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Endodontology
at a Glance
This title is also available as an e-book.
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Endodontology
at a Glance

Alix Davies
BDS (Hons), MFDS, MJDF, MClinDent, MEndo
Specialist in Endodontics/Clinical Tutor
King’s College London Dental Institute
& Specialist Practice, London, UK

Federico Foschi
BDS, MSc, PhD, FDS, FHEA
Consultant/Honorary Senior Lecturer in
Endodontics
King’s College London Dental Institute
& Specialist Practice, London, UK

Shanon Patel
BDS, MSc, MClinDent, MRD, PhD, FDS, FHEA
Consultant/Honorary Reader in Endodontics
King’s College London Dental Institute
& Specialist Practice, London, UK
This edition first published 2019
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Library of Congress Cataloging-in-Publication Data

Names: Davies, Alix, author. | Foschi, Federico, author. | Patel, Shanon, author.
Title: Endodontology at a glance / Alix Davies, Federico Foschi, Shanon Patel.
Description: Hoboken, NJ : Wiley-Blackwell, 2018. | Series: At a glance series |
Includes index. |
Identifiers: LCCN 2018034896 (print) | LCCN 2018035389 (ebook) | ISBN
9781118994719 (Adobe PDF) | ISBN 9781118994726 (ePub) | ISBN 9781118994702 (pbk.)
Subjects: | MESH: Dental Pulp Diseases—diagnosis | Dental Pulp
Diseases—therapy | Root Canal Therapy | Endodontics—methods | Handbooks
Classification: LCC RK351 (ebook) | LCC RK351 (print) | NLM WU 49 | DDC
617.6/342—dc23
LC record available at https://lccn.loc.gov/2018034896
Cover image: © Shanon Patel
Cover design by Wiley
Set in Minion Pro 9.5/11.5 by Aptara
Printed in Singapore

10 9 8 7 6 5 4 3 2 1
Dedications

Alix dedicates this book to her husband Paul, her children James and Isobel, and her parents Leigh
and John.

Federico dedicates the book to Martina, Alessandro and Arianna.

Shanon dedicates the book to Almas, Genie and Zarina.

v
Contents

Dedications v
About the companion website ix

Part 1 Disease processes in endodontology 1

1 The causes and sequelae of endodontic disease 2
2 Microbiology of apical periodontitis 4
3 Resorption 6

Part 2 Diagnosis 9
4 History taking 10
5 Examination and special tests 12
6 Pulp testing 14
7 Radiographic imaging for endodontics 16

Part 3 Endodontic therapy 19

8 Vital pulp therapy 20
9 Root canal morphology 22
10 Access cavity design 24
11 Mechanical preparation of the root canals 26
12 Irrigation 28
13 Root canal medicaments 30
14 Endodontic files 32
15 Endodontic armamentarium 34
16 Obturation 36
17 Root canal retreatment 38
18 Surgical endodontic treatment 40

Part 4 Pain and pain management 43

19 Odontogenic and non-odontogenic pain 44
20 Local anaesthesia in endodontics 46
21 Pain management in endodontics 48

Part 5 Outcome of endodontic treatment 51

22 Outcome of root canal treatment 52
23 Outcome of root canal surgery 54

vii
 Part 6 Endodontology and other aspects of dentistry 57
24 Endodontic–periodontic interface 58
25 Endodontic–orthodontic interface 60
26 Restoration of the endodontically treated tooth 62
27 Paediatric endodontics 64
28 Endodontics in the older population 66
29 Retain or replace? 68
30 Teeth whitening 70

Part 7 Trauma 73
31 Assessment of traumatic injuries 74
32 Management of crown fractures 76
33 Management of (crown-) root fractures 78
34 Management of luxation injuries 80
35 Management of avulsed teeth 82

Part 8 Risk management 85

36 Risk management in endodontics 86

Index 88

viii
About the
companion website

Don’t forget to visit the companion website for this book:

www.wiley.com/go/davies/endodontology

There you will find valuable material designed to enhance

your learning:
• Interactive multiple choice questions

ix
Disease processes in Part 1
endodontology

Chapters
1 The causes and sequelae of endodontic
disease 2
2 Microbiology of apical periodontitis 4
3 Resorption 6

1
 The causes and sequelae of
2

1
Part 1 Disease processes in endodontology

endodontic disease
Figure 1.1 Section of tooth showing Figure 1.2 Periapical Figure 1.3 Periapical radiograph of the LR6 showing
a carious lesion. Between this and the radiograph of the UL2 radiographic signs of chronic apical periodontitis associated
pulp, tertiary dentine deposition and showing radiographic with an existing root filling.
intratubular sclerosis can be seen. signs of chronic apical
Source: Courtesy of Ahmed Ali. periodontitis associated
with an infected necrotic
pulp.

Table 1.1 The roles of acute inflammatory mediators.

Mediator Source Role
Histamine Mast cells, basophils Vasodilatation, increased permeability
Prostaglandins Mast cells, leucocytes Vasodilatation
Leukotrienes Mast cells, leucocytes Increased permeability, leucocyte chemotaxis and adhesion
Platelet activating factor Mast cells, leucocytes Vasodilatation, increased permeability
Cytokines (IL1, TNF) Mast cells, macrophages Endothelial activation, fibroblast proliferation, neutrophil chemotaxis
Nitric oxide Macrophages, endothelium Vasodilatation
Complement Plasma Leucocyte chemotaxis and activation
Kinins Plasma Vasodilatation, increased permeability
Fibrinogen Plasma Chemotaxis and migration of neutrophils

Endodontology at a Glance. First Edition. Alix Davies, Federico Foschi and Shanon Patel. © 2019 John Wiley & Sons, Ltd. Published 2019 by John Wiley & Sons, Ltd.
Companion website: www.wiley.com/go/davies/endodontology
P
ulpitis is the inflammation of the pulp, whereas apical peri- the microorganisms penetrate into the inner dentine layers, 3
odontitis is the inflammation of the tissues surrounding the the toxins they produce cause significant pulpal inflammation.
apex of the tooth, including the periodontal ligament and If no treatment is provided, the bacteria eventually invade and

Chapter 1 The causes and sequelae of endodontic disease

the alveolar bone. Inflammation can be acute or chronic. colonise the pulp. The pulp is encased in a hard dentine shell
and can therefore not expand to accommodate large amounts
of fluid exudate. It also lacks sufficient collateral circulation.
Acute inflammation These factors limit the ability of the pulp to respond effectively
Acute inflammation is characterised by: to the insult. Pulpal inflammation can initially be reversible,
• Redness with removal of the irritants resulting in resolution of the
• Heat inflammation. However, as the immune challenge increases,
• Swelling the pulpal damage will advance beyond repair, resulting in
• Pain irreversible inflammation and progressive pulpal necrosis.
• Loss of function. Restorative procedures additionally may ‘push’ a tooth with
The redness and heat produced in an area of acute inflamma- pre-existing pulpal inflammation to irreversible pulpitis. This
tion are the results of vessel dilatation and increased blood flow occurs by overheating, desiccation or chemical irritation to the
to that area. Swelling is caused by the accumulation of tissue dentino-pulp complex. If rubber dam is not used, or poor fitting
exudates which contain neutrophils and inflammatory media- temporary restorations are placed, microleakage can also occur.
tors (Table 1.1). The exudate aims to dilute the toxins whilst the The risk of permanent damage is higher when the restorative
neutrophils ingest the pathogens by phagocytosis. Pain is felt work is close to the pulp and the dentine is permeable.
because of the swelling exerting pressure on nerve endings. Cer- A root canal with a necrotic pulp is the ideal environment
tain chemical mediators can also stimulate pain receptors. Swell- for bacterial colonisation as it provides a warm, moist, nutritious
ing and pain can result in loss of function of the inflamed area. and anaerobic environment. The reduced presence of oxygen can
also select aggressive anaerobic pathogens. The microorganisms
are protected from the host defences as there is no blood
Chronic inflammation circulation in the necrotic tissue. They derive their nutrients
Acute inflammation can be reversible by removal of the dam- from the necrotic pulp tissue, periradicular tissue fluids, saliva
aging stimulus. However, if it persists, chronic inflammation and metabolic by-products of other bacterial species.
ensues. Chronic inflammation is the result of a balance between Over time, the bacteria progress apically down the root
continued tissue damage and attempts by the host to eradicate the canal. Leakage of toxins and metabolic by-products through the
disease to produce some tissue repair. Macrophages are among apical foramen also stimulates the inflammatory response in
the main effector cells in chronic inflammation. They secrete the periapical tissues. Inflammatory mediators are released that
various inflammatory mediators and have a role in phagocyto- stimulate osteoclast differentiation. This results in apical bone
sis and antigen presentation. Lymphocytes additionally recog- resorption and production of an apical lesion surrounded by
nise foreign antigens by binding to them before proliferating to chronic inflammatory cells. This stage of the disease is described
mount an immune response by cell-mediated immunity (T lym- as chronic apical periodontitis associated with an infected
phocytes) or by humoral immunity (B lymphocytes). Symptoms necrotic tooth (Figure 1.2).
are usually limited at the chronic inflammation stage. The aim of root canal treatment is to reduce the bacterial load
and seal the canals to prevent further ingress of bacteria. However,
chronic inflammation can persist if inadequate disinfection is
Causes of apical periodontitis performed, with microorganisms remaining at levels sufficient to
Apical periodontitis is caused by bacterial infection of the pulp. stimulate an inflammatory response. If the root canal system and
In a healthy tooth, the pulp dentine complex is protected from coronal aspect of the tooth are not adequately sealed after root
oral microorganisms by the overlying enamel and cementum. canal treatment, bacteria can re-enter and cause recurrence of
However, these layers can be damaged by caries, cracks or frac- the apical inflammation. It can be difficult to identify if the cause
tures, tooth wear, restorative procedures or periodontal proce- of the inflammation is persistence of, or re-entry of bacteria (or
dures to produce portals of entry for microorganisms. both). This stage of the disease is described as chronic apical
As bacteria penetrate into dentine, they release toxins that periodontitis associated with an infected root-filled tooth
pass through the dentine tubules. The pulp responds to this by (Figure 1.3).
producing a layer of tertiary dentine as an additional protective Bacteria can egress through the apical foramen and, in some
layer. Increased intratubular mineral deposition may also reduce cases, cause suppuration that presents as an acute apical abscess
the permeability of the dentine (Figure 1.1). However, once or a chronic sinus tract.
 4

2 Microbiology of apical periodontitis

Part 1 Disease processes in endodontology

Figure 2.1 Stages in biofilm development.

Substrate
Dentine
Adsorption of inorganic and organic Attachment of planktonic Secondary colonisers are attracted
molecules to the root canal wall to microorganisms to produce to the monolayer, increasing its
produce a conditioning layer a monolayer thickness and complexity

Table 2.1 Advantages and disadvantages of culturing and molecular technology.

Method of Advantages Disadvantages

microorganism
detection
Culturing • Broad range allowing for growth of unanticipated species • A large number of microorganisms are uncultivatable
• Relative quantities of microorganisms can be ascertained • Some strains are ambiguous and not identifiable
• Widely available • Samples require immediate processing
• Pathogenicity and bacterial sensitivities can be performed • Cultivation can be time consuming and costly
• Low sensitivitiy

Molecular • High sensitivity and specificity • Information is mostly qualitative only, limited information
technology • Can detect cultivatable and non-cultivatable microorganisms about relative quantities
• Rapid technique • Assays can only detect a few species at a time
• Species can be detected directly from the clinical sample • Usually performed to search for target species
• Samples can be frozen for later analysis • Very expensive
• Can detect dead microorganisms

Table 2.2 Comparison between primary and persistent infection of the root canals.

Microbiological feature Primary apical periodontitis Persistent apical periodontitis

Numbers of bacteria per root canal 1000 to 100 000 000 1000 to 10 000 000

Number of species per canal 10 to 20 1 to 5 (10 to 20 in poorly treated canals)

Prevalent bacterial species (gram negative) Fusobacterium, Porphyromonas, Prevotella, Fusobacterium, Prevotella, Camplylobacter
Treponema, Campylobacter, Veillonella

Prevalent bacterial species (gram positive) Peptostreptococcus, Actinomyces, Peptostreptococcus, Proprionibacterium,

Eubacterium Lactobacillae, Enterococcus faecalis, Actinomyces

Presence of fungi Fungi less likely to be present Fungi more likely to be present

Presence of Enterococcus faecalis in canals Low prevalence Very high prevalence

Endodontology at a Glance. First Edition. Alix Davies, Federico Foschi and Shanon Patel. © 2019 John Wiley & Sons, Ltd. Published 2019 by John Wiley & Sons, Ltd.
Companion website: www.wiley.com/go/davies/endodontology
Which methods of sampling are used for Where do the bacteria reside in the root 5

bacterial detection? canal system?

Chapter 2 Microbiology of apical periodontitis

Apical periodontitis is caused by the presence of microorganisms Bacteria occur in the main canal as well as in accessory canals,
and their toxins in the root canals causing progressive inflam- isthmuses and deltas in the following habitats:
mation and necrosis of the pulp, followed by inflammation of 1 The lumen in planktonic form
the periapical tissues. Root canal treatment aims to reduce the 2 The canals walls as part of a biofilm
microbial load to a level that permits the body to amount an 3 The dentinal tubules.
effective immune response and promote healing. It has therefore A biofilm is a bacterial population that is embedded in a
been considered important to ascertain which microorganisms polysaccharide matrix and adheres to surfaces of solid–liquid
are present in the root canals of teeth with apical periodontitis interfaces (Figure 2.1). Biofilms are present in the root canal
to understand how the disease progresses, as well as how to system and occasionally are extraradicular. The biofilm is
­manage it. advantageous to the microorganism in the following ways:
Methods for isolation and detection of endodontic • Broader habitat range for growth: early colonisers alter the local
microorganisms fall into culturing and molecular technology environment and can increase nutrient availability and remove
(Table 2.1). For each, a sample must be taken from the root canal. waste products. This enables other bacterial species that would not
This is normally performed with paper points. This will normally have survived alone to attach to, and form part of the biofilm.
only allow sampling of microorganisms that are present in the • Increased metabolic diversity and efficiency: bacteria cohab-
main canal lumen. Files assist in collecting ‘scrapings’ from the iting in biofilms develop food webs whereby the metabolic by-
canal walls. Collection of bacteria from dentine tubules and products from one species become the main food source for
isthmuses is very difficult. another. Interactions between different species also allow more
effective breakdown and utilisation of host-derived substrates
Culturing compared with the actions of a single species alone.
The sample is transported in a medium that preserves viability • Protection from the host defences: the extracellular polysac-
whilst not enhancing growth. The microbes are then distributed charide resists phagocytosis from the host inflammatory cells. In
onto agar media or cultured in broths under aerobic or anaer- addition, various species can produce different enzymes to neu-
obic conditions. Species can then be identified by assessing tralise the host inflammatory mediators and also inactivate anti-
features including colony and cellular morphology, tolerance bacterial solutions that can be used to remove them during root
to oxygen, gram staining and metabolic end-product analy- canal treatment. Antibiotics usually require a level of bacterial
sis. Other tests that can be performed on the microorganisms activity to be effective. However, bacteria in biofilms often grow
include susceptibility to certain antibiotics, oxygen tolerance more slowly and are at the stationary phase of growth for longer.
and cell wall profile. This can result in enhanced antibiotic resistance.
• Genetic exchange: methods such as conjugation, transforma-
Molecular technology tion and transduction enable dissemination of virulence and anti-
Molecular technology enables identification of microorgan- biotic resistance genes within bacterial species of the biofilm.
isms without the need for culturing. It can more reliably iden- • Enhances pathogenicity: bacteria which individually have a low
tify bacteria, including those strains that show ambiguous virulence can still have a role in causing disease when they partake
phenotypes. Fungi can be identified by their 18S RNA gene. in a biofilm. Their role can be to assist the survival of more virulent
The clinical sample is solubilised, DNA extracted and spe- bacteria by improving adherence of the biofilm to host surfaces,
cific nucleic acid probes (primers) are added that are comple- obtaining nutrients from the host and evading host defences.
mentary to the target species being investigated. If the target
species is present, hybridisation will occur. The polymerase
chain reaction will then amplify the DNA to a level at which it How does the knowledge of the bacterial
can be detected. If the target species are absent in the sample, species and habitats influence endodontic
no hybridisation will occur and no DNA will be amplified.
Electrophoresis and fluorescent in situ hybridisation can be
treatment?
The complexity of intracanal infection requires treatment with
used to assist with separation and visual identification of the a broad spectrum antibacterial such as sodium hypochlorite.
strains present. Antimicrobial agents are far less effective at destroying bacteria
in biofilms than planktonic bacteria. They will therefore need to
be used in greater concentrations, or employed with techniques
Which bacteria are responsible for such as ultrasonic irrigation to disrupt the biofilms. Whilst
causing apical periodontitis? microorganisms present in the main root canal can be directly
The culturing and molecular biology techniques have revealed accessed and ideally eliminated by instrumentation and irriga-
the presence of more than 400 microorganisms. Different bacte- tion, those microbes that are located in lateral canals and dentine
ria dominate the canals in primary and persistent cases of apical tubules are more difficult to reach and can require other thera-
periodontitis (Table 2.2). peutic strategies to eliminate them (see Chapter 12).