Endodontic Microbiology E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch
• Veröffentlichungsjahr: 2017

Seitenzahl: 1289

Beschreibung

Endodontic Microbiology, Second Edition presents a comprehensive reference to the microbiology, pathogenesis, management, and healing of endodontic pathosis, emphasizing the importance of biological sciences in understanding and managing endodontic disease and its interaction with systemic health. * Provides a major revision to the first book to focus on the problems related to microbes in the root canal and periapical tissues * Updates current knowledge in endodontic pathosis, especially regarding next generation sequencing and microbial virulence * Presents useful diagrams, images, radiographs, and annotated histological images to illustrate the concepts * Emphasizes the importance of biological science in understanding and managing endodontic disease * Includes contributions from the leading researchers and educators in the field

Leseprobe

Endodontic Microbiology

Second Edition

Edited by

Ashraf F. Fouad

Freedland Distinguished Professor and ChairDepartment of EndodonticsSchool of Dentistry, University of North CarolinaChapel Hill, NC, USA

This edition first published 2017 © 2017 by John Wiley & Sons, Inc.

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Library of Congress Cataloging-in-Publication DataNames: Fouad, Ashraf F., editor. Title: Endodontic microbiology / edited by Ashraf F. Fouad. Description: Second edition. | Hoboken, NJ : John Wiley & Sons Inc., 2017. | Includes bibliographical references and index. Identifiers: LCCN 2016042792 | ISBN 9781118758243 (cloth) | ISBN 9781118975497 (Adobe PDF) | ISBN 9781118975503 (epub) Subjects: | MESH: Dental Pulp Diseases–microbiology | Dental Pulp Diseases–drug therapy | Periapical Diseases–microbiology |  Periapical Diseases–drug therapy | Anti-Infective Agents–therapeutic use | Root Canal Therapy Classification: LCC RK351 | NLM WU 230 | DDC 617.6/342–dc23 LC record available at https://lccn.loc.gov/2016042792

Cover images courtesy of the author

Dedication

To Amal, Fikry, Lori, Amani, George, Anthony Gade, and Edward; thank you for providing me the opportunity, the inspiration, the motivation, and the love.

Ashraf F. Fouad

CONTENTS

Contributors

Preface

Preface to the First Edition

Chapter 1: Microbial Perspectives in the Twenty-First Century

1.1 Introduction

1.2 Genomics

1.3 Molecular microbial ecology and the study of uncultivable bacteria

1.4 Intraspecies variation

1.5 Metagenomics and metatranscriptomics

1.6 Bacterial–bacterial communication

1.7 Host–bacterial interactions

1.8 Complex infectious diseases

1.9 The future

1.10 References

Chapter 2: Diagnosis, Epidemiology, and Global Impact of Endodontic Infections

2.1 Endodontic disease: irritation, inflammation, and infection of the pulp and periapical tissues

2.2 Primary diagnostic criteria: subjective symptoms and radiographic changes

2.3 Pulpal inflammation and infection: public health consequences

2.4 Epidemiology of endodontic diseases

2.5 Quality of root canal treatment and the development and persistence of apical periodontitis

2.6 Treatment strategies: prevention, treatment, and extraction

2.7 General oral health, oral health strategies, and tooth preservation as risk factors for oral infections

2.8 Conclusions

2.9 References

Chapter 3: Microbiology of Dental Caries and Dentinal Tubule Infection

3.1 Introduction

3.2 Oral biofilms associated with dental caries

3.3 Microbiota of dental caries

3.4 Microbial invasion of dentinal tubules

3.5 Clinical aspects of dental caries microbiota and dentinal tubule infection

3.6 Conclusions

3.7 References

Chapter 4: Culture-Based Analysis of Endodontic Infections

4.1 Introduction

4.2 Historical perspectives

4.3 Culture-based analysis in clinical practice

4.4 Clinical interpretations

4.5 Route of infection in vital and necrotic pulp

4.6 Apical periodontitis

4.7 Treatment aspects

4.8 Persisting infections at root-filled teeth

4.9 Culture versus molecular biology methods

4.10 Conclusions

4.11 References

Chapter 5: Molecular Analysis of Endodontic Infections

5.1 Introduction

5.2 Limitations of culture methods

5.3 Molecular biology techniques

5.4 Gene targets for microbial identification

5.5 PCR and its derivatives

5.6 Denaturing gradient gel electrophoresis

5.7 Terminal restriction fragment length polymorphism

5.8 DNA–DNA hybridization assays

5.9 Fluorescence in situ hybridization

5.10 Next-generation DNA sequencing technologies

5.11 Metagenomics

5.12 Advantages and limitations of molecular methods

5.13 Unraveling the endodontic microbiome with molecular biology methods

5.14 Microbial diversity in endodontic infections

5.15 Persistent and secondary intraradicular infections

5.16 Extraradicular infections

5.17 Other microorganisms in endodontic infections

5.18 Next-generation DNA sequencing analyses of the endodontic microbiome

5.19 Conclusions

5.20 References

Chapter 6: Extraradicular Endodontic Infections

6.1 Introduction

6.2 Brief review of the endodontic microorganisms in infected root canals

6.3 Pathways of microbial access to the dental pulp

6.4 Infection of the root canal space

6.5 Sequelae of pulp infection

6.6 Bacterial invasion of the periapical tissues

6.7 Microbial factors in periapical lesions

6.8 Bacterial evasion of host defense

6.9 Extraradicular endodontic infections

6.10 Treatment of endodontic infections

6.11 Conclusions

6.12 Acknowledgments

6.13 References

Chapter 7: Virulence of Endodontic Bacterial Pathogens

7.1 Introduction

7.2 Genetic aspects of bacterial virulence

7.3 Virulence factors

7.4 Virulence associated with endodontic microorganisms

7.5 Conclusions and future directions

7.6 References

Chapter 8: Viruses in Endodontic Pathosis

8.1 Introduction

8.2 General description of herpesviruses

8.3 Human cytomegalovirus

8.4 Epstein–Barr virus

8.5 Herpes simplex virus types 1 and 2

8.6 Varicella-zoster virus

8.7 Human herpesvirus-6

8.8 Human herpesvirus-7 and -8

8.9 Association between herpesviruses and apical disease

8.10 Pathogenesis of herpesvirus-associated apical disease

8.11 Model for herpesvirus-mediated apical disease

8.12 References

Chapter 9: Fungi in Endodontic Infections

9.1 General characteristics of fungi

9.2 Oral yeasts and carriage

9.3 Oral candidosis

9.4 Virulence factors and pathogenicity

9.5 Presence and pathogenicity of yeasts in different dental tissues

9.6 Antifungal activity of endodontic irrigating solutions and disinfectants

9.7 Conclusions

9.8 References

Chapter 10: Severe Head and Neck Infections

10.1 Introduction

10.2 Etiology and epidemiology

10.3 Microbiology

10.4 Anatomy and pathogenesis of spread

10.5 Diagnosis

10.6 Airway management

10.7 Medical and surgical management

10.8 References

Chapter 11: Endodontic Infections and Pain

11.1 Introduction

11.2 Biology of the pain system

11.3 Central sensitization

11.4 Persistent pain following endodontic therapy

11.5 Mechanisms of pain due to endodontic infections

11.6 Clinical strategies for treating pain due to endodontic infections

11.7 References

Chapter 12: Systemic Antibiotics in Endodontic Infections

12.1 Introduction

12.2 General principles of antibiotic prescribing

12.3 Efficacy of antibiotics

12.4 Classification and mode of action of antibiotics

12.5 Host factors

12.6 Antibiotic effectiveness and bacterial resistance in endodontics

12.7 Antibiotic toxicities, allergies, and superinfections

12.8 Role of antibiotics in clinical management of endodontic infections

12.9 Indications for prophylactic antibiotic therapy

12.10 References

Chapter 13: Topical Antimicrobials in Endodontics

13.1 Introduction

13.2 Challenges for topical antimicrobials in root canal disinfection

13.3 Requirements of endodontic topical antimicrobials

13.4 Classification of topical antimicrobials in root canal therapy

13.5 Conclusions

13.6 References

Chapter 14: Endodontic Infections in Incompletely Developed Teeth

14.1 Introduction

14.2 Review of tooth development as it relates to endodontic pathosis

14.3 Etiology, prevalence, and pathogenesis of pulp disease in incompletely developed teeth

14.4 Microbiology of endodontic infections in teeth from pediatric patients

14.5 Management of immature teeth

14.6 Orthodontic considerations in pathologically involved incompletely formed teeth

14.7 Stem cells for pulp and periodontal tissue regeneration

14.8 Recent innovations on the regeneration of tooth form

14.9 Conclusions and prospects

14.10 References

Chapter 15: Prognosis of Healing in Treated Teeth with Endodontic Infections

15.1 Introduction: The critical importance of prognosis

15.2 Outcome measures and criteria in assessment of endodontic prognosis

15.3 Levels of evidence in assessment of endodontic prognosis

15.4 Prognosis of primary apical periodontitis after initial treatment

15.5 Prognosis of posttreatment apical periodontitis after orthograde retreatment

15.6 Prognosis of posttreatment apical periodontitis after apical surgery

15.7 Prognosis of posttreatment apical periodontitis after intentional replantation

15.8 Etiology of persistent apical periodontitis after endodontic treatment

15.9 Conclusions

15.10 References

Chapter 16: Endodontic Infections and Systemic Disease

16.1 Introduction

16.2 Systemic pain syndromes that mimic endodontic pathosis

16.3 Jawbone radiolucencies that mimic endodontic pathosis

16.4 Systemic diseases or conditions that may influence the pathogenesis or course of endodontic pathosis

16.5 Systemic viral infections

16.6 Sickle cell anemia

16.7 Malignant neoplasms

16.8 Other systemic disease or abnormalities

16.9 Hormonal variation and pregnancy

16.10 Patients on systemic medications

16.11 Genetic and epigenetic variations

16.12 Can endodontic infections contribute to the pathogenesis of systemic disease?

16.13 References

Glossary

Index

EULA

List of Tables

Chapter 3

Table 3.1

Table 3.2

Chapter 4

Table 4.1

Table 4.2

Table 4.3

Table 4.4

Table 4.5

Table 4.6

Table 4.7

Table 4.8

Chapter 5

Table 5.1

Table 5.2

Table 5.3

Chapter 7

Table 7.1

Table 7.2

Chapter 8

Table 8.1

Table 8.2

Table 8.3

Chapter 9

Table 9.1

Table 9.2

Chapter 11

Table 11.1

Chapter 12

Table 12.1

Table 12.2

Table 12.3

Table 12.4

Table 12.5

Chapter 15

Table 15.1

Table 15.2

Table 15.3

Table 15.4

Chapter 16

Table 16.1

Table 16.2

Table 16.3

Table 16.4

List of Illustrations

Chapter 1

Fig. 1.1

Phylogenetic tree showing representatives of the domains Eukarya, Archaea, and Bacteria.

Chapter 2

Fig. 2.1

Minimal bone structural changes at the apex in conjunction with chronic pulpitis (a), necessitating endodontic treatment (b).

Fig. 2.2

Chronic apical periodontitis: incipient at mesial root, established at distal root of mandibular left first molar.

Fig. 2.3

Chronic apical periodontitis developing in 6 months after inadequate emergency treatment. The prognosis is reduced from > 95% to < 85%.

Fig. 2.4

The periapical index. The periapical condition is scored by comparison with a series of reference radiographs of teeth with known histology. Reproduced with permission from Ørstavik et al. (1986).

Fig. 2.5

Dichotomization of PAI scores applied to epidemiology. Blue line, teeth without apical periodontitis; red line, teeth with apical periodontitis. A minimum of false positives (healthy apical periodontium scored as diseased; blue cases in red sector) is acceptable at the expense of some false negatives (diseased teeth registered as healthy; red cases in blue sector).

Fig. 2.6

The prevalence of apical periodontitis in different populations. (a) Dugas et al. 2003; (b) Marques et al. 1998; (c) Frisk and Hakeberg 2005; (d) Loftus et al. 2005; (e) Buckley and Spangberg 1995; (f) DeCleen et al. 1993; (g) Eriksen 1991; (h) Dugas et al. 2003; (i) Kirkevang et al. 2001; (j) Frisk and Hakeberg 2005; (k) Chen et al. 2007; (l) Jiménez-Pinzón et al. 2004; (n) De Moor et al. 2000; (o) Saunders et al. 1997; (p) Sidaravicius et al. 1999; (q) Tsuneishi et al. 2005; (r) Kabak and Abbott 2005; (s) Segura-Egea et al. 2005.

Chapter 3

Figure 3.1

Potential routes of infection of coronal and radicular dentin. Bacterial invasion of coronal dentinal tubules toward the pulp space (a) occurs as a result of a breach in the integrity of the enamel from dental caries, enamel cracks/fractures, or restorative procedures. Invasion of tubules toward the pulp also occurs when the cementum is breached as a consequence of periodontal disease or procedures. If unchecked, bacteria within dentinal tubules will enter and infect the pulp chamber and root canal space, and bacterial biofilms (b) will develop. Subsequently, bacterial invasion of radicular dentin occurs from the pulpal surface toward the dentinocemental junction. Invasion in cervical and mid-root radicular dentin readily occurs (heavy invasion shown in c), while the amount and depth of invasion in apical dentin is low (d). Inflammatory periradicular disease (e) results from the bacterial infection.

Source:

Love 2004. Reproduced with permission of John Wiley and Sons.

Figure 3.2

The sequence of adherence and colonization of tooth surfaces by bacteria. (a) Primary colonizing bacteria existing as planktonic cells interact with the conditioning film (e.g., acquired pellicle, dentinal tubule fluid, serum) on the tooth surface using longer range interactions (e.g., pili) or shorter range molecular interactions. (b) The early colonizers form strong bonds with the surface molecules in the conditioning film or components of the tooth substrate (e.g., collagen) by a variety of mechanisms and multiple adhesins. In conjunction with adhesion, the bacteria perform other functions such as adapting to the available nutrition, intermicrobial signaling, and production of an extracellular matrix. (c) Late colonizing bacteria enter the community by coaggregation reactions contributing to sequential binding and colonization of the developing biofilm. In this regard,

Fusobacterium

has been shown to be an important bridging organism allowing interactions between nonbinding bacteria. Within the biofilm intricate processes and interactions, such as quorum sensing, metabolic communication, genetic exchange, and competitive interactions, further shape the membership of the complex community, ensuring efficient utilization of nutrients and reduced susceptibility to host defences or therapeutic methods (e.g., antimicrobials).

Source:

Love 2004. Reproduced with permission of John Wiley and Sons.

Fig. 3.3

Major species detected on acidic agar from severe early childhood caries (ECC) and caries-free children. Note the relationship of

Streptococcus mutans

and

S. wiggsiae

in ECC and the microbiota profile between health and disease.

Fig. 3.4

The caries process according to an extended caries ecologic hypothesis. This model proposes that dental plaque has a

dynamic stability stage

characterized by non-mutans streptococci (non-MS) and

Actinomyces

which maintain a stable plaque pH. This is disrupted when the plaque pH is lowered from bacterial acid production from a dietary change leading to an

acidogenic stage

accompanied by the possibility of tooth demineralization. An acidic plaque selects for acid-tolerant bacteria in the

aciduric stage

and conditions of tooth demineralization and dental caries. Our understanding of dental plaque composition suggests that the species in this model should be increased to include more

Streptococcus

species and more Gram-positive rod species than

Actinomyces

in the dynamic stability and acidogenic phases. The aciduric phase would include

Bifidobacterium

,

Scardovia,

and

Lactobacillus

species and mutans streptococci as in Table 3.1.

Source:

Takahashi and Nyvad 2011. Reproduced with permission of Sage Publications.

Fig. 3.5

Transmission electron micrograph demonstrating a colony of bacterial cells invading a radicular dentinal tubule. Note the close approximation of peripheral cells of the colony with the wall of the tubule indicative of cell attachment to tubule structure, an essential step in colonization.

Source:

Love 2004. Reproduced with permission of John Wiley and Sons.

Fig. 3.6

A model for tubule invasion by primary colonizing streptococci. Cell surface adhesins on

S. gordonii

attach the cells to unmineralized collagen within a tubule and the cells undergo a series of reactions resulting in chaining growth and invasion of the tubule.

Source:

Love 2002. Reproduced with permission of John Wiley and Sons.

Fig. 3.7

A model for tubule invasion by secondary colonizers. Secondary colonizers (

P. gingivalis

) may be able to attach to components of the dentine matrix but this does not allow them to invade a tubule (1, 2). The cells instead attach to primary colonizing bacteria (

S. gordonii

), which allows them to invade a tubule (3, 4).

Source:

Love 2002. Reproduced with permission of John Wiley and Sons.

Fig. 3.8

Regional variation in bacterial invasion of radicular dentine of an upper left canine with infection of the root canal system and resulting periapical inflammatory disease. Bacterial colonization of the root canal from a coronal to apical direction and more advanced dentinal tubule sclerosis in the apical radicular dentin results in low and superficial invasion of apical dentine (a) and heavy and deep invasion in mid-root and cervical radicular dentin (b).

Fig. 3.9

Photomicrograph showing resorption of cementum and dentin and exposure of dentinal tubules to the periradicular tissues. As a consequence, the tubules are patent on both the pulpal (inner) and external dentin surfaces and this results in enhanced permeability of the dentin and deeper bacterial invasion from the pulpal to the external root surface (haematoxin and eosin stain, x 200 magnification).

Fig. 3.10

Radiograph of an endodontically treated upper right first molar with four root canals. Successful disinfection of the root canal and radicular dentin is dependent on chemomechanical instrumentation of all of the root canal system to produce a well-centred canal flaring from the apical terminus (A) to the canal orifice (B) at the pulp chamber. The root filling materials should three-dimensionally fill the root canal space and form an apical seal at the apical terminus and extend coronally to fill the root canal at or 1–2 mm short of the canal orifice; however, the root filling should not extend into the pulp chamber. A coronal seal (C) is formed over the coronal extent of the root filling using a restorative material such as a zinc oxide/eugenol or glass ionomer cement material and a well-sealed permanent restoration (D) that returns the tooth to function and form is placed.

Fig. 3.11

A scanning electron micrograph of a dentin smear layer produced by instrumenting a root canal wall with an endodontic hand-file; note the presence of bacteria on the smear layer. The smear layer has occluded the underlying dentinal tubules and will inhibit the penetration of antimicrobial medicaments into dentinal tubules.

Fig. 3.12

A scanning electron micrograph of an instrumented root canal wall that was treated with an ethylene diamine tetraacetic acid/sodium hypochlorite regimen to remove the smear layer. The patent dentinal tubules allow maximum diffusion of antimicrobial medicaments into tubules to eradicate invading bacteria. Additionally, root canal filling materials can better form a seal with the root canal wall and occlude the tubules when the smear layer is removed.

Chapter 4

Figure 4.1

Histologic section showing a stained (blue) microbial invasion into the root canal. Courtesy of Dr Dominico Ricucci.

Figure 4.2

Microorganisms isolated by different investigators in initial samples from root canals with necrotic pulps. *Note that Gomes et al. (2005) only covers black-pigmented

Porphyromonas

and

Prevotella

species.

Figure 4.3

Mean percentage of anaerobic and facultatives after different times of experimental infection.

Figure 4.4

The main steps in the preparation and sterilization of the operation field before entering the root canal. Drawing by Mrs. Gunilla Hjort.

Figure 4.5

Microbiologic sampling from the root canal. Drawing by Mrs. Gunilla Hjort.

Figure 4.6

A molar tooth indicating the location where special attention has to be taken for reaching bacteria at sampling. (a) Longitudinal section. (b) Horizontal or cross-sectional view of a lower molar tooth.

Figure 4.7

The laboratory procedures of root canal samples in the Laboratory of Oral Microbiology at Göteborg University. Psp, polysaccharide producing.

Figure 4.8

Hypothetical outline of a stress protein response in biofilm communities of root canal bacteria. The stress induces production of stress proteins, which are released into the biofilm matrix. These proteins will provide beneficial effects for the community.

Figure 4.9

Histologic section of the apical region of a root showing resorbtion where present bacteria will be difficult to sample.

Figure 4.10

The predominant bacteria: (a) facultative anaerobic and (b) anaerobic bacteria in the main canal, dentine, and apical region of root canals of monkey teeth left open to the cavity for 7 days and then sealed for 6 months. Note the high number of enterics (G-facultative rods) typical for monkeys.

Figure 4.11

Mean viable counts of eight strains in percentage of total counts in samples from 12 teeth after 6 months (experimental infection). The eight strains were originally isolated from a monkey tooth (original infection), pure cultured in the laboratory and inoculated in equal numbers experimentally in 12 monkey teeth.

Figure 4.12

Total viable counts (10th logarithm) at various time points of each strain of the eight strain collection in wound chambers in rabbits followed for 35 days.

Figure 4.13

Histologic picture of the periapical area of a tooth in an immunized monkey. Note root resorption, cell infiltrate adjacent to the root and the thick fibrotic capsule. From Dahlén et al. 1982a.

Figure 4.14

Frequency of culture positive samples from 183 root canals undergoing treatment (first sample), 166 cases after the second appointment (second sample), 69 cases after the third appointment (third sample), and 9 cases after the fourth appointment (fourth sample). Courtesy of Dr. Chavez de Paz.

Figure 4.15

Microbial composition (%) between untreated teeth (Sundquist 1992a), teeth under treatment (Chavez de Paz et al. 2003), and root-filled teeth (Molander et al. 1998).

Figure 4.16

Pie charts showing the proportions of organisms isolated in studies of untreated necrotic pulps, cases undergoing treatment, and root-filled teeth with apical periodontitis. Courtesy of Dr. Chavez de Paz.

Chapter 5

Figure 5.1

The 16S rRNA gene (rDNA). Areas in orange correspond to variable regions, which contain information about the genus and the species. Primers designed on these regions are used in species-specific assays. Red areas correspond to conserved regions of the gene. Primers designed on these areas are used in broad-range assays.

Figure 5.2

Phylogenetic tree based on 16S rRNA gene comparisons showing several candidate endodontic pathogens, their respective phyla, and the clinical conditions they have been associated with. Scale bar shows number of nucleotide substitutions per site.

Figure 5.3

The 454 pyrosequencing approach. ADP, adenosine diphosphate; AMP, adenosine monophosphate; APS, adenosine 5′ phosphosulfate; ATP, adenosine triphosphate; dNDP, deoxynucleoside diphosphate; dNMP, deoxynucleoside monophosphate; dNTP, deoxynucleoside triphosphate; PPi, pyrophosphate.

Figure 5.4

Molecular biology methods used, or with potential to be used, in the study of endodontic infections. The choice for a particular technique will depend on the type of analysis to be performed. DGGE, denaturing gradient gel electrophoresis; PCR, polymerase chain reaction; T-RFLP, terminal restriction fragment length polymorphism.

Figure 5.5

Prevalence of

Tannerella forsythia

in primary endodontic infections as revealed by molecular studies using different methodologies.

Figure 5.6

Prevalence of

Treponema denticola

in primary endodontic infections as revealed by molecular studies using different methodologies.

Figure 5.7

Prevalence of named

Treponema

species in primary endodontic infections associated with different forms of apical periodontitis. Findings from the authors’ laboratory using group- and species-specific nested PCR.

Figure 5.8

Prevalence of four black-pigmented bacterial species in primary endodontic infections as revealed by culture and molecular studies.

Figure 5.9

Most prevalent bacterial species/phylotypes in asymptomatic and symptomatic primary endodontic infections. Findings from the authors’ laboratory using species-specific nested PCR.

Figure 5.10

Comparison of the prevalence of different bacterial species/phylotypes in acute apical abscess samples taken from two geographic locations.

Figure 5.11

Comparison of the prevalence of different bacterial species in primary endodontic infections of patients from two geographic locations.

Figure 5.12

Prevalence of

Enterococcus faecalis

in samples from root canal-treated teeth with apical periodontitis. Data from culture and molecular studies.

Figure 5.13

Relative abundance of the different bacterial phyla in symptomatic (acute) and asymptomatic (chronic) endodontic infections. (a) Overall data. (b) Data according to the clinical condition.

Chapter 6

Figure 6.1

Microbial location: (a) adhered to the root canal walls and inside the dentinal tubules; (b) suspended in the lumen of the root canal; (c) between the dentin and the gutta-percha filling material; (d) penetrating the dentinal tubules of root-filled teeth; (e,f) in the external root surface.

Figure 6.2

Treatment of acute apical abscess. Patient with history of acute pain, presenting pain on palpation and tenderness to percussion in the upper left first premolar tooth. (a) Swelling present in the left side of the patient's face. (b) The maxillary left second premolar shows a deep carious lesion. (c) Radiograph shows an apical widening in the tooth. (d) Surgical drainage and placement of a drain in the periapical region of the tooth, which remained for 24 hours. (e) Decrease of the patient's swelling. (f) Drain removal, root canal debridement, placement of a root canal medication for 7 days, coronal restoration. (g) Radiograph showing the root canal filling. (h) Restoration of tooth.

Figure 6.3

Resolution of persistent periapical infection by endodontic surgery. (a) Periapical radiograph after root canal treatment showing a large periapical lesion in the upper left first premolar tooth. (b) Radiographic evidence of healing of the periapical reaction 2 months after endodontic surgery. (c) Scanning electron microscopic (SEM) analysis of the removed root apex showing the buccal and lingual surfaces with extruded gutta-percha from the lingual foramen (arrow). (d) Higher magnification of the lingual foramen with extruded gutta-percha surrounded by resorption lacunae. (e) Lingual foramen presenting reproducing fungal forms. (f) Lateral of the extruded gutta-percha in the lingual foramen showing fungal forms attached to the filling material. (g) The surrounding resorptions and dentine of the lingual foramen, totally covered in a kind of “net,” probably an extracellular polymeric substance. (h) Radiographic review at 24 months postsurgery.

Source:

Ferreira et al. (2004). Reproduced with permission of John Wiley and Sons.

Figure 6.4

Persistent extraradicular infection in a root-filled asymptomatic human tooth: scanning electron microscopic analysis and microbial investigation after apical microsurgery. (a) A preoperative periapical radiograph showing the mandibular left first molar with an apparent radiolucency around the distal apex and widening of the periodontal ligament at the apex of the mesial root. (b) A postoperative radiograph after nonsurgical retreatment. (c) An immediate postoperative radiograph showing the resected distal root. (d) The 24-month radiograph follow-up, showing apical healing.

Figure 6.5

Persistent extraradicular infection in a root-filled asymptomatic human tooth: scanning electron microscopic analysis and microbial investigation after apical microsurgery. (a) Persistent sinus tract on the buccal alveolar mucosa associated with the distal apex of the lower left first molar. (b) Endodontic microsurgery: flap closure. (c) Root fragment for SEM examination. (d) SEM of extruded gutta-percha observed in the root apex was not removed after endodontic retreatment, noting in A the filling material after nonsurgical root canal retreatment and in B the previous root canal filling material that extruded through apical ledging during deobturation. (e) A, Uninstrumented apical foramen; B,C, bacterial colonies adhering to external radicular surface.

Chapter 7

Fig. 7.1

Examples of intracanal biofilms with different bacterial cell morphologies. (a) The predominance of cocci. Note the high concentration of cells in contact with the root canal wall (Taylor's modified Brown and Brenn, original magnification ×1000). (b) Predominance of filamentous forms. Note the irregular distribution of bacterial cells within the extracellular material (original magnification ×1000).

Fig. 7.2

Active biofilm dispersal and variant formation. Active dispersal of the parental strain and genetic variants, represented by different cell types, leads to subsequent attachment and colonization that can be initiated by either single variants, to generate clonal biofilms, or multiple variants, to form mixed-variant biofilms.

Fig. 7.3

Conjugative plasmid transfer in Gram-negative bacteria.

Fig. 7.4

Virulence factors associated with bacteria.

Fig. 7.5

Simplified map of the conjugative plasmid pAD1 originally isolated from

E. faecalis

DS16. Segments are described according to the functions encoded by genes contained within: (1) replication and maintenance; (2) regulation of pheromone response; (3) structural genes relating to conjugation; (4) unknown; (5) cytolysin biosynthesis; (6) unknown; (7) resistance to UV light; oriV, origin of replication; oriT, origin of transfer.

Fig. 7.6

Pheromone initiated conjugative plasmid transfer. The pheromone induces the appearance of a surface adhesin (aggregation substance) that facilitates the attachment of the donor and recipient cells. Aggregates give rise to conjugal channels through which the plasmid is transferred from the donor to the recipient cell.

Fig. 7.7

(a) Total DNA and (b) plasmid DNA analysis of endodontic

E. faecalis

. (a) Pulsed field gel electrophoresis (PFGE) of SmaI-digested genomic DNA. Note similarities between GS3–GS7, GS12, and GS21. Reference standard: lambda phage DNA. (b) Plasmid analysis of the same

E. faecalis

isolates. Lane M, molecular size marker (1 kb Plus DNA Ladder, Invitrogen); –, undigested; H, digested with HindIII. Strain designations are shown above the lane designations. Isolates classified based on PFGE pattern as clonal, GS3, GS12, and GS21 are similar in plasmid content. GS4 and GS5 appear to be alike in plasmid content. GS6 and GS7 each contain two similar small plasmids; however, GS6 has two additional plasmids.

Fig. 7.8

Horizontal gene transfer (HGT) in the root canal. Scanning electron micrographs showing accumulations of

E. faecalis

JH2-2/pAM81 and

S. gordonii

Challis-Sm (a) 24 hours and (b) 72 hours after inoculation into the root canal. (c) Bi-directional HGT of the plasmid pAM81 was confirmed by purification of the plasmid in transconjugants. pAM81 plasmid DNA from donor and transconjugant strains, digested with HindIII. Lanes 1 and 14, molecular size marker; lane 2,

E. faecalis

JH2-2/pAM81 (donor); lane 3,

S. gordonii

Challis-Sm (plasmid-free recipient); lane 4,

S. gordonii

Ch24RC; lane 5,

S. gordonii

Ch24F; lane 6,

S. gordonii

Ch72RC; lane 7,

S. gordonii

Ch72F; lane 8,

S. gordonii

Challis-Sm/pAM81 (donor); lane 9

, E. faecalis

JH2-2 (plasmid-free recipient); lane 10,

E. faecalis

J24RC; lane 11,

E. faecalis

J24F; lane 12,

E. faecalis

J72RC; lane 13,

E. faecalis

J72F. Plasmid DNA restriction fragments were separated by electrophoresis on 0.8% agarose gels in TBE buffer (3.5 hours at 50 V), stained with ethidium bromide, and visualized under ultraviolet light.

Fig. 7.9

Observation of human osteoblast-like MG63 cell apoptosis by Hoechst 33258 staining under a fluorescence microscope (original magnification, ×200). After MG63 cells were treated with different concentration of LTA from

E. faecalis

for 48 hours, Hoechst 33258 staining was used to assess apoptotic cells (arrows). The number of apoptotic cells was increased in a LTA–dose-dependent manner with marked morphologic changes found in cell apoptosis: condenser chromatin and disintegration of the nuclear membrane. (a) Control group; (b) 25 mg/mL LTA-treated group; (c) 50 mg/mL LTA-treated group; (d) 100 mg/mL LTA-treated group.

Fig. 7.10

Survival of gelatinase-positive

E. faecalis

OG1RF in dentinal tubules 8 months after obturation with gutta-percha and RoekoSeal. Negative control, no bacteria (A1 and inset in A2), absence of gelatinase-negative

E. faecalis

TX5128 (B1 and inset in B2) and presence of gelatinase-positive

E. faecalis

OG1RF (C1 and inset in C2). TX5198 is a gelatinase-negative mutant of OG1RF. Brown and Brenn stain.

Fig. 7.11

(a) Preoperative and (b) postoperative radiographs. (c) The patient presented 1 year and 8 months later with a sinus tract. (d) A gutta-percha point was inserted in the sinus tract, and a radiograph was taken. The radiolucent area was considerably increased. (e) Periradicular surgery was performed, and pathologic lesion specimen was obtained in its original relationship with the root apex. The circle indicates a likely communication between the center of the lesion and the sinus tract. (f,g) Overviews of the two sulfur granules (Taylor's modified Brown and Brenn; original magnification, ×50). (h) Higher power view from the center of the sulfur granule in (f). Concentration of intertwining bacterial filaments (original magnification, ×1000). (i) Periphery of the sulfur granule in (f). Bacterial filaments are arranged in dense aggregates at the periphery, surrounded by layers of an amorphous material. Concentrations of neutrophilic leukocytes appear on the outer surface, some of which are in close contact with the bacterial matrix (original magnification, ×400; original magnification of the inset, ×1000).

Chapter 8

Fig. 8.1

The replication of herpesviruses. A virion initiates infection by fusion of the viral envelope with the plasma membrane after attachment to the cell surface. The capsid is transported to the nuclear pore, where viral DNA is released into the nucleus. Viral transcription and translation occur in three phases: immediate early, early, and late. Immediate early proteins shut off cell protein synthesis. Early proteins facilitate viral DNA replication. Late proteins are structural proteins of the virus that form empty capsids. Viral DNA is packaged into preformed capsids in the nucleus. Viral glycoproteins and tegument protein patches in cellular membranes and capsids are enveloped. Virions are transported via endoplasmic reticulum and released by exocytosis or cell lysis.

Source:

Slots et al. 2002. Reproduced with permission of John Wiley and Sons.

Fig. 8.2

Herpesviruses in symptomatic endodontic pathosis.

Chapter 9

Fig. 9.1

A colony of

C. albicans

consisting of yeast cells and hyphal extensions on untreated enamel surface. The extracellular material indicating dense cellular activity can be observed in the middle of the colony (original magnification 1000×). Courtesy of Bilge Hakan Sen, Kamran Safavi, and Larz Spangberg.

Fig. 9.2

A colony of yeast cells on EDTA/NaOCl-treated cementum. The cells are in the stage of active budding (arrows) (original magnification 1500×). Courtesy of Bilge Hakan Sen, Kamran Safavi, and Larz Spangberg.

Fig. 9.3

A dense colony of

C. albicans

with numerous yeast cells on hyphal structures on untreated cementum surface (original magnification 550×). Courtesy of Bilge Hakan Sen, Kamran Safavi, and Larz Spangberg.

Fig. 9.4

Two hyphal extensions showing close attachment to the enamel surface with secreted extracellular mucous material (arrows) (original magnification 5000×). Courtesy of Bilge Hakan Sen, Kamran Safavi, and Larz Spangberg.

Fig. 9.5

A colony of yeast cells and hyphal structures grown on EDTA/NaOCl-treated radicular dentin. Note the penetration of hyphae (arrows) into dentinal tubules (original magnification 1100×). Courtesy of Bilge Hakan Sen, Kamran Safavi, and Larz Spangberg.

Fig. 9.6

Yeast cells migrating into the dentinal tubules. There are bud scars (arrows) on some of the cells (original magnification 5500×). Courtesy of Bilge Hakan Sen, Kamran Safavi, and Larz Spangberg.

Fig. 9.7

A colony of yeast cells and hyphae at the base of a smear-free dentin cavity. Note that part of the dentin is coated by an extracellular material (original magnification 1500×). Courtesy of Bilge Hakan Sen, Kamran Safavi, and Larz Spangberg.

Fig. 9.8

A dense mass of yeast and hyphae at the base of a smeared dentinal cavity (original magnification 550×). Courtesy of Bilge Hakan Sen, Kamran Safavi, and Larz Spangberg.

Fig. 9.9

(a) A dense colony of

C. albicans

particularly consisting of yeast cells on the smeared cavity wall (original magnification 750×). (b) Note that the yeast cells and hyphae are in close adaptation to the smeared surface (original magnification 1500×). Courtesy of Bilge Hakan Sen, Kamran Safavi, and Larz Spangberg.

Fig. 9.10

Bacteria (arrows) in dentinal tubules approximately 100 μm from the root canal wall in the middle third of root (original magnification 2000×). Courtesy of Bilge Hakan Sen, Beyser Piskin, and Tijen Pamir.

Fig. 9.11

Yeast cells on the root canal wall in the middle third (original magnification 1500×). Courtesy of Bilge Hakan Sen, Beyser Piskin, and Tijen Pamir.

Fig. 9.12

Yeast cells on the root canal wall in the apical third. Note that the cells are attached to each other and the dentinal wall with numerous organic strands (original magnification 5000×). Courtesy of Bilge Hakan Sen, Beyser Piskin, and Tijen Pamir.

Chapter 10

Fig. 10.1

Pathways of spread of odontogenic infections.

Fig. 10.2

Anatomic boundaries of the submandibular space.

Source:

Hohl et al. (1983).

Fig. 10.3

Anatomic boundaries of the sublingual space.

Source:

Hohl et al. (1983).

Fig. 10.4

Anatomic boundaries of the submental space.

Source:

Hohl et al. (1983).

Fig. 10.5

(a) Anatomic boundaries of the Ludwig's angina (

Source:

Hohl et al. 1983); (b) clinical example of Ludwig's angina.

Fig. 10.6

Anatomic boundaries of the buccal space.

Source:

Hohl et al. (1983).

Fig. 10.7

(a) Anatomic boundaries of the lateral pharyngeal space; (b) anatomic boundaries of the retropharyngeal space.

Source:

Hohl et al. (1983).

Fig. 10.8

Spaces involved as percentages of all cases.

Source:

Adapted from Poeschl et al. 2010 [151–156]. Reproduced with permission of Elsevier.

Fig. 10.9

(a) Anatomic boundaries of the submasseteric space; (b) anatomic boundaries of the pterygomandibular space; (c) anatomic boundaries of the superficial and deep temporal space.

Source:

Hohl et al. (1983).

Fig. 10.10

Anatomic boundaries of the canine space.

Source:

Hohl et al. (1983).

Fig. 10.11

Example of cancrum oris in an HIV patient.

Fig. 10.12

Clinical picture of a facial swelling and abscess of submandibular space.

Fig. 10.13

(a) Panorex showing gross decay of molar teeth; (b) CT scan of right submandibular, submasseteric, pterygomandibular, and lateral pharyngeal abscess formation; (c) clinical photo of patient.

Fig. 10.14

(a) Glidescope. (b) Fiberoptic intubation.

Fig. 10.15

Incision and drainage of left submandibular abscess.

Fig. 10.16

(a) Aspiration of right submandibular space abscess being performed under sterile conditions to avoid contaminant organisms; (b) incision and drainage of right submandibular space abscess.

Fig. 10.17

(a) Alar defect of infected wound; (b) wound thoroughly debrided and a bilobed local flap marked; (c) rotation and closure of local flap.

Fig. 10.18

(a) Upper lip debridement after a necrotizing infection; (b) example of a radial forearm free flap with the skin paddle based over the radial artery; (c) example of the raised flap prior to inset; (d) 1 month after upper lip reconstruction.

Chapter 11

Fig. 11.1

Direct and indirect mechanisms by which bacteria can activate pulpal or periradicular nociceptors. CGRP, calcitonin gene-related peptide; LPS, lipopolysaccharide; LTA, lipoteichoic acid; PAR, proteinase activated receptor; SP, substance P; TLR, toll-like receptor.

Fig. 11.2

The structure of lipopolysaccharides (LPS) and the pattern recognition receptor, TLR4, which detects LPS and its associated intracellular signaling molecules.

Fig. 11.3

Evaluation of the expression patterns of TLR4 and CD14 in human trigeminal sensory neurons. White arrows depict examples of neurons expressing both markers for each row of three images, and yellow arrows depict examples of neurons that express one but not both markers. Human trigeminal neurons were evaluated for colocalization of TLR4 (panel A), CD14 (panel J), with a marker for the capsaicin-sensitive subclass of nociceptors (TRPV1, panels B,C for TLR-4 and panels K,L for CD14.

Source:

Wadachi and Hargreaves (2006). Reproduced with permission of International and American Associations for Dental Research.

Chapter 12

Fig. 12.1

Penicillin structure and action. The penicillin β-lactam ring is seen to bind the penicillin-binding protein (PBP) and interfere with the peptidoglycan assembly process during bacterial cell wall formation. G, glycine; NAGA,

N

-acetylglucosamine; NAMA,

N

-acetyl-muramic acid. Data re-drawn from Hauser 2013.

Fig. 12.2

The cross-linking step during cell wall synthesis in

Staphylococcus aureus

. Transpeptidase cleaves the terminal D-alanine from a pentapeptide chain, which allows the next D-alanine to bind to the terminal glycine from an adjacent peptidoglycan strand. This cross-links the two peptidoglycan strands to provide stability to the cell wall. Penicillins and cephalosporins are structurally similar to the two terminal D-alanines and serve as substrates for transpeptidase. Therefore these agents will compete with the pepidoglycan D-alanines for this enzyme and thus limit the cross-linking within the cell walls.

Fig. 12.3

The three steps in protein synthesis. (a) Frame 1 represents the

initiation

step. In this example a small section of a strand of mRNA is depicted with three codons for three different amino acids (aa1, aa2, aa3). The anticodon for the tRNA carrying aa1 binds to the first codon to initiate protein synthesis. The

tetracycline

family of antibiotics can inhibit this first step in protein synthesis. (b) Frame 2 represents the

elongation

step. In this step the adjacent codon has been bound by the complementary tRNA which allows transpeptidation to occur (i.e., aa1 is freed from its tRNA and bound to the next aa). When this occurs the “donating” tRNA is released from the mRNA. (c) Frame 3 represents the

translocation

step. In this step, the ribosome repositions on the mRNA so that the tRNA carrying the growing peptide chain now occupies the correct location on the ribosome to pass the peptide chain on to the next amino acid. In this illustration, once the tRNA carrying aa3 attaches to the mRNA, the stage will be set for a repeat of the activity portrayed in Frame 2. Macrolide and lincosamide antibiotics will interfere with this third step in protein synthesis.

Fig. 12.4

Recommendations for antibiotic therapy in cases of symptomatic endodontic infections.

Source:

Fouad (2002). Reproduced with permission of John Wiley and Sons.

Fig. 12.5

Results of a randomized clinical trial (RCT) showing the incidence of bacteremia following single extraction and extraction with amoxicillin versus tooth brushing. Molecular analysis of bacteria was undertaken.

Source:

Adapted from Lockhart et al. (2008). Reproduced with permission of American Heart Association.

Chapter 13

Fig. 13.1

Different methods by which bacteria in a biofilm gain resistance against antimicrobials.

Fig. 13.2

Strategies to treat biofilm mediated infection.

Fig. 13.3

Challenges in the disinfection of endodontic biofilms.

Fig. 13.4

The principles of photodynamic effect.

Chapter 14

Fig. 14.1

Anatomy of apical papilla. (a) An extracted human third molar depicting root attached to the root apical papilla (open arrows) at developmental stage. (b) Hematoxylin and eosin (H&E) staining of human developing root (

R

) depicting epithelial diaphragm (open arrows) and apical cell rich zone (open arrowheads). (c) Harvested root apical papilla for stem cell isolation.

Source:

Adapted from Sonoyama et al. (2008). Reproduced with permission of Elsevier.

Fig. 14.2

(a) Immature maxillary central incisor with necrotic pulp. The apical portion of the canal is filled with a thick bacterial biofilm. Note the varying bacterial concentration (Taylor's modified Brown and Brenn, original magnification ×25). (b) Magnification of the rectangular area of the left root canal wall in (a). The apparently empty space between the dentin wall and the thick bacterial biofilm is a shrinkage artifact. Note the severe bacterial colonization of in dentinal tubules, some of which show bacteria up to the resorbed external radicular surface (original magnification ×100, inset ×400). (c) High power view from an area of the left canal wall coronal to the point indicated by the arrow in (a). The biofilm is filling the irregularities between the original calcospherites. No predentin can be seen (original magnification ×400). (d) Longitudinal section from a maxillary lateral incisor with necrotic and infected pulp, passing through the transition from predentin to dentin. Predentin appears colonized by some bacterial aggregations (original magnification ×400). (e) Apical third of a mandibular second premolar with necrotic and infected pulp. A thick bacterial biofilm is filling the canal as well as several areas of resorption present on the right canal wall (original magnification ×50). (f) High power view of the area demarcated by the rectangle in (e) (original magnification ×400). (g) Mesial root of a mandibular first molar exhibiting a large periapical radiolucency. Section of a mesio-distal plane showing lateral canals in the apical third (original magnification ×16). (h) Detail of the entrance of the lateral canals in (g). A bacterial biofilm is present on the walls of the main canal and of the lateral canals (original magnification ×50). (i) Detail of the apical root canal showing an apical ramification, colonized by bacteria (original magnification ×100). (j) Cross-cut section taken at the middle third of the root shown in (g). A wide isthmus connecting the two mesial canals is present, exhibiting a thick bacterial biofilm (original magnification ×16).

Fig. 14.3

Traditional apexification with calcium hydroxide. (a) Tooth 8 of an 11-year-old was necrotic with open apex. (b) The canal was cleaned and shaped and filled with calcium hydroxide every 3 months until an apical stop was detected. (c) The apical half of the canal was filled with gutta-percha and the remaining canal with composite.

Source:

Adapted from Huang (2008). Reproduced with permission of Elsevier.

Fig. 14.4

An open apex 8 with apex filled with mineral trioxide aggregate (MTA). (a) Before treatment. (b) Canal cleaned and shaped. (c) Apex filled with MTA plug. (d–g) Six-month, 3-year, 5-year, and 14.5-yr follow-up, respectively. Courtesy Dr. G. Bogen.

Fig. 14.5

(a) Radiograph showing a lower premolar of an 11-year-old patient having an extensive periradicular lesion. (b) Twenty-four-month radiograph after treatment showing complete root development.

Source:

Adapted from Banchs and Trope (2004). Reproduced with permission of Elsevier.

Fig. 14.6

Clinical case of a 10-year-old patient. (a) Radiograph showing an immature root of tooth 29 with an open apex and an extensive radiolucency at the periapical and mesial regions of the root. (b) Seven months after the initial treatment showing complete maturation of the root apex, healing of the periradicular bone, a significant increase of the calcified tissue in the root, decrease of root canal space, and the calcified coronal third of the root canal.

Source:

Adapted from Chueh and Huang (2006). Reproduced with permission of Elsevier.

Fig. 14.7

Clinical case of a 10-year-old patient. (a) Radiograph showing a radiolucent lesion at the periapical area of tooth 20 with a wide open apex (a gutta-percha point into the sinus tract). (b) Thirty-five months after the initial treatment revealing a market reduction of the root canal space and maturation of the root apex.

Source:

Adapted from Chueh and Huang (2006). Reproduced with permission of Elsevier.

Fig. 14.8

Histologic study of vital tissues formed in dog teeth after revitalization procedures. Thickened root resulting from the deposition of intracanal cementum (IC) onto dentin. Intracanl bone-like tissues (IB) scattered in the root canal space along with intracanal PDL-like tissues (IPL). (a) A sample showing vital tissues in the canal. A magnified view of the boxed region is shown in Inset a. Black arrows indicate cementocyte-like cells in IC; blue arrowheads indicate cementoblast-like cells lining against the IC. (b) A sample showing well-generated IPL extending from extracanal periodontal ligament (PL). (Inset b) Magnified view of the boxed region in (b). The yellow arrowheads indicate Sharpey's fibers. Yellow dashed lines, angles of ligament fibers. The black arrows indicate cementocyte-like cells in IC. Scale bars: a, Inset a, and b, 500 μm; Inset b, 200 μm.

Source:

Adapted from Wang et al. (2010). Reproduced with permission of Elsevier.

Fig. 14.9

Histologic study of a human tooth after revitalization treatment. (A) (a) Preoperative radiograph: tooth 9 exhibits incomplete formation of the root. Periapical radiolucency is present. (b) Postoperative radiograph: the periapical radiolucent area appears to be larger than the preoperative lesion, with sharp margins. (c) Follow-up radiograph taken 12 months after revitalization: the periapical radiolucency has resolved with only slight thickening of the periodontal ligament around the root apex. The canal space is reduced in size and the thickness of the canal walls is increased. (d) The patient presented after 25 months with complete crown fracture. Thickening of the root canal walls increased further. The periapical lesion completely resolved. (B) Histologic study of the tooth after extraction due to nonrestorability. (a) Section passing approximately at the center of the root canal. A mineralized tissue fills the apical portion of the canal (H&E; original magnification x16). (b) Detail of the apical portion in (a). An island of soft tissue is present in the calcified tissue apically (original magnification x25). The inset shows magnification of the ramification indicated by the lower arrow. Its lumen contains uninflamed connective tissue (original magnification x400). (c) A high-power view of the apical soft tissue in (b). Vital connective tissue with fibroblasts and abundance of collagen fibers. Absence of inflammatory cells (original magnification x400). (d) Magnification of the area indicated by the upper arrow in (b). The calcified tissue filling the apical canal is irregular and is demarcated apically by a cementum-like tissue, with some osteoblast-like lacunae. Increased root length is caused by deposition of cementum-like tissue (original magnification x400). (e) A high-power view of the area of the root canal wall indicated by the left arrow in (a). From left to right: area with high concentration of dentinal tubules (tubules are cut transversally by the microtome blade), area with less tubules, and calcified tissue with no dentin tubules (original magnification x400). (f) A high-power view of the area of the root canal wall indicated by the right arrow in (a). From right to left: area with high concentration of dentin tubules (cut obliquely by the microtome blade), area with only few tubules, and calcified tissue with no dentin tubules (original magnification x400).

Source:

Adapted from Shimizu et al. (2013). Reproduced with permission of Elsevier.

Fig. 14.10

Histologic study of a human tooth after revitalizatioin treatment. (A) (a) Peoperative radiograph of tooth 9. (b) A radiograph of the fractured tooth 3.5 weeks after revascularization. (c) A photograph of the extracted tooth. Note a small mass of soft tissue attached to the root apex (arrow). M, mineral trioxide aggregate plug. (B) Histology of the section of extracted revitalized tooth 9. (a) A loose connective tissue with few collagen fibers has filled the canal space up to the coronal MTA plug (H&E, original magnification x 200). The MTA plug was removed before histologic tissue processing. (b) High magnification of the square in (a) (the apical root canal). Flattened odontoblast-like cells lined along the predentin (solid arrows). Many blood vessels filled with red blood cells (open arrows). No mature nerve-like bundles along the blood vessels are observed. Most cells are spindle shaped. (c) High magnification of the rectangle in (a) (the apical foramen). There are fewer blood vessels (arrow) and cellular components at the apical foramen than in the canal. (d) High magnification of the square in (c) (part of the root apex). Layers of epithelial-like HERS (arrow) surrounding the root apex. Spaces in the tissue are artifacts caused by histologic preparation.

Source:

Adapted from Shimizu et al. (2012). Reproduced with permission of Elsevier.

Fig. 14.11

The survival of remaining pulp in a dog tooth after pulpectomy, root canal infection, disinfection, and receiving revitalization procedures. (a) Thickened inner root canal walls resulting partly from the thickened dentin on one side (left) and the deposition of intracanal cementum (IC) on the other side. (b) Magnified view from the top boxed region in (a). Blue arrowheads demarcate the dentin (D) and IC. The yellow arrowheads show the odontoblasts (od) and cementoblasts-like cells (c). (c) A magnified view of the right boxed region in (a). The IC extending from the dentinal wall toward the opposite of the canal forming a bridge. (d) A higher-magnification view of the odontoblast layer (od) from the left boxed region in (a). (Ea and Eb) Radiographs of the roots (*) showing pre- and post-experimental treatment, respectively (sample from group 2). Scale bars: (a) 500 μm, (b,c) 200 μm, and (d) 50 μm.

Source:

Adapted from Wang et al. (2010). Reproduced with permission of Elsevier.

Fig. 14.12

Swine SCAP/PDLSC-mediated root/periodontal structure as an artificial crown support for the restoration of tooth function in swine. (a) Extracted minipig lower incisor and root-shaped HA/TCP carrier loaded with SCAP. (b) Gelfoam containing 10 x 10

6

PDLSC (open arrow) was used to cover the HA/SCAP (black arrow) and implanted into the lower incisor socket (open triangle). (c) HA/SCAP-Gelfoam/PDLSC were implanted into a newly extracted incisor socket. A post channel was pre-created inside the root shape HA carrier (arrow). (d) The post channel was sealed with a temporary filling for affixing a porcelain crown in the next step. (e) The HA/SCAP-Gelfoam/PDLSC implant was sutured for 3 months. (f) The HA/SCAP-Gelfoam/PDLSC implant (arrow) was re-exposed and the temporary filling was removed to expose the post channel. (g) A pre-made porcelain crown was cemented to the HA/SCAP-Gelfoam/PDLSC structure. (h) The exposed section was sutured. (i,j) Four weeks after fixation, the porcelain crown was retained in the swine after normal tooth use as shown by open arrows. (k) After 3 months implantation, the HA/SCAP-Gelfoam/PDLSC implant had formed a hard root structure (open arrows) in the mandibular incisor area as shown by CT scan image. A clear PDL space was found between the implant and surrounding bony tissue (triangle arrows). (l,m) H&E staining showed that implanted HA/SCAP-Gelfoam/PDLSC contains newly regenerated dentin (D) inside the implant (L) and PDL tissue (PDL) on the outside of the implant (M). (n) Compressive strength measurement showed that newly formed bio-roots have much higher compressive strength than original HA/TCP carrier (*

P

 = 0.0002), but lower than that in natural swine root dentin (*

P

 = 0.003). BR, newly formed bio-root; HA, original HA carrier; NR, natural minipig root; PDLSC, periodontal ligament stem cells; SCAP, stem cells from apical papilla; TCP, tricalcium phosphate.

Source:

Sonoyama et al. (2006). http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000079. Used under CC BY 4.0 https://creativecommons.org/licenses/by/4.0/.

Chapter 15

Fig. 15.1

Primary infection healed after initial treatment. (a) Maxillary second molar with apical periodontitis extending along the mesial root surface, and associated sinus tract (traced with a gutta-percha cone). (b) Completed treatment. (c) At 8 years, radiographic and clinical normalcy suggest that the tooth has healed.

Fig. 15.2

Persistent infection healed after orthograde retreatment. (a) Maxillary first premolar with posttreatment apical periodontitis restored with a cast post and crown. (b) Completed retreatment with the original crown re-cemented in place. (c) At 4 years, radiographic and clinical normalcy suggest that the tooth has healed.

Fig. 15.3

Persistent infection healed after apical surgery. (a) Maxillary canine with a large excess of sealer and persistent infection. (b) Completed surgery, including root-end filling with MTA. (c) At 3 months, some bone deposition is suggested, but the lesion is not reduced. (d) At 6 months, the tooth is symptom free and the lesion appears to be healing. (e) At 1 year and 8 months, radiographic and clinical normalcy suggest that the tooth has healed.

Fig. 15.4

Persistent infection healed by scar formation (incomplete healing) after apical surgery. (a) Maxillary lateral incisor with a root filling extruded beyond the root end, and persistent apical periodontitis. (b) Completed surgery, including root-end filling with Super-EBA. (c) At 1 year, radiographic and clinical normalcy suggest that the tooth has healed with a small scar formed several millimeters from the root end. Courtesy of Dr. Richard Rubinstein.

Fig. 15.5

Persistent infection after initial treatment. (a) Maxillary lateral incisor with primary infection. (b) Completed treatment. (c) At 1 year, unchanged radiolucency suggests persistence of the infection.

Fig. 15.6

Healing dynamics after initial treatment. (a) Immediate postoperative radiograph of mandibular first molar with extensive primary infection, included in a clinical study. (b) At 18 months (termination of the study), residual smaller radiolucency at the mesial root tip suggests that healing is incomplete. (c) At 3.5 years, the area is completely healed. Extension of the study to four years would have captured the completion of healing. Adapted from Friedman et al. (1995).

Fig. 15.7

Primary infection healed by scar formation after initial treatment. (a,b) Mandibular lateral incisor and canine with primary infection associated with an orofacial fistula. (c) Completed treatment. (d,e) At 2 years, the fistula has healed with minimal scarring of the skin. The residual radiolucency may suggest persistence of infection. (f) Clinical view after reflection of a full thickness flap reveals a thick fibrous bundle connecting the periapical lesion and the soft tissues over the chin. Histologic examination of the dissected bundle confirmed it to be fibrous (scar) tissue. (g) At 6 months after surgery, further decreased radiolucency and better defined periodontal ligament space suggest healing in progress.

Fig. 15.8

Effect of advanced periodontal disease on the prognosis. (a) Mandibular lateral incisor with endodontic infection and advanced marginal periodontitis, resulting in extensive bone loss. (b) Completed treatment. (c) At 8 months, clinical normalcy and drastically decreased radiolucency suggest incomplete healing (tooth is still restored with a temporary filling). (d) At 3 years, recurrent bone loss because of advancing periodontal disease.

Fig. 15.9

Infection associated with perforation healed after orthograde retreatment. (a) Mandibular molar with a distal root perforation and associated bone loss. (b) Completed retreatment and perforation seal with MTA. (c) At 1.5 year, radiographic and clinical normalcy suggest that the tooth has healed. Regrettably, the tooth is not properly restored.

Fig. 15.10

Recurrent infection after apical surgery. (a) Maxillary lateral incisor with persistent infection. (b) Completed retrograde retreatment surgery, including a root filling with sealer and injectable gutta-percha. (c) At 6 months, radiographic and clinical normalcy suggest that the tooth has healed. (d) At 2.5 years, renewed radiolucency suggests recurrent infection.

Fig. 15.11

Root-end management with bonded Retroplast. (a) Clinical view of maxillary first molar with Retroplast “caps” bonded to the three roots. (b) Maxillary central incisor with persistent infection and extruded root filling. (c) At 9 years after surgery and bonding Retroplast at the root end, radiographic and clinical normalcy suggest that the tooth has healed. Courtesy of Dr. Vibe Rud.

Fig. 15.12

Persistent infection healed after repeat (second-time) surgery. (a) Maxillary lateral incisor with persistent infection after previous surgery, and a gutta-percha cone tracing the sinus tract. (b) Completed repeat surgery, comprising retrograde retreament and filling with MTA. (c) At 3 years radiographic and clinical normalcy suggest that the tooth has healed.

Fig. 15.13

Root-end cavity preparation with ultrasonic tips. (a) Assortment of ultrasonic tips for root-end cavity preparation. (b) Clinical view of root-end cavity preparation with an ultrasonic tip.

Fig. 15.14

Persistent infection healed after retrograde retreatment. (a) Maxillary second premolar with persistent infection. (b) Retrograde retreatment is carried out with ultrasonic files. (c) Completed surgery, including root filling with sealer and injectable gutta-percha. (d,e) At 1 and 7 years, respectively, radiographic and clinical normalcy suggest that the tooth has healed.

Fig. 15.15

Persistent infection healed after intentional replantation, where conventional treatment was unfeasible. (a) Maxillary first premolar with persistent infection, associated with palatal root perforation at the distal aspect, untreated palatal canal, buccal post perforation and total loss of the buccal bone plate. (b) Completed intentional replantation that included repair of two perforations and two root-end fillings, all with MTA. (c) At 3 months, the roots of both teeth have become realigned, and the radiolucency considerably decreased. (d) At 1 year and 4 months, radiographic and clinical normalcy suggest that the tooth has healed with two small scars remaining.

Chapter 16

Fig. 16.1

Percentage occurrence of nonendodontic lesions in biopsied clinical cases where the jawbone radiolucency was similar to a periapical lesion.

Source:

Adapted from Koivisto et al. (2012). Reproduced with permission of Elsevier.

Fig. 16.2

Periapical radiographs of multiple teeth with periapical radiolucencies that mimic endodontic pathosis. All these teeth responded normally to pulp testing. This patient had hyperparathyroidism secondary to kidney failure.

Fig. 16.3

Periapical radiograph taken 5 months after the herpes zoster infection. Endodontic treatment can be seen in maxillary left lateral and central incisors. Periapical radiolucent lesions can also be seen at the apices of left canine, first and second premolar. Except for the endodontic access openings, all teeth were intact with negligible carious involvement or minimal restorations.

Source:

Adapted from Goon and Jacobsen (1988). Reproduced with permission of Elsevier.

Fig. 16.4

Examples of teeth in which no apparent etiology other than sickle cell anemia was reported for the development of pulp necrosis and periapical lesions. Reproduced with permission from Andrews et al. 1983.

Fig. 16.5

Transmission electron micrograph of internalized

Porphyromonas endodontalis

. Internalized

P. endodontalis

(arrow) in human coronary artery endothelial cell following a 90-minute infection.

Source:

Dorn et al. (2002). Reproduced with permission of John Wiley and Sons.

Fig. 16.6

Mouse molar stained with universal bacterial PNA-FISH probe positive fluorescence (red) for bacteria in periapical tissues: (1) H&E stain of lesion (x200); (2) FISH stain of the same region at the same magnification (x200); (3) magnification of (2) (x1000) (unpublished data).

Fig. 16.7

Most likely relationships between endodontic disease and different systemic conditions according to available data. The question marks indicate doubtful associations or only at the level of animal models.

Guide

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