitivity of dentin: hydrodynamic mechanism in pulpal A-fiber activation Responses of intradental nerves to tissue injury and inflammation Local control of pulpal nociceptor activation Dentin hypersensitivity Pain symptoms and pulpal diagnosis References xiii xvii xix xxi Clinical pulp diagnosis and decision-making Kerstin Petersson and Claes Reit Introduction Evaluation of diagnostic information 11 11 11 17 22 25 25 29 29 33 33 33 33 36 38 40 44 44 45 46 49 49 49 v vi Contents Diagnostic accuracy Diagnostic strategy Clinical manifestations of pulpal and periapical inflammation Collecting diagnostic information Diagnostic methodology: assessment of pulp vitality Diagnostic methodology: evaluation of reported pain Diagnostic methodology: provocation/inhibition of pain Diagnostic methodology: evaluation of tooth discolorations Diagnostic classification References Caries pathology and management in deep stages of lesion formation Lars Bjørndal Enamel lesions without clinical cavitation Progressive stages of enamel–dentin lesions without surface cavitation and exposure of dentin to the oral environment Cavitation of the dentin lesion Concluding remarks on the natural history of dental caries Strategies for the management of deep caries Detailed treatment protocol for deep caries management References Treatment of vital pulp conditions Lars Bjørndal, Helena Fransson, and St´ephane Simon Introduction Indications and treatment concepts for preserving vital pulp functions Protocols for treatments aiming to preserve the vitality of the exposed pulp Factors of importance in preserving vital pulp functions Capping materials and healing patterns Tissue–biomaterial interaction and pulp healing Pulp-preserving treatments – a controversial treatment? Indications and treatment concepts for treating the irreversibly inflamed vital pulp (pulpectomy) Postoperative considerations Choosing between pulp-preserving vital pulp therapies and pulpectomy Concluding remarks on the avoidance of pulpectomy by vital pulp therapies Revitalization and/or regenerative endodontic procedures References Part 50 51 51 52 53 55 56 58 58 59 61 63 65 67 72 72 74 76 79 79 80 81 87 89 91 92 93 96 96 97 97 98 The Infected Necrotic Pulp and Apical Periodontitis Apical periodontitis Zvi Metzger, Anda Kfir, and Itzhak Abramovitz Introduction The nature of apical periodontitis Interactions with the infecting microbiota Treatment and healing of periapical lesions Persistence of periapical lesions Clinical manifestations and diagnostic terminology References 103 103 103 107 114 115 117 119 Contents Microbiology of the inflamed and necrotic pulp Luis E Ch´avez de Paz Introduction Historical background Clinical evidence Infections in root-filled teeth with persistent apical periodontitis Microbial pathogenesis of apical periodontitis Association of signs and symptoms with specific bacteria Biological evidence Extraradicular biofilms Ecological determinants for microbial growth in root canals Microbial interactions in biofilms Microbial resistance to antimicrobials Antibiofilm strategies Concluding remarks References Clinical diagnosis of pulp necrosis and apical periodontitis Dag Ørstavik Introduction Clinical features of pulp necrosis and root canal infections Radiographic features of apical periodontitis A strategy for the formulation of a periapical diagnosis Diagnostic challenges during treatment Special cases of endodontic infections An integrated approach to endodontic diagnosis References Part 10 123 123 123 124 126 128 129 131 133 134 134 136 137 138 138 143 143 144 147 153 153 154 162 165 Endodontic Treatment Procedures Endodontic emergencies Peter Jonasson, Maria Pigg, and Lars Bjørndal Introduction General diagnostic considerations and emergency principles The etiology and pathogenesis behind emergency scenarios Non-endodontic tooth pain – conditions of differential diagnostic interest Management of patients with acute dental pain References 11 vii Controlling the environment – the aseptic working field Merete Markvart and Pia Titterud Sunde Background Preparing teeth for rubber dam isolation and the development of an aseptic working field Rubber dam isolation Application of the rubber dam Disinfection of the working field Aseptic working procedures References 171 171 171 171 181 182 183 185 185 186 187 189 189 190 192 viii 12 Contents Access and canal negotiation: the first key procedural steps for successful endodontic treatment Ove A Peters and Ana Arias Introduction Principles of tooth development and tooth anatomy Individual analysis of the tooth, preoperative radiographs, and additional CBCT scans in complex cases Rubber dam isolation Access cavity preparation Canal negotiation References 13 Root canal instrumentation Lars Bergmans and Paul Lambrechts Introduction Principles of root canal instrumentation Root canal system anatomy Anatomical variations in teeth Procedural steps Endodontic instruments Instrumentation techniques Limitations of root canal instrumentation Preventing procedural mishaps References 14 Irrigation and disinfection Markus Haapasalo and Ya Shen Introduction Eradication of microorganisms from the root canal system Microbial reduction by instrumentation Root canal irrigation The apical root canal – a special challenge for irrigation Activation of irrigant flow Use of lasers in irrigation Wide-spectrum sound energy for cleaning the root canal system Intracanal medicaments Concluding remarks References 195 195 195 196 196 197 202 203 205 205 205 206 211 213 217 221 223 225 228 231 231 231 232 232 236 237 238 239 240 241 241 15 Root canal filling 247 15.1 Root canal filling materials Gottfried Schmalz and Birger Thonemann 248 Introduction Requirements Evaluation of specific materials References 248 249 253 272 15.2 Root canal filling techniques Amir-Taymour Moinzadeh and Hagay Shemesh Introduction Clinical objectives and in vitro investigations The root canal filling–dentin interface Root canal filling techniques Concluding remarks References 277 277 277 277 281 289 289 154 The Infected Necrotic Pulp and Apical Periodontitis (a) (b) (c) Fig 9.12 (a–c) Disease-characteristic radiographic signs of apical periodontitis A negative response to pulp testing and a radiographic appearance with bone loss at the apical end (or at other pulp orifices) that tapers off and meets the lamina dura further up the lateral aspect of the root is pathognomonic (disease-specific) for chronic apical periodontitis solutions, dressings) are often listed as likely causes of such pain or discomfort [41] However, the small to moderate tissue damage caused by endodontic treatment and medicaments is not very likely to give rise to strong, not to mention persistent, symptoms Thus inter-appointment pain is virtually nonexistent in case series of aseptically treated vital pulps [36] Rather, one may assume that in most cases of inter-appointment pain during treatment of apical periodontitis, it is the infection that exacerbates and causes an acute inflammation Inter-appointment pain during treatment of a vital pulp should also be seen as being most likely a response to an infection, either from residual, infected pulp tissue or from microbes introduced by a breach in the chain of asepsis The extent and duration will vary, but unless the infection is fuelled by a persistent locus outside the range of instruments and medicaments, symptoms normally subside within days Radiography is of little or no help; it may show lesions undetected in the primary diagnostic process, but hard-tissue changes from an inflammatory process will not show until after several days or more originating from the coronal aspect is a frequent cause of pulp infection with sequels (Fig 9.14) Vertical fractures originating from the apex [42] may cause a characteristic radiographic appearance, with a diffuse radiolucency along the side of the root [43] (Fig 9.15) Diagnosis of this condition is important as the root or the whole tooth must be extracted Horizontal root fractures, when infected, may show lesions developing from the periodontal ligament at the line of fracture [44] (see also Chapter 23) The tissues at the root tip may or may not be affected, depending on whether or not the pulp (or root filling) here is infected Tooth luxation will damage tissue at the apical foramen, which initiates a sterile inflammation with limited resorption of apical dentin and the lamina dura This is called transient apical periodontitis, and must be distinguished from inflammation caused by microbes as this condition may not need treatment [45] Developmental invaginations (and evaginations) produce morphological anomalies with an increased risk of pulpal and soft-tissue infection The characteristic radiographic and often clinical appearance simplify the diagnosis of such anomalies, but they pose severe challenges to treatment of the infection (Fig 9.16) Special cases of endodontic infections Root fractures and dental trauma; dens invaginatus Root fractures that initiate root infections may be seen as a variant of apical periodontitis An infraction Endodontic–periodontal lesions The “endo-perio lesion” is defined as an infection where there is continuity between infected tissues of the pulp and of the marginal periodontium [46] Infections Clinical diagnosis of pulp necrosis 155 Advanced concept 9.1 Criteria for systematic radiologic evaluation of endodontic treatment and disease Verbal descriptors of periapical health and disease (a) (b) A healthy apical periodontium has normal contours, width, and structure, or is widened only around excess filling material By strict criteria, a developing, unchanged, and even decreasing rarefaction is considered pathosis and treatment failure Source: from [33] Strindberg’s criteria are widely used in follow-up examinations of root-filled teeth This case is judged successful as the lesion is reduced to a widening around the excess root filling Visual descriptors of periapical health and disease The PeriApical Index (PAI) scoring system [34] r r r r r PAI 1: no inflammation or bone loss PAI 2: bone tissue changes suggestive of disease PAI 3: mineral loss without overt lesion formation PAI 4:well-defined radiolucent lesion PAI 5: lesion with bone tissue changes peripheral to the lesion 156 The Infected Necrotic Pulp and Apical Periodontitis Table 9.1 Diagnostic characteristics of pulp necrosis and periapical inflammations Disease term Pulp test Radiographic lesion Short pain Moderate pain Strong/lingering pain − − − − − −/+a −b + + + Chronic asymptomatic apical periodontitis − + − − − Chronic symptomatic apical periodontitis − + − + − Apical abscess with sinus tract − +c − + − Apical abscess − + − + + Pulp necrosis; no apical periodontitis Acute apical periodontitis a b c Pulp test usually negative, but acute pulpitis may progress to acute apical periodontitis with persistence of pulpal sensitivity Usually no radiographic lesion; condensing apical periodontitis in rare cases The sinus tract should be traced to the portal of exit of the infection from the pulp of the pulp may induce inflammation apically, but also, via lateral canals, at any location along the root or in the furcal area of multirooted teeth If and when there is pus formation from the pulpal infection that drains through the periodontal ligament and reaches the gingival or an existing periodontal pocket, we have by definition an endo-perio lesion of endodontic origin Conversely, if the infection in a periodontal pocket reaches a lateral canal or the apical delta of a vital, noninfected tooth, it may spread into the pulp causing necrosis and infection of pulp tissue, giving rise to an endo-perio lesion of periodontal origin (Fig 9.17) The latter is obviously a very rare situation: advanced marginal periodontitis affects a huge number of teeth and is routinely treated with aggressive scaling procedures, and both the infection and the treatment reach a high number of lateral canals, but pulp necrosis of periodontally involved and root-planed teeth is rare; pocket formation may proceed even to the root end without causing pulp necrosis and infection A true combined lesion may be defined as one where the periodontitis from an infected pulp meets up with the periodontitis from the marginal pocket, either at the apex or at the location of a lateral or furcal canal [46] It is wise to proceed with diagnostic procedures for pulpal and apical periodontal conditions and for marginal periodontitis separately From an endodontic point of view, a confirmed finding of a necrotic pulp is an indication for endodontic treatment irrespective of the state of the marginal periodontium If a deep periodontal pocket with limited lateral extension around the tooth is suspected to stem from the pulpal infection rather than from marginal plaque, mechanical periodontal treatment of that pocket should be postponed Sensibility test Negative Periapical radiographs No lesion No symptoms Pulp necrosis; no apical periodontitis Lesion Symptoms Acute, symptomatic apical periodontitis No signs or symptoms Chronic, asymptomatic apical periodontitis Clinical symptoms Chronic, symptomatic apical periodontitis Clinical signs SInus tract Swelling Apical abscess with sinus tract Apical abscess Fig 9.13 Flow diagram for arriving at clinical diagnoses of apical inflammatory conditions Note: In this scheme, the term acute apical periodontitis is reserved for painful conditions without a radiographically visible apical lesion Clinical diagnosis of pulp necrosis 157 Fig 9.14 An infraction line is clearly seen on opening of this tooth which is described in Case study 9.1 The infraction or crack probably served as portal of entry for microbes infecting the pulp and causing the symptomatology and ensuing acute apical periodontitis (a) (a) (b) (b) Fig 9.15 Vertical root fracture with apical periodontitis (a) The radiograph shows the typical diffuse destruction along the whole length of the root (b) The extracted tooth demonstrates the fracture originating from the apex and not quite reaching the crown portion of the tooth, which makes the clinical diagnosis of the fracture difficult Fig 9.16 Dens invaginatus The left upper lateral incisor has the diagnosis dens invaginatus, a developmental anomaly (a) The topography of this anomaly leads to caries, which again leads to apical periodontitis It is not easy to see whether it is the pulp itself or the soft tissues trapped in the invaginations which has become infected In either case, treatment can be extremely complicated, but was successful in this case (b) Source: Courtesy Dr Pia Titterud Sunde, University of Oslo 158 The Infected Necrotic Pulp and Apical Periodontitis (a) (b) Fig 9.17 An endo-perio lesion developing from a marginal infection on the distal aspect of a mandibular first molar The tooth responds positively to pulp testing due to persistent vitality in the mesial root, but the apical extent of the marginal infection has led to a retrograde infection of the pulp in the distal root Image (b) was taken year after (a) until a possible effect of the endodontic treatment can be observed, usually after 1–2 months Probing in such cases must be done gently to avoid undue damage to the cementum surface, which would prevent reattachment Root resorptions Resorptions frequently affect the pulp and may give rise to endodontic complications [47] The treatment decision is complex and depends on numerous factors apart from the pulpal and apical periodontal diagnoses Internal resorptions may be seen as an extended battlefield between infection in the coronal pulp and vital root pulp tissue Often the process has stopped due to necrosis of the apical pulp, in which case there is no vital tissue to keep the resorption going (Fig 9.18) A distinction of the coronal from the apical pulp diagnosis is hardly possible, as the nerves in the apical stump may be too distant to respond to pulp tests by electrical or thermal stimuli Moreover, the resorption may have reached the lateral periodontium, with or without root fracture, and false-positive responses are also possible Development of a lesion at the apex will confirm necrosis and infection of the apical pulp External root resorptions come in several varieties, and they also influence the pulp and thereby endodontic treatment decisions [47] Cervical root resorption is usually progressive in nature and gradually affects first coronal and later radicular dentin In later stages of cervical resorption therapeutic attempts at stopping the process virtually always compromise the pulp [48], and endodontic treatment becomes necessary more as a prophylactic measure than following infection of the pulp External infection-related root resorption may follow luxation and, especially, exarticulation of teeth [49, 50] Rapid resorption of tooth root substance may ensue if damage to the periodontium and disruption of root cementum exposes dentin tubules to an infected root canal Radiographic signs of resorption at the lateral aspect of the root are then a clear sign of pulp infection, which must be treated quickly to prevent progressive resorption and the development of apical periodontitis Replacement resorption (ankylosis) may be associated with pulp canal obliteration or necrosis Endodontic treatment may be indicated to prevent apical periodontitis, but the replacement of dentin by bone is unaffected (see Chapters 23 and 24 for more information on resorptions) Maxillary sinus involvement Apical periodontitis in roots protruding into the maxillary sinus may cause changes in the mucosal lining (swelling, hyperplasia) that become visible in radiographs (Fig 9.19) With continued activity of the root canal infection, an endodontically induced maxillary sinusitis may occur, with classical symptoms of this disease [51] Sinusitis may also induce symptoms in asymptomatic apical periodontitis in maxillary molar Clinical diagnosis of pulp necrosis (a) Fig 9.18 (a) Internal resorption with necrosis of the apical pulp and development of apical periodontitis (b) Healing 12 months after treatment Source: Courtesy of Dr Cecilie Herbjørnsen, Brage Tannklinikk (b) teeth, sometimes serving as a starting point for diagnosis of the affected tooth Differential diagnoses Sinusitis Usually, maxillary sinusitis proceeds without any involvement of the maxillary molars or premolars However, the inflammation may induce some sensitization of the nerve supply to the teeth in the area, and thus cause pulpitis-like symptoms and percussion sensitivity It is important to have precise recordings of the pulpal sensitivity of these teeth, to avoid improper 159 and irreversible pulp extirpation and root filling when the source of the infection is in the maxillary sinus Osteomyelitis Osteomyelitis is an infection of the medullary bone [52–54] The potential for spreading and the difficulties associated with treatment of this condition makes it important in endodontic diagnostic procedures An endodontic infection (periapical abscess, apical periodontitis) is one possible starting point for an osteomyelitis, and endodontic treatment may lead to resolution of the disease [55] Acute osteomyelitis has Fig 9.19 Swelling of the mucosa in the maxillary sinus associated with an infected upper first molar 160 The Infected Necrotic Pulp and Apical Periodontitis (a) Fig 9.20 (b) Osteomyelitis of the mandible symptoms of pain and fever; chronic osteomyelitis usually has acute episodes Radiographically, osteomyelitis may have features of bone destruction and/or production, and frequently shows a diffuse, characteristically “moth-eaten,” appearance (Fig 9.20) Normal structures Adjacent, normal structures often make radiographic assessment of the periapical conditions difficult The mandibular canal may be superimposed on the root end of mandibular molars, and the mental foramen may give the impression of a lesion of the first or second mandibular premolar (Fig 9.21) The normal appearance of the mandible in the molar region often displays large marrow spaces, which may appear as lesions of the roots of, particularly, second and third molars The nasal cavity may project over the apices of maxillary front teeth, and the maxillary sinus over premolars and first molars The incisive canal may have a cystic extension, which may even be secondarily infected, mimicking strongly symptomatic apical periodontitis of an upper central incisor [56, 57] If tracing of the lamina dura is difficult, these projections may give a false impression of apical lesions in maxillary teeth The zygomatic arch may obscure details of the apical area in upper molars Cemento-osseous dysplasia Cemento-osseous dysplasia [58, 59] is a poorly understood disease in the periapical bone area, which shows radiolucent and radiopaque areas alternating over time and in the bone There are no clinical signs or symptoms associated with this condition, which most often affects the lower front teeth in adult patients The radiolucent phases of cemento-osseous dysplasia can be indistinguishable from apical periodontitis, but a positive pulp test result must guard against unwarranted initiation of root filling procedures (Fig 9.22) Orofacial pain conditions Fig 9.21 Mental foramen projecting close to the apex of a mandibular second premolar Orofacial pain conditions are often related to one or several teeth, and may or may not reflect endodontic conditions Atypical odontalgia [60–62] is diagnosed when persistent, chronic or intermittent pain is ascribed to a particular tooth (or to a few neighboring teeth) by the patient, but no objective clinical or radiographic findings suggest dental pathosis or other oral disease Often, these cases may have features suggestive of neuropathic pain, mimicking pain from pulpitis or apical periodontitis, but they are actually caused by local or central sensitization of nerves serving that particular mouth area (see Chapter 22) Clinical diagnosis of pulp necrosis (a) (b) 161 (c) Fig 9.22 Cemento-osseous dysplasia Radiolucent area at the apex of the mandibular central incisors (a) is mistakenly diagnosed and treated as apical periodontitis (b) On follow-up a year later (c), the process involves a third root Vital pulps; no treatment was indicated Neuropathies and atypical odontalgia may occur in otherwise healthy patients, and must be distinguished from the dental pain sometimes presented by patients ă with certain psychic disorders, such as Munchausen syndrome, where the pain is part of a condition requiring psychiatric therapy and not dental treatment Temporo-mandibular joint afflictions may also give rise to symptoms mimicking dental pain As with atypical odontalgia, the absence of local signs and symptoms of disease will point to a condition outside the pulp and periapical tissues (see Chapter 22) Tumors of the jaw are frequently associated anatomically with tooth roots, and it is of course important to diagnose these conditions as quickly as possible The keratocystic odontogenic tumor (Fig 9.25) may be multilocular; most frequent in the posterior mandibular region, and believed to originate from the dental lamina The ameloblastoma is regularly multilocular and well characterized by trabeculae separating lobes in the lesion Malignant tumors of the jaw are rare and seldom a problem to distinguish from endodontic disease Cysts and tumors of the jaws Cysts and tumors of the jaws may be mistaken for endodontic lesions [63–66] In cases where there is a suggestion of such diseases, CBCT or other examinations may be indicated [27] As with most instances of diagnostic difficulty involving radiographic changes, a positive sensibility test of teeth in the area will strongly reduce the possibility for an endodontic origin of the lesion There are several jaw cysts that may mimic chronic apical periodontitis The incisive canal cyst (Fig 9.23) has been mentioned The lateral periodontal cyst (Fig 9.24) is believed to originate from remnants of the dental lamina in the lower premolar/canine area Careful tracing of an intact lamina dura around the root is often possible in this situation The simple or traumatic bone cyst is not a cyst but a cavity within the bone without an epithelial lining; it may extend up to and between the roots, but without compromising pulp vitality The giant cell granuloma is histologically described by its name; it often shows a multilocular appearance but may be mistaken for an apical periodontitis Fig 9.23 Incisive canal cyst 162 Fig 9.24 The Infected Necrotic Pulp and Apical Periodontitis Lateral periodontal cyst An integrated approach to endodontic diagnosis Clinical–radiological features and extent of infection Signs and symptoms must be related to a realistic concept of etiology and pathogenesis of the disease in (a) (b) question for a definite diagnosis In endodontics, it means that the inflammatory reactions of pulp and periapical tissues as registered and recorded by history, examination, and tests must be combined with some educated guesses: is there an infection, and if so, what is its localization, extent, and virulence? Apart from rare cases of recent trauma, all apical periodontal inflammatory reactions, signs, and symptoms are associated with a necrotic pulp and have an infectious etiology The issue of whether there is an infection is therefore quickly affirmed in the overwhelming majority of cases Asymptomatic teeth with necrotic pulps and no periapical lesion may not be infected; this diagnosis may, however, trigger a decision to treat the tooth endodontically in order to prevent future infection and periapical inflammation (see Key literature 9.2) The next issue is to determine localization and extent of the infection Apical periodontitis is primarily associated with infection of the pulp canal space; other locations for bacterial colonization and biofilm formation will be the dentinal tubules, the apical cementum, the surface of root filling material, and in the periapical granuloma (extraradicular infections) [67] (Fig 9.26) In tissue reactions leading to pus formation the bacteria will be contained in the abscess; if the bacteria outrun tissue defenses, they may spread through the submucosal or subcutaneous tissues as cellulitis Time is of the essence: the longer a root canal infection is left untreated, the greater the likelihood that peripheral elements of the tooth and surrounding tissues have become colonized (c) Fig 9.25 Keratocystic odontogenic tumor mimicking apical periodontitis associated with maxillary right canine and lateral incisor (a) Before surgery: all teeth test vital (b) After surgery, the canine and lateral incisor are devitalized and need endodontic treatment (c) After successful surgery and endodontic treatment, the keratocystic lesion is healing Clinical diagnosis of pulp necrosis 163 Key literature 9.2 Bacteriological status of teeth with a diagnosis of apical periodontitis Core concept 9.3 Relationship between tissue reactions and symptoms and the level of infection Sundqvist [6] r Sundqvist entered the pulp chambers of traumatized, intact necrotic maxillary front teeth that were either with or without apical radiolucencies (apical periodontitis) In all of 13 teeth without radiographic signs of apical periodontitis, no bacteria were recoverable by culture methods Contrarily, in 18 of 19 teeth with a periapical lesion, bacteria were found Clinical symptoms of acute inflammation occurred exclusively in teeth with radiolucencies The likelihood of experiencing symptoms increased with the number of bacterial species recovered Key learning point: A necrotic tooth with a lesion is infected; necrotic pulps without a lesion may be bacteria-free r r r Ricucci and Siqueira [67] Using histobacteriogical techniques, these workers documented bacterial infection in all but one of 107 teeth with radiographic signs of apical periodontitis after extraction or apicectomy Biofilm formation was demonstrated in 77% of the root canals, with 6% harboring extraradicular biofilms Biofilm formation was more prevalent in association with large lesions (82%) than in small (62%), and more in epithelialized lesions than in granulomas without epithelium Key learning point: Biofilm formation is an important aspect of apical periodontitis Finally, the infection’s virulence must be considered Chronic, asymptomatic lesions may have massive infection of the pulp, dentinal tubules, cementum surface, and even islands of microbes well established extraradicularly, but if the microbes have low virulence they pose a relatively small risk of immediate spreading or of causing systemic harm to the patient At the other extreme, infections with aggressive microbes may have the potential to spread and cause severe tissue damage, even to become life-threatening In between, acute symptoms of pain, swelling, and fever indicate active F E C D B A Fig 9.26 Pulpal and periapical infection: Bacterial colonization and biofilm formation in the pulp canal (A), lateral canals (B) and apical delta (C), dentinal tubules (D), cementum surface (E), and extraradicularly (F) r Pulp necrosis; no apical lesion visible: if symptoms: infected pulp space; if no symptoms: infection status unknown Chronic, asymptomatic and mildly symptomatic apical periodontitis: the pulp space, apical dentin, apical cementum, and possibly the periapical tissues are infected with biofilm formation Exacerbation: The infection has increased in virulence and/or the host has reduced capacity for defense Acute symptomatic apical periodontitis: a virulent infection of the pulp space has reached the periapical area Dentin, cementum, and periapical tissues may not yet have extensive biofilm formation Apical abscess: bacteria in and around the root canal multiply there with pus formation (whether from a primary acute periodontitis or from an exacerbating apical periodontitis) An abscess forms within the bone and may penetrate through the periodontium to tissue spaces (oral mucosa, subcutaneous tissues, mucosa of maxillary sinus or nasal cavity) Apical abscess with sinus tract: bacteria grow in a continuum from the root through the tissues and drain to the internal (sinus, nasal cavity) or external (oral cavity, skin) surface Key learning point: All these conditions are dependent on bacterial colonization of the root, and will heal if the infection of the dental tissues is eliminated infection which needs prompt treatment The relationship between clinical–radiographic diagnoses and the probable location of the underlying infection is shown in Core concept 9.3 A progression of disease from pulpal infection via acute, symptomatic to chronic apical periodontitis is given in Case study 9.1 Diagnosis and treatment options Asepsis is a guiding principle for all endodontic treatment In treatment of noninfected pulps, prevention of infection by maintaining asepsis is the sole purpose The selection of treatment modality for infection with apical periodontitis is highly dependent on the assessment of the level of infection as described earlier Thus, the choice between surgical removal (apicectomy, root resection/hemisection, extraction) and chemomechanical disinfection of the infected tissues is completely dependent on the localization of the microbes and their susceptibility to conservative, nonsurgical approaches Longstanding infection is likely to have massive infiltration of apical dentin [67–71] as well as a likelihood of extraradicular infection and cyst formation, all of which may strengthen indications for surgical removal of tissues in addition to ortho- or retrograde root filling Temporary measures for pain control by analgesics and control of 164 The Infected Necrotic Pulp and Apical Periodontitis Case Study 9.1 From chronic pulpitis to acute symptomatic apical periodontitis to asymptomatic or healing apical periodontitis Background; symptomatology Demographics Tentative diagnoses Level of infection No infection demonstrable Male, age 69, married, children, West European Medical history Noncontributory Dental history Well-preserved dentition Two months earlier: cusp fracture tooth 24 All-ceramic crown cemented with composite luting cement Tooth 37 occlusal infraction sealed with acid etch and composite Recent dental symptomatology January 20 Uneasy feeling left side, no localization possible, but teeth 24, 25, 26 suspected Normal sensibility to hot and cold food and drink Chewing ok Pulpitis? January 23 Strong pain, high doses of ibuprofen Still no localization Acute pulpitis January 25 No longer diffuse pain, 37 clearly percussion sensitive and tender to touch, chewing impaired Still no sensibility to hot or cold food or drinks Ibuprofen × 200 mg Acute pulpitis with partial necrosis; acute symptomatic apical periodontitis January 26 Reversion to more diffuse pain with 24, 25, and 26 apparently involved, but still percussion sensitivity of 37 Referred pain Spontaneous nose bleed from same side; patient has not had that before Bleeding tendency from ibuprofen usage Tooth 37 is now very sensitive to hot and cold, lingering Ibuprofen × 200 mg Acute pulpitis, partial pulp necrosis Infection of whole or part of pulp January 27 No more diffuse pain, percussion sensitive 37; chewing impaired; painful lymph nodes sublingually left side Ibuprofen Total pulp necrosis, acute symptomatic apical periodontitis Total pulp infection; potential for spreading January 29 Lymph node sensibility gone, minimal chewing sensibility Mildly symptomatic, chronic apical periodontitis Risk of spreading infection reduced January 30 All appears well, no symptoms Chronic apical periodontitis Total pulp infection; no spreading Infection of whole or part of pulp Seen by endodontist February Treatment: disinfection and filling 37 February 10 No anesthesia; no pulpal sensitivity; canals calcium hydroxide Infection of pulpal space reduced or eliminated February 11–13 Percussion sensitivity Infectious material extruded though apex during treatment February 17 Asymptomatic; root filled with little sealer surplus; cuspal reduction February 18–20 Two days of chewing discomfort February 20 Asymptomatic, fully functional From chronic pulpitis to acute apical periodontitis to asymptomatic and finally healing apical periodontitis: (a) November 12; (b) February 4; (c) February 17 Healing apical periodontitis Infectious material extruded though apex during treatment Healing apical periodontitis No infection Clinical diagnosis of pulp necrosis spreading infection by antibiotics are adjunct treatment modalities in acute cases References Gutmann JL, Baumgartner JC, Gluskin AH, Hartwell GR, Walton RE Identify and define all diagnostic terms for periapical/periradicular health and disease states J Endod 2009; 35: 1658–74 Tziafas D Experimental bacterial anachoresis in dog dental pulps capped with calcium hydroxide J Endod 1989; 15: 591–5 Williams TP, Brooks SL A longitudinal study of idiopathic osteosclerosis and condensing osteitis Dentomaxillofac Radiol 1998; 27: 275–8 Eliasson S, Halvarsson C, Ljungheimer C Periapical condensing osteitis and endodontic treatment Oral Surg Oral Med Oral Pathol 1984; 57: 195–9 Chazel JC, Tramini P, Valcarcel J, Pelissier B A comparative analysis of periapical health based on historic and current data Int Endod J 2005; 38: 277–84 Sundqvist G Bacteriological studies of necrotic dental pulps Odontological Dissertation, Ume˚a University, Sweden, 1976 Klausen B, Helbo M, Dabelsteen E A differential diagnostic approach to the symptomatology of acute dental pain Oral Surg Oral Med Oral Pathol 1985; 59: 297–301 Toure B, Kane AW, Diouf A, Faye B, Boucher Y Preoperative pain and medications used in emergency patients with irreversible acute pulpitis or acute apical periodontitis: a prospective comparative study J Orofac Pain 2007; 21: 303–8 Weissman J, Johnson JD, Anderson M, Hollender L, Huson T, Paranjpe A, et al Association between the presence of apical periodontitis and clinical symptoms in endodontic patients using cone-beam computed tomography and periapical radiographs J Endod 2015; 41: 1824–9 10 Kruse C, Spin-Neto R, Wenzel A, Kirkevang LL Cone beam computed tomography and periapical lesions: a systematic review analysing studies on diagnostic efficacy by a hierarchical model Int Endod J 2015; 48: 815–28 11 Carter LM, Layton S Cervicofacial infection of dental origin presenting to maxillofacial surgery units in the United Kingdom: a national audit Br Dental J 2009; 206: 73–8 12 Jespersen JJ, Hellstein J, Williamson A, Johnson WT, Qian F Evaluation of dental pulp sensibility tests in a clinical setting J Endod 2014; 40: 351–4 13 Nair PN Pathogenesis of apical periodontitis and the causes of endodontic failures Crit Rev Oral Biol Med 2004; 15: 348–81 14 Yoshioka T, Kikuchi I, Adorno CG, Suda H Periapical bone defects of root filled teeth with persistent lesions evaluated by cone-beam computed tomography Int Endod J 2011; 44: 245–52 15 Brynolf I A histological and roentgenological study of the periapical region of human upper incisors Odontol Revy Suppl 1967; 11 165 16 Kazzi D, Horner K, Qualtrough AC, Martinez-Beneyto Y, Rushton VE A comparative study of three periapical radiographic techniques for endodontic working length estimation Int Endod J 2007; 40: 526–31 17 Brynolf I Roentgenologic periapical diagnosis II One, two or more roentgenograms? 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