Endodontics E-Book: Principles and Practice

496 Pages·2020·17.6 MB·english

by  Mahmoud Torabinejad

Endodontics
Principles and Practice
SIXTH EDITION
Mahmoud Torabinejad, DMD, MSD, PhD
Affiliate Professor of Endodontics, Department of Endodontics, University of Washington Seattle, WA, USA
Adjunct Professor, Department of Endodontics
School of Dentistry, Loma Linda University, Loma Linda, CA, USA
Adjunct Professor, Department of Endodontics
University of Pacific Arthur A. Dugoni School of Dentistry;
Adjunct Professor, Department of Preventive and Restorative Dentistry, Section of Endodontics
University of California in San Francisco School of Dentistry
San Francisco, CA, USA
Ashraf F. Fouad, DDS, MS
Freedland Distinguished Professor
Vice-chair, Division of Comprehensive Oral Health
Adams School of Dentistry, University of North Carolina
Chapel Hill, NC, USA
Shahrokh Shabahang, DDS, MS, PhD
Associate Professor
Department of Endodontics
School of Dentistry
Loma Linda University
Loma Linda, CA, USA
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Preface
The primary responsibility of dentists has always been to relieve have newer clinically relevant information. In addition, it includes
dental pain and prevent tooth loss. Despite their efforts, many Expert Consult pin-code access for the first time.
teeth develop caries, suffer traumatic injury, or are impacted by This edition contains information regarding the pathogenesis
other disorders that may require endodontic care. Endodontics is a of pulp and periapical diseases, systemic consideration for patients
discipline of dentistry that deals with the morphology, physiology, who need endodontic intervention, endodontic radiology includ-
and pathology of the human dental pulp and periapical tissues, ing the use of CBCT, diagnosis and treatment planning, differ-
as well as the prevention and treatment of diseases and injuries ential diagnosis of pain and radiolucencies of non-pulpal origin,
related to these tissues. Its scope includes diagnosis and treat- endodontic case complexity and when to refer to an endodontist,
ment of pain of pulpal and/or periapical origin, vital pulp therapy, endodontic instruments, local anesthesia, emergency treatment,
regenerative endodontic procedures, nonsurgical root canal treat- management of vital pulp including regeneration of pulp-dentin
ment, surgical or non-surgical retreatment of cases with persistent complex, traumatic injuries, root canal anatomy, access prepara-
disease and internal bleaching of discolored teeth. Ultimately, the tions, cleaning and shaping, obturation, and temporization as well
primary goal of this discipline is to preserve the natural dentition. as restoration of endodontically treated teeth and bleaching. In
Root canal treatment is a well-tested procedure that has provided addition, it covers etiology, prevention, and treatment of acciden-
pain relief and has restored function and esthetics to patients for tal procedural errors, as well as treatment of cases with persistent
decades. Millions of patients expect preservation of their natural disease using nonsurgical and surgical approaches and their treat-
dentition. When root canal treatment is indicated, patients should ment outcomes that provide guidelines regarding the assessment
be aware that the procedure is safe and has a high success rate, if of these procedures.
properly performed. The other distinctive features of the new edition include mid-
As with other dental specialties, the practice of endodontics has chapter questions (online) so that the reader can check whether s/he
two inseparable components: art and science. The art consists of understand a concept and the rationale before moving to the next
executing technical procedures during root canal treatment. The topic in a chapter.
science includes the basic and clinical sciences related to biologi- The hard copy of this book is enhanced by online access (via
cal and pathological conditions that guide the art of endodontics the pin code on the inside front cover) to additional video clips
through the principles and methods of evidence-based treatment. for selected procedures. These features provide the reader with a
Evidence-based treatment integrates the best clinical evidence textbook that is concise, current, and easy to follow in an interac-
with the practitioner’s clinical expertise and the patient’s treatment tive manner.
needs and preferences. A principal objective of Endodontics: Prin- Endodontics: Principles and Practice is not intended to include
ciples and Practice is to incorporate recent evidence-based informa- all background information on the art and science of endodon-
tion regarding technological and scientific advances in the field of tics. At the same time, it is not designed to be a “cookbook” or
endodontics when available and when appropriate. a preclinical laboratory technique manual. The purpose of this
There are not enough endodontists to manage the endodontic textbook is to provide the reader with the basic information to
needs of the public, so general dentists must assist endodontists perform root canal treatment and to give the reader background
to preserve natural dentition. Their responsibility is to diagnose knowledge in related areas. It should be used as a building block
pulpal and periapical diseases and to perform uncomplicated root for understanding the etiology and treatment of teeth with pulpal
canal treatments. In fact, most of the endodontic procedures are and periapical diseases; then the reader can expand her or his end-
performed by generalists. Our textbook, written specifically for odontic experiences with more challenging cases. Providing the
dental students and general dentists, focusses on clinical content best quality of care is the guiding light for treatment planning and
and contains the information necessary for those who would like performing appropriate treatment.
to incorporate endodontics in their practice. This includes diagno- We would like to thank the contributing authors for sharing
sis and treatment planning as well as management of pulpal and their materials and experiences with our readers and with us; their
periapical diseases. In addition, the general dentist must be able to contributions improve the quality of life for millions of patients.
determine the case complexity and whether she or he can perform In addition, we acknowledge our colleagues and students who
the necessary treatment or if referral is the better option. provided cases and gave us constructive suggestions to improve
The new edition of this book focuses on clinical content and has the quality of our book.
removed some of the basic science since the readers have already
studied the basic sciences related to endodontic practice. We have Mahmoud Torabinejad
also overhauled the table of contents with many new contributors Ashraf F. Fouad
to combine and / or eliminate chapters to be more updated and Shahrokh Shabahang
2020
vi
List of Contributors
The editors would like to acknowledge and offer grateful thanks for the input of all previous editions’ contributors, without whom this
new edition would not have been possible.
Hamid Abedi, DDS MS MBA Anibal Diogenes, DDS, MS, PhD
Clinical endodontist, Irvine, CA, USA Professor and Vice Chair, Department of Endodontics,
University of Texas Health Science Center at San Antonio,
Kenneth Abramovitch, DDS, MS San Antonio, TX, USA
Professor and Chair, Department of Oral Pathology, Radiology
Melissa Drum, DDS, MS
and Medicine, University of Missouri – Kansas City, School
of Dentistry, Kansas City, MO, USA Professor, Advanced Endodontics Director, Division of
Endodontics, College of Dentistry, The Ohio State University,
Anita Aminoshariae, DDS, MS Columbus, OH, USA
Associate Professor, Endodontics, CWRU School of Dental
Brad Eli, DMD, MS
Medicine, Cleveland, OH, USA
Staff, Department of Dentistry, Scripps Memorial Hospital, La
Ana Arias, DDS, MS, PhD Jolla, CA, USA
Professor of Conservative Dentistry, School of Dentistry,
Mohamed I. Fayad, DDS, MS, PhD
Complutense University, Madrid, Spain
Clinical Associate Professor, Director of Research, Department
Adham A. Azim, BDS of Endodontics, University of Illinois, College of Dentistry,
Chicago, IL, USA
Division Head and Director of the Post-Graduate Program,
Periodontics and Endodontics, University at Buffalo, Buffalo,
Natasha M. Flake, DDS, PhD, MSD
New York, NY, USA
Associate Professor, Department of Endodontics, University of
Washington, Seattle, WA, USA
Brooke Blicher, DMD, Certificate in Endodontics
Clinical Endodontist, Upper Valley Endodontics, White River Ashraf F. Fouad, DDS, MS
Junction, Vermont; Freedland Distinguished Professor, Vice-chair, Division of
Clinical Instructor, Department of Restorative Dentistry and Comprehensive Oral Health, Adams School of Dentistry,
Biomaterials Science, Harvard School of Dental Medicine, University of North Carolina, Chapel Hill, NC, USA
Boston, MA, USA;
Assistant Clinical Professor, Department of Endodontics, Tufts Brian Goodacre, DDS, MSD
University School of Dental Medicine, Boston, MA, USA; Assistant Professor, Department of Prosthodontics, School of
Dental Staff, Department of Oral Surgery, Dartmouth Dentistry, Loma Linda University, Loma Linda, CA, USA
Hitchcock Medical Center, Lebanon, VT, USA
Charles J. Goodacre, DDS, MSD
Tatiana Botero, DDS, MS Distinguished Professor, Department of Restorative Dentistry, School
Clinical Associate Professor, Cariology Restorative Sciences and of Dentistry, Loma Linda University, Loma Linda, CA, USA
Endodontics, Ann Arbor, MI, USA
Robert Handysides, DDS
Sami Chogle, BDS, DMD, MSD Dean, Department of Endodontics, School of Dentistry, Loma
Chair and Program Director, Graduate Endodontics, Boston Linda University, Loma Linda, CA, USA
University, Boston, MA, USA;
Adjunct Associate Professor, Graduate Endodontics, Case Brad Johnson, DDS, MHPE
Western Reserve University, Cleveland, OH, USA Professor and Head, Director of Postdoctoral Endodontics,
Department of Endodontics, University of Illinois at Chicago,
William Herbert Christie, DMD, MS, FRCD(C) Chicago, IL, USA
Retired Professor, Senior Scholar, Department of Restorative
Dentistry, University of Manitoba, Winnipeg, Manitoba, James David Johnson, DDS, MS
Canada Clinical Professor and Chair, Department of Endodontics,
University of Washington School of Dentistry, Seattle, WA, USA
Blaine Cleghorn, DMD, MS
Professor and Assistant Dean, Faculty of Dental Clinical Mo Kang, DDS, PhD
Sciences, Dalhousie University, Halifax, Nova Scotia, Canada Professor and Chairman, Department of Endodontics, UCLA
School of Dentistry, Los Angeles, CA, USA
vii
viii LIST OF CONTRIBUTORS
Philip Michaelson, MS, DMD Christine Sedgley, MDS, MDSc, FRACDS, MRACDS(ENDO), PhD
Private Practice, Endodontics, Professional Endodontics, Inc., Professor and Chair, Department of Endodontology, Oregon
Chagrin Falls, OH, USA Health and Sciences University, Portland, OR, USA
W. Craig Noblett, DDS, MS Frank Setzer, DMD, PHD, MS
Volunteer Faculty, University of California, San Francisco, CA; Assistant Professor, Endodontic Clinic Director, and Predoctoral
Private practice, Fresno, CA Endodontic Program Director, Department of Endodontics,
University of Pennsylvania, Philadelphia, PA, USA
Ali Nosrat, DDS, MS, MDS
Clinical Assistant Professor, Department of Endodontics, School Shahrokh Shabahang, DDS, MS, PhD
of Dentistry, University of Maryland, Baltimore, MD, USA; Associate Professor, Department of Endodontics, School of
Private Practice, Centreville, VA, USA Dentistry, Loma Linda University, Loma Linda, CA, USA
John M. Nusstein, DDS, MS Renato Silva, DDS, MS, PhD
Professor and Chair, Division of Endodontics, College of Associate Professor, Department of Endodontics, University of
Dentistry, The Ohio State University, Columbus, OH, USA Texas Health Science Center at Houston, Houston, TX, USA
Avina Paranjpe, BDS, MS, MSD, PhD Tory Silvestrin, DDS, MSD, MSHPE
Associate Professor, Department of Endodontics, University of Chairman and Graduate Program Director, Department of
Washington, Seattle, WA, USA Endodontics, School of Dentistry, Loma Linda University,
Loma Linda, CA, USA
Masoud Parirokh, DMD, MSc
Distinguished Professor, Department of Endodontics, School of Fabricio B. Teixeira, DDS, MS, PhD
Dentistry, Kerman University of Medical Sciences, Kerman, Professor and Chair, Department of Endodontics, University of
Islamic Republic of Iran; Iowa, Iowa City, IA, USA
Distinguished Professor, Endodontology Research Center, Kerman
University of Medical Sciences, Kerman, Islamic Republic of Iran Yoshitsugu Terauchi, DDS, PhD
President, Endodontics, CT and MicroEndodontic Center,
Ove A. Peters, DMD, MS, PhD Yamato-shi, Kanagawa, Yamato City, Japan
Professor and Discipline Lead, Endodontics, School of Dentistry,
The University of Queensland, Brisbane, Qld, Australia Mahmoud Torabinejad, DMD, MSD, PhD
Affiliate Professor of Endodontics, Department of Endodontics,
Al Reader, DDS, MS University of Washington Seattle, WA, USA;
Professor, Division of Endodontics, College of Dentistry, The Adjunct Professor, Department of Endodontics, School of
Ohio State University, Columbus, OH, USA Dentistry, Loma Linda University, Loma Linda, CA, USA;
Adjunct Professor, Department of Endodontics, University of
Ilan Rotstein, DDS Pacific Arthur A. Dugoni School of Dentistry;
Professor and Chair, Endodontics, Orthodontics and General Adjunct Professor, Department of Preventive and Restorative
Practice Residency, Herman Ostrow School of Dentistry of USC, Dentistry, Section of Endodontics, University of California in
University of Southern California, Los Angeles, CA, USA; San Francisco, School of Dentistry, San Francisco, CA, USA
Associate Dean, Continuing Education, Herman Ostrow School
of Dentistry of USC, University of Southern California, Los Marco Aurelio Versiani, Lt. Col., DDS, MSc, PhD
Angeles, CA, USA Associate Researcher, Department of Restorative Dentistry,
Dental School of Ribeirão Preto, University of São Paulo,
Richard A. Rubinstein, DDS, MS, FACD Ribeirão Preto, São Paulo, Brazil
Adjunct Clinical Associate Professor, Cariology, Restorative Sciences
and Endodontics, University of Michigan, Ann Arbor, MI, USA Richard Walton, DMD, MS
Professor Emeritus, Department of Endodontics, University of
Nikita B. Ruparel, MS, DDS, PhD Iowa, Iowa City, IA, USA
Associate Professor, Department of Endodontics, UTHSCSA,
San Antonio, TX, USA Shane N White, BDentSc, MS, MA, PhD
Professor, UCLA School of Dentistry, Los Angeles, CA, USA
Mohammed Sabeti, DDS, MA
Clinical Professor, PRDS, University of California at San Anne E. Williamson, DDS, MS
Francisco, San Francisco, CA, USA Associate Professor, Endodontics, University of Iowa, Iowa City,
IA, USA
Nasser Said-Al-Naief, DDS, MS
Professor and Chair, OMFP Laboratory Director, Pathology and
Radiology, OHSU, Portland, OR, USA;
Hospital Staff, OMFS, School of Medicine, OHSU, Portland,
OR, USA;
Professor, Anatomic Pathology, School of Medicine, OHSU,
Portland, OR, USA
1
Pathogenesis of Pulp and
Periapical Diseases
CHRISTINE SEDGLEY, RENATO SILVA, AND
ASHRAF F. FOUAD
CHAPTER OUTLINE
Histology and Physiology of Normal Dental Pulp, 1 Normal Pulp, 11
Etiology of Pulpal and Periapical Diseases, 2 Reversible Pulpitis, 11
Microbiology of Root Canal Infections, 5 Irreversible Pulpitis, 11
Endodontic Infections Are Biofilm Infections, 5 Pulp Necrosis, 12
The Microbiome of Endodontic Infections, 6 Clinical Classification of Periapical (Apical) Conditions, 13
Pulpal Diseases, 8 Nonendodontic Pathosis, 15
LEARNING OBJECTIVES
After reading this chapter, the student should be able to: 6. D escribe the histopathological diagnoses of periapical lesions of
pulpal origin.
1. D escribe the histology and physiology of the normal dental
7. I dentify clinical signs and symptoms of acute apical periodon-
pulp.
titis, chronic apical periodontitis, acute and chronic apical
2. I dentify etiologic factors causing pulp inflammation.
abscesses, and condensing osteitis.
3. D escribe the routes of entry of microorganisms to the pulp and
8. D iscuss the role of residual microorganisms and host response
periapical tissues.
in the outcome of endodontic treatment.
4. C lassify pulpal diseases and their clinical features.
9. D escribe the steps involved in repair of periapical pathosis after
5. D escribe the clinical consequences of the spread of pulpal
successful root canal treatment.
inflammation into periapical tissues.
palisading layer that lines the walls of the pulp space, and their
Histology and Physiology of Normal Dental
tubules extend about two thirds of the length of the dentinal
Pulp tubules. The tubules are larger at a young age and eventually
become more sclerotic as the peritubular dentin becomes thicker.
The dental pulp is a unique connective tissue with vascular, lym- The odontoblasts are primarily involved in production of mineral-
phatic, and nervous elements that originates from neural crest ized dentin. They are connected by gap junctions that allow them
cells. It resides inside the tooth in a chamber with rigid walls. to form a semipermeable membrane. In addition, odontoblasts
The pulp contains odontoblasts, highly specialized cells with a play an important role in defense as they express Toll-like recep-
secretory function, which not only form dentin, but also interact tors (see later), cytokines, and defensins, among other immuno-
with dental epithelium early in tooth development to initiate the logic mediators.
formation of enamel. The pulp also contains fibroblasts, undiffer- Two main types of sensory fibers innervate the pulp: Aδ-fibers
entiated mesenchymal cells, collagen type I and II, proteoglycans, in the periphery and C-fibers in the central pulp. The Aδ-fibers
glycoproteins, and water1 (Fig. 1.1). are responsible for the sharp response to thermal changes. They
The histologic structure of the pulp is important, because it extend between the odontoblasts, lose their myelin sheath, and
reflects a unique architecture suited for the formation of dentin extend to a distance of 100 to 200 μm into the dentinal tubules.
and defense against invading pathogens. Odontoblasts form a The C-fibers are unmyelinated and are responsible for the dull
1
2 CHAPTER 1 Pathogenesis of Pulp and Periapical Diseases
A B
BV
PD
*
OD
C
OD
FB PD
D
• Fig. 1.1 Histologic section of (A) rat molar tooth showing coronal (B) and (C) radicular dental pulp in
higher magnification. Masson-Goldner trichrome staining. BV, Blood vessels; D, dentin; FB, fibroblasts;
OD, odontoblasts in odontoblastic layer; PD, predentin. An artifact (*) separating the predentin from the
odontoblastic layer. (Courtesy Dr. Claudia Biguetti.)
ache that affects patients with symptomatic irreversible pulpitis. Pulpal damage can occur because of impact injuries. Teeth
The pulp may also have Aβ-fibers and sympathetic fibers in the undergoing mild to moderate trauma and those with immature
walls of arterioles. apices have a better chance of pulpal survival in comparison with
The pulp vasculature plays a critical role in its response to irrita- those suffering severe injury or those with closed apices. Intrusion
tion. When the tooth first erupts into the oral cavity, the root apex is injuries are more likely to lead to pulp necrosis than are lateral or
immature, and there is ample blood supply to the pulp. Eventually, extrusion injuries4 (Fig.1.3).
the apex matures, and the ability of the pulp to withstand external Periapical tissues can be mechanically irritated and inflamed by
irritation, such as from trauma or caries, diminishes. However, the impact trauma, hyperocclusion, overinstrumentation of root canals,
pulp of the mature tooth has mechanisms to cope with increased perforation of the root, and overextension of root canal filling materi-
blood flow during inflammation, such as arteriovenous anastomoses als (Fig. 1.4). Inaccurate determination of root canal length is usually
and loops that can circulate and increase volume of blood when the the cause of overinstrumentation and subsequent inflammation. In
need arises. The pulp also contains an elaborate network of arteri- addition, lack of an adequate apical resistance form created during
oles and capillaries around the odontoblasts, which are high-meta- cleaning and shaping can cause overextension of filling materials into
bolic-rate cells, commonly known as the terminal capillary network.  the periapical tissues, causing physical and chemical damage (Fig. 1.5).
Application of forces beyond the physiologic tolerance of the
Etiology of Pulpal and Periapical Diseases periodontal ligament (PDL) during orthodontic tooth movement
results in disturbance of the blood and nerve supply of the pulp
Injury or irritation of pulpal or periapical tissues can result in tissue.5,6 In addition, orthodontic movement may initiate resorp-
inflammation. The reactions of the dental pulp to irritants are tion of the apex, usually without a change in vitality. 
largely dictated by the type and duration of a stimulus. These irri-
tants can be broadly classified as nonliving (mechanical, thermal, Chemical Irritants
or chemical) or living (microbial) (Video 1.1).
Antibacterial agents, such as silver nitrate, phenol with and without
Mechanical Irritants camphor, and eugenol, have been used to “sterilize” dentin after
cavity preparations. The effectiveness of many of these products
The potential for pulp irritation increases as more dentin is is questionable,7 and their cytotoxicity can cause inflammatory
removed during deep cavity preparations because dentinal per- changes in the underlying dental pulp.8 Other irritating agents
meability is greater closer to the pulp2 (Fig. 1.2). The removal include cavity cleansers, such as alcohol, chloroform, hydrogen
of tooth structure without proper cooling may also cause pulp peroxide, and various acids; chemicals present in desensitizers,
inflammation. Deep scaling and curettage may injure apical ves- cavity liners and bases; and temporary and permanent restorative
sels and nerves, resulting in pulpal damage.3 materials.
CHAPTER 1 Pathogenesis of Pulp and Periapical Diseases 3
AA B
• Fig. 1.2 Scanning Electron Microscopy of Human Dentin. Dentinal permeability is greater closer to
the pulp (A) than near the dentinoenamel junction (B) or the cementodentinal junction due to the higher
number of tubules per unit and bigger tubule diameter. Therefore the potential for pulp irritation increases
as more dentin is removed.
12
10 X X X X
8
s
nit
u
n
o 6
si
u
erf
P
4
2
• Fig. 1.4 Periapical radiograph showing overextension of root canal filling
0
material.
Splint rem 12 wks 24 wks 36 wks
Intrusion Extrusion
Lat lux X Control
• Fig. 1.3 Graphic representation of pulpal circulation subsequent to vari-
ous types of luxation injuries to teeth. Pulp circulation is measured in perfu-
sion units over a 36-week observation period.
Antibacterial irrigants used during cleaning and shaping of
root canals, intracanal medications, and some compounds pres-
ent in obturating materials are examples of potential chemical
irritants to periapical tissues.9,10 When testing the effects of anti-
microbial medications on dental pulp cells, researchers showed
that calcium hydroxide and lower concentrations of antibi-
otic pastes are conducive to cell survival and proliferation, but
more concentrated forms of antibiotic pastes have detrimental • Fig. 1.5 Improper instrumentation and extrusion of filling materials into
effects.11  the periapical tissues causes periradicular inflammation (arrows).
4 CHAPTER 1 Pathogenesis of Pulp and Periapical Diseases
Microbial Irritants identified as pattern recognition receptors (PRRs).18 PRRs recog-
nize PAMPs and initiate host defenses. G-protein coupled recep-
Although mechanical and chemical irritations are predominantly tors and Toll-like receptors (TLRs) are part of the innate immune
transient in nature, the most significant cause of inflammation is response and activate phagocytic functions to allow microbial
microbial. Studies have shown that even superficial carious lesions ingestion. G-protein coupled receptors bind to chemokines, lipid
in enamel are capable of attracting inflammatory cells in the mediators (e.g., platelet-activating factor, prostaglandin E2, and
pulp.12,13 The initial reaction of the pulp to these irritants is medi- leukotriene B ) or bacterial proteins, causing extravasation of
4
ated through the innate immune response. This early response to leukocytes and production of bactericidal substances. TLRs are
caries results in focal accumulation of chronic inflammatory cells, transmembrane proteins that are expressed by cells of the innate
such as macrophages, lymphocytes, and plasma cells.14 As caries immune system playing a central role in the initiation of cellular
progresses toward the pulp, the intensity and character of the infil- innate immune responses.19 These receptors recognize invading
trate change. Pulpal tissue may remain inflamed for long periods microbes and activate signaling pathways that launch immune
and may undergo eventual or rapid necrosis. This change depends and inflammatory responses to destroy the invaders. At least 13
on several factors: (1) the virulence of the microorganisms; (2) the TLRs have been discovered to date with different recognition
ability to circulate inflammatory fluids to avoid a marked increase abilities. Table 1.1 presents some of the currently identified TLRs
in intrapulpal pressure; (3) host resistance, including genetic and their specific interactions. 
variations; (4) the amount of circulation and (5) an important
factor, lymphatic drainage. Subsequently, microorganisms or their
byproducts and other irritants from the necrotic pulp diffuse from
the canal to the periapical region, resulting in the development of
an inflammatory lesion (Fig. 1.6).
Pulpal and periapical pathoses do not develop without the pres-
ence of bacterial contamination.15,16 Kakehashi and collaborators
created pulp exposures in conventional and germ-free rats.15 In the
germ-free rats, minimal inflammation only occurred throughout the
72-day observation period. Further, pulpal tissue in these a nimals
was not devitalized but rather showed calcific bridge formation by
day 14, with normal tissue apical to the dentin bridge (Fig. 1.7, A).
In contrast, infection, pulpal necrosis, and abscess formation
occurred by the eighth day in conventional rats (Fig. 1.7, B). The
bacteriological investigation by Sundqvist examining the flora of
human necrotic pulps supports the findings of Kakehashi and col-
laborators15 and Möller and coworkers.16 S undqvist examined previ-
ously traumatized intact teeth with necrotic pulps, with and without
apical pathosis. The root canals of teeth without apical lesions were
aseptic, whereas those with periapical pathosis had positive bacterial
cultures.17
Several mechanisms have been proposed for identification of
microorganisms as irritants by the immune system. Detection of • Fig. 1.6 Egress of irritants (closed arrow) from the root canal into the peri-
these pathogens can occur via interaction between pathogen-asso- apical tissue causes inflammation (open arrow) and replacement of normal
ciated molecular patterns (PAMPs) and specific receptors broadly periapical structures with a granulomatous tissue.
D
P
A B
• Fig. 1.7 A, No inflammation is seen in an exposed pulp (P) of a germ-free rat. Food particles and other
debris (D) are packed into the chamber. B, Periapical lesion is apparent in a conventional rat after pulp
exposure. (Courtesy Dr. H. Stanley.)