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Textbook of

ENDODONTICS

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Textbook of
ENDODONTICS
THIRD EDITION

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Nisha Garg MDS


(Conservative Dentistry and Endodontics)
Ex-Resident, Postgraduate Institute of Medical Education and Research

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Chandigarh, India
Ex-Resident, Government Dental College

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Patiala, Punjab, India
Presently Reader
Department of Conservative Dentistry and Endodontics

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Sri Sukhmani Dental College and Hospital
Dera Bassi, Punjab, India

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Amit Garg MDS

(Oral and Maxillofacial Surgery)
Ex-Resident, Government Dental College

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Postgraduate Institute of Medical Sciences
Rohtak, Haryana, India
Consultant Oral and Maxillofacial Surgeon

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Faridabad, Haryana, India

Foreword
Anil Chandra

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This book has been published in good faith that the contents provided by the authors contained herein are original, and is intended for
educational purposes only. While every effort is made to ensure accuracy of information, the publisher and the authors specifically disclaim
any damage, liability, or loss incurred, directly or indirectly, from the use or application of any of the contents of this work. If not specifically
stated, all figures and tables are courtesy of the authors. Where appropriate, the readers should consult with a specialist or contact the
manufacturer of the drug or device.

Textbook of Endodontics

First Edition: 2007


Second Edition: 2010
Third Edition: 2014
ISBN: 978-93-5090-952-2
Printed at

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Dedicated to

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Prisha

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Vedaant

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Contributors

Amit Garg Navjot Singh Khurana Sandhya Kapoor Punia


Consultant Oral and Lecturer Senior Lecturer
Maxillofacial Surgeon Department of Conservative Dentistry Department of Conservative Dentistry
Faridabad, Haryana, India and Endodontics and Endodontics
Government Dental College Darshan Dental College
Amita Patiala, Punjab, India Udaipur, Rajasthan, India

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Reader
Department of Conservative Dentistry Neelam Mittal Sanjay Miglani
and Endodontics Professor Associate Professor 
BRS Dental College and Hospital Faculty of Dental Sciences Faculty of Dentistry

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Panchkula, Haryana, India Institute of Medical Sciences Jamia Millia Islamia
Banaras Hindu University New Delhi, India
Anil Dhingra Varanasi, Uttar Pradesh, India

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Professor and Head Shinam Kapila Pasricha
Department of Conservative Dentistry Nisha Garg Senior Lecturer
and Endodontics Reader Department of Conservative Dentistry

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DJ Institute of Dental Department of Conservative Dentistry and Endodontics
Sciences and Research and Endodontics National Dental College
Dera Bassi, Punjab, India

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Modinagar, Uttar Pradesh, India Sri Sukhmani Dental
College and Hospital
Bobbin Gill Dera Bassi, Punjab, India Suresh K Saini
Consultant Endodontist Reader
Chandigarh, India Poonam Bogra Department of Prosthodontics
BRS Dental College and Hospital

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Senior Professor
Jaidev Dhillon Department of Conservative Dentistry Panchkula, Haryana, India
Professor and Head and Endodontics
Department of Conservative Dentistry DAV Dental College
Vikas Punia

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Senior Lecturer
and Endodontics Yamuna Nagar, Haryana, India
Department of Prosthodontics
BRS Dental College and Hospital
Darshan Dental College
Panchkula, Haryana, India RS Kang
Udaipur, Rajasthan, India
Associate Professor
JS Mann Department of Conservative Dentistry Yoshitsugu Terauchi DDD PhD
Associate Professor and Endodontics

Lecturer, Tokyo Medical and
Department of Conservative Dentistry Government Dental College Dental University
and Endodontics Patiala, Punjab, India Japan
Government Dental College
Patiala, Punjab, India Ruchi Vashisht
Reader
Manoj Hans Department of Conservative Dentistry
Reader and Endodontics
Department of Conservative Dentistry National Dental College
and Endodontics Dera Bassi, Punjab, India
Vyas Dental College and Hospital
Jodhpur, Rajasthan, India Sachin Passi
Principal and Head
Monia Sharma Department of Conservative Dentistry
Reader and Endodontics
Department of Periodontics Sri Sukhmani Dental
DAV Dental College College and Hospital
Yamuna Nagar, Haryana, India Dera Bassi, Punjab, India

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Foreword

It gives me immense pleasure to introduce you to the third edition of the Textbook of Endodontics. Past
several years have witnessed the publication of many new textbooks on the subject of endodontics
by well-known scholars and scientists. Several critically important paradigm shifts have occurred in
dentistry, particularly in the field of endodontics in the past decades, a shift towards the comprehensive
approach in the endodontic practice today. It is of foremost importance to put this work into the context
of the continuum of endodontic literature.

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Endodontics has become so important in the last several decades that books which condense all the

techniques and treatment options are certainly looked-for. Written by the two leading authorities on this
important aspect of dentistry, Drs Nisha Garg and Amit Garg have accumulated a tremendous amount

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of knowledge to summarize this important information into easy-to-read chapters. This compact yet
comprehensive work clearly portrays their efforts. The authors have invested extensive time and effort to freshly describe the
existing literature and have added interesting chapters like Endodontic Failures and Retreatment, Tooth Hypersensitivity, and

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Tooth Infractions. I am sure the new edition of the book will be equally appreciated by the undergraduate and postgraduate
students as well as the researchers.
I am delighted and honored to introduce and recommend the book, which will effectively bridge the gap between the

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scientific esoteric and practitioner’s daily need for relevant knowledge, and will become one of the most significant steps in
understanding the subject of endodontics. 

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Anil Chandra
Professor
Department of Conservative Dentistry and Endodontics
King George’s Medical University

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Lucknow, Uttar Pradesh, India

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Preface to the Third Edition

In presenting the third edition of the Textbook of Endodontics, we would like to express our appreciation in the kindly manner
in which the earlier editions were accepted by dental students and professionals across the country.
The scope of the third edition of this book is as earlier to be simple yet comprehensive Textbook of Endodontics that serves

as an introductory for dental students and a refresher source for general practitioners. The book attempts to incorporate most
recent advances in endodontics while at the same time not losing the sight of basics, therefore, making the study of endodontics
easier and interesting.

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In an attempt to improve the book further, many eminent personalities were invited to edit, write and modify the important

chapters in form of text and photographs. We would especially thank Dr Jaidev Dhillon, Dr Anil Dhingra, Dr Neelam Mittal,
Dr Poonam Bogra, Dr Sachin Passi, and Dr Manoj Hans for providing us clinical case-photographs and radiographs for better

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understanding of the subject.
We are indebted to Dr Poonam Bogra for writing an important chapter Biofilm in Endodontics for the book and editing

chapters, Access Cavity Preparation, Cleaning and Shaping of Root Canal System, Irrigation and Intracanal Medicaments.

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We fall lack of words to thank Dr Sri Rekha for critically evaluating the chapter; Working Length Determination, Endodontic

Instruments and Management of Traumatic Injuries.
We are thankful to Dr Sanjay Miglani for modifying chapter Internal Anatomy, Dr Navjot Singh Khurana for editing chapter

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Management of Traumatic Injuries, Dr Monia Sharma for Endodontic Periodontal Lesions, Dr Ruchi Vashisht for Obturation
of Root Canal System and Surgical Endodontics, Dr Shinam Pasricha for Tooth Infractions and Tooth Resorption, Drs Amita

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and Suresh Saini for Postendodontic Restorations, Dr Bobbin for Flare-ups, Drs Sandhya Kapoor Punia and Vikas Punia for
editing Geriatric Endodontics and Tissue Engineering.
We are specially thankful to Yoshitsugu Terauchi for sharing his new device for removal of the fractured instrument.

We are thankful to Dr RS Kang and Dr JS Mann for their constant support, motivation and encouragement. We are also

thankful to Dr Arundeep Singh, Dr Rahul Jain and Dr Gaurav Aggarwal for providing photographs and radiographs for the

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book. Also thankful to Dr Shaweta for helping us in sorting out the MCQs for the book.
We offer our humble gratitude and sincere thanks to Mr Avtar Singh (Chairman), and Mr Daman Jeet Singh, Sri Sukhmani

Dental College (SSDC), Dera Bassi, Punjab, India, for providing healthy and encouraging environment for our work.

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We would like to express our thanks to staff of Department of Conservative Dentistry and Endodontics, Sri Sukhmani Dental

College, Dera Bassi, Punjab, India, Dr Sachin Passi, Dr Rajnish Kumar and Dr Rahul Jain for their ‘ready to help’ attitude,
constant guidance and positive criticism which helped in improvement of the book.
It is hoped that all these modifications will be appreciated and render the book still more valuable basis for endodontic

practice.
We are thankful to Shri Jitendar P Vij (Group Chairman), Mr Ankit Vij (Managing Director), Mr Tarun Duneja (Director-

Publishing), Mr KK Raman (Production Manager), Mr Sunil Kumar Dogra (Production Executive), Mr Neelambar Pant
(Production Coordinator), Mr Manoj Pahuja (Senior Graphic Designer), Mr Binay Kumar (Proofreader), Mr Chandra Dutt
(Typesetter) and staff of M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India, for showing personal interest and
trying to the level best to bring the book in present form.

Nisha Garg
Amit Garg

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Preface to the First Edition

The amount of literature available in dentistry today is vast. Endodontics being no exception. However, during both our
graduation as well as postgraduation, we always felt the need for a book which would help us to revise and update our
knowledge. When we were doing undergraduation, there were no Indian authored books on endodontics. We were thus
motivated to frame a specialized, precise, concise, easy to read and remember yet, up-to-date Textbook of Endodontics.
The line diagrams are in an expressive interpretation of endodontic procedures, which are worked upon and simplified

to render them more comprehensive and comparable with real photographs. These illustrations (around 1200) are easy to

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remember and reproduce during examinations.
Emphasis is laid upon the language which is simple, understandable and exclusively designed for undergraduates,

postgraduates, general practitioners and teachers in the field.

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It took us more than three years to accomplish the arduous task of writing this book. This thrust for knowledge led us to link

everywhere, where we could Medline journals, books and more.
Nevertheless, a never-ending approach and internal craving of mind and soul finally resulted in publication of the book.

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God perhaps gave us some ability and showered his light on us, guiding us for this task.
Till the last week before the publication of the book, we were frantically looking for loopholes, missing information and any

important updates we might have missed out. To the best of our knowledge, we did everything we could. But for knowledge,

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one life is not enough. The sky is the limit.
We await the response of this first edition, which would improve us in the next editions to come.

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Nisha Garg
Amit Garg

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Contents

1. Introduction and Scope of Endodontics 1





History of Endodontics 1; Modern Endodontics 1; Patient Education 3





2. Pulp and Periradicular Tissue 7



Development of Dental Pulp 7; Histology of Dental Pulp 8; Supportive Elements 11;

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Innervation of Pulp 13; Anatomy of Dental Pulp 15; Pulp Chamber 15; Root Canal 15;







Functions of Pulp 17; Age Changes in the Pulp 18; Pulpal Calcifications/Pulp Stones/




Denticles 18; Calcific Metamorphosis 19; Periradicular Tissue 19

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3. Pathologies of Pulp and Periapex 22

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Pulp Pathologies 22; Etiology of Pulpal Diseases 23; Progression of Pulpal




Pathologies 24; Diagnostic Aids for Pulpal Pathology 25; Classification of Pulpal

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Pathologies 26; Barodontalgia/Aerodontalgia 27; Reversible Pulpitis/Hyperemia/




Hyperactive Pulpalgia 27; Irreversible Pulpitis 28; Chronic Pulpitis 30; Internal






Resorption 32; Pulp Necrosis 32; Pulp Degeneration 34; Periradicular

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Pathologies 35; Periapex Pathologies 36; Etiology of Periradicular Diseases 36; Diagnosis






of Periradicular Pathologies 37; Classification of Periradicular Pathologies 38; Acute




Apical Periodontitis 39; Acute Apical Abscess 39; Phoenix Abscess/Recrudescent




Abscess 41; Periapical Granuloma 42; Radicular Cyst/Cystic Apical Periodontitis 44;

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Chronic Alveolar Abscess 46; Persistent Apical Periodontitis 49; External Root




Resorption 49; Diseases of Periradicular Tissue of Nonendodontic Origin 49



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4. Endodontic Microbiology 51



Portals of Entry for Microorganisms 51; Classification of Microorganisms 53;



Microbial Virulence and Pathogenicity 54; Factors Influencing the Growth and Colonization of


Microorganisms 55; Microbial Ecosystem of the Root Canal 55;



Types of Endodontic Infections 56; Identification of the Bacteria 57; How to Combat




Microbes in the Endodontic Therapy? 59

5. Biofilm in Endodontics 61



Stages of Biofilm Formation 61; Types of Endodontic Biofilm 61; Ultrastructure of




Biofilm 62; Microbes in Endodontic Biofilms 62; Methods to Eradicate Biofilms 63





6. Rationale of Endodontic Treatment 65



Theories of Spread of Infection 65; Culprit of Endodontic Pathology 65; Portals for




Entry of Microorganisms 66; Inflammation 66; Nonspecific Mediators of Periradicular




Lesions 68; Antibodies (Specific Mediators of Immune Reactions) 71; Role of Immunity in




Endodontics 71; Endodontic Implications (Pathogenesis of Apical Periodontitis as Explained


by Fish) 71; Kronfeld’s Mountain Pass Theory 72; Rationale of Endodontic Therapy 73





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7. Diagnostic Procedures 74



Case History 74; Pulp Vitality Tests 82; Recent Advances in Pulp Vitality





Testing 85; Diagnostic Findings 87; Role of Radiographs in Endodontics 87;





Digital Radiography 91; Digital Dental Radiology 91; Phosphor Imaging System 93






8. Differential Diagnosis of Orofacial Pain 95



Pain 95; Diagnosis 95; Orofacial Pain 96; Sources of Odontogenic Pain 96;







Pulpal Pain 97; Periodontal Pain 98; Sources of Nonodontogenic Pain 99





9. Case Selection and Treatment Planning 103



Endodontic Therapy 103; Contraindications of Endodontic Therapy 104;



Treatment Planning 105; Medical Conditions Influencing Endodontic Treatment


Planning 106; Sequence of Treatment Delivery 107

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10. Asepsis in Endodontics 109



Rationale for Infection Control 109; Cross-infection 109; Objective

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of Infection Control 110; Universal Precautions 110; Classification of




Instruments 112; Instrument Processing Procedures/Decontamination


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Cycle 112; Disinfection 118; Antiseptics 119; Infection Control Checklist 120







11. Isolation of Teeth 122

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Isolation with Rubber Dam 122; Classification of Rubber Dam Clamps 124



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12. Pharmacology in Endodontics 131



Anxiety Control 131; Pain Control 132; Intrapulpal Injection 139;





Infection Control 141; Guidelines for Antibiotic Prophylaxis 143



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13. Endodontic Instruments 145



Classification of Endodontic Instruments 145; Group I Hand-operated

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Instruments 146; Group II Nonrotary Endodontic Instruments 152; Group III Rotary




Endodontic Instruments used with a Handpiece 155; Various Rotary Nickel Titanium


System 157; Profile System 158; Greater Taper File 158; Protaper File 158; Quantec File








System 160; Light Speed System 160; K3 Rotary File System 161; HERO 642 161; Race Files








(Reamers with Alternating Cutting Edges) 161; Real World Endo Sequence File 162; Wave




One System 162; Instrument Deformation and Breakage 163; Instruments used for Filling




Root Canals 166

14. Internal Anatomy 169



Pulp Cavity 169; Common Canal Configuration 171; Methods of Determining Pulp




Anatomy 172; Variations in the Internal Anatomy of Teeth 174; Factors Affecting Internal




Anatomy 180; Individual Tooth Anatomy 180; C-Shaped Canals 191; Classification of






C–Shaped Root Canals 191

15. Access Cavity Preparation 196



Instruments for Access Cavity Preparation 198; Guidelines for Access Cavity


Preparation 199; Access Cavity of Anterior Teeth 201; Access Cavity Preparation for




Premolars 203; Access Cavity Preparation for Maxillary Molars 204; Access Cavity Preparation




for Mandibular Molars 205; Clinical Managing Difficult Cases for Access Opening 206



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Contents xvii


16. Irrigation and Intracanal Medicaments 211



Ideal Requirements for an Irrigant 211; Functions of Irrigants 212; Factors that Modify





Activity of Irrigating Solutions 212; Commonly used Irrigating Solutions 213; Choice of an





Irrigant Solution 213; Normal Saline 213; Sodium Hypochlorite 214; Urea 216; Hydrogen









Peroxide 216; Urea Peroxide 217; Chlorhexidine 217; Chelating Agents 218; Ultrasonic








Irrigation 220; Newer Irrigating Solutions 221; Method of Irrigation 223; Endovac (Apical






Negative Pressure Irrigation System) 225; Intracanal Medicaments 227; Characteristics of





Intracanal Medicaments 227; Placement of Intracanal Medicament 232



17. Working Length Determination 235



Significance of Working Length 236; Different Methods of Working Length


Determination 238; Radiographic Method of Working Length Determination 238;



Grossman Method/Mathematical Method of Working Length Determination 239;


Electronic Apex Locators 240

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18. Cleaning and Shaping of Root Canal System 246



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Objectives of Biomechanical Preparation 247; Different Movements of


Instruments 249; Basic Principles of Canal Instrumentation 251; Techniques of Root Canal




Preparation 252; Standardized Preparation Technique (Conventional Technique) 253;

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Step Back Technique/Telescopic Canal Preparation/Serial Root Canal Preparation 253;


Modified Step Back Technique 257; Passive Step Back Technique 257; Coronal to




Apical Approach Technique 258; Step Down Technique 259; Crown Down Pressureless

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Technique 259; Hybrid Technique of Canal Preparation (Step Down/Step Back) 262;



Double Flare Technique 262; Modified Double Flared Technique 262; Balanced Force

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Technique 263; Reverse Balanced Force Preparation 264; Types of Crown Down Hand




Instrumentation Techniques 264; Modified Manual Step Down Technique 264; Profile




GT (Greater Taper) Technique 264; Quantec Instrument Technique 265; Protaper




Files 265; Engine Driven Preparation with NiTi Instruments 267; Profile System 267;






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Greater Taper Files (GT Files) 268; Light Speed System 268; K3 Rotary File System 270;





Real World Endo Sequence File 270; HERO 642 270; Wave One File System 271;





Canal Preparation using Ultrasonic Instruments 272; Canal Preparation using Sonic


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Instruments 273; Laser Assisted Root Canal Therapy 274; Evaluation Criteria of Canal




Preparation 274; Special Anatomic Problems in Canal Cleaning and Shaping 275



19. Obturation of Root Canal System 282



Timing of Obturation 284; Extent of Root Canal Filling 285; Materials




used for Obturation 286; Methods of Sealer Placement 301; Obturation




Techniques 301; Armamentarium for Obturation 302; Lateral Compaction



Technique 302; Variation of Lateral Compaction Technique 305; Chemical Alteration




of Gutta-percha 306; Vertical Compaction Technique 309; System B: Continuous




Wave of Condensation Technique 311; Lateral/Vertical Compaction of Warm Gutta-


percha 312; Sectional Method of Obturation/Chicago Technique 313; McSpadden




Compaction/Thermomechanical Compaction of the Gutta-percha 313; Thermoplasticized


Injectable Gutta-percha Obturation 313; Solid Core Carrier Technique 315; Obturation with



Silver Cone 318; Apical Third Filling 318; Postobturation Instructions 321; Repair following






Endodontic Treatment 322

20. Single Visit Endodontics 323



Advantages of Single Visit Endodontics 323; Disadvantages of Single Visit


Endodontics 323; Criteria of Case Selection 323; Contraindications of Single Visit




Endodontics 325

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21. Mid Treatment Flare-ups in Endodontics 326



Etiology 326; Mechanisms for Flare-ups 328; Clinical Conditions Related to




Flare-up 330; Management of Flare-ups 331



22. Endodontic Emergencies 335



Diagnosis and Treatment Planning 335; Pretreatment Endodontic



Emergencies 336; Conditions Requiring Emergency Endodontic


Treatment 337; Intratreatment Emergencies 341; Postobturation Emergencies 343





23. Endodontic Failures and Retreatment 345



Evaluation of Success of Endodontic Treatment 345; Causes of the Endodontic



Failures 346; Case Selection for Endodontic Retreatment 351; Steps of Retreatment 352





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24. Procedural Accidents 364



Inadequately Cleaned and Shaped Root Canal System 364; Instrument


Separation 368; Deviation from Normal Canal Anatomy 373; Inadequate Canal

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Preparation 375; Perforation 377; Obturation Related 383; Vertical Root






Fracture 384; Instrument Aspiration 385



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25. Surgical Endodontics 386



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Contraindications 387; Presurgical Considerations 388; Incision and




Drainage 388; Periradicular Surgery 389; Flap Designs and Incisions 391; Principles and






Guidelines for Flap Designs 391; Full Mucoperiosteal Flaps 391; Limited Mucoperiosteal

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Flaps 392; Flap Design Consideration in Palatal Surgery 393; Flap Reflection and




Retraction 394; Hard Tissue Management 395; Principles of Surgical Access to




Root Structure 395; Periradicular Curettage 396; Root-end Resection (Apicoectomy,



Apicectomy) 397; Root-end Preparation 400; Retrograde Filling 402; Reapproximation

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of the Soft Tissue 404; Replantation 404; Transplantation 405; Root Resection/






Amputation 405; Bicuspidization/Bisection 405; Endodontic Implants 409;





Postsurgical Care 409; Suturing 411; Postsurgical Complications 411

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26. Endodontic Periodontal Relationship 413



Pathways of Communication between Pulp and Periodontium 414; Impact of


Pulpal Diseases on the Periodontium 416; Impact of Periodontal Disease on Pulpal


Tissue 417; Etiology of Endodontic-periodontal Problems 417; Classification of Endodontic-




periodontal Lesions 417; Diagnosis of Endodontic-periodontal Lesions 419; Primary




Endodontic Lesions 420; Primary Endodontic Lesion with Secondary Periodontal


Involvement 421; Primary Periodontal Lesions 422; Primary Periodontal Lesions with




Secondary Endodontic Involvement 422; Independent Endodontic and Periodontal Lesions


which do not Communicate 426; True Combined Endo-Perio Lesions 426



27. Restoration of Endodontically Treated Teeth 428



Importance of Coronal Restoration 428; Factors Making Endodontically Treated Teeth


Different from Vital Teeth 429; Restorative Treatment Planning for Endodontically


Treated Teeth 430; Components of the Restored Tooth 432; Factors to be Considered




while Planning Post and Core 439; Preparation of the Canal Space and the


Tooth 447; Core 450; Custom-made Post 451; Core Fabrication 452; Investing and








Casting 452; Evaluation 452; Cementation 452





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Contents xix


28. Management of Traumatic Injuries 454



Classification of Dentofacial Injuries 454; Examination of Traumatic Injuries 455;




Crown Infraction 457; Crown Fracture 458; Complicated Crown Fracture 459;






Crown Root Fracture 463; Root Fracture 467; Luxation Injuries 471; Assessment of







Traumatic Injuries 477; Prevention of Traumatic Injuries 478



29. Pulpal Response to Caries and Dental Procedure 480



Response of Pulp to Dental Caries 481; Response of Pulp to Tooth Preparation 482;





Response of Pulp to Local Anesthetics 485; Effect of Chemical Irritants on Pulp 486;




Dentin Sterilizing Agents 486; Cavity Liner and Varnishes 486; Response




of Pulp to Restorative Materials 486; Restorative Resins 488; Effects of Pin




Insertion 488; Impression Material 489; Effects of Radiations on Pulp 489; Effect of






Heat from Electrosurgery 490; Effect of Lasers on Pulp 490; Defense Mechanism of




Pulp 490; Prevention of Pulpal Damage due to Operative Procedure 491; How does Pulp

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Recover? 491

30. Management of Discolored Teeth 492

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Classification of Discoloration 492; Bleaching 496; Contraindications for




Bleaching 496; Bleaching Agents 497; Home Bleaching Technique/Night Guard

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Bleaching 497; In-Office Bleaching 499; Bleaching of Nonvital Teeth 502; Effects of






Bleaching Agents on Tooth and its Supporting Structures 505

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31. Tooth Resorption 507



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Classification of Resorption 507; Cells Involved in Tooth Resorption 508; Mechanism of Tooth




Resorption 509; Factors Regulating Tooth Resorption 509; Internal Resorption 510; External






Root Resorption 516; Cervical Root Resorption (Extracanal Invasive Resorption) 522



32. Tooth Infractions 524

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Tooth Infractions 524; Vertical Root Fracture 529



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33. Tooth Hypersensitivity 531



Mechanism of Dentin Sensitivity 531; Incidence and Distribution of Dentin


Hypersensitivity 532; Etiology and Predisposing Factors 532; Differential




Diagnosis 534; Diagnosis 534; Treatment Strategies 534





34. Pediatric Endodontics 538



Anatomy of Primary Teeth 538; Pulp Treatment Procedures 540; Pulpotomy 542;





Pulpectomy for Primary Teeth 545; Apexification 548; Mineral Trioxide Aggregate 551





35. Geriatric Endodontics 554



Age Changes in the Teeth 554; Endodontics in Geriatric Patients 555;



Diagnosis and Treatment Plan 558

36. Lasers in Endodontics 561



History 561; Classification of Laser 562; Laser Physics 562; Type of Lasers 564;







Laser Interaction with Biological Tissues 564; Laser Safety in Dental Practice 565;



Soft and Hard Tissue Applications of Lasers in Dentistry 566

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Textbook of Endodontics

37. Magnification 569





Loupes 569; Surgical Operating Microscope 570; Endoscope 572; Orascope 572







38. Ethics in Endodontics 574



Principles of Ethics 574; Root Canal Ethics 574; Informed Consent 575;





Dental Negligence 575; Malpractice and the Standard of Care 576; Abandonment 577;





Malpractice Cases 577

39. Tissue Engineering 579



Strategies of Stem Cell Technology 579; Triad of Tissue Engineering 579; Dental Pulp




Stem Cells 582; Stem Cells from Human Exfoliated Deciduous Teeth 582; Periodontal




Ligament Stem Cells 582; Stem Cell Markers 582; Morphogens/Signaling Molecules 582;






Scaffold/Matrix 583; Approaches to Stem Cell Technology 583; Revascularization

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to Induce Apexification/Apexogenesis in Infected Non-vital Immature
Tooth 586; Apexification 586; Pulp Revascularization 586; Pulp Revascularization in






Immature Teeth 587; Mechanism of Revascularization 587; Advantages of




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Revascularization Procedure 588; Limitations of Revascularization Procedure 588



Index 591

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Introduction and Scope of
Endodontics 1
 History of Endodontics  Modern Endodontics  Patient Education



INTRODUCTION Prescience : 1776 to 1826



Age of discovery : 1826 to 1876
Endo is a Greek word for “Inside” and Odont is Greek word



Dark age : 1876 to 1926
for “Tooth”. Endodontic treatment deals inside of the tooth.



The renaissance : 1926 to 1976



Endodontics is the branch of clinical dentistry associated Innovation era : 1977 till date



with the prevention, diagnosis and treatment of pathosis of the
dental pulp and their sequelae. Prescience (1776 to 1826): In this era, endodontic therapy
Thus, the main aim of the endodontic therapy involves to: was concerned with the crude modalities like abscesses were

• Maintain vitality of the pulp. being treated with poultices or leeches and pulps were being
• Preserve and restore the tooth with damaged and necrotic cauterized using hot instruments.
pulp.
• Preserve and restore the teeth which have failed to the Age of discovery (1826 to 1876): In this era, the development
previous endodontic therapy. of anesthesia, gutta-percha and barbed broaches happened.
Thus we can say that the primary goal of endodontic The medications were created for treating pulpal infections
therapy is to create an environment within the root canal and the cements and pastes were discovered to fill them.
system which allows the healing and continued maintenance Dark age (1876 to 1926): In spite of introduction of X-rays
of the health of the periradicular tissue. and general anesthesia, extraction of tooth was the choice
Endodontics has been defined as art as well as science of of treatment than endodontics because theory of the focal

clinical dentistry; because in spite of all the factual scientific infection was main concern at that time.
foundation on which the endodontics is based, to provide an
The renaissance (1926 to 1976): In this era, endodontics was
ideal endodontic treatment is an art in itself.
established as science and therapy, forming its golden era. It
Before understanding what is root canal therapy, how and
showed the improvement in anesthesia and radiographs for
when it is performed and other facts regarding endodontic
better treatment results. The theory of focal infection was also
therapy, we should be familiar with the history of endodontics.
fading out, resulting in more of endodontics being practiced.
In 1943, because of growing interest in endodontics, the AAE,
HISTORY OF ENDODONTICS (TABLE 1.1) that is, the American Association of Endodontists was formed.
Endodontics has been practiced as early as second or third Innovation era: It is the period from 1977 onwards in
century BC. The history of endodontics begins in 17th century which tremendous advancements at very fast rate are being
and since then many advances, developments and research introduced in the endodontics. The better vision, better
work has been done continuously. techniques of biomechanical preparations, and obturation
Advances in endodontics have been made continuously, are being developed resulting in the simpler, easier and faster
especially after Pierre Fauchard (1678-1761) [Founder of endodontics with more predictable results.
modern dentistry] described the pulp very precisely in his Also the concept of single visit endodontics is now globally
textbook “Le Chirugien Dentiste”. accepted in contrast to multiple visits.
Latter in 1725, Lazare Rivere introduced the use of clove
oil as sedative and in 1746, Pierre Fauchard demonstrated
MODERN ENDODONTICS
the removal of pulp tissue. Dr Grossman, the pioneer of
endodontics divided the evolution of endodontics in four eras As we have seen, over the years, there has been a great improve
­
from 1776 to 1976, each consisting of 50 years. ment in the field of endodontics. Many researches have been

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Textbook of Endodontics

Table 1.1: History of endodontics


1725 Lazare Riviere Introduced clove oil for sedative property
1728 Pierre Fauchard First described the pulp tissue
1746 Pierre Fauchard Described removal of pulp tissue
1820 Leonard Koecker Cauterized exposed pulp with heated instrument and protected it with lead foil
1836 S Spooner Suggested arsenic trioxide for pulp devitalization
1838 Edwin Maynard Introduced first root canal instrument
1847 Edwin Truman Introduced gutta-percha as a filling material
1864 SC Barnum Prepared a thin rubber leaf to isolate the tooth during filling
1867 Bowman Used gutta-percha cones for filling of root canals
1867 Magitot Use of electric current for testing pulp vitality
1879 GA Mills Etiologic factor of pulp sequelae was lack of vitality in the tooth
1885 Lepkoski Substituted formations for arsenic to dry the nonvital pulp
1890 Gramm Introduced gold plated copper points for filling
1891 Otto Walkhoff Introduced camphorated chlorophenol as a medication
1895 Roentgen Introduced formocresol
1914 Callahan Introduction of lateral compaction technique
1918 Cluster Use of electrical current for determination of working length
1920 BW Hermann Introduced calcium hydroxide
1936 Walker Sodium hypochlorite
1942 Suzuki Presented scientific study on apex locator
1944 Johnson Introduced profile instrument system
1957 Nygaard Ostby Introduced EDTA
1958 Ingle and Levine Gave standardizations and guidelines for endodontic instruments
1961 Sparser Walking bleach technique
1962 Sunanda Calculated electrical resistance between periodontium and oral mucous
membrane
1967 Ingle Introduced standardized technique
1971 Weichman Johnson Use of lasers
1979 Mullaney et al. Use of step-back technique
1979 McSpadden McSpadden technique (Thermomechanical compaction)
1980 Marshall and Pappin Introduction of Crown down technique
1985-86 Roane, Sabala and Powell Introduction of balanced force technique
1988 Munro Introduced first commercial bleaching product
1989 Haywood and Heymann Nightguard vital bleaching
1993 Torabinejad Introduced MTA (Mineral trioxide aggregate)
2004 Pentron clinical laboratory Introduced Resilon

conducted and papers are being presented regarding the Various ways to reduce the levels of microbial infection,
advances, modifications and change in attitude regarding viz. chemical, mechanical and their combination have led to
endodontic therapy. In the past two decades, extensive studies development of newer antimicrobial agents and techniques
have been done on microbial flora of pulp and the periapical of biomechanical preparation for optimal cleaning and
tissue. The biological changes, role of innate and acquired shaping of the root canals.
immunological factors are being investigated in dental pulp To increase the efficiency of root canal instrumentation,
after it gets infected, healing of the periapical tissue after introduction of engine driven rotary instruments is made.
undergoing root canal therapy is also being investigated. Introduction of Nickel Titanium multitapered instruments

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Introduction and Scope of Endodontics 3


with different types of cutting tips have allowed the better, PATIENT EDUCATION
easier and efficient cleaning and shaping of the root canals.
The advent of endomicroscope in the field of endodontics Most of the patients who need endodontic treatment, are often
has opened the great opportunities for an endodontist. It curious and interested regarding the treatment. Following
is used in every phase of the treatment, i.e. from access information should be given to the patients in anticipation of
opening till the obturation of root canals. It makes the images frequently asked questions:
both magnified and illuminated, thus helps in making the
treatment more predictable and eliminating the guess work. Who Performs an Endodontic Therapy?
Introduction of newer obturation systems like system
B Touch and heat have made it possible to fill the canal three Generally, all dentists receive basic education in endodontic
dimensionally. Material like mineral trioxide aggregate (MTA), treatment but an endodontist is preferred for endodontic
a root canal repair material has made the procedures like therapy. General dentists often refer patients needing
apexification, perforation repair to be done under moist field. endodontic treatment to endodontists.
Since endodontics is based on the principles of inflammation,
pulp and periapical disease processes and treatments Who is an Endodontist?
available, the future of endodontics lies in redefining the
An endodontist is a dentist who undergoes a special training in
rationale of endodontic therapy using newer modalities and
diagnosing and treating the problems associated with inside
to meet the set of standards for excellence in the future.
of the tooth. To become specialists, they complete dental
school and an additional two or more years of advanced
Scope of endodontics (Fig. 1.1)
training in endodontics. They perform routine, difficult,
•  Vital pulp therapy (pulp capping, pulpotomy) complex endodontic procedures (including retreatment of
•  Diagnosis and differential diagnosis of oral pain previous root canals that have not healed completely) and
•  Root canal treatment of teeth with or without periradicular endodontic surgeries.

pathology of pulpal origin
•  Surgical management of pathology resulting form pulpal disease What is Endodontics?

•  Management of avulsed teeth (replantation) Endodontics is the diagnosis and treatment of inflamed
•  Endodontic implants and damaged pulps. Teeth are composed of protective hard
•  Root end resections, hemisections and root resections
covering (enamel, dentin and cementum) encasing a soft
living tissue called pulp (Fig. 1.2). Pulp contains blood vessels,
•  Retreatment of teeth previously treated endodontically nerves, fibers and connective tissue. The pulp extends from the
•  Bleaching of discolored teeth crown of the tooth to the tip of the roots where it connects to
•  Coronal restorations of teeth using post-and-cores. the tissues surrounding the root. The pulp is important during
a tooth’s growth and development. However, once a tooth is
fully mature it can survive without the pulp, because the tooth
continues to be nourished by the tissues surrounding it.

How does Pulp become Damaged?


Number of ways which can damage the pulp include tooth
decay (Figs 1.3 and 1.4), gum diseases, injury to the tooth by
accident.

Why do I Feel Pain?


When pulp becomes infected, it causes increased blood flow
and cellular activity, and pressure cannot be relieved from
inside the tooth. This causes pain. Pulp can even die without
causing significant pain.

How can You Tell if Pulp is Infected?


When pulp gets inflamed, it may cause toothache on taking
hot or cold, spontaneous pain, pain on biting or on lying
Fig. 1.1 The scope of endodontology down. A damaged pulp can also be noticed by drainage,

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4 
Textbook of Endodontics

Fig. 1.2 Normal anatomy of a tooth showing enamel,



dentin, cementum and pulp

Fig. 1.5 Tooth with infected pulp and abscess formation


swelling, and abscess at the root end (Fig. 1.5). Sometimes,
however, there are no symptoms.

Why do I need Root Canal Therapy?


Because tooth will not heal by itself, the infection may
spread around the tissues causing destruction of bone and
supporting tissues (Fig. 1.6). This may cause tooth to fall
out. Root canal treatment is done to save the damaged pulp
by thorough cleaning and shaping of the root canal system
and then filling it with gutta-percha (rubber like) material to
prevent recontamination of the tooth. Tooth is permanently
Fig. 1.3 Tooth decay causing damage to pulp restored with crown with or without post.

What are Alternatives to Root Canal Therapy?
If tooth is seriously damaged and its support is compromised,
then extraction is only alternative.

What is Root Canal Procedure?


Once the endodontic therapy is recommended, your
endodontist will numb the area by injecting local anesthetic.
After this a rubber sheet is placed around the tooth to isolate
it. Then the opening is made in the crown of the tooth and
very small sized instruments are used to clean the pulp from
pulp chamber and root canals (Fig. 1.7). After thorough
cleaning and shaping of root canals (Fig. 1.8), they are filled
with rubber like material called gutta-percha, which will
prevent the bacteria from entering this space again (Figs 1.9
Fig. 1.4 Radiograph showing carious exposure of pulp and 1.10).

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Introduction and Scope of Endodontics 5


Fig. 1.6 Radiograph showing periapical lesion

due to carious exposure

Fig. 1.9 Obturation of root canal system


Fig. 1.7 Cleaning and shaping of root canal system Fig. 1.10 Radiograph showing obturated canals


After completion of endodontic therapy, the endodontist
places the crown or other restoration so as to restore the tooth
to full function (Figs 1.11 and 1.12).

What are Risks and Complications?


It has been seen that more than 95 percent cases of endodontic
therapy are successful. However sometimes because of
unnoticed canal malformations, instrument errors a root
canal therapy may fail.

How many visits will it Take to


Complete this Treatment?
Nowadays most of the treatment can be completed in 1 to 2
visits. But treatment time can vary according to condition of
Fig. 1.8 Cleaned and shaped tooth the tooth.

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6 
Textbook of Endodontics

Will I have a Dead Tooth after Root


Canal Therapy?
No, since tooth is supplied by blood vessels present in
periodontal ligament, it continues to receive the nutrition
and remains healthy.

Will the Tooth need any Special Care or


Additional Treatment after Endodontic
Treatment?
One should not chew or bite on the treated tooth until it
has been restored by the dentist. The unrestored tooth is
susceptible to fracture, so visit the dentist for full coverage
restoration as soon as possible. Do not forget to maintain good
oral hygiene by brushing, flossing, and routine check-ups.

Can all Teeth be Treated Endodontically?


Most of the teeth can be treated endodontically. But
sometimes when root canals are not accessible, root is
severely fractured, tooth cannot be restored or tooth does not
Fig. 1.11 Complete restoration of tooth with crown placed have sufficient bone support, it becomes difficult to treat the

over the restored tooth tooth endodontically. However, advances in endodontics are
making it possible to save the teeth that even a few years ago
would have been lost.
Newer researches, techniques and materials have helped
us to perform the endodontic therapy in better way with
more efficiency. Since introduction of rotary instruments and
other technologies reduce the treatment time, the concept
of single visit is gaining popularity nowadays. It has been
shown that success of endodontic therapy depends on the
quality of root canal treatment and not the number of visits.
In the modern world single visit endodontics is becoming
quite popular.

QUESTIONS
1. What is scope of endodontics?
2. Define endodontics and explain in detail the stages of multiple
visit root canal treatment in 12.
Fig. 1.12 Complete endodontic treatment with root canal

obturation and crown placement BIBLIOGRAPHY
1. Balkwill FH. On the treatment of pulpless teeth. Br. Dent J.
1883;4:588-92.
2. Harding WE. A few practical observations on the treatment of
Will I feel Pain during or after Treatment? the pulp. J Brit Dent Assoc. 1883;4:318-21.
Nowadays with better techniques, and better understanding 3. Landers RR, Calhoun RL. One-appointment endodontic
therapy: a nationwide survey of endodontists. J Am Dent Assoc.
of anesthesia most of the patients feel comfortable during the
1970;80:1341.
treatment. But for first few days after therapy, one might feel 4. Soltanoff W. Comparative study of the single visit and multiple
sensation especially if pain and infection were present prior visit endodontic procedure. J Endod. 1978;4:278.
to the procedure. This pain can be relieved by medication. If 5. Wolch I. The one-appointment endodontic technique. J Can
severe pain or pressure persists, consult the endodontist. Dent Assoc. 1975;41:613.

vip.persianss.ir
Pulp and Periradicular Tissue
2
  Development of Dental     Anatomy of Dental Pulp   Pulpal Calcifications/Pulp Stones/
Pulp   Pulp Chamber Denticles
  Histology of Dental Pulp   Root Canal   Calcific Metamorphosis
  Supportive Elements   Functions of Pulp   Periradicular Tissue
  Innervation of Pulp   Age Changes in the Pulp

INTRODUCTION Dental pulp is:


The dental pulp is soft tissue of mesenchymal origin •  Soft tissue of mesenchymal origin.
•  Consists specialized cells, odontoblasts. 
located in center of a tooth. It consists of specialized cells,
•  O
  dontoblasts  arranged  peripherally  in  direct  contact  with 
odontoblasts arranged peripherally in direct contact with dentin matrix. 
dentin matrix. This close relationship between odontoblasts •  R  elationship  between  odontoblasts  and  dentin  is  known  as 
and dentin is known as “pulp-dentin complex” (Fig. 2.1). ‘pulp-dentin complex’.
The pulp is connective tissue system composed of cells, •  S  urrounded  by  rigid  walls  and  so  is  unable  to  expand  in 
ground substance, fibers, interstitial fluid, odontoblasts, response to injury.
fibroblasts and other cellular components. Pulp is actually a
microcirculatory system consists of arterioles and venules as Features of pulp which distinguish it from tissue found elsewhere
the largest vascular component. Due to lack of true collateral in the body:
circulation, pulp is dependent upon few arterioles entering •  P  ulp  is  surrounded  by  rigid  walls  and  so  is  unable  to  expand 
through the foramen. Due to presence of the specialized cells, in  response  to  injury  as  a  part  of  the  inflammatory  process. 
i.e. odontoblasts as well as other cells which can differentiate Therefore,  pulpal  tissue  is  susceptible  to  change  in  pressure 
into hard tissue secreting cells; the pulp retains its ability to affecting the pain threshold. 
form dentin throughout the life. This enables the vital pulp to •  T  here  is  minimal  collateral  blood  supply  to  pulp  tissue  which 
reduces its capacity for repair following injury.
partially compensate for loss of enamel or dentin occurring
•   The  pulp  is  composed  almost  entirely  of  simple  connective 
with age. The injury to pulp may cause discomfort and the tissue. At its periphery there is a layer of highly specialized cells, 
disease. Consequently, the health of pulp is important for the  odontoblasts.  Secondary  dentin  is  gradually  deposited  as 
successful completion of the restorative procedures. In this a  physiological  process  which  reduces  the  blood  supply  and 
chapter, we would discuss the comprehensive description of therefore, the resistance to infection or trauma.
pulp embryology, anatomy, histology, physiology and pulp •  T  he  innervation  of  pulp  tissue  is  both  simple  and  complex. 
changes with age. Simple  in  that  there  are  only  free  nerve  endings  and 
consequently the pulp lacks proprioception. Complex because 
of innervation of the odontoblast processes which produces a 
high level of sensitivity to thermal and chemical change.

DEVELOPMENT OF DENTAL PULP


The pulp originates from ectomesenchymal cells of dental
papilla. Dental pulp is identified when these cells mature and
dentin is formed.
Before knowing the development of pulp, we should
understand the development of the tooth. Basically the
development of tooth is divided into bud, cap and bell stage.
The bud stage (Fig. 2.2) is initial stage where epithelial
cells of dental lamina proliferate and produce a bud like
Fig. 2.1 Pulp-dentin complex projection into adjacent ectomesenchyme.

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8 Textbook of Endodontics

The cap stage (Fig. 2.3) is formed when cells of dental The cells of dental papilla appear as undifferentiated
lamina proliferate to form a concavity which produces cap mesenchymal cells, gradually these cells differentiate into
like appearance. It shows outer and inner enamel epithelia fibroblasts. The formation of dentin by odontoblasts heralds
and stellate reticulum. The rim of the enamel organ, i.e. where the conversion of dental papilla into pulp. The boundary
inner and outer enamel epithelia are joined is called cervical between inner enamel epithelium and odontoblast form the
loop. As the cells of loop proliferate, enamel organ assumes future dentinoenamel junction. The junction of inner and
bell stage (Fig. 2.4). outer enamel epithelium at the basal margin of enamel organ
The differentiation of epithelial and mesenchymal cells represent the future cementoenamel junction. As the crown
into ameloblasts and odontoblasts occur during bell stage. formation with enamel and dentin deposition continues,
The pulp is initially called as dental papilla; it is designated as growth and organization of pulp vasculature occurs.
pulp only when dentin forms around it. The differentiation of At the same time as tooth develops unmyelinated sensory
odontoblasts from undifferentiated ectomesenchymal cells is nerves and autonomic nerves grow into pulpal tissue.
accomplished by interaction of cell and signaling molecules Myelinated fibers develop and mature at a slower rate, plexus
mediated through basal lamina and extracellular matrix. of Raschkow does not develop until after tooth has erupted.
The dental papilla has high cell density and the rich vascular
supply as a result of proliferation of cells with in it. HISTOLOGY OF DENTAL PULP
When pulp is examined histologically, it can be distinguished
into four distinct zones from periphery to center of the pulp
(Fig. 2.5).

Zones of pulp are:


a.  Odontoblastic layer at the pulp periphery
b.  Cell free zone of Weil
c.  Cell rich zone
d.  Pulp core

a. Odontoblastic layer: Odontoblasts consists of cell bodies


and cytoplasmic processes. The odontoblastic cell bodies
form the odontoblastic zone whereas the odontoblastic
processes are located within predentin matrix. Capillaries,
Fig. 2.2 Development of tooth showing bud stage nerve fibers (unmyelinated) and dendritic cells may be
found around the odontoblasts in this zone.
b. Cell free zone of Weil: Central to odontoblasts is sub-
odontoblastic layer, termed cell free zone of Weil. It contains
plexuses of capillaries and small nerve fiber ramifications.

Fig. 2.3 Development of tooth showing cap stage

Fig. 2.4 Development of tooth showing bell stage Fig. 2.5 Zones of pulp

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Pulp and Periradicular Tissue 9

c. Cell rich zone: This zone lies next to subodontoblastic


layer. It contains fibroblasts, undifferentiated cells which
maintain number of odontoblasts by proliferation and
differentiation.
d. Pulp core: It is circumscribed by cell rich zone. It contains
large vessels and nerves from which branches extend
to peripheral layers. Principal cells are fibroblasts with
collagen as ground substance.

Contents of the pulp


•  Cells  i.  Odontoblasts 
    ii.  Fibroblasts
    iii.  Undifferentiated mesenchymal cells
    iv.  Defense cells
    –  Macrophages
    –  Plasma cells
    –  Mast cells
•  Matrix  i.  Collagen fibers
    –  Type I
    –  Type II Fig. 2.6 Diagram showing odontoblasts
    ii.  Ground substance
    –  Glycosaminoglycans
    –  Glycoproteins
    –  Water Odontoblasts
•  Blood vessels  Arterioles, venules, capillaries  •  Encountered first when pulp is approached from dentin. 
•  Lymphatics   Draining  to  submandibular,  submental  and  •  Number ranges from 59,000 to 76,000/mm2 in coronal dentin
deep cervical nodes •  Number is lesser in root dentin.
•  Nerves  i.  Subodontoblastic plexus of Raschkow •  Morphology reflects their functional activity. 
    i i.   Sensory afferent from Vth nerve and superior  •  Synthesize mainly type I collagen, proteoglycans.
cervical ganglion •  W
  hen irritated, secretes collagen and large crystals into tubule 
lumen, resulting in reduced permeability.

Structural or Cellular Elements


POINTS TO REMEMBER
Odontoblasts (Fig. 2.6) Similar characteristic features of odontoblasts, osteoblasts and
• They are first type of cells encountered when pulp is cementoblasts
approached from dentin. •  T  hey  all  produce  matrix  composed  of  collagen  fibers  and 
• The number of odontoblasts ranges from 59,000 to 76,000 proteoglycans capable of undergoing mineralization.
per square millimeter in coronal dentin, with a lesser •   All  exhibit  highly  ordered  RER,  Golgi  complex,  mitochondria, 
number in root dentin. secretory granules, rich in RNA with prominent nucleoli.
• In the crown of the fully developed tooth, the cell bodies Difference between odontoblasts, osteoblasts and cementoblasts
of odontoblasts are columnar and measure approximately •  O  dontoblasts  are  columnar  in  shape  while  osteoblasts  and 
500 µm in height, whereas in the midportion of the pulp, cementoblast are polygonal in shape.
they are more cuboidal and in apical part, more flattened. •  O  dontoblasts  leave  behind  cellular  processes  to  form  dentinal 
• The morphology of odontoblasts reflects their functional tubules  while  osteoblasts  and  cementoblast  are  trapped  in 
activity and ranges from an active synthetic phase to a matrix as osteocytes and cementocytes.
quiescent phase.
• Ultrastructure of the odontoblast shows large nucleus
which may contain up to four nucleoli. Fibroblasts (Fig. 2.7)
• Nucleus is situated at basal end. Golgi bodies are located • The cells found in greatest numbers in the pulp are
centrally. Mitochondria, rough endoplasmic reticulum fibroblasts.
(RER), ribosomes are distributed throughout the cell body. • ‘Baume’ refers them to mesenchymal cells/pulpoblasts or
• Odontoblasts synthesize mainly Type I collagen, pulpocytes in their progressive levels of maturation.
proteoglycans. They also secrete sialoproteins, alkaline • These are numerous in the coronal portion of the pulp,
phosphatase, phosphophoryn (phosphoprotein involved in where they form the cell-rich zone. These are spindle
extracellular mineralization). shaped cells which secrete extracellular components like
• Irritated odontoblast secretes collagen, amorphous collagen and ground substance.
material, and large crystals into tubule lumen which result • Fibroblasts eliminate excess collagen by action of lysoso-
in decreased permeability to irritating substance. mal enzymes.

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10 Textbook of Endodontics

• These cells are found throughout the cell-rich area and the
pulp core and often are related to blood vessels.
• When examined under light microscope, these cells appear
as large polyhedral cells possessing a large, lightly stained,
centrally placed nucleus with abundant cytoplasm and
peripheral cytoplasm extensions.
• In older pulps, the number of undifferentiated
mesenchymal cells diminishes, along with number of
other cells in the pulp core. This reduction, along with
other aging factors, reduces the regenerative potential of
the pulp.

Fig. 2.7 Histology of pulp showing fibroblasts Defense Cells (Fig. 2.8)


• Histiocytes and macrophages: They originate from
undifferentiated mesenchymal cells or monocytes. They
appear as large oval or spindle shaped cells which are
involved in the elimination of dead cells, debris, bacteria
• Fibroblasts of pulp are much like ‘Peter Pan’ because they and foreign bodies, etc.
“never grow up” and remain in relatively undifferentiated • Polymorphonuclear leukocytes: Most common form of
state. leukocyte is neutrophil, though it is not present in healthy
Fibroblasts
pulp. They are major cell type in microabscesses formation
•  Greatest in numbers.  and are effective at destroying and phagocytizing bacteria
•  ‘Peter Pan’ as they “never grow up”. and dead cells.
•  Remain in relatively undifferentiated state. • Lymphocytes: In normal pulps, mainly T-lymphocytes
are found but B-lymphocytes are scarce. They appear at
the site of injury after invasion by neutrophils. They are
Reserve Cells/Undifferentiated Mesenchymal Cells associated with injury and resultant immune response.
• Undifferentiated mesenchymal cells are descendants Thus their presence indicates presence of persistent
of undifferentiated cells of dental papilla which can irritation.
dedifferentiate and then redifferentiate into many cell • Mast cells: On stimulation, degranulation of mast cells
types. release histamine which causes vasodilatation, increased
• Depending on the stimulus, these cells may give rise to vessel permeability and thus allowing fluids and leukocytes
odontoblasts and fibroblasts. to escape.

Fig. 2.8 Cells taking part in defense of pulp

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Pulp and Periradicular Tissue 11

Extracellular Components SUPPORTIVE ELEMENTS


The extracellular components include fibers and the ground Pulpal Blood Supply
substance of pulp:
Teeth are supplied by branches of maxillary artery (Flow
chart 2.1). Mature pulp has an extensive and unique vascular
Fibers pattern that reflects its unique environment. Blood vessels
• The fibers are principally Type I and Type III collagen.
which are branches of dental arteries enter the dental pulp
• Collagen is synthesized and secreted by odontoblasts and
by way of apical and accessory foramina. One or sometimes
fibroblasts.
two vessels of arterioler size (about 150 µm) enter the apical
• The overall collagen content of the pulp increases with
foramen with sensory and sympathetic nerve bundles. The
age, while the ratio between Type I and Type III remains
arterioles course up through radicular pulp and give off
stable.
branches which spread laterally towards the odontoblasts
• Fibers produced by these cells differ in the degree of
layer and form capillary plexus. As they pass into coronal
cross-linkage and variation in hydroxyline content. Fibers
pulp, they diverge towards dentin, diminish in size and give
secreted by fibroblasts do not calcify.
rise to capillary network in sub-odontoblastic region (Fig.
• Collagen with age becomes coarser and can lead to
2.9). This network provides odontoblasts with rich source of
formation of pulp stones.
metabolites.
• In peripheral pulp, collagen fibers have unique arrange-
Blood passes from capillary plexus into venules which
ment forming von Korff’s fibers. These are corkscrew like
constitute the efferent (exit) side of the pulpal circulation
originating between odontoblasts and pass into dentin
and are slightly larger than corresponding arterioles. Venules
matrix.
enlarge as they merge and advance toward the apical foramen
Clinical Tips (Flow chart 2.2). Efferent vessels are thin walled and show
only scanty smooth muscle.
Fibers  are  more  numerous  in  radicular  pulp  than  coronal  and 
greatest  concentration  of  collagen  generally  occurs  in  the  most 
apical  portion  of  the  pulp.  This  fact  is  of  practical  significance  Lymphatic Vessels (Flow chart 2.3)
when a pulpectomy is performed during the course of endodontic  Lymphatic vessels arise as small, blind, thin-walled vessels
treatment. Engaging the pulp with a barbed broach in the region  in the coronal region of the pulp and pass apically through
of the apex affords a better opportunity to remove the tissue intact 
middle and radicular regions of the pulp. They exit via one or
than does engaging the broach more coronally, where the pulp is 
more gelatinous and liable to tear. two large vessels through the apical foramen.

Lymphatic can be differentiated from small venules in following


Ground Substance ways:
The ground substance of the pulp is part of the system of •  Presence of discontinuities in vessel walls.
•  Absence of RBC in their lumina.
ground substance in the body. It is a structureless mass with
gel like consistency forming bulk of pulp. Chief components
of ground substance are: Regulation of Pulpal Blood Flow
• Glycosaminoglycans Walls of arterioles and venules are associated with smooth
• Glycoproteins muscles which are innervated by unmyelinated sympathetic
• Water. fibers. When stimulated by electrical stimulus (e.g.
epinephrine containing local anesthetics), muscle fibers
Functions of ground substance contract, decreasing the blood supply (Fig. 2.10).
•  Forms the bulk of the pulp.
•  Supports the cells.
•  A
  cts as medium for transport of nutrients from the vasculature 
Pulpal Response to Inflammation
to the cells and of metabolites from the cells to the vasculature. Whenever there is inflammatory reaction, there is release of
lysosomal enzymes which cause hydrolysis of collagen and
Water content of the pulp is approximately 90 percent. the release of kinins. These changes further lead to increased
Depolymerization by enzymes produced by micro- vascular permeability. The escaping fluid accumulates in the
organisms found in pulpal inflammation may change ground pulp interstitial space. Since space in the pulp is confined
substance of the pulp. Alexander et al in 1980 found that these so, pressure within the pulp chamber rises. In severe
enzymes can degrade the ground substance of the pulp by inflammation, lymphatics are closed resulting in continued
disrupting the glycosaminoglycan-collagen linkage. increase in fluid and pulp pressure which may result in pulp
Alterations in the composition of ground substance necrosis.
caused by age or disease interfere with metabolism, reduced
cellular function and irregularities in mineral deposition. Effect of Posture on Pulpal Flow
Thus, the ground substance plays an important role in health In normal upright posture, there is less pressure effect in the
and diseases of the pulp and dentin. structures of head. On lying down, the gravitational effect

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12 Textbook of Endodontics

Flow chart 2.1 Arterial supply of teeth

Flow chart 2.2 Venous drainage of teeth Flow chart 2.3 Lymphatic drainage of teeth

disappears; there is sudden increase in pulpal blood pressure Clinical Correlation


and thus corresponding rise in tissue pressure which leads to
pain in lying down position. • Temperature changes
Another factor contributing to elevated pulp pressure – Increase in temperature:
on reclining position is effect of posture on the activity of i. A 10° to 15°C increase in pulp temperature causes
sympathetic nervous system. When a person is upright, baro- arteriolar dilation and increase in intrapulpal
receptors maintain high degree of sympathetic stimulation pressure of 2.5 mm Hg/°C but it is transient in nature.
which leads to slight vasoconstriction. Lying down will reverse ii. The irreversible changes occur when vasodilation is
the effect leading to increase in blood flow to pulp. In other sustained by heating the pulp to 45°C for prolonged
words, lying down increases blood flow to the pulp by removal periods, resulting in persistent increase in pulp
of both gravitational and baroreceptor effect. pressure.

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Pulp and Periradicular Tissue 13

occurs whereas there would be less hemorrhage if pulp


is extirpated closer to apex of the tooth. This is because of
increase diameter of the vessels in the central part of the
pulp.
• Aging: With increasing age, pulp shows decrease in
vascularity, increase in fibrosis, narrowing of diameter
of blood vessels and decrease in circulation. Finally, the
circulation becomes impaired because of atherosclerotic
changes and calcifications in the blood vessel leading to
cell atrophy and cell death.

INNERVATION OF PULP (FLOW CHART 2.4)


Dental pulp is abundantly innervated by both sensory as well
as autonomic nerve fibers (Fig. 2.11). The nerve fibers enter
the pulp through apical foramen along with blood vessels.
After entering the pulp, the nerve bundles run coronally
and divide into smaller branches until a single axons form
a dense network near the pulp-dentin margin, termed as
plexus of Raschkow. Also the individual axons may branch
into numerous terminal filaments which enter the dentinal
Fig. 2.9 Diagram showing circulation of pulp tubules (Fig. 2.12).
Pain is complex phenomenon which is in form of the
evoked potential in the tooth that initiated signals to the
brain. Regardless of the nature of sensory stimulus, i.e.
mechanical, chemical or thermal, almost all afferent impulses
from the pulp result in pain. The dental pulp contains both
sensory and motor nerves. The sensory nerves are encased
in myelin sheath. The myelin sheath is largely composed of
fatty substances or lipids and proteins. Myelin appears to be
internal proliferation of Schwann cells. The unmyelinated
fibers are surrounded by single layer of Schwann cells, but
in these myelin spirals are absent. The unmyelinated nerves
are usually found in autonomic nervous system. The nerve
fibers are classified according to their diameter, velocity of
conduction and function. The fibers having largest diameter
are classified as A fibers while those having smallest diameter
are classified as C fibers (Fig. 2.13). The A delta fibers are
faster conducting and are responsible for localized, sharp
dentinal pain. The C fibers are slower conducting fibers and
are considered responsible for dull and throbbing pain. The
pain receptors transmit their message to the central nervous
system at different rates depending upon size, diameter and
Fig. 2.10 Diagram showing regulation of pulpal blood flow
coating of the nerves.
Thermal, chemical or mechanical stimuli stimulate C
– Decrease in temperature: It has been seen that at fibers resulting in dull, poorly localized and throbbing pain.
temperature lower than – 2°C, the pulp tissue exhibits Electrical pulp tester stimulates A delta fibers first because
immediate pulpal pathology like vascular engorgement of their lower threshold. As the intensity of stimulus is
and necrosis. increased along with A delta fibers, some of the C fibers also
• Local anesthetics: The effect of local anesthetics on pulp get stimulated resulting in strong unpleasant sensation.
vasculature is mainly due to presence of vasoconstrictor in
anesthetic solution. For example, presence of epinephrine Difference between A-delta and C-fibers
in local anesthetic causes decrease in blood flow in the A-delta fibers C-fibers
pulp which is due to stimulation of a-adrenergic receptors •  H
  igh conduction   •  Slow conduction
located in pulpal blood vessels.   velocity (6–30 m/sec)    velocity (0.5–2 m/sec)
• General anesthetics: General anesthetics have shown to •  Myelinated  •  U
  nmyelinated
produce effect on the velocity of blood flow in the pulp. •  Pain is well localized   •  Not well localized
• Endodontic therapy: During endodontic therapy, if only •  Low threshold  •  H
  igh threshold
some part of pulp is extirpated, the profuse bleeding •  Sharp, quick and pricking pain  •  Dull and lingering pain

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14 Textbook of Endodontics

Flow chart 2.4 Nerve supply of teeth

Fig. 2.11 Nerve supply of teeth

Fig. 2.13 Diagram showing nerve fibers of pulp

A-delta nerve fibers


•  Most of myelinated nerve fibers are A-delta fibers.
•  A
  t  the  odontoblastic  layer,  they  lose  their  myelin  sheath  and 
anastomose  forming  network  of  nerves  called  “Plexuses  of 
Raschkow”. They send free nerve endings into dentinal tubules.
•  D
  iameter  of  these  fibers  ranges  from  2–5  µm  and  conduction 
velocity 6–30 m/s.
•  These are large fibers with fast conduction velocities.
•  P
  ain  transmitted  through  these  fibers,  is  perceived  as  sharp, 
quick and momentary type.
Fig. 2.12 Diagram showing nerve density 
•  Pain disappears quickly on removal of stimulus.
at different areas of the tooth

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Pulp and Periradicular Tissue 15

C-nerve fibers
•  C  -nerve fibers are small unmediated and fine sensory afferent 
nerves.
•  They have slow conduction velocities and high threshold.
•  D  iameter  of  C-fibers  ranges  from  0.3–1.2  µm  and  conduction 
velocity 0.5–2 m/s.
•  T  hey are stimulated by intense cold or hot stimuli or mechanical 
stimulation.
•   Even  in  presence  of  radiographic  lesion,  C-fibers  can  show 
response because these are more resistant to hypoxic conditions 
or compromised blood flow as compared to A-delta fibers.
•  T  hese are responsible for pain occurring during instrumentation 
of teeth.

Eighty  percent  of  nerves  of  pulp  are  C  fibers  and  remaining  are 
A-delta fibers.

ANATOMY OF DENTAL PULP Fig. 2.14 Diagram showing pulp cavity

Pulp lies in the center of tooth and shapes itself to miniature


form of tooth. This space is called pulp cavity which is divided
into pulp chamber and root canal (Fig. 2.14).
In the anterior teeth, the pulp chamber gradually merges
into the root canal and this division becomes indistinct (Fig.
2.15). But in case of multirooted teeth, there is a single pulp
chamber and usually two to four root canals (Figs 2.16 and
2.17). As the external morphology of the tooth varies from
person to person, so does the internal morphology of crown
and the root. The change in pulp cavity anatomy results from
age, disease, trauma or any other irritation.

PULP CHAMBER
It reflects the external form of enamel at the time of eruption,
but anatomy is less sharply defined. The roof of pulp chamber
consists of dentin covering the pulp chamber occlusally.
Canal orifices are openings in the floor of pulp chamber
leading into the root canals (Fig. 2.18).
A specific stimulus such as caries leads to the formation of
irritation dentin. With time, pulp chamber shows reduction
Fig. 2.15 Diagram showing pulp anatomy of anterior tooth
in size as secondary or tertiary dentin is formed (Fig. 2.19).

ROOT CANAL
Root canal is that portion of pulp cavity which extends from
canal orifice to the apical foramen. The shape of root canal
varies with size, shape, number of the roots in different teeth.
A straight root canal throughout the entire length of root is
uncommon. Commonly curvature is found along its length
which can be gradual or sharp in nature (Fig. 2.20). In most
cases, numbers of root canals correspond to number of roots
but a root may have more than one canal.
According to Orban, shape of the canal to large extent is
determined by shape of the root. Root canals can be round,
tapering elliptical, broad, thin, etc.
‘Meyer’ stated that roots which are round and cone shaped
usually contain one canal but roots which are elliptical with
flat or concave surface frequently have more than one canals
(Fig. 2.21). Fig. 2.16 Diagram showing pulp cavity of posterior tooth

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16 Textbook of Endodontics

Fig. 2.20 Straight and curved root canal

Fig. 2.17 Radiographic appearance of pulp cavity

Fig. 2.21 Diagram showing relationship between shape 


of root and number of root canals

Change in shape and location of foramen is seen during


posteruptive phase due to functional forces (tongue pressure,
mesial drift) acting on the tooth which leads to cementum
resorption and deposition on the walls of foramen. This whole
process resulted in new foramen away from the apex.

The total volume of all permanent pulp organs is 0.38 cc with mean 
of 0.02 cc.

The apical foramen is an aperture at or near the apex of a


root through which nerves and blood vessels of the pulp enter
or leave the pulp cavity (Fig. 2.22). Normally, it is present
near the apex but sometimes, opening may be present on
the accessory and lateral canals of root surface forming the
Fig. 2.18 Diagram showing opening of canal orifices   accessory foramina.
in the pulp chamber In young newly erupted teeth, it is wide open but as the
root develops, apical foramen becomes narrower. The inner
surface of the apex becomes lined with the cementum which
may extend for a short distance into the root canal. Thus we
can say that DCJ does not necessarily occur at the apical end
of root, but may occur within the main root canal (Figs 2.23A
to C).
Multiple foramina are frequent phenomenon in
multirooted teeth. Majority of single rooted teeth have single
canal which terminate in a single foramina. Continuous
deposition of new layers of cementum causes change in
foramen anatomy.

Average size of maxillary teeth is 0.4 mm and of mandibular teeth 
is 0.3 mm.

Accessory canals: They are lateral branches of the main


canal that form a communication between the pulp and
Fig. 2.19 Reduction in size of pulp cavity because 
periodontium. Accessory canals contain connective tissue
of formation of secondary and tertiary dentin and vessels and can be seen anywhere from furcation to apex

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Pulp and Periradicular Tissue 17

tissue may develop around it making a lateral canal from


radicular pulp.

FUNCTIONS OF PULP
The pulp lives for dentin and the dentin lives by the grace of
the pulp.

Pulp performs four basic functions


1.  Formation of dentin 
2.  Nutrition of dentin
3.  Innervation of tooth
4.  Defense of tooth.

1. Formation of dentin: It is the primary function of pulp


both in sequence and importance. Odontoblasts are
differentiated from the dental papilla adjacent to the
basement membrane of enamel organ which later deposits
dentin.
Fig. 2.22 Apical foramen through which nerves and blood vessels  Pulp primarily helps in:
enter or leave the pulp cavity •  Synthesis and secretion of organic matrix.
•  I  nitial  transport  of  inorganic  components  to  newly  formed 
matrix.
•  Creating an environment favorable for matrix mineralization.

2. Nutrition of dentin: Nutrients exchange across capillaries


into the pulp interstitial fluid. This fluid travels into the
dentin through the network of tubules formed by the
odontoblasts to contain their processes.
A B C 3. Innervation of tooth: Through the nervous system, pulp
transmits sensations mediated through enamel or dentin
Figs 2.23A to C Diagram showing cementodentinal junction to the higher nerve centers. Pulp transmits pain and senses
of temperature and touch.
Teeth are supplied by the maxillary and mandibular
divisions of the trigeminal (V) nerve. The dental nerve
divides into multiple branches as it traverses the bone.
At the apical alveolar plate, the A-delta and C axons enter
the periodontal ligament. Then the nerves enter the apical
foramina and unite to form common pulpal nerve. This
nerve proceeds coronally with afferent blood vessels and
latter divides into cuspal nerves at the coronal portion of
the tooth. On approaching the cell free zone of pulp, a
mixture of myelinated and nonmyelinated axons branch
repeatedly, forming a overlapping network of nerves, the
plexus of Raschkow. The nerve twigs either end among the
stroma of the pulp or terminate among the odontoblasts.
Fig. 2.24 Diagram showing accessory and lateral canals 4. Defense of tooth: Odontoblasts form dentin in response
to injury particularly when original dentin thickness has
been compromised as seen in caries, attrition, trauma or
but tend to be more common in apical third and in posterior restorative procedure. Odontoblasts also have the ability
teeth (Fig. 2.24). to form dentin at sites when dentin continuity has been
In other words, more apical and farther posterior the lost.
tooth, the more likely the accessory canals will be present. The formation of reparative dentin and sclerotic dentin
Exact mechanism of their formation is not known but they are defense mechanisms of the tooth.
occur in areas of premature loss of root sheath cells because Pulp also has the ability to elicit an inflammatory and
these cells induce formation of odontoblasts. They also immunologic response in an attempt to neutralize or
develop where developing root encounters a blood vessel. If eliminate invasion of dentin by caries causing micro-
vessel is located in this area, where dentin is forming; hard organisms and their by products.

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18 Textbook of Endodontics

AGE CHANGES IN THE PULP • Reduction in number of blood vessels, displaying


arteriosclerotic changes.
Pulp like other connective tissues, undergoes changes with • Earlier it was believed that collagen content increases with
time. These changes can be natural or may be result of injury age, but recent studies have found that collagen stabilizes
such as caries, trauma or restorative dental procedure. after completion of tooth formation. With age, collagen
Regardless of the cause, the pulp shows changes in forms bundle making its presence more apparent.
appearance (morphogenic) and functions (physiologic).
Physiologic Changes
Morphologic Changes
• Decrease in dentin permeability provides protective
• Continued deposition of intratubular dentin results in environment for the pulp.
reduction of tubule diameter. • Possibility of reduced ability of pulp to react to the irritants
• Reduction in pulp volume due to increase in secondary and repair itself.
dentin deposition (Fig. 2.25). Due to this root canal
appears very thin or seems to be totally obliterated.
• Presence of dystrophic calcification and pulp stones (Fig. PULPAL CALCIFICATIONS/
2.26). PULP STONES/DENTICLES
• Decrease in the number of pulp cells. Cells density
decreases to 50 percent by the age of 70. Pulp stones are nodular calcified masses appearing in either
• Degeneration and loss of myelinated and unmyelinated coronal and radicular pulp or both of these. The larger
axons. This results in decrease in sensitivity. calcifications are called denticles. It is seen that pulp stones
are present in at least 50 percent of teeth. Pulp stones may
form either due to some injury or natural phenomenon (See
Fig. 2.28).
Sometimes denticles become extremely large, almost
obliterating the pulp chamber or the root canal.
Pulp stones may be classified: (1) according to structure
(2) according to size (3) according to location.

Classification of pulp stone


•  According to structure 
–  True
  –  False
•  According to size
  –  Fine 
  –  Diffuse
•  According to location 
  –  Free 
  –  Attached
  –  Embedded
Fig. 2.25 Reduction in size of pulp volume

Fig. 2.26 Diagram showing pulp stones and reduced 


size of pulp cavity Fig. 2.27 Diagram showing true denticle

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Pulp and Periradicular Tissue 19

According to Structure • Embedded denticles are entirely surrounded by dentin.


Calcifications, are seen more in older pulps. This may be
They can be classified into true and false denticles. The due to increase in extent of cross linking between collagen
difference between two is only morphologic and not chemical. molecules.

True Denticle (Fig. 2.27) Clinical Significance of Pulp Stones


A true denticle is made up of dentin and is lined by
odontoblasts. These are rare and are usually located close Presence of pulp stones may alter the internal anatomy of the
to apical foramen. Development of true denticle is caused pulp cavity, making the access opening of tooth difficult. They
by inclusions of remnants of epithelial root sheath within may deflect or engage the tip of endodontic instrument. Since
the pulp. These epithelial remnants induce the cells of pulp the pulp stone can originate in response to chronic irritation,
to differentiate into odontoblast which form dentin masses the pulp chamber which appears to have diffuse and obscure
called true pulp stones. outline may represent large number of irregular pulp stones
which may indicate chronic irritation of the pulp.
False Denticles
Appear as concentric layers of calcified tissue. These appear CALCIFIC METAMORPHOSIS
within bundles of collagen fibers. They may arise around Calcific metamorphosis is defined as a pulpal response to
vessels. Calcification of thrombi in blood vessels called trauma that is characterized by deposition of hard tissue
phleboliths, may also serve as nidi for false denticles. All within the root canal space.
denticles begin as small nodules but increase in size by Calcific metamorphosis occurs commonly in young adults
incremental growth on their surface. because of trauma. It is evident usually in the anterior region
of the mouth and can partially or totally obliterate the canal
According to Size space radiographically.
The clinical picture of calcific metamorphosis is a tooth
According to size, there are fine and diffuse mineralizations.
with darker in hue than the adjacent teeth and exhibits a dark
Diffuse calcifications are also known as fibrillar or linear
yellow color because of decrease in translucency from greater
calcifications because of their longitudinal orientation. They
thickness of dentin under the enamel.
are found more frequently in the root canals, but can also be
The radiographic appearance of calcific metamorphosis
present in the coronal portion of the pulp. They are aligned
is partial or total obliteration of the pulp canal space with a
closely to the blood vessels, nerves or collagen bundles.
normal periodontal membrane space and intact lamina dura.
The mechanism of hard tissue formation during calcific
According to Location (Fig. 2.28) metamorphosis is characterized by an osteoid tissue which
• Free denticles are entirely surrounded by pulp tissue. is produced by the odontoblasts at the periphery of pulp
• Attached denticles are partially fused to the dentin. space or can be produced by undifferentiated pulpal cells
that undergo differentiation as a result of the traumatic
injury. This results in a simultaneous deposition of a dentin-
like tissue along the periphery of the pulp space and within
the pulp space proper. These tissues can eventually fuse with
one another, producing the radiographic appearance of a
root canal space that has become rapidly and completely
calcified.
The management of canals with calcific metamorphosis
is similar to the management of pulpal spaces with any form
of calcification.

PERIRADICULAR TISSUE (FIG. 2.29)


Periradicular tissue consists of cementum, periodontal
ligament and alveolar bone.

Cementum
Cementum can be defined as hard, avascular connective
tissue that covers the roots of the teeth. It is light yellow in
color and can be differentiated from enamel by its darker hue
and lack of luster. It is very permeable to dyes and chemical
Fig. 2.28 Free, attached and embedded pulp stones agents, from the pulp canal and the external root surface.

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20 Textbook of Endodontics

Fig. 2.29 Diagram showing periradicular tissue Fig. 2.30 Principal fibers of periodontal ligament

Types Periodontal Fibers


There are two main types of root cementum: The most important component of periodontal ligament is
1. Acellular (Primary) principal fibers. These fibers are composed mainly of collagen
2. Cellular (Secondary). Type I. Apart from the principal fibers, oxytalan and elastic
fibers are also present. The principal fibers are present in six
Acellular cementum
arrangements.
• Covers the cervical third of the root.
• Forms before tooth reaches the occlusal plane. Horizontal group: These fibers are arranged horizontally
• It does not contain cells. emerging from alveolar bone and attached to the root
• Thickness varies between 30 and 230 µm. cementum.
• Abundance of Sharpey’s fibers. Alveolar crest group: These fibers arise from the alveolar
• Main function is anchorage. crest in fan like manner and attach to the root cementum.
Cellular cementum These fibers prevent the extrusion of the tooth.
• Forms after tooth reaches the occlusal plane. Oblique fibers: These fibers make the largest group in
• It contains cells. periodontal ligament. They extend from cementum to bone
• Less calcified than acellular cementum. obliquely. They bear the occlusal forces and transmit them to
• Sharpey’s fibers are present in lesser number as compared alveolar bone.
to acellular cementum.
• Mainly found in apical third and interradicular region. Transseptal fibers: These fibers run from the cementum of
• Main function is adaptation. one tooth to the cementum of another tooth crossing over the
alveolar crest.
Periodontal Ligament (Fig. 2.30) Apical fibers: These fibers are present around the root apex.

Periodontal ligament is a unique structure as it forms a link Interradicular fibers: These fibers are present in furcation
between alveolar bone and cementum. It is continuous areas of multirooted teeth.
with connective tissue of the gingiva and communicates
with the marrow spaces through vascular channels in the Cells
bone. Periodontal ligament houses the fibers, cells and other The cells present in periodontal ligament are:
structural elements like blood vessels and nerves. • Fibroblast
Periodontal ligament comprises of the following • Macrophages
components: • Mast cells
• Periodontal fibers • Neutrophils
• Cells • Lymphocytes
• Blood vessels • Plasma cells
• Nerves. • Epithelial cells rests of Mallassez.

vip.persianss.ir
Pulp and Periradicular Tissue 21

Nerve Fibers
The nerve fibers present in periodontal ligament, are either of
myelinated or non-myelinated type.

Blood Vessels
The periodontal ligament receives blood supply from the
gingival, alveolar and apical vessels.

Functions
Supportive: Tooth is supported and suspended in alveolar
socket with the help of periodontal ligament.
Nutritive: Periodontal ligament has very rich blood supply. So,
it supplies nutrients to adjoining structures like cementum,
bone and gingiva via blood vessels. It also provides lymphatic
drainage.
Protective: These fibers perform the function of protection Fig. 2.31 Radiographic appearance of alveolar bone
absorbing the occlusal forces and transmitting to the
underlying alveolar bone.
Formative: The cells of PDL help in formation of surrounding play an important role in metabolism of bone. In healthy
structures like alveolar bone and cementum. conditions the crest of alveolar bone lies approximately 2 to 3
mm apical to the cementoenamel junction but it comes to lie
Resorptive: The resorptive function is also accomplished more apically in periodontal diseases. In periapical diseases,
with the cells like osteoclasts, cementoclasts and fibroblasts it gets resorbed easily.
provided by periodontal ligament.

QUESTION
Alveolar Bone (Fig. 2.31)
1. Write short notes on:
Bone is specialized connective tissue which comprises of • Zones of dental pulp
inorganic phases that is very well designed for its role as load • Odontoblasts
bearing structure of the body. • Accessory and lateral canals
• Innervation of pulp
• Functions of pulp
Cells • Age changes in the pulp
Cells present in bone are: • Pulp stones/denticles/pulpal calcifications
• Osteocytes
• Osteoblasts
• Osteoclasts.
BIBLIOGRAPHY
1. Bernick S. Differences in nerve distribution between erupted
Intercellular Matrix and non-erupted human teeth. J Dent Res. 1964;43:406.
Bone consists of two-third inorganic matter and one-third 2. Heverass KJ. Pulpal, microvascular, and tissue pressure. J Dent
Res. 1985;64:585.
organic matter. Inorganic matter is composed mainly of
3. Johnsen DC. Innervations of teeth: qualitative, quantitative
minerals calcium and phosphate along with hydroxyapatite,
and developmental assessment. J Dent Res. 1985;64:555.
carbonate, citrate, etc. while organic matrix is composed
4. Kim S. Regulation of pulpal blood flow. Dent Res. 1983;64:590.
mainly of collagen Type I (90%).
5. Linde A. The extracellular matrix of the dental pulp and dentin.
Bone consists of two plates of compact bone separated by J Dent Res. 1985;64:523.
spongy bone in between. In some area, there is no spongy 6. Mjör IA. Dentin-predentin complex and its permeability:
bone. The spaces between trabeculae of spongy bone are pathology and treatment overview. J Dent Res. 1985;64:621.
filled with marrow which consists of hemopoietic tissue 7. Pashley DH. Dentin-predentin complex and its permeability:
in early life and fatty tissue latter in life. Bone is a dynamic Physiologic overview. J Dent Res. 1985;64:613.
tissue continuously forming and resorbing in response to 8. Ruch JV. Odontoblast differentiation and the formation of
functional needs. Both local as well as hormonal factors odontoblast layer. J Dent Res. 1985;64:489.

vip.persianss.ir
Pathologies of  
Pulp and Periapex 3
  Pulp Pathologies   Internal Resorption   Acute Apical Abscess
  Etiology of Pulpal Diseases   Pulp Necrosis   Phoenix Abscess/Recrudescent 
  Progression of Pulpal Pathologies   Pulp Degeneration Abscess
  Diagnostic Aids for Pulpal    Periradicular Pathologies   Periapical Granuloma
Pathology   Periapex Pathologies   Radicular Cyst/Cystic Apical 
  Classification of Pulpal Pathologies   Etiology of Periradicular Diseases Periodontitis
  Barodontalgia/Aerodontalgia   Diagnosis of Periradicular     Chronic Alveolar Abscess
  Reversible Pulpitis/Hyperemia/  Pathologies   Persistent Apical Periodontitis
Hyperactive Pulpalgia   Classification of Periradicular    External Root Resorption
  Irreversible Pulpitis Pathologies   Diseases of Periradicular Tissue of 
  Chronic Pulpitis   Acute Apical Periodontitis Nonendodontic Origin

PULP PATHOLOGIES
INTRODUCTION
Dental pulp consists of vascular connective tissue contained
within the rigid dentin walls. It is the principal source of pain
in oral cavity and also a major site of attention in endodontics
and restorative procedures. Thus the knowledge to pulp is
essential not only for providing dental treatment, but also to
know the rationale behind the treatment provided.

Important features of pulp (Fig. 3.1)


•  Pulp is located deep within the tooth, so defies visualization.
•  It gives radiographic appearance as radiolucent line.
•  N
  ormal pulp is a coherent soft tissue, dependent on its normal 
hard  dentin  shell  for  protection. Therefore  once  exposed,  it  is 
extremely  sensitive  to  contact  and  temperature  but  this  pain 
does  not  last  for  more  than  1-2  seconds  after  the  stimulus  is 
removed.
•  P
  ulp  is  totally  surrounded  by  dentin  which  limits  the  area  for  Fig. 3.1 Relation of pulp with its surrounding structures
expansion and restricts the pulp’s ability to tolerate edema.
•  P
  ulp  has  almost  total  lack  of  collateral  circulation,  which 
severely  limits  its  ability  to  cope  with  bacteria,  necrotic  tissue 
and inflammation.
•  P
  ulp consists of unique cells, the odontoblasts, as well as cells 
that can differentiate into hard-tissue secreting cells. These cells 
form  dentin  and/or  irritation  dentin  in  an  attempt  to  protect 
pulp from injury (Fig. 3.2).
•  P
  ulpal responses are unpredictable. “Some pulps die if you look 
at them cross eyes, while others would not die even if you hit 
them with an axe”.
•  C
  orrelation of clinical signs and symptoms with corresponding 
specific histological picture is often difficult.
Fig. 3.2 Formation of irritation dentin

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Pathologies of Pulp and Periapex 23

ETIOLOGY OF PULPAL DISEASES • Anachoresis (Process by which microorganisms get


carried by the bloodstream from another source
I. Etiology of pulpal diseases can be broadly classified into: localize on inflamed tissue).
1. Physical 2. Traumatic
a. Mechanical • Acute trauma like fracture, luxation or avulsion of
i. Trauma tooth (Fig. 3.6).
• Acute trauma like fracture, or avulsion of tooth. • Chronic trauma including parafunctional habits like
• Iatrogenic dental procedures. bruxism.
ii. Pathologic wear like attrition, abrasion, etc. 3. Iatrogenic (Pulp inflammation for which the dentist’s
iii. Barodontalgia due to barometric changes. own procedures are responsible is designated as
b. Thermal dentistogenic pulpitis). Various iatrogenic causes of
• Heat generated by cutting procedures pulpal damage can be:
• Heat from restorative procedures • Thermal changes generated by cutting procedures,
• Heat generated from electrosurgical procedures during restorative procedures, bleaching of enamel,
• Frictional heat from polishing of restorations. electrosurgical procedures, laser beam, etc. can
2. Chemical cause severe damage to the pulp if not controlled.
• Acids from erosion • Orthodontic movement
• Use of chemicals like monomers, liners, bases, • Periodontal curettage
phosphoric acid, or use of cavity desiccants like • Periapical curettage
alcohol. • Use of chemicals like temporary and permanent
3. Bacterial fillings, liners, bases and use of cavity desiccants
• Caries such as alcohol.
• Microleakage around a restoration
• Periodontal pocket and abscess
• Anachoresis
II. WEIN classified causes of pulpal inflammation, necrosis
or dystrophy in a logical sequence beginning with the
most frequent irritant, microorganisms.
1. Bacterial: Most common cause of pulpal injury is
bacteria or their products which may enter the pulp
through a break in dentin either from:
• Caries (Figs 3.3 and 3.4)
• Accidental exposure
• Fracture
• Percolation around a restoration
• Extension of infection from gingival sulcus
• Periodontal pocket and abscess (Fig. 3.5)

Fig. 3.4 Radiograph showing carious exposure of pulp in first molar

Fig. 3.5 Periodontal disease causing pulpal inflammation; (1) Dental 


Fig. 3.3 Tooth decay causing pulpal inflammation plaque/calculus (2) Periodontal disease (3) Pulpal disease

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24 Textbook of Endodontics

Fig. 3.8 Response of pulp to various irritants


Fig. 3.6 Fracture of tooth can also cause pulpal inflammation

A B C D
Figs 3.9A to D Gradual response of pulp to microbial invasion

causes little or no pulpal inflammation, whereas extensive


operative procedures may lead to severe pulpal inflammation.
Fig. 3.7 Resorption of tooth
Depending on condition of pulp, severity and duration
of irritant, host response, pulp may respond from mild
inflammation to pulp necrosis (Fig. 3.8).
4. Idiopathic
These changes may not be accompanied by pain and thus
• Aging
may proceed unnoticed.
• Resorption; internal or external (Fig. 3.7)
Pulpal reaction to microbial irritation (Figs 3.9A to D)
Radiation injury to pulp
Pulp  cells  exposed  to  ionizing  radiation  may  become  necrotic,  Carious enamel and dentin contain numerous bacteria 
show vascular damage and the interference in mitosis of cells.  ↓
•  I  rradiation  also  affects  the  salivary  glands  causing  decreased  Bacteria penetrate in deeper layers of carious dentin
salivary flow, thereby increased predisposition to dental caries  ↓
and pulpal involvement.  Pulp is affected before actual invasion of bacteria via  
•  R  adiation  damage  to  teeth  depends  on  dose,  source,  type  of  their toxic byproducts 
radiation,  exposure  factor  and  stage  of  tooth  development  at  ↓
the time of irradiation. Byproducts cause local chronic cell infiltration 

When actual pulp exposure occurs, pulp tissue gets locally 
PROGRESSION OF PULPAL PATHOLOGIES infiltrated by PMNs to form an area of liquefaction necrosis  
Pulp reacts to above-mentioned irritants as do other at the site of exposure 
connective tissues. Degree of inflammation is proportional to ↓
intensity and severity of tissue damage. For example, slight Eventually necrosis spreads all across the pulp and periapical  
tissue resulting in severe inflammatory lesion
irritation like incipient caries or shallow tooth preparation

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Pathologies of Pulp and Periapex 25

Pulp Inflammation and its Sequel


The traditional theory which explained the pulpal
inflammation and its sequel was referred as strangulation
theory. Strangulation theory is no longer accepted and a
current theory explains the sequel of pulpal inflammation.

Strangulation Theory
It says that on irritation, there is local inflammation in pulp,
which results in vasodilation, increased capillary pressure
and permeability. These result in increased filtration from
capillaries into tissues, thus increased tissue pressure. By this,
thin vessel walls get compressed resulting in decreased blood
flow and increased venous pressure. This results in vicious
cycle, because increase in venous pressure further increase
capillary pressure. Consequently, choking/strangulation
of pulpal blood vessels occur because of increased tissue
pressure. This results in ischemia and further necrosis.
Fig. 3.10 Infectious sequelae of pulpitis
Current Theory
Many studies have shown that increase of pressure in one
area does not affect the other areas of pulp. Therefore local
inflammation in pulp results in increased tissue pressure in
inflamed area and not the entire pulp cavity.
It is seen that injury to coronal pulp results in local
disturbance, but if injury is severe, it results in complete stasis
of blood vessels in and near injured area. Net absorption of
fluid into capillaries in adjacent uninflammed area results
in increased lymphatic drainage thus keeping the pulpal
volume almost constant.

Limited increase in pressure within affected pulpal area is


explained by following mechanism:
•  I  ncreased  pressure  in  inflamed  area  favors  net  absorption  of 
interstitial fluids from adjacent capillaries in uninflamed tissues.
•  I  ncreased  interstitial  tissue  pressure  lowers  the  transcapillary 
hydrostatic pressure difference, thus opposes further filtration.
•  I  ncreased  interstitial  fluid  pressure  increases  lymphatic 
drainage.
•  B
  reak  in  endothelium  of  pulpal  capillaries  facilitate  exchange 
mechanism.

Infectious sequelae of pulpitis include apical periodontitis,


Fig. 3.11 Spread of pulpal inflammation to surrounding tissues
periapical abscess/cellulitis, and osteomyelitis of the jaw
(Fig. 3.10). Spread from maxillary teeth may cause purulent
sinusitis, meningitis, brain abscess, orbital cellulitis, and DIAGNOSTIC AIDS FOR PULPAL PATHOLOGY
cavernous sinus thrombosis. Spread from mandibular
teeth may cause Ludwig’s angina, parapharyngeal abscess, • Subjective symptoms: Most common being pain.
mediastinitis, pericarditis and empyema (Fig. 3.11). • Objective symptoms:
1. Visual and tactile inspection—3Cs
POINTS TO REMEMBER i. Color
Degree and nature of inflammatory response caused by microbial 
ii. Contour
irritants depends upon iii. Consistency
•  Host resistance 2. Thermal tests
•  Virulence of microorganisms i. Heat tests—isolation of tooth: Use of
•  Duration of the agent – Warm air
•  Lymph drainage – Hot water
•  Amount of circulation in the affected area – Hot burnisher
•  Opportunity of release of inflammatory fluids – Hot gutta-percha stick

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26 Textbook of Endodontics

ii. Cold tests: b. Acute pulpalgia


– Ethyl chloride spray • Incipient
– Ice pencils • Moderate
– CO2 snow (temperature –78°C) • Advanced
3. Electrical pulp testing c. Chronic pulpalgia
4. Radiographs d. Hyperplastic pulpitis
5. Anesthetic tests e. Pulp necrosis
6. Test cavity
Recent advances in diagnostic aids for pulpal pathology Retrogressive Changes
include: a. Atrophic papulosis
• Laser Doppler flowmetry b. Calcific papulosis
• Liquid crystal testing
• Hughes probeye camera Grossman’s Clinical Classification
• Infrared thermography 1. Pulpitis: Inflammatory disease of dental pulp
• Thermocouples a. Reversible papulosis
• Pulpoximetry i. Symptomatic (Acute)
• Dual wavelength spectrophotometry ii. Asymptomatic (Chronic)
• Plethysmography b. Irreversible pulpitis
• Xenon-133 radioisotopes i. Acute
a. Abnormally responsive to cold
CLASSIFICATION OF PULPAL PATHOLOGIES b. Abnormally responsive to heat
ii. Chronic
Baume’s Classification a. Asymptomatic with pulp exposure
Based on clinical symptoms: b. Hyperplastic pulpitis
• Asymptomatic, vital pulp which has been injured or c. Internal resorption
involved by deep caries for which pulp capping may be 2. Pulp degeneration
done. a. Calcific (Radiographic diagnosis)
• Pulp with history of pain which is amenable to b. Other (Histopathological diagnosis)
pharmacotherapy. 3. Necrosis
• Pulp indicated for extirpation and immediate root filling.
• Necrosed pulp involving infection of radicular dentin
POINTS TO REMEMBER
accessible to antiseptic root canal therapy. A  normal pulp  gives  moderate  response  to  pulp  test  and  this 
response subsides when the stimulus is removed. The tooth is free 
Seltzer and Bender’s Classification of  spontaneous  pain.  Radiograph  shows  an  intact  lamina  dura, 
absence  of  any  pulpal  abnormality,  calcifications,  and  resorption 
Based on clinical tests and histological diagnosis: (Fig. 3.12).
  Pulpitis  is  an  inflammation  of  the  dental  pulp  resulting  from 
Treatable without Pulp Extirpation and untreated  caries,  trauma,  or  multiple  restorations.  Its  principal 
symptom  is  pain.  Diagnosis  is  based  on  clinical  finding  and  is 
Endodontic Treatment confirmed in X-ray.
• Intact uninflamed pulp
• Transition stage
• Atrophic pulp
• Acute pulpitis
• Chronic partial pulpitis without necrosis.

Untreatable without Pulp Extirpation and


Endodontic Treatment
• Chronic partial pulpitis with necrosis
• Chronic total pulpitis
• Total pulp necrosis

Ingle’s Classification
Inflammatory Changes
a. Hyperreactive pulpalgia
• Hypersensitivity Fig. 3.12 Radiographic picture of normal teeth shows intact  
• Hyperemia. lamina dura, absence of pulp pathology

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Pathologies of Pulp and Periapex 27

BARODONTALGIA/AERODONTALGIA
It is pain experienced in a recently restored tooth during
low atmospheric pressure. Pain is experienced either
during ascent or descent. Chronic pulpitis which appears
asymptomatic in normal conditions, may also manifests as
pain at high altitude because of low pressure. It is generally
seen in altitude over 5000 feet but more likely to be observed
in 10,000 feet and above.

Rauch classified barodontalgia according to chief complaint:


Class I: In acute pulpitis, sharp pain occurs for a moment on ascent.
Class II: In chronic pulpitis, dull throbbing pain occurs on ascent.
Class III:  In  necrotic  pulp,  dull  throbbing  pain  occurs  on  descent 
but it is asymptomatic on ascent.
Class IV:  In  periapical  cyst  or  abscess,  severe  and  persistent  pain 
occurs with both ascent and descent. Fig. 3.13 Insertion of deep restoration causing pulp inflammation

REVERSIBLE PULPITIS/HYPEREMIA/ Symptoms


HYPERACTIVE PULPALGIA
• Reversible pulpitis is characterized by sharp pain lasting
This is the first stage where the pulp is symptomatic. There for a moment, commonly caused by cold stimuli.
is a sharp hypersensitive response to cold, but the pain • Pain does not occur spontaneously and does not continue
subsides when stimulus is removed. The patient may describe when irritant is removed.
symptoms of momentary pain and is unable to locate the • It may result from incipient caries and is resolved on
source of pain. This stage can last for month or years. removal of caries and proper restoration of tooth.

Definition Histopathology
Reversible pulpitis is mild-to-moderate inflammatory Reversible pulpitis may range from hyperemia to mild to
condition of the pulp caused by noxious stimuli in which moderate inflammatory changes limited to area of involved
the pulp is capable of returning to the normal state following dentinal tubules. It shows:
removal of stimuli. • Increased blood volume of pulp associated with increased
It is an indication of peripheral A delta fiber stimulation. intrapulpal pressure.
Determination of reversibility is the clinical judgment which • Edema of tissue.
is influenced by history of patient and clinical evaluation. • White cell infiltration.
• Reparative dentin formation.
Etiology
Pulpal irritation to external stimuli is related to dentin Diagnosis
permeability. Under normal circumstances, enamel and Patient’s symptoms and clinical tests.
cementum act as impermeable barrier to block the patency • Pain: It is sharp but of brief duration, ceasing when irritant
of dentinal tubules at dentinoenamel junction or dentino- is removed. It is usually caused by cold, sweet and sour
cemental junction. stimuli.
When caries and operative procedures interrupt this • Visual examination and history: May reveal caries,
natural barrier, dentinal tubules become permeable. So traumatic occlusion and undetected fracture.
inflammation can be caused by any agent which is capable of • Radiographs:
injuring pulp. It can be: – Show normal PDL and lamina dura, in other words
• Trauma normal periapical tissue.
– Accident or occlusal trauma – Depth of caries or restoration may be evident (Fig.
• Thermal injury 3.14).
– While tooth preparation with dull bur without coolant. • Percussion test: Shows negative response, i.e. tooth is
– Overheating during polishing of a restoration. normal to percussion and palpation without any mobility.
– Keeping bur in contact with teeth too long. • Vitality test: Pulp responds readily to cold stimuli. Electric
• Chemical stimulus—like sweet or sour foodstuff pulp tester requires less current to cause pain.
• Following insertion of a deep restoration (Fig. 3.13),
patient often complains of mild sensitivity to temperature
changes, especially cold. Such sensitivity may last for
Treatment
2 to 3 days or a week or longer but gradually, it subsides. • The best treatment of reversible pulpitis is prevention.
This sensitivity is symptomatic of reversible pulpitis. • No endodontic treatment is needed for this condition.

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28 Textbook of Endodontics

• Chemical, thermal, mechanical injuries of pulp may


induce pulp inflammation
• Reversible pulpitis when left untreated deteriorates into
irreversible pulpitis.

Symptoms
• A rapid onset of pain, which can be caused by sudden
temperature change, sweet or acidic food. Pain remains
even after removal of stimulus.
• Pain can be spontaneous in nature which is sharp,
piercing, intermittent or continuous in nature.
• Pain exacerbated on bending down or lying down due to
change in intrapulpal pressure.
• Presence of referred pain.
• In later stages, pain is severe, boring, throbbing in nature
Fig. 3.14 Radiograph showing deep restoration approximating the  which increases with hot stimulus. Pain is so severe that it
pulp in mandibular molars keeps the patient awake in night. The relief of pain can be
simply done by use of cold water. The patient may report
dental office with jar of ice water.
• Usually, a sedative dressing is placed, followed by per-
manent restoration when symptoms completely subside.
Diagnosis
• Periodic care to prevent caries, desensitization of hyper-
sensitive teeth and use of cavity varnish or base before • Visual examination and history: Examination of involved
insertion of restoration is recommended. tooth may reveal previous symptoms. On inspection,
• If pain persists despite of proper treatment, pulpal one may see deep cavity involving pulp (Fig. 3.15) or
inflammation should be considered as irreversible and it secondary caries under restorations (Fig. 3.16).
should be treated by pulp extirpation. • Radiographic findings:
– May show depth and extent of caries (Figs 3.17 and
POINTS TO REMEMBER 3.18).
Threshold to pain decreases in reversible pulpitis. It may be – Periapical area shows normal appearance but a slight
attributed to: widening may be evident in advanced stages of pulpitis.
•  R
  elease  of  mediators  (endogenous  allogenic  agents)  which  • Percussion: Tooth is tender on percussion (due to increased
initiate or lower the threshold of excitability. intrapulpal pressure as a result of exudative inflammatory
•  N
  europeptides  released  from  unmyelinated  C-fibers  mediate  tissue) (Fig. 3.19).
neurogenic  inflammation  which  results  in  hyperexcitability  of  • Vitality tests:
nerve endings.
– Thermal test: Hyperalgesic pulp responds more readily
to cold stimulation than for normal tooth, pain may
POINTS TO REMEMBER persist even after removal of irritant.
Reversible pulpitis
•  M
  ild  to  moderate  inflammatory  condition  in  which  the  pulp  is  Differences between transudate and exudate
capable  of  returning  to  the  normal  state  following  removal  of  Feature Transudate Exudate
stimuli. 
Definition Filtrate of blood plasma  Edema of inflamed 
•  Indicate peripheral A delta fiber stimulation.
but no changes in endo- tissue with increased 
•  Sharp pain lasting for a moment, commonly caused by cold. 
thelial permeability vascular permeability
•  Best treatment is prevention.
Character Noninflammatory edema Inflammatory edema
pH Greater than 7.3 Less than 7.3
IRREVERSIBLE PULPITIS
Specific gravity < 1.015 > 1.018
Definition P
  rotein  •  Less than 3 g/dL (low) •   More than 3 g/dL 
content (high)
“It is a persistent inflammatory condition of the pulp,
symptomatic or asymptomatic, caused by a noxious •   No tendency to  •   Tendency to 
stimulus”. It has both acute and chronic stages in pulp. coagulate coagulate
Cells Few cells Many inflammatory  
Etiology cells

• Most common cause of pulpitis is bacterial involvement of As the pulpal inflammation progresses, heat
pulp through caries intensifies the response because it has expansible effect

vip.persianss.ir
Pathologies of Pulp and Periapex 29

Fig. 3.15 Tooth decay causing pulpitis Fig. 3.18 Radiograph showing carious exposure of pulp in second 


premolar and first molar

Fig. 3.16 Secondary caries under restoration Fig. 3.19 Increased intrapulpal pressure causing pulpal pain

– Electric test: Less current is required in initial stages. As


tissue becomes more necrotic, more current is required
to generate the response.

Treatment
Pulpectomy, i.e. root canal treatment.

POINTS TO REMEMBER
A clinical guide as given by Carrotte in 2003 to determine the status 
of dental pulp in irreversible pulpitis.
•  A    history of spontaneous bouts of pain which may last from a few 
seconds to several hours
•  H   ot  and  cold  fluids  exacerbating  the  pain.  In  the  latter  stages, 
heat will be more significant and cold will relieve the pain
Fig. 3.17 Radiograph showing secondary caries under   •  P   ain  radiating  initially  but  once  the  periodontal  ligament  has 
restored first molar become involved; the pain will be more localized by the patient
•   The  tooth  may  become  tender  to  percussion,  once  the 
on blood vessels. Cold tends to relieve pain because of inflammation has spread to the periodontal ligament
•  A    radiographically visible widening of the periodontal ligament 
its contractile effect on vessels, reducing the intrapulpal
may be seen.
pressure.

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30 Textbook of Endodontics

at point of exposure (Fig. 3.20). Abscess is surrounded


POINTS TO REMEMBER by granulomatous tissue. This condition is also known as
Irreversible pulpitis pulpal granuloma.
•  P  ersistent  inflammatory  condition  of  the  pulp,  symptomatic  or 
asymptomatic, caused by a noxious stimulus.  • Hyperplastic form is overgrowth of granulomatous tissue
•  Pain can be spontaneous in nature. into carious cavity (Fig. 3.21).
•  Pain is sharp, piercing, intermittent or continuous. • Closed form of chronic pulpitis may occur from operative
•  Pain exacerbated on lying down. procedures, excessive orthodontic forces, trauma or
•  I  n later stages, pain is severe, boring, throbbing in nature which  periodontal lesions. Here carious lesion is absent.
increases with hot stimulus. 
•  Relief of pain can happen by use of cold water. 
•  Patient may report dental office with jar of ice water.

CHRONIC PULPITIS
It is an inflammatory response of pulpal connective tissue
to an irritant. Here pain is absent because of diminished
exudative inflammatory activity and corresponding decrease
in intrapulpal pressure to a point below threshold limits of
pain receptors.

Chronic pulpitis can be of three types:


1.  Ulcerative/open form
2.  Hyperplastic form
3.  Closed form.

Types
• Ulcerative form is a chronic inflammation of cariously
exposed pulp characterized by formation of an abscess Fig. 3.20 Carious exposure of first molar resulting in pulpitis

Differential diagnosis of reversible and irreversible pulpitis


Features Reversible pulpitis Irreversible pulpitis
Pain type Sharp and fleeting pain, usually dissipates after stimulus  Intense,  continuous  and  prolonged  pain  due  to 
is removed pressure of secondary irritants
Stimulus External stimulus, for example—heat, cold and sugar •  No external stimulus
•   Dead  or  injured  pulp  tissue  acts  as  secondary 
stimulant
Pain at night/postural No Yes
Pain localization Only with applied cold stimulus or PDL inflammation Only with applied heat stimulus or PDL inflammation
Referred pain Usually not found Common finding
History •  History of recent dental procedure History of:
•  S  ometimes cervical  erosion/abrasion •  Deep caries
•  Trauma
•  Extensive restoration
Percussion/occlusion If due to occlusion, percussion test is positive, otherwise  If  inflamed,  involved  PDL-percussion  test  is  positive, 
normal otherwise normal
Pulp tests
•  EPT Normal response Normal to elevated response
•  Cold Exaggerated response Pain relieved by cold occasionally
•  Heat Normal—exaggerated response Acute pain
Color change No Yes
Radiograph Caries, defective restoration without pulp protection Caries, defective restorations, PDL space enlargement
Treatment Removal  of  decay,  repair  of  defect,  restoration,  ZOE  Pulpectomy (single root), pulpotomy (multiple roots), 
dressing, occlusal adjustment occlusal adjustment

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Pathologies of Pulp and Periapex 31

Fig. 3.22 Hyperplastic form of pulpitis showing fleshy reddish pulpal 


Fig. 3.21 Hyperplastic form of chronic pulpitis mass filling the pulp chamber

Etiology – Chronic apical periodontitis in long standing cases.


– In young patients, low-grade long standing irritation
Etiology is same as that of irreversible pulpitis. It is normally stimulates periapical bone deposition, i.e. condensing
caused by slow and progressive carious exposure of pulp. osteitis. Radiograph shows areas of dense bone around
Nature of pulpal response depends on strength and duration apices of involved teeth.
of irritant, previous health of pulp and extent of tissue affected.
• Vitality tests
– Tooth may respond feebly or not at all to thermal test,
Signs and Symptoms unless one uses extreme cold
• Pain is absent because of low activity of exudative forces. – More than normal current is required to elicit the
Here proliferative granulomatous forces dominate. response by electric pulp tester.
• Symptoms develop only when there is interference with • Differential diagnosis: Hyperplastic pulpitis should be
drainage of exudates. differentiated from proliferating gingival tissue. It is done
• Hyperplastic form of chronic pulpitis is seen in teeth of by raising and tracing the stalk of tissue back to its origin,
children and adolescents in which pulp tissue has high i.e. pulp chamber.
resistance and large carious lesion permit free proliferation
of hyperplastic tissue. Since it contains few nerve fibers,
it is non-painful but bleeds easily due to rich network of Treatment
blood vessels. • Complete removal of pulp followed by its restoration
should be goal of the treatment. In case of hyperplastic
Histopathology pulpitis, removal of polypoid tissue with periodontal
curette or spoon excavator followed by extirpation of pulp
• Formation of sclerotic and irritation dentin should be done.
• Minimal amount of vasodilation and infiltration of cell, • If tooth is in nonrestorable stage, it should be extracted.
initially but when pulp is finally exposed, vasodilation and
cellular infiltration increases
• Surface of pulp polyp is usually covered by stratified
POINTS TO REMEMBER
squamous epithelium which may be derived from gingiva, Chronic pulpitis
desquamated epithelial cells of mucosa and tongue. •  P
  ain is absent due to diminished exudative inflammatory activity 
and decrease in intrapulpal pressure.
•  U
  lcerative  form  shows  formation  of  an  abscess  at  point  of 
Diagnosis exposure.
•  A  bscess is surrounded by granulomatous tissue so also called as 
• Pain: It is usually absent. pulpal granuloma.
• Hyperplastic form shows a fleshy, reddish pulpal mass •  H  yperplastic  form  is  overgrowth  of  granulomatous  tissue  into 
which fills most of pulp chamber or cavity (Fig. 3.22). It carious cavity. It is less sensitive but bleeds easily when probed.
is less sensitive than normal pulp but bleeds easily when •   In closed form carious lesion is absent.
probed. •  S  ymptoms appear only if there is interference with drainage of 
• Radiographic changes show exudates.

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32 Textbook of Endodontics

Fig. 3.23 Internal resorption of the tooth Fig. 3.24 Internal resorption of tooth causing perforation of root

INTERNAL RESORPTION
Internal resorption is initiated within the pulp cavity and
results in loss of substance from dentinal tissue (Fig. 3.23).

Etiology
Exact etiology is unknown.
Patient often presents with history of trauma or persistent
chronic pulpitis, or history of pulpotomy.

Mechanism of resorption
Pulp inflammation due to infection 

Alteration or loss of predentine and odontoblastic layer 

Undifferentiated mesenchymal cells come in contact with 
mineralized dentin Fig. 3.25 Radiograph showing internal resorption in distal root of 36

Differentiate into dentinoclasts 
↓ Treatment
Resorption results
• Pulp extirpation stops internal root resorption.
• Surgically, treatment is indicated if conventional treatment
Symptoms fails.

• Usually asymptomatic, recognized clinically through POINTS TO REMEMBER


routine radiograph. Internal resorption
• Pain occurs in cases of perforation of root (Fig. 3.24). •  Initiated within the pulp cavity
• ‘Pink tooth’ is the pathognomic feature of internal root •  Results in loss of substance from dentinal tissue.
resorption. •  Asymptomatic
•  Pain occurs if perforation of root.
•  “Pink tooth” appearance
Diagnosis •  Radiolucent enlargement of pulp canal
• Clinically: “Pink tooth” appearance •  Original root canal outline distorted
• Radiographic changes: (Fig. 3.25)
– Radiolucent enlargement of pulp canal
PULP NECROSIS
– Original root canal outline distorted
– Bone changes are seen only when root perforation into Pulp necrosis or death is a condition following untreated
periodontal ligament takes place. pulpitis. The pulpal tissue becomes dead and if the condition
• Pulp tests: Positive, though coronal portion of pulp is is not treated, noxious materials will leak from pulp space
necrotic, apical pulp could be vital. forming the lesion of endodontic origin (Fig. 3.26).

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Pathologies of Pulp and Periapex 33

Necrosis may be partial or total, depending on extent of Diagnosis


pulp tissue involvement.
• Pain: It is absent in complete necrosis.
The pulp necrosis is of two types:
• History of patient reveals past trauma or past history of
1. Coagulation necrosis: In coagulation necrosis, proto-
severe pain which may have lasted for some time followed
plasm of all cells becomes fixed and opaque. Cell mass is
by complete and sudden cessation of pain.
recognizable histologically, intracellular details lost.
• Radiographic changes: Radiograph shows a large cavity or
2. Liquefaction necrosis: In liquefaction necrosis, the
restoration (Fig. 3.28) or normal appearance unless there
entire cell outline is lost. The liquefied area is surrounded
is concomitant apical periodontitis or condensing osteitis.
by dense zone of PMNL (dead or drying), chronic
• Vitality test: Tooth is nonresponding to vitality tests. But
inflammatory cells.
multirooted teeth may show mixed response because
only one canal may have necrotic tissue. Sometimes teeth
Etiology with liquefaction necrosis may show positive response to
Necrosis is caused by noxious insult and injuries to pulp by electric test when electric current is conducted through
bacteria, trauma, and chemical irritation. moisture present in a root canal.
• Visual examination: Tooth shows color change like dull
or opaque appearance due to lack of normal translucency
Symptoms (Fig. 3.29).
• Discoloration of tooth—first indication of pulp death • Histopathology: Necrotic pulp tissue, cellular debris
(Fig. 3.27) and microorganisms are seen in pulp cavity. If there is
• History from patient concomitant periodontal involvement, there may be
• Tooth might be asymptomatic. presence of slight evidence of inflammation.

Fig. 3.26 Tooth decay resulting in pulpal necrosis Fig. 3.28 Radiograph showing a large restoration  


in molar resulting in infection of pulp

Fig. 3.27 Pulpal necrosis of 21 resulting in discoloration Fig. 3.29 Lack of normal translucency in nonvital 11

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34 Textbook of Endodontics

Treatment
Complete removal of pulp followed by restoration or
extraction of nonrestorable tooth.

POINTS TO REMEMBER
Pulp necrotic
•  Continued degeneration of acutely inflamed pulp.
•  Usually asymptomatic
•  Moderate to severe pain on biting pressure.
•  Treatment—Root canal therapy 

PULP DEGENERATION
Pulp degeneration is generally present in old age. It may be
the result of persistent mild irritation in young age. Usually,
pulp degeneration is induced by attrition, abrasion, erosion,
bacteria, operative procedures, caries, pulp capping and
reversible pulpitis. Fig. 3.31 Calcifications present in pulp
It may occur in following forms:

Atrophic Degeneration and Fibrosis Calcifications


• It is wasting away or decrease in size which occurs slowly
In calcific degeneration, the part of pulp tissue is replaced
as tooth grows old (Fig. 3.30).
by calcific material (Fig. 3.31). Mainly three types of
• There is gradual shift in ratio and quality of tissue elements.
calcifications are seen in pulp:
In this condition, the number of collagen fibers/unit area
1. Dystrophic calcifications
increases leading to fibrosis.
2. Diffuse calcifications
• Number and size of cells decrease so the cells appear as
3. Denticles/pulp stones.
“shrunken solid particles in a sea of dense fibers”.
• Fibroblastic processes are lost, cells have round and
pyknotic nuclei.
Dystrophic Calcifications
• They occur by deposition of calcium salts in dead or
• Dentinoblasts decrease in length, appear cuboidol or
degenerated tissue. Local alkalinity of destroyed tissues
flattened.
attracts the salts.
POINTS TO REMEMBER • They occur in minute areas of young pulp affected by
minor circulatory disturbances, in blood clot or around a
In atrophic degeneration and fibrosis
single degenerated cell.
•  Number of collagen fibers/unit area increases leading to fibrosis. 
•  Number and size of cells decrease
• They can also begin in the connective tissue walls of blood
•  Cells appear as “shrunken solid particles in a sea of dense fibers”. vessels and nerves and follow their course.

Diffuse Calcifications
• They are generally observed in root canals.
• The deposits become long, thin and fibrillar on fusing.

Denticles/Pulp Stones
These are usually seen in pulp chamber.

Classification of pulp stones


According to location (Fig. 3.32)
•  Free
•  Embedded
•  Attached
According to structure
•  True
•  False

True denticle: It is composed of dentin formed from


Fig. 3.30 Atrophic changes of pulp with age detached odontoblasts or fragments of Hertwig’s enamel root

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Pathologies of Pulp and Periapex 35

sheath which stimulates the undifferentiated cells to assume PERIRADICULAR PATHOLOGIES


dentinoblastic activity.
Periradicular tissue contains apical root cementum,
False denticle: Here degenerated tissue structures act as periodontal ligament and alveolar bone (Fig. 3.33).
nidus for deposition of concentric layers of calcified tissues. Apical periodontium consists of cellular and extracellular
components. Fibroblasts, cementoblasts, osteoblasts,
undifferentiated mesenchymal cells, epithelial cells rests
of malassez, blood vessels, lymphatics, sensory and motor
nerve fibers form its components.
Alveolar bone proper lines the alveolus. It consists of:
• Bundle bone: Peripheral bone
• Lamellated: Center of alveolar process

Fig. 3.32 Types of pulp stones according to location Fig. 3.33 Periodontium

Features of different forms of pulpitis


Features Reversible pulpitis Acute pulpitis Chronic pulpitis Hyperplastic pulpitis Pulp necrosis
Pain and  Mid pain lasting for a  Constant to severe  Mild and  Pain not present but it  Not present
stimulus moment pain caused by hot or  intermittent bleeds due to presence 
cold stimuli of rich network of blood 
vessels in granulomatous 
tissue into carious cavity
Stimulus Heat, cold or sugar •  Hot or cold •  Spontaneous
•  Spontaneous •   Dead/injured 
pulp tissue acts 
as secondary 
stimulus
Pulp test
•  Thermal Readily responds to  Acute pain to hot  No response No response No response
cold stimuli
•  Electric Normal response Normal to elevated  More current is  More current is required •   In cases of 
response required liquefaction 
necrosis, positive 
response is seen 
with electric tester
Radiograph •  Deep caries •  Deep caries •   Chronic apical  Same •  Large restoration
•  Defective restoration •  Defective restoration periodontitis 
•   Local condensing  Same •   Sometimes apical 
osteitis periodontitis or 
condensing osteitis
Treatment •  Removal of decay  •  Pulpotomy •  RCT •   Removal of polypoid  •  RCT/extraction
•   Restoration with  •   Root canal therapy •   Extraction of  tissue with curette/spoon 
pulp protection and  nonrestorable  excavator followed by 
occlusal adjustment tooth RCT

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36 Textbook of Endodontics

Symptoms of different forms of pulpitis


Symptoms X-ray findings Pulp vitality tests
Reversible pulpitis Asymptomatic or slight  No changes Gives response to vitality tests
symptoms to thermal stimulus
Irreversible pulpitis Asymptomatic or may have  No changes, except in long  Gives response
spontaneous or severe pain to  standing cases condensing 
thermal stimuli osteitis
Pulp necrosis None Depends on periapex status No response
Acute apical periodontitis Pain on biting or pressure Not significant Depending on status of pulp, 
response or no response
Chronic apical periodontitis Mild or none or no response Not significant Depending on pulp status, 
response
Acute apical abscess Pain and/or swelling Radiolucency at apical end No response
Chronic apical abscess Draining sinus Radiolucency No response
Condensing osteitis Varies according to status of pulp  Increased trabecular bone Depending on pulp status 
or periapex or no response response

Lamina dura is radiographic image of alveolar bone


proper.
Cementum: Two types of collagen fibers are present in
cementum.
1. Matrix fibers: Parallel to root surface; interwoven, mainly
consists of cementoblasts.
2. Sharpey’s fibers: Fibroblast is the main component of
Sharpey’s fibers.

PERIAPEX PATHOLOGIES
ETIOLOGY OF PERIRADICULAR DISEASES
Bacterial
• Root canal is unique, stringent ecological niche for
bacterial growth because of lack of oxygen. The primary Fig. 3.34 Sequelae of pulpal inflammation
nutrient source for root canal biotic is host tissues and
tissue fluids.
• Microorganisms in chronically infected root canals are • Anachoresis also accounts for microbial infection in teeth.
mainly anaerobic and gram-negative type. • Microorganisms may invade pulp from periodontal pocket
and accessory canals leading to development of lesion of
Most common microorganisms seen in periradicular diseases endodontic origin.
are:
•  Streptococcus Trauma
•  Peptostreptococcus
•  Provotella • Physical trauma to tooth, or operative procedures result
Black pigmented microorganisms in dental follicle desiccation or significant heat transfer
•  Porphyromonas causes sufficient damage to pulp and its blood supply.
•  Enterococcus • In cases of severe trauma to tooth, immediate interruption
•  Campylobacter of blood supply occurs resulting in necrosis of the pulp
•  Fusobacterium even though it is not infected.
•  Eubacterium • Persistent periapical tissue compression from traumatic
occlusion leads to apical inflammatory response.

Routes Factors-related to Root Canal Procedures


• Untreated pulpal infection leads to total pulp necrosis • It is impossible to extirpate pulp without initiating an
(Fig. 3.34). inflammatory response.

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Pathologies of Pulp and Periapex 37

Fig. 3.35 Inflammation of periradicular tissue resulting from  Fig. 3.36 Pain on percussion indicates inflammed periodontium


overextension of obturation material

• Using strong or excessive amounts of intracanal Intraoral Examination


medicaments between appointments may induce It includes examination of soft tissues and teeth to look for
periapical inflammation. discoloration, abrasion, caries, restoration, etc.
• Improper manipulation of instruments within root
canal or overinstrumentation can force dentinal debris, Clinical Periapical Tests
irrigating solution and toxic components of necrotic tissue
in the periapex. Percussion
• Over extended endodontic filling material may induce Indicates inflammation of periodontium (Fig. 3.36).
periapical inflammation by directly inducing foreign body
reaction which is characterized by presence of leukocyte Palpation
infiltration, macrophages and other chronic inflammatory Determines how far the inflammatory process has extended
cells (Fig. 3.35). periapically.

DIAGNOSIS OF PERIRADICULAR Pulp Vitality


• Thermal tests which can be heat or cold
PATHOLOGIES • Electrical pulp testing.

Chief Complaint Periodontal Examination


Patient usually complains of pain on biting, pain with It is important because periapical and periodontal lesion may
swelling, pus discharge, etc. mimic each other and require differentiation.
a. Probing: Determines the level of connective tissue
attachment. Probe can penetrate into an inflammatory
Dental History periapical lesion that extends cervically (Fig. 3.37).
Recurring episodes of pain, swelling with discharge, swelling b. Mobility: Determines the status of periodontal ligament.
which reduces of its own.
Radiographic Examination (Fig. 3.38)
Objective Examinations Periradicular lesions of pulpal origin have four characteristics
Extraoral Examination 1.  Loss of lamina dura apically.
2.  Radiolucency at apex regardless of cone angle.
General appearance, skin tone, facial asymmetry, swelling,
3.  Radiolucency resembles a hanging drop.
extraoral sinus, sinus tract, tender or enlarged cervical lymph 4.  Cause of pulp necrosis is usually evident.
nodes.

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38 Textbook of Endodontics

CLASSIFICATION OF PERIRADICULAR
PATHOLOGIES
Grossman’s Classification
1. Acute periradicular disease
a. Acute apical periodontitis
i. Vital
ii. Nonvital
b. Acute alveolar abscess
c. Phoenix abscess.
2. Chronic periradicular disease with areas of rarefaction:
a. Chronic apical periodontitis
• Chronic alveolar abscess
• Periapical granuloma
• Cystic apical periodontitis.
b. Persistent apical periodontitis.
3. Condensing osteitis
Fig. 3.37 Probing of tooth determines the  
4. External root resorption
level of connective tissue attachment
5. Disease of the periradicular tissues of nonendodontic
origin.

WHO Classification
K 04.4 – Acute apical periodontitis
K 04.5 – Chronic apical periodontitis (apical granuloma)
K 04.6 – Periapical abscess with sinus
K 04.60 – Periapical abscess with sinus to maxillary antrum
K 04.61 – Periapical abscess with sinus to nasal cavity
K 04.62 – Periapical abscess with sinus to oral cavity
K 04.63 – Periapical abscess with sinus to skin
K 04.7 – Periapical abscess without sinus
K 04.8 – Radicular cyst (periapical cyst)
K 04.80 – Apical and lateral cyst
K 04.81 – Residual cyst
K04.82 – Inflammatory paradental cyst.

Ingle’s Classification of
Pulpoperiapical Pathosis
A. Painful pulpoperiapical pathosis
1. Acute apical periodontitis
2. Advanced apical periodontitis
a. Acute apical abscess
b. Phoenix abscess
Fig. 3.38 Radiograph showing periapical lesion associated with 21 c. Suppurative apical periodontitis (chronic apical
abscess)
B. Nonpainful pulpoperiapical pathosis
Recent advances in radiography: 1. Condensing osteitis
• Digital subtraction radiography 2. Chronic apical periodontitis both incipient and
• Xeroradiography advanced stages.
• Digital radiometric analysis 3. Chronic apical periodontitis
• Computed tomography a. Periapical granuloma
• Radiovisiography b. Apical cyst
• Magnetic resonance imaging. c. Suppurative apical periodontitis.

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Pathologies of Pulp and Periapex 39

ACUTE APICAL PERIODONTITIS


Acute apical periodontitis is defined as painful inflam-
mation of the periodontium as a result of trauma, irritation
or infection through the root canal, regardless of whether
the pulp is vital or nonvital. It is an inflammation around
the apex of a tooth. The distinctive features of acute
apical periodontitis (AAP) are microscopic rather than A B C
roentogenographic, symptomatic rather than visible.

Etiology
• In vital tooth, it is associated with occlusal trauma, high
points in restoration, wedging or forcing object between
teeth. D E F
• In nonvital tooth AAP is associated with sequelae to pulpal
diseases. Figs 3.39A to F Management of acute apical periodontitis
• Iatrogenic causes can be over instrumentation of root
canal, pushing debris and microorganisms beyond apex, • Use of antibiotics, either alone or in conjunction with root
overextended obturation and root perforations. canal therapy is not recommended.
• If tooth is in hyperocclusion, relieve the occlusion.
• For some patients and in certain situations, extraction is
Signs and Symptoms an alternative to endodontic therapy.
• Tooth is tender on percussion
• Dull, throbbing and constant pain ACUTE APICAL ABSCESS (FIG. 3.40)
• Pain occurs over a short period of time It is a localized collection of pus in the alveolar bone at the root
• Negative or delayed vitality test apex of the tooth, following the death of pulp with extension
• No swelling of the infection through the apical foramen into periradicular
• Pain on biting tissue (Fig. 3.41).
• Cold may relieve pain or no reaction
• Heat may exacerbate pain or no reaction Etiology
• No radiographic sign; sometimes widening of periodontal
ligament space. • Most common cause is invasion of bacteria from necrotic
pulp tissue.
• Trauma, chemical or any mechanical injury resulting in
Histopathology pulp necrosis.
Inflammatory reaction occur in apical  
• Irritation of periapical tissue by chemical or mechanical
periodontal ligament treatment during root canal treatment.
↓ Tissue at surface of swelling appears taut and inflamed and
Dilatation of blood vessels  pus starts to form underneath it. Surface tissue may become
↓  inflated from the pressure of underlying pus and finally
Initiation of inflammatory response due to presence of  rupture from this pressure. Initially, the pus comes out in the
polymorphonuclear leukocytes and round cells  form of a small opening but latter it may increase in size or
↓ number depending upon the amount of pressure of pus and
Accumulation of serous exudate softness of the tissue overlying it. This process is beginning of
↓ chronic abscess.
Distention of periodontal ligament and  
extrusion of tooth, slight tenderness Pathophysiology of Apical Abscess Formation

If irritation continues Increase in pulpal pressure
↓  ↓
Loss of alveolar bone Collapse of venous circulation 

Hypoxia and anoxia of local tissue
Treatment ↓
• Endodontic therapy should be initiated on the affected Localized destruction of pulp tissue
tooth at the earliest (Figs 3.39A to F). ↓
• To control postoperative pain following initial endodontic Formation of pulpal abscess because of breakdown of PMNs, 
bacteria and lysis of pulp remnants
therapy, analgesics are prescribed.

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40 Textbook of Endodontics

Fig. 3.40 Periapical abscess

Fig. 3.42 Spread  of  apical  abscess  to  surrounding  tissues,  if  it  is 
not  treated;  (1)  Vestibular  abscess;  (2)  Periapical  abscess;  (3)  Palatal 
abscess; (4) Maxillary sinus

Fig. 3.41 Radiograph showing periapical abscess in relation to 21 Fig. 3.43 Swelling of mandibular area because of apical abscess

Features of Acute Apical Abscess Symptoms


•  Tooth is nonvital • In early stage, there is tenderness of tooth which is relieved
•  Pain by continued slight pressure on extruded tooth to push it
–  Rapid onset back into alveolus.
–  Readily  localized  as  tooth  becomes  increasingly  tender  to  • Later on, throbbing pain develops with diffuse swelling of
percussion overlying tissue.
–  Slight tenderness to intense throbbing pain
• Tooth becomes more painful, elongated and mobile as
–  Marked pain to biting
•  Swelling
infection increases in later stages.
–  Palpable, fluctuant  • Patient may have systemic symptoms like fever, increased
–  Localized sense of fullness WBC count.
•  Mobility • Spread of lesion towards a surface may take place causing
–  May or may not be present  erosion of cortical bone or it may diffuse and spread widely
•  Tooth may be in hyperocclusion leading to formation of cellulitis (Fig. 3.42). Location
•  Radiographic changes of swelling is determined by relation of apex of involved
–  No change to large periapical radiolucency tooth to adjacent muscle attachment (Fig. 3.43).

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Pathologies of Pulp and Periapex 41

Diagnosis
• Clinical examination.
• In initial stages, locating a tooth is difficult due to diffuse
pain. Location of the offending tooth becomes easier when
tooth gets slightly extruded from the socket.
• Pulp vitality tests give negative response.
• Tenderness on percussion and palpation.
• Tooth may be slightly mobile and extruded from its socket.
• Radiography helpful in determining the affected tooth as
it may show caries or evidence of bone destruction at root
apex.
Differential diagnosis of acute alveolar
abscess and periodontal abscess Fig. 3.44 Management of periapical abscess
Features Acute alveolar abscess Periodontal abscess
Pain type Pulsating, pounding,  Dull
continuous
Management of an Acute Apical Abscess
P
  ain localization Easily localized due to  Upon probing
percussive tenderness • Drainage of the abscess should be initiated as early as
P
  ain at night/ Pain continuous No possible. This may include:
postural a. Nonsurgical endodontic treatment (Root canal therapy)
(Fig. 3.44)
Mobility Yes Sometimes
b. Incision and drainage
Pulp tests c. Extraction
•  EPT No response Normal
•  Cold  No response Normal Considerations regarding the treatment of a tooth with peri­
•  Heat No response Normal apical abscess depend on following factors:
Swelling Yes, often to large size Occasionally •  Prognosis of the tooth
•  Patient preference
Radiograph Caries, defective  Possible foreign body 
•  Strategic value of the tooth
restorations or vertical bone loss
•  Economic status of the patient
Treatment •   Establish drainage  •   Removal of foreign 
(Incision and  body 
• In case of localized infections, systemic antibiotics provide
drainage) •  Scaling
•  Antibiotics •   Curettage, if 
no additional benefit over drainage of the abscess
•  NSAIDs necessary • In the case of systemic complications such as fever,
lymphadenopathy, cellulitis or patient who is immuno-
compromised, antibiotics should be given in addition to
Histopathology drainage of the tooth
• Relieve the tooth out of occlusion in hyperocclusion cases
Polymorphonuclear leukocytes infiltrate and   • To control postoperative pain following endodontic
initiate inflammatory response
therapy, nonsteroidal anti-inflammatory drugs should be
↓ given.
Accumulation of inflammatory exudates  
in response to active infection 
↓ PHOENIX ABSCESS/RECRUDESCENT
Distention of periodontal ligament 

ABSCESS
Extrusion of the tooth Phoenix abscess is defined as an acute inflammatory reaction
↓ superimposed on an existing chronic lesion, such as a cyst
If the process continues, separation of  or granuloma. In other words, phoenix abscess is an acute
 periodontal ligament 
exacerbation of a chronic lesion.

Tooth becomes mobile
↓ Etiology
Bone resorption at apex  Chronic periradicular lesions such as granulomas are in a
↓  state of equilibrium during which they can be completely
Localized lesion of liquefaction necrosis containing polymorpho-  asymptomatic. But sometimes, influx of necrotic products
nuclear leukocytes, debris, cell remnants and purulent exudates
from diseased pulp or bacteria and their toxins can cause

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42 Textbook of Endodontics

the dormant lesion to react. This leads to initiation of acute


inflammatory response. Lowered body defenses also trigger
an acute inflammatory response.

Symptoms
• Clinically, often indistinguishable from acute apical abscess
• At the onset, tenderness of tooth and extrusion of the tooth
from socket
• Tenderness on palpating the apical soft tissue.

Diagnosis
• Most commonly associated with initiation of root canal
treatment
• History from patient Fig. 3.45 Periapical granuloma present at the apex of nonvital tooth
• Pulp tests show negative response
• Radiographs show large area of radiolucency in the apex
created by inflammatory connective tissue which has
replaced the alveolar bone at the root apex.
• Histopathology of phoenix abscess shows areas of Clinical Features
liquefaction necrosis with disintegrated polymor-
phonuclear leukocytes and cellular debris surrounded by • Most of the cases are asymptomatic but sometimes pain
macrophages, lymphocytes, plasma cells in periradicular and sensitivity is seen when acute exacerbation occurs
tissues. • Tooth is not sensitive to percussion
• Phoenix abscess should be differentiated from acute • No mobility
alveolar abscess by patient’s history, symptoms and • Soft tissue overlying the area may/may not be tender
clinical tests results. • No response to thermal or electric pulp test
• Mostly, lesions are discovered on routine radiographic
examination.
Treatment
• Establishment of drainage Radiographic Features (Fig. 3.46)
• Once symptoms subside—complete root canal treatment.
• Mostly discovered on routine radiographic examination
POINTS TO REMEMBER • The earliest noticeable change seen is thickening of
periodontal ligament at the root apex.
Phoenix abscess
•  An acute exacerbation of a chronic lesion. • Lesion may be well circumscribed or poorly defined
•  Most commonly associated with initiation of root canal treatment. • Size may vary from small lesion to large radiolucency
•  I  nflux  of  necrotic  products  from  diseased  pulp  causes  the  exceeding more than 2 cm in diameter.
dormant lesion to react leading to initiation of acute inflammatory  • Presence of root resorption is also seen.
response. 
•  Pulp tests show negative response.
•  Radiograph-large area of radiolucency in the apex.
Histopathologic Features (Fig. 3.47)
• It consists of inflamed granulation tissue that is surrounded
by a fibrous connective tissue wall
PERIAPICAL GRANULOMA • The granulation consists of dense lymphocytic infiltrate
Periapical granuloma is one of the most common sequelae which further contains neutrophils, plasma cells,
of pulpitis. It is usually described as a mass of chronically histiocytes and eosinophils
inflamed granulation tissue found at the apex of nonvital • Sometimes, Russel bodies may also be present.
tooth (Fig. 3.45).
Treatment and Prognosis (Figs 3.48A to E)
Etiology of Periapical Granuloma Main objective in treatment is to reduce and eliminate
Periapical granuloma is a cell-mediated response to pulpal offending organisms and irritants from the periapical area.
bacterial products. Bacterial toxins cause mild irritation of • In restorable tooth, root canal therapy is preferred
periapical tissues. This leads to cellular proliferation and thus • In non-restorable tooth, extraction followed by curettage
granuloma formation. of all apical soft tissue.

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Pathologies of Pulp and Periapex 43

Fig. 3.46 Radiographic appearance of periapical granuloma Fig. 3.47 Histopathology of periapical granuloma

A B

C D

E
Figs 3.48A to E (A) Preoperative radiograph; (B) Working length radiograph; (C) Master cone radiograph;  
(D) Radiograph after obturation; (E) Follow-up after 3 months
Courtesy: Manoj Hans

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44 Textbook of Endodontics

POINTS TO REMEMBER
Periapical granuloma
•  Common sequelae of pulpitis. 
•  M
  ass  of  chronically  inflamed  granulation  tissue  at  the  apex  of 
non-vital tooth.
•  Usually asymptomatic
•  Pain and sensitivity occur when there is acute exacerbation. 
•  No response to thermal or electric pulp test

RADICULAR CYST/CYSTIC APICAL


PERIODONTITIS
The radicular cyst is an inflammatory cyst which results
because of extension of infection from pulp into the
surrounding periapical tissues.

Etiology Fig. 3.49 Cyst formation in periapical area

• Caries
• Irritating effects of restorative materials
• Trauma
• Pulpal death due to development defects.

Clinical Features
• The cyst is frequently asymptomatic. It is usually discovered
when periapical radiographs of tooth with nonvital pulp is
taken.
• Incidence – Males are affected more than females.
• Age – Peak incidence in third or fourth decades.
• Site – Highest in anterior maxilla
– In mandibular posterior teeth, separate small
cysts arise from each apex of multirooted
teeth.
• Slowly enlarging swelling, sometimes attains a large size.
• As the cyst enlarges in size, the covering bone becomes
thin in size and exhibits springiness due to fluctuation. Fig. 3.50 Pocket or bay cyst
• In maxilla, palatal expansion is mainly seen in case of
maxillary lateral incisor.
• The involved tooth is usually nonvital, discolored, in osmotic pressure. The result is fluid transport across
fractured or shows failed root canal. the epithelial lining into the lumen from the connective
tissue side. Fluid ingress assists in outward growth of the
cyst. With osteoclastic bone resorption, the cyst expands.
Pathogenesis Other bone-resorbing factors, such as prostaglandins,
Periapical granulomas are initiated and maintained by the interleukins, and proteinases, from inflammatory cells
degradation products of necrotic pulp tissue. Stimulation of and cells in the peripheral portion of the lesion permit
the resident epithelial rests of Malassez occurs in response additional cyst enlargement.
to the products of inflammation. Cyst formation occurs as a
result of epithelial proliferation, which helps to separate the Radiographic Features
inflammatory stimulus from the surrounding bone. When Radiographically, radicular cyst appears as round, pear
proliferation occurs within the body of the granuloma, it or ovoid-shaped radiolucency, outlined by a narrow radi-
plugs the apical foramen which limits the egress of bacteria opaque margin (Figs 3.51 and 3.52).
(Fig. 3.49). Sometimes, epithelial plugs protrude out from the
apical foramen resulting in a pouch connected to the root and
continuous with the root canal. This is termed as pocket or
Treatment (Figs 3.53A to G)
bay cyst (Fig. 3.50). Different options for management of residual cyst are:
• Breakdown of cellular debris within the cyst lumen • Endodontic treatment
raises the protein concentration, producing an increase • Apicoectomy

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Pathologies of Pulp and Periapex 45

Fig. 3.51 Radiographic appearance of radicular cyst Fig. 3.52 Radiographic picture of a periapical cyst

CBCT images 3 dimensional images above; Cross section images WRT 11 and 12 below

Fig. 3.53A Nonsurgical root canal treatment of right maxillary central and lateral incisor with a large periapical cyst  


using a new bioceramic sealer as an obturating material—with 1 month follow-up using CBCT

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46 Textbook of Endodontics

B C

D E

F G
Figs 3.53B to G (B) Preoperative radiograph showing PA radiolucency in relation to 11 and 12; (C) After removal of faulty prosthesis;  
(D) Working length determination; (E) Master cone selection; (F) Postobturation radiograph; (G) 4 months recall radiograph
Courtesy: Anil Dhingra

• Extraction (severe bone loss) of irritants from root canal system into periradicular area
• Enucleation with primary closure leading to formation of an exudate.
• Marsupialization (in case of large cysts).
Etiology
CHRONIC ALVEOLAR ABSCESS It is similar to acute alveolar abscess. It also results from pulpal
Chronic alveolar abscess is also known as suppurative necrosis and is associated with chronic apical periodontitis
apical periodontitis which is associated with gradual egress that has formed an abscess. The abscess burrows through the

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Pathologies of Pulp and Periapex 47

bone and soft tissue to form a sinus react stoma on the oral Radiographic examination shows diffuse area of
mucosa (Fig. 3.54). rarefaction. The rarefied area is so diffuse as to fade indistinctly
into normal bone (Fig. 3.55).
Symptoms
Differential Diagnosis
• Generally asymptomatic
• Detected either by the presence of a sinus tract or on Chronic alveolar abscess must be differentially diagnosed
routine radiograph from a granuloma or cyst, in which accurate diagnosis is
• In case of open carious cavity—drainage through root made by studying the tissue microscopically. It should also
canal sinus tract prevents swelling or exacerbation of be differentiated with cementoma which is associated with
lesion—can be traced to apex of involved tooth. vital tooth.

Diagnosis Treatment (Figs 3.56 and 3.57)


Chronic apical abscess may be associated with asymptomatic Removal of irritants from root canal and establishing
or slightly symptomatic tooth. Patient may give history of drainage is main objective of the treatment. Sinus tract
sudden sharp pain which subsided and has not reoccurred. resolve following root canal treatment removing the irritants.
Clinical examination may show a large carious exposure, Draining sinus is active with pus discharge surrounded
a restoration of composite, acrylic, amalgam or metal, or by reddish pink color mucosa. It can be detected by inserting
discoloration of crown of tooth. gutta-percha.
It is associated symptoms only if sinus drainage tract In healed sinus, pus discharge is absent and color of
become blocked. Vitality tests show negative response mucosa is normal (Figs 3.58 and 3.59).
because of presence of necrotic pulps.

Fig. 3.54 Sinus tract Fig. 3.55 Radiograph showing chronic alveolar abscess

A B C
Figs 3.56A to C Nonsurgical RCT of PA radiolucency. (A) Radiograph showing periradicular radiolucency IRT 35; (B) Access opening done and 
working length radiograph taken; (C) Radiograph after 3 months of obturation showing decrease in size of radiolucency
Courtesy: Neelam Mittal

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48 Textbook of Endodontics

A B

C D
Figs 3.57A to D (A) Extraoral sinus; (B) Source of sinus tracked using gutta-percha; (C) Postobturation radiograph;  
(D) Photograph showing healed sinus

Fig. 3.58 Preoperative photograph showing extraoral sinus in  Fig. 3.59 Postoperative photograph after 3 months  


submandibular region in relation with left mandibular first molar showing healed sinus

vip.persianss.ir
Pathologies of Pulp and Periapex 49

POINTS TO REMEMBER
Chronic alveolar abscess/suppurative apical periodontitis
•  R
  esults from pulpal necrosis and associated with chronic apical 
periodontitis that forms an abscess. 
•  A
  bscess  burrows  through  bone  and  soft  tissue  to  form  a  sinus 
tract.
•  Generally asymptomatic.
•  V
  itality  tests  show  negative  response  because  of  presence  of 
necrotic pulps.
•  Radiograph shows diffuse area of rarefaction. 

PERSISTENT APICAL PERIODONTITIS


It is post-treatment apical periodontitis in an endodontically
treated tooth. Enterococcus faecalis is found most consistently
reported organism in persistent apical periodontitis.
Fig. 3.60 Radiographic appearance of external root resorption

Etiology
• Usually apical periodontitis may persist because of
complexity of pulp space which cannot be reached by
• When replacement resorption/ankylosis occur, tooth
instruments or irrigants and thus obturation material.
becomes immobile with characteristic high percussion
• Nair listed following extraradicular factors which
sound.
contribute to persistent apical periodontitis:
– Foreign body reaction to gutta-percha
– Periapical biofilms Radiographic Features (Fig. 3.60)
– Cholesterol crystals • Radiolucency at root and adjacent bone.
– Periapical scar tissue • Irregular shortening or thinning of root tip.
– Actinomyces infection • Loss of lamina dura.

EXTERNAL ROOT RESORPTION Treatment (Fig. 3.61)


Resorption is a condition associated with either physiologic • Removal of stimulus of underlying inflammation.
or a pathologic process that results in loss of substance from a • Nonsurgical endodontic treatment should be tried first
tissues like dentin, cementum or alveolar none. before attempting surgical treatment.
In external root resorption, root resorption affects the
cementum or dentin of the root. It can be:
• Apical root resorption DISEASES OF PERIRADICULAR TISSUE OF
• Lateral root resorption NONENDODONTIC ORIGIN
• Cervical root resorption.
Periradicular lesions may arise from the remnants of
odontogenic epithelium.
Etiology
Periradicular inflammation due to: Benign Lesions
• Infected necrotic pulp
• Early stages of periradicular cemental dysplasia
• Over instrumentation during root canal treatment
• Early stages of monostatic fibrous dysplasia
• Trauma
• Ossifying fibroma
• Granuloma/cyst applying excessive pressure on tooth root
• Primordial cyst
• Replantation of teeth
• Lateral periodontal cyst
• Adjacent impacted tooth.
• Dentigerous cyst
• Traumatic bone cyst
Symptoms • Central giant cell granuloma
• Asymptomatic during development • Central hemangioma
• When root is completely resorbed, tooth becomes mobile • Hyperparathyroidism
• When external root resorption extends to crown, it gives • Myxoma
“Pink tooth” appearance • Ameloblastoma.

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50 Textbook of Endodontics

A B C D
Figs 3.61A to D Management of external root resorption of maxillary central incisor. (A) Preoperative radiograph showing external resorption; 
(B) Working length radiograph; (C) Radiograph after obturation; (D) Follow-up after 6 months

Radiographic Features of Lesions 7. Write short notes on:


• Phoenix abscess
of Nonodontogenic Origin • Radicular cyst
• Radiolucent areas • Differentiate acute abscess and chronic abscess
• Intact lamina dura. • Chronic hyperplastic pulpitis/pulp polyp.

Diagnosis
Teeth associated with nonodontogenic lesions are usually BIBLIOGRAPHY
vital. Final diagnosis is based on surgical biopsy and 1. Andreasen JO, Rud J. A histobacteriologic study of dental and
histopathological examination. periapical structure after endodontic surgery. Int J Oral Surg.
1972;1:272-81.
Malignant Lesions 2. Baume LJ. Diagnosis of diseases of the pulp. Oral Surg Oral
Med Oral Pathol. 1970:29:102-16.
They simulate endodontic periradicular lesions and are often 3. Bhasker SN. Periapical lesion: Types, incidence and clinical
metastatic in nature: features. Oral Surg Oral Med Oral Pathol. 1966;21:657-71.
• Squamous cell carcinoma 4. Byström A, Happonen RP, Sjögren U, Sundqvist G. Healing of
• Osteogenic sarcoma periapical lesions of pulpless teeth after endodontic treatment
• Chondrosarcoma with controlled asepsis. Endod Dent Taumotol. 1987;3:58-63.
• Multiple myeloma. 5. Dummer PMH, Hicks R, Huws D. Clinical signs and symptoms
in pulp disease. Int Endod J. 1980;13:27-35.
6. Hasler JE, Mitchell DF. Painless pulpitis. J Am Dent Assoc.
Diagnosis 1970;81:671-7.
• Involved tooth is vital: Occasionally, disruption of pulp 7. Marton IJ, Kiss C. Characterization of inflammatory cell
and sensory nerve may cause no response. infiltrate in dental periapical lesions. Int Endod J. 1993;26:
• Radiographic features: Lesions are associated with rapid 131-6.
and extensive loss of hard tissue, bone and tooth. 8. Michaelson PL, Holland GR. Is pulpitis painful? Int Endod J.
• Biopsy: Histological evaluation of diagnosis. 2002;35:829-32.
9. Morse DR, Seltzer S, Sinai I, Biron G. Endodontic classification.
J Am Dent Assoc. 1977;94:685-9.
QUESTIONS 10. Nair PNR, Sundqvist G, Sjögren U. Experimental evidence
1. Enumerate etiology of pulpal diseases. Write in detail about support the abscess theory of development of radicular
reversible pulpitis. cysts. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
2. Classify pulpal pathologies. What are clinical features of 2008;106:294-303.
irreversible pulpitis. 11. Nair PNR. New perspectives on radicular cysts: Do they heal?
3. Explain the etiology and classification of periradicular Int Endod J. 1998;31:155-60.
pathologies. 12. Pitt Ford TR. The effects of the periapical tissues of bacterial
4. Discuss differential diagnosis and treatment of pulp polyp contamination of filled root canal. Int Endod J. 1982;15:16-22.
(chronic hyperplastic pulpitis). 13. Seltzer S. Classification of pulpal pathosis. Oral Surg Oral Med
5. Classify diseases of pulp how will you differentiates between Oral Pathol. 1972;34:269-80.
hyperemia and acute pulpitis. 14. Torabinejad M. The role of immunological reactions in apical
6. Describe diagnosis and treatment plan of reversible and cyst formation and the fate of the epithelial cells after root
irreversible pulpitis. canal therapy: a theory. Int J Oral Surg. 1983;12:14-22.

vip.persianss.ir
Endodontic Microbiology
4
 Portals of Entry for Microorganisms  Factors Influencing the Growth and  Identification of the Bacteria



 Classification of Microorganisms Colonization of Microorganisms  How to Combat Microbes in the


 Microbial Virulence and  Microbial Ecosystem of the Root Canal Endodontic Therapy?


Pathogenicity  Types of Endodontic Infections

INTRODUCTION 1965: Kakehashi et al proved that bacteria are responsible for
Most of the pathologies of pulp and the periapical tissues pulpal and periapical disease.
1976: Sundqvist used different culturing techniques for identi­
are directly or indirectly related to the microorganisms.
fication of both aerobic and anaerobic organisms and concluded
Therefore to effectively diagnose and treat endodontic that root canal infections are multibacterial.
infection, one should have the knowledge of bacteria
associated with endodontic pathology. Since many years,
the interrelationship of microorganisms and the root canal
system have been proved. Leeuwenhoek observed infected PORTALS OF ENTRY FOR MICROORGANISMS
root canal of a tooth and found “cavorting beasties”. After
Microorganisms may gain entry into pulp through several
this, it took 200 years for WD Miller to make the correlation
routes. Most common portal of entrance for microorganisms
between microorganisms and pulpal or periradicular
to dental pulp is dental caries.
pathologies.
They can also gain entry into pulp cavity via mechanical or
Then in 1965, Kakehashi et al found that bacteria are the

traumatic injury, through gingival sulcus or via bloodstream.

main etiological factors in the development of pulpal and
periradicular diseases. Kakehashi et al proved that without
bacterial involvement only minor inflammation occurred in Source of entry of microorganisms into pulp
exposed pulp. •  Open cavity
So we have seen that a strong relationship occurs between •  Open dentinal tubules
•  Periodontal ligament or gingival sulcus

microorganisms and pulpal or periradicular diseases. All the
•  Anachoresis
surfaces of human body are colonized by microorganisms.
•  Faulty restorations.
Colonization is the establishment of bacteria in a living
host. It occurs if biochemical and physical conditions are
available for growth. Permanent colonization in symbiotic
relationship with host tissue results in establishment of
Entry through Open Cavity
normal flora. • This is the most common way of entry of microorganisms
Infection results if microorganisms damage the host and into the dental pulp.

produce clinical signs and symptoms. The degree of patho­ • When enamel and dentin are intact, they act as barrier to
genicity produced by microorganisms is called virulence. microorganisms (Fig. 4.1).
• When these protective layers get destroyed by caries
History of microbiology in association to endodontics (Fig. 4.2), traumatic injuries, fractures, cracks or restora­
17th century: AV Leeuwenhoek first described oral microflora.
tive procedures, microorganisms can gain access to the
1890: WD Miller (Father of oral microbiology) authorized book
“Microorganisms of human mouth”. pulp (Fig. 4.3).
1904: F Billings described theory of focal infection as a circumscribed
area of tissue with pathognomic microorganisms.
1909: EC Rosenow described theory of focal infection as localized or
Through Open Dentinal Tubules
generalized infection caused by bacteria traveling via bloodstream • Microorganisms can pass into the dentinal tubules and
from distant focus of infection. subsequently to the pulp (Fig. 4.4).
1939: Fish observed four distinct zones of periapical reaction in • Bacteria are preceded in the course of the tubules by their
response to infection.
breakdown products which may act as pulp irritants.

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52 
Textbook of Endodontics

Fig. 4.1 Normal tooth anatomy with protective layers of the pulp

Fig. 4.4 Entry of bacteria through decay into pulp


Fig. 4.2 Pulp infection from tooth decay

Fig. 4.5 Periodontal lesions causing inflammation of pulp

Anachoresis
Fig. 4.3 Radiograph showing deep carious lesion infecting the pulp Anachoresis refers to the attraction of blood borne bacteria

in the areas of inflammation. It is a process by which
microorganisms are transported in the blood to an area of
inflammation where they establish an infection. But whether
Through the Periodontal Ligament anachoresis contributes to pulpal or periradicular infection
or the Gingival Sulcus has not been determined.

• Microorganisms also gain entry into pulp via accessory and


Through Faulty Restorations
lateral canals which connect pulp and the periodontium.
• If periodontal disease or therapy destroys the protective • It has been seen that faulty restoration with marginal
covering, canal may get exposed to the microorganisms leakage can result in contamination of the pulp by bacteria.
present in the gingival sulcus (Fig. 4.5). • Bacterial contamination of pulp or periapical area can
• The removal of cementum during periodontal therapy also occur through broken temporary seal, inadequate final
exposes dentinal fluids to oral flora. restoration and unused post space (Figs 4.6 to 4.10).

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Endodontic Microbiology 53


Fig. 4.9 Periradicular infection as a result of poorly obturated canal


Fig. 4.6 Untreated canal and empty post space causing

root canal failure

Fig. 4.10 Poorly obturated canals resulting in root canal failure



Fig. 4.7 Radiograph showing faulty restoration

CLASSIFICATION OF MICROORGANISMS
(FIG. 4.11)
Microbial flora can be classified on the basis of:

Gram Stain Technique


Gram positive organisms, e.g. Streptococcus, Enterococcus,
-
Treponema, Candida, Actinomyces, Lactobacillus, etc.
Gram negative organisms, e.g. Fusobacterium, Campylo­

-
bacter, Bacteroides, Veillonella, Neisseria, etc.
• Obligate aerobes: The organisms which require oxygen
for their growth, e.g. tubercle bacilli.
• Facultative anaerobes: These organisms can grow in the
presence or absence of oxygen, e.g. Staphylococcus.
• Microaerophilic: They grow in an oxygen environment
but derive their energy only from fermentative pathways
that occur in absence of oxygen, e.g. Streptococcus, etc.
• Obligate anaerobes: These bacteria can grow only in

Fig. 4.8 Deep restoration may irritate the pulp absence of oxygen, e.g. Bacteroides, Fusobacterium.

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54  
Textbook of Endodontics

Fig. 4.11 Different types of microorganisms



MICROBIAL VIRULENCE Virulent factors
AND PATHOGENICITY •  Lipopolysaccharides (LPS)
•  Extracellular vesicles
Under normal conditions pulp and periapical tissues are •  Enzymes
sterile in nature, when microorganisms invade and multiply •  Fatty acids
in these tissues, endodontic infections result. •  Polyamines
•  capsule
•  Pilli
•  Pathogenicity is ability of microorganisms to produce a disease
•  Virulence is degree of pathogenicity.
Lipopolysaccharides
• Lipopolysaccharides (LPS) are present on the surface of
Virulence is directly related to pathogenicity. In 1965, gram negative bacteria.
-
Hobson gave an equation showing the relation of number • LPS have nonspecific antigens which are not neutralized
of microorganisms, their virulence, resistance of host and by antibodies.
severity of the disease. • They exert numerous biologic functions when released
from cells in the form of endotoxins.
• Endotoxins have capability to diffuse into the dentin.
Number of microorganisms ×
virulence of microorganisms = Severity of the disease
Various studies have shown the relationship between the
Resistance of host endotoxins and the periradicular inflammation.

Extracellular Vesicles
We can see that along with number of microorganisms,
• Extracellular vesicles are produced by gram-negative

their virulence is also directly related to the severity of the
bacteria in the form of endotoxins, outer membrane
disease.
fragments or blebs.

vip.persianss.ir
Endodontic Microbiology 55


• They have trilaminar structure similar to outer membrane Bacteriocins
of the parent bacteria. ese vesicles contain various
Some bacterias produce bacteriocins, which are antibiotic

TH
enzymes and toxic products which are responsible for
hemagglutination, hemolysis and bacterial adhesion. like proteins produced by one species of bacteria to inhibit
• Since they have antigenic properties similar to the parent another species of bacteria.
bacteria, they may protect bacteria by neutralizing specific
antibodies.
Coaggregation
Enzymes It is the existence of “symbiotic relationship” between some
bacterias which may result in an increase in virulence by the
• Enzymes produced by bacteria have numerous activities organisms in that ecosystem.
like they help in spread of the infection, neutralization of
immunoglobulin and the complement components.
• PMN leukocytes release hydrolytic enzymes which Bacterial Interrelationships
degenerate and lyse to form purulent exudates and have
adverse effects on the surrounding tissues. Interrelationships between certain bacteria can be comm­
ensal or antagonistic which affect their survival.
Fatty Acids
MICROBIAL ECOSYSTEM
• Various short chain fatty acids like propionic acid, butyric
acid are produced by anaerobic bacteria. OF THE ROOT CANAL
• These cause neutrophil chemotaxis, degranulation, phago- Since many years, various papers have been published
cytosis, and stimulate interleukin 1 production which regarding the microbial flora of the root canals, normal and
-
further causes bone resorption and periradicular diseases. infected both. But over past 5 to 10 years, difference in flora
has reported because of improved technology in sampling,
Polyamines culture techniques, culture media as well as more advanced
technology regarding isolation and identification of the
• These are biologically active chemicals found in the
microorganism.
infected canals.
Most commonly gram positive organisms are found in the
• Some of polyamines such as cadaverine, putrescine,

-
root canals, but gram negative and obligate anaerobes have
spermidine help in regulation of the cell growth,
-
also been found in the root canals. Usually the microorganisms
regeneration of tissues and modulation of inflammation.
which can survive in environment of low oxygen tension
• Other virulent factors like capsules present in gram
and can survive the rigors of limited pabulums are found in
-
negative black pigmented bacteria, enable them to
root canals. Most commonly seen bacteria in root canals is
avoid phagocytosis. Pilli may play an important role in
streptococci, others can be Staphylococcus, gram negative
attachment of bacteria to surfaces and interaction with

-
and anaerobic bacteria.
other bacteria.
In necrotic pulp, a mix of bacterial species is found. In

necrotic pulp, there is lack of circulation with compromised
FACTORS INFLUENCING THE GROWTH host defense mechanism; this makes pulp as a reservoir for
invading microbes.
AND COLONIZATION OF MICROORGANISMS
New nomenclature of Bacteroides species
Influence of Oxygen 1. Porphyromonas – Dark pigmented (asaccharolytic Bacteroides
 
-
­
species)
• A factor highly selective for the microbial flora of root
  • Porphyromonas asaccharolytica
canal is low availability of oxygen in infected root canals.


  • Porphyromonas gingivalis*
• In the initial stages, there is predominance of facultative


  • Porphyromonas endodontalis*


organisms but later they are replaced by anaerobic 2. Prevotella—Dark pigmented (saccharolytic Bacteroides species)
 
-
bacteria.   • Prevotella melaninogenica


  • Prevotella denticola


Nutritional Factors   • Prevotella intermedia


  • Prevotella nigrescens*


• Bacterias obtain their nutrition from tissue fluid and the   • Prevotella corporis


breakdown products of necrotic pulp tissue.   • Prevotella tannerae


• These nutrients are rich in polypeptides and amino acids, 3. Prevotella – Nonpigmented (saccharolytic Bacteroides species)

which are essential for growth of the bacteria.   • Prevotella buccae*


• Other source of nutrition for bacterias is inflammatory   • Prevotella bivia


  • Prevotella oralis
exudates containing serum and blood factors discharged


  • Prevotella oulorum
from related inflammatory processes in the remaining


*Most commonly isolated species of black pigmented bacteria.
pulp or the periapical tissues.
-
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56  
Textbook of Endodontics

Fig. 4.12 Interrelationship of various root canal microorganisms Fig. 4.13 Microorganisms in infected root canal


In necrotic pulps, tissue fluids and disintegrated cells

from necrotic tissue, low oxygen tension and bacterial
interactions are the main factors determining which bacteria
will predominate. The growth of one bacterial species may
be dependent on the other bacterial species which supplies
the essential nutrients. In the similar way, antagonistic
relationship may occur in bacteria, i.e. byproducts of some
bacterial species may kill or retard the growth of others
species. In other words, some byproducts can act either
as nutrient or as toxin depending on bacterial species
(Fig. 4.12).

Naidorf summarized following generalizations in relation to


organisms isolated from the root canals
•  Mixed infections are more common than single organisms
•  Pulp contains flora almost similar to that of oral cavity
•  Approximately 25 percent of isolated organisms are anaerobes Fig. 4.14 Abscess formation due to poorly obturated canal

•  Organisms isolated from flare-up as well as asymptomatic cases

are almost similar
•  Various researchers have identified wide variety of micro-
• Gram-positive anaerobes like Peptostreptococcus, Eubac­

organisms in the root canals which is partially related to personal
interest and culture techniques used by them. terium, Actinomyces and Streptococcus are also seen in
primary intra radicular infections.
-
TYPES OF ENDODONTIC INFECTIONS Secondary Intra-radicular Infections (Fig. 4.14)
According to location of infection in relation to root canal, it • These infections are introduced during or after the
can be classified as intra radicular and extra radicular. treatment.
-
-
• In these infections, those organisms are present which
were not prevalent during primary endodontic infections.
Intra-radicular Infections
• These organisms can enter the pulp cavity even after the
In intra radicular infections, microorganisms are present completion of endodontic treatment.
-
within the root canal system. These can be primary, secondary • Commonly found microorganisms in these infections
and persistent infections according to the time of organisms can be Pseudomonas aeruginosa, Staphylococcus, E. coli,
entry into the canal. E. faecalis and Candida sp.

Primary Intra-radicular Infections (Fig. 4.13) Persistent Intra-radicular Infections (Fig. 4.15)
• They are characterized by presence of mixed habitat, • In these infections, E. faecalis is most commonly found
mainly dominated by gram negative anaerobic bacteria organism.
-
like Porphyromonas, Prevotella, Fusobacterium, Dialister, • This organism plays a major role in etiology of persistent
Campylobacter and Treponema. periapical lesions.

vip.persianss.ir
Endodontic Microbiology 57


Fig. 4.15 Non healing of periapical lesion because of untreated canal Fig. 4.16 Periapical lesion due to root canal failure of 47

-

• E. faecalis is considered to be most common reason for
Microbiology of infected root canal
failed root canals and in canals with persistent infection. Obligate anaerobes Facultative anaerobes
• It is a gram-positive cocci and is facultative anaerobe.


Gram-negative bacilli Gram-negative bacilli


• Due to presence of following features, it can stay in root Porphyromonas* Capnocytophaga


canals even in adverse conditions: Prevotella** Eikenella


– It can persist in poor nutrient environment of root canal Fusobacterium


treated teeth. Campylobacter
– It can survive in presence of medicaments like calcium Bacteroides
Gram-negative cocci Gram-negative cocci


hydroxide.

Veillonella Neisseria
– It can stay alive in presence of irrigants like sodium

Gram-positive bacilli Gram-positive bacilli


hypochlorite Actinomyces Actinomyces

– It can convert into viable but noncultivable state.

Lactobacillus Lactobacillus



– It can form biofilms in medicated canals. Proprionibacterium



– It can penetrate and utilize fluid present in dentinal Gram-positive cocci Gram-positive cocci



tubules. Streptococcus Streptococcus

– It can survive in prolonged periods of starvation and Peptostreptococcus Enterococcus

Spirochetes Fungi


utilize tissue fluid that flow from periodontal ligament.

Treponema Candida
– It can survive in low pH and high temperature.



– It can acquire gene encoding resistance combined with *Dark pigmented bacteria
**Dark pigmented bacteria and nonpigmenting bacteria


natural resistance to antibiotics.
– It can establish mono-infections in medicated root canals.


Extra-radicular Infections (Fig. 4.16)
IDENTIFICATION OF THE BACTERIA
• Extra-radicular infections can be independent of intra-
radicular infections like apical Actinomyces or sequel of Following tests can be done to detect microorganisms and to
intraradicular infections, e.g. acute alveolar abscess. test which antibiotic they are sensitive to.
• Commonly found microorganisms in extra-radicular
infections are Actinomyces sp., Treponema sp., P. gingivalis, Gram’s Stain
F. nucleatum and P. endodontalis.
• It was developed by Christian Gram in 1884.
• It helps in differentiating bacterias in gram-positive and
The pathogenicity of Bacteroides is mainly related to the
gram negative organisms.
presence of lipopolysaccharides and peptidoglycans. These:
-
• Induce hormones like cytokinins which play an important role in
Culture


inflammations
• Stimulate B- lymphocytes
Culture taking method though done less these days, but it still


• Activate complement cascade


• Release various enzymes like collagenase holds its importance because of wide range of bacteria found


• Enhance production of various pain mediators like bradykinin, in the endodontic infections. The empirical administration


histamine and prostaglandins of antibiotics may not produce satisfactory results, in such
• LPS once released (as endotoxin) causes biological effects cases, culturing may provide a valuable information for better


including inflammation and bone resorption. antibiotic selection.

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Textbook of Endodontics

Principle of Culturing Anaerobic Culture Method


Culturing of root canals is done for two main reasons: • An anaerobic bacteria culture is a method used to grow
1. In cases of persistent infection, to grow and isolate the anaerobes from a clinical specimen.

microbial flora for antibiotic sensitivity and resistance • Anaerobic bacterial culture is performed to identify
profiles. bacteria that grow only in the absence of oxygen.
2. To assess the bacteriologic status of root canal system • The methods of obtaining specimens for anaerobic culture

before obturation and determine the effectiveness of and the culturing procedure are performed to ensure that
debridement procedure. the organisms are protected from oxygen.

Types of tissue cultures Culture Technique


• Cell culture: It is an in vitro growth of cells although the cells For culturing, samples can be obtained from either from an
 
proliferate they do not organize into tissue. infected root canal or from a periradicular abscess.
• Anaerobic culture: It is the culture which is carried out in the
 
absence of air. Sample from draining root canal
• Pure culture: It is a culture of a single cell species, without
• Isolate the tooth with a rubber dam. Disinfect the surface
 
presence of any contaminants.
• Primary culture: Refers to cultures prepared from tissues taken
of the tooth and surrounding area with betadine, chlor­
hexidine or NaOCl.
 
directly from animals.
• Secondary culture: It refers to a subculture derived from a primary • Gain access to the root canals using sterile burs and
 
culture. instruments.
• Plate culture: It refers to the culture which is grown on a medium, • If there is drainage, collect the sample using a sterile
 
usually agar or gelatin, on a Petri dish. needle and syringe or with use of sterile absorbent paper
• Streak culture: It refers to the culture one in which the medium is points. Place the aspirate in anaerobic transport media.
 
inoculated by drawing an infected wire across it.
• Suspension culture: It refers to a culture in which cells multiply Sample from dry canal
 
while suspended in a suitable medium. • To sample a dry canal, use a sterile syringe to place
• Slant culture: This culture is made on the surface of solidified
transport media into canal.
 
medium in a tube which has been tilted to provide a greater
surface area for growth. • Take the sample using a syringe or paper points and place
• Stab culture: In this culture, the medium is inoculated by the aspirate in anaerobic media.
 
thrusting a needle deep into its substance.
• Tissue culture: It refers to the culture in which maintenance or Sample from the abscess
 
growth of tissue, organ primordia, or the whole or part of an organ • Palpate the fluctuant abscess and determine the most
in vitro is done so as to preserve its architecture and function. dependent part of swelling.
• Disinfect the surface of mucosa with alcohol or iodophor.


• Penetrate a sterile 16 to 20 gauge needle in the surface and
Types of Culture Medium aspirate the exudates.
• Liquid (broth) • Inject this aspirate into anaerobic transport media.
• Solid (agar)
• Semisolid.
Culture Reversal
Liquid culture medium • Sometimes negative culture becomes positive after 24 to
• The original liquid media developed by Louis Pasteur 48 hours.
contained wine or meat broth. • So it is advised to allow more than 48 hours between taking
• In liquid media, nutrients are dissolved in water and culture and obturation.
bacterial growth is indicated by a change in the broth’s
appearance from clear to turbid. Advantages of culturing method
• Minimum of 106 bacteria per milliliter of broth are required • Culture helps to determine bacteriological status of root canal
for turbidity to be detected with unaided eye.

• It helps to isolate microbial flora for resistant profiles and for
 
• More of the bacterial growth is indicated by greater is the antibiotic sensitivity
turbidity. • Helps in identification of broad range of microorganisms.

Disadvantages of culturing method
Solid media
• Unable to grow several microorganisms which can give false
• It was developed by Robert Koch in 1881. It contained
 
negative results
pieces of potato, gelatin, and meat extract. • Strictly depend on mode of sample transport which must allow
• Since gelatin used to liquefy at 24°C, so he substituted it
 
growth of anaerobic bacteria
with agar. • Low sensitivity and specificity

• Time consuming
Bacteriological media: It consists of water, agar, growth

• Expensive and laborious.
enriching constituents like yeast extract, and blood.

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Endodontic Microbiology 59


Molecular Diagnostic Methods Advantages of PCR method
• PCR has remarkable sensitivity and specificity because each

 
Advantages of molecular methods distinct microbial species has unique DNA sequences
• They are helpful in detection of both cultivable and uncultivable • PCR can be used to detect virtually all bacterial species in a
 
 
microbial species sample
• They are more sensitive tests • It is also used to investigate microbial diversity in a given

 
• Molecular methods have greater specificity environment. Clonal analysis of microorganisms can also be

• They are less time consuming done by PCR method.

• Do not need special control for anaerobic bacteria Disadvantages of PCR method

• Are useful when a large number of samples are needed to be • Identify microorganisms qualitatively not quantitatively
 
analyzed for epidemiologic studies


• Detect only target microorganisms
• They do not require cultivation


• Difficult in microorganisms with thick wall like fungi

• They can be identified even when they are viable


• Possibility of false positive and negative results.

• They can be used during antimicrobial treatment



• Large number of samples can be stored at low temperature and
 
surveyed at once.
HOW TO COMBAT MICROBES
• To overcome disadvantages of culturing method, various IN THE ENDODONTIC THERAPY?
molecular diagnostic methods have developed. The microbial ecosystem of an infected root canal system
• Molecular diagnostic methods identify the microorgan­ and inflammatory response caused by it will persist until
isms using gene as a target which are unique for each source of irritation is completely removed. The main factor
species. These include DNA-DNA hybridization method, which is needed for successful treatment of pulp and
polymerase chain reaction method. periradicular inflammation is complete removal of the
source of infection such as microorganisms and their by
products, etc.
DNA-DNA Hybridization Method
Following measures should be taken to completely rid of
• This method uses DNA probes which target genomic DNA

these irritants:
or individual genes.
• Thorough cleaning and shaping of the root canal
• This method helps in simultaneous determination of the
system: Thorough cleaning and shaping followed by three
presence of a multitude of bacterial species in single or
dimensional obturation of the root canals have shown
multiple clinical samples and is especially useful for large
to produce complete healing of periradicular tissue
scale epidemiologic research.
(Figs 4.17A to C). Complete debridement of canal should
• In this method, segments of labeled, single strand DNA
be done with adjunctive use of irrigants like sodium
locate and bind to their complementary nucleic acid
hypochlorite which efficiently removes bacteria as well as
sequences.
their substrate from irregularities of canal system where
• After washing, the presence of bound label indicates the
instruments cannot reach such as fins, indentations, cul
presence of the target DNA sequence.

-
de sacs, etc.
-
• Oxygenating a canal simply by opening it is detrimental

Advantages of DNA-DNA hybridization method to anaerobes. Use of oxygenating agents as glyoxide can be
• Can be used for large scale epidemiological research of great help but care should be taken to avoid inoculation

• Allows simultaneous detection of multiple species of these oxygenating agents into periapical tissues.

• Microbial contaminants are not cultivated and their DNA is not • A tooth with serous or purulent or hemorrhagic exudate
 

amplified. should be allowed to drain with rubber dam in place for
Disadvantages of DNA-DNA hybridization method a time under supervision. An abscess which is a potent
• Cross reaction can occur on non-target microorganisms irritant, has an elevated osmotic pressure. This attracts

• Identifies only cultivable microorganisms more tissue fluid and thus more edema and pain. Drainage

• Does not detect unexpected by canal or by soft tissues decrease discomfort caused by

• Detects only target microorganisms.
inflammatory mediators.

• Antibiotics should also be considered as adjunctive in

severe infections. The choice of antibiotic agent should
Polymerase Chain Reaction Method be done on the knowledge of microorganisms associated
• Polymerase chain reaction (PCR) method involves in vitro with the endodontic infections.
replication of DNA, therefore it is also called as “genetic • Intracanal medicaments play an important role in

xeroxing” method. combating the microorganisms.
• Multiple copies of specific region of DNA are made by • Use of calcium hydroxide in canals with necrotic pulps

repeated cycles or heating and cooling. after instrumentation have shown to provide the beneficial

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60  
Textbook of Endodontics

A B C
Figs 4.17A to C (A) Infection of pulp which has progressed to alveolar abscess; (B) Complete cleaning and shaping

of root canal system; (C) Successful root canal therapy and healed periapical bone

results. Intracranial use of calcium hydroxide have shown BIBLIOGRAPHY


to increase the efficiency of sodium hypochlorite and
1. Baumgartner JC, Falkler WA Jr. Bacteria in the apical 5 mm of
also the effectiveness of antimicrobial agent. Calcium
infected root canals. JOE. 1991;17:380.
hydroxide powder is mixed with water or glycerin to 2. Byström A, Happonen RP, Sjögren U, Sundqvist G. Healing of
form a thick paste which is placed in pulp chamber with periapical lesions of pulpless teeth after endodontic treatment
amalgam carrier or a syringe. This paste is covered with a with controlled asepsis. Endod Dent Traumator. 1987;3:58.
sterile cotton pellet and access is sealed with temporary 3. Jose F Siqueira Jr, Isabela N Rocas. Clinical implications
restoration. and microbiology of bacterial persistence after treatment
Thus we can say that for successful endodontic outcome, procedures’. J Endod. 2008;34:1291-301.

one must have awareness of the close relationship between 4. Jose F Siqueira Jr. PCR methodology as a valuable tool for
endodontic infections and microorganisms. identification of endodontic pathogen. J Dent;2004;31:333-9.
5. Jose F Siqueira Jr. Taxododontic changes of bacteria associated
with endodontic infections. J Endodon. 2003;29(10):619-23.
6. Kakehashi S, Stanley HR, Fitzgerald RJ. ‘The effects of surgical
QUESTIONS exposures of dental pulps in germ free and conventional
1. What are different methods used for identification of bacteria. laboratory rats’. Oral Surg. 1965;20:340.
7. Nair PNR. ‘Light and electron microscopic studies of root canal


Write in detail about culture method?
2. Write short notes on: flora and periapical lesions’. J Endod. 1987;13:29-39.
8. Sjögren U, Figdor D, persson S, Sundqvist G. Influence


• Anachoresis
• Microbial virulence and pathogenicity of infection at the time of root filling on the outcome of
• Explain microbiology of infected root canals. endodontic treatment of teeth with apical periodontitis. Int
Endod J. 1997;30(5):297-306.

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Biofilm in Endodontics
5
 Stages of Biofilm Formation  Ultrastructure of Biofilm  Methods to Eradicate Biofilms



 Types of Endodontic Biofilm  Microbes in Endodontic Biofilms


Biofilm can be defined as a sessile multi-cellular microbial • Third stage involves the multiplication and metabolism of
community characterized by cells that are firmly attached attached microorganisms that ultimately will result in a
to a surface and enmeshed in a self produced matrix of structurally organized mixed microbial community.
extracellular polymeric substances. Bacterial biofilms are • Fourth stage involves detachment of biofilm microorganisms.

­
very prevalent in the apical root canals of teeth with primary
and post-treatment apical periodontitis. These bacterial TYPES OF ENDODONTIC BIOFILM
endodontic communities are often found adhered to or at
least associated with the dentinal canal walls, with bacterial Types of endodontic biofilm
cells encased in an extracellular amorphous matrix. In any •  Intracanal biofilms
natural environment, bacteria show the tendency to aggregate •  Extraradicular biofilms
in adherent microbic communities. The biofilm forms on any •  Periapical biofilms
surface that comes in contact with natural liquids. •  Biomaterial centered infections.

STAGES OF BIOFILM FORMATION (FIG. 5.1) Intracanal Microbial Biofilm


The formation of biofilm follows a series of developmental • Intracanal biofilm is microbial biofilm formed on the root
stages. canal dentin of infected tooth.
• First stage of biofilm formation involves the adsorption of • First identification of biofilm was earlier reported by Nair
macromolecules in the planktonic phase to the surface, in 1987 under transmission electron microscopy.
leading to the formation of a conditioning film. • Major bulk of the organisms existed as loose collections
• Second stage involves adhesion and co-adhesion of of cocci, rods, filaments and spirochetes apart from this
microorganisms and attachment may be strengthened bacterial condensations were seen as palisade structure
through polymer production and unfolding of cell surface similar to dental plaque seen on tooth surface.
structures. • Different morphologically distinct types of bacteria were
observed in these biofilms.

Fig. 5.1 Stages of biofilm formation



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Textbook of Endodontics

Extraradicular Microbial Biofilms


• Also termed as root surface biofilms, formed on the
root surface (cementum) adjacent to root apex of
endodontically infected teeth.
• Sites
– Teeth with asymptomatic periapical periodontitis


– Chronic periapical abscess associated with sinus tract.


• The extraradicular biofilms are dominated by cocci and
short rods, with cocci being attached to the tooth substrate.
• Filamentous and fibrillar forms were also observed in the
biofilm.
Fig. 5.2 Diagramatic representation of the structure of a mature biofilm


Abbreviations: N-Nutrients; M-Metabolic products; S-Signal molecules
Periapical Microbial Biofilms
• Periapical microbial biofilms are isolated biofilms found • Eighty-five percent by volume of the biofilm structure is
in the periapical region of an endodontically infected made up of matrix material, while 15 percent is made up
teeth. of cells.
• Microorganism involved are: • A fresh biofilm matrix is made of biopolymers, such as
– Actinomyces polysaccharides, proteins, nucleic acids, and salts.


– P. propionicum. • The structure and composition of a matured biofilm


modifies according to the environmental conditions,
Biomaterial Centered Infection like nutritional availability, nature of fluid movements,
physicochemical properties of the substrate, etc.
• Biomaterial centered infection (BCI) occurs when bacteria • The water channels, which are regarded as a primitive
adheres to an artificial biomaterial surface such as root circulatory system in a biofilm, intersect the structure
canal obturating materials and forms biofilms. of biofilm to establish connections between the
• Presence of biomaterial in close proximity to the host microcolonies. Presence of water channels facilitates
immune system can increase the susceptibility to BCI. efficient exchange of materials between bacterial cells and
• BCI usually reveals opportunistic invasion by nosocomial bulk fluid, which in turn helps to coordinate functions in a
organisms. Coagulase-negative Staphylococcus, S. aureus, biofilm community.
enterococci, streptococci, P. aeruginosa, and fungi are • The structural feature of a biofilm that has the highest
commonly isolated from infected biomaterial surfaces. impact in chronic bacterial infection is the tendency of
• Three phases of bacterial adhesion to biomaterial surface: microcolonies to detach from the biofilm community.
Phase 1: Transport of bacteria to biomaterial surface. During the process of detachment, the biofilm transfer

Phase 2: Initial, nonspecific adhesion phase. particulate constituents (cells, polymers, and precipitates)

Phase 3: Specific adhesion phase. from the biofilm to the fluid bathing the biofilm.

ULTRASTRUCTURE OF BIOFILM (FIG. 5.2) MICROBES IN ENDODONTIC BIOFILMS
A fully developed biofilm is described as a heterogeneous
Methods to isolate microbes
arrangement of microbial cells on a solid surface.
•  Culture
•  Microscopy
Microcolonies •  Immunological methods
•  Molecular biology methods
• The basic structural unit of a biofilm is the microcolonies
or cell clusters formed by the surface adherent bacterial
cells. Microorganisms involved in biofilm formation
•  E. faecalis
• Microcolonies are discrete units of densely packed
•  Coagulase–negative Staphylococcus
bacterial cell (single or multispecies) aggregates. •  Streptococci
• There is a spatial distribution of bacterial cells (micro •  Actinomyces species
­
colony) of different physiological and metabolic states •  P. propionicum
within a biofilm. •  Others: P. aeruginosa, fungi, Fusobacterium nucleatum, Porphy­

romonas gingivalis, Tannerella forsythensis, Actinomyces species
and P. propionicum.
Glycocalyx Matrix
• A glycocalyx matrix, made up of EPS, surrounds the micro- About 40 to 55 percent of the endodontic Microbiota in
colonies and anchors the bacterial cell to the substrate. primary infections is composed of species still uncultivated.

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Biofilm in Endodontics 63


Molecular studies investigating the breadth of bacterial MTAD
diversity in infected root canals have disclosed the occurrence
of uncultivated phytotypes belonging to several genera, MTAD has low pH and thus can act as a calcium chelator and
including: cause enamel and root surface demineralization. In addition,
• Synergistes it has been shown that it is a substantive medication (becomes
• Dialister absorbed and gradually released from tooth structures such
• Prevotella as dentin and cementum.
• Solobacterium
• Olsenella Tetraclean
• Fusobacterium
Pappen FG et al (2010) found that tetraclean is more effective
• Eubacterium
than MTAD against E. faecalis in planktonic culture and in
• Megasphaera
mixed-species in the in vitro biofilm as cetrimide in tetraclean
• Veillonella
improved the antimicrobial properties of the solutions,
• Selenomonas.
whereas Tween 80 present in MTAD seemed to have a neutral
or negative impact on their antimicrobial effectiveness.
METHODS TO ERADICATE BIOFILMS
Calcium Hydroxide
Sodium Hypochlorite
A commonly used intracanal medicament, has been shown
It is effective against biofilms containing P. intermedia, to be ineffective in killing E. faecalis on its own, especially
Peptostreptococcus micros, Streptococcus intermedius, Fuso­ when a high pH is not maintained. However, combination of
bacterium nucleatum and E. faecalis as it disrupts oxidative calcium hydroxide and camphorated paramonochlorophenol
phosphorylation and inhibits DNA synthesis of bacteria. completely eliminates E. faecalis. Two percent chlorhexidine
Dunavant et al (2006) concluded that both 1 percent NaOCl gel when combined with calcium hydroxide achieves a
and 6 percent NaOCl were more efficient in eliminating E. pH of 12.8 and can completely eliminate E. faecalis within
faecalis biofilm than the other solutions tested. dentinal tubules. Chlorhexidine and calcium hydroxide
when combined together have shown better antimicrobial
Chlorhexidine Digluconate properties than calcium hydroxide alone.

It is effective against both gram-positive and gram-negative


bacteria due to its ability to denaturate the bacterial cell wall Ultrasonically Activated Irrigation
while forming pores in the membrane. It kills E. faecalis cells Bhuva B et al (2010) found that use of ultrasonically activated
in 30 seconds or less in concentrations of 0.2 to 2 percent. irrigation using 1 percent sodium hypochlorite, followed by
Although in vitro studies have demonstrated the antibacterial root canal cleaning and shaping improves canal and isthmus
effect of CHX against E. faecalis to be superior to that of NaOCl, cleanliness in terms of necrotic debris/biofilm removal.
there are no in vivo studies yet available that would confirm
the better activity of CHX against this resistant species in the
infected root canal also. Ozone/Ozonated Water
Viera MR et al (1999) reported that Ozone in 0.1 to 0.3 ppm
QMiX concentration is able to completely kill bacteria after 15 or 30
minutes of contact time.
Qmix consists of EDTA, chlorhexidine, and detergent. It is as
effective as 6 percent NaOCl in killing 1-day old E. faecalis but
slightly less effective against bacteria in 3-week old biofilm. Lasers
Lasers induce thermal effect producing an alteration in the
Iodine bacterial cell wall leading to changes in the osmotic gradients
It is bactericidal, fungicidal, tuberculocidal, virucidal, and and cell death. Noiri et al found that Er:YAG irradiation
sporicidal as it penetrates into microorganisms and attacks reduces the number of viable cells in most of the biofilms
proteins, nucleotides, and fatty acids resulting in cell death. of A. naeslundii, E. faecalis, L. casei, P. acnes, F. nucleatum,
P. gingivalis and P. nigrescens.
EDTA
Plasma Dental Probe
It has little if any antibacterial activity. On direct exposure for
extended time, EDTA extracts bacterial surface proteins by It is effective for tooth disinfection. Plasma emission spectro
­
combining with metal ions from the cell envelope, which can scopy identifies atomic oxygen as one of the likely active
eventually lead to bacterial death. agents for the bactericidal effect.

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Textbook of Endodontics

Photoactivated Disinfection details of the biofilm lifestyle to be revealed and development


of various strategies for their complete eradication from root
It is a combination of a photosensitizer solution and low- canals.
power laser light. Photodynamic therapy/Light activated
therapy destroys an endodontic biofilm when a photo-
sensitizer selectively accumulated in the target cell is activated QUESTIONS
by a visible light of appropriate wavelength. 1. Define biofilm. What are different stages of biofilm formation.
2. What are different types of biofilms? Enumerate various
methods to eradicate biofilms.
Antibacterial Nanoparticles 3. Write short notes on:
Antibacterial nanoparticles bind to negatively charged • Ultrastructure of biofilm.
surfaces and have excellent antimicrobial and antifungal • Microbiology of biofilms.
activities. Studies have also shown that the treatment of
root dentin with ZnO nanoparticles, Chitosan-layer-ZnO BIBLIOGRAPHY
nanoparticles, or Chitosan nanoparticles produces an 80 to
95 percent reduction in the adherence of E. faecalis to dentin. 1. Czonstkowsky M, Wilson EG, Holstein FA. The smear layer in
endodontics. Dent Clin North Am. 1990;34:13-25.
2. Distel JW, Hatton JF, Gillespie MJ. Biofilm formation in
Endoactivator System medicated root canals. J Endod. 2002;28:689-93.
3. Donlan RM, Costerton JW. Biofilms: survival mechanisms of
It is able to debride into the deep lateral anatomy, remove the clinically relevant microorganisms. Clin Microbiol Rev. 2002;
smear layer and dislodge simulated biofilm clumps within 15:167-93.
the curved canals. 4. Dunavant TR, Regan JD, Glickman GN, Solomon ES, Honeyman
AL. Comparative evaluation of endodontic irrigants against
CONCLUSION Enterococcus faecalis biofilms. J Endod. 2006;32:527-31.
5. Hargreaves KM, Cohen S.  Pathways of the Pulp, 10th edn.
Ultrastructure of endodontic biofilms should be studied so as Mosby: Elsevier; 2012.
to provide a better understanding of its physiology, ecology, 6. Ingle JI, Bakland LK, Decker BC. Endodontics, 6th edn.
pathogenicity, and response to treatment. Unraveling the Elsevier; 2008.
specific composition of endodontic biofllms will require 7. Kishen A. Advanced therapeutic options for endodontic
biofilms. Endo Topics. 2012;22:99-123.
the integration of sophisticated microscopic and molecular
8. Nair PNR. Light and electron microscopic studies on root canal
microbiology approaches. This knowledge can be of utmost flora and periapical lesions. J Endod. 1987;13:29-39.
importance not only in promoting a refined understanding 9. Prabhakar J, Senthilkumar M, Priya MS, Mahalakshmi K,
of endodontic biofilms, but also in helping to develop better Sehgal PK, Sukumaran VG. Evaluation of antimicrobial efficacy
strategies for treatment. Moreover, it is very important of herbal alternatives (Triphala and green tea polyphenols),
to investigate the resilience, recovering ability, and fate MTAD, and 5% sodium hypochlorite against Enterococcus
of biofilm communities that are only partially aftected or faecalis biofilm formed on tooth substrate: an in vitro study.
disrupted by treatment. Another potential focus of study is the J Endod. 2010;36(1):83-6.
10. Ruddle CJ. Endodontic disinfection—tsunami irrigation.
susceptibility of the biofilm matrix to the effects of treatment
Endod Prac; 2008.
and its fate if left behind, so as to shed light on the issue of 11. Svensater G, Bergerholtz G. Biofilms in endodontic infections.
the remaining biofilm “carcass” in some way negatively Endo Topics. 2004;9:27-36.
influencing periradicular tissue healing. As the technologies 12. Usha HL, Kaiwar A, Mehta D. Biofilms in endodontics: new
for the study of biofilms in nature are being developed and understanding to an old problem. Int J Cont Dent. 2010;1(3):44-
becoming more advanced, the potential exists for further 51.

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Rationale of Endodontic
Treatment 6
 Theories of Spread of Infection  Antibodies (Specific Mediators of  Kronfeld’s Mountain Pass Theory



 Culprit of Endodontic Pathology Immune Reactions)  Rationale of Endodontic Therapy


 Portals for Entry of Microorganisms  Role of Immunity in Endodontics


 Inflammation  Endodontic Implications


 Nonspecific Mediators of Periradicular (Pathogenesis of Apical Periodontitis

Lesions as Explained by Fish)

Endodontic pathology is mainly caused by injury to the tooth Mechanism of Focal Infection
which can be physical, chemical or bacterial. Such injury can
results in reversible or irreversible changes in the pulp and There are generally two most accepted mechanisms
periradicular tissues. These resultant changes depend on the considered responsible for initiation of focal infection:
intensity, duration, pathogenicity of the stimulus and the host 1. Metastasis of microorganisms from infected focus by

defense mechanism. The changes that occur are mediated by either hematogenous or lymphogenous spread.
a series of inflammatory and immunological reactions (in 2. Carrying of toxins or toxic byproducts through blood

the vascular, lymphatics and connective tissue). All these stream and lymphatic channel to site where they may
reactions take place to eliminate the irritant and repair any initiate a hypersensitive reaction in tissues.
damage. For example: In scarlet fever, erythrogenic toxin liberated

However, certain conditions are beyond the reparative by infected streptococci is responsible for cutaneous
features of this disease.

ability of the body and need to be treated endodontically to
aid the survival of tooth.
Rationale of endodontic therapy is complete debridement Oral Foci of Infection

of root canal system followed by three-dimensional
obturation. Possible sources of infection in oral cavity which later on may
set up distant metastasis are:
• Infected periapical lesions such as:
THEORIES OF SPREAD OF INFECTION – Periapical granuloma


– Periapical abscess


Focal infection – Periapical cyst


It is localized or general infection caused by the dissemination of • Teeth with infected root canals.
microorganisms or toxic products from a focus of infection. • Periodontal diseases with special reference to tooth
Focus of infection extraction.
This refers to a circumscribed area of tissue, which is infected with
exogenous pathogenic microorganisms and is usually located near
a mucous or cutaneous surface. CULPRIT OF ENDODONTIC PATHOLOGY
Many studies have shown that root canal infections are
multibacterial in nature. In 1965, Kakehashi found that when
Theory Related to Focal Infection dental pulps of conventional and germ free rats were exposed
About a century ago, William Hunter first suggested that oral to their own oral microbial flora, the conventional rats
microorganisms and their products involved in number of showed pulpal and periapical lesions whereas the germ free
systemic diseases, are not always of infectious origin. rats did not show any development of lesion. So he described
In the year of 1940, Reimann and Havens criticized the importance of microorganisms for the development of pulpal

theory of focal infection with their recent findings. and periapical pathologies.

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Textbook of Endodontics

PORTALS FOR ENTRY OF MICROORGANISMS • Physical agents like cold, heat, mechanical trauma or
radiation.
(FIGS 6.1 AND 6.2) • Chemical agents like organic and inorganic poisons.
• Most common route for entering of microorganisms to • Infective agents like bacteria, viruses and their toxins.
dental pulp is dental caries. • Immunological agents like antigen-antibody cell mediated
• Microorganisms can also pass through open dentinal reactions.
tubules and subsequently to the pulp resulting in its
necrosis. Signs of Inflammation
• Microorganisms can enter into the pulp via accessory and
lateral canals which connect pulp and the periodontium. The Roman writer Celsus in 1st century AD gave four cardinal
• Anachoresis: Microorganisms are transported in the signs of inflammation:
blood to an area of inflammation where they establish an 1. Rubor (redness)


infection. 2. Tumor (swelling)


• Contamination of the pulp can also occur by bacteria 3. Color (hear)


through defective restorations with marginal leakage. 4. Dolor (pain).


Virchow later added the fifth sign function lasea (loss of


function).
INFLAMMATION (FIG. 6.3)
Inflammation is defined as the local response of living Inflammation is of Two Types
mammalian tissue to injury. 1. Acute inflammation dominated by polymorphonuclear
It is a body defense reaction in order to limit the spread

­
lymphocytes (PMNLs) and few macrophages.

or eliminate it or to remove consequent necrosed cells and 2. Chronic inflammation dominated by lymphocytes,
tissues. Following agents cause inflammation:

macrophages and plasma cells.

Tissue Changes Following Inflammation


As a result of inflammation tissues exhibit two types of
changes viz degenerative changes and proliferative changes.
1. Degenerative changes in the pulp can be:

• Fibrous
• Resorptive
• Calcific.
– Continuous degeneration of the tissue results in


necrosis. Suppuration is another form of degenera-
tion which is due to injury to polymorphonuclear
cells.
– This injury causes release of proteolytic enzymes


with resulting liquefaction of dead tissues thus
leading to formation of pus or suppuration.
Fig. 6.1 Radiograph showing poorly obturated canals

Fig. 6.2 Deep carious lesion resulting in pulp

necrosis and periapical lesion Fig. 6.3 Inflammatory cells present at the healing site

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Rationale of Endodontic Treatment 67


Three requisites which are necessary for suppuration: Macrophages (Fig. 6.7)
1. Tissue necrosis • When the PMNLs fail to remove the bacteria, the circulating

2. Polymorphonuclear leukocytes monocytes reach the site of inflammation and change into

3. Digestion of the necrotic material by proteolytic enzymes macrophages.
 
released by injured polymorphonuclear cells. • These macrophages are slow moving and remain at the
site of inflammation for a longer time (approximately
Clinical significance: An abscess can result even in 2 months). This result in development of chronic

absence of microorganisms because of chemical or inflammation.
physical irritation. It results in formation of sterile abscess.
2. Proliferative changes: Macrophages perform following functions:

• These are produced by irritants which are mild enough •  Help in phagocytosis and pinocytosis
•  Perform immunological function.
to act as stimulants. These irritants may act as both
•  Secrete lysosomal enzymes
irritant and stimulant, such as calcium hydroxide and •  Secrete complement protein and prostoglandins.
its effect on adjacent tissues. •  Provide antigen to the immunocomplement cells.
• In the approximation of the inflamed area, the irritant •  They act as scavenger of dead cells, tissues and foreign bodies.
may be strong enough to produce degeneration or •  They fuse with other macrophages to produce multinucleated


destruction, whereas at the periphery, the irritant may giant cells like osteoclasts, dentinoclasts and foreign body giant
be mild enough to stimulate proliferation. cells.
• The principal cells of proliferation or repair are the
fibroblasts, which lay down cellular fibrous tissues.
• In some cases, collagen fibers may be substituted by
a dense acellular tissue. In either case, it results in
formation of fibrous tissue.

Inflammatory Cells (Fig. 6.4)


Neutrophils (PMNLs) (Fig. 6.5)
• Along with basophils and eosinophils, polymorphonuclear
­
neutrophils are called granulocytes because of presence of
granules in the cytoplasm.
• Neutrophils are attracted to the site of injury within 24 hrs
and phagocytose the bacteria and cellular debris releasing
lactic acid.
• Because of its low pH, this lactic acid results in death of the
PMNLs and release of proteolytic enzymes (pepsin and
cathepsin) prostaglandins and leukotrienes.
• All these changes result in breakdown of the tissue, and
thus, formation of an abscess (dead PMNLs + debris).
Fig. 6.5 Neutrophil

Eosinophils (Fig. 6.6)
Eosinophils have many functional and structural similarities
with neutrophils like their formation in bone marrow,
phagocytosis, presence of granules in the cytoplasm,
bactericidal and toxic action against many parasites.

Fig. 6.4 Inflammatory cells Fig. 6.6 Eosinophil



Abbreviation: PMN: Polymorphonuclear

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Textbook of Endodontics

Fig. 6.7 Macrophage Fig. 6.8 Lymphocyte



Lymphocytes (Fig. 6.8) NONSPECIFIC MEDIATORS OF
• Lymphocytes are the most numerous cells (20%-45%) after PERIRADICULAR LESIONS
neutrophils.
• There are two types of lymphocytes seen in apical
Nonspecific mediators can be classified into following types:
periodontitis:
• Cell derived mediators:
1. T-lymphocytes

– Neuropeptides


• T-helper cells (Th): ey are present in the acute


– Eicosanoids/arachidonic acid derivatives
TH


phase of lesion expansion. – Cytokines


• T–suppressor cells (Ts): ey predominate in later – Lysosomal enzymes
TH


stages preventing rapid expansion of the lesion. – Platelet activating factor


2. B-lymphocytes: On getting signals from antigens and – Vasoactive amines


– Prostaglandins


T-helper cells, they transform into plasma cells and


• Plasma derived mediators
secrete antibodies. Their number increases in following

– The fibrinolytic system
conditions:


– The complement system
• Hypersensitivity state


– The kinin system
• Prolonged infection with immunological response.


• Extracellular matrix derived mediators

• Effector molecules.

Osteoclasts
• In the physiologic state, the preosteoclasts remain Cell Derived Mediators (Fig. 6.9)
dormant as monocytes in the periradicular bone.
• In case of apical periodontitis, they proliferate and fuse Neuropeptides
on stimulation by cytokines and other mediators to form • These are generated following tissue injury by the
osteoclasts. somatosensory and autonomic nerve fibers.
• These osteoclasts are responsible for demineralization • Neuropeptides include:
of the bone and enzymatic dissolution of organic matrix – Substance P (SP): Causes vasodilatation, increased


at the osteoclast-bone interface. This results in bone vascular permeability and increased blood flow.
resorption. – Calcitonin-gene related peptide (CGRP): Results in


vasodilatation.
Epithelial Cells
• Cytokines and other mediators stimulate the dormant cell Eicosanoids
rests of Malassez. The injury to cells results in release membrane phospho-
• These cells undergo division and proliferation which lipid, arachidonic acid which is metabolized by either
results in inflammatory hyperplasia. cyclooxygenase pathway or lipooxygenase pathway to form
­
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Rationale of Endodontic Treatment 69


prostaglandins (PGs) or leukotrienes (LTs) respectively, • Activates production of prostaglandins and pro

­
which are involved in inflammatory process. teolytic enzymes.
• Prostaglandins are of various types: • Enhances bone resorption.
– PGE2 • Inhibits bone formation.


– PGD2 IL1β is predominant in cases of periapical pathology.



– PGF2a 2. IL6: It is secreted by lymphoid and nonlymphoid cells




– PGI2 and causes inflammation under the influence of IL1,


• Leukotrienes: These are produced by activation of TNFα and interferon γ(IFN). It is seen in periapical
lipoxygenase pathway of arachidonic acid metabolism. lesions.
Studies have shown the presence of LTB4, LTC4, LTD4 3. IL8: It is produced by macrophages and fibroblasts



and LTE4 in periradicular lesions which cause different under the influence of IL1β and TNFα and is associated
effects on the tissues as shown in Flow chart 6.1. with acute apical periodontitis.
b. Chemotactic cytokines
Cytokines


1. TNF: They are seen in chronic lesions associated



• These are low molecular weight polypeptides secreted by with cytotoxic and debilitating effect. TNFα is seen in
activated structural and hematopoietic cells. chronic apical lesions and root canal exudates.
• Different cytokines such as interleukins and tumor necrosis 2. Colony stimulating factor (CSF): They are produced



factor (TNF) cause development and perpetuation of by osteoblasts and regulate the proliferation of PMNLs
periradicular lesions. and preosteoclasts.
a. Proinflammatory cytokines 3. Growth factors (GF): They are the proteins produced



1. IL1: The local effects of IL1 are: by normal and neoplastic that regulate the growth and


• Enhanced leukocyte adhesion to endothelial walls. differentiation of non-hematopoietic cells. They can
• Stimulate PMNLs and lymphocytes. transform a normal cells to neoplastic cells and are
known as transforming growth factors (TGF).
They are of two types:

i. TGF (produced by malignant cells)—not seen in
a
periapical lesions.
ii. TGF (produced by normal cells and platelets).
b
They counter the adverse effects of inflammatory host

response by:
• Activating macrophages.
• Proliferation of fibroblasts.
• Synthesis of connective tissue fibers and matrices.

Lysosomal Enzymes
Lysosomal enzymes such as alkaline phosphatase, lysozyme,
peroxidases, collagenase cause increase in vascular
permeability, leukocytic chemotaxis, bradykinin formation
Fig. 6.9 Inflammatory response to periapical lesion and activation of complement system.

Flow chart 6.1 Cell derived mediators

Abbreviation: PAF: Platelet activating factor

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Textbook of Endodontics

Platelet Activating Factor • This results in release of fibrinopeptides and fibrin


• It is released from IgE—sensitized basophils or mast cells. degradation products which cause increase in vascular
• Its actions include increase in vascular permeability, permeability and leukocytic chemotaxis.
chemotaxis, adhesion of leukocytes to endothelium and
bronchoconstriction. Complement System
Trauma to periapex can result in activation of kinin system
Vasoactive Amines which in turn activates complement system.
• Vasoactive amines such as histamine, serotonin are
present in mast cells, basophils and platelets. Kinin System
• Their release cause increase in tissue permeability, • These are produced by proteolytic cleavage of kininogen.
vasodilation used vascular permeability (Fig. 6.9). • Release of kinins cause smooth muscle contraction,
vasodilation and increase in vascular permeability (Flow
Prostaglandins chart 6.4).
• These are produced by activation of cyclo-oxygenase
pathway of arachidonic acid metabolism (Flow chart 6.2). Effector Molecules
• Studies have shown high levels of PGE2 in periradicular
lesions. Torbinejad et al found that periradicular The inflammatory process causes not only the destruction
bone resorption can be inhibited by administration of of the cells but also the extracellular matrix in the periapical
indomethacin, an antagonist of PGs. pathosis. The extracellular matrix is degraded by enzymatic
• This indicates that prostaglandins are also involved in the effector molecules by various pathways like:
pathogenesis of periradicular lesions. • Osteoclast regulated pathway
• Phagocyte regulated pathway
• Plasminogen regulated pathway
Plasma Derived Mediators (Flow chart 6.3) • Metalloenzyme regulated pathway [matrix metallo-
proteinases (MMPs)]
Fibrinolytic System
The collagen (proteins) based matrices are degraded by
• The fibrinolytic system is activated by Hageman factor

MMPs.
which causes activation of plasminogen.

Flow chart 6.3 Plasma derived mediators



Flow chart 6.2 Leukotrienes

Flow chart 6.4 Kinin system

Abbreviations: 5–HPETE: 5-hydroperoxyeicosatetraenoic acid;
5–HETE: 5-hydroxyeicosatetraenoic acid

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Rationale of Endodontic Treatment 71


ANTIBODIES (SPECIFIC MEDIATORS OF irritants from infected root canals into periapical area can
lead to formation and perpetuation of periradicular lesions. In
IMMUNE REACTIONS) contrast to pulp, periradicular tissue have unlimited source of
These are produced by plasma cells and are of two types: undifferentiated cells which can participate in inflammation
1. Polyclonal antibodies are nonspecific like IgE mediated and repair. Also these tissues have rich collateral blood supply

reactions which interact with antigen resulting in release and lymph drainage.
of certain chemical mediators like histamine or serotonin. Depending upon severity of irritation, duration and host,


2. Monoclonal antibodies like IgG and IgM, interact with response to periradicular pathosis may range from slight

the bacteria and their byproducts to form antigen- inflammation to extensive tissue destruction. Reactions
antibody complexes that bind to the platelets resulting in involved are highly complex and are usually mediated by
release of vasoactive amines thus increasing the vascular nonspecific and specific mediators of inflammation.
permeability and chemotaxis of PMNs.
The monoclonal antibodies exhibit antimicrobial effect. ENDODONTIC IMPLICATIONS

• In acute abscess, the complex enters the systemic (PATHOGENESIS OF APICAL PERIODONTITIS
circulation. The concentration of these complexes
return to normal levels after endodontic treatment. AS EXPLAINED BY FISH) (FIG. 6.10)
• In chronic lesions, the Ag-Ab complexes are confined Fish described the reaction of the periradicular tissues to
within the lesion and do not enter into the systemic bacterial products, noxious products of tissue necrosis, and
circulation. antigenic agents from the root canal. He established an
experimental foci of infection in the guinea pigs by drilling
ROLE OF IMMUNITY IN ENDODONTICS openings in the jaw bone and packing it with wool fibers
saturated with a broth culture of microorganisms. Fish in
The immune system of human being is a complex system 1939 said that the zones of infection are not an infection by
consisting of cells, tissues, organs as well as molecular themselves but the reaction of the body to infection. Thus
mediators that act together to maintain the health and well he concluded that the removal of this nidus of infection will
being of the individual. The cells and microbial irritants result in resolution of infection.
interact with each other via a number of molecular mediators
and cell surface receptors to result in various defense
Four well defined zones of reaction were found during the
reactions.
experiment:
Immunity is of two types: 1. Zone of infection or necrosis (PMNLs)

1. Innate immunity 2. Zone of contamination (Round cell inflitrate-lymphocytes)

3. Zone of irritation (Histiocytes and osteoclasts)

2.  Acquired/adaptive immunity.

4. Zone of stimulation (Fibroblasts, capillary buds and osteoblasts).
 
Innate Immunity
Zone of Infection
• It consists of cells and molecular elements which act as
barriers to prevent dissemination of bacteria and bacterial • In Fish's study, infection was confined to the center of the
products into the underlying connective tissue. lesion.
• The innate immunity is responsible for the initial non-
specific reactions.
• Cells providing innate immunity are neutrophils, mono-
cytes, eosinophils, basophils, NK cells, dendritic cells, and
odontoblasts.

Acquired/Adaptive Immunity
• It involves release of specific receptor molecules by
lymphocytes which recognize and bind to foreign antigens.
• Adaptive immunity is provided by:
– T lymphocytes that release T cell antigen receptors
– B lymphocytes that release B cell antigen receptors or
immunoglobulins.

Histopathology of Periapical Tissue


Response to Various Irritants
Root canal of teeth contains numerous irritants because
of some pathologic changes in pulp. Penetration of these Fig. 6.10 Fish's zones

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72  
Textbook of Endodontics

• This zone is characterized by polymorphonuclear leuko- After this, fibroblasts come in play and build fibrous


cytes and microorganisms along with the necrotic cells tissue, osteoblasts restrict the area by formation of sclerotic
and detructive components released from phagocytes. bone. Along with these if epithelial rests of Malassez are also
stimulated, it results in formation of a cyst.
Zone of Contamination
KRONFELD’S MOUNTAIN PASS
• Around the central zone, Fish observed the area of cellular
destruction. THEORY (FIG. 6.11)
• This zone was not invaded by bacteria, but the destruction Kronfeld had explained that the granuloma does not provide
was due to toxins discharged from the microorganisms in a favorable environment for the survival of the bacteria. He
the central zone . employed the Fish concept so as to explain the tissue reaction
• This zone is characterized by round cell infiltration, in and around the granulomatous area.
osteocyte necrosis and empty lacunae.
• Lymphocytes were prevalent everywhere. Zone A
He compared the bacteria in the infected root canal with
Zone of Irritation the invaders entrenched behind ‘high and inaccessible
• FISH observed evidence of irritation further away from the mountains’, the foramina serving as mountain passes.
central lesion as the toxins became more diluted.
• This is characterized by macrophages, histocytes and Zone B
osteoclasts. The degradation of collagen framework by
phagocytic cells and macrophages was observed while The exudative and granulomatous (proliferative) tissue of the
osteoclasts attack the bone tissue. granuloma represents a mobilized army defending the plains
• Ths histologic picture is much like preparation for repair. (periapex) from the invaders (bacteria). When a few invaders
enter the plain through the mountain pass, they are destroyed
Zone of Stimulation by the defenders (leukocytes). A mass attack of invaders
results in a major battle, analogous to acute inflammation.
• Fish noted that, at the periphery, the toxin was mild
enough to act as stimulant.
• This zone is characterized by fibroblasts and osteoblasts.
Zone C
In response to this stimulatory irritant, fibroblasts result in Only complete elimination of the invaders from their
secretion of collagen fibers. mountainous entrenchment will eliminate the need for a
• These collagen fibers act as wall of defense around the zone defense forces in the ‘plains’. Once this is accomplished, the
of irritation and as a scaffolding on which the osteoblasts defending army of leukocytes withdraws, the local destruction
synthesize new bone. created by the battle is repaired (granulation tissue) and the
So the knowledge gained in FISH study can be applied for environment returns to its normal pattern.

better understanding of reaction of periradicular tissues to a
nonvital tooth.
The root canal is the main source of infection. The micro

­
organisms present in root canal are rarely motile. Though
they do not move from the root canal to the periapical tissues;
but they can proliferate sufficiently to grow out of the root
canal. The metabolic byproducts of these microorganisms
or the toxic products of tissue necrosis may also get
diffused to the periradicular tissues. As the microorganisms
enter in the periradicular area, they are destroyed by the
polymorphonuclear leukocytes. But if microorganisms are
highly virulent, they overpower the defensive mechanism
and result in development of periradicular lesion.
The toxic byproducts of the microorganisms and the

necrotic pulp in the root canal are irritating and destructive to
the periradicular tissues. These irritants along with proteolytic
enzymes (released by the dead polymorphonuclear
leukocytes) result in the formation of pus. This results in
development of chronic abscess.
At the periphery of the destroyed area of osseous tissue,

toxic bacterial products get diluted sufficiently to act as
stimulant. This results in formation of a granuloma. Fig. 6.11 Kronfeld’s mountain pass theory

vip.persianss.ir
Rationale of Endodontic Treatment 73


This explains the rationale for the nonsurgical endodontic infection by completely obliterating the apical foramen

treatment for teeth with periapical infection. The complete and other portals of communication.
elimination of pathogenic irritants from the canal followed by
Rationale of surgical endodontic treatment: The rationale
the three dimensional fluid impervious obturation will result
of surgical endodontics is to remove the diseased tissue
in complete healing of periapical area.
present in the canal and around the apex, and retrofil the root
canal space with biologically inert material so as to achieve a
RATIONALE OF ENDODONTIC THERAPY fluid tight seal.
The rationale of root canal treatment relies on the fact that the
nonvital pulp, being avascular, has no defense mechanisms.
QUESTION
The damaged tissue within the root canal undergoes autolysis 1. What is rationale of endodontics? Explain in detail about fish



and the resulting break down products will diffuse into the zones.
surrounding tissues and cause periapical irritation associated
with the portals of exit even in the absence of bacterial BIBLIOGRAPHY
contamination. It is essential therefore, that endodontic
1. Abou-Rass, Bogen G. Microorganisms in closed periapical
therapy must seal the root canal system three dimensionally lesions. Int Endod J. 1998;31:39.
so as to prevent tissue fluids from percolating in the root 2. Alavi AM, Gulabivala K, Speight PM. Quantitative analysis



canal and toxic by-products from both necrotic tissue and of lymphocytes and their subsets in periapical lesions. Int
microorganisms regressing into the periradicular tissues. Endod J. 1998;31:233.
Endodontic therapy includes: 3. Baumgartner JC, Falkler (Ir) WA. Detection of immunoglobulin
• Nonsurgical endodontic treatment from explant cultures of periapical lesions. J Endod.
• Surgical endodontic treatment. 1991;17:105.
4. Fish EW. Bone infection. J Am Dent Assoc. 1939;26:691.
Nonsurgical endodontic treatment includes three phases: 5. Jontell M, Bergenholtz G, Scheynius K, Ambrose W. Dendritic
1. Access preparation: The rationale for this is to create a cells and macrophages expressing class I antigens in normal

straight line path for the canal orifice and the apex. rat incisor pulp. J Dent Res. 1988;67:1263.
2. Shaping and cleaning: The rationale for this is the 6. Kuo M, Lamster I, Hasselgren G. Host mediators in endodontic


exudates. J Endod. 1998;24:598.

complete elimination of vital or necrotic pulp tissue,
7. Lukic A, Arsenijevic N, Vujanic G, and Ramic Z. Quantitative
microorganisms and their byproducts.


analysis of immunocompetent cells in periapical granuloma:
3. Obturation: Main objective of obturation is to have a three Correlation with the histological characteristics of the lesions.

dimensional well fitted root canal with fluid tight seal so J Endod. 1990;16:119.
as to prevent percolation and microleakage of periapical 8. Robinson HB, Boling LR. The anachoretic effect in pulpitis.
exudate into the root canal space and also to prevent J Am Dent Assoc. 1949;28:268.

vip.persianss.ir
Diagnostic Procedures
7
  Case History   Diagnostic Findings   Digital Dental Radiology
  Pulp Vitality Tests   Role of Radiographs in Endodontics   Phosphor Imaging System
  Recent Advances in Pulp Vitality Testing   Digital Radiography

Diagnosis is defined as utilization of scientific knowledge for comprehensive medical and previous dental history should
identifying a diseased process and to differentiate from other be recorded. In addition, a description of the patient’s
disease process. In other words, literal meaning of diagnosis is symptoms in his or her own words should be noted.
determination and judgment of variations from the normal.
It is the procedure of accepting a patient, recognizing that Chief Complaint
he/she has a problem, determining the cause of problem and
developing a treatment plan which would solve the problem. It consists of information which promoted patient to visit a
There are various diagnostic tools, out of all these, art of clinician. Phenomenon symptoms or signs of deviation from
listening is most important. It also establishes patient-doctor normal are indicative of illness. The form of notation should
rapport, understanding and trust. be in patient’s own words.
Although diagnostic testing of some common complaints
may produce classic results but sometimes tests may produce Symptoms
wrong results, which need to be carefully interpreted by
clinician. Symptoms are defined as signs of departure from the normal.
The diagnostic process actually consists of four steps: They are indicator of illness.
1. First step: Assemble all the available facts gathered from
chief complaints, medical and dental history, diagnostic Symptoms can be:
•  S  ubjective symptom  are  told  by  the  patient. The  most  common 
tests and investigations.
subjective symptom is pain. 
2. Second step: Analyze and interpret the assembled clues to •  O
  bjective symptoms are ascertained by the clinician by different 
reach the tentative or provisional diagnosis. tests.
3. Third step: Make differential diagnosis of all possible
diseases which are consistent with signs, symptoms and
test results gathered. Subjective Symptoms
4. Fourth step: Select the closet possible choice.
The importance of making an accurate diagnosis cannot Pain
be overlooked. Many a times even after applying all the Once the patient completes information about his/her chief
knowledge, experience and diagnostic tests, a satisfactory complaint, a report is made which provides more descriptive
explanation for patient’s symptoms is not determined. In analysis about this initial information. It should include signs
many cases, nonodontogenic etiology is also seen as a source and symptoms, duration, intensity of pain, relieving and
of chief complaint. To avoid irrelevant information and to exaggerating factors, etc. Examples of type of the questions
prevent errors of omission in clinical tests, the clinician which may be asked by the clinician in recording the patient’s
should establish a routine for examination, consisting of chief complaints are as below:
complaint, past medical and dental history and any other • How long have you had the pain?
relevant information in the form of case history. • Do you know which tooth it is?
• What initiates pain?
• How would you describe the pain?
CASE HISTORY – Quality: Dull, sharp, throbbing, constant
The purpose of case history is to discover whether patient has – Location: Localized, diffuse, referred, radiating
any general or local condition that might alter the normal – Duration: Intermittent lasting for seconds, minutes or
course of treatment. As with all courses of treatment, a hours, constant

vip.persianss.ir
Diagnostic Procedures 75

Type of pain Reason for pain Provisional diagnosis


Location •  Localized pain Presence of proprioceptive A-beta fibers  •  Periodontal pain
present in periodontal ligament
•  Diffuse pain Lack of proprioceptive fibers in pulp •  Pulpal pain
Duration •  M
  omentary pain on stimulation •  Reversible pulpitis
•  S  pontaneous pain for long duration •  Irreversible pulpitis
Nature •  S  harp shooting momentary pain on  Stimulation of A-delta fibers because of  •  Dentinal pain
provoking movement of dentinal fluid present in  •  Reversible pulpitis
odontoblastic processes
•  Sharp shooting pain on mastication •  Irreversible pulpitis
•  Fracture of tooth
•  S  pontaneous dull, throbbing pain for long  Stimulation of C-fibers Irreversible pulpitis
duration
Stimulus •  Sweet and sour Due to stimulation of A-delta fibers present  •  Reversible pulpitis
in odontoblastic processes
•  Heat Vasodilatation caused by heat stimulates  •  Irreversible pulpitis
C-fibers of pulp
•  Cold Stimulation of A-delta fibers due to fluid  •  Dentin hypersensitivity
movement in odontoblastic processes
•  Heat and cold •  Early stages of irreversible pulpitis
•  S  timulated by heat and relieved by cold •  Late stages of irreversible pulpitis
•  On lying down or sleep •  Acute irreversible pulpitis

– Onset: Stimulation required, intermittent, spontaneous checklist of medical conditions which are needed to be taken
– Initiated: Cold, heat, palpation, percussion a special care.
– Relieved: Cold, heat, any medications, sleep.
In other words, history of present illness should indicate Checklist for medical history (Scully and Cawson)
severity and urgency of the problem. •  Anemia
•  Bleeding disorders
If a chief complaint is toothache but symptoms are too vague
•  Cardiorespiratory disorders
to establish a diagnosis, then analgesics should be prescribed •  Drug treatment and allergies
to help the patient in tolerating the pain until the toothache •  Endocrine disease
localizes. A history of pain which persists without exacerbation •  Fits and faints
may indicate problem of nonodontogenic origins. •  Gastrointestinal disorders
Pulpal pain can be sharp, piercing and lancinating. It is •  Hospital admissions and attendance
due to stimulation of A delta fibers. •  Infections
Dull, boring, excruciating or throbbing pain occurs if there is •  Jaundice
•  Kidney disease
stimulation of C-fibers. Pulp vitality tests are usually done to
•  Likelihood of pregnancy or pregnant itself
reach the most probable diagnosis. If pain is from periodontal
ligament, the tooth will be sensitive to percussion, chewing If there is any doubt about the state of health of patient,
and palpation. Intensity of pain gives an indication that pain consult medical practitioner before initiating endodontic
is of pulpal origin. Patient is asked to mark the imaginary treatment. Care should also be taken whether patient is
ruler with grading ranging from 0 to 10. on medication such as corticosteroids or anticoagulant
0 - No pain 10-Most painful therapy.
Mild to moderate pain can be of pulpal or periodontal According to standards of American Heart Association,
origin but acute pain is commonly a reliable sign that pain patient should be given antibiotic prophylaxis if there is
is of pulpal origin. Localization of pain also tells origin of high rise of developing bacterial endocarditis. For example
pain since pulp does not contain proprioceptive fibers; it is in cardiac conditions like prosthetic heart valves, rheumatic
difficult for patient to localize the pain unless it reaches the heart disease, previous bacterial endocarditis and complex
periodontal ligament. cyanotic heart diseases.

Medical History Objective Symptoms


There are no medical conditions which specifically Different tests performed by clinician are:
contraindicate endodontic treatment, but there are several • Visual and tactile inspection
which require special care. Scully and Cawson have given a • Percussion test

vip.persianss.ir
76 Textbook of Endodontics

• Palpation Percussion Test


• Periodontal examination Percussion test helps to evaluate the status of periodontium
• Mobility surrounding a tooth. Pain on percussion indicates
• Differential diagnosis inflammation in periodontal ligament which could be due to
• Radiographs trauma, sinusitis and/or PDL disease.
• Pulp vitality tests. Percussion can be carried out by gentle tapping with
gloved finger (Fig. 7.2) or blunt handle of mouth mirror (Fig.
7.3). Each tooth should be percussed on all the surfaces of
Visual and Tactile Inspection tooth until the patient is able to localize the tooth with pain.
For good visual and tactile, inspection, one requires good
vision, mouth mirror, explorer and good light. Before
conducting intraoral examination, check the degree of mouth POINTS TO REMEMBER
opening. For a normal patient, it should be at least two fingers •  D
  egree  of  response  to  percussion  is  directly  proportional  to 
(Fig. 7.1). During intraoral examination, look at the following degree of inflammation
structures systematically: •   Dull  sound  on  percussion  indicates  abscess  formation  while 
• The buccal, labial and alveolar mucosa sharp indicates inflammation
• The hard and soft palate •   Pain  on  percussion  is  indicative  of  possibility  of  following 
conditions:
• The floor of the mouth and tongue
   –  P
  eriodontal abscess
• The retromolar region    –  P
  ulp necrosis (Partial of total)
• The posterior pharyngeal wall and facial pillars    –  H
  igh points in restorations
• The salivary gland and orifices.    –  D
  uring orthodontic treatment
After examining this, general dental state should be
recorded, which include: Palpation
• Oral hygiene status
• Amount and quality of restorative work Palpation is done using digital pressure to check any
• Prevalence of caries tenderness in soft tissue overlying suspected tooth (Fig. 7.4).
• Missing tooth Sensitivity may indicate inflammation in periodontal tissues
• Presence of soft or hard swelling surrounding the affected tooth. Further palpation can tell any
• Periodontal status other information about fluctuation or fixation or induration
• Presence of any sinus tracts of soft tissue, if any (Fig. 7.5).
• Discolored teeth Palpation of salivary glands should be done extraorally.
• Tooth wear and facets Submandibular gland should be differentiated from lymph
• Check color, contour and consistency “three Cs” of hard nodes in the submandibular region by bimanual palpation
and soft tissues (Fig. 7.6).
• Normal tooth has translucent appearance. Any deviation
from normal translucency in form of discoloration, lack of Palpation of temporomandibular joint can be done by
translucency should be checked properly. Gingiva should standing in front of the patient and placing the index fingers
be checked for any deviation from normal pink and firm in the preauricular region. The patient is asked to open the
appearance. mouth and perform lateral excursion to notice (Fig. 7.7).

Fig. 7.1 Degree of mouth opening in a normal patient  Fig. 7.2 Percussion of tooth using gloved finger


should be at least two fingers

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Diagnostic Procedures 77

Fig. 7.3 Percussion of tooth using blunt handle of mouth mirror Fig. 7.5 Palpation of soft tissues

Fig. 7.4 Palpation of soft tissue using digital pressure Fig. 7.6 Bimanual palpation of submandibular gland

• Any restricted movement


• Deviation in movement
• Jerky movement
• Clicking
• Locking or crepitus.
Palpation of lymph nodes should be done to note
any lymph node enlargement, tenderness, mobility and
consistency (Fig. 7.8). The lymph nodes frequently palpated
are preauricular, submandibular, submental and cervical.

If any localized swelling is present, then look for:


•  Local rise in temperature
•  Tenderness
•  Extent of lesion
•  Induration
•  Fixation to underlying tissues, etc.
Fig. 7.7 Examination of temporomandibular joint

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78 Textbook of Endodontics

Fig. 7.8 Examination of lymph nodes  Fig. 7.9 Probing of a tooth determines the level of connective  


tissue attachment

Provisional diagnosis after examination of lymph nodes


Examination Provisional diagnosis
•   Enlargement of submental lymph  Infection of anterior teeth
nodes
•   Involvement of submandibular  Mandibular molar 
lymph nodes infection
•   Enlargement of lymph nodes at  May indicate tonsillar 
angle of mandible infection
•   Firm and tender palpable lymph  Acute infection
nodes associated with fever and 
swelling
•   Palpable lymph node not  Chronic infection
associated with pain
•   Hard-fixed lymph node with stone- Malignancy
like consistency Fig. 7.10 Probing interdentally can identify any rough or 
•  Matted, nontender lymph nodes Tuberculosis overextended proximal restoration

Periodontal Evaluation diagnosis, the clinician should get investigations done which
It can be assessed from palpation, percussion, mobility include lab investigations, radiographs, pulp vitality tests.
of tooth and probing (Figs 7.9 and 7.10). The mobility of a
tooth is tested by placing a finger (Fig. 7.11) or blunt end of Diagnostic Perplexities
the instrument (Fig. 7.12) on either side of the crown and There are certain conditions in which it is difficult to reach
pushing it and assessing any movement with other finger. proper diagnosis even after detailed history and examination.
These conditions can be:
Classification of Mobility • Idiopathic tooth resorption
Grade I: Distinguishable sign of tooth movement more • Treatment failures
than normal • Cracked tooth syndrome
Grade II: Horizontal tooth movement not more than 1 mm • Persistent discomfort
Grade III: Movement of tooth more than 1 mm or when tooth • Unusual radiographic appearances
can be depressed. • Paresthesia.

Differential Diagnosis Radiograph


Sometimes clinical signs and symptoms mimic each other they, In all endodontic cases, a good intraoral radiograph is
so have to be enumerated in different clinical conditions this mandatory as it gives excellent details and help in diagnosis
is known as differential diagnosis. It can include two or more and treatment planning. They help to diagnose tooth related
conditions. After differential diagnosis, to reach at definitive problems like caries, fractures, root canal treatment or any

vip.persianss.ir
Diagnostic Procedures 79

Fig. 7.11 Checking mobility of a tooth by palpating with fingers Fig. 7.13 Interpretation of radiograph according to appearance

Periapical lesions of endodontic origin have following


characteristic features (Fig. 7.14):
•   Loss of lamina dura in the apical region
•   Apparent etiology of pulpal necrosis 
•   Radiolucency remains at the apex even if radiograph is taken by 
changing the angle.

Radiographs help us in following ways:


•  Establishing diagnosis
•  Determining the prognosis of tooth
•  Disclosing the presence and extent of caries (Fig. 7.15)
•  Check the thickness of periodontal ligament
•  To see continuity of lamina dura
•  To  look  for  any  periodontal  lesion  associated  with  tooth  
(Fig. 7.16)
•   To see the number, shape, length and pattern of the root canals 
Fig. 7.12 Checking mobility of a tooth using   (Fig. 7.17)
blunt end of instrument •  To check any obstructions present in the pulp space
•  To check any previous root canal treatment if done (Fig. 7.18)
•  To  look  for  presence  of  any  intraradicular  pins  or  posts  
(Fig. 7.19)
•  To see the quality of previous root canal filling (Figs 7.20 and
previous restorations, abnormal appearance of pulp cavity 7.21)
or periradicular tissues, periodontal diseases and the general •  To see any resorption present in the tooth (Fig. 7.22)
•  To check the presence of calcification in pulp space
bony pattern.
•  To see root end proximal structures
•  Help  in  determining  the  working  length,  length  of  master 
gutta-percha  cone  and  quality  of  obturation  (Figs 7.23
Interpretation of radiograph according to appearance (Fig. 7.13) and 7.24)
Appearance Tentative finding •  During the course of treatment they help in knowing the level of 
instrumental errors like perforation, ledging and instrumental 
Black/Gray area a.  Decay separation (Fig. 7.25).
b.  Pulp
c.  Gingivae or space between teeth
Following lesions should be differentiated from the lesions of
d.  Abscess endodontic origin while interpreting radiographs:
e.  Cyst •  Periodontal abscess
White area a.  Enamel •  Idiopathic osteosclerosis
•  Cementomas
b.  Restoration (Metal, gutta-percha, etc.) •  Giant cell lesions
Creamy white area Dentin appears as creamy white area •  Cysts
White line around teeth Lamina dura around teeth •  Tumors

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80 Textbook of Endodontics

Fig. 7.14 Radiograph showing periapical lesion Fig. 7.17 Radiograph showing canal configuration 


of premolar and molars

Fig. 7.15 Radiograph showing caries in 36 Fig. 7.18 Radiograph showing endodontic 


treatment of premolars

Fig. 7.16 Radiograph showing periodontal involvement of 46 Fig. 7.19 Radiograph showing post and core treatment

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Diagnostic Procedures 81

Fig. 7.20 Radiograph showing poorly  Fig. 7.23 Working, length radiograph


obturated root canals

Fig. 7.21 Radiograph showing root canal fillings  Fig. 7.24 Master cone radiograph


of maxillary anterior teeth

Fig. 7.22 Radiograph showing external resorption Fig. 7.25 Radiograph showing instrument fracture

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82 Textbook of Endodontics

Disadvantages of radiographs Various types of pulp tests performed are:


•   They are only two dimensional picture of a three-dimensional  •  Thermal test
object   –  Cold test
•  Pathological changes in pulp are not visible in radiographs   –  Heat test
•   The initial stages of periradicular diseases produce no changes  •  Electrical pulp testing
in the radiographs  •  Test cavity
•   They do not help in exact interpretation for example radiographic  •  Anesthesia testing
picture  of  an  abscess,  inflammation  and  granuloma  is  almost  •  Bite test
same
•   Misinterpretation  of  radiographs  can  lead  to  inaccurate 
diagnosis Thermal Test
•   Radiographs  can  misinterpret  the  anatomical  structures  like 
incisive and mental foramen with periapical lesions In thermal test, the response of pulp to heat and cold is noted.
•   To know the exact status of multirooted teeth, multiple radio- The basic principle for pulp to respond to thermal stimuli is
graphs are needed at different angles which further increase the  that patient reports sensation but it disappears immediately.
radiation exposure. Any other type of response, i.e. painful sensation even after
removal of stimulus or no response are considered abnormal.
PULP VITALITY TESTS Cold test: It is the most commonly used test for assessing the
vitality of pulp. It can be done in a number of ways.
Pulp testing is often referred to as vitality testing. Pulp vitality
tests play an important role in diagnosis because these
• The most commonly used method for performing pulp
tests not only determine the vitality of tooth but also the
testing is spray with cold air directed against the isolated
pathological status of pulp. Pulp testers should only be used
tooth.
to assess the vital or nonvital pulp as they do not quantify the
• The other method is use of ethyl chloride (–4°C) in form of:
disease, nor do they measure the health and thus, should not
be used to assess the degree of pulpal disease. – Cotton pellet saturated with ethyl chloride (Fig. 7.26).
– Spray of ethyl chloride: After isolation of tooth with
Uses of pulp vitality testing rubber dam, ethyl chloride spray is employed. The ethyl
•   It  is  done  before  carrying  out  restorative  or  orthodontic  chloride evaporates so rapidly that it absorbs heat and
treatment so as to know status of the tooth/teeth even if teeth  thus, cools the tooth.
are asymptomatic and with normal radiographic appearance. • Frozen carbon dioxide (dry ice) is available in the form of
•   To  confirm  whether  radiolucent  area  present  at  apical  part  of  solid stick which is applied to facial surface of the tooth.
tooth is because of:
Advantage of using dry ice is that it can penetrate full
     –  Pulpal origin 
     –  Other pathological reasons
coverage restoration and can elicit a pulpal reaction to the
     –  Or it is a normal anatomic structure cold because of its very low temperature (–78°C).
• Another methods is to wrap an ice piece in the wet gauge
and apply to the tooth. The ice sticks can be prepared by
•  T  o  diagnose  oral  pain  whether  it  is  of  pulpal  or  periodontal 
filling the discarded anesthetic carpules with water and
origin or because of other reason.
•  T  o assess vitality of traumatized teeth (however vitality testing 
placing them in refrigerator.
of traumatized teeth is controversial). • Dichlorodifluoromethane (Freon) (–21°C) and 1, 1, 1,
•   To check the status of tooth especially which has past history of  2-tetrafluoroethane (–15 to –26°C) are also used as cold
pulp capping or deep restoration. testing material.

Sites of localization of acute dental infections


Teeth Usual exit from bone Site of localization
Mandibular incisors Labial Submental space, oral vestibule
Mandibular canine Labial Oral vestibule
Mandibular premolars Buccal Oral vestibule
Mandibular first molar Buccal or lingual Oral vestibule, buccal space, sublingual space
Mandibular second molar Buccal or lingual Oral vestibule, buccal space, sublingual space,
submandibular space
Maxillary central incisor Labial Oral vestibule
Maxillary lateral incisor Labial or palatal Oral vestibule, palatal
Maxillary premolars Buccal or palatal Oral vestibule, palatal
Maxillary molars Buccal or palatal Oral vestibule, buccal space, palatal

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Diagnostic Procedures 83

Fig. 7.26 Application of cotton pellet saturated with ethyl chloride Fig. 7.28 Application of hot burnisher to check vitality of tooth

precautions should be taken not to overheat it because in


this state, it is at higher temperature than required for pulp
testing and may result in pulpal injury.
• Hot burnisher, hot compound or any other heated
instrument may also be used for heat test (Fig. 7.28).
• Use of frictional heat produced by rotating polishing rubber
disc against the tooth surface is another method.
• Another method of heat test is to deliver warm water from
a syringe, on isolated tooth.
• Use of laser beam (Nd: YAG laser) is done to stimulate
pulp.

The preferred temperature for heat test is 150°F (65.5°C)


The patient may respond to heat or cold test in following possible 
ways:
•   Mild, transitory response to stimulus shows normal pulp
Fig. 7.27 Application of heated gutta-percha stick  •   Absence of response in combination with other tests indicates 
on tooth for heat test pulp necrosis. 
•   An  exaggerated  and  lingering  response  indicates  irreversible 
pulpitis.
   But there are certain conditions which can give false negative 
Clinical Tips response, i.e. the tooth show no response but the pulp could be 
possibly vital. These conditions can be:
Use of rubber dam is specially recommended when performing the  •   Recently  erupted  teeth  with  immature  apex—due  to 
test using the ice-sticks because melting ice will run on to adjacent  incompletely  developed  plexus  of  Rashkow.  Hence,  incapable 
teeth and gingivae resulting in false-positive result. of transmitting pain.
•   Recent  trauma—injury  to  nerve  supply  at  the  apical  foramen 
Heat test: Heat test is most advantageous in the condition or  because  of  inflammatory  exudates  around  the  apex  may 
where patient’s chief complaint is intense dental pain upon interfere the nerve conduction
contact with any hot object or liquid. •   Excessive  calcifications  may  also  interfere  with  the  nerve 
conduction.
Different methods used for heat test are: •   Patients on premedication with analgesics or tranquilizers may 
not respond normally.
• Direct warm air to the exposed surface of tooth and note
the patient response.
• If a higher temperature is needed to illicit a response, use
Electric Pulp Testing
heated gutta-percha stick, hot burnisher, hot water.
Heated gutta-percha stick (Fig. 7.27) is the most Electric pulp tester is used for evaluation of condition of
commonly used method for heat testing. In this method, the pulp by electrical excitations of neural elements within
tooth is coated with a lubricant such as petroleum jelly to the pulp. The pulp tester is an instrument which uses the
prevent the gutta-percha from adhering to tooth surface. gradations of electrical current to excite a response from the
The heated gutta-percha is applied at the junction of pulpal tissue. Pulp testers are available with cord which plug
cervical and middle third of facial surface of tooth and into electric outlets for power source (Fig. 7.29) they can
patient’s response is noted. While using gutta-percha stick, also be available as battery operated instrument (Fig. 7.30).

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84 Textbook of Endodontics

electrode. If gloves are not used, the circuit gets completed


when clinician’s finger, contact with electrode and
patient’s cheeks. But with gloved hands, it can be done by
placing patient’s finger on metal electrode handle or by
clipping a ground attachment on to the patient’s lip.
• Once the circuit is complete, slowly increase the current
and ask the patient to point out when the sensation occurs.
• Each tooth should be tested 2 to 3 times and the average
reading is noted. If the vitality of a tooth is in question, the
pulp tester should be used on the adjacent teeth and the
contralateral tooth, as control.

Disadvantages of electric pulp testing


Following conditions can give rise to wrong results:
•  False positive response in:
Fig. 7.29 Electric pulp tester   –   Teeth  with  acute  alveolar  abscess,  because  gaseous  or 
liquefied  products  within  the  pulp  canal  can  transmit 
electric current.
    –   Electrode may contact gingival tissue thus giving the false 
positive response.
    –   In multirooted teeth, pulp may be vital in one or more root 
canals and necrosed in others, thus eliciting a false positive 
response. 
•   In  certain  conditions,  it  can  give  false  negative  response,  for 
Fig. 7.30 Battery operated pulp tester
example:
    –   Recently traumatized tooth
    –   Recently erupted teeth with immature apex.
    –   Patients with high pain threshold
    –   Calcified canals
    –   Poor battery or electrical deficiency in plug in pulp testers.
    –   Teeth with extensive restorations or pulp protecting bases 
under restorations
    –   Patients premedicated with analgesics or tranquilizers, etc.
    –   Partial  necrosis  of  pulp  sometimes  is  indicated  as  totally 
necrosis by electric pulp tester.

Test Cavity
This method should be used only when all other test methods
are inconclusive in results. Here a test cavity is made with
high speed number 1 or 2 round burs with appropriate air
and water coolant. The patient is not anesthetized while
Fig. 7.31 Checking vitality of tooth using electric pulp tester performing this test. Patient is asked to respond if any painful
sensation occurs during drilling. The sensitivity or the pain
felt by the patient indicates pulp vitality. Here the procedure
A positive response indicates the vitality of pulp. No response is terminated by restoring the prepared cavity. If no pain is
indicates nonvital pulp or pulpal necrosis. felt, cavity preparation may be continued until the pulp
chamber is reached and later on endodontic therapy may be
Procedure carried out.
• Before starting the procedure, patient must be explained
about the method. This will be helpful in reducing the
Anesthesia Testing
anxiety of patient.
• Isolation of the teeth to be tested is one of the essential When patient is not able to specify the site of pain and when
steps to avoid any type of false positive response. This can other pulp testing techniques are inconclusive, the selective
be done by using 2” × 2” gauge piece. anesthesia may be used. The main objective of this test is to
• Apply an electrolyte on the tooth electrode and place it on anesthetize a single tooth at a time until the pain is eliminated.
the facial surface of tooth (Fig. 7.31). Precaution should It should be accomplished by using intraligamentary
be taken to avoid it contacting adjacent gingival tissue or injection. Injection is administered to the most posterior
restorations; this will cause false positive response. tooth in the suspected quadrant. If the pain persists, even
• Confirm the complete circuit from electrode through after tooth has been fully anesthetized, then repeat the
the tooth, to the body of the patient and then back to the procedure to the next tooth mesial to it. It is continued until

vip.persianss.ir
Diagnostic Procedures 85

the pain disappears. If source of pain cannot be determined, pulp vitality as it provides an objective differentiation
repeat the same technique on the opposite arch. between necrotic and vital pulp tissue.

Bite Test Recently Available Pulp Vitality Tests


This test helps in identifying a cracked or fractured tooth. This • Laser Doppler flowmetry (LDF)
is done if patient complains of pain on mastication. Tooth is • Pulp oximetry
sensitive to biting if pulpal necrosis has extended to the • Dual wavelength spectrophotometry
periodontal ligament space or if a crack is present in a tooth. • Measurement of temperature of tooth surface
In this patient is asked to bite on a hard object such as cotton • Transillumination with fiberoptic light
swab, tooth pick or orange wood stick with suspected tooth • Plethysmography
and the contralateral tooth (Fig. 7.32). Tooth slooth is • Detection of interleukin—1 beta
another commercially available device for bite test. It has a • Xenon—133
small concave area on its top which is placed in contact with • Hughes probeye camera
the cusp to be tested (Fig. 7.33). Patient is asked to bite on it. • Gas desaturation
Pain on biting may indicate a fractured tooth. • Radiolabeled microspheres
• Electromagnetic flowmetry.
Bite test
Pain present on biting—apical periodontitis
Pain present on release of biting force—cracked tooth.
Laser Doppler Flowmetry
Laser Doppler flowmetry (LDF) was developed by Tenland in
1982 and later by Holloway in 1983. The technique depends
RECENT ADVANCES IN PULP on Doppler principle in which a low power light from a
VITALITY TESTING monochromatic laser beam of known wavelength along a
The assessment of pulp vitality is a crucial diagnostic fiberoptic cable is directed to the tooth surface, where the
procedure in the practice of dentistry. Current routine light passes along the direction of enamel prisms and dentinal
methods rely on stimulation of A delta nerve fibers and give no tubules to the pulp.
direct indication of blood flow within the pulp. These include The light that contacts a moving object is Doppler shifted,
thermal stimulation, electrical or direct dentine stimulation. and a portion of that light will be back scattered out of tooth
These testing methods have the potential to produce an into a photodetector. Some light is reflected off moving
unpleasant and occasionally painful sensation and inaccurate red blood cells in pulpal capillaries and as a consequence
results. In addition, each is a subjective test that depends on frequency broadened. The reflected light is passed back to
the patient’s perceived response to a stimulus as well as the the flow meter where the frequency broadened light, together
dentist’s interpretation of that response. with laser light scattered from static tissue, is photo-detected
Recent studies have shown that blood circulation and not for strength of signal and pulsatility (Fig. 7.34).
innervation is the most accurate determinant in assessing

Fig. 7.32 Patient is asked to bite on cotton swab or hard  


object for bite test

Fig. 7.33 Tooth slooth Fig. 7.34 Working of LDF

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86 Textbook of Endodontics

Since, red blood cells represents the majority of moving rather than arteries in the pulp and its rigid encapsulation by
objects within the tooth, measurements of Doppler shifted surrounding dentine and enamel make it difficult to detect a
back scattered light may be interpreted as an index of pulpal pulse in the pulp space. This method measures oxygenation
blood flow. changes in the capillary bed rather than the supply vessels and
The resulting photocurrent is processed to provide a hence does not depend on a pulsatile blood flow.
blood flow measurement. The blood flow measured by laser
Doppler technique is termed as ‘flux’, which is proportional Advantages of DWLS
to the product of average speed of blood cells and their
concentration. • In case of avulsed and replanted teeth with open
Pulp is a highly vascular tissue, and cardiac cycle blood apices where the blood supply is regained within first 20
flow in the supplying artery is transmitted as pulsations. These days but the nerve supply lags behind. Repeated readings
pulsations are apparent on laser Doppler monitor of vital for 40 days in such teeth reveal the healing process.
teeth and are absent in nonvital teeth. The blood flux level in • It uses visible light which is filtered and guided to the tooth
vital teeth is much higher than for nonvital teeth. Currently by fiberoptics, unlike laser light where eye protection is
available flowmeters display the signal on a screen, from which necessary for patient and the operator.
the clinician can interpret whether pulp is vital or nonvital. • Noninvasive test.
• An objective test.
Advantages of laser Doppler flowmetry • Instrument is small, portable and inexpensive.
•  An objective test
•  Accurate to check vitality
Measurement of Surface Temperature
Disadvantages of laser Doppler flowmetry
•   Cannot be used in patients who cannot refrain from moving or 
of Tooth
if tooth to be tested cannot be stabilized This method is based on the assumption that if pulp becomes
•  M
  edications  used  in  cardiovascular  diseases  can  affect  the  nonvital, the tooth no longer has internal blood supply, thus
blood flow to pulp
should exhibit a lower surface temperature than that of its
•  Requires higher technical skills to achieve
•  Use of nicotine also affect the blood flow to pulp
vital counterparts.
•  Expensive Fanibund in 1985 showed that it is possible to differentiate
by means of crown surface temperature, distinct difference
between vital and nonvital teeth. He used a thermistor unit
Pulp Oximetry consisting of two matched thermistors connected back to
Pulp oximetry is a noninvasive device for determining back, one measuring the surface temperature of the crown
pulp vitality. The principle of this technology is based on (measuring thermistor) while the other acting as a reference
modification of Beer’s law and the absorbency characteristics thermistor. The tooth to be tested was dried with gauze and
of hemoglobin in red and infrared range. the thermistor unit was positioned so that the measuring
The pulp oximeter is a noninvasive oxygen saturation thermistor contacted the center of the buccal surface of the
monitor in which liquid crystal display oxygen saturation, crown. The reference thermistor was suspended in air, close
pulse rate and plethysmographic wave form readings. The to it, but not touching either the measuring thermistor or the
probe consists of red and infrared light-emitting diodes enamel surface.
opposite a photoelectric detector. Clinically the detection of a Equilibrium was then achieved between the temperatures
pulse should be enough to establish pulp vitality or necrosis. of the thermistors, the crown surface and the immediate
A distinctive advantage of this technique is its objectivity environment by holding the measuring unit in the described
and lack of dependence on sensory response which position until a steady state was established for at least 20
eliminates the need for application of an unpleasant stimulus seconds. Stimulation of the crown surface was carried out
to the patient. by means of a rubber-polishing cup fitted to a dental contra-
angle handpiece. The recordings were continued for a period
Advantages of pulp oximetry of time following the stimulation period. It was found that a
•   Effective and objective method to evaluate pulp vitality difference was obtained between the critical period for vital
•   Useful  in  cases  of  traumatic  injuries  where  the  blood  supply  and nonvital teeth and the difference corresponded with a
remains intact but nerve supply is damaged specific temperature change.
•   Pulpal  circulation  can  be  detected  independent  of  gingival 
circulation
•   Easy to reproduce pulp pulse readings Transillumination with Fiberoptic Light
•   Smaller and cheaper pulp oximeters are now available.
It is a system of illumination whereby light is passed through
Disadvantages of pulp oximetry
Background absorption associated with venous blood.
a finely drawn glass or plastic fibers by a process known as
total internal reflection.
By this method, a pulpless tooth that is not noticeably
Dual Wavelength Spectrophotometry discolored may show a gross difference in translucency
Dual wavelength spectrophotometry (DWLS) is a method when a shadow produced on a mirror is compared to that of
independent of a pulsatile circulation. The presence of arterioles adjacent vital teeth.

vip.persianss.ir
Diagnostic Procedures 87

Detection of Interleukin-I Beta in Human


Periapical Lesion
The inflammatory periapical lesions are common sequelae
of infected pulp tissue. Numerous cell types including PMN
leukocytes, T and B lymphocytes, macrophages and plasma
cells are found in these tissues.
These inflammatory cells produce interleukin-1 (IL-1),
which acts as a mediator of various immunologic and
inflammatory responses.
This lymphocyte activating factor IL-1 is responsible for
osteoclast activation which results in bone resorption which
is frequently a feature of inflammatory response.
Fig. 7.35 Normal radiographic features of teeth
Plethysmography
It is a method for assessing the changes in volume and has
been applied to the investigation of arterial disease because stages of periradicular diseases produce no changes in the
the volume of the limb or organ exhibits transient changes radiographs. They are only two dimensional picture of a three
over the cardiac cycle. Plethysmography in limb or digit dimensional object. It must be emphasized that a poor quality
can be performed using air filled cuffs or mercury in rubber radiograph not only fails to yield diagnostic information but
strain gauges. As the pressure pulse passes through the limb also causes unnecessary radiation to the patient.
segment, a wave form is recorded which relates closely to that To reduce the amount of radiation exposure and to
obtained by intra-arterial cannulation. The same principle improve the quality of radiograph, continuous efforts have
can be used to assess tooth vitality. Presence or absence of a been made since the discovery of X-ray in 1895.
wave form can indicate the status of the tooth.
In order to decrease the radiation exposure, certain newer
methods have been introduced which include:
DIAGNOSTIC FINDINGS •   Use  the  paralleling  technique  instead  of  bisecting  angle 
Once the patient has been evaluated and the clinical technique
•  Faster radiographic films.
examination along with tests are completed, a diagnosis
•  Digital radiographic techniques.
is made. The findings of examination are arranged in a •  Use of electronic apex locator to assist in endodontic treatment.
rational manner so as to diagnose the pulpal or periapical
diseases. Once the correct diagnosis is made, the treatment
plan should be made. Basically the pulpal diseases can be History of dental radiology
1895  WC Roentgen  Discovery of X-rays
reversible pulpitis, irreversible pulpitis or the necrotic pulp.
1896  O Walkhoff  First dental radiograph
The periapical diseases can be acute apical periodontitis, 1901  WH Rollins  P  resented first paper on dangers of 
chronic apical periodontitis, acute or chronic apical abscess X-rays
or condensing osteitis. 1904  WA Price   Introduction of bisecting technique
1913  Eastman  Introduction of pre-wrapped 
ROLE OF RADIOGRAPHS IN ENDODONTICS   Kodak company  dental films
1920  Eastman  Introduction of machine made 
Radiographs play an important role in diagnosis of the dental   Kodak company  film packets
diseases. The interpretation of radiographs should be done 1925  HR Raper   Introduction of bitewing technique
in a systematic manner. The clinician should be familiar with 1947  FG Fitzgerald   Introduction  of  paralleling  cone 
technique
normal radiographic landmarks.

Normal radiographic landmarks are (Fig. 7.35):


Enamel: It is the most radiopaque structure. Principles of Radiography
Dentin: Slightly darker than enamel.
For diagnostic purposes in endodontics, the number of
Cementum: Similar to dentin in appearance.
Periodontal ligament: Appears as a narrow radiolucent line around  radiographs required, depends on situations. A properly
the root surface. placed film permits the visualization of approximately three
Lamina dura: It is a radiopaque line representing the tooth socket. teeth and at least 3 to 4 mm beyond the apex. In most of the
Pulp cavity: Pulp chamber and canals are seen as radiolucent lines  cases, a single exposure is needed to get the information
within the tooth. on root and pulp anatomy. Basically there are two types of
techniques for exposing teeth viz; bisecting angle technique
Though the radiographs play an important role in dentistry and paralleling technique.
but they have a few shortcomings. For example, pathological In bisecting angle technique (Fig. 7.36) the X-ray beam is
changes in pulp are not visible in radiographs, also the initial directed perpendicular to an imaginary plane which bisects

vip.persianss.ir
88 Textbook of Endodontics

Fig. 7.36 Bisecting angle technique


Fig. 7.37 Paralleling technique

the angle formed by recording plane of X-ray film and the To limit this problem, Walton gave a modified paralleling
long axis of the tooth. This technique can be performed technique in which central beam is oriented perpendicular
without the use of film holders, it is quick and comfortable to radiographic film but not to teeth. Modified paralleling
for the patient when rubber dam is in place. But it also has technique covers the disadvantages of paralleling technique.
certain disadvantages like incidences of cone cutting, image
distortion, superimposition of anatomical structures and Cone Image Shift Technique
difficulty to reproduce the periapical films. The concept of technique is that as the vertical or horizontal
In paralleling technique (Fig. 7.37), the X-ray film is placed angulations of X-ray tube head change, the object buccal
parallel to the long axis of the tooth to be exposed and the or closest to the tube head moves to opposite side of
X-ray beam is directed perpendicular to the film. radiograph when compared to lingual object (Figs 7.38
and 7.39). In other words, we can say that the cone image
Advantages of paralleling technique are: shift technique separates and identifies the facial and
•  Better accuracy of image lingual structures.
•  Reduced dose of radiation As the cone position moves from parallel either towards
•  Reproducibility horizontal or vertical, the object on the film shifts away from
•   Better  images  of  bone  margins,  interproximal  regions  and 
the direction of cone, i.e. in the direction of central beam.
maxillary molar region
When two objects and the film are in fixed position and
Disadvantages the tube head is moved, images of both objects moving in
Difficult to use in patients with 
opposite direction, the resultant radiograph shows lingual
•  Shallow vault
•  Gag reflex
object that moved in the same direction as the cone and the
•  When rubber dam is in place buccal object moved in opposite direction. This is also known
•  Extremely long roots as “SLOB” rule (same lingual opposite buccal).
•  Uncooperative patients
•  Tori Synonyms of cone image shift technique
•  BOR (Buccal object rule)
Cone angulation is one of the most important aspects •  SLOB (Same lingual opposite buccal)
•  BOMM (Buccal object moves most)
of radiography because it affects the quality of image. As
•  Clark’s rule
we have seen that paralleling technique has been shown •  Walton’s projection
to be superior to bisecting angle technique especially in
reproduction of apical anatomy of the tooth.
To simplify the understanding of SLOB rule, Walton gave an easy 
method. Place two fingers directly in front of open eyes so that one 
As  the  angle  increases  away  from  parallel,  the  quality  of  image  finger  is  superimposed  on  the  other.  By  moving  the  head,  from 
decreases.  This  happens  because  as  the  angle  is  increased,  one way and the other, the position of finger, relative to each other 
the  tissue  that  the  X-rays  must  pass  through  includes  greater  shifts. The same effect is produced with two superimposed roots 
percentage of bone mass thus anatomy becomes less predictable. when center beam is shifted.

vip.persianss.ir
Diagnostic Procedures 89

Fig. 7.39 As X-ray tube head changes, the object buccal or closet to 


the tube head moves to opposite side of radiograph when compared 
to lingual object

2. Vertical bitewing film: In this, film is oriented vertically


so as to record more of root area. It is done in cases of
extensive bone loss.

Advantages
•  Helps in detecting interproximal caries
Fig. 7.38 Cone-shift technique •  Evaluate periodontal conditions
•  Evaluate secondary caries under restorations 
•   Help  in  assessing  alveolar  bone  crest  and  changes  in  bone 
Advantages of ‘SLOB’ rule height by comparing it with adjacent teeth.
•   It  helps  in  separation  of  overlapping  canals,  for  example,  in 
maxillary premolars and mesial canals of mandibular molars
•  T  he working length radiographs are better traced from orifice to  Safety concerns of X-rays
the apex by this technique •   Through X-rays are harmful but dental X-rays are safe because 
•  I  t  helps  to  locate  the  root  resorptive  processes  in  relation  to  of  their  low  level  of  radiation  exposure.  Moreover,  to  avoid 
tooth excessive  exposure,  one  should  use  lead  apron  to  cover  body 
•   This  technique  is  helpful  in  locating  a  canal  in  relation  to  and high speed film. 
radiopaque margin, such as bur in the access opening •   To take X-ray of pregnant patient, lead shield should be used to 
•   It is useful in identification of anatomic landmarks and pathosis cover body including the womb area. Moreover X-rays should 
•   This  rule  is  also  used  to  increase  the  visualization  of  apical  be taken if necessary.
anatomy  by  moving  anatomic  landmarks  such  as  zygomatic 
process or the impacted tooth
•   It also helps to identify the angle at which particular radiograph  Advantages of Radiographs in Endodontics
was made, even if information was not recorded
•   It  helps  to  identify  the  missed  canals  or  calcified  canals  and  In endodontics, the radiographs perform essential functions
sometimes the canal curvature. in three main areas, viz; diagnosis, treatment and recall.
Disadvantages of ‘SLOB’ rule
•   It results in blurring of the object which is directly proportional  Diagnosis
to  cone  angle. The  clearest  radiograph  is  achieved  by  parallel  • Radiographs help to know the presence of caries which
technique, so when the central beam changes direction relative  may involve or on the verge of involving the pulp. Depth of
to object and the film, object become blurred. caries, restoration, evidence of pulp capping or pulpotomy,
•   It causes superimposition of the structures. Objects which have 
etc. could be evaluated on seeing the radiograph (Fig. 7.40).
natural  separation  on  parallel  technique,  with  cone  shift;  they 
may move relative to each other and become superimposed. For  • The radiographs help to know the root and pulpal anatomy,
example in case of maxillary molars, all three separate roots are  i.e. normal and abnormal root formation, curvature of the
visible  on  parallel  radiographs  but  an  angled  radiograph  may  canal, number of roots and the canals, any calcifications if
move palatal root over the distobuccal or mesiobuccal root and  present in the canal and variation in the root canal system,
thus decreasing the ability to distinguish apices clearly. i.e. presence of fused or extra roots and canals (Fig. 7.41),
any bifurcation or trifurcation in the canal system if
Bitewing Radiographs present.
• Radiographs help to know the pulp conditions present
Bitewing radiographs include the crowns of maxillary and inside the tooth like pulp stones, calcification, internal
mandibular teeth and alveolar crest in the same film. resorption, etc.
Two types • A good quality preoperative radiograph provide
1. Horizontal bitewing films: In this beam is aligned information on orientation and depth of bur relative to the
between the teeth parallel to occlusal plane. pulp cavity (Fig. 7.42).

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90 Textbook of Endodontics

Fig. 7.40 Extent of caries/restoration   Fig. 7.43 Radiograph showing periodontal involvement 


can be seen on radiograph of mandibular first molar

• Other conditions like resorption from the root surface, i.e.


external resorption, thickening of periodontal ligament
and extent of periapical and alveolar bone destruction can
be interpreted by viewing the radiographs (Fig. 7.43).
• They also help to identify the numerous radiolucent
and radiopaque structures which often lie in the close
proximity to the tooth. These must be distinguished and
differentiated from the pathological lesions.

Treatment
The radiographs exposed during the treatment phase are
known as working radiographs. Working radiographs are
made while rubber dam is in place, i.e. these radiographs are
exposed during treatment phase.
• Working length determination: In this, radiograph
establishes the distance from the reference point to apex
Fig. 7.41 Radiograph showing extra root in first molar
till which canal is to be prepared and obturated (Fig. 7.44).
By using special cone angulations, some superimposed
structures can be moved to give clear image of the apical
region.
• Master cone radiographs: It is taken in the same way as
with working length radiograph. Master cone radiograph
is used to evaluate the length and fit of master gutta-
percha cone (Fig. 7.45).
• Obturation: Radiographs help to know the length, density,
configuration and the quality of obturation (Fig. 7.46).

Recall
• Radiographs are essential to evaluate the post-treatment
periapical status (Figs 7.47A and B).
• The presence and nature of lesion that have occurred after
the treatment are best detected on radiographs. These
lesions may be periapical, periodontal or non-endodontic.
Fig. 7.42 Preoperative radiograph can provide information on 
• Recall radiographs help to know the success of treatment
orientation and depth of the angulation of handpiece by evaluating the healing process.

vip.persianss.ir
Diagnostic Procedures 91

Fig. 7.44 Working length radiograph Fig. 7.46 Radiograph showing obturated 36

A B
Fig. 7.45 Master cone radiograph Figs 7.47A and B Radiograph showing comparison of size of periapical 
radiolucency. (A) Preoperative; (B) 6 months post-treatment

DIGITAL RADIOGRAPHY identifying them, but machines are able to discriminate at


density level beyond what human eye can see.
Digital imaging uses standard radiology techniques with film
to record the image, and then subjects the finished image to Advantages
digital processing to produce the final result. •   The amount of information available from these radiographs is 
The backlog film image is converted to a digital signal by greater than from radiographs that have not been digitized.
a scanning device, such as videocamera. First the image is •  The storage of radiographs and quality of image is better.
divided into a grid of uniformly sized pixels, each of which is •  Photographs of radiographs can be produced.
assigned a gray scale value based on its optical diversity. This Disadvantages
value is stored in computer. •   The  radiation  dose  to  the  patient  is  the  same  as  that  used  for 
One of the most useful operations is a comparison of conventional radiographs. 
images called digital subtraction. The computers can compare •   Requires equipment to print photographs or even for scanning 
two images, this property can be used to see the progression of radiographs.
of disease over time and evaluation of treatment outcomes of
endodontic therapy. DIGITAL DENTAL RADIOLOGY
Another use is the detection of lesion on radiographs. This
is where an endodontist can use this application for diagnosis. Images in digital form can be readily manipulated, stored and
The computers can detect lesion with pattern recognition retrieved on computer. Furthermore, technology makes the
and boundary determination. Sometimes density changes transmission of images practicable. The general principles of
on radiographs are so subtle that human eye has trouble digital imaging are:

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92 Textbook of Endodontics

• The chemically produced radiograph is represented by


data that is acquired in a parallel and continuous fashion
known as analog.
• Computers use binary (0 or 1) language, where information
is usually handled in 8 character words called bytes.
• If each character can be either 0 or 1. This results in 28
possible combinations (words) that is 256 words. Thus
digital dental images are limited to 256 shades of gray.
• Digital images are made up of pixels (picture elements),
each allocated a shade of gray.
• The spatial resolution of a digital system is heavily
dependent upon the number of pixels available per
millimeter of image.

Methods of digital dental radiology


•  One uses charged couple devices.
•  Other uses photo stimulable phosphor imaging plates.

Both methods can be used in dental surgery with


conventional personal computers.
Digital imaging system requires an electronic sensor or Fig. 7.48 Sensor used for RVG
detector, an analog to digital converter, a computer, and a
monitor or printer for image of the components of imaging
system. It instructs the X-ray generator when to begin and
end the exposure, controls the digitizer, constructs the
image by mathematical algorithm, determines, determines
the method of image display, and provides for storage and
transmission of acquired data.
The most common sensor is the charge-coupled device
(CCD), the other being phosphor image.
When a conventional X-ray unit is used to project the
X-ray beam onto the sensor, an electronic charge is created,
an analog output signal is generated and the digital converter
converts the analog output signal from CCD to a numeric
representation that is recognizable by the computer.
The radiographic image then appears on the monitor
and can be manipulated electronically to alter contrast,
resolution, orientation and even size.

The CCD System


The CCD is a solid state detector containing array of
X-ray or light sensitive phosphores on a pure silicon chip.
These phosphors convert incoming X-rays to a wavelength
that matches the peak response of silicon. Figs 7.49 Different sizes of sensors available
RVG
RVG is composed of three major parts: removed from mouth after each exposure, the time to take
1. The radio part consists of a conventional X-ray unit, a multiple images is greatly reduced.
precise timer for short exposure times and a tiny sensor to 2. The ‘visio’ portion of the system receives and stores
record the image (Figs 7.48 and 7.49). Sensor has a small incoming signals during exposure and converts them
(17 × 24 mm) receptor screen which transmits information point by point into one of 256 discrete gray levels. It
via fiberoptic bundle to a miniature CCD. The sensor is consists of a video monitor and display processing unit
protected from X-ray degradation by a fiberoptic shield (Fig. 7.50). As the image is transmitted to the processing
and can be cold sterilized for infection control. Disposable unit, it is digitized and memorized by the computer.
latex sheath is also used to cover the sensor when it is in The unit magnifies the image four times for immediate
use (Fig. 7.48). Because the sensor does not need to be display on video monitor and has additional capability

vip.persianss.ir
Diagnostic Procedures 93

Two sizes of phosphor plates (size similar to conventional


intraoral film) packets are provided. They have to be placed
in plastic light-tight bags, before being placed in the mouth.
They are then positioned in the same manner as film packets,
using holders, incorporating beam-aiming devices, and
are exposed using conventional dental X-ray equipment.
The dose is highly reduced. The image is displayed and
manipulated. A hard copy can be obtained if necessary.

Advantages
•  Low radiation dose (90% reduction)
•  Almost instant image (20–30 seconds)
•   Wide  exposure  latitude  (almost  impossible  to  burn  out 
information)
•  Same size receptor as films
•  X-ray source can be remote from PC
•  Image manipulation facilities.
Fig. 7.50 Visio part displays the captured image
Disadvantages
•  Cost
•  Storage of images (same as with CCD systems)
of producing colored images. It can also display multiple •  Slight in convenience of plastic bags.
images simultaneously, including a full mouth series on
one screen. A zoom feature is also available to enlarge a
portion of image up to face-screen size.
QUESTIONS
3. The ‘graphy’ part of RVG unit consists of digital storage
apparatus that can be connected to various print out or 1. Define diagnosis. Enumerate various diagnostic techniques in
mass storage devices for immediate or later viewing. endodontics. Describe in detail on electric pulp tester.
2. Enumerate the various diagnostic aids in endodontics and
describe in detail on thermal testing.
Advantages 3. Describe the various pulp vitality tests. Add a note on the
•  Low radiation dose recent method to determine the vascularity of the tooth.
•   Increased  diagnostic  capability  through  digital  enhancement  4. What are the various methods employed to detect the vitality of
and enlargement of specific areas for closer examination a tooth.
•  Elimination of image distortion from bent radiographic film 5. Discuss role of radiographs in endodontics.
•  Possible to alter contrast and resolution 6. Write short notes on:
•  Instant display of images • Pulp vitality tests
•   Film less X-rays means, no dark room, no messy processing and  • Thermal test for pulp vitality
no any problems/faults associated with developing of film • Recent advances in pulp vitality testing
•  Full mouth radiographs can be made within seconds • Role of radiograph in endodontics
•  Storages and archiving of patient information • Digital radiography
•  Transfer of images between institutions (teleradiology) • RVG/radiovisiography
•   Infection control and toxic waste disposal problems associated  • Electric pulp testing
with radiology are eliminated. • Diagnostic aids in endodontics
Disadvantages • Test cavity
•  Expensive • Thermal testing
•  Large disc space required to store images • RVG
•   Bulky sensor with cable attachment, which can make placement  • SLOB rule
in mouth difficult • Electric pulp tester
•  Soft tissue imaging is not very nice. • Interpretation of vitality tests
• False positive and false negative readings in electric pulp
testing
• Laser Doppler flowmetry.

PHOSPHOR IMAGING SYSTEM


BIBLIOGRAPHY
Imaging which uses photostimulable phosphor is also
1. Bhasker SN, Rappaport HM. Dental vitality tests and pulp
called as an indirect digital imaging technique. The image is status. J Am Dent Assoc. 1973;86:409-11.
captured on a phosphor plate as analog information and is 2. Carrottem P. Endodontics: part 2 diagnosis and treatment
converted into a digital format when the plate is processed. planning. British Dent J. 2004;197:231-38.

vip.persianss.ir
94 Textbook of Endodontics

3. Cave SG, Freer TJ, Podlich HM. ‘Pulp-test responses in 8. Narhi MVO. The neurophysiology of the teeth. Dent Clin North
orthodontic patients’. Aust Orthodont J. 2002;18:27-34. Am. 1990;34:439-48.
4. Dummer PMH, Hicks R, Huws D. ‘Clinical signs and symptoms 9. Schnettler JM, Wallace JA. Pulse oximeter as a diagnostic tool
in pulp disease’. Int Endod J. 1980;13:27-35. of pulp vitality. J Endod. 1991;17:488-90.
5. Hyman JJ, Cohen ME, Lakes G. The predictive value of 10. Stark MM, Kempler D, Pelzner RB, Rosenfeld J, Leung RL,
endodontic diagnostic tests. Oral Surg. 1984;58:343-46. Mintatos S. Rationalization of electric pulp testing methods.
6. Kells BE, Kennedy JG, Biagioni PA, Lamey PJ. Computerized Oral Surg Oral Med Oral Pathol. 1977;43:598-606.
infrared thermographic imaging and pulpal blood flow: Part 2. 11. Yanipiset K, Vongsavan N, Sigurdsson A, Trope M. The
Rewarming of healthy human teeth following a controlled cold efficacy of laser Doppler flowmetry for the diagnosis of
stimulus. Int Endod J. 2000;33:448-62. revascularization of reimplanted immature dog teeth. Dent
7. Mickel AK, Lindquist KAD, Chogle S, Jones JJ, Curd F. Electric Traumatol. 2001;17:63-70.
pulp tester conductance through various interface media. J
Endod. 2006;32:1178-80.

vip.persianss.ir
Differential Diagnosis of
Orofacial Pain 8
 Pain  Sources of Odontogenic Pain  Sources of Nonodontogenic Pain



 Diagnosis  Pulpal Pain


 Orofacial Pain  Periodontal Pain


Orofacial pain is the field of dentistry related to diagnosis and • Intensity
management of chronic, complex facial pain and orofacial • Aggravating factors
disorders. Orofacial pain, like pain elsewhere in the body, • Precipitating factors
is usually the result of tissue damage and the activation of • Past medical and dental history
nociceptors, which transmit a noxious stimulus to the brain. • Psychologic analysis
Orofacial disorders are complex and difficult to diagnose due • Review of systems.
to rich innervations in head, face and oral structures. Ninety
percent of orofacial pain arises from teeth and adjoining Location
structures. As a dentist, one must be trained to diagnose and The patient’s description of the location of his or her
treat acute dental pain problems. complaint identifies only site of pain. So, it is the dentist’s
responsibility to determine whether it is the true source of
PAIN pain or the referred pain.
Dorland’s Medical Dictionary defines pain as “A more or less
localized sensation of discomfort, distress or agony resulting Onset
from the stimulation of nerve endings”. It indicates that pain It is important to record the conditions associated with initial
is a protective mechanism against injury. International onset of pain. Sometimes it may facilitate in recognizing the
Association for the Study of Pain (IASP) has defined pain as etiology of pain.
“an unpleasant sensory and emotional experience associated
with actual or potential tissue damage, or described in terms Chronology
of such damage.” Chronology of pain should be recorded in a following pattern:
• Initiation
DIAGNOSIS • Clinical course and temporal pattern
– Mode
For establishing the correct diagnosis, the dentist must record


– Periodicity
all relevant information regarding signs, symptoms, history of
– Frequency
present complaint, past medical and dental history.


– Duration.


History of Pain
Quality
The history is an important part of diagnosis, it should assess It should be classified according to how pain makes the
the present location of the pain, its causative and aggravating patient feel.
factors and a detailed description of the pain since its origin. • Dull, gnawing or aching
History of pain includes the following: • Throbbing, pounding or pulsating
• Sharp, recurrent or stabbing pain
Chief Complaint • Squeezing or crushing pain.
• Location
• Onset Intensity
• Chronology Intensity of pain is usually established by distinguishing
• Quality between mild, moderate and severe pain. A visual analog

vip.persianss.ir
96  
Textbook of Endodontics

scale is used to assess the intensity of pain. The patient OROFACIAL PAIN
is given a line on which no pain is written on one end and
at other end there is most severe pain which patient has Orofacial pain can be basically divided into odontogenic

­
experienced. A scale of 0-10 is used to assess the pain, (dental pain) and nonodontogenic pain (nondental). Dental
0-being no pain while 10 being the maximum pain possible. pain may have origin in the pulpal tissue or the periradicular
• Pain index : 0-10 (Fig. 8.1) tissue. Nondental pain can be in form of myofacial toothache,
• Pain classification : Mild vascular headache, cluster headache, sinusitis, trigeminal
Moderate neuralgia.


Severe

SOURCES OF ODONTOGENIC PAIN
Aggravating Factors
Aggravating factors always help the clinician in diagnosis. Dental Pain of Pulpal Origin (Fig. 8.2)
These can be local or conditional. Local factors can be in Dental pulp is richly innervated by A and C nerve fibers.
form of irritants like heat, cold, sweets and pain on biting, etc. The nerves of the pulp include primary afferent fibers that
Conditional factors include change of posture, activities and are involved in pain transmission and sympathetic efferent
hormonal changes, etc. fibers which modulate the microcirculation of the pulp.
Local factors Conditional factors The sympathetic efferent fibers reduce the flow of the blood
through pulp by stimulating smooth muscle cells encircling

• Sweets • Change of posture
• Chewing • Time of day the arterioles. Four types of nerve endings are present in pulp:
• Palpation • Activities 1. Marginal fibers

• Heat • Hormonal 2. Simple predentinal fibers

• Cold 3. Complex predentinal fibers
• Percussion 4. Dentinal fibers.

POINTS TO REMEMBER
Stimulation of A, fibers produce a sharp, piercing or stabbing
sensation while C, fibers produce dull, burning, and aching sensation
that is usually harder to endure.

The pulpal pain is of threshold type, i.e. no response



occurs until threshold level is increased. Pulp may respond to
Fig. 8.1 Rating scale to check intensity of pain ranging from (0-10) chemical, mechanical, electrical or thermal stimulation but

Fig. 8.2 Neurophysiology of pulpal pain

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Differential Diagnosis of Orofacial Pain 97


not to ordinary masticatory functions. Pulpal pain cannot be compounds, fluoride compounds like sodium fluoride,
localized by the patient. A basic feature of pain of pulpal origin stannous fluoride, iontophoresis, restorative resins and
is that it does not remain the same for long periods. Generally dentin bonding agents.
it resolves, becomes chronic or involves the periodontal
structure. Reversible Pulpitis
In reversible pulpitis, pain occurs when a stimulus (usually
Dental Pain of Periodontal Origin cold or sweets) is applied to the tooth. When the stimulus is
Periodontal pain is deep somatic pain of the musculoskeletal removed, the pain ceases within 1 to 2 seconds, i.e. it should
type because of presence of proprioceptor fibers. Patient can return to normal with removal of cause. The common causes
localize the pain of periodontal origin. Therefore, periodontal of reversible pulpitis are caries, faulty restorations, trauma or
pain presents no diagnostic problems because the offending any recent restorative procedures.
tooth can be readily identified. This localization can be

­
identified by applying pressure to the tooth axially and laterally. Diagnosis
When the periodontal pain involves many teeth, one may Diagnosis is made by careful history and clinical examination.

consider occlusal overstressing which could be due to occlu If there is discrepancy between the patient’s chief complaint,

­
sal interferences or parafunctional habits such as bruxism. symptoms and clinical examination, obtain more information
from the patient. It is important to note that both pulpal
Sources of odontogenic pain
and periapical diagnosis should be made before treatment
Pulpal pain
•  Dentinal sensitivity is initiated. If tooth is sensitive to percussion, then look for
•  Reversible pulpitis bruxism and hyperocclusion.
•  Irreversible pulpitis
•  Necrotic pulp. Treatment
Periodontal pain • Removal of the cause if present (caries, fractured
•  Acute apical periodontitis restoration, exposed dentinal tubules).
•  Acute periapical abscess • If recent operative procedure or trauma has taken place,
•  Chronic apical periodontitis
then postpone the additional treatment and observe the
•  Periodontal abscess
•  Pericoronitis.
tooth.
• If pulp exposure is detected, go for root canal treatment.

PULPAL PAIN Irreversible Pulpitis


Irreversible pulpitis develops, if inflammatory process
Dentinal Sensitivity progresses to involve pulp. Patient may have history of
In the absence of inflammation, dentinal sensitivity is spontaneous pain or exaggerated response to hot or cold that
the mildest form of pulp discomfort. The pain is often lingers even after the stimulus is removed. The involved tooth
characterized as a short, sharp, shock and it is brought on usually presents an extensive restoration and/or caries.
by some stimulating factor such as hot or cold, sweet, sour,
acid or touch. It is not pathologic, but is rather, fluid flow Diagnosis
in the dentinal tubules which stretches or compresses the Diagnosis is usually made after taking thorough history and
nerve endings that pass alongside the tubular extensions of clinical examination of the patient.
the pulp odontoblasts. Dentinal sensitivity may also develop • Patient usually gives a history of spontaneous pain.
when dentin is exposed from gingival recession or following • Tooth is hypersensitive to hot or cold that is prolonged in
periodontal surgery. duration.
• Pulp may be vital or partially vital.
Diagnosis • In certain cases of irreversible pulpitis, the patient may
• Apply the irritant which starts the painful reaction-hot or arrive at the dental clinic with a glass of ice/cold water.
cold, sweet or sour or scratching with an instrument. In these cases, cold actually alleviates the patient’s pain
­
• All diagnostic tests such as electric pulp test, percussion and thus, can be used as a diagnostic test. Cooling of the
and radiographs give normal response. dentin and the resultant contraction of the fluid in the
tubules relieves the pressure on pulpal nerve fibers caused
Treatment by edema and inflammation of the pulp.
After diagnosis, dentinal hypersensitivity can be treated by
home use of desensitizing dentifrices containing strontium Treatment
chloride, fluorides and potassium nitrate. Various agents can Complete removal of pulpal tissue should be done, i.e.
be use to occlude the dentinal tubules like varnishes, calcium endodontic therapy.

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98 
Textbook of Endodontics

Necrotic Pulp Diagnosis


• Spontaneous dull, throbbing or persistent pain is present.
It results from continued degeneration of an acutely inflamed
• Tooth is extremely sensitive to percussion.
pulp. Literal meaning of necrosis is death, i.e. pulpal tissue
• Mobility may be present.
becomes dead because of untreated pulpal inflammation. In
• On palpation, tooth may be sensitive.

­
pulpal necrosis, there is progressive breakdown of cellular
• Vestibular or facial swelling in seen in these patients.
organization with no reparative function. It is frequently
• Pulp tests show negative results.
associated with apical radiolucent lesion. In case of
multirooted teeth, one root may contain partially vital pulp,
whereas other roots may be nonvital. Treatment
• Drainage.
• Complete extirpation of pulp.
Diagnosis • Appropriate analgesics and antibiotics if necessary.
• Tooth is usually asymptomatic; may give moderate to
severe pain on biting pressure (It is not symptom of
necrotic pulp but it indicates inflammation ). Chronic Apical Periodontitis
• Pulp tests show negative response but in case of It is caused by necrotic pulp which results from prolonged
multirooted teeth, it can give false positive results. inflammation that erodes the cortical plate making a
periapical lesion visible on the radiograph. The lesion contains
Treatment granulation tissue consisting of fibroblasts and collagen.
Complete removal of pulpal tissue that is root canal treatment.
Diagnosis
PERIODONTAL PAIN • It is usually asymptomatic but in acute phase may cause a
dull, throbbing pain.
Acute Apical Periodontitis • Pulp tests show nonvital pulp.
It is the inflammation of periodontal ligament which is caused • There is no pain on percussion.
by tissue damage, extension of pulpal pathology or occlusal • Radiographically, it is usually associated with periradicular
trauma. Tooth may be elevated out of the socket because of radiolucent changes.
the built up fluid pressure in the periodontal ligament. Pain
remains until the bone is resorbed, fluid is drained or irritants Periodontal Abscess
are removed.
Acute periodontal abscess is an virulent infection of an
existing periodontal pocket. It can also occur because of
Diagnosis
apical extension of infection from gingival pocket.
• Check for decay, fracture lines, swelling, hyperocclusion
or sinus tracts.
• Patient has moderate to severe pain on percussion. Diagnosis
• Mobility may or may not be present. • Tooth is tender to lateral percussion.
• Pulp tests are essential and their results must be correlated • When sinus tract is traced using gutta-percha, it points
with other diagnostic information in order to determine if towards the lateral aspect of the tooth.
inflammation is of pulpal origin or from occlusal trauma.
• Radiographs may show no change or widening of Treatment
periodontal ligament space in some cases. Root planning and curettage.

Treatment Pericoronitis
• Complete removal of pulp.
• Occlusal adjustment. It is inflammation of the periodontal tissues surrounding the
erupting third molar.
Acute Periapical Abscess
Acute periapical abscess is an acute inflammation of periapical Diagnosis
tissue characterized by localized accumulation of pus at the • Deep pain which radiates to ear and neck.
apex of a tooth. It is a painful condition that results from an • May be associated with trismus.
advanced necrotic pulp. Patients usually relate previous
painful episode from irreversible pulpitis or necrotic pulp. Treatment
Swelling, tooth mobility and fever are seen in advanced cases. Operculectomy and surgical removal of tooth if required.

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Differential Diagnosis of Orofacial Pain 99


SOURCES OF NONODONTOGENIC PAIN • Usually arise with or without pulpal or periradicular
pathology.
As dental pain is considered one of the most common cause • Tooth pain is not relieved by anesthetizing the tooth; rather
of orofacial pain, the dentist can be easily drawn to diagnosis local anesthesia given at affected muscle may reduce the
of pain of odontogenic origin. There are many structures in toothache.
the head and neck region which can simulate the dental pain.
Such types of pain are classified under heterotrophic pain. Diagnosis
Heterotrophic pain can be defined as any pain felt in an area These muscular pains as nonodontogenic tooth is purely
other than its true source. based on lack of symptoms after diagnostic tests such as pulp
There are three general types of pain: testing, percussion and local anesthesia block.

1. Central pain Several therapeutic options used in the management of

2. Projected pain


muscular pain are:

3. Referred pain. • Restriction of functional activities within painless limit

Referred pain is a heterotrophic pain, i.e. felt in an area • Occlusal rearrangement

innervated by a different nerve, from the one that mediates • Deep massage
the primary pain. Referred pain is wholly dependent upon the • Spray and stretch technique
original source of pain. It cannot be provoked by stimulation • Ultrasound therapy
where the pain is felt while it can be accentuated only by • Local anesthesia at the site of trigger points
stimulation the area where primary source of pain is present. • Analgesics.
Referred pain can be of odontogenic or nonodontogenic
origin.
Neurovascular Toothache
The most common neurovascular pain in the mouth and face
Odontogenic Referred Pain
is migraine. This category of pain includes three subdivisions
In this pain originates from pulpally involved tooth and of primary headache. These are:
is referred to adjacent teeth/tooth or proximating deep • Migraine
and superficial structures. For example, pain from pulpal • Tension type headache
involvement of mandibular second or third molar is referred • Cluster headache.
to ear. This pain is diagnosed by selective anesthesia technique. These neurovascular entities can produce relatively local-

ized pains that match with sign and symptoms with the tooth-
Nonodontogenic Referred Pain ache. These accompanying toothaches are usually mistaken
for true odontogenic pains and can be treated as separate
In this pain originates from deep tissues, muscles, joints, entities. Unfortunately there are several clinical characteris-
ligaments, etc. and is perceived at a site away from its origin. tics that could misguide clinician in diagnosis and treatment.
Pain arising from musculoskeletal organs is deep, dull,
aching and diffuse type. Pain form cutaneous origin is of Features of Neurovascular Toothache
sharp, burning and localized (e.g. pain of maxillary sinusitis The following characteristics are found commonly in
and may result pain in maxillary premolars). neurovascular toothache are:
• The pain is deep, throbbing, spontaneous in onset,
Myofascial Toothache variable in nature and pulsatile. These are characteristics
which simulate pulpal pain.
Any deep somatic tissue in the head and neck region has
• The pain is predominantly unilateral.
tendency to induce referral pain in the teeth. In these
• Accompanying toothache shows periods of remission
structures, pains of muscular origin appear to be the most
that imitates the pain-free episodes or temporal behavior
common. Muscles which are commonly affected are
found in neurovascular pain.
masseter, temporalis but in some cases medial, and lateral
• Headache is considered as the main symptom. It is most
pterygoid and digastric muscles are also affected.
often accompanied by toothache.
• Recurrence is characteristic finding in neurovascular pain.
Characteristic Findings of Muscular Toothache Sometimes, the pain may undergo remission after dental
• Nonpulsatile, diffuse, dull and constant pain. treatment has been performed in these teeth. It usually
• Pain increases with function of masticatory muscles. For appears for certain period of time and may even spread to
example, pain is increased when chewing is done because adjacent teeth, opposing teeth or the entire face.
of effect on masseter muscle. • Autonomic effects such as nasal congestion, lacrimation,
• Palpation of the involved muscles at specific points (trigger rhinorrhea and edema of the eyelids and face is seen.
points)* may induce pain. Sometimes edema of the eyelids and face might lead to
*Trigger points are hyperexcitable muscle tissues which confusion in diagnosis as these features bear a resemblance
may feel like taut bands or knots. to abscess.

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100 Textbook of Endodontics

Migraine of jaw pain, i.e. occurring in number of patients secondary to
cardiac pain. Sometimes, patient presents dental complaints
Migraine has been divided into two main types: as the chief complaint rather than having pain in substernal
1. Migraine with aura. region, it creates confusion in diagnosis for dental pain. A

2. Migraine without aura. lack of dental cause for dental pain should always be an

alerting sign. Anesthetizing the lower jaw or providing dental
Features of Migraine treatment does not decrease the tooth pain, it indicates
• Commonly found between the age group 20 to 40 years. that primary source of pain is not the tooth. Usually the
• Visual auras are most common. These usually occur 10 to cardiac toothache is decreased by taking rest or a dose of
30 minutes prior to the onset of headache pain (Migraine sublingual nitroglycerin. A complete medical history should
with aura) be taken when cardiac toothache is suspected and should be
• Pain is usually unilateral, pulsatile or throbbing in nature immediately referred to cardiac unit in hospital.
• More common in females In brief, characteristics of cardiac toothache are:


• Patient usually experiences nausea, vomiting, photo • Pain is of sudden in onset, gradually increasing in intensity,

­
phobia diffuse with cyclic pattern that vary in intensity from mild
• Various drugs used in the management of migraine are to severe.
sumatriptan, b-blockers, tricyclic antidepressants and • Tooth pain is increased with physical activities.
calcium channel blockers. • Chest pain is usually associated.
• Pain is not relieved by anesthesia of lower jaw or by giving
analgesics.
Cluster Headache
• Commonly found in the age group 20 to 50 years Neuropathic Pain
• Cluster headaches derive their name from the temporal Neuropathic pain is usually caused by abnormalities in the
behavior and usually occur in series, i.e. one to eight neural structures themselves. Neuropathic pain is sometimes
attacks per day misdiagnosed as psychogenic pain because local factors can
• More common in males than females not be visualized.
• Pain is unilateral, excruciating and continuous in nature Neuropathic pain can be classified into different categories:
and usually found in orbital, supraorbital or temporal

• Neuralgia
region • Neuritis
• Autonomic symptoms such as nasal stuffiness, lacri- • Neuropathy.
mation, rhinorrhea or edema of eyelids and face are
usually found
• Standard treatment is inhalation of 100 percent oxygen. Neuralgia
The behavior of neurovascular variants should be well Paroxysmal, unilateral, severe, stabbing or lancinating
pain, usually are the characteristics of all paroxysmal

appreciated to avoid any unnecessary treatment and
frustration felt by patient and clinician. Although the term neuralgias. The pain is usually of short duration and lasts for
neurovascular toothache is nondescriptive, but it has few seconds.
given the dentist an important clinical entity that has been Trigeminal neuralgia
misdiagnosed and mistreated in the past. • It is also known as ‘Tic Doulourex’ which has literal
meaning of painful jerking.
Signs and symptoms of neurovascular headache that mimic the • Usually characterized by paroxysmal, unilateral, sharp,
toothache are: lancinating pain typically confined to one or more
•  Periodic and recurrent nature branches of 5th cranial nerve.
•  Precise recognition of painful tooth • Even slight stimulation of ‘Trigger points’ may elicit sharp,
•  Absence of local dental etiology. shooting pain.
• Sometimes trigger points are present intraorally. These
are stimulated upon chewing which may led to diagnosis
Cardiac Toothache of odontogenic pain. Intraoral trigger points always create
Severe referred pain felt in mandible and maxilla from area confusion in diagnosis if not properly evaluated.
outside the head and neck region is most commonly from • Local anesthesia given at the trigger point reduces the
the heart. Cardiac pain is clinically characterized by attacks.
heaviness, tightness or throbbing pain in the substernal • It rarely crosses midline.
region which commonly radiates to left shoulder, arm, neck • Frequently occur in persons over the age of 50 years.

and mandible. Cardiac pain is most commonly experienced • Attacks generally do not occur at night.
on the left side rather than right. In advanced stages, the • Absence of dental etiology along with symptoms of
patient may complain of severe pain and rubs the jaw and paroxysmal, sharp, shooting pain always alert the dentist
chest. In present time, dentist should be aware of incidence to include neuralgia in the differential diagnosis.

vip.persianss.ir
Differential Diagnosis of Orofacial Pain 101


• Treatment includes surgical and medicinal. Usually have multiple dental procedures completed before reaching
medicinal approach is preferred. It includes adminis a final diagnosis.

­
tration of carbamazepine, baclofen, phenytoin sodium Clinical characteristics of neuropathy
and gabapentin, etc. • Also called atypical odontalgia.
• More common in women.
Neuritis • Frequently found in 4th or 5th decades of life.
Neuritis literally means inflammation of nerve. It is usually • Tooth pain remains constant or unchanged for weeks or
observed as heterotopic pain in the peripheral distribution of months.
the affected nerve. It may be caused by traumatic, bacterial • Constant source of pain in tooth with no local etiology.
and viral infection. In neuritis, the inflammatory process • Pain usually felt in these patients is—dull, aching and
elevates the threshold for pricking pain but lowers it for persistent.
burning pain. The characteristics of pain in neuritis are: • Most commonly affected teeth are maxillary premolar and
• Pain has a characteristic burning quality along with easily molar region.
localization of the site. • Response to local anesthesia is equal in both pulpal
• It may be associated with other sensory effects such as toothache and atypical odontalgia.
hyperesthesia, hypoesthesia, paresthesia, dysesthesia and
anesthesia. Sinus or Nasal Mucosal Toothache
• Pain is nonpulsatile in nature.
Sinus and nasal mucosal pain is also another source which can
• Pain may vary in intensity.
mimic toothache. It is usually expressed as pain throughout
Peripheral neuritis is an inflammatory process occurring
the maxilla and maxillary teeth.

along the course of never trunk secondary to traumatic,
Clinical characteristics of sinus or nasal mucosal tooth
bacterial, thermal or toxic causes. Neuritis of superior dental

­
ache are:
plexus has been reported when inflammation of sinus is
• Fullness or pressure below the eyes.
present. The dental nerves frequently lie just below the lining
• Increased pain when palpation is done over the sinus.
mucosa or are separated by very thin osseous structure.
• Increased pain sensation when head is placed lower than
These nerves are easily involved due to direct extension.
the heart.
Symptoms usually seen along with antral disease are pain,
• Local anesthesia of referred tooth/teeth does not
paresthesia and anesthesia of a tooth, gingiva or area
eliminated pain while topical anesthesia of nasal
supplied by infraorbital nerve. Mechanical nerve trauma
mucosa  will eliminate the pain if etiology lies in nasal
is more common in oral surgery cases. It usually arises from
mucosa.
inflammation of the inferior dental nerve either due to trauma
• Different diagnostic aids used to diagnose sinus disease
or infection.
include paranasal sinus view, computed tomography
Acute neuritis cases are always misdiagnosed and
imaging and nasal ultrasound.

remain untreated. Most of the times, dental procedures
are done to decrease the symptoms of neuritis as these are
difficult to diagnose. These unnecessary dental procedures
Psychogenic Toothache
further act as aggravating factors for neuritis, making it This is a category of mental disorders in which a patient
chronic. may complain of physical condition without the presence
of any physical signs.
Treatment of neuritis In these cases, always think of psychogenic toothache. No
• Treatment of acute neuritis is based on its etiology.

damage to local tissue is typical in heterotrophic pain entities.
• If bacterial source is present, antibiotics are indicated. It must be noted that psychogenic pain is rare. So, all other
• If viral infection is suspected, antiviral therapy should be

possible diagnoses must be ruled out before making the
started. diagnosis of psychogenic pain.
• If there is no infections, steroids should be considered. The following features are usually found in these diseases

are:
Neuropathy • Pain is observed in multiple teeth.
This is the term used for localized and sustained pain • Precipitated by severe psychological stress.
secondary to an injury or change in neural structure. • Frequent changes in character, location and intensity of
Atypical odontalgia has been included in neuropathy. pain.
Atypical odontalgia means toothache of unknown cause. It is • Response to therapy varies which can include lack of
also known as “Phantom tooth pain” or “dental migraine”. response or unusual response.
Most patients who report with atypical odontalgia usually • Usually referred to psychiatrist for further management.

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102 Textbook of Endodontics

Different type of conditions along with nature of pain, QUESTION
aggravating factors and duration
1. Write short notes on:



Condition Nature of pain Aggravating Duration • Dentin hypersensitivity
factors • Enumerate sources of odontogenic pain
Odontalgia Stabbing, throbbing Hot, cold, lying Hours • Acute periapical abscess
intermittent down, tooth to days • Enumerate sources of nonodontogenic pain
percussion • Trigeminal neuralgia
• Referred pain.
Trigeminal Lancinating, Light touch on Second to
neuralgia excruciating, skin or mucosa minutes
episodic BIBLIOGRAPHY
Cluster Severe ache, Sleep, alcohol Hours 1. Hargreaves KM, et al. Adrenergic regulation of capsaicin-



headache episodic retro-orbital sensitive neurons in dental pulp. J Endod. 2003;29(6):397-9.
component 2. Henry MA, Hargreaves KM. Peripheral mechanism of
Cardiogenic Temporary pain in Exertion Minutes odontogenic pain. Dent Clin North Am. 2007;51(1):19-44.
left side of mandible, 3. Merrill RL. Central mechanisms of orofacial pain. Dent Clin
episodic North Am. 2007;51(1):45-59.
4. Merrill RL. Orofacial pain mechanisms and their clinical
Sinusitis Severe ache, Tooth Hours, application. Dent Clin North Am. 1997;41:167-88.
throbbing, percussion, days
nonepisodic involve lowering of
multiple maxillary head
posterior teeth

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Case Selection and
Treatment Planning 9
 Endodontic Therapy  Treatment Planning  Sequence of Treatment Delivery



 Contraindications of Endodontic  Medical Conditions Influencing


Therapy Endodontic Treatment Planning

The aim of endodontic treatment is to treat or prevent apical restoration (usually crown preparation) and eliminate fear of
periodontitis. Every single tooth starting from central incisor to pulp exposure (Figs 9.4A to C). Elective endodontics allows
third molar can be a potential candidate for root canal therapy. to do more predictable and successful restorative dentistry.
According to treatment point of view, four factors determine
the decision to do or not to do a root canal treatment. These
factors are accessibility, restorability, strategic value of a tooth
and general resistance of patient which ensures success. In
this chapter we will discuss indications, contraindications
and treatment planning regarding endodontic therapy.

ENDODONTIC THERAPY
Actual Reason for Endodontic Therapy
If there is pulp involvement due to caries, trauma, etc. (Figs
9.1 to 9.3) the tooth must be treated endodontically and
restored with proper restoration.

Elective Endodontics
Sometimes elective endodontic is done with crack or heavily
restored tooth, to prevent premature loss of cusp during their Fig. 9.2 Deep restoration irt 47 approximating pulp

indicates endodontic treatment

Fig. 9.1 Carious exposure of pulp resulting Fig. 9.3 Radiograph showing deep caries irt 37


in pulp necrosis and periapical lesion indicating root canal treatment

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104 Textbook of Endodontics

A
Fig. 9.5 When severe attrition of teeth results in sensitivity and


discomfort, endodontic treatment is done for desensitization

Devitalization of Tooth
In patients with attrited teeth, rampant caries or recurrent
decay and smooth surface defects, it is wise to do desensitiza­
tion of the teeth so that patients do not feel discomfort to cold
or sweets (Fig. 9.5).

Endodontic Emergency
B Sometimes patient comes with acute dental pain, in such
cases endodontic therapy is often indicated before a complete
examination and treatment plan doing.

CONTRAINDICATIONS OF
ENDODONTIC THERAPY
There are only few true contraindications of the endodontic
therapy. Otherwise any tooth can be treated by root canal
treatment.

Mainly there are following four factors which influence the


decision of endodontic treatment:
1. Accessibility of apical foramen.

2. Restorability of the involved tooth.

3. Strategic importance of the involved tooth.
C

4. General resistance of the patient.

Figs 9.4A to C Heavily restored teeth sometime
Therefore, before deciding the endodontic treatment,

indicate elective endodontic therapy

multiple factors should be considered. Following cases are
considered poor candidates for endodontic treatment:
• Nonrestorable teeth: Such teeth with extensive root caries,
furcation caries, poor crown/root ratio, with fractured root
Inadequate Restorations are contraindicated for endodontic treatment. Because
in such cases even the best canal filling is futile if it is
Patients with cracked or carious teeth having crowns, when impossible to place the restoration.
want patch up of the crown margins or use preexisting crown • Teeth in which instrumentation is not possible: Such

even after another restorative procedures show high degree teeth with sharp curves, dilacerations, calcifications,
of restorative failure. In such cases, endodontic treatment dentinal sclerosis are treatment difficulties.
followed by optimal restoration of the tooth provide high • Poor accessibility: Occasionally trismus or scarring from

success rate. surgical procedures or trauma, systemic problems, etc.

vip.persianss.ir
Case Selection and Treatment Planning 105


may limit the accessibility due to limited mouth opening. A treatment plan for gaining the patient compliance and


These result in poor prognosis of the endodontic therapy. to have success in the pain management should progress as

­
• Untreatable tooth resorption: Resorptions which are follows:
extremely large in size make the endodontic treatment • Treatment of acute problem includes first step of
almost impossible for such teeth. endodontic treatment which comprises of access opening,
• Vertical tooth fracture: Teeth with vertical root fractures extirpation of pulp and allowing drainage through pulp
pose the hopeless prognosis. space.
• Nonstrategic teeth: There are two major factors • Oral hygiene instructions, diet instructions.
which relegate a strategic tooth to the hopeless status; • Temporary restoration of carious teeth, scaling and
restorability and periodontal support. The tooth that polishing.
cannot be restored or that has inadequate, amenable • Definitive restorations of carious teeth.
periodontal support is hopeless. Evaluation of the oral • Complete root canal treatments of required teeth.
cavity can decide whether tooth is strategic or not, for • Do endodontic surgery if needed.
example if a person has multiple missing teeth, root • Evaluate the prognosis of treated teeth.
canal of third molar may be needed. But in case of well • Provide post endodontic restorations.
maintained oral hygiene with full dentition, an exposed
third molar can be considered for extraction. Factors Affecting Treatment Planning
• Evaluation of the clinician: Clinician should be honest

while dealing with the case. Self evaluation should be done • Chief complaint regarding pain and swelling requires
for his experience, capability to do the case, equipment he urgent treatment and planning for definitive solution.
has or not for the completion of the case. • Previous history of dental treatment (solve the residual
• Systemic conditions: Most of the medical conditions do problems of previous dental treatment).

not contraindicate the endodontic treatment but patient • Medical history (identify factors which can compromise
should be thoroughly evaluated in order to manage the dental treatment).
case optimally. • Intraoral examination (to know the general oral condition
first before focusing on site of complaint so as not to miss
POINTS TO REMEMBER the cause).
• Extraoral examination (to differentially diagnose the chief
For predictable and successful endodontic therapy, following steps
are needed and skipping a step may lead to the endodontic failure
complaint).
or less desirable result: • Oral hygiene.
• Take proper history and medical history of the patient • Periodontal status (to see the periodontal foundation for

• Make accurate diagnosis and treatment planning long term prognosis of involved tooth).

• Obtain adequate anesthesia • Teeth and restorative status (to identify replacement of

• Isolate the tooth using rubber dam missing teeth, status of the remaining dentition).

• Utilize adequate visualization and lighting • Occlusion (to check functional relationship between

• Obtain straight line access to the canals opposing teeth, parafunctional habits, etc.).

• Complete biomechanical preparation of the tooth
• Special tests (to explore the unseen tissues).

• Efficient and safe use of nickel titanium files
• Diagnosis (repeat the series of conclusion).

• Copiously irrigate at all stages
• Treatment options (evaluate various options to decide the

• Obturate the canal three dimensionally

• Give the coronal restoration to tooth. best choice for long term benefit of the patient).

Factors affecting outcome of endodontic treatment
TREATMENT PLANNING •  Health and systemic status of patient
•  Previous restoration
The treatment planning signifies the planning of the •  Root canal anatomy
management of the patient’s dental problems in systematic •  Presence or absence of periapical pathology
and ordered way that assumes a complete knowledge of •  Complexity of root canal system
patient needs, nature of problem and prognosis of the •  Periodontal health of tooth
treatment. •  Presence or absence of root resorption
•  Skill of clinician
Thus the stage of assessment of a complete picture overlaps
•  Patient’s cooperation.

with the stages of decision making, treatment planning and
treatment phase.
Factors Affecting Healing after
POINTS TO REMEMBER Endodontic Treatment
The treatment planning consists of following phases: • Cleaning and shaping of apical third of canal is more
•  Establishing the nature of the problem important than middle third. Apical third should be
•  Decision making thoroughly cleaned and sealed so that microorganisms
•  Planning required to deliver the selected treatment.
cannot reach the periapical tissues.

vip.persianss.ir
106 Textbook of Endodontics

• When there is periapical radiolucency, prognosis is poorer •  Some degree of congestive •  Reduce the level of stress and



when compared to a normal tooth. heart failure may be present anxiety while treating patient
• When there is perforation on root surface, it should be •  Chances of excessive •  Keep the appointments



sealed at the earliest for better prognosis. bleeding when patient is on short and comfortable
• When there is open apex, it is difficult to seal the canal aspirin
because of its shape. In such teeth, before obturation, •  If pacemaker is present, •  Use local anesthetics



apex locators can cause without epinephrine
apexification using calcium hydroxide or MTA should be
electrical interferences •  Antibiotic prophylaxis is
attempted for developing apical barrier.


given before initiation of the
• When there is persistent acute infection in previously treatment
treated tooth, nonsurgical endodontic treatment should Prosthetic valve or implants
be tried before attempting surgical endodontics.
•  Patients are at high risk for •  Prophylactic antibiotic
• When there is apical third fracture, and pulp is vital,



bacterial endocarditis coverage before initiation
stabilize the tooth. •  Tendency for increased of the treatment


– If pulp is nonvital, attempt endodontic treatment bleeding because of •  Consult physician for any



– If it is difficult to negotiate fractured segment, check it prolonged use of antibiotic suggestion regarding patient
periodically. therapy treatment
– If radiolucency appears, manage the case surgically. Leukemia


• In retreatment cases, care should be taken to remove any Patient has increased tendency •  Consult the physician
previous root canal filling. If it cannot be retrieved from for: •  Avoid treatment during acute


periapical tissues, surgical resection of root tip should be •  Opportunistic infections stages


considered. •  Prolonged bleeding •  Avoid long duration


• In case of endodontic-periodontal lesion, if extensive •  Poor and delayed wound appointment

healing •  Strict oral hygiene instructions
destruction of periodontal attachment is present,


•  Evaluate the bleeding time and
prognosis is poor.


platelet status
• If alveolar bone destruction involves more than half •  Use of antibiotic prophylaxis


of the root, attempts should be made to improve the Cancer
periodontal status. In case of grade III mobility, prognosis Usually because of radio •  Consult the physician prior to
is poorer.
-

therapy and chemotherapy treatment
• If crown is extensively damaged that it cannot be restored, •  These patients suffer from •  Perform only emergency


root canal treatment should not be attempted. xerostomia, mucositis, treatment if possible
trismus and excessive •  Symptomatic treatment

bleeding of mucositis, trismus and
MEDICAL CONDITIONS INFLUENCING •  Prone to infections xerostomia
ENDODONTIC TREATMENT PLANNING

because of bone marrow •  Optimal antibiotic coverage

suppression prior to treatment
•  Strict oral hygiene regimen
Medical condition Modifications in

treatment planning Bleeding disorders
In cases of hemophilia, •  Take careful history of the
Patients with valvular

thrombocytopenia, prolonged patient
disease and murmurs bleeding due to liver disease, •  Consult the physician for

Patients are susceptible Prophylactic antibiotics are broadspectrum antibiotics, suggestions regarding the
to bacterial endocarditis advocated before initiation of the patients on anticoagulant patient
secondary to dental endodontic therapy therapy patient experiences •  Avoid aspirin containing

treatment •  Spontaneous bleeding compounds and NSAIDs
•  Prolonged bleeding •  In thrombocytopenia cases,

Patients with hypertension •  Petechiae, ecchymosis and replacement of platelets is

hematoma done before procedure
•  In these patients, stress •  Give premedication
•  Prophylactic antibiotic

and anxiety may further •  Plan short appointments

coverage to be given
increase chances of
•  In case of liver disease, avoid
myocardial infarction or

drugs metabolized by liver
cerebrovascular accidents
Renal disease
­
•  Sometimes antihyper­ •  Use local anesthetic with


tensive drugs may cause minimum amount of •  In this patient usually has •  Prior consultation with


postural hypotension vasoconstrictors hypertension and anemia physician
•  Intolerance to nephrotoxic •  Check the blood pressure
Myocardial infarction


drugs before initiation of treatment
•  Stress and anxiety can •  Elective endodontic treatment •  Increased susceptibility to •  Antibiotic prophylaxis screen


opportunistic infections the bleeding time


precipitate myocardial is postponed if recent
infarction or angina myocardial infarction is •  Increased tendency for •  Avoid drugs metabolized and


present, i.e. < 6 months bleeding excreted by kidney

vip.persianss.ir
Case Selection and Treatment Planning 107


Diabetes mellitus Sequence of treatment delivery consists of three stages:
•  Patient has increased •  Take careful history of the 1. Initial treatment



tendency for infections and patient 2. Definitive treatment


poor wound healing •  Consult with physician prior to 3. Patient recall check up



•  Patient may be suffering treatment

from diseases related to •  Note the blood glucose levels


cardiovascular system, •  Patient should have normal


kidneys and nervous system meals before appointment
like myocardial infarction, •  If patient is on insulin therapy,
SEQUENCE OF TREATMENT DELIVERY

hypertension, congestive he/she should have his
heart failure, renal failure regular dose of insulin before Initial Treatment
and peripheral neuropathy appointment
•  Schedule the appointment The initial treatment mainly aims at providing the relief from

early in the mornings symptoms for example incision and drainage of an infection
•  Antibiotics may be needed with severe pain and swelling, endodontic treatment of a case

•  Have instant source of sugar of acute irreversible pulpitis, etc.

available in clinic
Halting the progress of primary disease, i.e. caries or
•  Patient should be evaluated for


periodontal problem comes thereafter. Finally the patient

the presence of hypertension,
myocardial infarction or renal is made to understand the disease and its treatment which
failure further increases his/her compliance to the treatment. This
Pregnancy approach is beneficial for the long term prevention of the
•  In such patients the harm •  Do the elective procedure in dental caries and periodontal disease.


to patient can occur via second trimester
radiation exposures, •  Use the principles of
Definite Treatment

medication and increased ALARA while exposing patients
level of stress and anxiety to the radiation Definitive treatment involves root canal treatment, surgical
•  In the third trimester, •  Avoid any drugs which can treatment, endodontic retreatment or the extraction of


chances of development cause harm to the fetus teeth with hopeless prognosis. In this phase tooth is given
of supine hypotension are •  Consult the physician to verify
endodontic treatment with final restoration to maintain its

increased the physical status of the
patient and any precautions if form, function and esthetics.
required for the patient
•  Reduce the number of
Patient Recall Check Up

oral microorganism (by
chlorhexidine mouth wash)
Regular patient recall is integral part of the planning process.
-
•  In third semesters, don’t place
It involves taking patient history, examination, diagnosing

patient in supine position for
prolonged periods again for assessment of the endodontic treatment.
Anaphylaxis
Before the clinician starts the endodontic therapy, a

number of issues arise related to the treatment planning.
Patient gives history of •  Take careful history of the
These include maintaining asepsis of the operatory and

severe allergic reaction on patient
administration of: •  Avoid use of agents to which infection control measures, premedication and administra­

•  Local anesthetics patient is allergic tion of local anesthesia followed by review of radiographs and
•  Certain drugs •  Always keep the emergency kit complete isolation of the operating site.

•  Latex gloves and rubber available

dam sheets •  In case the reaction develops:

– Identify the reaction
SUMMARY

– Call the physician

– Place patient in supine
Efficient and successful endodontics begins with proper case
 
position
– Check vital signs
selection. The clinician must know his/her limitations and
select cases accordingly. Since success of endodontic treatment

– If vital signs are reduced,
depends upon many factors which can be modified to get better
 
inject epinepherine tongue
– Provide CPR if needed before initiating the treatment. Therefore accurate and thorough

– Admit the patient preparation of both patient as well as tooth to be treated should

Abbreviation: ALARA: As low as reasonably achievable be carried out to achieve the successful treatment results.

vip.persianss.ir
108 Textbook of Endodontics

QUESTIONS BIBLIOGRAPHY
1. What is criteria for tooth selection for endodontic treatment? 1. Chambers IG. The role and methods of pulp testing in oral



2. Discuss different factors affecting case selection for endodontic diagnosis: a review. Int Endod J. 1982;15:1.
treatment. 2. Elfenbaum A. Causalgia in dentistry: an abandoned pain



3. Discuss various factors invested in the prognosis and success sundrome. Oral Surg. 1954;7:594.







of endodontic treatment. 3. Murray CA, Saunders WP. Root canal treatment and general
4. Discuss the principles of endodontic treatment. health: a review of literature. Int Endod J. 2000;33:1.
5. Discuss indications and contraindications for root canal 4. Newton JT, Buck DJ. Anxiety and pain measures in dentistry: a
treatment. guide to their quality and application. J Am Dent Assoc. 2000;
6. Write short notes on: 131:1449.
• Indications and contraindications of endodontic therapy 5. Weckstein MS. Basic psychology and dental practice. Dent Clin
• Role of medical history in endodontics. North Am. 1970;14:379.

vip.persianss.ir
Asepsis in Endodontics
10
 Rationale for Infection Control  Classification of Instruments  Antiseptics



 Cross-infection  Instrument Processing Procedures/  Infection Control Checklist



 Objective of Infection Control Decontamination Cycle

 Universal Precautions  Disinfection


Endodontics has long emphasized the importance of CROSS-INFECTION
aseptic techniques using sterilized instruments, disinfecting
solutions and procedural barriers like rubber dam. Dental Cross-infection is transmission of infectious agents among
professionals are exposed to wide variety of microorganisms patients and staff within a clinical environment.
in the blood and saliva of patients, making infection
Different routes of spread of infection
control procedures of utmost importance. The common
•  Patient to dental health care worker (DHCW).
goal of infection control is to eliminate or reduce number •  DHCW to patient.
of microbes shared between the people. The procedures of •  Patient to patient.
infection control are designed to kill or remove microbes or •  Dental office to community.
to protect against contamination. •  Community to patient.

RATIONALE FOR INFECTION CONTROL Different Routes of Spread of Infection


The deposition of organisms in the tissues and their growth
Patient to Dental Health Care Worker
resulting in a host reaction is called infection. The number
It can occur in following ways:
of organisms required to cause an infection is termed as the
• Direct contact through break in skin or direct contact
infective dose.
with mucous membrane of dental health care worker
(DHCW).
Factors affecting infective dose are:
• Indirect contact via sharp cutting instruments and needle
•  Virulence of the organism
•  Susceptibility of the host stick injuries.
•  Age, drug therapy, or pre-existing disease, etc. • Droplet injection by spatter produced during dental
procedures and through mucosal surfaces of dental team.
Microorganisms can spread from one person to another
via direct contact, indirect contact, droplet infection and Dental Health Care Worker to the Patient
airborne infection (Flow chart 10.1). Direct contact occurs It occurs by:
by touching soft tissues or teeth of patients. It causes • Direct contact, i.e. through mucosal surfaces of the patient.
immediate spread of infection by the source. • Indirect contact, i.e. via use of contaminated instruments
Indirect contact results from injuries with contaminated and lack of use of disposable instruments.

sharp instruments, needle stick injuries or contact with • Droplet infection via inhalation by the patient.
contaminated equipment and surfaces.
Droplet infection occurs by large particle droplets spatter Patient to Patient

which is transmitted by close contact. Spatter generated It occurs by use of contaminated and nondisposable
during dental procedures may deliver microorganisms to the instruments.
dentist.

POINTS TO REMEMBER Dental Office to the Community


It occurs:
•  Airborne infection involves small particles of < 5 µm size • When contaminated impression or other equipment
•  These microorganisms remain airborne for hours and can cause
contaminate dental laboratory technicians.

infection when inhaled.
• Via spoiled clothing and regulated waste.

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110 Textbook of Endodontics

Flow chart 10.1 Chain of infection


Community to the Patient These are as follows:

• Immunization: All members of the dental team (who are
Community to the patient involves the entrance of
exposed to blood or blood contaminated articles) should
microorganisms into water supply of dental unit. These
be vaccinated against hepatitis B.
microorganisms colonize inside the water lines and thereby
• Use of personal protective barrier techniques, that is use
form biofilm which is responsible for causing infection.
of protective gown, face mask, protective eyewear, gloves,
etc. These reduce the risk of exposure to infectious material
POINTS TO REMEMBER
and injury from sharp instruments.
For an infection to be transmitted, the following conditions are • Maintaining hand hygiene.
required:
•  A pathogenic organism.
•  A source which allows pathogenic organism to survive and Personal Protection Equipment

multiply.
•  Mode of transmission.
Barrier Technique
•  Route of entry. The use of barrier technique is very important, which includes
•  A susceptible host. gown, face mask, protective eyewear and gloves (Fig. 10.1).
Protective gown: Protective gown should be worn to prevent
OBJECTIVE OF INFECTION CONTROL contamination of normal clothing and to protect the skin of
the clinician from exposure to blood and body substances.
The main objective of infection control is elimination • The clinician should change protective clothing when it
or reduction in spread of infection from all types of becomes soiled and if contaminated by blood.
microorganisms. • Gown can be reusable or disposable for use. It should

Basically two factors are important in infection control: have a high neck and long sleeves to protect the arms from

1. Prevention of spread of microorganisms from their hosts. splash and spatter.

2. Killing or removal of microorganisms from objects and • Protective clothing must be removed before leaving the

surfaces. workplace.
• Protective clothing should be washed in the laundry with
UNIVERSAL PRECAUTIONS health care facility.
It is always recommended to follow some basic infection Facemasks: A surgical mask that covers both the nose and
control procedures for all patients, termed as “universal mouth should be worn by the clinician during procedures.
precautions”. Though facemasks do not provide complete microbiological

vip.persianss.ir
Asepsis in Endodontics 111


Head caps: Hairs should be properly tied. Long hairs should
be either covered or restrained away from face. To prevent
hair contamination head caps must be used.
Protective eyewear: Clinician, helping staff and patient must
protect their eyes against foreign bodies, splatter and aerosols
which arise during operative procedures using protective
glasses.
Eyewear protects the eyes from injury and from microbes such as
hepatitis B virus, which can be transmitted through conjunctiva.

Gloves: Gloves should be worn to prevent contamination


of hands when touching mucous membranes, blood, saliva
and to reduce the chances of transmission of infected
microorganisms from clinician to patient.

Gloves should be:


•  Good quality, sterile for all types of surgical procedures and


Fig. 10.1 Personal protective equipment showing mouth mask, nonsterile for all clinical procedures and changed after every
patient

gloves, eyewear, head cap
•  Well fitted and nonpowdered since the powder from gloves can


contaminate veneers and radiographs and can interfere with
wound healing
•  Made-up of ‘low extractable latex protein’ to reduce the

possibility of allergy.

Some important points regarding use of gloves:


• Gloves are manufactured as disposable items meant to be
used for only one patient.
• A new pair of gloves should be used for each patient and
may need to be changed during a procedure.
• Gloves should be changed between patients and when
torn or punctured.
• Overgloves or paper towels must be used for opening
drawers, cabinets, etc.
• Handwashing should be performed immediately before
putting on gloves. Similarly handwashing after glove
removal is essential.
• Gloves must be worn when handling or cleaning materials
or surfaces contaminated with body fluids.
Fig. 10.2 Removal of facemask should be done by grasping it  • Some persons can show allergic reactions to gloves

only by its strings, not by mask itself due to latex (polyisoprene) or antioxidants such as
mercaptobenzothiazole. Ensure that latex free equipment
and nonlatex gloves (polyurethane or vinyl gloves) are
protection but they prevent the splatter from contaminating
used on patients who have a latex-allergy.
the face.
• Person with skin problems (if related to use of glove)
• Masks should be changed regularly and between patients.
should be assessed properly.
• The outer surface of mask can get contaminated with
• Latex gloves should be used for patient examinations and
infectious droplets from spray or from touching the mask
procedures and should be disposed off thereafter.
with contaminated fingers, so should not be reused.
• Heavy utility gloves should be worn when handling and
• If the mask becomes wet, it should be changed between
cleaning contaminated instruments and for surface
patients or even during patient treatment.
cleaning and disinfection.
• The maximum time for wearing masks should not be
more than one hour, since it becomes dampened from
respiration, causing its degradation. Hand Hygiene
• In order to greater protection against splatter, a chin Hand hygiene significantly reduces potential pathogens on
length plastic face shields must be worn, in addition to the hands and is considered the single most critical measure
face masks. for reducing the risk of transmitting organisms to patients and
• To remove mask, grasp it only by its strings, not by the dentists. The microbial flora of the skin consist of transient
mask itself (Fig. 10.2). and resident microorganisms.

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112 Textbook of Endodontics

Transient flora, which colonize the superficial layers of CDC Recommends:

the skin, are easier to remove by routine handwashing. They • Critical and semicritical instruments are to be heat
are acquired by direct contact with patients or contaminated sterilized.
environmental surfaces. • Semicritical items sensitive to heat should be treated with
Resident flora, attached to deeper layers of the skin are high level disinfectant after cleaning.

more resistant to removal and less likely to be associated with • Noncritical items can be treated intermediate to low level
such infections. disinfectant after cleaning.
The purpose of surgical hand antisepsis is to eliminate

transient flora and reduce resident flora for the duration of Definitions
a procedure to prevent introduction of organisms in the
Cleaning: It is the process which physically removes contamination
operative wound, if gloves become punctured or torn. but does not necessarily destroy microorganisms. It is a prerequisite
For most routine dental procedures washing hands with before decontamination by disinfection or sterilization of instru

plain, nonantimicrobial soap is sufficient. For more invasive

­
ments since organic material prevents contact with microbes,
procedures hand antisepsis with either an antiseptic inactivates disinfectants.
solution or alcohol-based handrub is recommended. Disinfection: It is the process of using an agent that destroys germs
or other harmful microbes or inactivates them, usually referred to
Indications for hand hygiene
chemicals that kill the growing forms (vegetative forms) but not
•  At the beginning of patient
the resistant spores of bacteria.
•  Between patient contacts
•  Before putting on gloves Antisepsis: It is the destruction of pathogenic microorganisms
•  After touching inanimate objects existing in their vegetative state on living tissue.
•  Before touching eyes, nose, face or mouth Sterilization: Sterilization involves any process, physical or chemical,
•  After completion of case that will destroy all forms of life, including bacterial, fungi, spores
•  Before eating, drinking and viruses.
•  Between each patient Aseptic technique: It is the method which prevents contamination
•  After glove removal of wounds and other sites, by ensuring that only sterile objects and
•  After barehanded contact with contaminated equipment or fluids come into contact with them; and that the risks of airborne

surfaces and before leaving treatment areas contamination are minimized.
•  At the end of the day.
Antiseptic: It is a chemical applied to living tissues, such as skin
or mucous membrane to reduce the number of microorganisms
Handwash Technique present, by inhibition of their activity or by destruction.
• Removal of rings, jewelry and watches. Disinfectant: It is a chemical substance, which causes disinfection.
• Cover cuts and abrasions with waterproof adhesive It is used on nonvital objects to kill surface vegetative pathogenic
dressings. organisms, but not necessarily spore forms or viruses.
• Clean fingernails with a plastic or wooden stick.
• Scrub hands, nails and forearm using a good quality liquid
soap preferably containing a disinfectant.
• Rinse hands thoroughly with running water.
INSTRUMENT PROCESSING PROCEDURES/
• Dry hands with towel. DECONTAMINATION CYCLE
Instrument processing is the collection of procedures
CLASSIFICATION OF INSTRUMENTS
which prepare the contaminated instruments for reuse.
The center for disease control and prevention (CDC) classified For complete sterilization process, instruments should be
the instrument into critical, semicritical and noncritical processed correctly and carefully (Flow chart 10.2).
depending on the potential risk of infection during the use
of these instruments. These categories are also referred to as
Steps of instrument processing
Spaulding classification (by Spaulding in 1968).
•  Presoaking (Holding)
Classification of instrument sterilization •  Cleaning
•  Corrosion control
Category Definition Examples •  Packaging
Critical Where instruments enter •  Surgical blades and •  Sterilization

or penetrate into sterile instruments •  Monitoring of sterilization
tissue, cavity or blood •  Surgical dental bur •  Handling the processed instrument.

stream
Semicritical Which contact intact •  Amalgam condenser

mucosa or nonintact skin •  Dental handpieces Presoaking (Holding)

•  Mouth mirror It facilitates the cleaning process by preventing the debris

•  Saliva ejectors
from drying.

Noncritical Which contact intact skin •  Pulse oximeter
Procedure:

•  Stethoscope

•  Light switches • Wear puncture resistant heavy utility gloves and personnel

•  Dental chair protective equipment.

vip.persianss.ir
Asepsis in Endodontics 113


Flow chart 10.2 Instrument processing procedure


Fig. 10.3 Ultrasonic cleaner


• Place loose instruments in a perforated cleaning basket
and then place the basket into the holding solution.
Disadvantages: This procedure is not recommended
as there are maximum chances of direct contact with
Holding solution for instruments can be:
•  Neutral pH detergents
instrument surfaces and also of cuts and punctures.
•  Water 2. Ultrasonic cleaning (Fig. 10.3): It is excellent cleaning

•  Enzyme solution. method as it reduces direct handling of instruments. So,
it is considered safer and more effective than manual
• Perforated cleaning basket reduces the direct handling of scrubbing.
instruments. So, chances of contamination are decreased. Procedure:

• Holding solution should be discarded at least once a day • Mechanism of action: Ultrasonic energy generated in

or earlier if seems to be soiled. the ultrasonic cleaner produces billions of tiny bubbles
• Avoid instrument soaking for long time as it increases the which, in further, collapse and create high turbulence
chances of corrosion of instruments. at the surface of instrument. This turbulence dislodges
• It aids in the subsequent cleaning process by removing the debris.
gross debris. • Maintain the proper solution level.
• Use recommended cleaning solution.
POINTS TO REMEMBER • Time may vary due to:
The advantage of cleaning procedure is that it reduces the bio- – Nature of instrument
burden, i.e. microorganisms, blood, saliva and other materials. – Amount of debris


– Efficiency of ultrasonic unit.


Usually the time ranges vary from 4 to 16 minutes.
Cleaning • After cleaning, remove the basket/cassette rack and
wash under tap water. Use gloves while washing under
Methods used for cleaning:
•  Manual scrubbing
tap water as the cleaning solution is also contaminated.
•  Ultrasonic cleaning • Discard the solution at least daily.
•  Mechanical-instrument washer. 3. Mechanical–instrument washer: These are designed to

clean instruments in hospital set-up. Instrument washer
has also the advantage that it reduces the direct handling
1. Manual scrubbing: It is one of the most effective methods
of the instrument.

for removing debris, if performed properly.
Procedure:
Control of Corrosion by Lubrication

• Brush delicately all surfaces of instruments while sub-
merged in cleaning solution. It prevents damage of instruments because of drying. For
• Use long-handled stiff nylon brush to keep the scrub- rust-prone instruments, use dry hot air oven/chemical vapor
bing hand away from sharp instrument surfaces. sterilization instead of autoclave. Use sprays rust inhibitor
• Always wear heavy utility gloves and personnel protec- (sodium nitrite) on the instruments.
tive equipment.
• Use neutral pH detergents while cleaning. Packaging
• Instruments’ surfaces should be visibly clean and free It maintains the sterility of instruments after the sterilization.
from stains and tissues. Unpacked instruments are exposed to environment when

vip.persianss.ir
114 Textbook of Endodontics

Fig. 10.4 Peel-pouches for packing instruments Fig. 10.5 Ultraviolet chamber for storage of sterile instruments


sterilization chamber is opened and can be contaminated Table 10.1: Sterilization method and type of packaging material
by dust, aerosols or by improper handling or contact with
contaminated surfaces. Sterilization method Packaging material
Varieties of packaging materials are available in the market Autoclave •  Paper or plastic peel-pouches
such as self-sealing, paper-plastic and peel-pouches. Peel- Wrapped cassettes •  Plastic tubing (made-up of nylon)
pouches are the most common and convenient to use (Fig. •  Thin clothes (Thick clothes are not


advised as they absorb too much heat)
10.4).
•  Sterilization paper (paper wrap)
Packs should be stored with the following considerations (Table Chemical vapor •  Paper or plastic pouches
10.1): •  Sterilization paper
•  Instruments are kept wrapped until ready for use
Dry heat •  Sterilization paper (paper wrap)
•  To reduce the risk of contamination, sterile packs must be
•  Nylon plastic tubing (indicated for dry

handled as little as possible

heat)
•  Sterilized packs should be allowed to cool before storage;
•  Wrapped cassettes

otherwise condensation will occur inside the packs
•  Sterile packs must be stored and issued in correct date order.

The packs, preferably, are stored in UV chamber (Fig. 10.5) or
• Filtration
drums which can be locked.
– Candles


– Membranes


Methods of Sterilization – Asbestos pads


Sterilization is process by which an object, surface or medium • Radiation
is freed of all microorganisms either in the vegetative or spore Chemical agents:
state (Table 10.1). • Alcohols
– Ethanol


Classification of Sterilizing Agents – Isopropyl alcohol


Physical agents: • Aldehydes
• Sunlight – Formaldehyde


• Drying – Glutaraldehyde


• Cold • Halogens
• Dry heat – Iodine


– Flaming – Chlorine




– Incineration • Dyes


– Hot air oven – Acridine




• Moist heat – Aniline


– Boiling • Phenols


– Steam under pressure – Cresol




– Pasteurization – Carbolic acid




vip.persianss.ir
Asepsis in Endodontics 115


• Metallic salts gases since they stop the steam from reaching the inner part of
– Ethylene oxide the packs.


– Formaldehyde • For packaging of autoclaving instruments, one should


– Beta propiolactone use porous covering so as to permit steam to penetrate


• Surface active agents through and reach the instruments.
• The materials used for packaging can be fabric or sealed
The accepted methods of sterilization in dental practice are: paper or cloth pouches (Fig. 10.7) and paper-wrapped
•  Moist/steam heat sterilization cassettes.
•  Dry heat sterilization
• If instruments are to be stored and not used shortly after
•  Chemical vapor pressure sterilization
•  Ethylene oxide sterilization.
sterilization, the autoclave cycle should end with a drying
phase to avoid tarnish or corrosion of the instruments.

Moist/Steam Heat Sterilization Phases


Sterilization process is composed of three main phases:
Autoclave 1. Pretreatment phase/heat-up cycle: All air is virtually
• Autoclave provides the most efficient and reliable method


expelled by a number of pulses of vacuum and the
of sterilization for all dental instruments.
introduction of steam, so that the saturated steam can
• It involves heating water to generate steam in a closed
affect the instruments during second phase.
chamber resulting in moist heat that rapidly kills
2. Sterilizing phase/sterilization cycle:
microorganisms (Fig. 10.6).

• The temperature increases adequately up to the degree
Use of saturated steam under pressure is the most efficient, at which sterilization is to take place.
quickest, safest, effective method of sterilization because: • Actual sterilizing period (also called Holding Time)
•  It has high penetrating power starts when the temperature in all parts of the autoclave
•  It gives up a large amount of heat (latent heat) to the surface chamber and its contents has reached the sterilizing

with which it comes into contact and on which it condenses as temperature.
water. • This should remain constant within specified
temperature throughout the whole sterilization phase.
Types of Autoclaves 3. Post-treatment phase/depressurization cycle: In this

Two types of autoclaves are available: phase either the steam or the revaporized condensed
1. Downward (gravitation) displacement sterilizer: This is water is removed by vacuum to ensure that the goods are
dried rapidly.

nonvacuum type autoclave.
2. Steam sterilizers (autoclave) with pre- and postvacuum

processes. Three Main Factors Required for
Effective Autoclaving
Packaging of Instruments for Autoclaving 1. Pressure: It is expressed in terms of psi or kPa.

• For wrapping, closed containers such as closed metal 2. Temperature: For effective sterilization the temperature

trays, glass vials and aluminum foils should not be used, should be reached and maintained at 121°C. As the

Fig. 10.6 Autoclave for moist heat sterilization Fig. 10.7 Cloth pouches for instrument wrapping


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116 Textbook of Endodontics

temperature and pressure increases, superheated steam
Packaging material requirements for dry heat
is formed. This steam is lighter than air, thus rises to the •  Should not be destroyed by temperature used.
upper portion of the autoclave. As more steam is formed, •  Should not insulate items from heat.
it eliminates air from autoclave. The reason of complete
Acceptable materials
elimination of air is to help superheated steam to penetrate •  Paper and plastic bags
the entire load in the autoclave and remain in contact for •  Wrapped cassettes
the appropriate length of time. •  Paper wrap
3. Time: A minimum of 20 to 30 minutes of time is required •  Aluminum foil

after achieving full temperature and pressure. •  Nylon plastic tubing
Unacceptable materials
Plastic and paper bags which are not able to withstand dry heat
Clinical Tips


temperature.
•  Higher the temperature and pressure, shorter is the time

required for sterilization. Recommended temperature and duration of hot oven
•  At 15 psi pressure, the temperature of 121°, the time required
Hot air oven

is 15 minutes.
•  At 126°C, time is 10 minutes. Temp°C 141°C 149°C 160°C 170°C 180°C
•  At 132°C, time is 3 minutes at 27 to 28 lbs—flash sterilization.
Time 3 hr 2.5 hr 2 hr 1 hr 30 min

Advantages of autoclaving Mechanism of Action


•  Time efficient • The dry heat kills microorganisms by protein denaturation,
•  Good penetration coagulation and oxidation.
•  The results are consistently good and reliable
• Organic matter such as oil or grease film must be removed
•  The instruments can be wrapped prior to sterilization.
from the instruments as this may insulate against dry heat.
Disadvantages of autoclaves • Instruments which can be sterilized in dry hot oven are
•  Blunting and corrosion of sharp instruments
glassware such as pipettes, flasks, scissors, glass syringes,
•  Damage to rubber goods.
carbon steel instruments and burs. Dry heat does not
corrode sharp instrument surfaces. Also it does not erode
glassware surfaces.
Dry Heat Sterilization • Before placing in the oven, the glassware must be dried.
It is alternative method for sterilization of instruments. This The oven must be allowed to cool slowly for about 2 hours
type of sterilization involves heating air which on further as glassware may crack due to sudden or uneven cooling.
transfers energy from air to the instruments. In this type of
sterilization, higher temperature is required than steam or Rapid heat transfer (forced air type): In this type of
chemical vapor sterilization. sterilizer, a fan or blower circulates the heated air throughout
the chamber at a high velocity which, in turn, permits a more
rapid transfer of heat energy from the air to instruments,
Conventional Hot Air Oven thereby reducing the time.
The hot air oven utilizes radiating dry heat for sterilization
as this type of energy does not penetrate materials easily. Temperature/Cycle recommended
So, long periods of exposure to high temperature are usually 370°F–375°F–12 minutes for wrapped instruments
required. 370°F–375°F–16 minutes for unwrapped instruments.

Packaging of Instruments for Dry Heat Advantages of dry heat sterilization


• Dry heat ovens usually achieve temperature above 320°F •  No corrosion is seen in carbon-steel instruments and burs
(160°C). •  Maintains the sharpness of cutting instruments
• The packs of instrument must be placed at least 1 cm apart, •  Effective and safe for sterilization of metal instrument and

for air to circulate in the chamber. mirrors
• In conventional type of hot air oven, air circulates by •  Low cost of equipment
•  Instruments are dry after cycle
gravity flow, thus it is also known as Gravity convection.
•  Industrial forced draft types usually provide a larger capacity at
• The type of packaging or wrapping material used should

reasonable price
be able to withstand high temperature otherwise it may get •  Rapid cycles are possible at higher temperatures.
char.

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Asepsis in Endodontics 117


• Use system in ventilated room.
Disadvantages of dry heat sterilization
•  Poor penetrating capacity of dry heat
• Space should be given between the instruments that are
•  Long cycle is required because of poor heat conduction and to be sterilized in the chamber for better conduction and

poor penetrating capacity penetration.
•  High temperature may damage heat sensitive items such as • Water should not be left on the instruments.

rubber or plastic goods
•  Instruments must be thoroughly dried before placing them in
Ethylene Oxide Sterilization (ETOX)

sterilization
•  Inaccurate calibration and lack of attention to proper settings
This sterilization method is best used for sterilizing complex

often lead to errors in sterilization
•  Heavy loads of instruments, crowding of packs and heavy instruments and delicate materials.
Ethylene oxide is highly penetrative, noncorrosive gas

wrapping easily defeat sterilization


•  Generally not suitable for handpieces above 10.8°C with a cidal action against bacteria, spores and
•  Cannot sterilize liquids viruses.
•  May discolor and char fabric.

Mechanism of Action
Chemical Vapor Sterilization It destroys microorganisms by alkylation and causes
denaturation of nucleic acids of microorganisms.
Sterilization by chemical vapor under pressure is known as
The duration that the gas should be in contact with the
chemical vapor sterilization. In this, special chemical solution


material to be sterilized is dependent on temperature,
is heated in a closed chamber, producing hot chemical vapors
humidity, pressure and the amount of material.
that kill microorganisms.
Temperature, pressure and time required for completion
of one cycle is 270°F (132°C) at 20 lb for 30 minutes. Chemical Advantages
vapor sterilizer is also known as chemiclave. •  It leaves no residue.
•  It is a deodorizer.
•  Good penetration power.
Mechanism of Action •  Can be used at a low temperature.
• Coagulation of protein •  Suited for heat sensitive articles, e.g. plastic, rubber, etc.
• Cell membrane disruption Disadvantages
• Removal of free sulfhydryl groups •  High cost of the equipment.
• Substrate competition. •  Toxicity of the gas.
•  Explosive and inflammable.
Contents of chemical solution: The solution contains various
ingredients which are as follows:
•  Active ingredient – 0.23% formaldehyde Irradiation


•  Other ingredient – 72.38% ethanol + acetone +


water and other alcohols Ionizing Radiation (X-rays, Gamma Rays and

High-Speed Electrons)
Four cycles are required for this sterilizer which are as follows: Ionizing radiations are effective for heat labile items. They
1.  Vaporization cycle
are commonly used by the industry to sterilize disposable
2.  Sterilization cycle
3.  Depressurization cycle
materials such as needles, syringes, culture plates, suture
4.  Purge cycle (which collects chemicals from vapors in the material, cannulas and pharmaceuticals sensitive to heat.
High energy gamma rays from cobalt-60 are used to sterilize

chamber at the end of cycle).
such articles.
Advantage
Eliminates corrosion of carbon steel instruments, burs and pliers. Nonionizing Radiation
Disadvantages (Ultraviolet Light and Infrared Light)
•  The instruments or items which are sensitive to elevated • Ultraviolet rays:

temperature are damaged
– Ultraviolet (UV) rays are absorbed by proteins and
•  Sterilization of liner, textiles, fabric or paper towels is not
nucleic acids and kill microorganisms by the chemical

recommended
•  Dry instruments should be loaded in the chamber. reactions.

– Their main application is purification of air in operating


rooms to reduce the bacteria in air, water and on the
Precautions to be Taken contaminated surfaces.
• Use gloves and protective eyewear while handling the • Infrared:

chemical solution. – It is used for sterilizing a large number of syringes


• Use paper/plastic peel-pouches or bags recommended for sealed in metal container, in a short period of time.
use in chemiclave. – It is used to purify air in the operating room.


vip.persianss.ir
118 Textbook of Endodontics

Fig. 10.8 Glass bead sterilizer Fig. 10.9 Files placed in glass bead sterilizer


Glass Bead Sterilizer Methods of Disinfection
It is rapid method of sterilization which is used for sterilization Disinfection by Cleaning
of instruments (Fig. 10.8). It uses table salt which consists Cleaning with a detergent and clean hot water removes
approximately of 1 percent sodium silico-aluminate, sodium almost all pathogens including bacterial spores.
carbonate or magnesium carbonate. So it can be poured more
readily and does not fuse under heat. Salt can be replaced
by glass beads provided the beads are smaller than 1 mm in Disinfection by Heat
diameter because larger beads are not efficient in transferring Heat is a simple and reliable disinfectant for almost anything
the heat to endodontic instruments due to presence of large except living tissues. Mechanical cleaning with hot water
air spaces between the beads. provides an excellent quality of disinfection for a wide variety
The instruments can be sterilized in 5 to 15 seconds at a of purposes.

temperature of 437 to 465°F (260°C) even when inoculated
with spores. Low Temperature Steam
Most vegetative microorganisms and viruses are killed
Advantages when exposed to steam at a temperature of 73°C for 20
•  Commonly used salt is table salt which is easily available and minutes below atmospheric pressure. This makes it a useful

cheap procedure to leave spoiled instruments safe to handle prior
•  Salt does not clog the root canal. If it is carried into the canal, it
to sterilization.

can be readily removed by irrigation.
Disadvantage
Handle portion is not sterilized, therefore instruments are not Disinfection by Chemical Agents
entirely ‘sterile’ (Fig. 10.9). They are used to disinfect the skin of a patient prior to surgery
and to disinfect the hands of the operator.
Glass bead sterilizer Disadvantages of using chemicals:
•  Fast method • No chemical solution sterilizes the instruments immersed
•  Uses table salt which consists 1 percent sodium silico-aluminate, in it.

sodium carbonate or magnesium carbonate
• There is a risk of producing tissue damage if residual
•  Salt can be replaced by glass beads
•  Instruments can be sterilized in 5 to 15 seconds solution is carried into the wound.
•  Temperature is 437 to 465°F (260°C).
Levels of Disinfectant
DISINFECTION Alcohols—Low Level Disinfectant
• Ethanol and isopropyl alcohols are commonly used as
It is the term used for destruction of all pathogenic organisms, antiseptics.
such as, vegetative forms of bacteria, mycobacteria, fungi and • Possess some antibacterial activity, but they are not
viruses, but not bacterial endospores. effective against spores and viruses.

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Asepsis in Endodontics 119


Method of Sterilizing conditions Advantages Disadvantages
sterilization
Dry heat •  Hot air oven •  160°C for 60–120 •  No corrosion •  Poor penetration of dry heat




minutes •  Instruments are dry after cycle •  Long cycle of sterilization



•  Rapid heat •  190°C for 6–12 minutes •  Low cost of equipment •  Damage to rubber and plastic




transfer •  Higher temperature may


damage the instruments
Moist heat •  Autoclave •  121°C at 15 psi for 15 •  Better penetration of moist heat •  Dulling and corrosion of sharp




minutes •  Rapid and effective method of instruments


sterilization •  Damage to plastic and rubber


•  Flash autoclave •  134°C for 3–10 minutes •  Does not destroy cotton or cloth •  Instruments need to be air dried




products at the end of cycle
•  Used for most of instruments


Chemical •  Chemical •  127–131°C at 20 psi for •  Short sterilization cycle •  Requires adequate ventilation




vapor pressure 20 minutes •  Lack of corrosion of instrument •  Instruments should be dried



sterilization •  Effective method before sterilization


•  May emit offensive vapor smell


•  Chemical vapors can damage


sensitive instruments
Chemical •  Ethylene oxide •  Good penetration •  Expensive



sterilization •  Nontoxic •  Explosive and inflammable


•  Heat sensitive articles can be •  Toxicity of gas


sterilized

• Act by denaturing proteins. Glutaraldehyde


• To have maximum effectiveness, alcohol must have a 10 • Toxic, irritant and allergenic.
minutes contact with the organisms. • A high level disinfectant.
• Instruments made of carbon steel should not be soaked in • Active against most vegetative bacteria, fungi and bacterial
alcoholic solutions, as they are corrosive to carbon steel. spores.
• Rubber instruments absorb alcohol thus their prolonged • Frequently used for heat sensitive material.
soaking can cause a reaction when material comes in • A solution of 2 percent glutaraldehyde (Cidex), requires
contact with living tissue. immersion of 20 minutes for disinfection; and 6 to 10
hours of immersion for sterilization.
Phenolic Compounds—Intermediate Level, • Safely used on metal instruments, rubber, plastics and
porcelain.
Broad Spectrum Disinfectant
• Activated by addition of sodium bicarbonate, but in its
• The phenolic compounds were developed to reduce their
activated form, it remains potent only for 14 days.
side effects but are still toxic to living tissues.
• At high concentration, these compounds are protoplasmic
poison and act by precipitating the proteins and destroy ANTISEPTICS (FIG. 10.10)
the cell wall.
• These compounds are used for disinfection of inanimate Antiseptic is a chemical disinfectant that can be diluted
objects such as walls, floors and furniture. sufficiently to be safe for application to living tissues like
• They may cause damage to some plastics and they do intact skin, mucous membranes and wounds.
not corrode certain metals such as brass, aluminum and
carbon steel.
Alcohols
Aldehyde Compounds—High Level Disinfectant • Two types of alcohols are used ethyl alcohol and isopropyl
Formaldehyde alcohol.
• Broad spectrum antimicrobial agent. • Used for skin antisepsis.
• Flammable and irritant to the eye, skin and respiratory • Their benefit is derived primarily in their cleansing action.
tract. • The alcohols must have a prolonged contact with the
• Has limited sporicidal activity. organisms to have an antibacterial effect.
• Used for large heat sensitive equipment such as ventilators • Ethyl alcohol is used in the concentration of 70 percent as
and suction pumps excluding rubber and some plastics. a skin antiseptic.
• Not preferred due to its pungent odor and because 18 to 30 • Isopropyl alcohol is used in concentration of 60 to 70
hours of contact is necessary for cidal action. percent for disinfection of skin.

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120 Textbook of Endodontics

Disinfection of dental material
Material Disinfectant Technique
Cast lodophor Soaking for 10 min
Wax records Iodoform, NaOCl Immersion
Alginate impression Iodophors, NaOCl Soaking for less
Phenolic compound than 10 min

Sterilization of the dental equipment


Instrument Method
Mouth mirror, probes, explorer Autoclave
Endodontic instruments—files, Autoclave
reamers, broaches
Steel, burs Disposable
Carbide and diamond burs Autoclave
Local anesthetic cartridges Presterilized/disposable
Fig. 10.10 Hand disinfectant
Needles Disposable

Rubber dam equipment
Aqueous Quarternary Ammonium •  Carbon steel clamps and metal Dry heat, ethylene oxide,

frames autoclave
Compounds •  Punch Dry heat, ethylene oxide
• Benzalkonium chloride (Zephiran) is the most commonly Gutta-percha points Dip in 5.2% sodium
used antiseptic. hypochlorite for 1 min and
• It is well-tolerated by living tissues. then rinse with ethyl alcohol

Iodophor Compounds
INFECTION CONTROL CHECKLIST
• Used for surgical scrub, soaps and surface antisepsis.
• Usually effective within 5 to 10 minutes. Infection Control during the
• Discolor surfaces and clothes. Pretreatment Period
• Iodine is complexed with organic surface-active agents
such as polyvinyl-pyrrolidine (Betadine, Isodine). Their • Utilize disposable items whenever possible.
activity is dependent on the release of iodine from the • Ensure before treatment that all equipment have been
complex. sterilized properly.
• Concentrated solutions have less free iodine. Iodine is • Remove avoidable items from the operatory area to
released as the solution is diluted. facilitate a thorough cleaning following each patient.
• These compounds are effective against most bacteria, • Identify those items that will become contaminated
spores, viruses and fungi. during treatment, for example, light handles, X-ray unit
heads, tray tables, etc. Disinfect them when the procedure
is complete.
Chloride Compounds • Review patient records before initiating treatment.
• Commonly used are sodium hypochlorite and chlorine • Place radiographs on the X-ray view box before starting
dioxide. the patient.
• Sodium hypochlorite has rapid action. • Preplan the materials needed during treatment to avoid
• A solution of 1 part of 5 percent sodium hypochlorite with opening of the cabinets and drawers once the work is
9 parts of water is used. started.
• Chlorous acid and chlorine dioxide provides disinfection • Use separate sterilized bur blocks for each procedure to
in 3 minutes. eliminate the contamination of other, unneeded burs.
• Always keep rubber dam kit ready in the tray.
• Follow manufacturer’s directions for care of dental unit
Diguanides water lines (DUWL).
• Chlorhexidine is active against many bacteria. • Clinician should be prepared before initiating the
• Gets inactivated in the presence of soap, pus, plastics, etc. procedure, this includes the use of personal protective
• Mainly used for cleaning skin and mucous membrane. equipment (gown, eyewear, masks and gloves) and hand
• As a 0.2 percent aqueous solution or 1 percent gel it can be hygiene.
used for suppression of plaque and postoperative infection. • Update patient’s medical history.

vip.persianss.ir
Asepsis in Endodontics 121


Chairside Infection Control • Sterilize the hand pieces whenever possible. In general
hand piece should be autoclaved but the hand piece which
• Treat all patients as potentially infectious.
cannot be heat sterilized, should be disinfected by the use
• Take special precautions while handling syringes and
of chemicals. Clean the handpiece with a detergent and
needles.
water to remove any debris. Sterilize it.
• Use a rubber dam whenever possible.
• Waste that is contaminated with blood or saliva should be
• Use high volume aspiration.
placed in sturdy leak proof bags.
• Ensure good ventilation of the operatory area.
• Handle sharps items carefully.
• Be careful while receiving, handling, or passing sharp
• Remove personal protective equipment after clean-up.
instruments.
Utility gloves should be washed with soap before removal.
• Do not touch unprotected switches, handles and other
• At the end, thoroughly wash hands.
equipment once gloves have been contaminated.
• Avoid touching drawers or cabinets, once gloves have
been contaminated. When it becomes necessary to do so, QUESTIONS
ask your assistant to do this or use another barrier, such as
overglove to grasp the handle or remove the contaminated 1. What is rationale of infection control? Mention different routes



of infection transmission?
gloves and wash hands before touching the drawer and
2. Define sterilization and disinfection. Describe the various
then reglove for patient treatment.



methods to achieve sterilization of endodontic arma-
mentarium.
Infection Control during the 3. Write short notes on:


Post-treatment Period • Glass bead sterilizer.
• Autoclave.
• Remove the contaminated gloves used during treatment, • Asepsis in endodontics.
wash hands and put on a pair of utility gloves before • Infection control during endodontic procedures.
beginning the clean up. • Sterilization of rotary equipments.
• Continue to wear protective eyewear, mask and gown • Different routes of infection transmission.
• Sterilization of endodontic instruments.
during clean up.
• Dispose of blood and suctioned fluids which have been
collected in the collection bottles during treatment. BIBLIOGRAPHY
• After disposing of blood and suctioned fluids, use 0.5%
chlorine solution to disinfect the dental unit collection 1. Association reports: current status of sterilization instruments


bottle. Keep the solution in the bottle for atleast 10 minutes. devices, and methods for the dental office; LADA. 1981;102:
683-9.
• Clean the operatory area and disinfect all the items not
2. Charles H Stuart. Enterococcus faecalis: its role in root canal
protected by barriers.


treatment failure and current concepts in retreatment;
• Remove the tray with all instruments to sterilization area J endodon. 2006;32(2):93-8.
separate from the operatory area. 3. Chris H Miller. Cleaning, sterilization and disinfection. JADA.


• Never pick up instruments in bulk because this increases 1993;24:48-56.
the risk of cuts or punctures. Clean the instruments 4. Chris H Miller. Sterilization and disinfection. JADA. 1992;123:
manually or in an ultrasonic cleaner. 46-54.

vip.persianss.ir
Isolation of Teeth
11
 Isolation with Rubber Dam  Classification of Rubber Dam Clamps


The complexities of oral environment present obstacles to the Barnum, a New York dentist in 1863 (Figs 11.1A to E).
endodontic procedures starting from diagnosis till the final
treatment is done. In order to minimize the trauma to these Advantages of using a rubber dam
surrounding structures and to provide comfort to the patient, •  It is raincoat for the teeth
the clinician needs to control that field. While performing any •  It helps in improving accessibility and visibility of the working


operative procedure, many structures require proper control area
so as to prevent them from interfering the operating field. •  It gives a clean and dry aseptic field while working

•  It protects the lips, cheeks and tongue by keeping them out of
These structures together constitute the oral environment.

the way
•  It helps to avoid unnecessary contamination through infection
Following components of oral environment need to be con-

control
trolled during operative procedures:
•  It protects the patient from inhalation or ingestion of
•  Saliva

instruments and medicaments
•  Moving organs
•  It helps in keeping teeth saliva free while performing a root
–  Tongue

canal so that tooth does not get decontaminated by bacteria
–  Mandible
present in saliva
•  Lips and cheek
•  It improves the efficiency of the treatment
•  Gingival tissue

•  It limits bacterial laden splash and splatter of saliva and blood
•  Buccal and lingual vestibule.

•  It potentially improves the properties of dental materials

•  It provides protection of patient and dentist.
Advantages of moisture control

Disadvantages of using a rubber dam
Patient related factors: •  Takes time to apply
•  Provides comfort to patient •  Communication with patient can be difficult
•  Protects patients from swallowing or aspirating foreign bodies •  Incorrect use may damage porcelain crowns/crown margins/
•  Protects patient’s soft tissues—tongue, cheeks by retracting

traumatize gingival tissues

them from operating field. •  Insecure clamps can be swallowed or aspirated.
Operator related factors: Contraindications of use of rubber dam
•  A dry and clean operating field •  Asthmatic patients
•  Infection control by minimizing aerosol production •  Allergy to latex
•  Increased accessibility to operative site •  Mouth breathers
•  Improved properties of dental materials, hence better results •  Extremely malpositioned tooth

are obtained •  Third molar (in some cases).
•  Protection of the patient and operator
•  Improved visibility of the working field and diagnosis.
•  Less fogging of the dental mirror
•  Prevents contamination of tooth preparation POINTS TO REMEMBER
•  Hemorrhage from gingiva does not enter operative site.
Rubber dam
•  Introduced by Barnum, a New York Dentist in 1863
•  It is raincoat for the teeth
ISOLATION WITH RUBBER DAM •  Improves accessibility, visibility, gives clean and dry aseptic

Isolation of the tooth requires proper placement of the rubber field, and protects patient from inhalation of instruments and
dam/dental dam. It helps to isolate the pulp space from saliva medicaments.
•  Contraindicated in asthmatic patients, mouth-breathers, and
and protects oral tissues from irrigating solutions, chemicals

third molar cases.
and other instruments. Rubber dam was introduced by

vip.persianss.ir
Isolation of Teeth 123


A B

C D

E
Figs 11.1A to E Photographs showing RCT under rubber dam. (A) Rubber dam application; (B) Access opening under rubber dam; 

(C) Working length radiograph; (D) Master cone insertion under rubber dam; (E) Radiograph after obturation

Courtesy: Jaidev Dhillon

Rubber dam can be defined as a flat thin sheet of latex/non-


Rubber dam accessories

latex that is held by a clamp and frame which is perforated •  Lubricant/petroleum jelly
to show the tooth/teeth to protrude through the perforations •  Dental floss
while all other teeth are covered and protected by sheet •  Rubber dam napkin.
(Figs 11.1A to E).

Rubber dam equipment


•  Rubber dam sheet
Rubber Dam Sheet (Fig. 11.2)
•  Rubber dam clamps • The rubber dam sheet is normally available in size 5 × 5 or
•  Rubber dam forceps 6 × 6 squares in green or black color
•  Rubber dam frame
• It is available in three thicknesses, i.e. light, medium and
•  Rubber dam punch.
heavy

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124 Textbook of Endodontics

Fig. 11.2 Rubber dam sheet Fig. 11.3 Rubber dam clamps



• The middle grade is usually preferred as thin is more prone
to tearing and heavier one is more difficult to apply
• Latex-free dam is necessary as number of patients are
increasing with latex allergy
• Flexi dam is latex-free dam of standard thickness with no
rubber smell.

Thickness of rubber dam sheet


Thin - 0.15 mm


Medium - 0.20 mm


Heavy - 0.25 mm


Extra heavy - 0.30 mm


Special heavy - 0.35 mm


Rubber Dam Clamps
• Rubber dam clamps, to hold the rubber dam onto the tooth
are available in different shapes and sizes (Fig. 11.3).
• Clamps mainly serve two functions:
1. They anchor the rubber dam to the tooth.


2. Help in retracting the gingiva. Fig. 11.4 A clamp should contact tooth from all sides



Bland Clamps
• Bland clamps are usually identified by the jaws, which are
flat and point directly towards each other.
CLASSIFICATION OF RUBBER DAM CLAMPS
• In these clamps, flat jaws usually grasp the tooth at or On the Basis of Jaw Design
above the gingival margin.
• They can be used in fully erupted tooth where cervical • Bland
constriction prevents clamp from slipping off the tooth. • Retentive.

Retentive Clamps On the Basis of Material Used


• As the name indicates, these clasps provide retention by • Metallic
providing four-point contact with the tooth. • Nonmetallic/plastic.
• In these, jaws are usually narrow, curved and slightly
inverted which displace the gingivae and contact the tooth Metallic: Traditionally, clamps have been made from tem-
below the maximum diameter of crown (Fig. 11.4). pered carbon steel and more recently from stainless steel.
Both flanges are further subdivided into: Nonmetallic/plastic: Nonmetallic are made from polycarbon-
• Winged ate plastic. Advantage of nonmetallic clamps is that these do
• Wingless. not appear radiopaque on radiographs (Fig. 11.5).

vip.persianss.ir
Isolation of Teeth 125


Fig. 11.5