Textbook of Endodontology 2nd Edition

Textbook of Endodontology

Textbook of Endodontology Second Edition Edited by Gunnar Bergenholtz Preben Hørsted-Bindslev Claes Reit

This edition first published 2010 © 2003 Blackwell Munksgaard © 2010 Blackwell Publishing Ltd Blackwell Publishing was acquired by John Wiley & Sons in February 2007. Blackwell’s publishing programme has been merged with Wiley’s global Scientific, Technical, and Medical business to form Wiley-Blackwell. First edition published 2003 Second edition 2010 Registered office John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, United Kingdom Editorial offices 9600 Garsington Road, Oxford, OX4 2DQ, United Kingdom 2121 State Avenue, Ames, Iowa 50014-8300, USA For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com/wiley-blackwell. The right of the author to be identified as the author of this work has been asserted in accordance with the Copyright, Designs and Patents Act 1988. 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 the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher. Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought. Library of Congress Cataloging-in-Publication Data Textbook of endodontology/edited by Gunnar Bergenholtz, Preben Hørsted-Bindslev, Claes Reit. — 2nd ed. p. ; cm. Includes bibliographical references and index. ISBN 978-1-4051-7095-6 (hardback: alk. paper) 1. Endodontics. I. Bergenholtz, Gunnar. II. Hørsted-Bindslev, Preben. III. Reit, Claes. [DNLM: 1. Dental Pulp Diseases—therapy. 2. Periapical Diseases—therapy. WU 230 T355 2010] RK351.T49 2003 617.6⬘342—dc22 2009024733 A catalogue record for this book is available from the British Library. Set in 9.5/12.5pt Palatino by Gray Publishing, Tunbridge Wells, Kent Illustrations by Jens Lund Kirkegaard Printed in Singapore 1—2010

Contents List of Contributors Preface 1

Introduction to endodontology Claes Reit, Gunnar Bergenholtz and Preben Hørsted-Bindslev Endodontology The dawn of modern endodontology The objective of endodontic treatment Clinical problems and solutions The diagnostic dilemma The tools of treatment Extraction and dental implant? References

Part 1 2

The dentin–pulp complex: structures, functions and responses to adverse influences Leif Olgart and Gunnar Bergenholtz

Dentinal and pulpal pain Matti Närhi Introduction Classification of nerve fibers Morphology of intradental sensory innervation Function of intradental sensory nerves under normal conditions 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

4

1 1 2 3 3 5 6 6 6

The Vital Pulp

Introduction Constituents and normal functions of the dentin–pulp complex Basal maintenance Appropriate responses of the healthy pulp to non-destructive stimuli Responses to external threats Effects of potentially destructive stimuli References 3

xi xiii

Treatment of vital pulp conditions Preben Hørsted-Bindslev and Gunnar Bergenholtz Introduction Clinical scenarios Treatment options Factors influencing choice of treatment Management of exposed pulps by direct pulp capping/partial pulpotomy Pulpectomy

11 11 11 18 19 19 23 30 33 33 33 33 36 37 39 42 42 43 44 47 47 47 48 50 52 59 v

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Contents

Emergency treatment References 5

Endodontics in primary teeth Ingegerd Mejàre Introduction The normal pulp Pulpal inflammation in the primary tooth Wound dressings – characteristics, modes of action and reported clinical success rates Objectives of pulp treatment Operative treatment procedures Indications and contraindications for pulp treatment in primary teeth Future directions References

65 69 73 73 73 73 75 79 79 85 85 88

Part 2 The Necrotic Pulp 6

The microbiology of the necrotic pulp Gunnel Svensäter, Luis Chávez de Paz and Else Theilade Introduction Evidence for the essential role of microorganisms in apical periodontitis Routes of microbial entry to the pulpal space Modes of colonization Ecological determinants for microbial growth in root canals Methods for studying the root canal microflora Composition of the endodontic microflora Association of signs and symptoms with specific bacteria Concluding remarks References

7

Apical periodontitis Zvi Metzger, Itzhak Abramovitz and Gunnar Bergenholtz Introduction The nature of apical periodontitis Interactions with the infecting microbiota Clinical manifestations and diagnostic terminology References

8

Systemic complications of endodontic infections Nils Skaug and Vidar Bakken Introduction Acute periapical infections as the origin of metastatic infections Chronic periapical infections as the origin of metastatic infections References

9

Treatment of the necrotic pulp Paul Wesselink and Gunnar Bergenholtz Introduction Objectives and general treatment strategies Scheme for a routine procedure in root canal therapy Considerations in complex cases

95 95 95 96 97 98 103 106 109 110 110 113 113 113 118 123 126 128 128 128 135 138 140 140 140 143 152

Contents

Effects of root canal therapy on the intracanal microbiota Management of symptomatic lesions References

Part 3 10

The surgical microcope Pierre Machtou

Root canal instrumentation Lars Bergmans and Paul Lambrechts Introduction Principles of root canal instrumentation Root canal system anatomy Procedural steps Endodontic instruments Instrumentation techniques Limitations of root canal instrumentation Preventing procedural mishaps References

12

Root canal filling materials Gottfried Schmalz and Preben Hørsted-Bindslev Introduction Requirements Gutta-percha cones Sealers Materials for retrograde fillings (root-end fillings) and replantation Mandibular nerve injuries References

13

153 153 156

Endodontic Treatment Procedures

Introduction Components Ergonomics and working techniques Microinstrumentation Critical steps Concluding remarks References 11

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Root filling techniques Paul Wesselink Introduction Specific objectives Selecting a root canal filling material Root filling techniques for gutta-percha Root filling techniques employing gutta-percha and sealer Procedures prior to root canal filling Assessing root filling quality Filling of the pulp chamber and coronal restoration Conclusions and recommendations References

163 163 163 164 167 167 168 168 169 169 169 170 174 180 183 186 188 190 193 193 194 198 202 214 215 216 219 219 219 219 221 224 229 229 230 231 231

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Contents

Part 4 Diagnostic Considerations and Clinical Decision Making 14

Diagnosis of pulpal and periapical disease Claes Reit and Kerstin Petersson Introduction Evaluation of diagnostic information Diagnostic strategy Clinical manifestations of pulpal and periapical inflammation Collecting diagnostic information Diagnostic classification References

15

Diagnosis and management of endodontic complications after trauma John Whitworth Introduction Common dental injuries Dental trauma and its consequences General considerations in the management of dental trauma Diagnostic quandaries – to remove or review the pulp after trauma? Pulp regeneration – the dawn of a new era? References

16

The multidimensional nature of pain Ilana Eli and Peter Svensson Introduction Neurobiological factors affecting the pain experience Psychological factors affecting the pain experience Gender and pain Special populations Management and treatment of pain Concluding remarks References

17

Clinical epidemiology Claes Reit and Lise-Lotte Kirkevang Introduction Clinical epidemiology Diagnosis Cause Prevalence, frequency and incidence Risk for apical periodontitis Treatment Prognosis Longevity of root filled teeth Back to the case References

18

Endodontic decision making Claes Reit The outcome of endodontic treatment Factors influencing treatment outcome Prevalence of endodontic “failures”

235 235 235 237 238 238 247 253 255 255 255 258 267 273 274 274 277 277 278 280 282 284 285 287 287 290 290 290 292 292 293 295 296 296 297 298 298 301 301 302 304

Contents

Variation in the management of periapical lesions in endodontically treated teeth Clinical decision making: descriptive projects Endodontic retreatment decision making: a normative approach Concluding remarks References

Part 5 19

The root filled tooth in prosthodontic reconstruction Eckehard Kostka

Non-surgical retreatment Pierre Machtou and Claes Reit Introduction Indications Access to the root canal Access to the apical area Instrumentation of the root canal Antimicrobial treatment Preventive retreatment Prognosis References

21

304 305 306 311 311

The Root Filled Tooth

Introduction Problems associated with root filled teeth as abutments Core build-ups Clinical techniques Prosthodontic reconstruction References 20

ix

Surgical endodontics Peter Velvart Introduction General outline of the procedure Pain control after surgery Bone healing Prognosis References

317 317 317 322 325 327 332 335 335 335 335 339 342 344 346 346 346 348 348 349 361 362 362 364

Failures after surgical endodontics Thomas von Arx

366

Index

371

List of Contributors Editors Gunnar Bergenholtz

Institute of Odontology, The Sahlgrenska Academy at University of Gothenburg, Sweden

Preben Hørsted-Bindslev

School of Dentistry, Faculty of Health Sciences, Aarhus University, Denmark

Claes Reit

Institute of Odontology, The Sahlgrenska Academy at University of Gothenburg, Sweden

Contributors Itzhak Abramovitz

Hebrew University and Hadassa Faculty of Dental Medicine, Hebrew University, Jerusalem, Israel

Thomas von Arx

School of Dental Medicine, University of Berne, Switzerland

Vidar Bakken

Faculty of Medicine and Dentistry, University of Bergen, Norway

Lars Bergmans

School of Dentistry, University of Leuven, Belgium

Luis Chávez de Paz

Faculty of Odontology, Malmö University, Sweden

Ilana Eli

The Maurice and Gabriela Goldschleger School of Dental Medicine, Tel Aviv University, Israel

Lise-Lotte Kirkevang

School of Dentistry, Faculty of Health Sciences, Aarhus University, Denmark

Eckehard Kostka

School of Dental Medicine, Charité, Medical Faculty of the Berlin Humboldt University, Germany

Paul Lambrechts

School of Dentistry, University of Leuven, Belgium

Pierre Machtou

Denis Diderot School of Dentistry, Paris 7 University, France

Ingegerd Mejàre

Faculty of Odontology, Malmö University, Sweden

Zvi Metzger

The Maurice and Gabriela Goldschleger School of Dental Medicine, Tel Aviv University, Israel

Matti Närhi

Faculty of Medicine, University of Kuopio, Finland

Leif Olgart

Karolinska Institute, Stockholm, Sweden

Kerstin Petersson

Faculty of Odontology, Malmö University, Sweden

Gottfried Schmalz

School of Dentistry, University of Regensburg, Germany xi

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List of Contributors

Nils Skaug

deceased

Gunnel Svensäter

Faculty of Odontology, Malmö University, Sweden

Peter Svensson

School of Dentistry, Faculty of Health Sciences, Aarhus University, Denmark

Else Theilade

School of Dentistry, Faculty of Health Sciences, Aarhus University, Denmark

Peter Velvart

Private practice, Zürich, Switzerland

Paul Wesselink

Academic Center for Dentistry Amsterdam (ACTA), The Netherlands

John Whitworth

School of Dental Science, Newcastle University, UK

Preface The Textbook of Endodontology is intended to serve the educational needs of dental students, as well as of dental practitioners seeking updates on endodontic theories and techniques. The primary aim has been to provide an understanding of the biological processes involved in pulpal and periapical pathologies and how that knowledge impinges on clinical management, and to present that information in an easily accessible form. Therefore, we have supplemented the core text with numerous figures and photographs, as well as with boxes highlighting key facts, important clinical procedures and key research. Case studies are given at the end of some chapters in order to further illustrate topics described in the text. In these various ways, the book provides information both at a foundation level, and at a more detailed level for the graduating student and practitioner. The key information boxes are color coded as an easyto-use navigational aid for readers. Core concepts are colored pink, while advanced concepts are purple. Clinical procedures are coded green and key literature boxes are blue. Although not designed to provide a comprehensive review of the literature, this book is also intended to

stimulate the reader to delve into the research that forms our current knowledge base in endodontology. To aid the reader, a selective reference list is provided and comments have been added to especially weighty or useful references. Important and interesting investigations are presented in the core and advanced concept boxes, and we hope that these features will encourage the student to carry on with his or her own exploration of the subject area. This is the second edition of the book, which features three new chapters reflecting the use of the surgical microscope, diagnosis and management of endodontic complications subsequent to dental trauma, and endodontic epidemiology. The dedicated support of our coauthors – 23 highly respected clinicians and scientists – who, in addition to the editors, have contributed to this book, is greatly appreciated. We thank them all sincerely for their time, effort and endurance during the editing process. Gunnar Bergenholtz Preben Hørsted-Bindslev Claes Reit

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Chapter 1

Introduction to endodontology Claes Reit, Gunnar Bergenholtz and Preben Hørsted-Bindslev

Endodontology The word ”endodontology” is derived from the Greek language and can be translated as ”the knowledge of what is inside the tooth”. Thus, endodontology concerns structures and processes within the pulp chamber. But what about ”knowledge”? What does it actually mean to ”know” things? Most people would probably say that knowledge has something to do with truth and providing reasons for things. It is often believed that dental and medical knowledge is simply scientific knowledge – science is based on research and deals with how things are constructed and work. But as practicing dentists we also need other types of knowledge. Although it is important to know about tooth anatomy and how to produce good root canal preparations for example, we must also develop good judgment and ability to make the ”right” clinical decisions. There are at least three different forms of knowledge that the dental practitioner requires and, in a tradition that goes all the way back to Aristotle, we will refer to the Greek terms for these forms: episteme, techne and phronesis (1).

Episteme Episteme is the word for theoretical–scientific knowledge. The opposite is doxa, which refers to “belief” or “opinion”. There is a massive body of epistemic knowledge within endodontology, for example on the biology of the pulp, the microorganisms that inhabit root canals, the procedures and materials used in the clinical practice of endodontology (endodontics) and the outcome of endodontic therapies. Science produces “facts”. It must be understood that modern science is an industry and is affected by many factors, both internal and external. Although this is not the place to discuss the philosophy of science, the concept of “truth” and the growth of scientific knowledge is not unproblematic. There has been substantial contemporary philosophical discussion reflecting on epistemic knowledge, and the interested reader is referred to one of the many good introductory texts that are available (3).

The results of science are presented in lectures, articles and textbooks. So from a student’s point of view the learning situation is rather straightforward, provided that the subject is structured well and ample time given for reading and reflection. This book, in large part, is composed of epistemic knowledge.

Techne The first person to challenge the deeply intrenched theoretical concept of knowledge was the British philosopher Gilbert Ryle. In his book The Concept of Mind (10) he introduces “knowing-how” and distinguishes it from “knowing-that”. “Knowing-how” is practical in nature and concerns skills and the performance of certain actions. This concept of knowledge implies the ability not only to do things, but also to understand what you are doing. To say that you have practical knowledge, it is not enough to produce things out of mere routine or habit. You have to “know” what you are doing and be able to argue about it. Practice must be combined with reflection. The idea that there is a tacit or silent dimension of knowledge has had a great impact on the contemporary discussion. Michael Polanyi, for example, said that “We know more than we can tell” (9). When trying to explain how we master practical things such as riding a bicycle or recognizing a face, it is not possible to articulate verbally all the knowledge that we have. Certain important aspects are “tacit”. Likewise, it is not sufficient to teach students about root canal preparation simply by asking them to read a book or presenting the subject matter in a lecture. It has to be demonstrated. Knowledge is very often transmitted by the act of doing. A substantial body of endodontic knowledge must be characterized as techne. It is not possible to learn all about the procedures in endodontology by studying a textbook. Observing a good clinical instructor, watching other dentists at work, performing the procedures oneself and reflecting on what has been learned are all important. 1

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Introduction to endodontology

Phronesis According to Aristotle, phronesis is the ability to think about practical matters. This can be translated as “practical wisdom” (5) and is concerned with why we might decide to act in one way rather than in another. When thinking about the “right” action or making the “right” decision we enter the territory of moral philosophy. The person who has practical wisdom has good moral judgment. Modern ethical thinking has been influenced significantly by ideas that originated during the enlightenment. Morality is concerned with human actions and there are certain principles that can separate “right” from “wrong” decisions. Jeremy Bentham (2) and the utilitarians launched the utility principle and Immanuel Kant (6) invented the categorical imperative, each creating a tradition with great impact on today’s medical ethics and decision making. Aristotle, on the other hand, believed that there are no explicit principles to guide us. He understood practical wisdom as a combination of understanding and experience and the ability to read individual situations correctly. He thought that phronesis could be learnt from one’s own experience and by imitating others who had already mastered the task. He stressed the cultivation of certain character traits and the habit of acting wisely. The clinical situation demands that the dentist exercises practical wisdom, “to do the right thing at the right moment”. In order to develop phronesis, theoretical studies of moral theory and decision-making principles might be helpful. Neoaristotelians such as Martha Nussbaum (8) have suggested that reading literature should be part of any academic curriculum, the idea being that it increases our knowledge and understanding of other people. However, the essence of phronesis has to be learnt from practice.

Concepts of endodontology From the above it can be concluded that endodontology encompasses not only theoretical thinking but also the practical skills of a craftsperson and the practical thinking needed for clinical and moral judgment. Unfortunately, through the years, undue prestige has been given to theoretical–scientific thinking and this has hindered the development of a rational discussion of the other types of knowledge. The serious student of endodontology has to investigate all three aspects, but, as argued above, there are limits to what can be communicated within the covers of a textbook.

The dawn of modern endodontology It all started with a speech at the McGill University in Montreal. In the morning of October 3, 1910, Dr William

Hunter gave a talk entitled “The role of sepsis and antisepsis in medicine”. Hunter said that: “In my clinical experience septic infection is without exception the most prevalent infection operating in medicine, and a most important and prevalent cause and complication of many medical diseases. Its illeffects are widespread and extend to all systems of the body. The relation between these effects and the sepsis that causes them is constantly overlooked, because the existence of the sepsis is itself overlooked. For the chief seat of that sepsis is the mouth; and the sepsis itself, when noted, is erroneously regarded as the result of various conditions of ill-health with which it is associated – not, as it really is, an important cause or complication. “Gold fillings, gold caps, gold bridges, gold crowns, fixed dentures, built in, on, and around diseased teeth, form a veritable mausoleum of gold over a mass of sepsis to which there is no parallel in the whole realm of medicine or surgery. The whole constitutes a perfect gold trap of sepsis.” The cited text was published in the Lancet in 1911. But Hunter’s words rapidly spread and were intensively discussed among laymen and given banner headlines in the newspapers. Essentially, Hunter proposed that microorganisms from a dental focus of infection can spread to other body compartments and cause serious systemic disease. The fear that illnesses and even those of chronic or of unknown origin were caused by oral infections, brought thousands of people to the waiting rooms of dentists with demands to have their teeth removed. As a result of the focal infection theory teeth were extracted in enormous numbers. Although not directly stated by Hunter, teeth with necrotic pulps were seen as one of the main causes of “focal infection”. Laboratory studies had disclosed the presence of bacteria in the dead pulp tissue. In the 1920s, dental radiography came into general use and radiolucent patches around the apices of teeth with necrotic pulps indicating an inflammatory bone lesion were possible to detect. If such teeth were extracted and cultured, microorganisms were often recovered from the attached soft tissue. It became virtually incontestable that pulpally diseased teeth should be removed. Reflecting on this period in the history of dentistry, Grossman (4) wrote: “The focal infection theory promulgated by William Hunter in 1910 gave dentistry in general, and root canal treatment in particular, a black eye from which it didn’t recover for about 30 years.” However, in hindsight, this period can also be regarded as the dawn of modern endodontology. Researchers started to question and oppose the clinical consequences of the focal infection theory. Microbiologists began mapping out the microflora of infected root canals. Pathologists

Introduction to endodontology

investigated the reaction patterns of the pulp and periapical tissues and came to understand the protective power of the host defense mechanisms. Clinicians invented aseptic methods to treat the root canal, and radiography made it possible to confine the procedures to within the root canal space. It was further demonstrated that root canal infections could be combated successfully and it became obvious that root canal infections were not such a serious threat to the human organism as once believed. Pulpally compromised teeth could therefore be spared and endodontic treatment became a necessary skill of the modern dentist.

The objective of endodontic treatment The consequences of inflammatory lesions in the pulp and periapical tissue (Fig. 1.1) have tormented humankind for thousands of years. Historically, therefore, the main task of endodontic treatment has been to cure toothache due to inflammatory lesions in the pulp (pulpitis) and the periapical tissue (apical periodontitis). For a long period of time a commonly used method to remedy painful pulps was to cauterize the tissue with a red-hot wire or with chemicals such as acid. In 1836, arsenic was introduced to devitalize the pulp, a method that would be used for well over 100 years. Procedures to remove the pulp without toxic chemicals were introduced in the early part of the 19th century and small, hooked instruments were used. The advent of local anesthesia at the beginning of the 20th century made pulpectomy a painless procedure. Signs of root canal infection, such as abscesses with fistulae, were also dealt with historically using highly toxic chemicals. These substances were introduced to the root canal, and forced through the foramen into the fistula. Often the treatment was more damaging than the

3

disease condition itself, and the tooth and parts of the surrounding bone were often lost in the process. While relief of pain is still a primary goal of endodontic treatment, patients also may want to exclude the compromised tooth, as both a general and local health hazard. This means that intra- as well as extraradicular infections should be eradicated and that materials implanted in the root canal should be innocuous and not cause adverse tissue reactions or systemic complications. Using modern endodontic treatment procedures, these treatment objectives can be attained in the large majority of cases.

Clinical problems and solutions The vital pulp Under normal, physiological conditions the pulp is well protected from injury and injurious elements in the oral cavity by the outer hard tissue encasement of the tooth and an intact periodontium (Fig. 1.2). When the integrity of these tissue barriers is breached for any reason, microorganisms and the substances they produce may gain access to the pulp and adversely affect its healthy condition. The most common microbial challenge of the pulp derives from caries. Even in its early stages substances from caries-causing bacteria may enter the pulp along the exposed dentinal tubules. Like any connective tissue, the pulp responds to this with inflammation. Inflammation has an important aim to neutralize and eliminate the noxious agents. It also organizes subsequent repair of the damaged tissue. Thus, the pulp may react in a manner that allows it to sustain the irritation and remain in a functional state. Yet, when caries has extended to the vicinity of the pulp, the response may take a destructive course and result in severe pain and death (necrosis) of the tissue. Areas of important knowledge

Endodontic treatment concepts

Pulp capping Dentin reactions

Pulpal inflammation

Pain mechanisms

Fig. 1.1 A medieval skull found in Denmark showing teeth with serious attrition. In the first left molar the pulp chamber is exposed and the alveolar bone is resorbed around the root apices, indicating a once-present periapical inflammation due to necrosis of the pulp followed by root canal infection.

Pulpectomy

Fig. 1.2

The scope of endodontology: the vital pulp.

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Introduction to endodontology

An inflamed or injured pulp may have to be removed and replaced with a root filling – a procedure termed pulpectomy. This measure is undertaken especially in cases when the condition of the pulp is such that an inflammatory breakdown is deemed imminent. A manifest infection may otherwise develop in the root canal system. A pulpectomy procedure is carried out under local anesthesia and with the use of specially designed root canal instruments. These instruments remove the diseased pulp and prepare the canal system so that it can be filled properly. The purpose of the filling is to prevent microbial growth and multiplication in the pulpal chamber. Thus, pulpectomy is a measure primarily aimed at preventing the development of a manifest root canal infection and painful sequelae. Pulpectomy may also be carried out any time a pulp is directly exposed to the oral environment. This may occur after clinical excavation of caries or after a traumatic insult or iatrogenic injury. If the exposure is fresh and the pulp judged not to be seriously inflamed it may not have to be removed. If the open wound is treated with a proper dressing and protected from the oral environment by pulp capping, healing and repair of the wound

Core concept 1.1

are possible. For common terminologies used to specify the endodontic disease conditions and their treatments, see Core concept 1.1.

The necrotic pulp As mentioned above, injury to the pulp may lead to necrosis of the tissue (Fig. 1.3). The necrotic pulp is defenseless against microbial invasion and will allow microorganisms indigenous to the oral cavity to reach the pulp chamber, either along an open direct exposure or through uncovered dentinal tubules or cracks in the enamel and dentin. Lateral canals exposed as a result of progressive marginal periodontitis may also serve as pathways for bacteria to reach the pulp. The specific environment in the root canal, characterized by the degrading pulp tissue and lack of oxygen, will favor a microbiota dominated by proteolytic, anaerobic bacteria. These microorganisms may organize themselves in clusters and in microbial communities attached to the root canal walls as well as inside the dentinal tubules of the root. In these positions microorganisms stay protected from host defense mechanisms and can therefore multiply rapidly to large numbers. Microorganisms attempt to

Common terms and expressions used for endodontic disease conditions and treatment procedures

Pulpitis

Inflammation of the dental pulp. Symptomatic and asymptomatic pulpitis, as well as irreversible and reversible pulpitis, are commonly used terms to specify lesions with and without painful symptoms. The terms total and partial pulpitis are also in use.

Pulp necrosis

Pulp death. Pulp chamber is devoid of a functional pulp tissue. Necrosis can be more or less complete, i.e. partial or total.

Apical periodontitis

Inflammatory reaction of the tissues surrounding the root apex of a tooth. Symptomatic/asymptomatic apical periodontitis and acute/chronic apical periodontitis, respectively, are applied to indicate lesions with and without overt clinical symptoms such as pain, swelling and tenderness. Dental or apical granuloma is a histological term for an established lesion. Apical, periapical and periradicular are interchangeable terms to state the location of the process at or near the root tip.

Pulp capping

Treatment procedure aimed at preserving a dental pulp that has been exposed to the oral environment.

Partial pulpotomy

Treatment procedure by which the most (often inflamed) superficial portion (1–2 mm) of the coronal pulp is surgically removed with the aim of preserving the remaining tissue.

Pulpotomy

Treatment procedure by which the entire coronal pulp tissue is surgically removed with the aim of preserving the remaining tissue. The term pulpotomy is also used to describe a pain-relieving procedure in an emergency treatment of symptomatic pulpitis.

Pulpectomy

Treatment procedure by which pulp tissue (often inflamed) is surgically removed and replaced with a root filling.

Root canal treatment (RCT)

Treatment of teeth with necrotic pulps where root canals are often infected.

Non-surgical retreatment

Treatment of root filled teeth with clinical and/or radiographic signs of root canal infection, where root fillings are removed, canals disinfected and refilled. May also be carried out to improve the technical quality of previous root fillings.

Surgical retreatment

Treatment procedure by which the root apex of a tooth is surgically accessed to manage a root canal infection that has not been successfully treated by RCT. Retrograde endodontics or surgical endodontics are other terms for this procedure.

Introduction to endodontology

Areas of important knowledge

Endodontic treatment concepts

Areas of important knowledge

5

Endodontic treatment concepts

Restoration of the root filled tooth

Pulp necrosis

Root canal treatment

Intracanal microbiota

Non-surgical retreatment Microbiota of the filled canal Surgical retreatment

Periapical tissue reactions

Reasons for treatment “failure”

Fig. 1.3

Fig. 1.4

The scope of endodontology: the necrotic pulp.

invade the periodontal tissues via the apical foramen or any other portal of exit from the root canal, and may do so before the host defense has been effectively organized. Once established, however, organisms will normally be held back but not eliminated from the root canal space. A chronic inflammatory lesion will ensue, normally around the root tip, and remain for as long as no treatment is initiated. The periapical tissue reaction is often visible in a radiograph as a localized radiolucency because the adjacent bone has been resorbed in the course of the inflammatory process. The condition may or may not be associated with pain, tooth tenderness and various degrees of swelling. Treatment of the necrotic pulp is by root canal treatment (RCT) and is aimed to combat the intracanal infection. The canal is cleaned with files in order to remove microbes as well as their growth substrate. Owing to the complex anatomy of the root, instruments cannot reach all parts of the canal system and therefore antimicrobial substances are added to disinfect the canal. In order to avoid reinfection and to prevent surviving microbes from growing, the canal is then sealed with a root filling.

The root filled tooth Pulpectomy and RCT do not always lead to a successful clinical outcome. For example, a tooth may continue to be tender or periapical inflammation may persist. Such treatment “failures” are often associated with defective root fillings, which allow organisms from the initial microbiota to survive in the root canal or new bacteria to enter via leakage along the margins of the coronal restoration (Fig. 1.4).

The scope of endodontology: the root filled tooth.

The root canal in such cases may be retreated using either a non-surgical or a surgical approach. In non-surgical retreatment the root filling is removed and the canal is reinstrumented. Antimicrobial substances are applied to kill the microbes and the space is refilled. Crowns, bridges and posts may mean that it is sometimes not feasible to reach the root canal in a conventional way. In such cases, a surgical retreatment may be attempted. A mucoperiosteal flap is then raised and entrance to the apical part of the root made through the bone. Surgical retreatment often involves cutting of the root tip, instrumentation of the apical root portion and placement of a filling at the apical end.

The diagnostic dilemma The disease processes in the pulp and periapical tissues take place in a concealed body compartment that normally is not available for direct inspection. Instead, the clinician has to rely on indirect information to assess the condition of the tissue and reach a diagnosis. The reliance on indirect signs and symptoms entails the risk of making false-positive and false-negative diagnoses. For example, the patient’s report of pain has been found to be an inaccurate sign because there is no exact relationship between the amount of tissue damage and level of pain encountered. Furthermore most inflammatory episodes within the pulp or periapical bone pass by without symptoms. Another factor is that the discriminatory ability of the intrapulpal nerves is not perfect, which means that if a patient has toothache due to pulpitis there is a high risk that he or she may “point out the wrong tooth”. Nevertheless a patient’s experience of pain and especially its character serve as important

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Introduction to endodontology

indicators of an endodontic disease condition. Along with pulp vitality testing and radiographic examination, the disease history is a prime source of diagnostic data. Yet, to avoid erroneous diagnoses all data have to be interpreted with utmost care and with in-depth knowledge of possible errors and the factors that influence diagnostic accuracy.

The tools of treatment To many dentists, RCT can best be described by using Winston Churchill’s words on golf: “An impossible game with impossible tools”. The complexity of root canal anatomy, the relative stiffness of root canal instruments, being unable, often, to visualize the area properly, and the lack of space in the mouth provide substantial challenges to the skill and patience of the dentist. Intracanal work is exceptionally demanding; this is clearly demonstrated by numerous radiographically based epidemiological surveys, which repeatedly report that many root fillings do not meet acceptable technical standards. Because clinical outcome is strongly related to the quality of treatment, the high frequency of substandard performances is a subject of great concern to the profession. The last 10–15 years have seen a tremendous technological development that facilitates endodontic treatment and enhances the potential to increase its overall standard (7). For example, the advent of super-flexible nickel–titanium alloy has made it possible to fabricate instruments that are highly flexible and can follow the anatomy of the root canal and therefore produce good quality canal preparations. Furthermore, systems have been developed that allow the instruments to be maneuvered by machine rather than by hand, improving finescale manipulation and decreasing operator fatigue. The surgical microscope has brought light and vision into the pulp chamber. Working under high magnification, it is now far easier to remove mineralizations, locate small root canal orifices and control intracanal procedures than with the naked eye or with loupes. However, high-quality microscopes are expensive and, thus far, the technology has found limited adoption by dentists other than those specialized in endodontics. In the midst of this technological boom it must not be forgotten that endodontics is primarily about controlling infection. While the intracanal work is aimed to eliminate infectious elements and give space for the subsequent root filling, this effort would be futile if measures were not undertaken to prevent oral contaminants from entering the root canal space during the procedure. Luckily, there are few medical treatments that can be carried out as aseptically as endodontic therapy. Shielding the tooth with a rubber dam is the oldest and still the most effective way to ensure that the operation field remains

Fig. 1.5 Rubber dam isolated tooth, which is in the process of being disinfected.

sterile (Fig. 1.5). This measure also facilitates the procedure and is critically important to the clinical success of endodontic therapy.

Extraction and dental implant? Extraction and placement of dental implants to replace endodontically compromised teeth has gained popularity in recent years. Such a measure can certainly be a valuable option in cases of severely damaged teeth that either have a hopeless prognosis or cannot be provided with a proper restoration. Yet, dental implants must not be overused or misused because an endodontic treatment, for example, may appear complicated. Clearly endodontic therapy represents a very realistic opportunity to restore most teeth with diseased pulps to a healthy state. Indeed endodontic therapy has reached a level of sophistication today that dentists, with proper knowledge and training, can carry out the procedures with a high rate of success. Epidemiological data have furthermore shown that endodontically treated teeth maintain a functional place in the oral cavity for long periods of time (11).

References 1. Aristotle (Iruin T, ed.). Nicomachean Ethics. London: Hackett Publishing, 1988. 2. Bentham J. Introduction to the Principles of Morals and Legislation (1789) (Burns JH, Hart DLA, eds). London: Methuen, 1982. 3. Chalmers AF. What is this Thing called Science? Buckingham: Open University, 1999. 4. Grossman LI. Endodontics 1776–1996: a bicentennial history against the background of general dentistry. J. Am. Dent. Assoc. 1976; 93: 78–87. 5. Hughes GJ. Aristotle on Ethics. London: Routledge, 2001.

Introduction to endodontology

6. Kant I. Foundations of the Metaphysics of Morals (1785). Indianapolis: Bobbs–Merrill, 1959. 7. Molander A, Caplan D, Bergenholtz G, Reit C. Improved root-filling quality among general dental practitioners educated in nickel titanium rotary instrumentation. Int. Endod. J. 2007; 40: 254–60. 8. Nussbaum M. Poetic Justice. The Literary Imagination and Public Life. Boston: Beacon Press, 1995.

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9. Polanyi M. Personal Knowledge: Towards a Postcritical Philosophy. London: Routledge, 1958. 10. Ryle G. The Concept of Mind. London: Penguin, 1949. 11. Salehrabi R, Rotstein I. Endodontic treatment outcomes in a large patient population in the USA: an epidemiological study. J. Endod. 2004; 30: 846–50.

Part 1

The Vital Pulp

9

Chapter 2

The dentin–pulp complex: structures, functions and responses to adverse influences Leif Olgart and Gunnar Bergenholtz Introduction The extent to which the dental pulp will sustain impairment in the clinical setting depends on its potential to oppose bacterial challenges and withstand injury by various forms of trauma. To understand the biological events that operate and most often prevent the pulp from suffering a permanent breakdown, the specific biological functions of both dentin and pulp under pathophysiological conditions will be addressed in this chapter. These two tissue components of the tooth form a functional unit that often is referred to as the dentin–pulp complex (Fig. 2.1).

Constituents and normal functions of the dentin–pulp complex Dentin and dentinal tubules Dentin provides elasticity and strength to the tooth that enable it to withstand loading forces by mastication and trauma. Dentin also elicits important defense functions aimed at preserving the integrity of the pulp tissue.

Enamel Pulp Dentin

The dentin–pulp complex Cementum

Fig. 2.1 The soft tissue of the pulp is surrounded by dentin and enamel or cementum. Inset depicts the interface zone between dentin and pulp.

Under normal, healthy conditions, when dentin is covered by enamel and cementum, fluid in the dentinal tubules can contract or expand to impinge on the cells in the pulp in response to thermal stimuli applied on the tooth surface. Hence, dentin of the intact tooth can transform external stimuli into an appropriate message to cells and nerves in the pulp – a feature that is useful clinically to test its vital functions (see Chapter 14). A sensory transducer function triggered by elastic deformation is also in effect to detect overload resulting in reflex withdrawal and sharp transient pain. When enamel and cementum are damaged for any reason, the exposed dentinal tubules serve as pathways to the pulp for entry of potentially noxious elements in the oral environment including bacterial macromolecules, which may provoke inflammation (4). The deeper the injury the more tubules become involved (Fig. 2.2). In the periphery there are about 20 000 tubules per square millimeter, each having a diameter of 0.5 μm. At the pulpal ends the tubular apertures occupy a greater surface area because the tubules converge centrally and become wider (2.5–3 μm) (20). Thus, at the inner surface of dentin there are more than 50 000 tubules per square millimeter. In root dentin, especially towards the apex, the tubules become more widely spaced. Also, in the pulpal portion of root dentin they are thinner and have a smaller diameter (ca. 1.5 μm). There are extensive branches between the tubules that allow intercommunication. Movement of particulate matter and macromolecules by way of the dentinal tubules may occur not only from the external environment to the pulp but also in the opposite direction. Hence, following injury which has resulted in disruption of the tight junctions that normally hold the odontoblasts together (71), fluid in the pulp may enter the tubules and bring plasma proteins with antimicrobial properties (41). The potential for elements to permeate the dentinal tubules is normally greatly restricted by a variety of tissue structures, including collagen fibers and cellular processes. The odontoblasts normally extend cytoplasmic processes into the tubules. Controversy exists, however, 11

12

The Vital Pulp

The odontoblast – a multifunctional cell The most recognized function of the odontoblasts is to form and maintain dentin. Like many other tissuesupporting cells, odontoblasts also contribute to host defense. By lining the periphery of the pulp with cellular extensions into dentin they are, thus, in the unique position of being the first cell to encounter and react to noxious elements entering dentin from the oral environment (Fig. 2.4). Upon challenge the odontoblasts generate and release a multitude of molecules that can help to defeat invading microorganisms. The response also gives rise to activation of specific receptors present on adjacent cells, vessels, nerves and on the odontoblast itself (Advanced concept 2.1). Thus, the odontoblasts, together with local resident defense cells and blood-borne invading cells, have a broad repertoire of response patterns and play important roles in activating both innate and adaptive immune responses of the pulp (for reviews see Refs 23, 24) (Fig. 2.5).

Tubules near the enamel

Tubules near the pulp

Dentin formation Fig. 2.2 Density of dentinal tubules in various portions of the crown region in teeth. It has been estimated that the surface area taken by cross cut tubules is ca. 2–3% in the periphery. Near the pulp the dentinal tubules assume ca. 25% of the surface area (61).

as to how far. While some believe that these processes extend all the way to the enamel or cementum junctions others contend that only the innermost part (0.5–1 mm) of dentin is filled (15). A large number of the tubules also contain nerve terminals. Furthermore, cells belonging to the immunosurveillance system of the pulp extend dendrites into the tubules of the predentin layer (52). Consequently, the space available in the tubules for the transport of particulate matter and macromolecules is normally much smaller than the tubular space per se (61) (Fig. 2.3). This is especially true at their pulpal ends. Dentin

Predentin

The original odontoblasts, here also termed primary odontoblasts, produce dentin both during tooth development and after completion of root formation. The fact that intratubular cellular processes stay behind makes dentin tubular in nature. Owing to the continued function of the odontoblasts, the pulpal space gradually narrows over time and in old individuals it may become so small that endodontic treatment is difficult. The odontoblasts may also produce new dentin at an increased rate in response to mild stimuli: e.g. during initial precavitated stages of enamel caries (10); by slowly progressing caries in general (9); or following a shallow preparation for restorative purposes. This type of new dentin has been termed reactionary dentin (67) (see also Core concept 2.1).

Pulp Odontoblasts

Nerves

Dentinal tubule

Dendritic cell

Fig. 2.3 Cellular extensions of odontoblasts, nerves and cells of the immune system (dendritic cells) occupy the pulpal ends of the dentinal tubules.

The dentin–pulp complex: structures, functions and responses to adverse influences

Advanced concept 2.1 Role of odontoblasts in pulpal immunity

Core concept 2.1

Odontoblasts are supplied with a multitude of receptors, which enable them to sense and respond to microbial elements and thereby alert the immune system. Thus, several members of the Toll receptor family have been identified on odontoblasts (19, 23). Upon activation of such receptors production of proinflammatory cytokines and chemokines is initiated; these, in turn, recruit immune cells. Recent observations suggest that odontoblasts are more potent attractants than pulpal fibroblasts in this respect (67). Odontoblasts may also release antimicrobial peptides with the capability of direct killing both Gram-positive and Gram-negative bacteria (18). Odontoblasts furthermore respond to proinflammatory cytokines secreted by adjacent resident cells and invading immune cells. Specific substances that regulate vascular permeability and angiogenesis are also released upon microbial challenges (70). Consequently, the strategic peripheral position of the odontoblast and its varied spectrum of response patterns make the cell a prime mover of the pulp’s defense to both externally and internally derived adverse influences.

Primary dentin: dentin formed by primary odontoblasts.

Dentinal repair Following injury or irritation (e.g. by a restorative procedure or rapidly progressing caries), the primary odontoblasts may die. Because these cells are postmitotic cells, they are unable to regenerate by cell division. New dentin may nevertheless be formed. Such dentinal repair appears to occur through the activity of so-called repairing odontoblasts or secondary odontoblasts. The precursor of these cells is thought to be a population of postnatal Dentin Predentin Odontoblasts Cell-free zone Cell-rich zone

13

Terms used for different types of dentinogenesis

Reparative dentin: dentin formed in response to injury by either primary or secondary odontoblasts (repairing odontoblasts). Equivalent terms commonly used are irregular secondary dentin, irritation dentin and tertiary dentin. Note that primary dentin and secondary dentin are terms sometimes used to designate dentin formed by primary odontoblasts before and after termination of root development, respectively. Consequently, the term tertiary dentin has emerged to denote dentin formed in response to irritation or injury. The current text makes no such distinction.

stem cells that are present in the pulp tissue proper (22). Following their recruitment and upregulation, a mineralizing matrix is laid down on the dentinal wall. Repair by secondary odontoblasts is also possible against an appropriate wound-healing agent applied to treat direct exposure of the pulp (see Chapter 4). Hence, a new generation of odontoblast-like cells, capable of making new dentin locally, can evolve in the pulp upon injury. Secondary odontoblasts produce dentin at a rate that is dependent on the extent and duration of the injury. The development of this hard tissue leads to an increase in dentin thickness (Figs 2.6 and 2.7). It should be noted that dentin formed by secondary odontoblasts is more irregular and amorphous and contains fewer dentinal tubules than primary dentin (11). These tubules will not necessarily be in direct line with the tubules of the primary dentin (Fig. 2.8). Consequently, a complex of primary and reparative dentin becomes less permeable to externally derived matter. It also follows that such dentin is less sensitive to thermal, osmotic and evaporative stimuli (12; see also Chapter 3). The quality of the new hard tissue is not always as good as that of primary dentin. When it is formed rapidly, e.g. following an ischemic injury by dental trauma, it may become highly porous and contain areas filled with soft tissue. Although the pulpal space in radiographs may appear

Fig. 2.4 Tissue section stained with hematoxylin and eosin showing dentin, predentin and pulp tissue proper with odontoblasts lining the periphery.

2

a 1

b

c

Fig. 2.5 The odontoblast has many functions which change during tooth development, maturation and injury of teeth. (a) Sensor: 1. affected from outside by antigens, mechanical forces, thermal gradients; 2. bombarded from inside by circulating hormones, paracrine and autocrine substances. (b) Secretory cell: a. for dentin lay down, b. for maintenance, c. for immune defense. (c) Pain mediator: acting as a transducer between external stimuli and pulpal sensory nerves.

14

The Vital Pulp

Fig. 2.6 Microphotograph showing hard tissue repair following a cavity preparation (arrow). The circle indicates bulk of new dentin being formed.

Fig. 2.7 Clinical photograph of anterior lower teeth showing extensive loss of tooth structure due to tooth wear. Reparative dentin formed in the pulp has prevented direct exposure of the tissue to the oral environment.

completely obliterated, these areas are large enough to give room for bacterial growth and multiplication in case of an ensuing infectious exposure (Fig. 2.9). Similarly, hard-tissue repair of pulpal wounds may occasionally show gross defects, which makes it highly permeable to bacteria and bacterial elements. Therefore, hard-tissue deposition in the pulp, although adding to the defense potential of the tissue in certain instances, should be viewed as a scar tissue.

Nerves Pulpal nerves monitor painful sensations. By virtue of their peptide content they also play important functions in inflammatory events and subsequent tissue repair

Fig. 2.8 Tissue section of an interface zone between primary dentin and reparative dentin as indicated by arrows. Note that the dentinal tubules are less numerous in the secondary dentin than in the primary dentin to the left. Also, few of the tubules are in direct line with those of the primary dentin, thus making the entire complex less permeable. Pulpal tissue and nuclei of pulp cells are to the right. (Courtesy of Dr Lars Bjørndal and with permission of Caries Research, Karger.)

Fig. 2.9 Series of radiographs of a tooth in a patient who suffered a luxation injury at a young age. Hard tissue is successively deposited in the pulp. Arrow indicates change in status between the 15-year and 20-year follow-up radiographs. In the radiograph to the right, a periapical radiolucency is seen, suggesting pulpal infection. (From Robertson et al. (65) with permission of the Journal of Endodontics.)

(Fig. 2.10). In addition, they control dentin formation (Fig. 2.10). There are two types of nerve fiber that mediate the sensation of pain: A-fibers conduct rapid and sharp pain sensations and belong to the myelinated group, whereas C-fibers are involved in dull aching pain and are thinner and unmyelinated. The A-fibers, mainly of the A-delta type, are preferentially located in the periphery of the pulp, where they are in close association with the odontoblasts and extend fibers to many but not all dentinal tubules. The C-fibers typically terminate in the pulp

The dentin–pulp complex: structures, functions and responses to adverse influences

Storage Release

Transport

15

Trigeminal ganglion

Production of SP CGRP NKA

Transport

Impulse propagation

Fig. 2.10 A large portion of the sensory fibers, including C-fibers and some A-delta fibers, contain vasoactive neuropeptides such as calcitonin gene-related peptide (CGRP), substance P (SP) and neurokinin A (NKA). The neuropeptides are produced in the trigeminal cell bodies and are transported via axonal flow to the nerve terminals in the pulp, where they are stored. In addition to their effect on pulpal blood flow and vessel permeability, SP and CGRP exert stimulatory effects on the growth of pulpal cells, such as fibroblasts and repairing odontoblasts. They are also active in the recruitment of immunocompetent cells in response to bacterial exposures.

tissue proper, either as free nerve endings or as branches around blood vessels (56). The nature of A- and C-fibers and their respective roles in pain transmission are described in Chapter 4. Nerves belonging to the autonomic nervous system, such as sympathetic vasoconstrictor fibers, are also present (48). They enter the pulp together with blood vessels and sensory axons. Histochemically, they can be traced in the pulp via their content of noradrenaline and neuropeptide Y. Upon release, these substances result in contraction of the smooth-muscle sphincters in arteries and small arterioles apical to and within the pulp (58). Both sensory and sympathetic nerves stimulate dentin formation as evidenced by reduced dentin formation in the absence of sensory nerves and after sympathectomy, respectively (32). Sensory and sympathetic nerves also interact in pulpal inflammation. For example, an intact innervation is significant for recruitment and activation of cells of the immune system (see Key literature 2.1). As yet, there is little evidence that parasympathetic vasodilator blood flow control plays an important role in the local function and defense of the pulp.

Vascular supply Current knowledge of the vascular architecture of the pulp has been influenced greatly by the use of the microvascular resin cast method (Fig. 2.11) (68). This technique

Key literature 2.1 Based on experimental studies Haug and Heyeraas (25) suggested that immune responses are subjected to modulation by the sympathetic nervous system (SNS) in dental tissues. The SNS was shown to inhibit the production of proinflammatory cytokines, while stimulating the production of anti-inflammatory cytokines. In rat dental tissues, it was found that the SNS is significant for recruitment of inflammatory cells such as CD 43+ granulocytes. Sympathetic nerves appeared to have an inhibitory effect on osteoclasts, odontoclasts, and on IL-1alpha production. The SNS stimulated reparative dentin production, since reparative dentin formation was reduced after sympathectomy. Sprouting of sympathetic nerve fibers occurs in chronically inflamed dental pulp, and neural imbalance caused by unilateral sympathectomy recruits immunoglobulin-producing cells to the rat dental pulp. In conclusion, this article presents evidence in support of interactions between the sympathetic nervous system and cells producing hard tissue, and pulpal inflammation.

allows resin to fill up even the smallest capillaries of the pulp. A vascular cast is then obtained, which, following corrosion of surrounding tissue structures, can be examined in the scanning electron microscope. In all developmental stages the crown pulp shows a larger vascular network than the root pulp. In more central portions of the pulp the vascular network is less dense than in peripheral pulp. Anastomosis between

16

The Vital Pulp

(a)

(c)

(b)

(d)

Fig. 2.11 Series of microphotographs of the vascular network in the pulp of teeth. (a) In the young tooth of dogs there is a dense terminal capillary network in the pulp–dentin border zone. (b) The superficial capillary network in the odontoblast region in a view perpendicular to the pulpal surface. (c) Blood vessels in the distal root canal of a mature dog premolar. The superficial capillaries drain directly into large venules (V). In the mature tooth, continuous dentin formation and narrowing of the pulp cavity lead to remodeling of the vascular tree. (d) The vascular network of an adult human tooth. With a narrow apical foramen, the number of arterioles is reduced to 5–8 and venules to 2–3 (40). The number of main vessels, arterioles and venules in the central pulp is also reduced and the typical hairpin loops of the terminal capillary network become less pronounced. The detailed vascular architecture of the pulp is similar in cat, dog and human teeth. (Courtesy of Dr K. Takahashi.)

incoming and outgoing blood vessels has been observed in the central pulp of adult animal teeth (40) and seems to be more frequent in the apical pulp than in the crown pulp (38). Shunt connections between supplying and draining pulpal vessels have also been found just outside the apical foramen in the periodontal ligament (69). It is reasonable to assume that these shunts provide control of blood perfusion through the pulpal tissue. Hence, in the case of a local inflammatory event causing increased resistance to pulpal blood flow, arteriovenous shunts may come into play and redirect incoming blood.

Lymphatics Both morphological and functional studies in animals show the existence of lymphatic vessels in the pulp (8, 26). These vessels are important to adjust for increased colloid osmotic pressures exerted by proteins and macromolecules accumulating extracellularly in inflamed areas. Another important function is to serve as pathways to the regional lymph nodes for antigen-presenting cells.

The dentin–pulp complex: structures, functions and responses to adverse influences

Immune defense The dentin–pulp complex is uniquely organized to offset microbial threats from caries and other breaches of the outer hard tissue encasement of the tooth to the oral environment. While permeable to bacterial elements by virtue of the dentinal tubules, dentin nonetheless carries out an important filter function of significance to the pulp’s immune defense. Primarily two mechanisms account for this effect: (i) the peripherally directed flow of dentinal fluid, and (ii) the absorbance of bacteria and bacterial macromolecules to the inner walls of the tubules (63). Thereby, dentin is able to temper exposures of noxious elements to the pulp, allowing it to adapt and organize an effective immune defense response. Constituents making up the innate immune defense of the pulp include resident tissue cells, viz. odontoblasts and immune cells, nerves and vessels (Fig. 2.12). The basal set up of immune cells is limited to antigenpresenting cells (APCs), macrophages and T-lymphocytes (T-cells) of the memory type (23). Neither B-cells nor mast cells are residents of the normal pulp and will not appear in the tissue unless there is an inflammatory event. APCs in the normal pulp are of two types. One has a pronounced dendritic configuration and belongs to the family of dendritic cells (DCs). The other is of the monocyte/macrophage lineage. Both constitutively carry class II MHC molecules on their cell surface. This molecule, found on all cells capable of antigen presentation, is a gene product of the major histocompatibility complex (MHC) and acts as a stimulatory molecule in T-cell activation both locally and in the regional lymph nodes.

Sensory nerves

17

The DCs in the pulp are strategically positioned in the periphery of the tissue, where foreign antigens are most likely to enter (Figs 2.12 and 2.13). Here, they compete for available space with the odontoblasts and make contact with these cells via their cytoplasmatic processes (52). Pulpal DCs are also in close proximity with nerve tissue elements and blood vessels in the paraodontoblastic region, suggesting interactive potentials (53, 54). The primary function of DCs is to alert the immune system for an effective subsequent elimination, and not to directly combat invading microorganisms. In peripheral sites, like the pulp, they occur in an immature

Fig. 2.13 Tissue section showing dendritic cells (stained brown) within the odontoblastic and subodontoblastic layer. Immunohistochemical staining was carried out with OX6-antibody, which is a marker for class II MHC molecules.

Blood vessel

Lymph vessel

Pulp

Dentin

Odontoblasts Dendritic cell

Fibroblast

Stem cell

Macrophage class II

Macrophage non-class II

Memory T-cell

Fig. 2.12 Constituents of primary significance in the defense of the pulp against foreign substances, including bacterial elements, make up the innate “first line of defense”.

18

The Vital Pulp

Secondary immune response

II

6 5

Local APC

Sensory nerves

Blood vessel

T-cell

I

4

DC

1

Lymph vessel

3 2

Primary immune response

Lymph node

Fig. 2.14 Antigen-specific T-cells are developed in the pulp following primary (I) and secondary (II) antigen exposures along dentinal tubules. Dendritic cells (1 in figure) capture protein antigen for processing to peptide fragments and carry (2) and present peptide fragments in the context of the class II molecules on their cell surface to naïve T-cells in the regional lymph nodes (3: primary immune response). Following clonal expansion, these cells enter the circulation (4 in figure). Following their patrolling of tissues as memory T-cells, they may participate in secondary immune responses at local sites, e.g. in the pulp (5 in figure), if exposed to the appropriate antigen by local APC (6 in figure). This route constitutes adaptive pathogen-specific immunity.

state. Maturation to become professional APCs (capable of activating T-cells that have not been exposed to antigen before, so-called naïve T-cells) comes from capturing incoming foreign antigens. Upon exposure they usually start migrating to the regional lymph nodes. Once there, fragments of the antigen bound to the class II MHC molecule will be shown to the appropriate naïve T-cells that become activated in a primary immune response (Fig. 2.14). DCs are particularly effective in microbial sensing, capturing and processing foreign antigens and are thus a key initiator of the adaptive immune response. The class II molecule-expressing macrophages are distributed in a remarkably high number in the pulp and seem to form a dense network together with pulpal DCs (33, 34). Like other connective tissues, macrophages in the pulp are heterogeneous in terms of phenotype and function. While there are those serving in local antigen presentation, there is also a large population of non-class II molecule-expressing, resident macrophages (histiocytes), primarily located perivascularly with primary functions in phagocytosis.

Basal maintenance Blood flow It is assumed that odontoblasts and nerve endings, especially during tooth development, have a high energy

demand. This may also be true in mature teeth. Hence, although there is limited collateral circulation, the peripheral pulp is well vascularized (see Fig. 2.11) The blood flow through the young adult pulp during resting conditions is relatively high compared with that of other oral tissues (50). In the adult dog, blood flow per 100 g of tissue is ca. 40 ml/min in teeth with a fully formed apex. By comparison, in the gingiva it is ca. 30 ml/min. The dense capillary network in peripheral pulp also allows filtration of fluid from the blood vessels, thereby supplying the dentinal tubules with fluid. In old teeth blood perfusion becomes successively lower.

Local control The level of the resting blood flow in the pulp is to a great extent controlled by the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP). Both CGRP and SP maintain a continuous relaxation of feeding arterioles (7). This continuous influence on the blood supply to the pulp depends on a basal release of the peptides without apparent nerve activation. Nitric oxide (NO) – a short-lived gas molecule that is produced enzymatically in the endothelial cell lining of vessels – also serves to maintain a physiological blood perfusion of the pulp (37). It has a powerful vasodilator action and, unlike neuropeptides, causes relaxation of the draining venules in the pulp under physiological conditions (7) (see Advanced concept 2.2).

The dentin–pulp complex: structures, functions and responses to adverse influences

19

Advanced concept 2.2 Mechanisms regulating pulpal blood flow

Advanced concept 2.3

The physiological regulation of blood flow and tissue pressures in the pulp has been studied in some detail in animal teeth. For example, treatment with antagonists to neuropeptides, or axotomy leading to degeneration of the sensory innervation, almost halves the pulpal blood flow and reduces the interstitial fluid pressure in the pulp. Pharmacological blocking of nitric oxide (NO) production also reduces blood flow but, at the same time, increases tissue pressure. Thus, when the physiological action of NO is intact, flow resistance in draining vessels is low (dilated vessels), allowing appropriate blood flow, volume and tissue pressure in the pulp (8). The constitutive NOproducing enzyme (eNOS) is activated by normal pulse-dependent shear stress in pulpal vessels (37).

A transient increase in pulpal blood flow is produced by electrical or noxious stimulation of adjacent tissues and teeth, as demonstrated in anesthetized animals (57). Thus pinching or insertion of an injection needle in the vestibular oral mucosa and delivery of a short train of electrical impulses to the lip or adjacent teeth give rise to a blood flow increase several minutes in duration. This phenomenon demonstrates the extensive branching of sensory nerves in and around teeth and their wide receptive fields, implying that spreading of neurogenic vascular reactions may take place between different oral tissues within the same nerve territory.

Remote control The regulatory control of pulpal blood flow also involves autonomic nerves. This remote system influences blood circulation in the pulp as well as in adjacent tissues within the same innervation territory. Although parasympathetic vasodilator nerves do not seem to play a significant role, there is firm evidence for sympathetic vasoconstrictor control in the dental pulp. The system does not seem to be active tonically and may not support local moment-to-moment demands of the tissue. However, physical and mental stresses trigger sympathetic vasoconstriction in the oral region, including the pulp, as part of the general fight-and-flight reaction (58). In general terms, both the sympathetic and the parasympathetic systems operate at the general or segmental levels and tend to ignore the needs of an individual tissue such as the pulp. Therefore, the locally active mechanisms, such as the blood flow control, most favorably meet the nutritional demands of the healthy pulp. Suitable adjustment of blood flow in the pulp is mainly the result of a balance between the locally governed relaxing factors and a certain myogenic constrictive tone of the vessels.

Spreading of vascular reactions

tion, which is immediately followed by a brief, sharp pain, alerting the individual to further withdrawal. This is an important alarm system protecting the tooth from overload leading to crown or root fractures by mastication forces, for example (59). In parallel there is a transient increase in blood perfusion in the pulp (49). This is part of an instant local defense reaction and is brought about by the fine terminal branches of sensory nerves supplying both cells in the odontoblast region and small feeding arterioles deeper in the pulp. Excitation of the most terminal branches in the peripheral area of the pulp results in a reflex propagation of impulses in adjacent nerve terminals belonging to the same nerves (axon reflex) (59). Because these nerves contain vasodilating neuropeptides, it takes only a few seconds for a short-lasting (