Ebook Textbook of endodontology (3/E): Part 1

(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

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

Blackwell Munksgaard (1e, 2003); Blackwell Publishing Ltd (2e, 2010)

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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 9 8 7 6 5 4 3 2 1

List of contributors xiii

Lars Bjørndal and Alastair J Sloan

Responses of the healthy dentin–pulp complex to nondestructive stimuli 25The dentin–pulp complex and responses to external injuries 25

Inge Fristad and Matti N¨arhi

Morphology of intradental sensory innervation 33

Sensitivity of dentin: hydrodynamic mechanism in pulpal A-fiber activation 38Responses of intradental nerves to tissue injury and inflammation 40Local control of pulpal nociceptor activation 44

Kerstin Petersson and Claes Reit

v

Diagnostic accuracy 50

Clinical manifestations of pulpal and periapical inflammation 51

Diagnostic methodology: assessment of pulp vitality 53Diagnostic methodology: evaluation of reported pain 55Diagnostic methodology: provocation/inhibition of pain 56Diagnostic methodology: evaluation of tooth discolorations 58

Lars Bjørndal

Progressive stages of enamel–dentin lesions without surface cavitation and exposure of dentin

Concluding remarks on the natural history of dental caries 72

Detailed treatment protocol for deep caries management 74

Lars Bjørndal, Helena Fransson, and St´ephane Simon

Indications and treatment concepts for preserving vital pulp functions 80Protocols for treatments aiming to preserve the vitality of the exposed pulp 81Factors of importance in preserving vital pulp functions 87

Tissue–biomaterial interaction and pulp healing 91Pulp-preserving treatments – a controversial treatment? 92Indications and treatment concepts for treating the irreversibly inflamed vital pulp

Choosing between pulp-preserving vital pulp therapies and pulpectomy 96Concluding remarks on the avoidance of pulpectomy by vital pulp therapies 97Revitalization and/or regenerative endodontic procedures 97

Clinical manifestations and diagnostic terminology 117

8 Microbiology of the inflamed and necrotic pulp 123

Luis E Ch´avez de Paz

Ecological determinants for microbial growth in root canals 134

A strategy for the formulation of a periapical diagnosis 153

An integrated approach to endodontic diagnosis 162

Merete Markvart and Pia Titterud Sunde

Preparing teeth for rubber dam isolation and the development of an aseptic

12 Access and canal negotiation: the first key procedural steps for successful endodontic treatment 195

Ove A Peters and Ana Arias

Principles of tooth development and tooth anatomy 195Individual analysis of the tooth, preoperative radiographs, and additional CBCT scans in

Lars Bergmans and Paul Lambrechts

Markus Haapasalo and Ya Shen

Eradication of microorganisms from the root canal system 231

The apical root canal – a special challenge for irrigation 236

Wide-spectrum sound energy for cleaning the root canal system 239

Gottfried Schmalz and Birger Thonemann

Amir-Taymour Moinzadeh and Hagay Shemesh

Clinical objectives and in vitro investigations 277

Part 4 The Endodontically Treated Tooth

Kishor Gulabivala and Yuan-Ling Ng

Distribution of remaining tooth structure and restorability 299Principles of restoration of root-treated teeth 300Timing of restoration after endodontic treatment 301

Study designs commonly used in endodontic research 317

Frank Setzer and Bekir Karabucak

Why might the initial treatment be unsuccessful? 327When may further intervention be considered? 329

Access to the root tip 368

Nigel Foot and John Whitworth

Common local anesthetic agents in endodontics 382Standard methods of local anesthesia for endodontics 383

Measures to preempt or overcome challenging local anesthesia 387

Lene Baad-Hansen and Peter Svensson

Atypical odontalgia/persistent dentoalveolar pain 399

Temporomandibular disorder pain – referred pain 401

Consequences of pulp breakdown and infection after trauma 411General considerations in the management of dental trauma 416Diagnostic quandaries: to remove or review the pulp after trauma? 422

24 Medicolegal considerations 427

Lars Bjørndal, Shiv Pabary, and John Whitworth

Ethical considerations – the concepts of beneficence and nonmaleficence 427

Endodontic procedures as complex interventions with scope for imperfection,

Professional indemnity/malpractice insurance 430

Severe odontogenic infections that may compromise systemic health 443Suspicion of locally aggressive or neoplastic lesions 444

Inhalation or aspiration of dental instruments or materials 445Allergic responses that may compromise systemic health 445

Lars Bjørndal Section of Cariology and Endodontics, Department of Odontology, Faculty of Health and

Medical Sciences, University of Copenhagen, Copenhagen, Denmark

Lise-Lotte Kirkevang Department of Dentistry and Oral Health, Aarhus University, Aarhus, Denmark

Department of Endodontics, Institute of Clinical Dentistry, Faculty of Dentistry,University of Oslo, Oslo, Norway

John Whitworth School of Dental Sciences, Newcastle University/Newcastle Hospitals NHS Foundation

Trust, Newcastle, UK

Contributors

Itzhak Abramovitz Department of Endodontics, The Hebrew University and Hadassah Faculty of Dental

Medicine, Jerusalem, Israel

Ana Arias Department of Conservative Dentistry, School of Dentistry, Complutense University,

Madrid, Spain

Lene Baad-Hansen Section of Orofacial Pain and Jaw Function, Department of Dentistry and Oral Health,

Aarhus University, Aarhus, DenmarkScandinavian Center for Orofacial Neurosciences (SCON)

Lars Bergmans Leuven BIOMAT Research Cluster, Department of Oral Health Sciences, Section

Endodontics, KU Leuven, Leuven, Belgium

Luis E Ch´avez de Paz Endodontics, Department of Dental Medicine, Karolinska Institute, Huddinge, Sweden

Nigel Foot The Briars Dental Centre, Newbury, UK

Eastman Dental Institute, University College, London, UK

Helena Fransson Department of Endodontics, Faculty of Odontology, Malm ¨o University, Malm ¨o, Sweden

Inge Fristad Department of Clinical Dentistry, Endodontics, Faculty of Medicine and Dentistry,

University of Bergen, Bergen, Norway

Kishor Gulabivala Unit of Endodontology, Department of Restorative Dental Sciences, Eastman Dental

Institute, Faculty of Medical Sciences, University College London, UK

Markus Haapasalo Division of Endodontics, University of British Columbia Faculty of Dentistry, Vancouver,

Canada

Peter Jonasson Department of Endodontology, Institute of Odontology, The Sahlgrenska Academy,

University of Gothenburg, Gothenburg, Sweden

xiii

Bekir Karabucak Department of Endodontics, University of Pennsylvania School of Dental Medicine,

Philadelphia, PA, USA

Anda Kfir Department of Endodontology, The Goldschleger School of Dental Medicine, Tel Aviv

University, Tel Aviv, Israel

Thomas Kvist Department of Endodontology, Institute of Odontology at The Sahlgrenska Academy,

University of Gothenburg, Gothenburg, Sweden

Paul Lambrechts Leuven BIOMAT Research Cluster, Department of Oral Health Sciences, Section

Endodontics, KU Leuven, Leuven, Belgium

Merete Markvart Section of Cariology and Endodontics, Department of Odontology, Faculty of Health and

Medical Sciences, University of Copenhagen, Copenhagen, Denmark

Zvi Metzger Department of Endodontology, The Goldschleger School of Dental Medicine, Tel Aviv

University, Tel Aviv, Israel

Amir-Taymour Department of Endodontology, Academic Center for Dentistry Amsterdam (ACTA),

University of Amsterdam and VU University, Amsterdam, The Netherlands

Moinzadeh

Peter Musaeus Center for Health Sciences Education (CESU), Aarhus University, Aarhus, Denmark

Matti N¨arhi Oral Physiology, University of Eastern Finland, Department of Dentistry and Biomedicine,

Kuopio, Finland

Yuan-Ling Ng Unit of Endodontology, Department of Restorative Dental Sciences, Eastman Dental

Institute, Faculty of Medical Sciences, University College London, UK

Dag Ørstavik Department of Endodontics, Institute of Clinical Dentistry, Faculty of Dentistry, University

of Oslo, Oslo, Norway

Shiv Pabary InDental Practice, Gateshead, UK

School of Dental Sciences, Newcastle University, Newcastle, UKPostgraduate Medico-Legal Tutor, Health Education England North East

Ove A Peters Department of Endodontics, University of the Pacific, Arthur A Dugoni School of

Dentistry, San Francisco, CA, USA

Kerstin Petersson Department of Endodontics, Faculty of Odontology, Malm ¨o University, Malm ¨o, Sweden

Maria Pigg Department of Endodontics, Faculty of Odontology, Malm ¨o University, Malm ¨o, Sweden

Claes Reit Department of Endodontology, Institute of Odontology at The Sahlgrenska Academy,

University of Gothenburg, Gothenburg, Sweden

Tara Renton Oral Surgery, King’s College London, London, UK

Vibe Rud Private Practice, Clinic for Surgery and Endodontics, Copenhagen, Denmark

Gottfried Schmalz Department of Conservative Dentistry and Periodontology, University of Regensburg,

Regensburg, GermanyDepartment of Periodontology, University of Bern, Bern, Switzerland

Frank Setzer Department of Endodontics, University of Pennsylvania School of Dental Medicine,

Philadelphia, PA, USA

Hagay Shemesh Department of Endodontology, Academic Center for Dentistry Amsterdam (ACTA),

University of Amsterdam and VU University, Amsterdam, The Netherlands

Ya Shen Division of Endodontics, University of British Columbia Faculty of Dentistry, Vancouver,

Canada

St´ephane Simon School of Dentistry, Universit´e de Paris Diderot, Paris, France

Alastair J Sloan Cardiff Institute for Tissue Engineering & Repair, Oral and Biomedical Sciences, School of

Dentistry, College of Biomedical and Life Sciences, Cardiff, Wales, UK

Luc van der Sluis Center of Dentistry and Oral Hygiene, University Medical Center Groningen, University of

Groningen, Groningen, The Netherlands

Pia Titterud Sunde Department of Endodontics, Institute of Clinical Dentistry, Faculty of Dentistry, University

of Oslo, Oslo, Norway

Peter Svensson Section of Orofacial Pain and Jaw Function, Department of Dentistry and Oral Health,

Aarhus University, Aarhus, DenmarkScandinavian Center for Orofacial Neurosciences (SCON)Department of Dental Medicine, Karolinska Institute, Huddinge, Sweden

Birger Thonemann Private Practice, D ¨usseldorf, Germany

Department of Conservative Dentistry and Periodontology, University of Regensburg,Regensburg, Germany

With appreciation we, the prior editors, want to

con-gratulate the new editors, Drs Lars Bjørndal, Lise-Lotte

Kirkevang, and John Whitworth for their hard work

and well-mannered effort in conducting the revision of

Textbook of Endodontology By attracting both old and

new authors the latest developments in the biology,

diagnosis, and treatment of endodontic conditions are

now available While the basic concepts and

struc-ture of the previous two editions have been retained

in terms of the Core concept, Clinical procedure and

Advanced concept text boxes, descriptions of key

lit-erature, and extensive references, several new chapters

have been commissioned and prior chapters have been

thoroughly reviewed Overall the book gives the reader

a broad perspective on the endodontic field All authors

originate from Europe and its neighboring countries,

including Turkey and Israel, even though some of themhave their professional sites in the United States Inessence many of the chapters have authors from a newgeneration of endodontists and they have all providedtext that is well worth studying Therefore, we believethat the time spent on each chapter will be very valu-able For undergraduate and postgraduate students inparticular this book provides a rich source for learningthat will show what the discipline of endodontology can

do today to preserve the original dentition

Gunnar BergenholtzPreben Hørsted-Bindslev

Claes Reit

April 2018

xvii

A decade has passed since the second edition of

Text-book of Endodontology, and its founding editors, Gunnar

Bergenholtz, Preben Hørsted-Bindslev, and Claes Reit,

deserve our unreserved thanks for their legacy to the

endodontic community It is with the greatest respect,

humility, and some degree of awe that a new editorial

team steps into their shoes, to fan the flames and bring

this new edition to life

Much has developed and changed in the last 10 years,

but core principles remain unchanged We remain

com-mitted to the educational needs of undergraduate and

postgraduate dental students and general

practition-ers who wish to update their knowledge of

contempo-rary endodontic research and practice The third edition

remains true to the textbook’s founding principles,

pro-viding information on the biological processes of

pul-pal and periapical disease and how this influences

clin-ical decision-making and practice New line drawings

and clinical images are included and we have retained

core concept, advanced concept, clinical procedure, and

key literature boxes for ease of assimilation We hope the

individual chapters work well together, and have

sign-posted readers to related chapters where this may be

helpful

Many of the original authors were enthusiastic to

revise and update their well-received chapters and we

are grateful to those who allowed the updating of their

previous work as part of a comprehensive revision New

for this edition are distinctive chapters on local

anes-thesia, asepsis, access and canal negotiation, irrigation

and disinfection, emergency management, and colegal considerations Aspects of diagnosis, deep cariesmanagement, decision-making for endodontic retreat-ment, orofacial pain, and clinical epidemiology alsoreceive greater emphasis A final chapter provides help-ful insights on the pressures facing young dentists asthey transition from dental school to independent prac-tice and strive to remain true to core principles of train-ing Readers may also find single best answer questionsuseful to gauge their knowledge and understanding

medi-We are extremely grateful to all contributing authors,and to their long-suffering partners and families whohave supported them through the writing and editorialprocess Furthermore, we wish to express our sinceregratitude to the entire team from Wiley, and in particu-lar special editing and project manager Dr Nik Prowse,who has supported us during the process Thank you allvery much

As global sales of paper books once again exceedthose of electronic versions, we hope this traditional textwill provide readers with an attractive, user-friendly,and informative resource This project is very muchalive and we welcome the observations and construc-tive feedback of students and colleagues on this thirdedition

Lars BjørndalLise-Lotte KirkevangJohn Whitworth

January 2018

xix

This book is accompanied by a companion website:

www.wiley.com/go/bjorndal/endodontology

The website includes:

r Interactive multiple-choice questions

xxi

Introduction to endodontology

John Whitworth, Lise-Lotte Kirkevang, and Lars Bjørndal

Endodontology

The word “endodontology” derives from the Greek

lan-guage and can be translated as “the knowledge of what

is inside the tooth.” Thus, endodontology concerns all

structures and processes within the tooth, with

particu-lar reference to the dental pulp and the space it occupies

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 being able to provide reasons for things It is often

believed that dental and medical knowledge is simply

scientific knowledge – truth that is supported by

scien-tific research to provide reasons for disease processes

and justification for clinical actions But as practicing

dentists, scientific knowledge is not always sufficient,

and although it is important to know about the anatomy

of the pulp space and the fatigue failure of engine-driven

endodontic files, we must also develop sound judgment

and the ability to make correct clinical decisions, often

in the face of uncertainty The knowledge required by

dental practitioners is therefore complex and

multi-dimensional and can be considered within Aristotle’s

domains of “episteme,” “techne,” and “phronesis” [1]

Episteme

Episteme is the word for theoretical, scientifically

sup-ported knowledge, the opposite being doxa, which

refers to common beliefs or opinions that may not be

so grounded in “hard” evidence The body of epistemic

knowledge in endodontology is enormous, spanning

from fundamental pulp biology to the clinical risk

factors associated with root canal treatment failure

The knowledge generated by science, however, is often

less certain than we would wish, and subject to the

weakness of study design, the bias of conflicting

inter-ests, and a lack of obvious translation to the realities of

“wet-fingered” dentistry Nevertheless, efforts are made

to present scientific knowledge in a balanced waythrough lectures, articles, and textbooks, so from astudent’s point of view, learning requires ample time forreading and opportunities for discussion and reflection.This book, in large part, is composed of epistemicknowledge

Techne

A substantial element of learning endodontology must

be characterized as techne, or “knowing how,” which

embraces elements of practical skill, craft, and artistry

It is not always possible to explain every detail of how

we perform technical acts, such as negotiating a lenging root canal with delicate tactile sense or riding abicycle around a corner without falling off In this way,

chal-it is not sufficient to teach students how to shape a rootcanal solely by asking them to read a book or attend alecture Their knowledge must be supplemented withpractical experiences, both observing and doing, and bydiscussion and personal reflection to understand thechallenges they encounter, develop cognitive and prac-tical strategies to overcome them, and to help them dobetter next time

It is not possible to learn all about the procedures

in endodontology by studying a textbook Observing agood clinical instructor, watching other dentists at work,performing the procedures oneself, and reflecting onwhat has been learnt are all important The preclini-cal simulation laboratory provides an essential environ-ment in which to embed new factual knowledge andtranslate it into practical reality

Phronesis

According to Aristotle, phronesis is the ability to think

about practical matters and then acquire the ability to act

Textbook of Endodontology, Third Edition Edited by Lars Bjørndal, Lise-Lotte Kirkevang, and John Whitworth.

© 2018 John Wiley & Sons Ltd Published 2018 by John Wiley & Sons Ltd.

Companion Website: www.wiley.com/go/bjorndal/endodontology

1

in the “right” way in any given circumstance The

prac-tice of clinical dentistry demands that wisdom is

exer-cised, “to do the right thing at the right moment,” acting

in the best interest of the patient, even if it is difficult or

costly for the dentist to do so Examples might include

the use of rubber dam to control asepsis in all

endodon-tic procedures, or being honest with patients and seeking

a practical solution when when things have gone wrong

Again, this cannot be fully developed by reading a book;

the essence of phronesis must be learnt from practice

Concepts of endodontology

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 The serious student of

endodontology must investigate all three aspects, and

although this textbook will contain many pointers to the

development of technical skills and clinical judgment,

there are understandable limits to what can be achieved

without hands-on experience combined with diligent

reflection

The objective of endodontic treatment

The consequences of inflammatory lesions in the dental

pulp and periapical tissues have tormented humankind

for thousands of years (Fig 1.1) and historically, the

main task of endodontic treatment was to cure toothache

caused by inflammation in the pulp (pulpitis) and the

periapical tissues (apical periodontitis) For a long time,

this was achieved by cauterizing pulp tissues with

hot wires, applying toxic chemicals such as arsenic or

Fig 1.1 A medieval skull found in Denmark showing teeth with serious

attrition In the mandibular left first molar the pulp chamber is exposed and

the alveolar bone is resorbed around the root apices, indicating that this

per-son had been suffering from periapical inflammation caused by an infected,

necrotic dental pulp.

formaldehyde, or by incising soft tissues to drain pus;all extremely painful in the era before local anesthetic.Although the relief of pain is still a primary goal ofendodontic treatment, much of the pulpal and periapi-cal disease that we encounter is painless, and the empha-sis should be on managing the cause of disease, invari-ably microbial infection, and promoting conditions thatare compatible with the healing and repair of tissues.This means that all steps of the endodontic proceduresdescribed in this book, ranging from caries managementand vital pulp therapies to surgical retreatment and thefinal coronal restoration, should be guided by efforts toeliminate and exclude microorganisms from the pulpspace, the periapical tissues, and, by extension, fromother parts of the body With meticulous infection con-trol, the treatments described should allow predictabletissue healing and the preservation of functional teeth inthe large majority of cases

Clinical problems and solutions

Core concepts 1.1 and 1.2 provide a summary of mon pulpal and periapical conditions and the treatmentprocedures to manage them

com-The vital pulp

Under normal physiological conditions, the dental pulp

is sterile and well protected from injury by hard tissuesand an intact periodontium But when the integrity ofthese tissue barriers is breached for any reason, microor-ganisms and the substances they produce may enter thepulp and adversely affect its health The most commonmicrobial challenge is from dental caries Even at anearly stage of caries progression, the immunocompetentpulp is aware, because substances from the cariogenicbiofilm may reach the dental pulp and its odontoblastcells along patent dentinal tubules Like any connectivetissue, the pulp responds with innate and adaptiveimmunity, which has an important role in neutralizingand eliminating the noxious agents Inflammationwithin the pulp can be seen as a two-edged sword,with the early stages providing a “necessary” defensiveresponse, contributing to hard-tissue deposition and tothe repair of damaged soft tissues Thus, the pulp mayreact in a manner that allows it to sustain the irritationand remain in a functional state Yet when caries hasactively progressed to the vicinity of the pulp, theresponse may take a destructive course leading to tissuenecrosis followed by large-scale microbial invasion.These processes may or may not be painful In an idealworld, it would be possible to control all risk factorsfor caries, but caries remains highly prevalent, and ifdamage is to be limited, practitioners should recognize

Core concept 1.1 Recommended diagnostic terminology and synonyms for endodontic conditions

Pulpal

r Normal pulp: A clinically asymptomatic pulp that responds within

normal limits to pulp sensibility testing (synonym: healthy pulp).

r Pulpitis: Inflammation of the dental pulp.

r Reversible pulpitis: Inflammation of the pulp that if treated should

allow the pulp to return to normal.

r Irreversible pulpitis: Inflammation of the pulp that is incapable of

healing Symptomatic (painful) and asymptomatic (painless) forms

are recognized.

r Pulp necrosis: Pulp death The pulp chamber is devoid of functional

pulp tissue with varying degrees of pulp breakdown within the root

canals.

Additional terms to denote teeth that have already received treatment:

although these terms do not denote the presence of a pathological

con-dition, they are widely adopted to describe the state of teeth that

com-monly present to treatment providers in practice.

r Previously initiated treatment : A tooth that presents with evidence

of emergency treatment for pain relief, but without the completion

of a permanent root filling.

r Previously treated: A tooth containing a permanent root canal filling

(synonym: root-filled).

Periapical

r Normal apical tissues: Teeth presenting with no clinical symptoms

or clinical/radiographic signs of periapical disease.

r Apical periodontitis: Inflammatory reaction in the tissues

surround-ing the root of a tooth, usually caused by pulp space infection, but

sometimes perpetuated by infection or foreign bodies that have become established within the periapical tissues Inflammation of the periapical tissues can also be caused by traumatic injuries, but this is often sterile and short lived (transient).

r Symptomatic apical periodontitis: Inflammation producing clinical symptoms, and usually accompanied by clinical and/or radiographic signs that indicate the presence of disease or traumatic injury (synonym: acute apical periodontitis) The term acute apical peri- odontitis may also refer to the very painful first stages of the peri- apical inflammatory reaction where bone destruction has not yet occurred and there is no evidence of a periapical radiolucency.

r Asymptomatic apical periodontitis: Inflammation producing no ical symptoms but with clinical and/or radiographic signs that indicate the presence of disease (synonym: chronic apical peri- odontitis).

clin-r Condensing osteitis: A form of apical periodontitis characterized by the slow deposition of bone, usually around the apex of a tooth and associated with low-grade inflammation (synonym: periapical osteosclerosis).

r Apical abscess: A purulent lesion associated with an infected,

necrotic pulp.

r Acute apical abscess: An inflammatory reaction characterized by

the rapid onset of painful periapical symptoms, pus formation, and swelling of associated tissues (synonyms: suppurative apical peri- odontitis, phoenix abscess).

r Chronic apical abscess: An inflammatory reaction characterized by gradual onset, little or no discomfort, and the intermittent discharge

of pus through an associated sinus tract (synonym: apical titis with fistula).

periodon-Core concept 1.2 Common treatment procedures to manage endodontic disease conditions

r Deep caries management: Treatment procedure that aims to

pre-serve vital pulp functions by avoiding direct exposure of pulp tissue

to the oral environment Recognized approaches include:

– selective carious tissue removal (one visit) (synonym: partial caries

removal) and

– stepwise carious tissue removal (two visits) (synonym: stepwise

excavation).

r Pulp capping: Treatment procedure that aims to preserve vital pulp

functions after direct exposure of pulp tissue to the oral environment

(direct pulp cap).

r Pulpotomy: Treatment procedure that aims to preserve vital pulp

functions by surgically removing superficial pulp tissue (partial

pulpotomy) or the entire coronal pulp (pulp chamber pulpotomy).

r Pulpectomy: Treatment procedure in which a vital pulp is removed,

the root canal system is instrumented and cleaned, and a permanent

root canal filling is placed (synonym: root canal treatment of a tooth containing vital pulp tissue).

r Root canal disinfection: Treatment procedure in which a necrotic/

infected pulp is removed, the root canal system is instrumented, cleaned, and disinfected, and a permanent root canal filling is placed (synonym: root canal treatment of a tooth containing necrotic/infected pulp tissue).

r Nonsurgical retreatment: Treatment of a previously treated tooth

with clinical and/or radiographic signs of root canal infection, where root filling materials are removed to facilitate the disinfection and refilling of the pulp space Also undertaken to improve the technical quality of previous treatment.

r Surgical retreatment: Treatment of a previously treated tooth by gical means to manage infection or other pathology that has not responded to nonsurgical management.

sur-(a) Selective carious removal (b) Pulp capping

(e) Root canal disinfection (f) Non-surgical retreatment

(g) Surgical retreatment

and treat precavitated carious lesions without operative

intervention, and approach the operative treatment

of lesions that have progressed more extensively in a

way that will avoid direct pulp exposure to the mouth

(Fig 1.2a) Even in the case of frank pulp exposure after

traumatic injury or during operative dentistry,

espe-cially in the young, it may be possible to preserve vital

pulp functions by pulp-capping or pulpotomy procedures

(Fig 1.2b,c)

When the dental pulp is judged to be irreversibly

inflamed or if the pulp is likely to be compromised by

a restorative procedure (e.g., decoronation of a tooth as

an overdenture abutment), pulp tissue may be removed

and replaced with a root filling – a procedure termed

pulpectomy (Fig 1.2d) Clinically, pulp tissue is

asepti-cally removed under local anesthesia, canals are shaped

with instruments to accommodate a root canal filling, the

pulp space is irrigated to remove residual pulp tissue

and microorganisms, and the canal is filled before

restor-ing the cavity Pulpectomy is highly successful and aims

to prevent significant infection from establishing within

the pulp space, which would inevitably lead to the

exten-sion of inflammatory changes into the periapical tissues

It is easy to become complacent about the

predictabil-ity of pulpectomy, yet in common with all

endodon-tic procedures, failure to exercise stringent asepsis may

result in established pulp space infection and the

devel-opment of apical periodontitis in the long term All

of these technically exacting and often minimally

inva-sive procedures are greatly assisted by magnification

and enhanced illumination, ideally from an operating

microscope

The necrotic or infected pulp space associated

with apical periodontitis

Pulp tissue may become necrotic after traumatic

disrup-tion of its blood supply, or as a consequence of microbial

infection Necrotic pulp tissue is defenseless againstmicrobial invasion and the entry of oral microorganismsafter frank pulpal exposure or through dentinal tubules

as a consequence of extremely deep caries, suddencracks, and fractures, as well as operative dentistry orperiodontal disease/instrumentation, will soon result inpulp space infection Established infections are typically

in biofilm formation and colonize canal walls, pulpspace irregularities, and dentinal tubules They are alsofrequently interspersed with residual necrotic tissue.The host has no means of eliminating infection from theavascular pulp space, and the percolation of microbialcomponents into the periapical tissues leads inevitably

to the extension of inflammatory disease into the tissuessurrounding the tooth Although localized periapicalinflammation (apical periodontitis) is the most com-monly studied, serious and potentially life-threateningextension is possible (acute apical abscess; spreadingcellulitis), as is the potential for more widespread effects

on general health Apical periodontitis can remainundetected and untreated for long periods of time,particularly if there are no symptoms, and may expandsignificantly, discharge to the mouth through a sinustract, or undergo cystic change

Although the treatment of a necrotic/infected pulp

space or root canal disinfection (Fig 1.2e) is an aseptic

pro-cedure with much in common with pulpectomy, the aim

is not just to eliminate necrotic tissue but to disrupt andremove biofilm infection from the complexities of thepulp space The emphasis on disinfection is thus high-lighted, and only in the presence of a clean canal can

a well-executed root filling and coronal restoration serve favorable conditions for periapical healing

pre-The endodontically treated tooth

Although the treatment of pulpitis and apical odontitis is usually successful, painful symptoms are

an immature tooth with an extremely deep carious lesion is aseptically amputated at the floor of the pulp chamber and dressed with a capping agent before sealing the tooth against infection In favorable conditions, the remaining pulp tissue remains vital, completes root formation and lays down a protective layer

of tertiary reparative dentin beneath the capping material (d) Pulpectomy The removal of an irreversibly inflamed pulp and its aseptic replacement with a root canal filing and sound coronal restoration prevents root canal infection and the development of periapical inflammation (e) Root canal disinfection Infection of the necrotic pulp causes inflammation in the periapical tissues and is treated by shaping, disinfecting and filling the pulp space under strict asepsis and sealing the crown to prevent new infection The central image shows the tooth with complete caries excavation, isolated with rubber dam and the canal being irrigated with sodium hypochlorite solution to eliminate microorganisms and necrotic pulp tissue Healing of apical periodontitis is predictable if infection can be adequately managed (f) Nonsurgical retreatment A poorly conducted endodontic treatment, coupled with leakage of the coronal restoration promoted infection of the root canal system and the failure of apical periodontitis to heal Disinfection of the pulp space, followed by root canal filling and a sound coronal restoration predictably results in periapical healing (g) Surgical retreatment A tooth with a satisfactory root canal treatment and sound coronal restoration presents with persistent apical periodontitis The cause in this case is extraradicular infection associated with biofilm formation on the external root surface and established infection in the periapical tissues Disinfection of the root canal will not eliminate the infection, which must be approached surgically Resection of the root end, followed by the preparation and sealing of an apical cavity, eliminates infection and allows periapical healing without disturbing the coronal restoration.

not always controlled and the periapical tissues do not

always heal This is often associated with imperfections

in the initial treatment, including suboptimal infection

control, missed anatomy, or other technical challenges

that might have been identified by more careful

diagno-sis, more advanced imaging of the tooth, or greater

atten-tion to detail during the initial endodontic treatment or

final restoration In these circumstances, retreatment may

be considered In nonsurgical retreatment (Fig 1.2f), the

root canal system is re-entered from the mouth under

aseptic conditions, the causes of treatment failure are

identified and managed, the canal system is disinfected,

and the root canal densely filled before providing a

seal-ing coronal restoration to promote periapical healseal-ing

In surgical retreatment (Fig 1.2g) persistent infections are

approached surgically, usually by resecting the root tip,

and managing and pulp space infection by creating a

root-end cavity and sealing it tightly with a root-end

fill-ing Retreatment procedures are technically demanding

and are made easier and more predictable with

magnifi-cation and enhanced illumination

The diagnostic dilemma

To many, the process of endodontic diagnosis is as much

an art as a science Dentists are often confronted by

dis-ease processes in the pulp and periapical tissues that

have few or no symptoms, or by symptoms referred to

or from adjacent teeth or other structures There are no

laboratory investigations, such as blood tests, that can

provide objective insights, and the tissues under

investi-gation are generally hidden from view Clinicians must

therefore rely on imperfect, indirect tests, such as the

application of cold or an electronic stimulus to the teeth,

or the interpretation of two-dimensional radiographic

images to diagnose pulp and periapical conditions and

select an appropriate treatment Throughout this

text-book, considerable attention is given to the process of

pulp and periapical diagnosis, the dilemmas that may

arise, and the care that must be exercised in reaching

conclusions

The outcome dilemma

The meaning of “success” also demands some

intro-duction To some, the elimination of painful symptoms

and the preservation of a tooth in comfortable function

is a key measure of success For others, the slightest

radiographic evidence of periapical inflammation,

even in the absence of clinical symptoms and signs,

suggests an uncertain outcome or treatment failure The

outcome dilemma is highlighted by the widespread use

of three-dimensional imaging with its potential to detect

persistent lesions that would not have been identified by

traditional radiographic methods As healthcare sionals, we should strive to control inflammatory disease

profes-by managing the cause, which is invariably microbialinfection Throughout this textbook, an optimal treat-ment outcome will be defined by the absence of clinicalsigns and symptoms of inflammatory disease, and bythe radiographic preservation or re-establishment of alamina dura and normal periapical bony structure

The tools of treatment

To many dentists, endodontic procedures can bedescribed by Winston Churchill’s words on golf: “Animpossible game with impossible tools.” The complex-ity of root canal anatomy, the relative stiffness of manyinstruments, the inability to visualize the area of workproperly, and the lack of space in the mouth providesubstantial challenges to the skill and patience of thedentist Intracanal work is exceptionally demanding andthis is clearly demonstrated by numerous radiographi-cally based epidemiological surveys, which repeatedlyshow that many root canal fillings fall below acceptabletechnical standards Because clinical outcome is stronglyrelated to the quality of treatment, the high frequency ofsuboptimal treatment is a subject of great concern to theprofession

The last 15–20 years have seen tremendous ical developments that facilitate endodontic treatmentand enhance the potential to improve standards [2].Many of these have made the previously impossible pos-sible, by broadening the scope of teeth that can be suc-cessfully treated, by empowering dentists who do nothave specialist skills, and by making procedures moreefficient and enjoyable for dentists and patients alike.The widespread adoption of ultra-flexible engine-driveninstruments for shaping root canals is a prime example,though one danger of this technological focus and theability to instrument and root-fill teeth quickly is that the

technolog-Fig 1.3 Rubber dam-isolated tooth in the process of being disinfected prior

to pulp access.

focus on asepsis and the stringent management of

infec-tion may have been undermined

Luckily, there are few medical treatments that can be

carried out as aseptically as endodontic procedures and

shielding the tooth with a rubber dam is the oldest and

still the most effective way to ensure that the operation

field remains sterile (Fig 1.3) It is this, combined with

a range of infection-controlling measures to be

imple-mented at each stage of endodontic treatment, that helps

to preserve teeth damaged by disease or trauma and that

will return them to long-term health and function [3]

3 Salehrabi R, Rotstein I Endodontic treatment outcomes in

a large patient population in the USA: an epidemiological

study J Endod 2004; 30: 846–50.

The Vital Pulp

9

The dentin–pulp complex: structure,

functions, threats, and response

to external injury

Lars Bjørndal and Alastair J Sloan

Introduction

There is uncertainty in the literature whether dentin and

pulp should be considered separate entities or if they

form an integrated biological unit [1] It is

understand-able that clinicians who conduct treatment on enamel

and dentin (caries management, restorative procedures)

or pulp (endodontic procedures) may consider them

separately (Fig 2.1) Yet the hypersensitivity

encoun-tered when scratching exposed dentin surfaces with a

sharp probe or drying with air may remind them that

dentin is vital, connected with pulp tissue and that both

tissues play important roles in responding to external

injury

There are marked differences in the structure,

func-tions, and chemistry of dentin and pulp, both

embry-ologically and in mature teeth, yet their

interconnec-tion is beyond quesinterconnec-tion When physiological and

patho-logical reactions are encountered in one, accompanying

changes can be expected in the other The first cells to

sense danger and react to environmental stimuli are the

odontoblasts, which maintain an intimate relationship

with dentin throughout the life of the tooth

Odonto-blasts retain their formative capacity, enabling them to

secrete dentin matrix in response to post-eruptive

den-tal injury They also participate in complex signaling

and control processes in collaboration with other cellular

populations within the pulp

The dentin–pulp complex reacts both to

physiolog-ical changes and to localized external stimuli such as

wear (Fig 2.2), and to accidental or iatrogenic injuries

Responses to caries and trauma are considered more

fully in Chapters 5 and 23, respectively

The odontoblast and the dentin–pulp complex

The primary odontoblast, dentinal tubules,and branching

Human odontoblasts align themselves at the periphery

of the pulp, adjacent to the predentin layer (Fig 2.3a,b).They maintain this position throughout odontogene-sis and for the life of the healthy tooth [2] Their cellbodies appear cylindrical in the coronal pulp cham-ber and more cubic in the root [3] This may reflectthe different activity levels of odontoblasts in differentregions of the tooth In its simplest terms, the odon-toblast is a formative, collagen-producing cell, layingdown predentin matrix for mineralization Odontoblastcell bodies are intimately related, with cell-to-cell con-tacts forming tight junctions and well-defined intercel-lular space, allowing communication between odon-toblasts The sprouting of fine collagen fibrils can beobserved in the intercellular spaces closest to the pre-dentin (Fig 2.3c) In histological sections, the odonto-blast layer appears to consist of 3–4 rows of cell bod-ies in pseudostratified arrangement, but this reflects thesummation of several layers of dentinal tubules Theactual odontoblast:dentinal tubule ratio is 1:1 [4], witheach odontoblast extending a single cytoplasmic processforming a single tubule (Fig 2.3d)

Primary odontoblasts (those responsible for primarydentinogenesis during tooth formation) are postmitoticcells Cellular transformation occurs during the stages ofprimary and secondary dentinogenesis (Fig 2.4) Eachstage is characterized by the presence and activity of

Textbook of Endodontology, Third Edition Edited by Lars Bjørndal, Lise-Lotte Kirkevang, and John Whitworth.

© 2018 John Wiley & Sons Ltd Published 2018 by John Wiley & Sons Ltd.

Companion Website: www.wiley.com/go/bjorndal/endodontology

11

Dentin Pulp

Cementum Dentin–pulp complex

Enamel

Fig 2.1 Macroscopic view of a bisected mandibular molar showing pulp

tissue surrounded by dentin and enamel Note the relatively deep position of

the pulp chamber roof, which is about level with the cervical region of the

crown Magnified region illustrates the relationship of odontoblast cell bodies

aligned at the dentin/pulp interface, and the underlying pulp tissue with

cell-free and cell-rich zones, blood vessels (red), and nerve fibers (blue), some of

which extend into dentinal tubules.

distinctive intracellular organelles and by distinctive

functions [2, 5] relating to the secretory status of the cell

[6] (see Core concept 2.1)

The first primary dentin laid down (mantle dentin)

can be viewed along the enamel–dentin junction (EDJ)

As the thickness of dentin increases by the central

move-ment of secretory odontoblasts, their cell bodies become

Fig 2.2 Incisal view of lower anterior teeth are shown with a marked wear exposing the primary dentin, and original location of the pulp chamber Deposi- tion of hard tissue (arrows) has prevented the direct exposure of pulp tissue to the oral environment There is a sliding transition between secondary dentin formation diminishing the pulp cavity over time and the tertiary dentin laid down due to the localized external stimuli caused by the wear.

more tightly packed along the diminishing ence of the pulp space Estimates suggest a density of

circumfer-8000 secretory odontoblasts per mm2at the occlusal EDJ,and more than 20 000 per mm2 in cuspal regions Inthese peripheral regions, the dentinal tubules of youngadults have an estimated diameter of 0.5 μm Half waythrough dentinogenesis, odontoblast density increases

to 30 000–36 000 per mm2 When primary dentin is plete, secretory odontoblasts line the pulp chamber at

OB-c

OP

Fig 2.3 (a) Human odontoblasts align beneath

pre-dentin (black asterisk) with subjacent fully mineralized

dentin (white asterisk) (b) Higher magnification of the

cylindrical cell bodies of postmitotic young and mature

odontoblasts with polarized nuclei (N) Framed area is

shown in (c) (c) Early deposition of predentin collagen

fibrils (CF) is noted between odontoblasts cell bodies

(OB-c) close to the predentin matrix Cell-to-cell contacts

or tight junctions (black arrows) define the

intercellu-lar spaces and allow communication between adjacent

odontoblasts (d) Detail of the odontoblast processes (OP)

entering predentin matrix with the presence of collagen

fibrils (transverse plane) (white arrows).

Core concept 2.1 The odontoblast cycle

(see Fig 2.4)

During primary dentinogenesis, odontoblasts are described as

secre-tory [2] and have the features of actively secreting cells as they lay

down predentin matrix When formation of the crown is complete

and the tooth erupts into the mouth, odontoblasts within the

coro-nal pulp downregulate their secretory activity, and become mature

cells [2], characterized by the presence of autophagic vacuoles This

autophagic activity is suggested to be a survival mechanism, involved

in cellular maintenance and homeostasis The subsequent aging of

mature odontoblasts to become old odontoblasts [2] is characterized

by the accumulation of lipofuscin, an aging or “wear and tear”

pig-ment that is found in many tissues of the body, reflecting the previous

intense activity of the cells.

a density of approximately 58 000 per mm2, with

tubu-lar diameters of 2.5–3.0 μm in the innermost microns of

dentin (Fig 2.5) The thickness of coronal dentin, and

the consequent length of dentinal tubules in this region,

is approximately 2.5–3.5 mm [7] The convergence and

widening of dentinal tubules in deep coronal dentin is

reflected in a more open and porous tissue as the pulp

is approached In root dentin, tubular densities are less

Fig 2.5 Schematic representation of the increasing density and diameter

of dentinal tubules in deep coronal dentin In young teeth, more than 75% of the innermost dentin may be made up of large dentinal tubules.

OP

GC

GC

AV Ly

LF Mitochondrion

RER

N

N N

Aging

Fig 2.4 Schematic representation of the life cycle of human odontoblasts, being secretory, mature, and old During tooth development, secretory odontoblasts are the primary dentin- forming cells After tooth eruption, dentin matrix secretion is performed by mature and aging odontoblasts Mature odontoblasts are charac- terized by the presence of autophagic vacuoles (AV) The progress of aging from mature to old odontoblasts is characterized by the accu- mulation of lipofuscin (LF) or “age pigment.”

GC, Golgi complex; JC, junctional complexes;

Ly, lysosome; M, mitochondria; N, nucleus; OP, odontoblastic process; PC, primary cilium; RER, rough endoplasmic reticulum; SG, secretory granules (see also Core concept 2.1) Source: Reproduced from [2] with permission of SAGE.

than in the crown and diminish apically [8, 9] Tubule

diameters close to the pulp in root dentin are

approxi-mately 1.5 μm

Dentinal tubules contain numerous anastomosing

branches and lateral extensions [9] The largest are

observed in mantle dentin along the EDJ The

“foot-prints” of these major, Y-shaped branches, often 0.5–

1.0 μm in diameter, are illustrated in Fig 2.6 Smaller

microbranches are observed, predominately in coronal

dentin, with diameters of 50–100 nm (Fig 2.6) In root

dentin, branches of 300–700 nm diameter are also noted

Branching is generally increased in areas where the

dis-tance between main dentinal tubules is relatively large

All of this reflects the interconnectedness of odontoblasts

during dentinogenesis and throughout the life of the

tooth This may facilitate communication in response to

internal and external stimuli Core concept 2.2 provides

a classification of dentinogenesis

Clinical implications of dentin microstructure

Variation in the density and branching of dentinal

tubules is clinically significant in terms of dentin

perme-ability, with clinical implications for the management of

deep dentin after traumatic injury, during operative

den-tistry, bonding of adhesive materials, and in the

diag-nosis and management of dental pain The deeper the

injury, the greater the number and diameter of tubules

involved and the greater the potential risk to the pulp

In general terms, the area occupied by tubules increases

threefold from the EDJ to the pulp chamber [10] In a

Core concept 2.2 Classification of dentin

r Primary dentin: Dentin laid down by secretory odontoblasts prior

to tooth eruption.

r Secondary dentin: Continued, physiological deposition of tubular dentin by secretory, mature, and old odontoblasts after tooth erup- tion The rate and thickness of secondary dentin deposition is not influenced by external injury or irritants.

r Tertiary dentin: Dentin laid down in localized regions in response

to external stimuli, and of two phenotypes:

– Reactionary: Tubular dentin laid down predominantly by

upreg-ulated primary odontoblasts (Fig 2.7) Depending on the nature and degree of injury, some of the cells involved may be sec- ondary odontoblast-like cells.

– Reparative: An initial layer of atubular dentin, followed by

tubular dentin produced by secondary odontoblast-like cells recruited to the site of injury following the death of primary odontoblasts.

very young tooth, 75% of the pulpal wall in a deep ity may be taken up by large, open dentinal tubules (seeFig 2.5) [7] For this reason, it may be more helpful toconsider deep cavity reparations in young teeth as proce-dures conducted within an intracellular soft tisssue envi-ronment comprising odontoblast processes rather than ahard, impervious mineralized tissue Even if the externalarea of an injury appears relatively small, the depth ofpenetration can have a significant bearing on the threatposed to the pulp The influence of dentin microstructure

cav-on reacticav-on patterns to caries is discussed in Chapter 5

Enamel

Dentin

EDJ

PD

Fig 2.6 (a) Thin undemineralized tooth

section disclosing the enamel–dentin

junc-tion (EDJ) Large, Y-shaped branching of

dentinal tubules is observed in the outermost

mantle dentin (arrows) The apparent

exten-sion of some tubules into enamel also reveals

a past embryonic stage reflecting the

inter-connectedness of ectodermal and

mesenchy-mal tissues at the start of amelo- and

dentino-genesis (b) Thin, undemineralized section

showing numerous microbranches (arrows)

between dentinal tubules The globular

cal-cospherites that characterize the

relation-ship between fully mineralized dentin and

predentin (PD) are noted at the interface

between the two tissues.

b c

2 a

1

Fig 2.7 The odontoblast has many tions that change during tooth development, maturation, and injury (a) Sensor: 1 Detect- ing antigens entering dentin, mechanical forces, thermal gradients; 2 Bombarded from inside by circulating hormones, paracrine (cell-to-cell communication) and autocrine (chemical or hormonal communication between cells) substances (b) Secretor: lay- ing down dentin matrix, and for maintenance and immune defense (c) Pain mediator: acting as a transducer between external stimuli and pulpal sensory nerves.

func-Dentinal tubules follow an S-shaped course in the bulk

of coronal dentin, but in root dentin they are straighter

and align more perpendicular to the root canal walls

This is relevant in the management of root ends during

endodontic surgery (see Chapter 20)

The odontoblast as a multifunction cell

Primary odontoblasts are responsible for primary and

secondary dentinogenesis (see Core concept 2.2) As the

tooth ages, mature and old odontoblasts show signs of

reduced cellular function [11, 12], but may be reactivated

to secrete tertiary reactionary dentin matrix following

mild stimulation [13] The main life-long function of the

odontoblast is to form and maintain dentin and preserve

the architecture of the pulp by expressing various

adhe-sion molecules These molecules are essential to

main-tain relationships between the cellular, hard-tissue, and

matrix components of the dentin–pulp complex (see

sec-tion on The dental pulp)

The positioning of odontoblasts, with their

cytoplas-mic processes extending into dentin, places them

ide-ally to intercept and react to noxious elements

enter-ing exposed dentinal tubules from the mouth (Fig 2.7)

When challenged, they generate and release a multitude

of molecules that are active against invading

microor-ganisms Their response also activates toll-like receptors

(TLR) that are present on the odontoblast itself,

adja-cent cells, blood vessels, and nerves These receptors

are able to recognize microbial elements and form part

of the pulpal immune response, due to the subsequent

production of a range of cytokines and chemokines

(see Advanced concept 2.1) Thus, the odontoblasts,

together with local resident and bloodborne defense

cells, have a broad repertoire of response patterns and

play important roles in activating both innate and

adap-tive immune responses within the pulp (see section on

Immune responses in the dentin–pulp complex)

The odontoblast process and the content of

dentinal tubules

It is uncertain how far odontoblast processes extend

into mature dentin Some have argued that they extend

the full thickness of dentin, from the EDJ to the pulp,and actively grow during the secretion of primarydentin Others have argued that only the innermost0.5–1 mm of dentin maintains odontoblast processes[19, 20] Many dentinal tubules also contain sensorynerve terminals Furthermore, cells belonging to theimmune-surveillance system of the pulp extend den-drites (dendritic cells) into the tubules of the predentinlayer [21] Besides cellular processes and nerve fibers,the intratubular environment also includes collagen fib-rils (Fig 2.8), and calcium phosphate deposits Con-sequently, the space available within dentinal tubulesfor the transport of particulate matter and macro-molecules is considerably smaller than the overalltubular cross-section However, external stimuli thatcause fluid movement within the dentinal tubules may

Advanced concept 2.1 Role of odontoblasts in

pulpal immune defense

Odontoblasts are supplied with pattern recognition receptors (PRRs), enabling them to sense and respond to microbial elements by recog- nizing their ligands (pathogen associated molecular patterns, PAMPs) and thereby form part of the immune system [14] A main group

of the PRRs is the toll-like receptor (TLR) family, which has been identified on the surface of odontoblasts [15, 16] After a PAMP–TLR interaction the subsequent activation of the nuclear factor kappa B (NF-κB) intracellular signaling pathway leads to the production of proinflammatory cytokines and chemokines, such as interleukin 1α (IL-1α), IL-1β, IL-8, and tumor necrosis factor-α (TNFα), which in turn recruit immune cells The NF-κB pathway is in fact modulat- ing the inflammatory response in many cells Observations suggest that odontoblasts are more potent attractants than pulpal fibroblasts [17] Odontoblasts may also release antimicrobial peptides that are capable of directly killing Gram-positive and Gram-negative bacte- ria Odontoblasts furthermore respond to proinflammatory cytokines secreted by adjacent resident cells and immune cells that invade the pulp from the circulation Specific substances that regulate vascular permeability and angiogenesis are also released following microbial challenge [18] In summary, the odontoblast is a multifunctional cell and a prime mover in identifying danger and coordinating the pulp’s defensive response (see also Fig 2.7).

PD

OP

Fig 2.8 (a) Transmission electron

micro-graph showing a transverse undemineralized

tooth section between dentin (D) and

pre-dentin (PD) The area occupied by tubules is

apparent (b) Higher magnification shows an

odontoblast process (OP) inside one of the

tubules The collagen network of predentin

is also shown, with darker fibrils undergoing

mineralization Fine collagen fibers are also

seen within the dentinal tubules (arrow).

stimulate odontoblasts/nerve complexes and represent

a unique mechanosensory system, giving the

odonto-blasts a pivotal role in signal transduction [22, 23] This

may be instrumental in identifying the flexural loads on

teeth, and may partly explain the vulnerability of

pulp-less teeth to fracture

The odontoblast and tertiary dentin

The secretory activity of mature and old odontoblasts

can be upregulated following dental injury, with the

secretion of tertiary reactionary dentin matrix in

local-ized regions of the pulp, as seen during carious

progres-sion (Fig 2.9, Core concept 2.2) In pulp horns, where

dentin may be exposed by physiological wear of the

cusp tip (Fig 2.2), dentinal tubules can be occluded by

dentin with a partly atubular nature, preventing directexposure of the pulp tissue to the oral environment.The atubular nature may reflect the programmed death(apoptosis) of some of the tightly packed odontoblasts inthis region of the pulp (see Advanced concept 2.2) Even

in teeth which have not been subject to external injurythis pattern can be observed, confirming this physiolog-ical phenomenon [24]

In contrast, an acute external injury (e.g., cavity ration into dentin, or excessive drying with compressedair) may cause the sudden aspiration of odontoblastcell bodies into the dentinal tubules, where they willdegenerate and promote pulp inflammation [28] Fol-lowing the loss of primary odontoblasts, tertiary repar-ative dentin matrix is secreted by new odontoblast-likecells (see Core concept 2.2 and Fig 2.10) In the case

prepa-(a)

*

RD PRD

OB RD

OB

RDM

Fig 2.9 (a) Light microscopic overview

of interface between dentin and reactionary

dentin subjacent to a carious lesion Note

that the tubules are less numerous in the

reactionary dentin (RD), and a few tubules

(arrows) are in direct continuity with those of

the primary dentin Mature odontoblasts (OB)

and “reactionary dentin matrix” (RDM) are

apparent Source: Courtesy of Lars Bjørndal.

(b) A similar transmission electron

micro-scopic overview of the mature odontoblasts

(OB) layer aligning a wide region of

“pre-reactionary dentin” (PRD) and the subjacent

reactionary dentin (RD) with odontoblast

pro-cesses (arrows), making reactionary dentin

less permeable (c) Higher magnification of

the mature odontoblasts (OB) shown in (b)

reveals intracellular organelles (white

aster-isk, e.g., rough endoplasmic reticulum and

secretory granules) presumably related to an

upregulated status and activity leading

reac-tionary dentin deposition.