Oral and Dental

Version 3

Therapeutic Independent evaluation

' Guidelines of the evidence
What's new
in Oral and Dental 3
Some of the new information and major
changes included in Therapeutic Guidelines:
Oral and Dental , version 3.

To help dentists and medical practitioners determine the likely cause of

acute dental pain, an expanded guide to common causes, and their
management, has been included. Nonsteroidal anti- inflammatory drugs
(NSAIDs) are preferred for acute dental pain but can cause significant
adverse effects; details are included on how to determine whether NSAID
use is appropriate for a patient. Opioids have a limited role in the treatment
of dental pain; if they are indicated, advice is included on minimising
potential harms. Analgesic dosing in children requires dose calculations;
for simplicity, calculated doses for common preparations of ibuprofen and
paracetamol have been included.

Antibiotic therapy is not a substitute for dental treatment of acute

odontogenic infections, but is sometimes required adjunctively. The
indications for antibiotic therapy (including for patients who present to a
medical practitioner) are clarified in a new table. To support antimicrobial
stewardship, new advice is included on how to explain the potential
harms of antibiotic therapy to patients, and manage patients who report
hypersensitivity to antimicrobials.
It is crucial that oral mucosal lesions are assessed for ‘ red flag’ features
(summarised in a new box) that require further investigation. To aid
recognition of oral mucosal lesions, new photos are included of common
>ral mucosal diseases. New information is also included on red, white and
pigmented lesions, and a new table outlines the features and management
of oral candidiasis and Candida -associated lesions.
Dental practitioners often treat patients with complex medical conditions
for whom dental treatment may need to be modified, because of the
condition or the medication used to treat it. New sections are included on
dental treatment for patients who are immunocompromised, or who have a
cardiac implanted electronic device, a bleeding disorder, or diabetes that is
treated with an SGLT2 inhibitor.
Before an oral or dental procedure, patients taking antithrombotic drugs
must be evaluated for the risk of bleeding related to patient factors or
.
the procedure Management is determined by the assessment findings
and knowledge of the antithrombotic drug(s) used, and may include
local haemostatic measures, specialist referral, or temporary interruption
of antithrombotic therapy (in consultation with the patient’s medical
.
practitioner) Specific advice is included for common antithrombotics.

A flow chart is included to help practitioners assess the risk of medication -

related osteonecrosis of the jaw (MRONJ) in patients taking
antiresorptive or antiangiogenic drugs who require a bone- invasive dental
procedure. Advice is also included on managing patients at risk of MRONJ.

Patients at risk of adrenocortical insufficiency may need their corticosteroid

dose increased before certain procedures—specific advice is included.
Antibiotic prophylaxis is rarely needed for dental procedures. The topic on
antibiotic prophylaxis outlines when antibiotics are and are not indicated.
To aid choice of local anaesthetic, a new table outlines the properties of
commonly used preparations. Although the dose required is usually much
lower than the maximum dose of local anaesthetic, the maximum dose
should always be calculated; an example calculation is included.
Safe and effective use of anxiolysis to facilitate a dental procedure
requires careful patient assessment and perioperative management, and
appropriate drug choice. New guidance helps identify patients at increased
risk of adverse outcomes; a summary of the advantages and disadvantages
of benzodiazepines and nitrous oxide aids drug choice; and a patient
information sheet (printable from eTG complete ) summarises the principles
of perioperative management of patients receiving anxiolysis.
To support medical practitioners treating patients with common oral and
dental conditions, guidance on triage and management is included, together
with new information on oral hygiene, dental anatomy and terminology, and
the dental numbering system.
A new section is included on peri-implant mucositis and peri-implantitis.

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Version 3, 2019

Oral and Dental Expert Group

Therapeutic Guidelines Limited, Melbourne

.•
Therapeutic
" "*
XI I 1 H

Guidelines
Copyright © 2019 Therapeutic Guidelines Limited
All rights reserved. Apart from any fair dealing for the purpose Contents
of private study, criticism, or review as permitted under
the Copyright Act 1968 , no part of this publication may be
reproduced, stored in a retrieval system, scanned or transmitted
in any form without the permission of the copyright owner.
Tables, boxes, figures and photos vii
Suggested citation:
Oral and Dental 3 Expert Group ... xiii
Oral and Dental Expert Group. Therapeutic guidelines: oral and dental.
Version 3. Melbourne: Therapeutic Guidelines Limited; 2019. Acknowledgments xv
Key information xvii
First published 2007
Reprinted 2008 Topics
Reprinted 2009
Version 2 2012
Principles of diagnosis and management in dental practice 1
Reprinted 2013 Dental prescriptions and prescription-writing 9
Reprinted 2014
Practical information on using drugs in dentistry 15
Reprinted 2016
Reprinted March 2017 Dental caries 63
Reprinted November 2017
Periodontal and peri -implant diseases 71
Reprinted 2018
Reprinted 2019 Acute odontogenic infections 79
Version 3 2019
Salivary gland infections 89
Oral mucosal disease 93
Halitosis 125
Publisher and distributor: Orofacial pain 129
Therapeutic Guidelines Limited
Bruxism 149
Ground Floor, 473 Victoria Street
West Melbourne, Victoria 3003 Trismus 151
Australia
Dental management of patients with medical conditions .... 153
Telephone + 61393291566
Antibiotic prophylaxis for dental procedures 189
Telephone 1800061260 ( within Australia)
Facsimile + 61393265632 Local anaesthetics in dentistry 201
Email sales@tg.org.au
Website < www.tg.org.au >
Anxiolysis (minimal sedation) for dental procedures 211
Complications after oral surgery 221

£5
ISBN 978-0-9925272 -9- 7 Dental and maxillofacial trauma 225
MIX
Paper from Medical emergencies in dental practice 233
FSC
responsible sources

Printed in Australia by Adams Print FSC* C110099

v
 Guidance for medical practitioners managing oral and dental issues. 261
Tables, boxes, figures
Appendices and photos
Appendix 1. Drug use in pregnancy and breastfeeding. 277

Index 287

Tables
Table 1. Antimicrobial stewardship strategies applicable to general
dental practice 24
Table 2. NSAIDs commonly used in dentistry 44
Table 3. Major adverse effects of NSAIDs 44
Table 4. Adverse effects with short-term use of opioids 52
Table 5. Advantages and disadvantages of immediate- release
opioids commonly used in dentistry 54
Table 6. Properties of topical corticosteroids used on the oral mucosa.... 55
Table 7. Recommended concentration of fluoride toothpaste according
to age and risk of dental caries 67
Table 8. Examples of topical fluoride applications for patients at
elevated risk of dental caries 68
Table 9. Acute odontogenic infections: features and overview of
management 80
Table 10. Common risk factors for oral candidiasis 114
Table 11. Overview of oral candidiasis and Candida -associated
lesions 115
Table 12. A guide to differentiating and managing acute dental pain .... 132
Table 13. Weight- based dose and approximate volumes of ibuprofen
liquid for children 142
Table 14. Weight- based dose and approximate volumes of
paracetamol liquid for children 143
Table 15. Signs and symptoms of temporomandibular disorders. 144
Table 16. Risk of prolonged bleeding following oral and dental
procedures 157

vi vii
 Table 17. Stages of osteonecrosis of the jaw 165 Box 9. Patient instructions for applying a topical corticosteroid to
the oral mucosa 56
Table 18. Dental procedures and their requirement for surgical
antibiotic prophylaxis 190 Box 10. Dental treatment options for acute localised odontogenic
infections 82
Table 19. Local anaesthetics for infiltration or regional block in
dentistry 205 Box 11. Potential causes of salivary gland swelling 90

Table 20. Maximum safe single doses of local anaesthetics available in Box 12. ‘Red flag’ features of oral mucosal disease 94
208
dental cartridges in Australia Box 13. Drugs frequently associated with dry mouth 122
Table 21. Advantages and disadvantages of oral benzodiazepines and Box 14. Practical advice for patients with dry mouth 124
inhaled nitrous oxide for anxiolysis in dentistry 214
Box 15. Common causes of halitosis 125
Table 22. Pharmacokinetic properties of benzodiazepines used in
dentistry 217 Box 16. Factors that influence the choice of analgesics for acute
dental pain 137
Table 23. Management of bleeding after oral surgery 224
Box 17. Common triggers of bruxism 150
Table 24. Signs and symptoms of hyperventilation syndrome 254
Box 18. Important patient- related
factors that increase the risk of
Table 25. Initial assessment of the severity of an acute asthma prolonged bleeding from an oral or dental procedure in
attack in adults and children 255
patients taking antithrombotic drugs 156
Table 26. Signs of airway obstruction 257
Box 19. Local haemostatic measures for oral and dental procedures
Table 27. Common dental problems encountered by medical in patients taking antithrombotic drugs 158
262
practitioners Box 20. History taking to assess the risk of medication- related
Table 28. Drugs used in the management of oral and dental osteonecrosis of the jaw 167
conditions in pregnancy and breastfeeding 282
Box 21. Management advice for patients at risk of medication- related
osteonecrosis of the jaw undergoing a bone- invasive dental
Boxes procedure 171
Box 1. General principles of managing oral and dental conditions.... 1 Box 22. Management of a patient with stable diabetes undergoing
a dental procedure in an outpatient setting. 180
Box 2. Examples of antimicrobials used in dentistry with good oral
bioavailability 17 Box 23. Principles for appropriate prescribing of surgical antibiotic
prophylaxis in dentistry 191
Box 3. Guidance for intravenous to oral switch 18
Box 24. Cardiac conditions for which endocarditis prophylaxis is
Box 4. Examples of dental indications for which a short duration of recommended for patients undergoing a procedure listed
therapy (less than 7 days) is appropriate 19
in Box 25 194
Box 5. Explaining the harms of antibiotic therapy 20
Box 25. Dental procedures for which endocarditis prophylaxis is
Box 6. Common misconceptions about antimicrobial allergy 26 recommended for patients with a cardiac condition listed in
Box 24 195
Box 7. Questions to ask in an antibiotic allergy assessment 29
Box 26. A worked example of calculating the maximum volume of a
Box 8. Patients who should not be prescribed an NSAID by a dentist 46
safe single dose of local anaesthetic 207
viii ix
 Box 27. Patient groups at increased risk of adverse outcomes with Figures
213
anxiolysis (minimal sedation) Figure 1. Example of the format required for a legal prescription
Box 28. Instructions for patients having anxiolysis (minimal sedation) written by a dentist 14
216
for a dental procedure Figure 2. Suggested management of patients reporting hypersensitivity
Box 29. Initial assessment and management of an avulsed tooth 226 to penicillins 32

Box 30. Management of urticaria and angioedema 238 Figure 3. Beta- lactam structure and side-chain similarity 36

Box 31. Management of anaphylaxis 239 Figure 4. Stages of dental caries and its sequelae 63

Box 32. Management of syncope 241 Figure 5. Anatomical location of localised odontogenic infections and
associated conditions 81
Box 33. Management of angina or an acute coronary syndrome 242
Figure 6. Assessing the risk of medication- related osteonecrosis of
Box 34. Management of cardiac arrest 243
the jaw before a bone-invasive dental procedure in a patient
Box 35. Management of hypoglycaemia 244 treated with an antiresorptive or antiangiogenic drug 168
Box 36. Management of methaemoglobinaemia 246 Figure 7. Possible sites of persistent bleeding after tooth extraction 223
Box 37. Management of stroke 247 Figure 8. Basic life support flow chart 235

Box 38. Management of seizures 248 Figure 9. Primary teeth eruption and exfoliation pattern 268

Box 39. Management of temporary paralysis of the periocular Figure 10. Secondary teeth eruption pattern 269
muscles 249
Figure 11. Anatomy of the tooth and surrounding tissues 270
Box 40. Management of chemical eye injuries 251
Figure 12. The Federation Dentaire Internationale (FDI) dental
Box 41. Management of foreign bodies lodged on the surface of numbering system 272
the eye 251

Box 42. Management of penetrating eye injuries 252 Photos

Box 43. Management of unilateral blindness following injection of Photo 1. Early carious lesions and cavities 64
local anaesthetic containing a vasoconstrictor 253
Photo 2. Squamous cell carcinoma of the left ventral surface of
Box 44. Management of unilateral blindness following injection of the tongue 96
dermal fillers 253
Photo 3. Squamous cell carcinoma of the right anterior ventral
Box 45. Management of hyperventilation syndrome 254 surface of the tongue 97

Box 46. Management of an acute asthma attack 256 Photo 4. Squamous cell carcinoma of the left mandibular alveolus . 97
Box 47. Preventive measures to minimise the risk of inhaled or Photo 5. Leukoplakia of the ventral surface of the tongue and floor
swallowed objects 258 of mouth 98

Box 48. Management of an inhaled or swallowed object 259 Photo 6. Erythroplakia of the right postero-lateral surface
of the tongue 99
Photo 7. Papilloma of the right maxillary labial mucosa 100

x xi
 Photo 8. Oral lichen planus of the left buccal mucosa showing
102
Oral and Dental 3
Expert Group
characteristic white striations
Photo 9. Oral lichenoid lesion due to contact hypersensitivity to an
amalgam filling 102

Photo 10. Geographic tongue lesion of the right lateral border

of the tongue 104

Photo 11. Amalgam tattoo 105 Dr Caroline Hall (chair)

Medical Advisor, Therapeutic Guidelines Limited, Melbourne, Victoria
Photo 12. Hairy tongue 106
Dr Paul Buntine
Photo 13. Persistent traumatic ulcer of the right posterior lateral Emergency Physician, Box Hill Hospital
margin of the tongue 107 Director of Emergency Medicine Research, Eastern Health
Photo 14. Minor aphthous ulcer of the mandibular labial mucosa .... 108 Adjunct Senior Lecturer, Monash University, Melbourne, Victoria

Photo 15. Intraoral lesions caused by the herpes simplex virus 110 Professor Ivan Darby
Chair and Head of Periodontics, Melbourne Dental School, The University
Photo 16. Mucous membrane pemphigoid affecting the mandibular of Melbourne, Melbourne, Victoria
gingivae 113
Dr Lee Fong
Photo 17. Avulsed primary and secondary teeth 227 General Practitioner, Adamstown
Photo 18. Patient with right- sided facial palsy 249 GP Clinical Lead, Hunter New England Local Health District
Senior Clinical Director, Hunter Primary Care, Newcastle, New South
Wales
Professor Albert Frauman
Professor of Clinical Pharmacology and Therapeutics, The University of
Melbourne
Director, Department of Clinical Pharmacology and Therapeutics, Austin
Health, Melbourne, Victoria
Dr Nicole Heaphy
Head of Oral Medicine, Royal Dental Hospital of Melbourne, Melbourne,
Victoria
Dr R Mark Hutton
General Dentist, Mount Gambier, South Australia
Dr Angus Kingon
Oral Surgeon, Sydney, New South Wales
Associate Professor David Looke
Senior Staff Specialist in Infectious Diseases and Clinical Microbiology,
Princess Alexandra Hospital
Associate Professor, School of Clinical Medicine, The University of
Queensland, Brisbane, Queensland
xii xiii
 Associate Professor John Matthews
General Dental Practitioner ( retired)
Current Board Member, Melbourne Dental Clinic, The University of
Melbourne, Melbourne, Victoria
Ms Hazel Moore
Editor, Therapeutic Guidelines Limited, Melbourne, Victoria
Dr Kate Morlet-Brown
Oral and Maxillofacial Surgeon, Fremantle, Western Australia
Adjunct Associate Professor Geraldine Moses
Consultant Clinical and Drug Information Pharmacist, Mater Public Hospital
Adjunct Associate Professor, School of Pharmacy, The University of
Queensland, Brisbane, Queensland
Consultant Pharmacist to the Australian Dental Association
Dr Paul Sambrook
Head of Unit, Oral and Maxillofacial Surgery, Royal Adelaide Hospital
Clinical Director, Oral and Maxillofacial Surgery, Adelaide Dental Hospital
Senior Lecturer, The University of Adelaide, Adelaide, South Australia
Dr Sue-Ching Yeoh
Oral Medicine Specialist, Sydney, New South Wales
Members of the expert group have provided declarations of interest as per
Therapeutic Guidelines Limited’s policy on conflict of interest. For more
information, see < www.tg.org.au>.
xiv
Acknowledgments
The expert group thanks colleagues who have contributed to the develop-
ment of this manuscript. In particular:
Dr Luke Grzeskowiak
NHMRC Early Career Research Fellow, Adelaide Medical School,
Robinson Research Institute, The University of Adelaide
Senior Pharmacist, SA Pharmacy, Flinders Medical Centre, Adelaide,
South Australia
Ms Tamara Lebedevs
Senior Pharmacist and Antimicrobial Stewardship Pharmacist, Women
and Newborn Health Service, King Edward Memorial Hospital, Perth,
Western Australia
Professor Laurence Walsh
Professor of Dental Science, The University of Queensland, Brisbane,
Queensland
Members of the Antibiotic 16 Expert Groups, who revised the sections
'Prevention of infective endocarditis’, ‘Surgical antibiotic prophylaxis for
patients with a pre-existing joint prosthesis’, ‘Surgical antibiotic prophy-
laxis for patients with a pre-existing breast implant ' and ‘Antimicrobial
hypersensitivity'. For a list of members of the Antibiotic 16 Expert
Groups, see < www.tg.org.au/the- organisation/expert-groups/> .
The individuals listed above have provided declarations of interest as per
Therapeutic Guidelines Limited’s policy on conflict of interest. For more
information, see < www.tg.org.au >.
The expert group thanks colleagues from Melbourne Dental School, The
University of Melbourne, who have contributed photographs to this manu-
script. In particular Dr Antonio Celentano, Dr Rita Hardiman and Professor
Michael McCullough.
Previous versions of these guidelines form the basis for this revised version.
The expert group thanks colleagues who have worked on previous versions:
P Abbott, C Daly, J Dowden, A Goss, M McCullough, J Manski-Nankervis, R
Moulds, J Pope, L Roller, N Savage, M Tennant, LTeoh.
xv
 Ms Hazel Moore gratefully acknowledges the assistance of Dr Leigh - Anne
Claase (Chief Executive Officer, Therapeutic Guidelines Limited [TGL]), Ms
Key information
Susan Daskalakis (Senior Editor, TGL) , Ms Jessica Gibney (Senior Editor,
TGL) , Ms Melanie Rosella (Senior Editor, TGL), Ms Erin Spiric (Assistant
Editor, TGL), Mr Jacob Warner (Editor, TGL) and Mr Albert Chau (Typesetter
and Electronic Publisher).
Independence
The Therapeutic Guidelines evaluation network and other healthcare pro -
fessionals provide valuable feedback on the use of the guidelines in clinical Therapeutic Guidelines Limited (TGL) is an independent, not-for-profit
practice. organisation. Key factors for this independence are:
• financial self-sufficiency; TGL derives an income solely from the
sales of its products, and receives no funding from government or
commercial organisations, including the pharmaceutical industry
• implementation of a strict conflict of interest policy for Directors,
members of the company, staff, members of expert groups and
external reviewers.

Conflicts of interest in expert groups are minimised by careful selection of

members. Any remaining conflicts are declared and managed during the
guideline development process in accord with the TGL conflict of interest
policy, which is available on the TGL website < www.tg.org.au >.

Production process
The process used to produce these guidelines is described on the TGL
website < www.tg.org.au > .

Dosing regimens
The dosing regimens in the text generally apply to nonpregnant adults of
average size; higher or lower doses are appropriate for some patients.
Children’s doses have not been assessed for suitability in neonates; when
doses are given for neonates, they apply to full-term neonates only, unless
otherwise specified.
Where more than one drug regimen is listed for an indication, the number
next to the regimen shows its place in therapy (eg i for first-line
therapy, 2 for second- line therapy) . Drugs that are equally appropriate for
a given indication are marked with the same number.

xvi xvii
 References
All references are published in eTG complete. In print versions of the guide-
lines, a comprehensive list of references is not included because space is
limited.
Principles of diagnosis
Evaluation and feedback and management in
Guideline users are encouraged to comment on the content or format by
emailing < feedback@tg.org.au >.
dental practice
Disclaimer
These guidelines are an acceptable basis for management of patients, but
there may be sound reasons for modifying therapy in certain patients or
Overview of diagnosis and management
specific institutions. The complexity of clinical practice requires that users
The information included in this topic is appropriate for dental practice and
understand the individual clinical situation and exercise independent pro-
may not be applicable to other areas of medicine.
fessional judgment when basing therapy on these guidelines. Particularly
in complicated situations, these guidelines are not a substitute for expert The general principles of managing oral and dental conditions are sum -
advice. marised in Box 1 ( below).
These guidelines do not provide comprehensive drug information. Box 1. General principles of managing oral and dental
Prescribers should consider the particular harm-benefit profile of a drug
conditions
in each patient, taking into account adverse effects, contraindications, the
potential for drug interactions and other drug characteristics. • Identify the disease and its cause—establish a diagnosis.
• Provide acute care.
• Address the cause to prevent recurrence.
• Address the effect of the disease.
• Restore normal function.
• Monitor healing. <D
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• Provide ongoing monitoring and management, particularly for chronic or
recurrent diseases. li.
re Q

The process of establishing a diagnosis begins by taking a thorough his- 8CD +« -

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tory (see p.2) , conducting a clinical examination, and performing diagnostic O
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tests if appropriate ( see p.3). The clinician uses this information to estab- tUDTJ

lish a diagnosis, based on a knowledge of oral and dental diseases, and

gc
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the systemic diseases that can manifest in the mouth. Clinicians should o §
also consider the possibility that the patient’s symptoms may be an i/ i E

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adverse effect of a drug. 5

It is usually possible to establish a diagnosis for dental problems before §

starting treatment (unless emergency or acute treatment is required) . If £E
xviii 1
 the diagnosis is unclear, the clinician should either defer treatment while
awaiting further information (eg test results), or refer the patient to a spe-
cialist (for information on referral, see p.6) .
It is essential to identify the cause of the disease because addressing
the cause is an integral part (and usually the first stage) of managing the
disease. The cause may be simple (eg dental caries as a cause for pulp
disease) or complex (eg a systemic disease with oral manifestations).
Complex conditions may require other management in addition to dental
treatment, and consultation with or referral to the patient’s medical prac -
titioner (for information on referral, see p.6) . Risk factors for the disease
should also be identified and modified, if possible, as part of the overall
management of the patient. If the cause is not addressed, full or rapid
recovery may not be achievable, or an acute condition may progress to
become chronic.
Once the diagnosis and cause have been established, the clinician should
decide an appropriate management strategy. There is a distinction
between ‘management’ and ‘treatment ’. Treatment refers to a systematic
course of medical or surgical care, whereas management encompasses
the overall handling of the patient and their health issues in a sensitive
manner, in addition to treatment.
Drug therapy or irreversible dental treatment should not be started until the
diagnosis has been confirmed. The approach of ‘let’s try this and see if it
helps’ or ‘just in case’ is not recommended—it may expose the patient to
incorrect or inappropriate treatment, or mask signs or symptoms that could
indicate a particular diagnosis.
75
Most conditions that lead patients to visit their dentist require dental or
oral treatment (for the process of rational treatment, see p. 4) . Drugs are
0
-oc
Q
usually only needed adjunctively, with consideration of the likely benefit
and potential adverse effects (for the role of drugs, see p.4) .
than leading questions (eg ask the patient what particular things cause
dental pain, rather than asking if hot or cold drinks cause pain) .
Take a medical history, which includes:
• age and weight, particularly for children
• medical conditions
• pregnancy and breastfeeding status
• a comprehensive medication history, including:
- prescription medicines
- over-the-counter and nonprescription medicines
- complementary medicines (eg vitamins, supplements, herbal
medicines)
- smoking status (past or current)
- alcohol intake
- use of illicit drugs
- history of allergies and adverse reactions to drugs
• capacity assessment—assess the patient’s overall capacity to provide
an accurate history, understand and consent to treatment, and
understand and adhere to post-treatment care requirements.
Consult the patient’s carer, medical practitioner or other healthcare prac -
titioner, if needed to complete the history. If the patient is unsure of the
medicines they are taking, ask them to obtain a current list from their
medical practitioner, pharmacist or electronic health record, to bring to the
next appointment. Crosscheck the medicine list with the medical history—
there may be conditions the patient has forgotten to mention or has not
disclosed. See also Box 20 (p.167) for history taking in relation to use of
drugs associated with osteonecrosis of the jaw.
0
A complete history also includes the patient’s social history (eg family, M

occupation, recreation) .
03
75 C 2.
o At each appointment, check the patient’s history for any changes.
03 Q
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Taking a history O
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When a patient attends a dental practice, establish the reason for their Examination and diagnostic tests .S
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Z3 visit.
Before starting the clinical examination, a provisional diagnosis may be evi -
|
o
Take a dental history, which includes an overview of the patient’s previous
~
0 dental problems and treatment, and a detailed history of the presenting dent. Target the examination and diagnostic tests to confirm the diagnosis iS §
to condition. This assists with forming a provisional diagnosis—several and identify the tooth or tissues that are affected. 0.100
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potential diagnoses (ie differential diagnoses) may be likely. Ask specific Choose tests that are evidence-based, and will aid in decision making; i
• TO
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questions to narrow the field—open-ended questions are more effective involve the patient in the decision to undergo a test. Diagnostic
2 3
 confirmation is particularly important if the dental treatment required for
the provisional diagnosis is irreversible (eg root canal, tooth extraction) .
However, the clinical benefit of performing a diagnostic test should out-
weigh any associated risks. Cumulative radiation exposure, particularly in
childhood and adolescence, has been associated with an increased inci-
dence of cancer. Aim to achieve the lowest possible radiation exposure
while maximising the diagnostic value of the test. For information on radia-
tion exposure during pregnancy, see p. 7.
The process of rational treatment
After taking a patient history and establishing a diagnosis, determine the
therapeutic objective (eg pain relief, treating infection) and choose an
appropriate treatment; involve the patient in this decision. In dentistry,
drugs are usually an adjunct to dental treatment (for the role of drugs, see
below) .
Starting treatment involves:
• providing the patient with information about the condition and the
reasons for treatment
• performing appropriate oral or dental treatment
• if required, recommending appropriate drug therapy, writing an
accurate prescription ( see p.12) and providing the patient with the
required information (see p.13).
Monitoring progress involves:
75
g • reviewing the patient
g • deciding whether to stop, continue or change the treatment.
c The above process is in line with Australia’s National Strategy for Quality
Use of Medicines .
75
o-
J (0 Q
«5
0 The role of drugs
0
| Overview of drug use in dental practice
~ In dental practice, drugs are usually an adjunct to dental treatment.
5 Appropriate dental treatment can minimise or avoid the need for drugs
(eg dental treatment of a localised odontogenic infection usually avoids
co
the need for antibiotics). The use of drugs can often be deferred until the
response to dental treatment has been reviewed. If drugs are necessary,
4 5
they are more likely to be effective if the cause of the disease has been
addressed and dental treatment has been provided. Drug choice is based
on efficacy, safety, suitability (eg adherence issues, patient comorbidities,
drug formulation) , and cost.
Inappropriate prescribing can lead to ineffective and unsafe treatment,
exacerbate or prolong illness, distress or harm the patient, be costly, and,
for antimicrobials, contribute to antimicrobial resistance in the wider com-
munity. In Australia, medication- related problems cause approximately
250 000 hospital admissions annually, and up to 400 000 presentations
to emergency departments annually.* This does not include adverse medi -
cation events for which the patient does not present to hospital. Many
adverse medication events can be prevented by taking a detailed history
and prescribing rationally.
Patients often attend a dental appointment with an expectation of a
particular treatment (eg analgesics, antibiotics) , which may have been
influenced by advertising, unrealistic expectations or drug dependence.
Always consider alternatives to drug treatment and involve the patient in
.
treatment decisions Patients are more likely to choose conservative treat-
ment strategies when a shared decision- making approach is adopted.
Consider the likely benefits and potential harms of drug therapy. If drug
therapy is appropriate, choose an evidence-based treatment for the
condition, with consideration of individual patient factors. Evaluate drug
information to determine the therapeutic value; new and expensive drugs
should be critically evaluated in comparison to established treatments.
Off-label prescribing
‘ Off- label’ use refers to use of a drug in a manner (eg indication, dose, Q)
route of administration, patient group) that is not approved by the 2
Australian Therapeutic Goods Administration (TGA)-listed product infor-
mation. The manufacturer of the medicine does not carry any legal .
responsibility for off- label prescribing— should an issue arise, such as .<£/ 75
a serious adverse reaction, legal liability lies solely with the prescribes Oc -
> +•
c a>
—
Appropriate off- label prescribing requires sufficient evidence to support effi- tUO 'D
.~o2 c
cacy and safety, an overall favourable harm-benefit ratio and the consent
of the patient.1 "
og
* Pharmaceutical Society of Australia (PSA). Medicine safety: Take care. Canberra: PSA; 'o
. TO
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2019.
• g TO
t For further information on off-label prescribing, see the Council of Australian Therapeutic £ £
Advisory Groups publication Rethinking Medicines Decision-making in Australian Hospitals:
Guiding Principles for the Quality Use of Off- label Medicines.
 Overprescribing and underprescribing
It is important that the dose, duration of treatment and quantity of drugs
prescribed are correct and clearly stated on the prescription.
Overprescribing is wasteful, can cause unnecessary adverse effects, and
increases the opportunity for overdose. Of particular concern are drugs that
cause dependence or are prone to abuse (eg opioids, benzodiazepines) ,
and drugs that have a narrow therapeutic index (ie the therapeutic dose is
very close to the toxic dose) . Overprescribing of antimicrobials can lead to
increased antimicrobial resistance.
Underprescribing is also wasteful and potentially harmful, particularly
because it can result in ineffective treatment.
Sporting authorities and the use of drugs
Sporting authorities prohibit the use of some drugs by athletes competing
in sporting events. Some of the drugs prohibited in sport may be prescribed
or administered by dentists. Most elite athletes are aware of the require-
ments for their particular sport.
Information about drugs and their status for sporting participants is
available from the Australian Sports Anti - Doping Authority (ASADA) ,
1300 027 232 or < www.asada.gov.au/substances >, and from the World
Anti-Doping Agency (WADA) , < www.wada -ama.org/en > .
75
M
Referral
0
o When referring a patient to another practitioner (eg specialist, medical
-oc
Clinical records
Clinical records should be kept in accordance with the Dental Board of
Australia guidelines on dental records.
Dental treatment during pregnancy and
breastfeeding
Most dental treatment can be carried out safely during pregnancy.
In general, elective treatment is best performed in the second trimester
(ie the fourth, fifth and sixth months) of pregnancy. Elective procedures
requiring general anaesthesia or intravenous sedation should be deferred
until after the birth and, preferably, until after breastfeeding has stopped.
If the patient is unsure if she is pregnant, defer treatment decisions until
pregnancy status is known.
If intraoral radiographs are necessary for assessment or diagnosis of infec-
tion or trauma, there is no reason, on radiation protection grounds, to
defer them. The Australian Radiation Protection and Nuclear Safety Agency
( ARPANSA ) guidelines* state that intraoral radiographs are not contraindi-
cated during pregnancy; however, a leaded drape is recommended when
the X-ray beam is directed downwards towards the patient’s trunk (eg when
taking occlusal views of the maxilla).
For information on the use of drugs during pregnancy and breastfeeding,
see Appendix 1 (pp.277-86) .
0

ll.
practitioner) , a written referral should be provided. The referral should <2
CD outline the presenting oral or dental complaint, suspected diagnosis (if
75 known) and relevant patient details. The referral should be recorded in the
o-
J CD Q
patient’s history. The referring clinician should ensure the patient attends
</ 5
o
the appointment, and communicate with the other clinician about the
E0 patient’s condition.

3
Likewise, if a medical practitioner has referred a patient to a dentist, the
CD dentist should communicate with the medical practitioner (eg provide feed-
—
0
.2» back to the medical practitioner in writing). CA C
4
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0
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* Code of practice and safety guide for radiation protection in dentistry: Radiation protection
series No. 10. Australian Radiation Protection and Nuclear Safety Agency; 2005.
6 7
Dental prescriptions and
prescription- writing

Overview of legislation about

prescriptions and prescribing
The information included in this topic is appropriate for dental practice and
may not be applicable to other areas of medicine.
For legislation pertaining to obtaining, possessing, prescribing, supplying
or administering drugs in each of the states and territories*, see p.10.
Dentists should follow the appropriate legislation for their state or territory.
Overall, the requirements for what constitutes a legal prescription does not
vary significantly between the states and territories.
Dentists may prescribe prescription- only drugs and drugs available over-
the-counter, provided the drug is for the dental treatment of a patient
under their care and the prescription complies with the relevant state or
territory legal requirements. Prescriptions must be written for use by only
the person named on the prescription. A prescription must not be written
under a person’s name to obtain stock for use in the practice on multiple
patients.

Additional caution should be exercised when prescribing drugs of

dependence. o
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V)
Additional caution should be exercised when prescribing drugs of depend-
*0
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ence. Dentists should be aware of the relevant legislation for their state
or territory pertaining to prescribing drugs of dependence. Drugs of
dependence include some Schedule 4 drugs (eg benzodiazepines) and all
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2
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Schedule 8 drugs, as outlined in the relevant state and territory legislation.

75 z
Xs o
* The roles of prescribing and supplying of drugs to patients are usually separated to avoid a
conflict of interest and promote medication safety. If a dentist decides to supply drugs to Q
o £.
Q
patients, they must ensure that dispensing is performed to the standard of a pharmacist,
with appropriate labelling and documentation.
9
 In most states and territories, dentists can prescribe a drug of dependence For more information, see the Poisons Standard and the relevant state or
for a patient under their care provided all the following points are fulfilled: territory Acts and Regulations, listed below.
• they do so in accordance with legal requirements
Australian Capital Territory
• they have taken all reasonable steps to ascertain the identity of that Drugs of Dependence Act 1989
person
Drugs of Dependence Regulation 2009
• they have ensured that a therapeutic need exists
Medicines, Poisons and Therapeutics Goods Act 2008
• the drug is required for dental treatment.
Medicines, Poisons and Therapeutics Goods Regulation 2008
Misuse of drugs of dependence, particularly opioids, is increasingly preva-
lent. Drug-dependent and drug- seeking patients can present to a dental New South Wales
practice. Be circumspect if a patient demands drugs of dependence and Poisons and Therapeutic Goods Act 1966
exhibits a good level of knowledge or a preference for a specific drug. Poisons and Therapeutic Goods Regulation 2008
When prescribing drugs of dependence, dentists should be familiar with:
• the Prescription Shopping Programme Northern Territory
• any state-based real-time prescription monitoring services Medicines, Poisons and Therapeutic Goods Act 2017
• the state or territory legislative requirements to notify authorities of Poisons and Dangerous Drugs Regulations 2004
fraudulently obtained prescriptions of drugs of dependence.
Queensland
Legislation about prescribing for staff, family members or for the purpose Health Act 1937
of self- administration varies between the states and territories; however, Health ( Drugs and Poisons ) Regulation 1996
generally, self- prescribing and prescribing for staff or family members are
not recommended. South Australia
Controlled Substances Act 1984
The Pharmaceutical Benefits Schedule includes a number of medicines
that are subsidised by the Pharmaceutical Benefits Scheme ( PBS) if Controlled Substances (Poisons) Regulations 2011
prescribed by a dentist. For more information, see the PBS website < www.
Tasmania
pbs.gov.au/browse/dental >. Some medicines are not subsidised by the
PBS, so the patient will pay the full cost of the medicine. If the nonsubsi-
75 Poisons Act 1971
0 dised medicine is a prescription- only medicine, they can be prescribed as a Poisons Regulations 2008
‘private’ or ‘non - PBS ’ prescription.
Q
o Victoria
c
0 Dentists may not order repeat prescriptions. Drugs, Poisons and Controlled Substances Act 1981
75 Drugs , Poisons and Controlled Substances Regulations 2017
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£ Legislative Acts and Regulations relevant Western Australia ru

1
if
Medicines and Poisons Act 2014 c 'CUD
to prescriptions and prescribing Medicines and Poisons Regulations 2016
3
The Poisons Standard classifies medicines and chemicals into o «
.9 Schedules 1 to 10. State and territory legislation regulates the availability £ .2
CD of medicines and chemicals, based on their classification in the Poisons
Standard . Be aware that the regulations in each state and territory can vary
CL
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significantly.
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10 11
 • Use plain English.
The prescription • Do not use abbreviations or Latin terms, except for standard
recommended abbreviations (eg mg for milligram, mL for millilitres).*
tool
A prescription is a legal document; it is a written communication • Do not abbreviate microgram, nanogram, international or
unit.
a prescriber and a pharmacist , for preparing and dispensing a • Avoid using decimal points if possible (eg write quantities less
between
drug for a patient. Who may write prescriptions and how they
should be than 1gram as milligrams, and quantities less than 1milligram as
(see
written are outlined in the appropriate state and territory legislation micrograms).
p.ll). • If using a decimal point, put a ‘0’ in front of the point (eg ‘
0.5’, not
To reduce the potential for error, the prescriber must provide
a prescrip- . .
‘ 5’)
.
tion that is legible, clear and unambiguous Although computer-
generated • Limit the number of items on a prescription to three (or one if
prescriptions can be easier to read than handwritten prescriptions, errors prescribing a Schedule 8 drug).
can still occur. • Use computer-generated prescriptions if possible.
Essential information required for a legal prescription written by a
dentist • If space is unused on the prescription, put a line across the area to
varies slightly between the states and territories, but generally
comprises: prevent the addition of items .
• prescriber's name, address, telephone number and qualifications
• Dentists may not order repeat prescriptions.
• patient's full name (given and family names), address, age and date of
birth (for children, include the patient’s weight) The prescription and the patient
• date the prescription is written When prescribing drugs, provide the patient with specific information
• drug name in full (preferably generic or approved name) the drug, including:
about
• drug strength (eg 250 mg, 500 mg) • the generic or approved name of the drug
• drug form (eg tablet, capsule or mixture) • the expected effects of the drug and what it is used for
• quantity of drug to be supplied • instructions on how to take or use the drug, including the dose, route,
• drug dose, route of administration, frequency and duration of duration, and frequency of administration (eg whether to take the
treatment medicine regularly or as needed)
• clear instructions for the patient (in English)—it is not appropriate to • potential adverse effects and what to do if they occur
3 write ‘take as directed'
• other precautions (eg possible interactions, maximum dose)
S
a • any further instructions necessary for the pharmacist • when to return for review
-O • the words 'for dental treatment only’ • permission to contact you if necessary.
cz • handwritten signature of the prescriber.
75 Patients often do not remember the verbal instructions they are given o
prescrip-
o Figure 1 (p.14) is an example of the format required for a legal during a consultation, so it is preferable to give written
instructions as well.
is?
(0
tion written by a dentist. If the prescription is for an item included in the Consumer medicine information (CMI) leaflets are available for the majority
8

it
Pharmaceutical Benefits Scheme (PBS ) , the dentist 's unique prescriber of medicines prescribed in Australia, and should be offered
when a drug is
number must be on the prescription. PBS prescription pads are available prescribed or dispensed. Consumer medicine information
leaflets are avail-
, a PBS
from Medicare Australia. If the prescription is for a non-PBS item able from pharmacies, some clinical software packages and

it
o the PBS must be online (eg IMPS
prescription form may be used, but all references to MedicineWise website <www.nps.org.au>).
£ '.
out and the form endorsed with the words 'Private Prescription

II
crossed
8
Points to note when writing a prescription include;
• Aim to make the prescription tamper-proof (unalterable); use indelible
For further detail, see the Australian Commission on Safety and
Quality in Healthcare
publication Recommendations for Terminology, Abbreviations and
ink. Medicines Documentation .
Symbols Used in

12 13
 Figure 1. Example of the format required for a legal
prescription written by a dentist

Dr J Smith BDSc
Address Practical information on
Telephone number
PBS prescribing number using drugs in dentistry

Patient’s Medicare number 12 3 4 5 6 7 8 9

Principles of antimicrobial use in dental
Patient’s name Miss Jane Citizen
practice
Patient’s address 1 Sample St, Sample Town
Appropriate antimicrobial prescribing in
Date of birth : 1112 / 2014 Age: 5 yrs Weight: 18 kg
dental practice
This topic outlines the principles of appropriate antimicrobial use in den-
[ vfPBS RPBS Brand substitution tistry (in hospital and community settings). Appropriate antimicrobial
not permitted therapy improves patient outcomes, reduces unnecessary antimicrobial
use and reduces adverse consequences for the patient and the commu-
Rx nity. For a more comprehensive discussion, see ‘Principles of antimicrobial
Phenoxymethylpenicillin 50 mg/ mL suspension use' in eTG complete.
100 mLxl Appropriate antimicrobial prescribing includes the following steps:
• decide whether antimicrobial therapy is indicated—the majority of
Give 225 mg ( 4.5 mL), 4 times a day at 6 - hourly
Tz infections that present in dental practice require dental treatment
intervals for 5 days
0
to address the source of infection. Antibiotic therapy may also be
o required but is not a substitute for dental treatment
-O • select an antimicrobial for the indication that is consistent with
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appropriate clinical guideline recommendations, or based on advice 3
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Consider patient factors such as history of antimicrobial c
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0 hypersensitivity ( see pp.25-37), recent antimicrobial use, and .2
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pregnancy and breastfeeding
• document the antimicrobial therapy in the patient’s medical record or ES^
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Signature medication chart, including the indication and the intended duration of
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.2 1 / 1 2 / 2019 therapy before further review or cessation.

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The antimicrobial regimens recommended in these guidelines are chosen
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2 with respect to the optimal route of administration ( see p.16) and duration 5E
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15
14
 Prophylactic , empirical and directed
antimicrobial therapy
Antimicrobial use may be prophylactic, empirical or directed against an
identified pathogen.
Prophylactic antimicrobial therapy aims to prevent infection when there
is a significant clinical risk of infection developing. There are limited indica -
tions for antibiotic prophylaxis for the prevention of infective endocarditis
(see pp.192-9) , and surgical antibiotic prophylaxis is usually not required
for common dental procedures (see pp.189-92).
Empirical antimicrobial therapy is used to treat an established infection
when the pathogen has not been identified. Antimicrobial choice is based
on the clinical presentation and the expected antimicrobial susceptibility of
the most likely or important pathogen ( s).
Review empirical therapy as soon as possible.
• In hospitalised patients, review therapy daily.
• If the diagnosis excludes infection, stop antimicrobial therapy.
• If a pathogen is not identified, re-evaluate the need for antimicrobial
therapy. If ongoing antimicrobial therapy is considered necessary,
consider de-escalation (eg change parenteral therapy to oral therapy,
or change a broad- spectrum to a narrower- spectrum antimicrobial).
• If a pathogen is identified, follow the principles of directed therapy.
Directed antimicrobial therapy is used to treat an established infection
when the pathogen has been identified, and an antimicrobial with activity
75 against the pathogen can be selected.
<D
Q Preliminary microbiology results (eg Gram stain) may allow targeting of
-co antimicrobial therapy before definitive results are available; modify ongoing
a: therapy once the pathogen and susceptibility are known.
75
Oral therapy is usually associated with less serious adverse effects than
parenteral therapy. It also has the advantage of lower drug and administra-
tion costs.
The antimicrobials listed in Box 2 ( below) have good oral bioavailability and
can often be given orally rather than intravenously, provided:
• they are appropriate for the indication
• they have adequate tissue penetration for the infection being treated
• the patient can tolerate oral administration.
For children unable to swallow tablets, the availability of a suitable drug
formulation can affect antimicrobial choice.
If the oral route is unsuitable, the enteral route (eg nasogastric [ NG],
nasoenteric, percutaneous endoscopic gastrostomy [ PEG ] ) may be used.
Box 2. Examples of antimicrobials used in dentistry with
good oral bioavailability
• clindamycin
• doxycycline
• metronidazole
• trimethoprim + sulfamethoxazole
Parenteral therapy
Parenteral antimicrobial administration (usually intravenous, but occa-
sionally intramuscular if intravenous access is difficult and a suitable
formulation is available) is required when:
• oral administration is not tolerated or not possible
• gastrointestinal absorption is likely to be significantly reduced
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accentuates already poor bioavailability

° Choosing the optimal route of administration • an oral antimicrobial with a suitable spectrum of activity is not
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a5 • higher doses than can be easily administered orally are required to 75
g Oral and enteral therapy achieve an effective concentration at the site of infection
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• urgent treatment is required for severe and rapidly progressing
For the majority of infections, oral antimicrobial therapy is appropriate, .£ o
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infection.
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Parenteral (eg intravenous, intramuscular) therapy ( see p.17) is required
under specific circumstances.
75
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If parenteral therapy is used initially, reassess the need for ongoing par-
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parenteral therapy is required, switch to oral or enteral therapy once the
16 17
 patient is clinically stable and is able to tolerate oral intake. Guidance
on when to switch from intravenous to oral therapy is provided in Box 3
( below) .
Box 3. Guidance for intravenous to oral switch
It is often appropriate to switch a patient’s therapy from the intravenous to oral
route when all of the following apply [NB1]:
• clinical improvement
• fever resolved or improving
• no unexplained haemodynamic instability
• tolerating oral intake with no concerns about malabsorption
• a suitable oral antimicrobial with the same or similar spectrum, or an oral
formulation of the same drug, is available. For children, a suitable paediatric
formulation is available.
NBl: Does not apply to infections that require high tissue concentrations or prolonged
intravenous therapy.
Other routes of administration
Topical administration of antibiotics is associated with the emergence of
resistant organisms and can cause hypersensitivity reactions.
Tips for optimising the antimicrobial dosage
regimen
« duration of therapy (less than 7 days) is appropriate
When selecting a dosage regimen for antimicrobial therapy, patient factors,
s the pharmacokinetic and pharmacodynamic properties of the drug, and
O
potential drug interactions should be taken into account.
o
In certain patients with altered pharmacokinetics (eg altered drug clear-
CD
n ance or volume of distribution), dosing can be difficult and expert advice
Monitoring of antimicrobial blood concentration is used to improve effi-
cacy and minimise dose-related toxicity of drugs with a narrow therapeutic
index. Monitoring may also be used to optimise dosage regimens in other
circumstances (eg patients with septic shock or who require intensive care
support).
Choosing the duration of antimicrobial
therapy
The duration of therapy for some indications is based on clinical practice
because it is not clearly defined from published studies. In general, use the
shortest possible duration of therapy, consistent with the condition being
treated and the patient’s clinical response.
If antibiotic therapy is necessary for dental infections, a short duration of
therapy is usually sufficient because the key component of management
is dental treatment. Box 4 (below) gives examples of dental indications for
which a short duration of antibiotic therapy is appropriate. However, there
are certain indications that require prolonged therapy (eg osteomyelitis).
Advice on duration is included in the clinical topics in these guidelines.
Prolonged duration of antimicrobial therapy is associated with an increased
risk of adverse reactions, Clostridium difficile infection, candidiasis and
selection of antibiotic -resistant organisms, as well as increased costs.
Box 4. Examples of dental indications for which a short
• spreading odontogenic infections without severe or systemic features
• infection following dentoalveolar surgery
• necrotising gingivitis •
3>
3

o may be required. Examples include: Types of adverse effects of antimicrobials §

0 • patients with septic shock or who require intensive care support §
1 • patients with severe burns
Consider benefits versus harms of antimicrobial
• patients with fluid sequestration into a third space (eg bleeding,
a ascites)
therapy
s • patients with cystic fibrosis All antimicrobials can cause adverse effects, so consider the benefit-harm — -a
£ tv=<A
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5 • pregnant women profile when deciding whether to prescribe an antimicrobial. Adverse effects
& obese patients.
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• are usually minor or self-limiting but serious adverse effects, including )

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death, occur rarely. Adverse effects of antimicrobials can be classified as
CD
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direct or indirect (see p.20).
18 19
 Discuss the benefits and harms of antimicrobial therapy with patients. The
infection. Minimising exposure to antibiotics reduces the risk of developing
C. difficile infection.
benefits vary depending on the infection; Box 5 (below) provides guidance
on explaining the harms. Candida species are normal flora in the gastrointestinal and genitourinary
tracts, but antibiotic therapy disrupts the normal flora, and infection caused
Box 5. Explaining the harms of antibiotic therapy by Candida species can develop (eg a local mucocutaneous infection such
as oral or vulvovaginal candidiasis, or invasive infection in immunocompro-
Adverse effects of antibiotics include diarrhoea, rash or more serious
mised or critically ill patients) .
hypersensitivity reactions.
Antibiotics disrupt the balance of bacteria in the body (the microbiome) . While the Antimicrobial use is associated with an increased risk of colonisation
consequences of this are not fully understood, it can cause problems ranging from or infection with a drug-resistant pathogen . For example, acquisition of
mild yeast infections (eg thrush) through to more serious infections (eg Clostridium vancomycin-resistant enterococci (VRE) has been associated with previous
.
difficile ) treatment with antimicrobials, particularly vancomycin and cephalosporins.
Antibiotics can also cause bacteria to become resistant to treatment so that future The risk of colonisation with methicillin- resistant Staphylococcus aureus
infections are harder to treat. Multidrug-resistant bacteria (known as ‘superbugs’) ( MRSA) has been correlated with the frequency and duration of prior
can spread between people, affecting other family members and the community. antibiotic therapy, particularly quinolones and cephalosporins. For more
information on antimicrobial resistance, see below.
Direct adverse effects The microbiome is an ecological community of commensal, symbiotic
and pathogenic organisms found in (and on) all multicellular organisms,
Always check if a patient has a history of adverse drug reactions before
including humans. Emerging data on changes to the human microbiome
prescribing an antimicrobial. Adverse drug reactions to antimicrobials are
after antimicrobial use suggest that such changes may have implications
most commonly non-immune- mediated, pharmacologically predictable
for patient health that, while not well understood, may be far- reaching. An
reactions (eg nausea, vomiting, diarrhoea) or immune-mediated nonsevere
intact microbiome is part of the body’s defence against infection.
delayed reactions (eg maculopapular rash), which do not necessarily pre-
clude further use of the drug.
However, occasionally the reaction is a severe or life-threatening
The importance of antimicrobial resistance
immune- mediated hypersensitivity reaction, which can be immediate (eg
75 anaphylaxis) or delayed (eg drug rash with eosinophilia and systemic symp- What is antimicrobial resistance?
toms [ DRESS], Stevens-Johnson syndrome / toxic epidermal necrolysis
[SJS/TEN]) , and subsequent exposure to the drug could be fatal. For fur-
0 Unlike other drugs, the use of antimicrobials in one patient can influence
future efficacy in other patients. The development and spread of antimicro-
Q
ther discussion on types of antimicrobial hypersensitivity, see pp.25-37.
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bial resistance is a major problem for society. .E
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Always check if a patient has a history of hypersensitivity before
prescribing an antimicrobial.
In the general sense, antimicrobial resistance means that an organism
has either natural resistance to an antibiotic (intrinsic resistance) , or has
c
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acquired a resistance mechanism (acquired resistance) . Although the .2
ECD Indirect adverse effects mechanisms are complex, resistance usually develops due to selective 03 £»
£ pressure exerted by the widespread presence of antimicrobial drugs in the g£
3 Indirect adverse effects of antimicrobials include effects on both com- environment, together with the facilitated transfer of organisms (or their
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mensal and environmental flora. genetic material) within the environment, in both healthcare and commu- •“

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nity settings. 75 £
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The gastrointestinal tract can become colonised with C. difficile after anti-
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The concept of resistance also applies to laboratory antimicrobial suscep- o tuo
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31 biotic use, because antibiotics can disrupt the normal gastrointestinal tract tibility testing and reporting, where a categorisation of ‘resistant ’ implies CL -O
flora. A proportion of colonised patients progress to develop C. difficile ‘ likely to fail treatment’ with the antibiotic.

21
20
 Antimicrobial resistance is increasing in many pathogens. Emergence of
resistance to ‘reserve’ antibiotics—such as quinolones, carbapenems,
vancomycin, colistimethate sodium (colistin)—is a major public health
challenge.
Antimicrobial use and emergence of resistance
Appropriate antimicrobial use delays the emergence of resistance and
minimises the prevalence of resistance after it has emerged.
To ensure that antimicrobials remain effective for treating important infec -
tions, it is crucial to reduce inappropriate antimicrobial prescribing, particularly
of beta-lactamase inhibitor combinations (eg amoxicillin + clavulanate), ceph-
alosporins, quinolones, carbapenems and vancomycin.
Useful resources about antimicrobial resistance are available from:
• Australian Commission for Safety and Quality in Health Care < www.
safetyandquality.gov.au/>
• NPS MedicineWise < www.nps.org.au/medical-info/clinical-topics/
reducing-antibiotic - resistance >
• Centers for Disease Control and Prevention < www.cdc.gov/
drugresistance/index.html >.
An introduction to antimicrobial stewardship
What is antimicrobial stewardship?
TO
§
^
Antimicrobial stewardship (AMS) promotes optimal antimicrobial pre-
scribing. The aim of an antimicrobial stewardship program is to improve
c QUO
patient outcomes and reduce adverse consequences associated with anti-
microbial use, including antimicrobial resistance, toxicity and unnecessary
£ u
-
i
costs. Antimicrobial stewardship is an important strategy for preserving
Q these strategies can be applied in dental settings, including within Primary
- the effectiveness of the antimicrobials that are currently available, in the
£ face of rising antimicrobial resistance. Evidence shows that antimicrobial
^
~
stewardship activities can reduce inappropriate antimicrobial use, which is
associated with improved patient care.
o Managing antimicrobial drug shortages
o The Australian Antimicrobial Stewardship Clinical Care Standard describes
is standards for safe, high-quality care of any person who receives antimi-
o. crobial therapy. These standards apply to prescribing in community and
§ hospital settings.
JZ
22
For more information about antimicrobial stewardship, see the Australian
Commission on Safety and Quality in Health Care publication Antimicrobial
Stewardship in Australian Health Care 2018 , available online.
Antimicrobial stewardship in hospitals
In Australia, national safety and quality standards require all health service
organisations to have an effective antimicrobial stewardship (AMS) program
in place, which is assessed for accreditation. For a comprehensive discus-
sion on antimicrobial stewardship programs in hospitals, see ‘Principles of
antimicrobial use’ in eTG complete.
Antimicrobial stewardship in the community
setting
Most antimicrobial use occurs in the community setting, so general dental
practice is an important focus for antimicrobial stewardship (AMS).
Community- based dental practitioners can use many strategies to opti-
mise antimicrobial prescribing. Efforts to avoid antibiotic use for infections
when the likelihood of benefit is low (eg localised odontogenic infections) ,
or selection of narrow- spectrum antibiotics rather than broad-spectrum
antibiotics ( where possible) , can have a major impact on population- wide
antimicrobial consumption. Continued improvements in this area are likely
to positively impact antimicrobial resistance over time.
Importantly, community- based dental practitioners can also have a positive
influence on the beliefs of individual patients and the broader community
about antimicrobial use and antimicrobial resistance. For patient resources,
see p.24.
.E
The Australian Commission on Safety and Quality in Health Care is devel- D
(
oping antimicrobial stewardship strategies for general practice. Many of
c
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Health Networks and general dental practices, and by general dental prac - c
titioners and other staff—for examples, see Table 1 (p.24) .
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There have been problems with the supply of antimicrobial drugs in w
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Australia. The National Centre for Antimicrobial Stewardship has developed '£3 </)
a set of fact sheets about shortages of antimicrobials, outlining patient
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management and the use of alternative antimicrobials when a particular ol -5
drug is not available—see < www.ncas-australia.orgfeducation >.
23
 Table 1. Antimicrobial stewardship strategies applicable to Antimicrobial hypersensitivity
general dental practice
‘Hypersensitivity’ is a broad term for unpredictable adverse drug reactions,
Component of general Strategies for antimicrobial stewardship ( AMS)
dental practice which can be caused by immune- mediated or other mechanisms. ‘Allergy ’
refers to an immune- mediated mechanism. In this topic, ‘immune-medi-
Primary Health Networks Promote Antibiotic Awareness Week.
ated hypersensitivity’ and ‘allergy’ are used interchangeably.
Establish a local antimicrobial stewardship advisory group.
Promote antimicrobial stewardship through education, It is common for patients to report a history of allergy to an antimicro-
information resources and tools for schools, childcare bial—usually penicillin—and this can present a clinical dilemma. If the
centres and community groups.
antimicrobial is administered to an allergic patient, a severe reaction can
General dental practice Promote the Antimicrobial Stewardship Clinical Care occur; however, it is known that many patients who report an allergy tol-
owners Standard [NB1].
erate the drug if it is administered again. A patient history of antimicrobial
Ensure staff have access to Therapeutic Guidelines: Oral
and Dental .
allergy often dates back to a reaction that occurred in childhood; it is com -
monly described as a rash, with vague features not typical of an immediate
Encourage participation in audit and feedback on
antimicrobial prescribing at a practice level. immune- mediated (IgE) hypersensitivity reaction. In fact, few childhood
reactions are reproducible in adulthood, and over 90% of reported peni -
General dental Participate in online learning modules on antimicrobial
practitioners stewardship. cillin allergies can be excluded by skin testing and oral provocation.
Demonstrate commitment to antimicrobial stewardship
using a ‘commitment poster’. Over 90% of reported penicillin allergies can be excluded by
Prescribe according to Therapeutic Guidelines: Oral and antibiotic allergy testing.
Dental .
Specify the duration of antimicrobial therapy on the Careful assessment and confirmation of antimicrobial hypersensitivity
prescription. ensures that patients with serious infections are not unnecessarily denied
Use shared decision making with consumers for the most effective treatment, or treated unnecessarily with broad- spectrum
antimicrobial decisions, when appropriate. antibiotics. Recent studies (including Australian data) found that when an
Participate in audit and feedback activities for prescribing antimicrobial allergy was recorded on a medication chart, patients were
of antimicrobials.
more likely to receive inappropriate antibiotic therapy and have inferior
15 General dental practice Implement infection control and prevention strategies clinical and microbiological outcomes.
staff according to national guidelines.
<D Accurate and detailed information about antimicrobial hypersensitivity must
O Provide displays (eg posters, videos, information
C pamphlets) for consumers. be documented in the patient’s medical record. If a reported allergy is sub- •OD
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include information about how the allergy has been excluded.

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0 Patient resources to promote appropriate use patient’s medical record accordingly. .2
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of antimicrobials
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.9 priate use of antibiotics and antibiotic resistance—see Antibiotics, and systemic symptoms [ DRESS], Stevens-Johnson syndrome / toxic epi - -o
c <D
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0 explained and Antibiotic resistance: the facts , available on their website. dermal necrolysis [SJS/TEN ]), or after allergy is confirmed on testing. For o - •

information on anaphylaxis, see p.238.

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Discuss the benefits and harms of antimicrobial therapy with patients. The
benefits vary depending on the infection; Box 5 (p.20) provides guidance Common misconceptions about antimicrobial allergy are clarified in Box 6
5E
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on explaining the harms. ( p.26).
24 25
 Box 6. Common misconceptions about antimicrobial allergy
Misconception: Antimicrobial allergy is lifelong.
Antimicrobial allergy is likely to wane over time and many people who report an
allergic reaction in childhood are able to tolerate the drug as an adult.
Misconception: All childhood rashes associated with beta- lactam antibiotics are
due to allergy.
Childhood rashes are commonly caused by a viral infection or a drug-virus
interaction rather than drug allergy, and are often not reproducible upon a
supervised challenge when the patient is well .
Misconception: Documented antimicrobial allergies are always true allergies.
In an Australian review of antimicrobial prescribing, up to 20% of documented
severe reactions including extensive urticaria, compromised airway, angi-
oedema, hypotension, collapse or anaphylaxis. The reaction occurs soon
after exposure to a drug, typically within minutes to 2 hours. Anaphylaxis
is more likely with parenteral rather than oral administration. For penicil-
lins, anaphylaxis occurs at an estimated rate of 1 to 4 cases per 10 000
courses. A clear history of an IgE-mediated reaction means the drug
( and sometimes related drugs) should not be administered again unless
appropriate precautions can be taken (eg according to a desensitisation
protocol) , or after specialist advice on the basis of relevant skin testing
followed by oral provocation.
Not all immediate hypersensitivity reactions are severe.

Delayed immune- mediated (T- cell)

‘allergies’ were pharmacologically predictable non-immune -mediated adverse
reactions (eg gastrointestinal intolerance).
Misconception: Cephalosporin cross-reactivity in patients allergic to penicillin is
hypersensitivity reactions
around 10%.
Delayed immune- mediated hypersensitivity reactions are usually the
Recent reviews have found that overall, only 1to 2% of patients with a confirmed result of T-cell (not IgE) mediated mechanisms, and produce a range of
penicillin allergy have a cephalosporin allergy ( for cross-reactivity between beta syndromes commonly characterised by maculopapular rash (exanthem) .
.
lactams, see p 34). These reactions typically occur after more than one dose of a drug, with an
onset days after starting treatment. However, delayed immune-mediated
Types of antimicrobial hypersensitivity hypersensitivity can occur more rapidly on rechallenge (within 6 hours) .

Type A versus Type B reactions Delayed hypersensitivity reactions are far more common than
immediate reactions; the majority are not severe.
Type A adverse drug reactions are pharmacologically predictable reactions
75 (eg gastrointestinal intolerance). Type B reactions are unpredictable reac - Delayed hypersensitivity reactions are far more common than immediate
<D tions mediated by immunological or other mechanisms. The most common reactions. They often occur in patients with a viral infection and can be due
G
types of immune- mediated reactions are immediate IgE- mediated (Type to the infection or a drug-virus interaction; consequently, such reactions •OX)
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well. In particular, a mild maculopapular rash caused by a penicillin, espe-
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cially amoxicillin or ampicillin, is not strongly predictive of a future reaction c
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and many patients tolerate the drug if it is administered at a later time. c
syndrome. These are usually caused by direct mast-cell degranulation, and
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26 27
 • Stevens-Johnson syndrome / toxic epidermal necrolysis (SJS/TEN) —a
rare, acute and potentially fatal skin reaction caused by acute Box 7. Questions to ask in an antibiotic allergy assessment
keratinocyte death, resulting in fulminant epidermal skin and epithelial
Severity and type of reaction
mucosal loss similar to burn injuries.
Do you remember the details of the reaction?
• Acute generalised exanthematous pustulosis (AGEP) —characterised
How was the reaction managed? Did it require treatment or hospitalisation?
by dozens to hundreds of pin-sized pustules on a background of
erythema, often with fever and leucocytosis, and rarely, organ Timing
involvement; can have a quick onset following drug administration (eg How long after taking the antibiotic did the reaction occur?
1day) . How many years ago did the reaction occur?
• Acute interstitial nephritis (AIN) —a T-cell mediated hypersensitivity
reaction most commonly associated with penicillins; causes kidney Antibiotic use since reaction
dysfunction and can include eosinophilia, fever and exanthematous Are there other antibiotics that have you taken without problems since the
reaction?
rash.
• Serum sickness—characterised by vasculitic or urticarial rash,
arthralgia/arthritis, fever, hypocomplementaemia and sometimes Specific tests
proteinuria. Serum sickness is triggered more commonly by cefaclor
than other cephalosporins, and also by sulfonamides; the onset is When to do allergy testing
typically several days after starting treatment.
• Drug-induced liver disease. The role of allergy testing is largely limited to assessing patients with a his-
tory of immune-mediated hypersensitivity. Seek expert advice if considering
A delayed severe hypersensitivity reaction is a contraindication to further allergy testing.
drug exposure—including desensitisation—because this can be fatal.
Allergy testing is most accurate when performed as early as possible
after the patient has recovered from the acute reaction (usually at least
Further drug exposure—including desensitisation—is
6 weeks after the reaction) , because results may become negative over
contraindicated following a delayed severe reaction.
time. Allergy tests can be negative even in patients who have true allergy; a
negative test result in the presence of a strong history can be a false nega -
Diagnosis of antimicrobial hypersensitivity tive result and requires specialist interpretation.
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The clinical history is critically important in the diagnosis of antimicrobial Skin testing, including skin - prick and intradermal testing with immediate
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hypersensitivity. If hypersensitivity is reported, ask about the nature and reading, is the standard method used in specialised centres to test for
immediate (IgE- mediated) hypersensitivity. These tests have good sen-
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severity of the reaction, timing, how it was managed, and whether the o
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patient knows if other antibiotics have been tolerated since the reaction
for phenoxymethylpenicillin, benzylpenicillin, amoxicillin and ampicillin.
.2
(see Box 7, p.29). 03 1

3 Common pharmacologically predictable antimicrobial adverse reactions

Intradermal tests have better diagnostic sensitivity than skin- prick tests,
but there is a higher risk of adverse reactions.
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internal organ involvement); in many cases these reactions do not justify
avoiding the antimicrobial in future. sensitivity than for immediate reactions.
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28 29
 Skin tests for penicillin hypersensitivity should be performed by specialists, Management of patients reporting
using both the penicillin major and minor determinants—these increase
hypersensitivity to penicillins
the sensitivity of testing.
Managing a patient who reports hypersensitivity to penicillins depends on
In vitro tests many factors. Consider whether antimicrobial therapy is necessary, and the
balance of benefits and harms.
In the context of immediate reactions, a significant elevation of mast-cell
tryptase concentration detected in a blood sample collected 1to 4 hours If the details of the reaction are not clear, take a clinical history to deter-
after a reaction may be helpful to identity mast-cell degranulation. mine the nature and severity of the reaction, how it was managed, and
whether the patient knows if other antibiotics have been tolerated since—
Other in vitro tests for IgE- mediated hypersensitivity are available for ben- see Box 7 (p.29).
zylpenicillin, phenoxymethylpenicillin, amoxicillin and cefaclor through
commercial laboratories; however, such testing is of limited utility, with One common scenario is a patient reporting a childhood history of penicillin
allergy that is unclear. In this situation, keep in mind that many childhood
concerns about false-positive and false- negative results.
rashes associated with beta-lactam antibiotics are caused by a viral infec -
tion or a drug-virus interaction, rather than true antibiotic allergy. These
Drug provocation testing reactions are rarely severe and patients can potentially be rechallenged
Drug provocation testing, also called drug challenge, graded challenge or under specialist guidance.
test dosing, is the controlled administration of a drug in order to diagnose Although it is not possible to give clear guidance to cover all situations,
hypersensitivity. It is often used to confirm tolerance to an antimicrobial Figure 2 ( p.32) provides a guide for generalists to manage some common
when skin-prick or intradermal tests are negative or equivocal. penicillin hypersensitivity scenarios in which a beta - lactam antibiotic is
Drug provocation testing should only be performed under medical super- the preferred drug. This is a simplified summary of a complex field; the
Antibiotic Expert Groups recognise that there are regional variations in how
vision, after consultation with a specialist, in a safe environment where
severe allergic reactions such as anaphylaxis can be managed, and after penicillin hypersensitivity is managed, and that specialists may choose to
obtaining informed consent from the patient.
manage their patients differently after weighing up the benefits and harms
in an individual.
In carefully selected patients (eg those with a history of benign rash in
75 childhood or other delayed nonsevere skin reaction) and with specialist When selecting an antimicrobial in a patient with penicillin hypersensi-
tivity, it is important to understand how R1 side-chains affect the risk of
0 advice, direct oral challenge without prior skin testing can be considered
o when therapy with phenoxymethylpenicillin or amoxicillin is required. In cross- reactivity between beta lactams—for cross-reactivity between beta
o
patients with delayed nonsevere hypersensitivity, prolonged oral provoca - lactams, see p.34. OJD
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tion (5 to 7 days) following a supervised single- dose provocation is often In patients known or strongly suspected to have immediate hypersensitivity <>
75
used to ensure true delayed hypersensitivity is not missed. Do not perform
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Mo 75 £»
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International Consensus on drug allergy. Allergy 2014;69(4):420 -37.
30 31
 Figure 2. Suggested management of patients reporting
hypersensitivity to penicillins
Penicillin hypersensitivity reported by a patient in

:
whom a beta -lactam antibiotic is the preferred drug

;
i
i
History of immediate (IgE-mediated) History of delayed (T-cell
History of penicillin History of
penicillin hypersensitivity (typically AND cephalosporin non-immune-mediated
mediated) penicillin
occurs within 1to 2 hours of drug immune- mediated adverse effect
hypersensitivity (typically (eg gastrointestinal
exposure) hypersensitivity
occurs days after starting
intolerance)
treatment, but can occur
more rapidly on rechallenge)

I i I
Delayed nonsevere penicillin Avoid all beta Safe to administer
Immediate severe Immediate nonsevere Delayed severe penicillin
penicillin hypersensitivity penicillin hypersensitivity hypersensitivity (usually a lactams, except for any beta lactam.
hypersensitivity (eg severe
(eg extensive urticaria, (eg mild urticaria or maculopapular rash or benign aztreonam [NB6] .
cutaneous adverse reaction
compromised airway, immediate rash) [NB3] or significant organ childhood rash; not a severe
angioedema, hypotension, cutaneous adverse reaction

i
involvement such as acute
collapse or anaphylaxis) [ NB3] and no significant organ
interstitial nephritis)
involvement)

i Avoid penicillins.
i i
Avoid penicillins and
Safe to administer most
cephalosporins. Avoid Avoid penicillins and .
Avoid penicillins However, in a Refer to specialised Remove penicillin
allergy from the
cephalosporins [NB1]. non-urgent situation and under antibiotic allergy
Safe to administer a
cefalexin and cefaclor in cephalosporins [NB4],
specialist guidance, consider a testing centre . patient’s medical
patients with amoxicillin Safe to administer a record or annotate the
non-beta - lactam antibiotic single dose of a penicillin followed
or ampicillin allergy. non-beta -lactam antibiotic or true nature of the
or aztreonam . aztreonam.
by a prolonged (5 to 7 day)
reaction.
Can consider a
Safe to administer a provocation test .
carbapenem [NB2) or Can consider a carbapenem
75
carbapenem [ NB2 ] . aztreonam . [NB2 ].
Safe to administer a cephalosporin
In patients with a history of a mild
reaction or a reaction that occurred
<U In the distant past [ NB5].
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c perform desensitisation perform desensitisation
Avoid desensitisation in
or aztreonam. .E
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(see eTG complete ) . (see eTG complete ) .
delayed severe
ID
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- In a non-urgent situation,
consider specific allergy
In a non- urgent situation,
consider specific allergy
hypersensitivity because
further drug exposure can
Penicillins include: phenoxymethylpenicillin, benzylpenicillin, amoxicillin, ampicillin,
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testing and drug testing and drug be fatal . c
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1 supervision (where such supervision (where such ceftriaxone, cefotaxime, ceftazidime, cefepime
CD testing is available) . testing is available).
Carbapenems include: imipenem, meropenem, ertapenem
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2 NB1: In a critical situation, a cephalosporin can be considered in this group after undertaking a risk-benefit analysis
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and assessment of potential side chain cross reactivity (see p.34) Seek expert advice. NB 4: There is limited evidence on the safety of cephalosporins in patients with a history of penicillin-associated 75 c
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C3 approximately 1%: therefore, carbapenems can be considered in supervised settings. However, in patients considered.
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with a history of a severe cutaneous adverse reaction (eg drug rash with eosmophilia and systemic symptoms NB5: In patients who have had a recent reaction, consider avoiding cephalosponns with the same or similar R1
CD ( DRESS ], Stevens-Johnson syndrome / toxic epidermal necrolysis [ SJS/TEN ], acute generalised side - chain as the implicated penicillin (see p.34).
-3 exanthematous pustulosis [ AGEP ] ) , consider a carbapenem only in a critical situation when there are limited O
NB6: However, avoid aztreonam in patients hypersensitive to ceftazidime: these drugs have the same R1
treatment options.
side -chain, so there is a risk of cross -reactivity.

32 33
 Cross- reactivity between beta lactams
Immune-mediated penicillin hypersensitivity was historically thought
to be due solely to the beta -lactam ring structure that is common to all
beta- lactam antibiotics (penicillins, cephalosporins, carbapenems and
monobactams). However, recent evidence and clinical experience suggests
that most reactions occur in response to antigenic molecules in the R1
side-chain that distinguishes individual penicillins and cephalosporins from
one another. Drugs with the same or similar R1side-chains are more likely
to cross- react (see Figure 3, p.36) .
The prevalence of cross- reactivity between beta lactams is not known pre-
cisely. It is a common misconception that cephalosporin allergy occurs in
approximately 10% of patients who are allergic to a penicillin. However,
recent reviews show that overall, only 1to 2% of patients with a confirmed
penicillin allergy have a cephalosporin allergy. Cross-reactivity is more likely
in patients with an amoxicillin or ampicillin allergy who receive cefalexin or
cefaclor, due to their similar R1side-chains.
Beta-lactam cross- reactivity is more likely in patients with
amoxicillin or ampicillin allergy who receive cefalexin or cefaclor,
due to their similar R1side-chains .
Cefazolin has no common side-chains with other beta lactams so is often
tolerated in patients with a penicillin or cephalosporin allergy.
Cefazolin has no common side- chains with other beta lactams so
is often tolerated in penicillin or cephalosporin allergy.
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c no cross- reactivity between penicillins and monobactams.
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3 biotic is the preferred drug, antimicrobials to avoid based on potential
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cross- reactivity due to identical or similar R1side-chains are:
• amoxicillin or ampicillin allergy—avoid cefalexin and cefaclor (except in
delayed nonsevere hypersensitivity; see Figure 2 [p.32] for guidance)
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-SZ
• ceftazidime allergy—avoid aztreonam.
34
In patients with immediate severe penicillin hypersensitivity (eg anaphy-
laxis, angioedema) , avoid penicillins and cephalosporins in most situations;
however, in a critical situation when a beta lactam is the preferred drug, a
cephalosporin can be considered after undertaking a risk-benefit analysis
ond assessment of potential side-chain cross-reactivity (eg for sepsis,
meningitis, endocarditis) . Seek expert advice.
In patients with delayed severe penicillin hypersensitivity (eg drug rash
with eosinophilia and systemic symptoms [ DRESS], Stevens-Johnson syn-
drome / toxic epidermal necrolysis [SJS/TEN ] ) , do not use cross-reactivity
to guide treatment and avoid all penicillins and cephalosporins—see
f igure 2 (p.32) for guidance.
In patients with delayed severe penicillin hypersensitivity, do not
use cross-reactivity to guide treatment.
Cross- reactivity between sulfonamides
Antibiotic sulfonamides (eg sulfamethoxazole, sulfadiazine, dapsone [ a
sulfone antibiotic closely resembling sulfonamide antibiotics]) are often
avoided in patients who are allergic to nonantibiotic sulfonamides (eg
frusemide). However, this is usually not necessary because, with one
exception, there is no cross- reactivity between antibiotic and nonantibiotic
sulfonamides. (The exception is sulfasalazine, a nonantibiotic sulfonamide
that is structurally similar to sulfonamide antibiotics; avoid sulfasalazine in
patients with antibiotic sulfonamide allergy, and vice versa.)
Furthermore, evidence shows that the rate of immune-mediated
cross- reactivity within the antibiotic sulfonamide group (eg between sul-
famethoxazole and dapsone) is lower (9 to 12%) than previously thought •OJO
( 20%), and therefore these antibiotics could be used in a patient with a .Ec/
history of nonsevere allergy to another antibiotic sulfonamide. However,
)
33
this does not apply in patients with anaphylaxis or a severe cutaneous c
adverse reaction such as drug rash with eosinophilia and systemic symp -
o
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toms ( DRESS) or Stevens-Johnson syndrome / toxic epidermal necrolysis .2
I S^
( SJS/TEN). cS
For more information about allergy to sulfonamides, including a patient
information sheet, see the Australasian Society of Clinical Immunology and C 0
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 Figure 3. Beta- lactam structure and side- chain similarity
General structure of penicillins I xnmples of beta -lactam antibiotics grouped by side -chain similarity (cont ) .
Beta-lactam antibiotic R1side -chain [ NB1]
ceftriaxone, cefotaxime
find cefepime

N 0

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General structure of cephalosporins
cefuroxime
0 S
H
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beta -lactam dihydrothiazine

ring ring N 0
H
N
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C R2 ceftazidime
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Examples of beta -lactam antibiotics grouped by side -chain similarity (H3C) 2CO

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36 37

Antimicrobial drugs used in dentistry
This topic covers practical information on using the antimicrobial (anti-
bacterial, antifungal or antiviral) drugs recommended for oral and dental
infections in these guidelines. For comprehensive drug information,
including precautions, contraindications, adverse effects ahd drug interac -
tions, consult an appropriate drug information resource. If prescribing an
antimicrobial drug, consider the benefit-harm profile of the drug in the
individual patient; this requires knowledge of the patient’s medical history
and concomitant medications, including prescription, over-the-counter and
complementary medicines.
For a more comprehensive discussion of antimicrobial drugs, in particular
susceptibility, see the Antibiotic topics in eTG complete.
Antibacterial drugs used in dentistry
Cephalosporins used in dentistry
Cephalosporins are beta -lactam antibiotics (ie they contain a beta -lactam
ring in their structure). In the majority of patients, cephalosporins do not
cause significant adverse effects; however, some patients are hypersensi -
tive to one or more beta -lactam antibiotics (for information on antimicrobial
hypersensitivity, see pp.25-37).
Widespread use of cephalosporins is linked to an increasing prevalence of
75 infections caused by methicillin-resistant Staphylococcus aureus (MRSA) ,
0)
vancomycin-resistant enterococci (VRE), multidrug-resistant Gram-negative
o bacteria and Clostridium difficile .
T5
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a:
Moderate- spectrum cephalosporins: cefalexin and
significant adverse effects; however, some patients are hypersensitive
to one or more beta- lactam antibiotics (for information on antimicrobial
hypersensitivity, see pp.25-37) .
Narrow-spectrum penicillins: benzylpenicillin and
phenoxymethylpenicillin
Narrow-spectrum penicillins are active against numerous oral patho-
gens, including Peptoniphilus (formerly Peptostreptococcus ) species,
Actinomyces species, most Streptococcus species and other oral anaer-
obes (eg Fusobacterium species) . They are inactivated by strains that
produce beta- lactamase enzymes.
Uonzylpenicillin (penicillin G) is given parenterally. For susceptible infec -
tions (eg spreading odontogenic infection with severe or systemic features),
it is the treatment of choice because of its narrow spectrum of activity.
Phenoxymethylpenicillin (penicillin V) is given orally. For susceptible
organisms, phenoxymethylpenicillin is preferred to amoxicillin because of
its narrower spectrum of activity. Food impairs the absorption of phenoxy-
methylpenicillin. Ideally, it should be dosed at 6-hourly intervals, but for
practical purposes four-times-daily dosing, evenly spaced during waking
hours, is often used (eg half an hour before each meal and at bedtime) .
Narrow- spectrum penicillins with antistaphylococcal
activity: dicloxacillin and flucloxacillin
Dlcloxacillin and flucloxacillin are active against streptococci and staphy-
lococci, but inactive against MRSA. They are recommended as first-line
treatment for many skin and soft tissue infections (eg acute suppurative
sialadenitis). "OJD
.E
f ood impairs the absorption of dicloxacillin and flucloxacillin. Ideally, they
( j)

75
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Cefalexin and cefazolin have a similar spectrum of antibacterial activity. tlmes- daily dosing, evenly spaced during waking hours, is often used (eg c
CD
half an hour before each meal and at bedtime). .2
ECD
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They are active against streptococci and staphylococci, but inactive against IS
MRSA and some anaerobes. In some circumstances, cefalexin and cefa- Rarely, flucloxacillin is associated with cholestatic jaundice, particularly in
zolin can be used as a penicillin alternative in patients hypersensitive to older patients on prolonged therapy. Cholestatic jaundice can occur after si
3
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oral or intravenous administration, and up to 6 weeks after treatment. “ -O
penicillins (for information on antimicrobial hypersensitivity, see pp.25-37). c d )
.2
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Dicloxacillin appears to cause less irreversible hepatotoxicity, but causes
more interstitial nephritis.
75 c
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| Penicillins are beta - lactam antibiotics (ie they contain a beta-lactam ring
.
in their structure) In the majority of patients, penicillins do not cause
39
38
 Moderate- spectrum penicillins: amoxicillin and ampicillin
Amoxicillin and ampicillin are active against the pathogens treated by
benzylpenicillin and phenoxymethylpenicillin; however, they have a broader
spectrum of activity. They are inactivated by strains that produce beta-
lactamase enzymes.
Broad- spectrum penicillins (beta- lactamase inhibitor
combinations): amoxicillin + clavulanate
The beta - lactamase enzyme inhibitor, clavulanate, has little inherent
antibacterial activity; it inhibits the beta- lactamase enzymes produced by
several bacteria, including S. aureus and Bacteroides fragilis . The spectrum
of activity of amoxicillin ( see above) is significantly broadened when com -
bined with clavulanate.
Kidney impairment, patients who are taking a high dose of trimethoprim or
other drugs that can cause hyperkalaemia) .
Glycopeptides used in dentistry
The primary indication in dental practice for the parenteral glycopeptide,
vancomycin, is treatment of infection with MRSA. It is not as effective as
beta lactams in the treatment of S. aureus infections that are susceptible
to beta lactams.
Vancomycin is associated with selection of glycopeptide- resistant bacteria
( eg VRE, vancomycin - intermediate S. aureus [ VISA ]).
For information on vancomycin dosing and monitoring, see ‘Principles of
vancomycin use’ in eTG complete .

Because of its broad spectrum of activity, amoxicillin + clavulanate has a

limited role in the treatment of odontogenic infections. It is used when
.
narrower- spectrum regimens are not suitable Additional treatment
for anaerobic bacteria (eg metronidazole) is usually not required with
amoxicillin+clavulanate.
Intravenous amoxicillin + clavulanate has an emerging role in Australia and
is recommended for a limited number of infections in the guidelines.
Folic acid antagonists used in dentistry:
trimethoprim and sulfamethoxazole
15
| Trimethoprim and sulfamethoxazole (a sulfonamide) act by inhibiting bac -
O terial folate production.
T3
c The primary indication in dental practice for the combination of
trimethoprim -{- sulfamethoxazole (cotrimoxazole) is treatment of S. aureus
Lincosamides used in dentistry
The lincosamides, clindamycin and lincomycin, are active against most
rtnaerobic bacteria (eg Peptoniphilus [ formerly Peptostreptococcus ] species,
Porphyromonas gingivalis , Prevotella oralis , B. fragilis) and some aerobic
bacteria (egS. aureus , most Streptococcus species).
In dental practice, lincosamides should be reserved for the treatment of
uusceptible infections in patients hypersensitive to penicillins.
Although clindamycin is inherently more active than lincomycin, for most
indications the same dosage is appropriate. In these guidelines, clinda -
mycin is ranked preferentially to lincomycin because there are more clinical
data to support its use.
Clindamycin and lincomycin have similar adverse effects; they can both to
cause antibiotic -associated diarrhoea. .£cf
)

15 3
— J
infections in patients hypersensitive to penicillins, and community- associ- There is no oral liquid formulation of clindamycin currently marketed in C

'
Australia; however, a 10 mg mL clindamycin solution can be made by o
Q
-CD ated methicillin-resistant S. aureus (CA -MRSA) infections. _
dispersing the contents of a 150 mg capsule in 15 ml of water. The solu-
c
.2
tion should be shaken or stirred until an even dispersion is formed and the IS
^
£ Some patients are hypersensitive to sulfonamide antibiotics (for informa-
§
• tion on antimicrobial hypersensitivity, see pp.25-37) . required volume should be measured immediately. The dose can be mixed
’

=
tD
3
Trimethoprim inhibits tubular secretion of creatinine, which can elevate with juice or soft food to disguise the taste before administration. The solu- fil
c CD
£ serum creatinine without any true decrease in glomerular filtration rate. tion should be prepared immediately before administering each dose, and •” T3

<D
CD
Trimethoprim also inhibits tubular excretion of potassium and can cause
hyperkalaemia. Monitor serum potassium after 3 days of treatment with tri-
uny remaining solution should be discarded. 15 .£
o
+3
O
—(/)
'OJO
_c methoprim in patients at increased risk of hyperkalaemia ( eg patients with
CD
£ -o
3

40 41
 Nitroimidazoles used in dentistry
The nitroimidazole, metronidazole, has activity against most anaerobic
bacteria (eg Peptoniphilus [formerly Peptostreptococcus ] species, R gingi -
valis, P. oralis, B. fragilis ).
Metronidazole can cause nausea, vomiting, flushing, headache and palpi-
tations if taken concomitantly with alcohol. Advise patients to avoid alcohol
during treatment and for at least 24 hours after completing the course of
metronidazole.
In these guidelines, the recommended dosage of metronidazole is 400 mg
orally or 500 mg intravenously, 12 -hourly. The 12- hourly dosing regimen is
based on pharmacokinetic data and minimum inhibitory concentrations of
the pathogens involved, in addition to limited clinical studies and extensive
clinical experience with its use.
Tetracyclines used in dentistry
Tetracyclines have a broad spectrum of antibacterial activity.
Doxycycline is the preferred tetracycline for dental indications. Doxycycline
has not been associated with tooth discolouration, enamel hypoplasia or
bone deposition, even in children younger than 8 years, so is increasingly
used in this age group. However, use is limited by the lack of a suitable
commercially available formulation (eg an oral liquid formulation).
Oesophagitis can occur with oral doxycycline. Oral doxycycline should be
taken with food and a large glass of water, and the patient should remain
re upright after administration. Photosensitivity reactions can occur with tetra -
0 cyclines; warn patients to avoid sun exposure.
Q
D
re Antifungal drugs used in dentistry
re
o This topic covers
i/> Azole antifungals used in dentistry
o §
Miconazole and clotrimazole are broad-spectrum antifungals available in
1 topical preparations either alone or in combination with hydrocortisone.
S
C!3 Use of topical azoles on the skin is generally well tolerated. Oral miconazole
s .
gel can cause mild gastrointestinal adverse effects Systemic absorption of
8a. miconazole can occur when applied topically to the oral mucosa. Azoles
: have many clinically significant drug interactions, so consult an appropriate
re resource on drug interactions (for resources, see p.61) if starting or stop-
ping azoles in patients taking other drugs.
42
Polyene antifungals used in dentistry
Topical nystatin and amphotericin B are active against Candida spe-
cios. They are poorly absorbed orally and not absorbed through the
mucosa when applied topically, so do not cause systemic effects or drug
Interactions.
Nystatin suspension has a high sucrose content (approximately 50%),
which may promote plaque accumulation and tooth decay. Otherwise,
topical intraoral polyenes have few adverse effects. Taking amphotericin
lozenges after food reduces the risk of nausea.
Antiviral drugs used in dentistry
Aciclovir and famciclovir are guanine analogue antivirals with activity
ngainst herpes simplex virus .
Oral famciclovir is available in a single dose without a prescription, as a
pharmacist-only (Schedule 3) medicine for the treatment of recurrent
herpes simplex virus infection of the lips (herpes simplex labialis or cold
sores).
Topical aciclovir is the preferred topical antiviral for recurrent herpes
simplex virus infection of the lips because it requires 5 applications per
day, whereas penciclovir (an alternative) requires 6 applications per day.
Adherence can be challenging because of the frequency of application
required. Topical aciclovir should not be applied to mucous membranes (eg
in the mouth, eye or vagina) because it may be irritant.
Drugs used to treat acute pain in
W)
dentistry <Zin
practical information on drugs used to treat acute pain §
.
in dentistry For comprehensive drug information, including precautions,
contraindications, adverse effects and drug interactions, consult an
appropriate drug information resource. If prescribing an analgesic drug
or local anaesthetic, consider the benefit-harm profile of the drug in the
Individual patient; this requires knowledge of the patient’s medical history
and concomitant medications, including prescription, over-the-counter and
c o
•“ O -
complementary medicines. U>
U
i/
no
For a more comprehensive discussion of analgesic drugs, see 'Principles of re re
-
analgesic and anti-inflammatory drug use for musculoskeletal conditions in al a
adults’ and the Analgesic topics in eTG complete.
43
 r

- For
For information on local anaesthetics used in dentistry, see pp.201 9. NSAIDs are the preferred drug class for acute dental pain; however, they
a more comprehensive discussion of local anaesthetics, see the Analgesic con cause significant renal, cardiovascular, gastrointestinal, respiratory and
topics in eTG complete. luiematological adverse effects—these are summarised in Table 3 ( p. 44).

Nonsteroidal anti-inflammatory drug use in The risk of harm from NSAIDs increases with increasing age,
higher doses, longer durations of treatment, and concomitant use
dentistry of some drugs.
Nonsteroidal anti- inflammatory drugs (NSAIDs) include nonselective cyclo-
oxygenase (COX) inhibitors and COX-2-selective inhibitors (the latter group Assessing whether NSAID use is appropriate
is sometimes referred to as coxibs). Table 2 (below) shows NSAIDs com -
NSAIDs are the preferred analgesics for acute dental pain because of their
monly used in dentistry.
nnti - inflammatory actions, efficacy for bone pain and ability to reduce
opioid requirements, nausea and vomiting, and improve pain relief when
Table 2. NSAIDs commonly used in dentistry
used as a component of multimodal analgesia.*
NSAID Frequency of oral administration [ NB1]
Before prescribing an NSAID, weigh these potential benefits against the
nonselective potential harms (see Table 3, p.44) in the individual; the risk of harm
ibuprofen 3 or 4 doses daily depends on patient factors (see below) and the NSAID used. Consider
naproxen 1or 2 doses daily [NB2]
Accessing the patient’s electronic health record to obtain more information
on their health status. If unsure of the safety of short-term NSAID use for
M patient, consult a medical practitioner. For information on choosing an
COX-2 selective
celecoxib 1or 2 doses daily Analgesic regimen for patients at risk of NSAID-related toxicity, see p.48.
NSAID = nonsteroidal anti- inflammatory drug; COX = cyclo-oxygenase
There is a low risk of harm when NSAIDs are used short-term by healthy
people who are not taking other medicines. However, even in these
NB1: The frequency of administration gives an indication of the drug'
s half-life (eg ibuprofen has
a short half-life so requires frequent dosing).
NB2: Immediate- release naproxen is dosed twice daily and modified-release naproxen patients steps should be taken to minimise harm; for practical advice to
minimise harms when prescribing short-term NSAIDs for acute dental pain,
is dosed
once daily.
75 see p. 49.
0)
Table 3. Major adverse effects of NSAIDs Conversely, NSAID use is contraindicated in some people and should be
avoided in others because of a significant risk of harm —see Box 8 (p.46)
Q
o
for patients who should not be prescribed an NSAID by a dentist. If par-
*OJ0
c System Adverse effects .£
acetamol is not expected to provide sufficient analgesia in these patients,
CD to
75 renal impaired kidney function, acute kidney failure 3

o cardiovascular
consider alternative pain management strategies or refer the patient to a c
o
increased blood pressure, fluid retention, worsening of heart
in failure, thrombosis, myocardial infarction, stroke, cardiovascular medical practitioner. c
CD death .2
Deciding whether it is safe to prescribe NSAIDs in patients with risk factors 75 E*
for NSAID - induced renal, cardiovascular or gastrointestinal toxicity is more
CD gastrointestinal oesophageal, gastric, duodenal and small bowel ulceration, upper
abdominal pain, gastric erosions, gastrointestinal bleeding
3
complex ( see pp.46-7) . Consider the cumulative risk of NSAID toxicity if O
— -o C
more than one risk factor is present.
C3 4
c <u
respiratory bronchospasm in patients with NSAID-exacerbated respiratory
.2» *”
— disease [NB1] 75 .E
o -
CD
haematological The use of NSAIDs in elderly patients (see p. 47) and pregnant or breast-
feeding women (see pp.47-8) requires extra consideration.
impaired platelet function [ NB1] £
* (!)
CD O tuO
NSAID = nonsteroidal anti- inflammatory drug 2E
- -O
o
JZ NB1: This adverse effect occurs with nonselective NSAIDs, but not COX Q
-2-selective NSAIDs. * Although most of the evidence for NSAIDs as part of multimodal analgesia comes from
postoperative pain, the findings are considered relevant for most acute pain settings. 45
44
 Box 8. Patients who should not be prescribed an NSAID by
a dentist
• patients with severe kidney impairment (eGFR of less than 30 mL/min)
• patients with severe heart failure
• patients with an active gastrointestinal ulcer or gastrointestinal bleeding
• patients with bleeding disorders
• patients taking corticosteroids or anticoagulants
• patients with multiple risk factors for increased NSAID toxicity (eg elderly
patients with a history of gastrointestinal bleeding)
eGFR = estimated glomerular filtration rate: NSAID = nonsteroidal anti-inflammatory drug
Renal toxicity
Acute kidney injury is a serious adverse effect associated with all NSAIDs.
Risk factors for NSAID-induced acute kidney injury include:
• older age
• pre-existing kidney impairment
• volume depletion (eg dehydration, sepsis) or effective arterial volume
depletion (eg due to heart failure, cirrhosis, nephrotic syndrome)
• current use of angiotensin converting enzyme inhibitors (ACEIs),
angiotensin II receptor blockers (ARBs), diuretics or other nephrotoxic
drugs.
The risk of acute kidney injury is cumulative—for example, the risk is sig-
nificantly increased if an NSAID is co-administered with an ACEI plus a
n diuretic, or if an older patient taking an NSAID develops an acute illness
s
Q
associated with dehydration.
O To choose an appropriate analgesic regimen for patients at increased risk
cu of renal toxicity, see p. 48 . hove comorbidities and take other drugs that increase their risk of NSAID-
g rolated adverse effects.
o
Cardiovascular toxicity
1 Although all NSAIDs can cause cardiovascular toxicity, not all are equally
likely to do so—evidence is evolving. Furthermore, the relationship between
5 duration of NSAID use and onset of toxicity is not fully understood. It is
clear that the risk of cardiovascular toxicity increases with longer dura-
Risk factors for increased cardiovascular toxicity with NSAID use include:
• established cardiovascular disease (eg myocardial infarction, stroke)
• risk factors for cardiovascular disease (including smoking, older age,
elevated blood pressure, dyslipidaemia and diabetes) .
II a decision is taken to use an NSAID in a patient at increased risk of
cardiovascular toxicity, see p.48 for suitable choices.
Gastrointestinal toxicity
Itisk factors for increased gastrointestinal toxicity with NSAID use include:
• older age
• history of upper gastrointestinal bleeding or peptic ulcer disease
• Helicobacter pyiori infection
• current use of drugs that increase the risk of upper gastrointestinal
bleeding or perforation (eg anticoagulants, antiplatelet drugs, selective
serotonin reuptake inhibitors [SSRIs], serotonin and noradrenaline
reuptake inhibitors [SNRIs], systemic corticosteroids)
• significant comorbidity
• smoking.
II a decision is taken to use an NSAID in a patient at increased risk of
gustrointestinal toxicity, see p.49 for suitable choices.
Elderly people
Assess the need for NSAIDs in elderly people particularly carefully. Elderly
( Kiopleare generally at increased risk of renal, cardiovascular and gastro-
intestinal adverse effects of NSAIDs. Elderly people are also more likely to
'3
3
If a decision is taken to use an NSAID in an elderly patient, see p.48 for
§
suitable choices; NSAIDs with a short half-life are preferred (see Table 2, §
p.44) .
ES
Women who are pregnant or breastfeeding fit
~ -o4
C )

s.
Q
tions of therapy and higher doses. Short-term use (ie less than 5 days) of
NSAIDs does not significantly increase the risk of cardiovascular events,
If possible, avoid NSAIDs throughout pregnancy. The safety of NSAID use
( luring the first 8 weeks of pregnancy is uncertain. NSAIDs should not be
B E
O —
V </>
£5 and can reduce the requirement for opioids. o eo
jy used beyond 32 weeks of gestation because they can be associated with to 3

adverse maternal and fetal outcomes. £ -5

46 47

There are fewer data on the use of C0X-2-selective NSAIDs than nonselec -
tive NSAIDs in pregnancy, so if a decision is taken to use an NSAID in
a pregnant woman up to 32 weeks’ gestation, a nonselective NSAID
is
preferred.
Do not use NSAIDs in pregnant women beyond 32 weeks’
gestation.
Small amounts of NSAIDs are excreted into breast milk; however, these
amounts are unlikely to cause harm to breastfed infants. Ibuprofen is the
.
preferred NSAID for women who are breastfeeding Advise breastfeeding
mothers to feed their baby just before taking their medication, to minimise
the amount of drug in the breastmilk.
See Appendix 1(pp.277-86) for more information on NSAID use in preg-
nancy and breastfeeding.
Choosing an analgesic regimen for patients at
increased risk of NSAID-related toxicity
Consult with a medical practitioner if unsure of the safety of short-term use
of an NSAID for a particular patient.
Recognise patients that should not be prescribed NSAIDs by a dentist (see
.
Box 8, p.46) If paracetamol is not expected to provide sufficient analgesia
p.47),
Recognise patients at increased risk of gastrointestinal toxicity see
(
and:
• avoid nonselective NSAIDs (eg ibuprofen, diclofenac, naproxen
)
• use a COX-2-selective NSAID (eg celecoxib * )
for
• if a COX-2-selective NSAID cannot be used, use paracetamol alone
mild to moderate pain (for analgesic regimens, see p .140 for children
or p.138 for adults), or, in adults, paracetamol with oxycodone for
severe pain (for analgesic regimens, see p.139).
In patients who have had NSAID-induced bronchospasm:
• avoid nonselective NSAIDs (eg ibuprofen, diclofenac, naproxen)
• use a COX-2-selective NSAID (eg celecoxib).
Practical advice to minimise harms when
prescribing short- term NSAIDs for acute dental
pain
acute
To minimise harms in all patients prescribed short-term NSAIDs for
dental pain, advise the patient to:
• take the NSAID regularly (rather than as required) using the lowest
effective dose
• use the NSAID for the shortest duration possible, and not more than
5 days—the risk of adverse effects may increase after 5 days of
use

_ns paracetamol and, as soon as possible, stop

in these patients, consider alternative pain management strategies or refer • combine the NSAID with
the patient to a medical practitioner. the NSAID then use paracetamol alone
• seek review if the NSAID is still required after 5 days to avoid
Recognise patients at increased risk of renal toxicity (see p.46), and: inadvertent long-term use.
c
Q • consult a medical practitioner to determine if NSAID use is adverse
Il Is no longer advised that NSAIDs be taken with food to reduce
appropriate, unless paracetamol alone is expected to provide sufficient
there is no evidence to support this approach . Additionally,
ra analgesia. effects, because
, reduces the rate of !§
g taking NSAIDs with food delays the peak concentration
O Recognise patients at increased risk of cardiovascular toxicity (see p.46), absorption, and can result in less effective relief of acute pain. §
jg and: §
E
T5
• consider that ineffective pain relief can cause tachycardia, which may
cause adverse cardiovascular effects
Paracetamol use in dentistry
I aracetamol has analgesic and antipyretic actions and a low incidence
of P
E. <£
5 • avoid diclofenac and C0X- 2-selective NSAIDs other than celecoxib ’ effects compared with other analgesic drugs. However , in over-
g • use celecoxib or ibuprofen (naproxen can be used, but has a higher
adverse
dose, it can lead to severe hepatotoxicity.
c 0
•“ -o
U< >
•

o risk of gastrointestinal adverse effects) but limit treatment to 5 days

/
S • if celecoxib, ibuprofen and naproxen cannot be used, use paracetamol
a?
alone for mild to moderate pain (for analgesic regimens, see p.140 effects than 0. -o
h1
for children or p.138 for adults), or, in adults, paracetamol with * C0X - 2-selective NSAIDs have a lower risk of gastrointestinal adverse
if the patient is taking low -
nonselective NSAIDs; however, this advantage may be reduced
48 oxycodone for severe pain (for analgesic regimens, see p.139). dose aspirin concurrently . 49
 Although generally less effective than NSAIDs for acute dental pain, par • be familiar with the opioids suitable for use in dentistry and the
f- - a
acetamol is the drug of choice when NSAIDs are contraindicated because formulations in which they are available (for information on choosing
of its favourable safety profile. suitable opioid, see p.53)
,
Paracetamol is used in combination with other analgesics for the treatment • know how to manage potential drug interactions and adverse effects
verbal and written education to patients about
of acute dental pain because this can result in enhanced pain manage and provide appropriate
ment, or synergistic analgesia. As a component of multimodal
- sedative effects (for advice on managing the harms of opioids, see
analgesia,
paracetamol reduces the requirement for opioids. -
P 52)
• prescribe the lowest dose for the shortest duration possible, because
Paracetamol is available in multiple formulations (eg immediate-release, long-term opioid use often starts with the use of opioids to treat
acute
modified- release) and in combination with other drugs. Therefore, patients pain
should be advised to consider the paracetamol content of all their medica- the legislation about prescriptions and prescribing of drugs of
tions, to avoid inadvertent ingestion of higher than recommended doses.
• consider
dependence (see pp.9-10) .
In adults with significant liver disease, or who are underweight, cachectic
or frail, reduced doses are often inappropriately used. This may Prescribe the lowest dose of opioid for the shortest duration
result in
inadequate analgesia and, consequently, use of more harmful analgesics possible, because long-term opioid use often starts with the use
Therapeutic doses are not hepatotoxic in these patient groups, but
. of opioids to treat acute pain.
there
is an increased risk of liver damage if supratherapeutic
doses (ie doses
greater than 4 g in 24 hours) are inadvertently taken. Harms of opioids
In obese children, the dose of paracetamol should be calculated spec -
using Unnerally, when given in equianalgesic doses, opioids have a similar
ideal body weight rather than actual body weight (see also Table
14, and incidence of adverse effects; however, there can be significant
p.143).
Interpatient variability. Elderly or frail patients may be particularly sensitive
When prescribing paracetamol, the dose should be stated in grams or to opioids, so require careful monitoring.
mil-
ligrams rather than the number of tablets or volume of liquid,
unless the Hnrms associated with opioids include:
exact formulation to be administered has been specified.
• adverse effects—serious adverse effects (eg opioid-induced
75 ventilatory impairment, accidental death) are more likely to occur
g Opioid use in dentistry when opioids are used in high doses or concomitantly with other
sedative drugs (eg benzodiazepines, alcohol, cannabis). Table 4 .52
(p )
Q
In combination with nonopioid analgesics and nonpharmacological - opioid use ; for a
O lists adverse effects that can occur with short term
measures (eg dental treatment), an opioid may be used for acute severe
more detailed discussion of the adverse effects of opioids, see the
1
03
nociceptive dental pain in adults (eg pain associated with major
s
o —
trauma,
severe postoperative pain) for analgesic regimens, see p.139. Opioids
Analgesic topics in eTG complete
§
should not be used for pain that is chronic, neuropathic or nociplastic, or • aberrant behaviour (eg diversion, nonmedical use, abuse,
8
1
for pain in children, except by specialists. —
addiction) the risk of opioid abuse is high; in some studies, opioid
abuse was reported in more than 20% of patients taking long-term
I
Safe prescribing of opioids in dentistry requires the practitioner to: opioids for chronic noncancer pain
13
§2 ^
o • be familiar with the indications for which opioid use is appropriate • risk of overdose—increased opioid prescribing rates have been c o
• be familiar with the suitability of opioid use in specific populations associated with a significant increase in the number of fatalities •” TJ

5
2
(eg elderly or frail patients, opioid-tolerant patients)
because there is
significant interpatient variability in the response to opioids
involving opioids
• neuroadaptive and physiological changes (eg opioid tolerance,
«
o —
C
'43 </)
o ‘OJO
opioid dependence, opioid-induced hyperalgesia) —may occur after
£2 -S
a; • weigh potential benefits of opioid use in an individual against potential 3

harms (for harms of opioids, see p.51) 7 to 10 days of use.

50 51
 Table 4. Adverse effects with short-term use of opioids [NB1] Constipation is a frequent adverse effect of opioids—advise patients to
System Adverse effects obtain a stimulant laxative ( eg docusate with senna) if it becomes an
respiratory opioid-induced ventilatory impairment (excessive
Issue.
sedation with
or without a decrease in respiratory rate [NB2]), which is more
marked during sleep Choice of opioid in dentistry
accidental death t in
Immediate-release opioids commonly used for acute pain managemen
increased risk of sleep-disordered breathing (central or obstructive
apnoea) dentistry include oxycodone , tramadol and tapentadol . Tramadol and tap -
have
ontadol are sometimes referred to as atypical opioids, because they
cough suppression
multiple mechanisms of action in addition to mu- opioid receptor agonism
.
neurological delirium, sedation, dysphoria or euphoria, miosis, impaired
rec -
cognition Despite significant clinical experience with its use, codeine is no longer
because its use is associated with more
other adverse effects can occur in patients with renal impairment ommended for pain management
cardiovascular bradycardia, vasodilation and hypotension (including postural harm than benefit.
—
hypotension) usually only seen after the use of large
intravenous Table 5 ( p.54) summarises the advantages and disadvantages of opioids
doses during anaesthesia or if the patient is hypovolaemic
commonly used in dentistry.
dermatological pruritus [NB3]

—
widespread urticaria suggests an allergic response
gastrointestinal nausea, vomiting, constipation, spasm of the sphincter of Oddi Corticosteroids used in dentistry
urinary urinary retention and difficulty with micturition, increased external
Ibis topic covers practical information on using corticosteroids in dentistry
.
sphincter tone, decreased detrusor muscle tone a-
I or comprehensive drug information, including precautions, contraindic
NBl: For a more detailed discussion of the adverse effects of opioids, drug
in eTG complete.
see the Analgesic topics tions, adverse effects and drug interactions, consult an appropriate
resource . For a more comprehens ive discussion of corticoster-
NB2: A decrease in respiratory rate is an unreliable indicator of opioid information
-induced ventilatory dulatory drug use for rheumatolo gical
impairment, which can coexist with a normal respiratory rate.
Sedation is a more sensitive oids, see ‘Principles of immunomo
indicator of opioid-induced ventilatory impairment. diseases in adults’ in eTG complete.
NB3: Opioid-induced pruritus is not associated with a rash and is
thought to be due to an action
If prescribing a corticosteroid, consider the benefit-harm profile of the
on opioid receptors. drug
75 ’s medical
in the individual patient; this requires knowledge of the patient
Q>
history and concomitant medications, including prescription, over -
the-
-c
Q
Adverse effects can be limited by using the lowest dose for the tary medicines .
a shortest counter and complemen
duration possible.
"CUD

CO oral .E
75 Corticosteroids are used in the management of many dental and n )

Provide appropriate verbal and written education to patients and their

o-
3
s
mucosal inflammatory conditions . In dentistry, routes of administra tion of
c
carers about the sedating effects of opioids, including: o
Corticosteroids include: c
• topical (on the oral mucosa ) —see pp.55-6
CO
o • not to drive or operate machinery
.2
o • how to recognise the signs of excessive sedation (eg not being able to
• intradental (within a tooth)—see p.56 75
.2
3
stay awake or be roused from sleep)
• systemic (oral, intramuscular or intravenous administration) —see £ 7o
CD • to seek medical attention if they become excessively
sedated (because
this can be an early indicator of ventilatory impairment) or experience
.
p 57. •” -D
c 0 )

0
Q
2
. other concerning adverse effects. The route of administration should be tailored to the clinical situation
dentistry, intradental or topical corticostero ids are preferred because
. In
they
75
o
+o3
—c
if )
TOO

^
is
ero associated with fewer systemic adverse effects, and a local effect 2E
-
0
-0 Advise patients and their carers of the sedating effects of opioids ol
often sufficient. Local intraoral injection of corticoster oids is not appro - O

priate nor recommended for dental procedures. 53

52
 Table 5. Advantages and disadvantages of immediate- Topical corticosteroids used in dentistry
release opioids commonly used in dentistry , mouthwashes,
In dentistry, topical corticosteroids (eg creams, ointments oral
Opioid Advantages and disadvantages iprays) are used to manage the symptoms of immune- mediated
or per-
Commonly used in pain management mucosal diseases, including conditions that present with recurrent
substantial clinical experience with
mstent oral ulceration. Although there is
oxycodone preferred opioid for severe acute nociceptive dental pain
in these use of topical corticosteroids , this practice is off- label and sup-
guidelines because of: intraoral
• widespread experience with its use l>orted by little published evidence.
• fewer drug interactions than tramadol potency cortico-
In the general practice setting, only mild or moderate
utoroid creams or ointments should be used. Potent
• more predictabele pharmacokinetics and greater efficacy than or very potent creams
codeine
corticosteroids , should not be
tramadol
or ointments, or other formulations of topical , .
alternative in patients who cannot tolerate other opioids or who are potency
allergic to opiate derivatives ntnrted without specialist advice. Table 6 (below) lists the relative
wide range of potential adverse effects and drug interactions, i > 1 corticosteroid creams and ointments .
including
serotonin toxicity [NB1]
on the
tapentadol alternative in patients who cannot tolerate other opioids or who are Tnble 6. Properties of topical corticosteroids used
allergic to opiate derivatives oral mucosa .
more potent opioid effect than tramadol Drug [ NB2] Strength
Comparative potency
immediate-release oral formulations are not available on the PBS on oral mucosa [NB1]
No role in pain management
Suitable to prescribe without specialist advice
codeine there is no good evidence that codeine (even in doses of 60 hydrocortisone acetate 1%
mg) is mild
any more effective than paracetamol or NSAIDs, or improves
analgesia triamcinolone acetonide 0.02%
when combined with paracetamol or an NSAID moderate
codeine-containing preparations have been abused betamethasone valerate 0.02%, 0.05%
codeine is a prodrug that is metabolised to morphine—there is
significant interpatient variability in this conversion, and Do not prescribe without specialist advice
some patients
experience either minimal analgesic effect or morphine
toxicity betamethasone valerate 0.1%
potent
there is a known increased risk of toxicity in certain patient groups, 0.1%
including: methylprednisolone
<D aceponate
a • patients who are ultrarapid metabolisers of codeine
~a • breastfeeding mothers betamethasone dipropionate 0.05% •op

cu • children younger than 12 years 0.1%

mometasone furoate tf)
• children 12 to 18 years who have recently had a
tonsillectomy and/ 0.05% in optimised
or adenoidectomy for obstructive sleep apnoea [NB2] betamethasone dipropionate
O
very potent
vehicle §
NSAID = nonsteroidal anti-inflammatoiy drug; PBS = Pharmaceutical
CD NB1: Signs of serotonin toxicity include altered mental status (eg
Benefits Scheme
clobetasol propionate [NB3] 0.025 to 0.05% §
agitation, anxiety, restlessness,
1
confusion), autonomic stimulation (eg increased heart rate,
increased blood pressure,
NHL : Topical corticosteroids are more potent when applied to
the oral mucosa than when S£
2
fever, sweating, dilated pupils) and neuromuscular excitation (eg
. tremor, clonus,
applied to the skin. 5
s hyperreflexia, myoclonus, rigidity)
and an ointment.
NB2: For more detail, see the Therapeutic Goods Administration ( )
TGA Medicines Safety Update
NB2: All formulations in this table are available as both a cream
registered for use in Australia, but
— -o
c o
B
u
for codeine (Volume 8, Number 5). NU3: Clobetasol propionate as a cream or ointment is not
-sas.htm > or
is via the Special Access Scheme < www.tga.gov.au/hp/access
available
.
compounding pharmacies Use only under specialist supervision.
& -O JD
M CO
*0
a3 SE
£ £
54 55
 r
Prolonged or sustained use of moderate, potent or very potent topical being treated and where
twment. The form used depends on the condition
corticosteroids requires regular monitoring. Use of these higher potency Ihn compound is to be placed.
corticosteroids increases the risk of systemic absorption, either through the with
oral mucosa or if inadvertently swallowed. Adrenal suppression Combination corticosteroid and antibiotic pastes (eg triamcinolone
has been used within the root canal system
documented with the use of high-potency topical corticosteroids. clindamycin or demeclocycline) can be
Of (i tooth (intracanal application). Pastes can be used:
Local adverse effects include superimposed candidiasis, mucosal atrophy,
capillary fragility, telangiectasia, delayed wound healing and • during endodontic treatment
pigmentation. Predisposing factors for candidiasis include
altered • to reduce periapical inflammation and pain associated with irreversible
immune compro- pulpitis or an infected root canal system
mise, smoking, denture use and hyposalivation. resorption
• to prevent and manage several forms of inflammatory root
Select a topical corticosteroid based on potency, lesion size and ( eg internal inflammatory resorption, external apical inflammatory
location,
and the patient's preference and ability to adhere to
instructions. Creams resorption, external lateral inflammatory resorption)
are water-based and easily applied to the oral mucosa, whereas oil-based and
• to reduce external replacement resorption following tooth avulsion
ointments may be more difficult to apply; however, patients may have a intrusive luxation injuries.
preference because of taste, texture and ease of use.
other
Combination corticosteroid and antibiotic cements typically contain the
The patient's pharmacist or medical practitioner may not be familiar
with lubstances (eg calcium hydroxide , zinc oxide, eugenol ). To prepare
intraoral use of topical corticosteroids. Provide patients with written instruc paste. The paste is
- Oernent, a powder and liquid are mixed to form a
tions that can be shared with their healthcare practitioner to explain , and sets to form a hard cement.
the plnced on the dentine or exposed pulp
practice. See Box 9 ( below) for instructions on application :
of topical corti- Cements can be used
costeroids to the oral mucosa.
• within the crown of a tooth as part of a cavity lining or base
Box 9. Patient instructions for applying a topical • as an indirect pulp cap
corticosteroid to the oral mucosa • as a direct pulp cap
• as a pulpotomy agent before restoring cavities in teeth that have
• It is not necessary to dry the mucosa first.
reversible pulpitis.
• Apply a pea-sized amount of the cream or ointment to a clean
fingertip, then
Systemic corticosteroids used in dentistry
TO smear a thin layer onto the affected area.
§ • Hold in the mouth for 1to 2 minutes without swallowing, and then spit
excess.
out
a or dental
Systemic corticosteroids are rarely appropriate for treating oral
D
• Follow the dentist's instruction for frequency of application. they are associated with significant adverse effects— •M
conditions because
used in
local applications are usually effective (for topical corticosteroids 3i
TO '

• Ideally, apply the corticosteroid after meals or oral hygiene practices. TO

o
TO
• Although the cream will be labelled 'For external use only', use on the oral (Jnntistry, see pp.55 - 6).
mucosa is safe—systemic absorption from the mouth is minimal if used as should only be prescribed by a dental specialist:
is instructed.
Systemic corticosteroids §
Indications for systemic corticosteroids include:
• severe postoperative swelling
5 Intradental corticosteroids used in dentistry • severe trauma
Intradental corticosteroid and antibiotic combinations can be used
to
• periapical nerve sprouting and acute apical periodontitis following —c -aa>
3 manage pulp and periapical diseases, which are caused by bacteria
and
removal of acutely inflamed pulp
inflammation. Dental treatment is also required. • Inflammatory mucosal disease.
Q.
2
5S
— of postopera- -S
0
I Two forms of corticosteroid and antibiotic combinations are
commercially
Do not routinely use systemic corticosteroids for the control £
tive pain and swelling.
. .
available
U1
for intradental use—a water-soluble paste and a hard-setting
56 57
 Iwiyond the gingival crevice or
.
periodontal pocket Patients should
be
is
Mouthwashes and other topical Informed that the principal treatment
for chronic periodontal disease
and meticu-
with debridement of involved teeth
formulations used in dentistry
.
litolossional intervention
inii' oral hygiene. Although
for periodontal disease,
they are not appropriate as the
antiseptic mouthwashes can be
sole treatment
beneficial in some
This topic covers practical information on using mouthwashes and other with gingivitis (see p.71)
use in patients
topical formulations in dentistry. For comprehensive drug information, circumstances (eg for short-term ) when inflammation restricts normal
including precautions, contraindications, adverse effects and drug inter- Of necrotising gingivitis (see p.73
actions, consult an appropriate drug information resource. If prescribing Inothbrushing) .
a mouthwash or another topical formulation, consider the benefit-harm
profile of the drug in the individual patient; this requires knowledge of the
patient's medical history and concomitant medications, including prescrip-
Chlorhexidine some
fungicidal, and has activity against
tion, over-the-counter and complementary medicines. Clilorhexidine is bactericidal and surfaces so is effective over a pro-
oral
viruses. Chlorhexidine adsorbs
onto
on a clean tooth surface, but
longed period. It prevents plaque formation
Mouthwashes used in dentistry (loos not reduce pre-existing plaque
.
Antiseptic mouthwashes (see below) decrease the number of microorgan- include mouthwash (as chlorhexidine
isms in the oral cavity and can be used for periodontal disease, dental
Immoral chlorhexidine formulations and 0.2%), gel and a slow-release
gluconate in concentrations of 0.12
%
caries, and pre- and post- procedural mouth rinsing. periodontal pockets.
formulation for local delivery into
Fluoride mouthwashes (see p.60) have significant benefits in patients at mouthwash was inactivated by
II was previously thought that chlorhexidine toothpaste; however,

.
high risk of dental caries, but should only be used on the recommendation sulfate used in standard
Hie detergent sodium lauryl unlikely that there is
of a dentist. case. Although it is
re' oarch has shown this is not the gel, further
Anti-inflammatory and analgesic mouthwashes (eg benzydamine; see p.60) mi interaction between
sodium lauryl sulfate and chlorhexidine
this.
provide symptomatic relief of some inflammatory oral mucosal diseases. evidence is required to confirm
, irritate mucosal surfaces and
Lubricating mouthwashes (eg artificial salivary products, sodium bicarbo- Chlorhexidine can cause skin reactions ,
Interrupt wound healing. Intraoral
use can cause a burning sensation
nate) can provide temporary symptomatic relief of dry mouth (see p.121). ; it can also cause brown
formation
S altered taste and increased calculus buccal cavity and margins of dental
decolouration of the teeth, tongue
§ Alcohol-containing mouthwashes may be associated with oral cancer, ,
be professionally
Q and should be avoided if possible. In addition, patients with oral mucosal . Extrinsic staining is not permanent and can w>
restorations recommended for short
removed from the teeth. Chlorhexidine
-a disease and dry mouth should avoid alcohol-containing mouthwashes is usually 3)
because they cause profound drying of the oral mucosa. adverse effects . 3
periods of up to 2 weeks to minimise
CC
§
£ has been reported, sometimes
so severe as to be life
°
a)
Topical antiseptics for intraoral use Chlorhexidine allergy
threatening. If a patient reports a
history of allergy to chlorhexidine
, including topical
, it must
application.
§
it
S Antiseptic mouthwashes decrease the number of microorganisms in the ho avoided via all routes of administration IS
oral cavity.
—-
p
c a>
O Antiseptic mouthwashes can reduce plaque formation but do not reduce Hydrogen peroxide o
£ existing plaque, which must be removed with mechanical cleaning.
topical hydrogen peroxide has
antiseptic properties. Short-term use of low-
adversely
U
S Antiseptic mouthwash is not required as part of a standard oral hygiene mouthwash (eg 1.5%) does not o fj)
routine (for more information on oral hygiene, see p.273).
i dncentration hydrogen peroxide
of the mouth. However , higher concentra - 22
to
nffoct the hard or soft tissues can cause ol -O
Oj (eg 30 to 35% ), such as in tooth-bleaching products,
—
i The use of antiseptic mouthwashes in periodontal disease is controversial. tions
They are only effective against supragingival plaque, and are not effective 59
58
 hydroxyapa -
mucosal burns. Reversible hypertrophy of the papillae of the
tongue can moro resistant to future acid challenge than the carbonated
occur with continued use of hydrogen peroxide mouthwash. enamel .
lltnu of normal tooth
high concentrations.
fluoride ions have an antimicrobial effect at very
Other topical antiseptics formulations with a low pH (eg acidulated phosphate fluoride) also have
Cetylpyridinium chloride is a quaternary ammonium compound mime antimicrobial activity.
with , gel, foam and
surfactant, detergent and antibacterial properties; intraoral
formulations I luoride formulations; include toothpaste, mouthwash
.
include mouthwash, gargle and lozenges Some formulations
combine varnish. The . recommended
i concentration of fluoride toothpaste varies
on the use
cetylpyridinium chloride with a local anaesthetic or an anti-
inflammatory. HI cording to age and risk of dental caries
. For more information
Povidone-iodine has antibacterial, antifungal and antiviral properties Of fluoride for dental caries , see p.66.
;
intraoral formulations include mouthwash and gargle. Povidone-iodine
can
cause irritation of skin and mucous membranes. It is absorbed
damaged skin so application over a large area of broken skin is
through Casein phosphopeptide-amorphous calcium
not recom- phosphate
mended. Povidone-iodine should not be used during pregnancy or
lactation
because it can cause hypothyroidism in the neonate. .
i nttoin phosphopeptide-amorphous calcium phosphate CPP-ACP
( )
, which combine with fluoride
con-
Mouthwashes containing essential oils (eg eucalyptol, menthol thymol, Irtins bioavailable calcium and phosphate ions
include sugar-
to promote enamel remineralisation. CPP-ACP formulations
methyl salicylate) have been found to have antiseptic
properties and and varnish, some of which also contain fluoride.
reduce plaque formation, but there is limited independent lino chewing gum, paste
evidence of proteins. For more informa -
benefit. Avoid CPP-ACP in patients with allergies to milk
tion on the use of CPP- ACP for dental caries, see p.69 .
Triclosan is not recommended.

Topical intraoral benzydamine Sources of drug information

_ Benzydamine is a nonsteroidal anti-inflammatory drug (NSAID) with anal
gesic properties, used for temporary relief of painful
inflammatory oral
- Recommended sources of drug information include the
books, electronic resources and websites:
following journals,

2 mucosal conditions. Benzydamine formulations include

mouthwash,
5
®
intraoral gel and spray, in concentrations of 0.15 to 1% . Some formula- Journals
tions combine benzydamine with an antiseptic.
the Australian Dental M
Aimlralian Dental Journal ( ADJ) (can be accessed via
Awociation website < www.ada.org.au >)
ra Local adverse reactions of benzydamine, such as numbness,
burning, 3
ro erythema and rash, have been occasionally reported
. Systemic adverse Amtralian Prescriber < www.nps.org.au/australian -
prescriber > g
O reactions are uncommon.
in
tu
3
*
books and electronic resources
| Topical remineralising agents independently prepared source of §£
Australian Medicines Handbook (AMH)—
; also includes drug interactions, calculators
nvidonce -based drug information
o Fluoride nod average weight and height for children ; updated electronically biannually
e <D
“o -
»nd in print annually (can be accessed via the Australian
Dental Association as
o
cp
Fluoride significantly reduces the incidence of dental caries
applied fluoride promotes enamel remineralisation
. Topically
Website < www .ada .org.au > )
'3
o ntt
m
through the formation of E2
—
i
fluoride-containing apatites (eg fluorhydroxyapatite, fluorapatite),
which are o. -o

60 61
 Therapeutic Guidelines —a source of accurate, independent and practical
.
treatment advice for a wide range of clinical conditions eTG complete
integrates all Therapeutic Guidelines topics in a searchable digital product
.
< www.tg org.au>
AusDI —provides a comprehensive up -to- date medicines database that includes Dental caries
independent drug monographs, product summaries, and pharmaceutical
company information (can be accessed via the Australian Dental Association
website < www.ada.org.au> )
MIMS —contains product information as provided by pharmaceutical companies Pathology and diagnosis of dental caries
and approved by the Therapeutic Goods Administration

Any recent textbook on clinical pharmacology Dental caries (tooth decay) is a pathological process resulting in localised
destruction of tooth tissue.
Websites Dental plaque ( a complex biofilm of mixed bacteria and their by-products)
Is a prerequisite for dental caries development. Frequent exposure to
Pharmaceutical Benefits Scheme ( PBS) < www.pbs.gov.au>
dietary sugar and carbohydrates leads to an increase in the population
Australian Dental Association < www.ada.org.au > of cariogenic bacteria in the biofilm. Cariogenic bacteria produce organic
acids, which lower the pH of the biofilm, resulting in enamel demineralisa -
.
NPS MedicineWise < www.nps org.au >
tion ( loss of carbonated hydroxyapatite).

Figure 4 (below) and Photo 1(p.64) show the stages of dental caries.

Figure 4. Stages of dental caries and its sequelae

enamel
15
© © ©
0
o
o pulp
c mucosa
03
15
o
to
OJ
£CD
zs bone to
O .2
.9 5
(
o
CD
Cl
CD
© 15
M

CD 0
JZ
1. carious ‘white spot’ .
3 large cavity involving the pulp O
2. initial cavity 4. periapical abscess
62 63
 Photo 1. Early carious lesions and cavities
Dental caries management strategies
Prevention and minimal intervention management of dental caries
( before cavitation has occurred) can involve several strategies that promote
remineralisation and arrest further decay. Individualise the management
approach by tailoring strategies to the patient’s risk factors, such as:
• dietary modification, avoiding sucrose in sticky forms and limiting
other sugars (eg acidic drinks) and carbohydrates as snacks between
meals
• plaque reduction by cleaning the teeth
brushing at least twice a day with a toothpaste containing fluoride
early carious lesions (white spots) cavities (see p.66)
interdental cleaning (eg flossing), preferably immediately before
Early carious lesions present as white spots on the tooth that have a brushing*
relatively intact surface. Early diagnosis of carious lesions maximises the • tooth surface modification
opportunities for their arrest and reversal. They can be accurately assessed using remineralising agents (eg fluoride; see p.66)
and monitored by either traditional methods (eg visual and radiographic placing fissure sealants and other adhesive materials that protect
techniques), or newer technologies involving laser and light-induced the tooth surface
fluorescence.
• saliva modification
Continued subsurface demineralisation leads to cavitation. If untreated, addressing causes of dry mouth (see p.121)
cavitation gradually progresses through the enamel and dentine towards using low-acid, sugar-free chewing gum or lozenges, or nonacidic
the dental pulp, leading to: coarse foods (eg carrots) to increase salivary flow and buffering
• pulpitis capacity of saliva .
• pulp necrosis
n Additional strategies for patients at elevated risk of dental caries
M • infection of the root canal system Include acidulated or higher concentration fluoride products (see p.66),
Q
<1) • apical periodontitis non -fluoride remineralising agents (see p.69) or chlorhexidine (see p.70).
o • periapical abscess (for management, see p.81) Perform a thorough assessment of the patient (eg age, other medications,
03 • spreading odontogenic infection (for management, see pp.82-6). disease risk) and use clinical judgment to determine an appropriate individ-
g ualised management strategy. For further information on individual dental
o caries management protocols, see the International Caries Classification
co Dental caries risk assessment nnd Management System < www.iccms- web.com> .
If cavitation has occurred, remove the infected tooth structure and
Dental caries risk assessment involves quantification of risk factors such as restore the cavity using minimally destructive methods and adhesive dental
5 diet, saliva quality and quantity, plaque characteristics, oral hygiene habits, materials. o>
and use of fluoridated products.
S
•
8
8_ Early modification of these factors is part of the primary preventive
Q
strategy (for management strategies, see p.65). The International Caries 15
2
0
Classification and Management System provides further information on 0)
individual dental caries risk assessment and management protocols (see ‘ Although there is little evidence to suggest interdental cleaning (flossing or interdental O
brushing) reduces caries, it is an important part of oral hygiene that reduces interdental
64 < www.iccms-web.com>). plaque. 65
 Fluoride Table 7. Recommended concentration of fluoride
toothpaste according to age and risk of dental
Toothpastes containing fluoride significantly reduce the incidence of dental caries [NB1]
.
caries Fluoride promotes enamel remineralisation through the formation of
Toothpaste for people not at elevated risk of dental caries
fluoride-containing apatites (eg fluorhydroxyapatite, fluorapatite) , which are
more resistant to future acid challenge than the carbonated hydroxyapa child younger than 18 months twice -daily brushing without toothpaste
-
tites of normal tooth enamel. Toothpastes that do not contain fluoride
provide little protection against dental caries.
child 18 months to younger than
6 years twice daily, pea-sized amount [NB2] '
500 to 550 ppm (0.5 to 0.55 mg g) fluoride

1000 to 1500 ppm (1to 1.5 mg/g) fluoride

child 6 years to adolescent
twice daily
Toothpastes that do not contain fluoride provide little protection
against dental caries . adolescent or adult 1000 to 1500 ppm (1to 1.5 mgfg) fluoride
twice daily

The recommended concentration of fluoride toothpaste varies according Toothpaste for people at elevated risk of dental caries [NB3]
to age and risk of dental caries (see Table 7; p.67). Children up child younger than 18 months twice-daily brushing with toothpaste may be
to
6 years of age are at increased risk of dental fluorosis— a mineralisation recommended [NB2]
disorder of the teeth caused by excessive ingestion of fluoride during the child 18 months to younger than 1000 ppm (1mg/g) fluoride twice daily [NB2]
tooth-forming years. In patients with dental fluorosis, the porosity of the 6 years OR
subsurface enamel is increased and discolouration can occur (eg white more frequent use of 500 to 550 ppm (0.5 to
spots, mottling) . 0.55 mg/g) fluoride [NB2]

To minimise ingestion of fluoride, after brushing the teeth, toothpaste child 6 years to adolescent more frequent use of 1000 to 1500 ppm (1to
1.5 mg/g) fluoride [ NB 2 ]
should be spat out and not swallowed. The mouth should not be rinsed,
to
allow increased uptake of fluoride from the saliva. adolescent or adult
OR
^
5000 ppm (5 m g) fluoride twice daily

Do not rinse the mouth after brushing with fluoride toothpaste. more frequent use of 1000 to 1500 ppm (1to
1.5 mg/g) fluoride
To ppm = parts per million
c Use other topical fluoride products ( eg mouthwash, gel, varnish) in patients rinse the mouth after use to allow
NBl: Spit out fluoride products to minimise ingestion; do not
at elevated risk of dental caries (see Table 8; p.68). increased uptake of fluoride from the saliva.
Q
T3 NB2: Advise parents of the risk of fluorosis and the need to supervise
.
toothbrushing
c Water fluoridation is an effective, inexpensive and safe community health
NB3: Toothpaste use may be varied as needed, based on the dentist
’s clinical judgment.
measure to prevent dental caries. Individuals without access to community
i

0
- .
water fluoridation are at elevated risk of dental caries— see Table 7 (p 67)
- for recommended fluoride toothpaste concentrations or Table 8 (p.68) for

^—^
other topical fluoride products. Fluoride supplements in the form of drops
or tablets are no longer recommended because of limited efficacy and the
risk of dental fluorosis. C/)
o 2
.9
Fluoride supplements in the form of drops or tablets are no longer c5
o
Q
Q.
recommended . 15
2 4
jjj
o <1>
x: a

66 67
 Table 8. Examples of topical fluoride applications for
patients at elevated risk of dental caries [NB1]
Formulation Usual directions for use
neutral fluoride mouthwash Use in adults and children 6 years or older daily. Patients
220 ppm (0.22 mg/mL) should rinse in the mouth for 1minute at a time of day
when toothpaste is not used [NB2].
neutral fluoride mouthwash Use in adults and children 6 years or older weekly or
900 ppm (0.9 mg/mL) more frequently if indicated. Patients should rinse in the
mouth for 1minute at a time of day when toothpaste is
not used (NB2 ].
neutral fluoride toothpaste Use in adults and adolescents twice daily for
5000 ppm ( 5 mg/g) toothbrushing instead of 1000 to 1500 ppm (1to
1.5 mg) fluoride toothpaste, continued indefinitely
[ NB2 ].
Although available over-the-counter, it must be
recommended by a dental practitioner.
fluoride varnish 22 600 ppm Use in adults and children 1year or older usually twice a
(22.6 mg/mL)
year depending on dental caries risk.
Applied by a dental practitioner to all at-risk dental
surfaces.
acidulated phosphate Use in adults and children 10 years or older usually twice
fluoride gel or foam a year depending on dental caries risk.
12 300 ppm (12.3 mg/g)
Applied by a dental practitioner for up to 4 minutes using
trays—evacuate excess [ NB2 ].
Acidulated phosphate fluoride is preferred to neutral
fluoride products because it has better enamel uptake;
however, avoid acidulated gels and foams in patients
with ceramic crowns and bridgework, direct restorations
75 containing glass particles, or poor salivary flow (eg
patients undergoing head or neck irradiation).
Q)
a neutral fluoride gel or foam Use in adults and children ( age restriction variable)
a 5000 to 9000 ppm (5 to usually twice a year depending on dental caries risk.
c 9 mg/ g )
CO Can be used for patients with ceramic crowns and
75 bridgework, direct restorations containing glass particles,
or poor salivary flow (eg patients undergoing head or
O neck irradiation).
(0
o Applied by a dental practitioner for up to 4 minutes using
—
trays evacuate excess [NB2].
o
Adults can use neutral fluoride gel or foam at home,
5
3 according to recommended instructions.
o .2
silver fluoride formulations Use in adults and children (age restriction variable)
.42
^ usually twice a year or as recommended by a dentist.
0
Q . Applied by a dental practitioner to arrest carious lesions,
CO but can stain teeth black.
0
C <u
| continued next page
68
Table 8. Examples of topical fluoride applications for
patients at elevated risk of dental caries [NB1]
(cont. )
formulation Usual directions for use
fluoride + CPP- ACP Use in adults and children for noncavitated white spot
900 ppm+10% cream lesions twice daily after brushing with usual fluoride
toothpaste.
Patients should apply the cream to the teeth, hold in
the mouth for 3 to 5 minutes, spit out excess and avoid
rinsing the mouth [ NB2 ].
Use in adults and children for noncavitated white spot
fluoride+CPP-ACP
lesions usually twice a year depending on dental caries
22 600 ppm (22.6 mg/
mL) + 2% varnish risk.
Applied by a dental practitioner to all at-risk dental
surfaces.
CPP ACP = casein phosphopeptide-amorphous calcium phosphate
NB1: Treatment choice is based on clinical judgment and requires a complete assessment of the
patient (eg age, other medications, disease risk).
NB2: Spit out fluoride products to minimise ingestion; do not rinse the mouth after use to allow
increased uptake of fluoride from the saliva.
Non- fluoride remineralising agents
There are a number of topical applications claiming to lead to remineralisa-
tion of a decalcified tooth surface. However, most international guidelines
acknowledge that further research is required before recommending wide-
spread use of other remineralising agents in dental caries management
plans—fluoride remains first- line therapy for the primary prevention and
treatment of dental caries.
Emerging evidence suggests casein phosphopeptide-amorphous calcium
phosphate (CPP- ACP) in combination with fluoride can reverse dental
caries in the early stages of the disease (noncavitated lesions). CPP ACP
-
products should not replace fluoride interventions, but may be discussed
as an additional treatment in motivated patients. Use clinical judgment to
determine if CPP- ACP is an appropriate option in patients at elevated risk (/)
of dental caries. For practical information on using CPP- ACR see p.61.
CO
o
75
Q
69
 Chlorhexidine
Chlorhexidine has a limited role in prevention of dental caries in patients at
elevated risk. Chlorhexidine prevents plaque formation on a cleaned tooth
surface and may reduce the level of cariogenic bacteria in the mouth. Periodontal and peri-
However, further evidence is needed to assess whether this prevents dental
caries. Use clinical judgment to determine if chlorhexidine is an appropriate implant diseases
option in patients at elevated risk of dental caries; if indicated, use:

1 chlorhexidine + fluoride 0.2%+0.0033% (15 ppm) gel (pea-sized

amount) brushed on to the teeth daily or weekly*

OR
Gingivitis
1 chlorhexidine 0.5% gel (pea- sized amount) brushed on to the Gingivitis (inflammation of the gingivae) is the most mild and common
teeth daily or weekly.* form of periodontal disease. Record the periodontal status of all patients
because approximately 50% of the population have periodontal disease.
The low concentration of fluoride in the combination formulation is not Gingivitis is associated with the accumulation of dental plaque (a complex
clinically significant, so it should be used in addition to the recommended blofilm of mixed bacteria and their by-products) and calculus at the gin-
fluoride toothpaste (see Table 7; p.67). Recent research has shown that gival margins. Bacterial by-products diffuse into the adjacent gingival tissue
chlorhexidine is not inactivated by the detergent sodium lauryl sulfate used cousing a nonspecific inflammatory response.
in standard toothpaste, so they can be used at the same time. For prac-
tical information on using chlorhexidine, see p.59. Inflammation of the gingival tissues results in red and swollen gums that
bleed easily. Gingivitis is not painful and does not destroy the periodontal
For dental caries management, chlorhexidine gel is preferred to ligament or alveolar bone. However, if it is not managed appropriately, gin -
mouthwash; givitis can progress to periodontitis (for management of periodontitis, see
• alcohol-containing chlorhexidine mouthwashes may increase the risk .
|) 72 ). Figure 5 ( p.81) shows the location of gingivitis around the teeth.
ra of oral cancer, and cannot be used in children younger than 12 years
With appropriate management, gingivitis is reversible; resolution of
§ • alcohol-free chlorhexidine mouthwashes have a short expiry after
Inflammation can be expected within 1month. Strategies include:
o opening.
D • removing plaque and calculus with thorough debridement
• smoothing any irregularities on the teeth (eg rough edges of fillings)
2 that allow plaque to accumulate J2
o • improving oral hygiene through patient education (for information on
oral hygiene, see p.273) .
I
=o
Antibiotic therapy is not required for gingivitis. "D

a <o
Antibiotic therapy is not required for gingivitis. n
S
s If pain and inflammation associated with gingivitis restrict oral hygiene
§ 3
& practices, consider short-term use of a mouthwash to reduce plaque
Q (S)
o to
CL)

* When used for more than a few days, chlorhexidine may cause a superficial discolouration
formation; use: .
«5 .<2
Q O

of the teeth and fillings (see p.59 for more information).

70 71
 .
l chlorhexidine 0.2% mouthwash 10 mL rinsed in the mouth for
1minute then spat out 8- to 12-hourly for 5 to 10 days*
OR
l chlorhexidine 0.12% mouthwash 15 mL rinsed in the mouth for
1minute then spat out, 8- to 12-hourly for 5 to 10 days.*
Periodontitis
Periodontitis is characterised by the loss of bone and tissues that sup-
port the teeth (eg periodontal pocket formation, gingival recession) —see
Figure 5 (p.81). It is often associated with halitosis and an unpleasant
taste in the mouth. In severe periodontitis, the teeth may become loose
or drift, allowing spaces to develop between the teeth. Pain is not usually
a feature until the late stages of the disease. Assess and record the peri-
odontal status of all patients because approximately 50% of the population
have periodontal disease.
Gram - negative anaerobic bacteria are involved with the initiation and pro-
gression of periodontitis, with Porphyromonas gingivalis recognised as the
key pathogen.
Risk factors for the development and progression of periodontitis include
smoking and poorly controlled diabetes.
_ Periodontitis is classified by its stage (severity of disease and complexity of
management) and grade (biological features such as rate of progression)
2 The disease usually presents as chronic and slowly progressing, with brief
acute episodes. The amount of plaque, calculus and bleeding usually cor-
TO
®
responds with the disease severity.
ns Rarely patients present with a rapidly progressing form of periodontitis
TO (previously known as aggressive or early-onset periodontitis) characterised
O by rapid attachment loss and alveolar bone destruction. Unlike the usual
.£
presentation, the severity of periodontal destruction does not correlate with
the amount of plaque and calculus. This presentation is more common in
g
- patients with a family history of the condition. Specialist management of
^ rapidly progressing periodontitis is required.
ip Periodontitis in children is rare and usually associated with systemic dis-
TO ease (eg leukaemia, type 1diabetes, cyclic neutropenia)—refer for urgent
specialist review.
ro
0
* When used for more than a few days, chlorhexidine may cause a superficial discolouration
of the teeth and fillings (see p.59 for more information).
72
Successful management of periodontitis requires removal of bacterial
deposits, improved patient oral hygiene, control of risk factors and con-
tinued follow up. Strategies include:
• thorough debridement to remove supragingival and subgingival plaque
and calculus. Local anaesthetics may be needed
• polishing, reshaping or replacing defective fillings
• providing patients with advice on oral hygiene (for information on oral
hygiene, see p.273)
• collaborating with the patient’s medical practitioner to modify risk
factors (eg smoking, diabetes management)
• providing regular supportive periodontal care.
lor patients with severe periodontitis, specialist referral is usually required.
Poriodontal surgery may be indicated if the patient has not responded to
nonsurgical debridement.
Antibiotic therapy is rarely required for periodontitis.
Antibiotic therapy is rarely required for periodontitis; only consider anti-
biotic therapy for the following patients, preferably under the care of a
periodontist:
• patients with rapidly progressing periodontitis
• patients with periodontitis that has not responded to dental treatment
• immunocompromised patients, including patients with poorly
. controlled diabetes.
Necrotising periodontal disease
Necrotising periodontal disease is an acute painful condition characterised
2
by gingival bleeding and necrosis or ulceration of the interdental papillae,
I
which is often covered with a greyish pseudomembrane. It is usually
Associated with halitosis and can be associated with swollen glands (lym-
phadenopathy) and fever.
=
TO
TO
Necrotising periodontal disease is classified by the extent of inflammation
TO
or necrosis. TO
• Necrotising gingivitis (previously known as acute necrotising ulcerative
gingivitis [ANUG]) affects the interdental papillae and gingivae; if ~a c/5
not managed appropriately, it can spread to involve the bone. For £o0.2
0
• 0
management of necrotising gingivitis, see p.74. Necrotising gingivitis - -O
Q
most commonly occurs in young adult smokers and rarely occurs in
73
 .
children Children thought to have necrotising gingivitis should be
assessed for acute herpetic gingivostomatitis (for information on oral
mucocutaneous herpes, see p.110) . OR
• Necrotising periodontitis affects the periodontium and results in bone
.
loss Promptly refer for specialist management.
• Necrotising stomatitis affects the periodontium, bone and soft tissues
of the oral cavity. Promptly refer for specialist management.
Management of necrotising gingivitis
Thorough debridement of plaque and necrotic debris is necessary for
successful management of necrotising gingivitis. However, it may not be
possible to complete debridement at the initial presentation because
necrotising gingivitis can be associated with significant pain.
Begin management of necrotising gingivitis with:
• gentle removal of as much plaque and necrotic debris as possible,
using local anaesthetics if necessary
• local irrigation with chlorhexidine 0.2% mouthwash or hydrogen
peroxide 3% solution. Chlorhexidine mouthwash or hydrogen peroxide
solution (as below) may also be used if pain limits the patient’s ability
to mechanically clean their teeth
• antibiotic therapy (as below)
i hydrogen peroxide 1.5% solution 10 mL, rinsed in the mouth for
1minute then spat out, 12 -hourly until pain has reduced
2 chlorhexidine 0.2% mouthwash 10 mL rinsed in the mouth for
1minute then spat out, 8- to 12-hourly until pain has reduced*
OR
chlorhexidine 0.12% mouthwash 15 mL rinsed in the mouth for
2
1minute then spat out, 8- to 12 -hourly until pain has reduced.*
Review the patient in 48 to 72 hours; perform a periodontal examination
and provide the patient with advice on oral hygiene. Perform thorough
debridement as soon as possible to prevent recurrence.
A poor response to treatment or recurrence of symptoms is usually due to
inadequate debridement or a lack of improvement in oral hygiene, rather
than an ineffective antibiotic regimen. If the infection has not responded
to appropriate management (complete debridement, antibiotic therapy,
Improved oral hygiene) within 2 weeks, refer for specialist management.
Treatment failure is usually due to inadequate debridement or
poor oral hygiene, rather than ineffective antibiotic therapy.

• analgesics (to select an appropriate analgesic regimen for acute dental

pain, see p.137)
• advice to stop smoking.
Periodontal abscess
A periodontal abscess most often occurs in patients with pre-existing perio-
Profoundly immunocompromised patients (for guidance on assessing
Q)
a patient’s degree of immune compromise, see p.181) or patients with dontal disease or in those who are immunocompromised (eg patients with
poorly controlled diabetes). Symptoms include swelling of the gums and
O
TJ severe cases of necrotising gingivitis require prompt referral for specialist !
c
03 management in addition to the management above.
discomfort. Pain is often difficult to localise, and is not severe enough to M

7u Interfere with sleep. 2

Q.
o- For antibiotic therapy of necrotising gingivitis, use:
i

It is important to differentiate a periodontal abscess from a periapical E

c6 abscess, because a periodontal abscess requires local periodontal treat-
2
CD metronidazole 400 mg orally, 12- hourly for 3 to 5 days.
ECD ment. Figure 5 (p.81) shows the locations of periodontal and periapical
CD
Q .
5 If pain and inflammation restrict oral hygiene practices, recommend short- Abscesses. For the management of periapical abscess, see p.81. o
c
=
o
3
term use of a mouthwash to reduce plaque formation; use: Management of periodontal abscess includes:
cu
.2
75
• draining the abscess (with local anaesthetics) through the periodontal c </>
CD
Cl
i hydrogen peroxide 3% solution 5 mL, mixed with 5 mL of warm
water, rinsed in the mouth for 1minute then spat out, 12 - hourly
pocket beneath the swelling or, less commonly, through an incision in -0oo o<CD>
/

5 the external surface of the gingival swelling Q)

until pain has reduced <5 .2
- -a
CD
11 Q
OR ' When used for more than a few days, chlorhexidine may) cause a superficial discolouration
of the teeth and fillings (see p.59 for more information . 75
74
 • removing plaque and calculus deposits with thorough debridement
Management of peri- implantitis
• irrigating the area with water, saline solution or local anaesthetic
solution. Management of peri-implantitis includes:
• nonsurgical debridement of the implant
• providing advice on improving oral hygiene (see pp.273-5) and
In severe cases, tooth extraction may be necessary to drain pus ade-
quately, followed by thorough irrigation and curettage of the socket. smoking cessation
Specialist management is required if a periodontal abscess does not • encouraging regular dental review, including maintenance of the
respond to local intervention. implant.
If the patient is profoundly immunocompromised (for guidance on In addition to the above strategies, the following interventions are often
assessing a patient’s degree of immune compromise, see p.181) , treat as required:
for spreading odontogenic infections without severe or systemic features • surgical intervention
( see p.82).
• surface decontamination, with or without hard tissue augmentation
In the rare event that a periodontal abscess has spread into surrounding • soft tissue grafting
tissues or caused systemic signs and symptoms of infection, it should be • antibiotic therapy (as below)
treated as an odontogenic infection (see pp.79-86).
• specialist referral.
Despite appropriate treatment, some implants will show continued bone
Peri- implant diseases loss and require removal.

Peri -implant diseases are caused by plaque accumulation around an Tor antibiotic therapy of peri-implantitis, in conjunction with other interven-
osseointegrated dental implant. Peri -implant mucositis involves nonde- tions, consider using:
structive reversible inflammation of the soft tissues, similar to gingivitis. amoxicillin 500 mg orally, 8- hourly for 7 days
Peri-implantitis involves destruction of the bone support of the implant,
and can lead to loss of the implant. PLUS

Peri - implant disease is more likely if the dental implant is not professionally metronidazole 400 mg orally, 12-hourly for 7 days.
75 maintained, or if a patient smokes, has a history of periodontitis, has poor
0 oral hygiene or is unable to clean their implant. Peri-implantitis is associ- l or patients with hypersensitivity to penicillins (see pp.31-5), use metro-
Q
o
ated with excess cement or poor fit of dental implant components. nidazole as a single drug (see above) .
c
03
Management of peri-implant mucositis is
Q.
2
o £
- Management of peri-implant mucositis includes: :z
• nonsurgical debridement of the implant 0
~
Q -
o • providing advice on improving oral hygiene (see pp.273-5) and o
C
smoking cessation CD
CD
.y • encouraging regular dental review, including maintenance of the 75
implant. c </>
o o>
0 O jg
Antibiotic therapy is not required. o
CD •£ 0
CD 5- .<2
Antibiotic therapy is not required for peri- implant mucositis.
0 O -
76 77
Acute odontogenic infections
Acute odontogenic (tooth-related) infections are common and can affect:
• dental pulp—secondary to restoration breakdown, dental caries or loss
of tooth structure from trauma
• periodontal tissues—most commonly due to advanced periodontitis
• pericoronal tissues—most commonly from partially erupted mandibular
third molars.
If an odontogenic infection is ignored or not appropriately treated, it can
progress to a localised abscess or spread to the soft tissues of the face
or neck. Rare but serious complications include Ludwig angina, airway
compromise, sepsis, or spread to the bone, brain, neck or mediastinum.
Immunocompromised patients are prone to rapidly spreading infection.
Persistent dental pain and swelling after dentoalveolar surgery could be
due to alveolar osteitis (dry socket; see p.222) or a postoperative infection
( see p.87).

Osteomyelitis of the jaw is an important differential diagnosis in patients

with an unresolved oral infection with systemic features and localised
bone pain or tenderness. If osteomyelitis of the jaw is suspected, refer the
patient to hospital; expert advice is needed. Differential diagnoses include
osteonecrosis ( which can be medication-related osteonecrosis of the jaw;
see p.164) and osteoradionecrosis (which occurs in patients undergoing
radiation therapy; see p.175). <f )
c
.2

Approach to managing acute odontogenic £

.E
infections .9
c
<D
<00
An acute odontogenic infection requires prompt management with dental o
treatment (eg extraction, root canal) or surgical intervention, to address c
o
the source of the infection. Antibiotic therapy is not a substitute for TJ
O
dental treatment, but may be required if dental treatment is not likely to 0)
be received within 24 hours. Whether the patient can be managed in the 3
O
community or requires hospital admission depends on the severity of the <
Infection (see Table 9; p.80) .
79
 Seek expert advice for patients with recurrent infection who have received
antibiotics but not dental treatment.
Localised odontogenic infections
An odontogenic infection is considered to be localised if it causes dental
Antibiotic therapy is not a substitute for dental treatment of pain without facial swelling or systemic features. Localised odontogenic
odontogenic infection.
infections can involve periapical, pericoronal or periodontal abscesses—
see Figure 5 (below) for their anatomical location. Signs of abscess include
Odontogenic infection is usually polymicrobial, involving anaerobic and
visible pus, a localised swelling on the gum or fluctuant tissue. However,
aerobic oral bacteria. Metronidazole is used in conjunction with a penicillin
dental pain may be the only sign of a periapical abscess.
because of increased rates of resistance to penicillins in some oral bac-
teria (eg Prevotella oralis ) . However, amoxicillin+ clavulanate has adequate
anaerobic activity, so can be used as a single preparation. Figure 5. Anatomical location of localised odontogenic
infections and associated conditions
Table 9. Acute odontogenic infections: features and
overview of management ©
Clinical features Management overview 'enamel

localised dental pain outpatient dental treatment

odontogenic
dentine
abscess (localised swelling if dental treatment is not likely
infection (see p.81) on the gum or fluctuant
2
to be received within 24 hours, 3
tissue) medical practitioners can start pulp
pus may be visible antibiotic therapy; however,
ensure the patient receives
no facial swelling dental treatment 4
no severe or systemic
features of infection
spreading
odontogenic
facial swelling
dental or facial pain
outpatient dental treatment
followed by oral antibiotic ©
infection without therapy
severe or systemic abscess (localised swelling
15
©
if dental treatment is not likely
features ( see p.82) on the gum or fluctuant
tissue) to be received within 24 hours,
<D medical practitioners can start
O pus may be visible
-o antibiotic therapy; however,
c no severe or systemic ensure the patient receives
1. pericoronal infection 4. periodontitis (bone loss) —see p.72 c
if )
cu features of infection dental treatment
.M
2
2. pericoronal abscess .
5 periodontal abscess—see p 75 .
o
i
— 3. gingivitis—see p.71 6. periapical inflammation (apical
periodontitis) or abscess a
to spreading severe features such as provide appropriate support of .£
o
odontogenic significant facial swelling airway, breathing and circulation The key to successful management of localised odontogenic infection is .2
c
infection with and pain, trismus, neck
CD
severe or systemic swelling, difficulty swallowing,
urgent transfer to a hospital with dental treatment to drain pus and address the source of infection—see <D
= Box 10 (p.82) for treatment options. Antibiotic therapy is not required
an oral and maxillofacial surgeon o
3 features (see p.84) difficulty breathing or airway or other appropriate expert
CD c
.42
compromise because dental treatment removes the source of infection and bacte- o
-* systemic features such as
surgical intervention and
intravenous antibiotic therapy raemia caused by treatment resolves rapidly. T3
O
CD pallor, sweating, tachycardia,
Cl 0)
CD an axillary temperature above
38°C [NB1] or sepsis
CD Do not routinely give antibiotic therapy after dental treatment for O
-C
.
NB1: Oral temperatures are unreliable for infections originating in the mouth a localised odontogenic infection. <

80 81
 However, if an infected tooth breaks during an extraction and there is a • surgical or dental treatment (endodontic or periodontal treatment, or
delay in removing residual root or bone fragments, antibiotic therapy is tooth extraction) to address the source of infection
indicated—see p.83 for a suggested antibiotic regimen. If the tooth is not • oral antibiotic therapy, ideally started after samples are taken for
infected, antibiotic therapy is not required. culture.

Antibiotic therapy is not a substitute for dental treatment of
localised odontogenic infection.
Patients with localised odontogenic infection may present to a medical
practitioner; promptly refer the patient to a dentist for treatment. If dental
treatment is not likely to be received within 24 hours, start antibiotic
therapy ( see p.83 for an appropriate antibiotic regimen). However, antibi-
otic therapy is not a substitute for dental treatment so ensure the patient
sees a dentist. Offer systemic analgesics for the treatment of dental pain
(to select an appropriate analgesic regimen for acute dental pain, see
p.137) . For pericoronal infections, irrigate the area with sterile saline solu-
tion, and recommend rinsing with warm saline or chlorhexidine mouthwash
until dental treatment can take place.
Box 10. Dental treatment options for acute localised
odontogenic infections
It may not be possible to achieve adequate analgesia with local anaes-
thetics in patients with spreading odontogenic infection; however, this
should not delay dental treatment. Anxiolysis (minimal sedation) (see
pp.211-20) or general anaesthesia may be required. Once the source of
infection has been addressed, start antibiotic therapy.
Patients with spreading odontogenic infection may present to a medical
practitioner; refer the patient to a dentist for prompt treatment. If dental
treatment is not likely to be received within 24 hours, start antibiotic
therapy ( as below) . However, antibiotic therapy is not a substitute for
dental treatment so ensure the patient sees a dentist. Offer systemic anal-
gesics for the treatment of dental pain (to select an appropriate analgesic
regimen for acute dental pain, see p.137) .
For antibiotic therapy of spreading odontogenic infections without systemic
or severe features, use:

Periapical abscess
i
12 -hourly for 5 days '
metronidazole 400 mg (child: 10 mg kg up to 400 mg) orally,

• endodontic (root canal) treatment PLUS EITHER

• tooth extraction

75
Periodontal abscess
i phenoxymethylpenicillin 500 mg (child: 12.5 m kg up
to 500 mg) orally, 6- hourly for 5 days ^
• periodontal treatment (debridement) —see p.75
CD
OR
Q • tooth extraction
o 2 amoxicillin 500 mg (child: 15 mg/kg up to 500 mg)
c Pericoronal infection, including abscess orally, 8- hourly for 5 days </)
03 C
75 • tooth extraction (treatment of choice) .2
o-
OR ( as a single preparation)
• remove or recontour the opposing tooth
a
i

2 amoxicillin +clavulanate 875 +125 mg (child 2 months or older: .E

22.5 + 3.2 mg/kg up to 875 +125 mg) orally, 12 -hourly for 5 days.
0
.2
0 c

= 5 Spreading odontogenic infections without For patients hypersensitive to penicillins ( see pp.31-5) , use:
0
•OD
o
0
.2 severe or systemic features clindamycin 300 mg (child: 7.5 mg/kg up to 300 mg) orally,
c
o
^ 8- hourly for 5 days.*
4
O
o_
0 o
A spreading odontogenic infection that has caused facial swelling but no 0
T
0 severe or systemic features can be managed in an outpatient dental set- D
ting. Management involves:
o
<
J0

• drainage of pus, with culture and susceptibility testing of pus samples * An oral liquid formulation of clindamycin is not commercially available but can be
prepared, if required, by dispersing a capsule in liquid: see p.41 for instructions.
82 83
 Review the patient 48 to 72 hours after starting treatment to check
response. Advise the patient to seek prompt dental review if their condition
deteriorates or if the infection has not resolved within 5 days.
Review patients within 48 to 72 hours of starting treatment.
If the infection has not responded to treatment, ensure:
• the source of infection has been addressed
• pus was drained adequately—computed tomography (CT) may be
required to check for locules requiring drainage
• the infection is susceptible to the current antibiotic regimen—if the
results of culture and susceptibility testing are available, modify
antibiotic therapy accordingly.
Failing this, or if the patient’s condition has deteriorated, seek expert
advice from an oral and maxillofacial surgeon—transfer to an inpatient
facility may be required.
Spreading odontogenic infections with
severe or systemic features (including
Ludwig angina)
Severe features of a spreading odontogenic infection include significant
facial swelling and pain, trismus, swelling of the neck, difficulty swallowing
and difficulty breathing. Systemic features include pallor, sweating, tachy-
cardia, and an axillary temperature above 38°C ( oral temperatures are
<D
Q unreliable for infections originating in the mouth) . The infection can rap-
o idly become life threatening because of the risk of airway obstruction and
c </ )
a: sepsis. Ludwig angina is a severe spreading infection involving the bilateral
Tu submandibular, sublingual and submental spaces, with cellulitis.
Management of spreading infection with severe or systemic features
Involves:
• maintaining a patent airway (do not lie the patient flat)
• resuscitation
• draining pus by incising affected spaces and placing drains
• removing the tooth or otherwise addressing the source of infection
• obtaining blood and other samples for culture and susceptibility testing
• intravenous antibiotic therapy.
Spreading odontogenic infections can be associated with sepsis (for
definitions of sepsis in children and adults, see ‘Principles of managing
sepsis and septic shock’ in eTG complete ) . For patients with sepsis, start
antibiotic therapy within 1 hour of presentation to medical care; antibi-
otics should be given immediately after appropriate samples are taken
for culture. Obtain blood samples and other relevant samples as soon as
possible, but not if doing so will delay antibiotic administration. For non-
antibiotic management of sepsis, see ‘Early intervention for sepsis or septic
shock’ in eTG complete.
For empirical antibiotic therapy of spreading odontogenic infection with
severe or systemic features (including Ludwig angina) , in conjunction with
surgical intervention, use:
i benzylpenicillin intravenously
patients requiring intensive care support: 2.4 g (child: 50 mg/kg
up to 2.4 g) 4-hourly
patients not requiring intensive care support: 1.8 g (child:
50 mg/kg up to 1.8 g) 4- hourly
PLUS
c
metronidazole 500 mg (child: 12.5 mg/kg up to 500 mg)
.-2
intravenously, 12- hourly M

o £
Arrange urgent transfer of patients who have a spreading infection with OR (as a single preparation) .£
CD
£CD
severe or systemic features to a hospital that has an oral and maxillofacial
surgeon or another appropriate expert.
.c2
2 <U
OJD
I
3 O
CD Arrange urgent transfer of patients with a spreading infection with c
.2 severe or systemic features to a hospital that has an oral and O
T3
0
maxillofacial surgeon or another appropriate expert. O
Q_ ©
Co
3
0 O
J3
<
84 85
 2 amoxicillin + clavulanate intravenously
adult: 1+ 0.2 g 6-hourly* t
child 3 months or older: 25 + 5 mg kg up to 1+0.2 g 6-hourly
^ .*§
For patients with immediate nonsevere or delayed nonsevere hypersensi-
tivity to penicillins (see pp.31-5) , use:
'
cefazolin 2 g (child: 50 mg kg up to 2 g) intravenously, 8-hourly;
for adults requiring intensive care support, use 6- hourly dosing
PLUS
metronidazole 500 mg (child: 12.5 mg/kg up to 500 mg)
intravenously, 12 -hourly.
For patients with immediate severe or delayed severe hypersensitivity to
penicillins (see pp.31-5), as a single- drug regimen, use:
i clindamycin 600 mg (child: 15 mg/kg up to 600 mg)
intravenously, 8-hourly
Infection following dentoalveolar surgery
Infection following dentoalveolar surgery (eg tooth extraction, implant
placement and associated procedures) is uncommon, and its incidence
is not reduced by surgical antibiotic prophylaxis. Before diagnosing post-
operative dental infection, exclude postsurgical inflammation and alveolar
osteitis ( dry socket; see p.222). Signs and symptoms of postoperative
dental infection include:
• cellulitis adjacent to the surgical site
• fluctuant surgical site
• purulent discharge from the surgical site
• pain and swelling that is worsening or is not improving 48 hours after
surgery.
If postoperative dental infection is associated with severe symptoms (eg
significant facial swelling and pain, trismus, swelling of the neck, dif-
ficulty swallowing, difficulty breathing) , follow the management advice on
pp.84-5.

OR Management of postoperative dental infection not associated with severe

symptoms requires:
2 lincomycin 600 mg (child: 15 mg/kg up to 600 mg) intravenously,
• draining pus
8- hourly.
• addressing the source of infection, including removing residual root or
tooth fragments if demonstrated on X-ray
Modify therapy based on the results of cultures and susceptibility testing.
Switch to oral therapy once swelling and trismus subside (and the patient • analgesia and rehydration therapy.
TO can swallow) and purulent discharge from the drains slows. If results of Most postoperative dental infections can be managed by dental treatment
susceptibility testing are not available for oral continuation therapy, use the alone. However, if the patient is immunocompromised or has systemic
appropriate regimen on p.83.
0
o features of infection (eg pallor, sweating, tachycardia, axillary tempera -
ture above 38°C* ) , consider using antibiotic therapy in addition to dental
~o
c Stop oral antibiotic therapy once the drains are not producing any purulent (/)
c
TO
discharge, signs and symptoms have resolved, the white cell count has treatment. If antibiotic therapy is indicated, the regimens for spreading .2
o*-
TO
returned to normal and the patient is afebrile. odontogenic infections without severe or systemic features are appropriate M

( see p.83).
</ j .£
0
* At the time of writing, there is limited clinical evidence to determine the optimal dosage Review the patient 48 to 72 hours after starting treatment to check .c2
ECD regimen of intravenous amoxicillin+ clavulanate. For adults with a spreading odontogenic response. Advise the patient to seek prompt dental review if their condition
infection with severe or systemic features, a reasonable alternative regimen is 2 +0.2 g 0
=3 intravenously, 8-hourly. deteriorates or if the infection has not resolved within 5 days. 'OJD
o
CD t If the abscess has been adequately drained, consider reducing the dose of c
.2 o
-
+» amoxicillin+ clavulanate to 1+ 0.2 g intravenously, 8-hourly. a
CD f At the time of writing, there is limited clinical evidence to determine the optimal dosage o
CL
co regimen of intravenous amoxicillin + clavulanate. For children who weigh 40 kg or more 0
0 with a spreading odontogenic infection with severe or systemic features, a reasonable 3
O
jC alternative regimen is 2 +0.2 g intravenously, 8-hourly.
§ If the abscess has been adequately drained, consider
<
reducing the dose of
amoxicillin + clavulanate to 25 + 5 mg/kg up to 1+ 0.2 g intravenously, 8-hourly. * Oral temperatures are unreliable for infections originating in the mouth. 87
86
Salivary gland infections

Diagnosing salivary gland infections

Swelling of a parotid, submandibular or sublingual salivary gland may indi-
cate salivary gland infection; however, a noninfective cause of swelling (eg
.
salivary gland obstruction) is more likely Box 11 (p.90) outlines potential
causes of salivary gland swelling. Benign masseteric hypertrophy, lymphad-
enopathy or acute spreading odontogenic infections may be mistaken for
salivary gland swelling.
Investigations or imaging (eg ultrasound or computed tomography [CT])
may be necessary to determine the diagnosis.

Acute suppurative sialadenitis (including

parotitis)
Acute suppurative sialadenitis (including parotitis) is usually caused by
Staphylococcus aureus , though occasionally it is polymicrobial in adults.
The glands are enlarged, often hot and tense, and pus may be expressed
from the gland duct. The patient is usually systemically unwell, dehydrated
and has difficulty swallowing.
Management of acute suppurative sialadenitis includes:
• urgent referral to hospital for surgical review <r )
c
• rehydration .2
M
• culture and susceptibility testing of blood samples
• if the swelling is fluctuant, intraductal or surgical drainage; send pus £
.2
for culture and susceptibility testing o
c
• antibiotic therapy, given intravenously initially (see p.90) then orally J2
once the patient can swallow (see p.91) . 0D

rc
If S. aureus is identified in a blood culture, treat as S. aureus bacteraemia >
( see ‘ Staphylococcus aureus bacteraemia ’ in eTG complete ) . If the results 15
cr >
of blood culture indicate a polymicrobial bacteraemia, seek expert advice.
89
 Box 11. Potential causes of salivary gland swelling In some regions, based on local community acquired-MRSA susceptibility
patterns, clindamycin or lincomycin is a suitable alternative to vancomycin:
Inflammatory causes
• acute bacterial infection (acute suppurative sialadenitis; see pp.90-2) caused i clindamycin 600 mg (child: 15 mg/kg up to 600 mg)
by Staphylococcus aureus , streptococci or mixed anaerobes intravenously, 8- hourly; switch to oral therapy once the patient can
• viral infections (eg mumps, coxsackievirus infection, Epstein-Barr virus [EBV ] swallow
infection)
• chronic infections (eg tuberculosis, actinomycosis) OR
• autoimmune disease (eg Sjogren syndrome) 2 lincomycin 600 mg (child: 15 mg/kg up to 600 mg) intravenously,
Obstructive causes 8-hourly; switch to oral therapy once the patient can swallow.
• stones (sialadenitis)
• trauma for patients with immediate nonsevere or delayed nonsevere hypersen-
• mucous retention (ranula) sitivity to penicillins (see pp.31-5) and without risk factors for MRSA, use:

Metabolic causes
• obesity
'
cefazolin 2 g (child: 50 mg kg up to 2 g) intravenously, 8- hourly;
switch to oral therapy once the patient can swallow.
• hypothyroidism
• alcoholic liver disease For patients with immediate severe or delayed severe hypersensitivity to
• malnutrition (eg eating disorder) penicillins (see pp.31-5) and without risk factors for MRSA , use clinda-
Tumours
mycin or lincomycin as above.
• benign (eg pleomorphic adenoma, monomorphic adenoma)
• malignant (eg mucoepidermoid carcinoma, adenoid cystic carcinoma, Oral continuation therapy for acute
adenocarcinoma, lymphoma)
suppurative sialadenitis
Drug or food hypersensitivity
Initiate oral continuation therapy once the patient can swallow. If the
75 rosults of culture and susceptibility testing are available, modify oral
Intravenous antibiotic therapy for acute therapy accordingly. If the results of susceptibility testing are not available,
o use:
Q suppurative sialadenitis
o
c i dicloxacillin 500 mg (child: 12.5 mg/kg up to 500 mg) orally,
(Q Initiate empirical antibiotic therapy for acute suppurative sialadenitis in
6-hourly for a total of 10 days (intravenous plus oral)
75 conjunction with local intervention or drainage; use:
o-
i (/)

OR c
c/ 5 flucloxacillin 2 g (child: 50 mg/kg up to 2 g) intravenously, .2
0
1
0
6- hourly; switch to oral therapy once the patient can swallow. i
'
flucloxacillin 500 mg (child: 12.5 mg kg up to 500 mg) orally,
6- hourly for a total of 10 days ( intravenous plus oral). .£
2
0 For patients with risk factors for methicillin-resistant Staphylococcus aureus u
CD c
(MRSA) infection ( see ‘Risk factors for infection with methicillin- resistant For patients with risk factors for methicillin-resistant Staphylococcus aureus 20
.2
Staphylococcus aureus (Box 2.31) ’ in eTG complete ) , use: ( MRSA) infection (see ‘Risk factors for infection with methicillin - resistant «
0
CL Staphylococcus aureus (Box 2.31) ’ in eTG complete ) for whom results of TO
2 vancomycin intravenously; see ‘Principles of vancomycin use’ in susceptibility testing are not available, use: £
0
eTG complete for dosage and principles of use; switch to oral c/>
therapy once the patient can swallow.
90 91
 i trimethoprim+sulfamethoxazole 160+800 mg (child 1month or
older: 4+ 20 mg/kg up to 160+800 mg) orally, 12-hourly for a
total of 10 days (intravenous plus oral)

Oral mucosal disease

OR
2 clindamycin 450 mg (child: 10 mg/kg up to 450 mg) orally,
8-hourly for a total of 10 days (intravenous plus oral).*

For patients with immediate nonsevere or delayed nonsevere hypersen-

.
sitivity to penicillins (see pp 31-5) and without risk factors for MRSA, use:
cefalexin 500 mg (child: 12.5 mg/kg up to 500 mg) orally,
6- hourly.
For patients with immediate severe or delayed severe hypersensi
-
tivity to penicillins ( see pp.31-5) and without risk factors for MRSA, use
trimethoprim+sulfamethoxazole or clindamycin as above.
Assessment of oral mucosal disease
Oral mucosal lesions are common. They can be due to physiological
changes, local disease, an oral manifestation of a skin condition, an
Adverse drug reaction or systemic disease (eg gastrointestinal disease).
Successful management of an oral mucosal disease requires an accurate
diagnosis .
Assessing an oral mucosal lesion involves taking a full patient history
(Including a medication history), performing a thorough extraoral and
Intraoral examination and using diagnostic investigations where appro-
priate. Have a high index of suspicion for oral cancer—see p.95 for risk
(actors for oral cancer. If any ‘red flag' features are present ( see Box 12;
p.94), the diagnosis is not clear, or the patient has not responded to initial
treatment, early referral to an appropriate specialist is required.*

Failure to respond to initial treatment, an unclear diagnosis or the

presence of any suspicious features could indicate malignancy.
To
<o Some oral mucosal diseases are associated with significant morbidity and
Q mortality, particularly oral potentially malignant disorders and oral cancer
g ( see p.95). Oral potentially malignant disorders include:
• oral leukoplakia (see p.98)
(0

<5
• oral erythroplakia (see p.99)
o
• chronic hyperplastic candidiasis (see p.116) 0)
u)
1
• actinic cheilitis
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to
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1 • oral lichen planus (see p.101) .-12
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a • oral submucous fibrosis To
s • discoid lupus erythematosus o
o
5Q. • dyskeratosis congenita
£
£ • epidermolysis bullosa.
a? To
• An oral medicine specialist is the most appropriate specialist to diagnose and manage O
* An oral liquid formulation of clindamycin is not commercially available but can be oral mucosal disease, but may not be accessible; an oral surgeon, dermatologist or
g2 .
prepared, if required, by dispersing a capsule in liquid; see p 41 for
instructions. .
otorhinolaryngologist are other options 93
 • oral mucositis ( see p.120)
Box 12. ‘Red flag’ features of oral mucosal disease
• amalgam tattoo (see p.104)
• oral ulcers that have lasted for more than 2 weeks • geographic tongue (see p.103)
• orals ulcers that recur
• hairy tongue (see p.105).
• nontraumatic oral ulcers in children
There are physiological causes of oral mucosal discolourations (eg Fordyce
• pigmented lesions on the oral mucosa
spots [ectopic sebaceous glands], leukoedema), which do not require
• red, white or mixed red and white lesions on the oral mucosa of unknown origin
active management.
or with features of potentially malignant disease, such as:
- induration
- ulceration with rolled margins Oral cancer
- fixation to underlying tissues
- lesions in high-risk sites (eg lateral tongue, floor of mouth) Oral cancer is associated with significant morbidity and mortality. Early
presentations of oral cancer are usually asymptomatic, whereas late
• facial or oral paraesthesia presentations include pain, discomfort, reduced mobility of the tongue,
• persistent oral mucosal discomfort with no obvious cause increased mobility of the teeth or an inability to wear dentures. Oral cancer
• lumps or swellings, including lymphadenopathy varies in appearance and can mimic many other oral mucosal diseases—
• swelling, pain or blockage of a salivary gland, suggestive of salivary gland see Photos 2, 3 and 4 (pp.96-7).
disease (eg see Box 11 on p.90 for common causes of salivary gland swellings)
• suspected allergy or adverse reaction to dental materials (eg oral lichenoid Oral cancer can mimic many other oral mucosal diseases, so early
lesion; p.103) specialist referral is required for investigation and biopsy of any
suspicious lesion.
• dry mouth that is not adequately relieved with artificial salivary products and
nonpharmacological methods (see Box 14; p.124) Any suspicious lesion needs early specialist referral for investigation and
• dry mouth caused by systemic disease biopsy (for guidance on assessing an oral lesion, see pp.93-4) * .
• suspected oral manifestations of systemic disease (eg syphilis, Behget
Squamous cell carcinoma is the most common oral malignancy, which
syndrome, HIV, inflammatory bowel disease, lichen planus, pemphigoid)
arises from the epithelium of the oral cavity. Oral squamous cell carci-
75 • lesions occurring in immunocompromised patients (eg patients with neutropenia
noma can affect any part of the oral mucosa; however, it most commonly
or HIV infection)
o occurs on the lateral surfaces of the tongue, the floor of the mouth or the
o
o gingivae.
c
Oral potentially malignant disorders can become malignant at the site of
03 the lesion, but also predict an increased risk of cancer at other sites in the Risk factors for oral squamous cell carcinoma include:
0
a
O— mouth, even in clinically normal appearing oral mucosa. • advanced age
• male gender
(/)
The following conditions can be managed in general practice, provided 0
<f )
• smoking or tobacco use
.2
0 there are no ‘red flag’ features present that would warrant referral (see 03
£0 Box 12 above): • alcohol use
0

• recurrent aphthous ulcerative disease ( see p.107)

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3 • infection by oncogenic viruses (eg human papillomavirus) 75
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• traumatic oral ulcers (see p.106) • personal or family history of squamous cell carcinoma of the head and (
o
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o
• oral candidiasis (see pp.114-9) neck 3
• angular cheilitis ( see p.116) E
0
• history of cancer therapy
GJ
• oral mucocutaneous herpes simplex virus (see p.110) 75
* The treating specialist should perform the biopsy of an oral mucosal lesion. In rural or
0
si O
• dry mouth (see p.121) remote areas where a delay in specialist review is expected, seek expert advice on biopsy

94 —
technique a punch biopsy is not appropriate. 95
 • prolonged immunosuppression Photo 3. Squamous cell carcinoma of the right anterior
• areca nut (betel quid) chewing. ventral surface of the tongue
Genetic susceptibility, environment, occupation and diet may also con-
tribute to the development of oral squamous cell carcinoma.
Cancers originating from the salivary glands and supporting nonepithelial
tissues are less common than squamous cell carcinoma. Metastatic can-
cers to the oral soft tissues and jawbones commonly originate from primary
malignancies in the breast, prostate, kidneys or lungs. Leukaemia and lym-
phoma may also present in the oral cavity.

Photo 2. Squamous cell carcinoma of the left ventral surface

of the tongue

Photo 4. Squamous cell carcinoma of the left mandibular

alveolus

15
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96 97
 Oral leukoplakia
Leukoplakia is a clinical term for a nonremovable white lesion that is not
easily recognisable as any particular condition and therefore requires fur-
ther investigation. Oral leukoplakia may be homogenous (uniform lesion
often with a fissured surface) , or nonhomogeneous (with surface irregu-
larity and textural or colour variation [ eg speckled ]) —see Photo 5 (below).
Some oral leukoplakia lesions show histologic evidence of dysplasia, carci-
noma in situ or invasive squamous cell carcinoma—for information on oral
cancer, see p.95. The malignant transformation rate for oral leukoplakia is
variably reported, but ranges between 0.13 to 34%, with a mean annual
transformation rate of 3.8% per year.
Oral erythroplakia
Erythroplakia is a clinical term for a potentially malignant fiery red lesion
that cannot be attributed to any particular condition (see Photo 6, below) .
Lesions are usually asymptomatic and isolated, and commonly appear on
the floor of the mouth, tongue, soft palate and buccal mucosa. Lesions
may appear as smooth, velvety, granular or nodular plaques, often with
clear margins. Oral erythroplakia most commonly affects middle- aged and
elderly men.
Approximately 70 to 90% of oral erythroplakia lesions are
carcinoma in situ or squamous cell carcinoma upon presentation.

Refer patients with oral leukoplakia to an appropriate specialist for biopsy
and monitoring.*
Biopsy of a persistent undiagnosed oral white patch is required to
exclude epithelial dysplasia, carcinoma in situ and squamous cell
carcinoma.
Urgent referral to a specialist for biopsy of oral erythroplakia lesions is
essential because approximately 70 to 90% are carcinoma in situ or squa-
mous cell carcinoma upon presentation*—for information on oral cancer,
see p.95. Periodic review and repeated biopsy by the managing specialist
Is recommended for all patients with oral erythroplakia, because malignant
I
transformation is common.

Photo 5. Leukoplakia of the ventral surface of the tongue Photo 6. Erythroplakia of the right postero-lateral surface
and floor of mouth of the tongue

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i
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remote areas where a delay in specialist review is expected, seek expert advice on biopsy remote areas where a delay in specialist review is expected, seek expert advice on biopsy
—
technique a punch biopsy is not appropriate. technique —a punch biopsy is not appropriate.
98 99
 Human papilloma virus-related oral
lesions
Human papilloma viruses (HPV) can cause a wide range of oral mucosal
lesions. The virus is usually transmitted by direct contact with a lesion.
Squamous papilloma is the most common oral HPV lesion, appearing as
a protruding growth with small finger- like projections ( see Photo 7, below).
Sexually transmitted HPV infections can cause oral HPV lesions called con-
dyloma acuminata. Verruca vulgaris—the common wart—is also caused by
HPV infection and may present in the oral cavity. Both condyloma acumi-
nata and verruca vulgaris can be clinically similar to squamous papilloma.
Oncogenic types of HPV are now recognised as a cause of some squamous
cell carcinoma, particularly of the posterior tongue, tonsillar region and oro-
pharynx. These appear to be a distinct entity, separate to the oral cancers
associated with alcohol and tobacco use. For information on oral cancer,
see p.95.
Refer patients with suspected HPV lesions to an appropriate specialist for
biopsy and management. *
Photo 7. Papilloma of the right maxillary labial mucosa
15
Oral lichen planus
Lichen planus is an uncommon idiopathic immune- mediated condition that
can affect the skin, hair, nails, and oral and genital mucosae. For manage-
ment of lichen planus not occurring in the mouth, see ‘Lichen planus’ in
eTG complete .
Oral lichen planus typically occurs on the buccal mucosa, tongue and
gingivae. In the nonerosive form of the disease, the lesions consist of a
characteristic reticular pattern of white striations or plaques (see Photo 8;
.
p.102) Erosive oral lichen planus presents as erythematous, ulcerated
or eroded areas of mucosa, which are often painful. Symptoms include
stinging or burning, especially with spicy or acidic food. Oral lichen planus
Is associated with an increased risk of oral squamous cell carcinoma (for
Information on oral cancer, see p.95).
Oral lichen planus is associated with an increased risk of oral
squamous cell carcinoma.
Refer patients with suspected oral lichen planus to a specialist for biopsy,
definitive diagnosis and management.* Differential diagnosis should
oxclude oral lichenoid lesions (see p.103). If lichen planus occurs on the
gingival tissues, management includes improving oral hygiene and peri-
odontal health. Patients with oral lichen planus require ongoing review by
an oral medicine specialist because of the chronic nature of the condition
and the potential for malignant transformation.
If biopsy- proven oral lichen planus becomes symptomatic, treat with:

G betamethasone dipropionate 0.05% cream or ointment topically

-a
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0
to the lesions, twice daily after meals, until symptoms resolve.
*
15
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resolved. If the patient ’s symptoms have not improved after 3 weeks of 0
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£0 of the lesion changes, advise patients to return to their treating specialist.
0
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0 15
* The treating specialist should perform the biopsy of an oral mucosal lesion. In rural or remote areas where a delay in specialist review is expected, seek expert advice on biopsy o
remote areas where a delay in specialist review is expected, seek expert advice on biopsy technique—a punch biopsy is not appropriate.
100
—
technique a punch biopsy is not appropriate. t For instructions on applying a topical corticosteroid to the oral mucosa, see Box 9 (p.56).
101
 Photo 8. Oral lichen planus of the left buccal mucosa
showing characteristic white striations Oral lichenoid lesion
Oral lichenoid lesions (see Photo 9; p.102) are similar in appearance to
idiopathic oral lichen planus ( see p.101) .
Lichenoid mucosal reactions can be caused by:
• contact hypersensitivity to dental restorations
• hypersensitivity reactions to drugs, particularly:
drugs that lower blood pressure (eg beta blockers, angiotensin
converting enzyme inhibitors, diuretics [particularly
hydrochlorothiazide])
- nonsteroidal anti-inflammatory drugs (NSAIDs)
drugs that treat thyroid disorders
• medical conditions:
hepatitis C infection, particularly in patients with the human
leukocyte antigen HLA -DR6 allele (which is common in people of
Mediterranean descent)
thyroid disorders
- chronic graft-versus-host disease.
Photo 9. Oral lichenoid lesion due to contact hypersensitivity
to an amalgam filling Refer patients with a suspected oral lichenoid lesion to an appropriate
specialist for definitive diagnosis and management.
In the case of contact hypersensitivity to an amalgam filling, replacement
of the implicated amalgam filling may result in partial or full resolution of
the lesion. However, removal of all amalgam fillings is not recommended.
To
0
Q
o Geographic tongue
c
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Geographic tongue (erythema migrans) is a benign condition affecting up
To
O to 5% of the population. It manifests as migratory red lesions and usually
Involves the dorsal surface of the tongue, but sometimes extends to the 0
* /5
0 floor of the mouth and buccal mucosa. The red patches have a central
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0
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Occasionally the central red patch is sensitive, but not painful. If pain or
ZJ
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o
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0 history of the condition. Some patients have atopic allergies, or can relate To
the lesions to particular foods or stress. Histologically, the lesions are psori- o
asiform, but geographic tongue is not related to a specific condition.
102 103
 Management of geographic tongue is not required beyond correct diag- Photo 11. Amalgam tattoo
nosis and reassurance. If any ‘red flag’ features of oral mucosal disease
are present ( see Box 12; p.94), refer to an appropriate specialist.

Photo 10. Geographic tongue lesion of the right lateral

border of the tongue

Hairy tongue
Hairy tongue occurs when excessively long and hyperkeratinised filiform
papillae of the tongue become stained by an accumulation of epithelial
cells, exogenous material or chromogenic microorganisms (see Photo 12;
p,106) . It is usually black, but may be other colours and can occur with the
15 Amalgam tattoo use of chlorhexidine mouthwash, after a course of antibiotics or in patients
0 who have limited oral intake (eg with percutaneous endoscopic gastros-
o
o
Amalgam tattoos are a common cause of exogenous oral discolouration . tomy [ PEG] feeding).
C They result from the iatrogenic mucosal implantation of amalgam particles
03 If any ‘red flag’ features of oral mucosal disease are present ( see Box 12;
-
15
s
during the course of a dental procedure. They are usually small, macular
and blue-grey to black in colour. Amalgam tattoos are usually found in
.
p 94), refer to an appropriate specialist.
o
close proximity to amalgam- restored teeth or where such teeth were previ- Management of hairy tongue primarily involves identifying and addressing 0
i/) </>
0 ously present ( see Photo 11; p.105). the cause. Other strategies include improving oral hygiene (see pp.273-5), 03
0
0 brushing the tongue gently with a toothbrush and using sodium bicarb-
Amalgam tattoos are benign and do not require treatment, beyond correct
onate mouthwash. A sodium bicarbonate mouthwash can be made by
T3
0 diagnosis. To confirm the diagnosis, metallic amalgam particles may be evi- 15
CD adding half a teaspoon of sodium bicarbonate powder to a glass of warm
dent on X-ray. If the diagnosis is not confirmed or if any ‘red flag’ features
<D
water. The mouthwash can be rinsed in the mouth on waking and at any
o
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of oral mucosal disease are present ( see Box 12; p.94), refer patients to
time during the day.
5
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104 105
 Photo 12. Hairy tongue Persistent ulcers (lasting more than 2 weeks despite addressing the cause
of trauma—see Photo 13, below) or recurrent ulcers require investigation;
refer to an appropriate specialist.

Photo 13. Persistent traumatic ulcer of the right posterior

lateral margin of the tongue

Traumatic oral ulcers

Oral ulceration due to trauma is common and can be associated with:
• eating rough, sharp or hot foods
• sharp broken teeth or dental restorations
• toothbrushing
• oral prostheses or orthodontic appliances
• chemical burns (eg following incorrect use of tooth-bleaching Recurrent aphthous ulcerative disease
products).
Recurrent aphthous ulcerative disease is the most common cause of non-
Address causes of trauma, including changing oral hygiene practices, traumatic ulcers of the oral mucosa. The disease has an immune-mediated
75
M smoothing sharp edges of teeth or restorations, adjusting prostheses or pathogenesis and is characterised by the periodic eruption of painful
0 placing wax on orthodontic appliances. ulceration of the oral mucosa. Aphthous ulcers can occur acutely with
O
smoking cessation, but these usually resolve with time, or can be triggered
TJ Most traumatic ulcers resolve spontaneously if the cause of the trauma
C by trauma (eg toothbrushing, orthodontic appliances) —to address causes
n has been adequately addressed. However, if any ‘red flag’ features of oral
of oral trauma, see p.106.
75 mucosal disease are present (see Box 12; p.94), refer to an appropriate
o specialist. The ulcers usually occur on the mucosa of the cheek, lip and floor of the
>
(/
mouth, but can occasionally affect the mucosa of the gingivae and hard
CD A salt water mouthwash is antiseptic and may provide symptomatic relief.
ECD If temporary pain relief is required, apply a topical anaesthetic or analgesic
2 to the ulcer, such as:
CD
.42 benzydamine 1% gel (adult and child 6 years or older) topically to
^
CD
the ulcer, 2 - to 3- hourly as necessary.
Q_
CD
CD

106
 • Major aphthous ulceration
- less common form
Management of recurrent aphthous
- presents as larger lesions (10 mm or more in diameter) ulcerative disease
- can persist for up to 6 weeks (and occasionally months) If an aphthae- like ulcer occurs in a child, refer for further investigation I
- heal with submucosal scarring. because it could be a sign of systemic disease.
• Herpetiform aphthous ulceration For management of aphthous ulcers in patients receiving palliative care,
rare see ‘Management of specific oral problems in palliative care’ in eTG
- presents as recurrent crops of nonvesicular small ulcers (1to complete .
2 mm in diameter) that coalesce to form larger ulcers
Topical corticosteroid treatment can produce rapid healing of minor aph-
- heal within 1to 2 weeks
thous ulcers, particularly if used in the prodromal or pre-ulcerative stage.
- not caused by the herpes virus, so do not have a cluster pattern. The aim is to treat the lesion rather than prevent further outbreaks; for
Assessment of aphthous ulcers involves taking a thorough history and adults, use:
examination; see also ‘red flag’ features of oral mucosal disease (Box 12;
hydrocortisone 1% cream or ointment topically to the lesions, 2 to
P - 94) . In children, investigate for systemic causes of nontraumatic ulcera- 3 times daily after meals.*
tion. In adults who have additional symptoms, investigate for a systemic
cause. Systemic causes of aphthous ulcers include:
If pain relief is required for minor aphthous ulcers in adults, apply a top-
• iron, vitamin B12, folate or zinc deficiency
ical anaesthetic or analgesic to the ulcers, such as:
• coeliac disease
• ulcerative colitis benzydamine 1% gel topically to the lesions, 2- to 3-hourly as
• Behget syndrome necessary.
• PFAPA (periodic fever, aphthous stomatitis, pharyngitis, cervical
adenitis) syndrome in children. Lidocaine viscous solution is an alternative topical anaesthetic for hospital
settings (but be aware of the higher cost) ; for adults, use:
Deficiencies should be treated only on laboratory confirmation—see
75 ‘Vitamin, mineral and trace element deficiencies’ in eTG complete for lidocaine 2% viscous solution, use the lowest dose necessary
management. up to 15 ml_, rinsed in the mouth for 30 seconds then spat out,
3 - hourly as necessary; maximum 8 doses in 24 hours.
CD
O
u Photo 14. Minor aphthous ulcer of the mandibular labial
c
CD
mucosa Ulcers that are not improving after 2 weeks are potentially malignant—refer
75
o—
to a specialist for management and biopsy.1
"
i

CO Seek specialist advice for patients with major or herpetiform aphthous CD

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ulceration or immunocompromised patients with neutropenic ulceration.
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-C t The treating specialist should perform the biopsy of an oral mucosal lesion. In rural or O
remote areas where a delay in specialist review is expected, seek expert advice on biopsy
technique a punch biopsy is not appropriate.
— 109
108
 To reduce the risk of virus transmission, advise patients with an active
Oral mucocutaneous herpes herpes simplex virus infection to avoid direct contact of the lesion with
other people.
Primary oral mucocutaneous herpes Treat minor primary oral mucocutaneous herpes with supportive man-
For the management of herpes simplex infection in neonates, see agement (ie oral fluids, antipyretic drugs and analgesia). Apply a topical
‘Neonatal herpes simplex infection’ in eTG complete . anaesthetic or analgesic, such as:
Primary oral mucocutaneous herpes simplex virus (HSV) infection (herpetic benzydamine 1% gel (adult and child 6 years or older), topically to
gingivostomatitis) often occurs in childhood with fever, painful intraoral the lesions, 2 - to 3- hourly as necessary.
lesions, systemic symptoms (eg malaise, lethargy) and cervical lymphad-
.
enopathy Intraoral herpes simplex virus lesions begin as blisters and
If this is not available, lidocaine viscous solution is an alternative topical
.
ulcerate rapidly—see Photo 15 (below) Healing occurs within several days
anaesthetic for hospital settings (but be aware of the higher cost):
in infants, but can take up to 2 weeks in older children. During this time, it
may be difficult to eat and drink and hospital admission may be required . lidocaine 2% viscous solution
Herpetic gingivostomatitis is rare in adults, but can be severe and present
adult: use the lowest dose necessary up to 15 mL, rinsed in the
with dehydration due to severe odynophagia.
mouth for 30 seconds then spat out, 3-hourly as necessary;
While herpes simplex virus is the most common virus to cause mouth maximum 8 doses in 24 hours
ulcers, other viruses (eg varicella zoster virus, coxsackie virus, cytomeg- child 3 years or older: use the lowest dose necessary up to
alovirus) may be the cause. Intraoral herpes simplex virus lesions may 0.2 mlVkg (maximum 5 mL) , rinsed in the mouth for 30 seconds
resemble those seen in necrotising gingivitis ( see p.73 for management of then spat out, 3 -hourly as necessary; maximum 4 doses in
necrotising gingivitis) ; however, necrotising gingivitis is rare in children and 24 hours*
is confined to the gingival tissues, while herpetic gingivostomatitis lesions
child younger than 3 years: use the lowest dose necessary up to
are widespread and affect all soft tissues in the mouth.
0.2 mL/kg (maximum 1.25 mL), applied to the affected areas
with a cotton swab, 3 - hourly as necessary; maximum 4 doses in
Photo 15. Intraoral lesions caused by the herpes simplex
24 hours.*
virus
75
If the pharynx is affected in adults and children older than 12 years, lido -
<D
Q caine viscous solution can be gargled and swallowed.
*
o
c Management of primary oral mucocutaneous herpes differs for the fol-
co
lowing patients, so referral to a medical practitioner is required:
75-
i

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(/) • immunocompromised patients 0
(/)

• patients with HIV.

CD 0
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children. Use the lowest dose necessary for the shortest duration, and do not exceed the
CD
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maximum recommended dose. Do not administer lidocaine viscous solution to infants or o
children for teething pain due to the risk of serious adverse effects (eg seizures, cardiac
offects, death) .
110 111
 Recurrent oral mucocutaneous herpes
Recurrent oral mucocutaneous herpes simplex virus (HSV) infection follows
latent reactivation of the virus. Lesions usually occur on the lips (herpes
simplex labialis or cold sores) , but can also occur on the intraoral mucosa
or other areas of skin.
Lesions are usually preceded by the prodromal stage, lasting several hours
to days, which features pain, burning, tingling or itching. Recurrences are
usually mild and infrequent, and their frequency can be minimised with sun
.
protection Herpes simplex virus reactivation may be complicated by ery-
thema multiforme ( see ‘Erythema multiforme’ in eTG complete ) .
A herpes simplex virus lesion affecting the oral mucosa cannot be dif-
ferentiated from an aphthous or traumatic ulcer using microbiological
testing—most adults will have positive serology for the herpes simplex virus
from previous exposure, and viral DNA may be detected on swabs of aph-
thous or traumatic ulcers. Instead, diagnosis requires a thorough history
and clinical examination.
To reduce the risk of virus transmission, advise patients with an active
herpes simplex virus infection to avoid direct contact of the lesion with
other people.
For a minor recurrence of oral mucocutaneous herpes, episodic antiviral
therapy may reduce its duration; use:
Mucous membrane pemphigoid
Mucous membrane pemphigoid is an uncommon autoimmune vesicu-
lobullous disorder that affects stratified squamous epithelium. It occurs
predominantly on the gingivae and palate ( see Photo 16, below) . Mucous
membrane pemphigoid presents as large, painful and persistent ero-
sions, and is characterised by subepithelial splitting, with bulla or vesicle
formation. The lesions heal with variable amounts of scarring. Differential
diagnosis includes pemphigus vulgaris (see ‘Pemphigus vulgaris’ in eTG
complete ) .
Refer patients with suspected mucous membrane pemphigoid to an appro-
priate specialist for biopsy and definitive diagnosis.* Management usually
requires long-term use of immunosuppressive therapy. Ophthalmologist
review is necessary because there is a risk of blindness with mucous mem-
brane pemphigoid.
Photo 16. Mucous membrane pemphigoid affecting the
mandibular gingivae

i aciclovir (adult and child older than 3 months) 5% cream topically,

5 times daily (every 4 hours while awake) for 5 days, started at
75 the first sign of recurrence or during the prodromal stage
<D OR
O
T3
c i famciclovir (adult) 1500 mg orally, as a single dose, taken at the
first sign of recurrence or during the prodromal stage.
03
75
o-
i

Using aciclovir cream for longer than recommended has no benefit. o

ID
(D
ID
03
<D
£CD Management of recurrent oral mucocutaneous herpes differs for the fol-
£
lowing patients, so referral to a medical practitioner is required: o
Z3
CD • patients with severe recurrences of herpes (with systemic signs and 75
ID
.2 symptoms, or if the patient has difficulty eating or swallowing) O
o
3
CD • patients with generalised or chronic herpes infection (with crusted E
CL
lesions and ulceration) 75
2
0 • immunocompromised patients * The treating specialist should perform the biopsy of an oral mucosal lesion. In rural or O
-
i

jC
• patients with HIV. remote areas where a delay in specialist review is expected, seek expert advice on biopsy
technique a punch biopsy is not appropriate.
— 113
112
 Oral candidiasis and Candida - associated Table 11. Overview of oral candidiasis and Candida -
lesions associated lesions
Pseudomembranous candidiasis
Candida species are a commensal organism of the oral cavity. Oral candidi- Clinical features
asis is an opportunistic infection that is uncommon in healthy individuals; creamy white curd, papules and plaques that are
however, it occurs relatively commonly in neonates. Table 10 (below) lists sometimes removable
common risk factors for oral candidiasis. Table 11 (pp.115-7) gives an red , raw and often bleeding base
overview of the clinical features, predisposing factors and management of generally asymptomatic
oral candidiasis and Candida -associated lesions. If any ‘red flag’ features may affect the oropharynx
of oral mucosal disease are present (see Box 12; p.94), refer to an appro- if the dorsal tongue is affected, autoinoculation of the
priate specialist. palate may occur

Predisposing factors
Table 10. Common risk factors for oral candidiasis
see Table 10 (p.114) for risk factors for oral
Local factors Systemic factors candidiasis
neonates
dentures immune compromise (eg poorly controlled diabetes)
salivary gland hypofunction drugs (eg systemic corticosteroids, antibiotics) Management

corticosteroid inhalers address predisposing factors

poor oral hygiene use topical antifungal therapy for oral candidiasis (see
p.118)
smoking
if the infection affects the oropharynx, refer for
specialist management
For management of oral candidiasis in patients receiving palliative care,
Erythematous candidiasis
see ‘ Management of specific oral problems in palliative care’ in eTG
complete. Clinical features
sensitive red lesions commonly affecting the palate
Management of oral candidiasis in immunocompromised patients requires and tongue
75 specialist advice.
g the tongue may appear depapillated and smooth
<D
O Patients with undiagnosed HIV infection may present initially with oral can - Predisposing factors
"o didiasis. For patients with HIV, see ‘Oropharyngeal candidiasis in adults with see Table 10 (p.114) for risk factors for oral
rc HIV infection’ in eTG complete for advice on systemic antifungal therapy. candidiasis
75 broad- spectrum antibiotic therapy
o Management
(/
> address predisposing factors <D
o >
(/

use topical antifungal therapy for oral candidiasis (see CO

CD
0 p.118) .<2
~o
=3
o continued next page
75
.9 (/
>
o
o
o 3
CZ
2 E
o
JZ
75
O

114 115
 Table 11. Overview of oral candidiasis and Candida -
Table 11. Overview of oral candidiasis and Candida -
associated lesions (cont.)
Hyperplastic candidiasis
Denture-associated erythematous stomatitis ( denture stomatitis)
Clinical features
asymptomatic, nonremovable white plaques that may
appear nodular
usually affects the retro-commissures, anterior buccal
mucosa and lateral tongue
may be bilateral
may resemble oral leukoplakia (see p.98) or oral
cancer (see p.95)
Predisposing factors
see Table 10 (p.114) for risk factors for oral candidiasis
Management
address predisposing factors
may be associated with epithelial dysplasia—refer to a
specialist for biopsy and management [NB1]
Angular cheilitis (angular stomatitis)
Clinical features
painful erythema and Assuring of the corners of the
mouth
usually caused by a mixed infection of Candida ,
Staphylococcus aureus and Streptococcus species
often associated with intraoral candidiasis
associated lesions (cont.)
Clinical features
sensitive erythematous lesions confined to denture -
bearing areas, particularly the palate
may appear punctate, or smooth and red
nodular hyperplasia may be observed
Predisposing factors
see Table 10 (p.114) for risk factors for oral candidiasis
ill-fitting dentures
suboptimal oral and denture hygiene
dietary factors
Management
advise patient to optimise denture hygiene and to
remove dentures at night, clean them, then store
them dry overnight ( for denture hygiene advice, see
-
P 275)
dental review to assess fit of dentures
if symptoms do not resolve after 1month of optimal
oral and denture hygiene, use topical antifungal
therapy for oral candidiasis (see p.118) applied inside
the mouth and to the dentures
Median rhomboid glossitis

Predisposing factors Clinical features

75 rhomboid area of depapillation and erythema in the
see Table 10 (p.114) for risk factors for oral candidiasis
midline of the dorsal tongue
0 deep skin folds around the mouth (associated with
O worn down teeth, ill- fitting dentures or not wearing may be fissured or nodular
D
autoinoculation of the palate may occur
*

C dentures)
cu iron, folate or vitamin B12 deficiency usually asymptomatic although it may sting or burn
75
o-
i Crohn disease Predisposing factors

in
granulomatous disease
see Table 10 (p.114) for risk factors for oral candidiasis 0
CD atopic and seborrhoeic dermatitis (/)
Management 03
0
2
CD Management address predisposing factors .12o
Z5 dental review to assess dental or denture-related use topical antifungal therapy for oral candidiasis (see
CD causes p.118) 75
.9 address predisposing factors
in
o
o
D
( use topical antifungal therapy for angular cheilitis (see 3
Q-
03 -
P 119) E
75
NB1: The treating specialist should perform the biopsy of an oral mucosal lesion.
CD treat oral candidiasis if present, with topical antifungal In rural or
ZZ
therapy for oral candidiasis (see p.118) on biopsy O
remote areas where a delay in specialist review is expected, seek expert advice
continued next page technique—a punch biopsy is not appropriate .
116
 Antifungal therapy for oral candidiasis
For management of oral candidiasis in patients with HIV infection, see
‘Oropharyngeal candidiasis in adults with HIV infection’ in eTG complete.
For management of oral candidiasis in patients receiving palliative care,
see ' Management of specific oral problems in palliative care' in eTG
complete .
Management of oral candidiasis in immunocompromised patients requires
specialist advice.
Antifungal therapy is not always necessary for oral candidiasis and
Candida -associated lesions—see Table 11 (pp.115-7) for indications for
antifungal therapy. Successful treatment relies on adequate contact time
between the antifungal and the affected mucosa, so advise patients not to
eat or drink directly after administration.
Treat oral candidiasis in neonates and children younger than 2 years with
a topical antifungal. In infants, apply the dose in the front of the mouth to
.
avoid choking Use:
i nystatin 100 000 units/mL suspension 1mL topically (then
swallowed), 4 times daily, after feeding, for 7 to 14 days; continue
treatment for 2 to 3 days after symptoms resolve*
OR
2 miconazole 2% gel 1.25 mL topically (then swallowed), 4 times
daily, after feeding, for 7 to 14 days; continue treatment for at
« least 7 days after symptoms resolve.
5
o hydrocortisone 1% cream topically to the angles of the mouth,
a Treat oral candidiasis in adults and children 2 years and older with;
m i miconazole 2% gel 2.5 mL topically (then swallowed) , 4 times
5 daily, after food, for 7 to 14 days; continue treatment for at least
o 7 days after symptoms resolve
£ OR
I amphotericin B 10 mg lozenge sucked (then swallowed), 4 times
o daily, after food, for 7 to 14 days; continue treatment for 2 to
B 3 days after symptoms resolve
5
& OR
sz
118
* Nystatin suspension contains sucrose.
3 nystatin 100 000 units/mL suspension 1mL topically (then
swallowed), 4 times daily, after food, for 7 to 14 days; continue
treatment for 2 to 3 days after symptoms resolve.*
Advise patients with dentures to use miconazole or nystatin, because the
antifungal should be applied to the fitting surface of the dentures at least
twice a day. Dentures should be removed from the mouth at night, then
.
cleaned and stored in a dry environment overnight For instructions on
cleaning dentures, see p.275.
Evaluate patients with intractable candidiasis for systemic disease (eg dia-
betes, HIV infection).
Antifungal therapy for angular cheilitis
Treat angular cheilitis with a topical antifungal cream; use:
i clotrimazole 1% cream topically to the angles of the mouth, twice
daily for at least 14 days; continue treatment for 14 days after
symptoms resolve
OR
2 miconazole 2% cream topically to the angles of the mouth, twice
daily for at least 14 days; continue treatment for 14 days after
symptoms resolve.
A mild topical corticosteroid can be used in addition to the topical anti-
fungal, to treat the associated inflammatory dermatitis; use:
twice daily until inflammation subsides.
Combination products containing a topical corticosteroid and antifungal are
available, but should only be used until inflammation subsides. Treatment a)
should be completed with a topical antifungal alone, for 14 days after </ >
symptoms resolve.
a
.
If oral candidiasis is present, treat with antifungal therapy (see p 118) .
.2
-o
w
Seek specialist advice for persistent angular cheilitis. Treatment for mixed g
Infection may be required or it may be a symptom of a systemic condition,
O
such as Crohn disease or granulomatous disease. E
O
‘ Nystatin suspension contains sucrose. 119
 If pain is not adequately managed with topical measures, systemic anal-
Oral mucositis gesics may be required— seek advice from the patient’s multidisciplinary

Oral mucositis presents as painful inflammation, redness, swelling

team .
and ulceration of the oral mucosal surfaces caused by radiotherapy, Establish preventive oral care regimens, and regularly assess the oral
chemotherapy or other drugs. Oral mucositis is a type of stomatitis (an cavity. Patients with profound mucositis have difficulty performing oral
inflammatory condition of the oral tissues). Other causes of stomatitis hygiene measures effectively, though this should be encouraged neverthe-
include salivary gland hypofunction (for management of dry mouth, see less. Chlorhexidine limits exposure to water-borne pathogens, and can be
p.121) and vitamin deficiencies. Take a thorough history and examination used when pain and discomfort restrict oral hygiene practices; use:
to identify the cause.
chlorhexidine 0.2% mouthwash alcohol-free, 10 mL rinsed in the
Oral mucositis can lead to significant problems with eating, drinking and mouth for 1minute then spat out, 8- to 12-hourly (use diluted
adherence to medication. Patients undergoing treatment of cancer who with 10 mL of water if stinging occurs) .*
develop mucositis have an increased risk of systemic infection and require
longer hospital admissions.
Chlorhexidine gel is an alternative oral hygiene adjunct to mouthwash, and
Patients should be dentally fit before starting chemotherapy or head may provide some lubrication and ease discomfort; use:
and neck radiotherapy, particularly if the treatment will result in severe
chlorhexidine 0.5% gel alcohol-free, apply 2 to 3 times daily to all
mucositis and reduced salivary flow. For more information on the dental
management of patients receiving chemotherapy or head and neck radio-
mucosal surfaces and gingival margins * .
therapy, see p.174 and p.175.
Nutritional support for patients with mucositis is important. Encourage
patients to avoid irritant foods (eg acidic, spicy, salty, dry or abrasive
Management of oral mucositis foods). Refer patients for specialist nutritional advice if mucositis is severe.
For management of oral mucositis in patients receiving palliative care, see
‘ Management of specific oral problems in palliative care’ in eTG complete.
Dry mouth
For management of oral mucositis in children, seek expert advice.
15 The subjective feeling of dry mouth (xerostomia) is a relatively common
Manage oral mucositis in conjunction with a multidisciplinary team, which
condition that may or may not occur in the context of salivary gland hypo-
function (an objective reduction in the quantity and the quality of saliva) .
0 includes addressing the cause, symptomatic relief, oral care regimens and
o nutritional advice.
~o
c Many physiological and pathological conditions and drugs can cause
salivary gland hypofunction or dry mouth. Common causes of dry mouth
o: Initial and regular ongoing assessment of oral pain is essential . Lubricants
15 and analgesic mouth solutions may reduce pain and inflammation.
o- Include:
i

Artificial salivary products can be applied as necessary for transient relief of

oral dryness. If a topical analgesic is needed, use: • dehydration 0
0 CO
• alcohol 03
0
0 1 benzydamine hydrochloride 0.15% solution 15 mL, rinsed in • anxiety .2
0 the mouth for 30 seconds then spat out, 1.5- to 3-hourly as • mouth breathing
O
CD 15
• drugs ( see Box 13; p.122).
necessary (use diluted with 15 mL of water if stinging occurs)
1
co
o
OR o
If common causes have been excluded, investigate for less common med-
0 3
CL
E
2 2 lidocaine 2% viscous solution, use the lowest dose necessary ical conditions associated with dry mouth (eg Sjogren syndrome) .
0 15
-£= up to 15 mL, rinsed in the mouth for 30 seconds then spat out, o
3- hourly as necessary; maximum 8 doses in 24 hours. • When used for more than a few days, chlorhexidine may cause a superficial discolouration
120 of the teeth and fillings (see p.59 for more information). 121
 Box 13. Drugs frequently associated with dry mouth [NB1] Management of dry mouth
• anticholinergic drugs
For management of dry mouth in patients receiving palliative care, see
• antihistamines Management of specific oral problems in palliative care’ in eTG complete.
• drugs to lower blood pressure
Encourage patients to have a dental review and any necessary dental treat-
- angiotensin converting enzyme inhibitors
ment before starting a drug that can cause dry mouth.
- angiotensin II receptor blockers
Review the patient's medications and, in conjunction with the prescriber,
- alpha blockers
slop any non-essential medications that can cause a dry mouth.
- beta blockers
- diuretics Management strategies for patients with dry mouth include:
• inhaled bronchodilators • ensuring adequate hydration
- beta2 agonists (eg salbutamol) • ensuring good oral hygiene (see pp.273-5)
- muscarinic antagonists (eg tiotropium) • regular dental examination and treatment every 3 to 6 months
• opioids • topical remineralising agents to prevent tooth decay (see p.65)
• symptomatic relief.
• psychotropic drugs
- antidepressants Options for the symptomatic relief of dry mouth include:
- antipsychotics • artificial salivary products or other oral lubricants (eg bicarbonate
- illicit drugs (eg marijuana, cocaine) mouthwash) (however, effects may be too transient to be of significant
- psychostimulants (eg amfetamines) benefit)
• urinary antispasmodics • products that stimulate saliva, such as throat lozenges or chewing
gum (however, many products are acidic or have a high sugar content,
NBl: Dry mouth is likely to be more severe if these drugs are used in combination.
which can cause further tooth decay).
Dry mouth is a debilitating adverse effect of head and neck radiotherapy, Box 14 (p.124) outlines nonpharmacological advice for patients with dry
75 with the degree of salivary flow reduction dependent on the dose and mouth.
c region of the radiation (see also p.175 for the dental management of
I( symptomatic measures are inadequate, or if dry mouth is a symptom of
a patients undergoing head and neck radiotherapy). .
systemic disease, refer patients to an appropriate specialist
c Chronic dry mouth can have a profound effect on the oral environment and

o
—
to
w
can contribute to:
• tooth decay (dental caries; see pp.63-70) and erosion
is • periodontal disease (see pp.71-6) o
</>
£ • oral mucosal disease (see pp.93-124) 03
<D
3 • oral candidiasis (see p.114) .<2
-D
a • difficulty with the retention of dentures 75
s • difficulty with chewing, swallowing and speech g
o
E • altered sense of taste.
so5 - E
-C
75
O

122 123
 Box 14. Practical advice for patients with dry mouth

To manage your dry mouth:

• ensure you are adequately hydrated—drink at least 1.5 litres of tap water a day
• chew food thoroughly before swallowing because chewing stimulates saliva flow Halitosis
• chew sugarless gum or suck sugarless sweets (avoid fruit flavours)
• avoid smoking cigarettes
• avoid acidic foods
• limit your caffeine and alcohol intake, especially in the evening Diagnosis of halitosis
- add milk to tea or coffee to reduce the drying effect
Halitosis is an unpleasant noxious odour emanating from the oral cavity.
• avoid mouthwashes and other oral preparations that contain alcohol
• trial various over-the- counter dry mouth products or bicarbonate mouthwash Halitosis can have a self-limiting, intraoral or extraoral cause (see Box 15,
below) . Definitive diagnosis can be difficult and requires a thorough dental
- a bicarbonate mouthwash can be made by adding half a teaspoon of
bicarbonate powder to a glass of warm water. Rinse with mouthwash on and medical history. Examination of the nose, tonsils, mucosal surfaces of
waking and at any time during the day. the pharynx and oral cavity, and teeth is required.

To prevent oral and dental consequences of dry mouth: Box 15. Common causes of halitosis
• ensure you have good oral hygiene
• have regular dental examinations Self-limiting causes
• avoid acidic beverages (eg wine, fruit juices, soft drinks, sports drinks) or limit • dry mouth from mouth breathing or snoring
their consumption to meal times • odour-causing foods (eg garlic, onions, spices)
• limit your sugar intake and avoid sugary snacks. • smoking and alcoholic beverages

Intraoral causes
• poor oral hygiene (eg food particles between the teeth, on the tongue and
75 around the gums)
CD • intraoral bacteria
Q
~o
- tongue colonisation
c - dental caries
03
- periodontitis
75
o • acute infections within the mouth including:
</ j - dental abscess
CD
- oral candidiasis
£O - necrotising gingivitis
2
D • salivary gland hypofunction
O
• tonsillar pathology
.2
- chronic caseous tonsillitis .<2
in

I
CD
Cl - peritonsillar abscess
CD
CD
• oral cancer CD
DC continued next page X

125
124
 Box 15. Common causes of halitosis (cont.) Perceived halitosis ( without detectable oral malodour) may reflect a psy-
chological illness. Other people ’s behaviour, or perceived behaviour, such
Extraoral causes as covering the nose or averting the face, is typically misinterpreted by
• acute pharyngeal infections (eg streptococcal pharyngitis, glandular fever) these patients as an indication that their breath is offensive.
• respiratory Devices that objectively measure volatile sulfur compounds give variable
- postnasal drip results, are costly and are not recommended.
- sinusitis
Poor oral hygiene or a poorly designed denture or bridge can result in accu-
intranasal foreign bodies
mulation of dental plaque and food debris, which can worsen halitosis.
-

- bronchitis
- bronchiectasis
- lung abscess Management of halitosis
- respiratory tract cancer
• gastrointestinal
Initial management of halitosis requires identifying and addressing the
- Zenker diverticulum cause (see Box 15; p.126).
- gastrocolic fistulae
- Helicobacter pylori infection (not well established) Management of self-limiting causes of halitosis includes:
- gastro - oesophageal reflux disease (not well established) • improving oral hygiene, including tongue cleaning (see pp.273-5)
• advanced kidney disease • avoiding odour-causing foods, smoking and alcoholic beverages
• advanced liver disease • addressing the cause of mouth breathing, if identified
• trimethylaminuria • considering a trial of other nonspecific measures, such as:
• ketoacidosis (eg starvation, protein-only diet, diabetes) - chewing sugar-free gum to stimulate saliva
- ensuring adequate hydration
Self -limiting causes of halitosis are common on waking, usually due to
- reducing caffeine intake.
low salivary flow and lack of oral cleansing during sleep. Oral malodour
is the result of microbial degradation of various substrates into volatile Management of intraoral causes of halitosis depends on the origin of the
75 compounds (eg sulfur) . The dorsal surface of the tongue is the most likely malodour—see Box 15 ( p.126) . Promote oral hygiene for patients with an
location of the microbial population causing halitosis. Self- limiting causes intraoral cause of halitosis (see pp.273-5). If improved oral hygiene and
0)
o of halitosis can be rectified by eating, rinsing the mouth with water and management of intraoral causes does not resolve halitosis, referral to a
u
c
oral hygiene. Other causes of self-limiting halitosis include food (eg garlic, medical practitioner is appropriate to investigate for extraoral causes.
CD onion, spices), smoking and alcoholic beverages.
75
O -
i
Intraoral causes of halitosis include poor oral hygiene or underlying
pathology, most commonly intraoral infections (eg periodontal infections,
Promote oral hygiene for patients with transient or intraoral
causes of halitosis.
f/5
0 pericoronitis). Although halitosis is the result of a complex interaction
If an extraoral cause of halitosis is identified, manage as required; referral
between several bacterial species, the most active bacteria are Gram -
may be necessary.
0

U
negative anaerobes that are associated with periodontal disease.
(J
Refer patients with persistent or recurrent halitosis to a specialist (eg oral
. 9 Poor oral hygiene results in accumulation of dental plaque and medicine specialist, periodontist) .
0
food debris, which can worsen halitosis. .US2 )
Patients with psychogenic halitosis present a diagnostic and treat-
i
Cl
2 Extraoral causes of halitosis include systemic conditions, such as res- ment challenge, and, despite reassurance, may require psychological
0
assessment.
03
J0
piratory infections, gastrointestinal disorders, advanced kidney disease and X
ketoacidosis.
126 127
Orofacial pain

Overview of orofacial pain for dentists

Pain is ‘ an unpleasant sensory and emotional experience associated with
actual or potential tissue damage, or described in terms of such damage’.*
Pain is a subjective experience influenced by both sensory inputs received
by the brain (eg in response to inflammation) and the brain ’s interpretation
of these inputs in the context of other available information. For example,
a patient’s pain experience may be influenced by their coping strategies,
previous experiences with pain and pain relief, and their confidence in the
clinician’s ability to diagnose and manage their condition.
Orofacial pain has many causes, only some of which are dental. If the
patient’s pain is not of dental origin, refer them for medical assessment. If
the patient’s pain is of dental origin, assess the type of pain ( nociceptive,
neuropathic or nociplastic) and its duration (acute or chronic), because
these factors affect the optimal treatment strategy.
Nociceptive pain arises from activation of nociceptors (receptors in skin
and deep tissues that are sensitive to potentially noxious stimuli) due
to threatened or actual tissue damage (eg inflammation in irreversible
pulpitis).
Neuropathic pain arises from injury or disease of the somatosensory
nervous system. It is often described as a burning or tingling sensation.
Oral neuropathic pain is not uncommon. It can be difficult to diagnose,
and investigation by a dental specialist (eg oral medicine specialist, oral
surgeon, oral and maxillofacial surgeon) may be required.
Nociplastic pain is a diagnosis of exclusion; it is considered when nocicep-
tive and neuropathic pain have been ruled out. In nociplastic pain states, .E
central sensitisation is the key contributor, rather than ongoing pathology.
TO
CL
75
o
£o
* Merskey H, Bogduk N, editors for IASP Task Force on Taxonomy. Classification of chronic O
pain: descriptions of chronic pain syndromes and definitions of pain terms. 2nd ed.
Seattle: International Association for the Study of Pain; 1994.
129
 Pain managed by dentists is usually acute dental pain (see pp.130-43) .
Such pain:
• is usually nociceptive
• usually resolves rapidly with appropriate dental treatment, but may
require short-term use of analgesics
• serves a protective biological function—it alerts the body to a potential
threat, prevents the body from further harm, and can teach the body
to avoid similar harm in the future.
Chronic pain (also referred to as persistent pain) may be associated with
ongoing pathology; however, often the originating pathology is no longer
evident and pain persists because of lasting changes within the nervous
system. Such pain:
• may be nociceptive, neuropathic, nociplastic or mixed
• can be difficult to diagnose because there may not be any obvious
pathology
• may result in anxiety, fear, depression, loss of sleep and impaired
social functioning; these factors may also affect a patient’s pain
experience
• requires a sociopsychobiological (biopsychosocial) approach to
assessment and management; see the Analgesic topics in eTG
complete. Analgesics have a limited role.
Causes of chronic orofacial pain include temporomandibular disorders (see
p.144) and burning mouth syndrome (see p.146) .
If a patient with chronic orofacial pain presents with dental pain, determine
15
•M whether the pain is a symptom of their chronic pain condition or associ-
0 ated with a dental pathology. Do not undertake dental treatment unless a
o dental pathology is confirmed to be causing the pain.
a • following surgical procedures that cause postoperative pain
c • when a patient has presented to a medical practitioner and is unable
cu
_
15s
Acute dental pain
o certain indications ( see Table 12; p.132 6) and the patient should
< />
CD Acute dental pain is usually inflammatory in nature. Table 12 (pp.132-6)
i
:
0 outlines common causes of acute dental pain. Also consider cond-
0
itions that are less common, difficult to diagnose or not of dental origin
o (eg trigeminal neuralgia may be mistaken for pulpitis). Refer patients for
.9 medical assessment if their orofacial pain is not of dental origin.
0 o
Cl
CD Dental treatment is the most effective means of reducing pain of
0
the teeth and surrounding tissues.
130
Dental treatment is the most effective means of managing acute pain of
the teeth or surrounding tissues. Drug therapy has a more limited role and
should only be used if necessary.
Patients with dental pain presenting to a
medical practitioner
If a patient with dental pain presents to a medical practitioner and is
unable to see a dentist promptly, interim treatment may be needed—see
Table 12 (pp.132-6) for initial management of common causes of dental
pain. However, the medical practitioner should stress the importance of
seeing a dentist, because dental treatment is often the definitive treatment
of conditions causing dental pain.
If dental review is not immediately available, the medical practitioner may
consider a panoramic X- ray—an orthopantomogram (OPG) —to exclude
serious pathologies (eg gross dental caries, jaw fractures, jaw lesions such
as cysts).
Indications for analgesics for acute dental
pain
Analgesics modify the sensation of pain but do not address its cause.
Therefore, for acute dental pain, analgesics should only be used as an
adjunct to dental treatment in the following circumstances:
• when the patient’s pain cannot be eliminated or adequately controlled
by dental treatment and other required drugs (eg antibiotic therapy for
spreading infection)
to see a dentist promptly—interim analgesics should be offered for
-
be reminded that dental treatment is necessary to treat the cause of
pain.
Analgesics should only be used as an adjunct to appropriate .£
dental treatment. cu
CL
The analgesic regimens in this topic are only suitable for nociceptive pain.
15
-o2
For neuropathic or nociplastic pain, further investigations and other man-
o
agement approaches are required ( see p.129 for further information) .
131
w Therapeutic Guidelines: Oral and Dental
Table 12. A guide to differentiating and managing acute dental pain
Description of pain and
associated features
intermittent dental pain that is experienced
when the tooth is exposed to a stimulus (eg hot,
cold or sweet food or drinks) and resolves once
the stimulus is removed
severe dental pain that is experienced when
the tooth is exposed to a stimulus (eg hot,
cold or sweet food or drinks)
pain persists as a dull throbbing ache after
the stimulus is removed, and can become
continuous
Table 12. A guide to differentiating and managing acute dental pain (cont.)
Description of pain and
associated features
dental pain that presents as a dull throbbing
ache, and is not triggered by a stimulus such
as hot, cold or sweet food or drinks
tooth may be sore to bite on
tenderness of the tooth to pressure and
on biting
w
CJ Orofacial pain
Likely cause and suggested management
Likely cause: reversible pulpitis
Initial management by medical practitioners
advise the patient to avoid food or drink that provokes pain
cover any obvious cavity with an inert material (eg chewing gum, Blu Tack)
advise the patient to see a dentist as soon as possible
analgesics and antibiotic therapy are not indicated
Dental treatment
simple restoration or desensitisation treatment is required
Likely cause: irreversible pulpitis
Initial management by medical practitioners
advise the patient to avoid food or drink that provokes pain
offer analgesics— NSAIDs are preferred if the patient can use them (see p.137)
cover any obvious cavity with an inert material (eg chewing gum, Blu Tack)
if symptoms are severe, consider local anaesthesia of the affected tooth for temporary pain relief ( for
information on local anaesthetics in dentistry, see pp.201-9)
advise the patient to see a dentist as soon as possible
antibiotic therapy is not indicated
Dental treatment
endodontic treatment (root canal) or extraction is usually needed
continued next page
Likely cause and suggested management
Likely cause: infected root canal system with acute periapical inflammation (apical periodontitis)
Initial management by medical practitioners
offer analgesics—NSAIDs are preferred if the patient can use them (see p.137)
advise the patient to see a dentist urgently
antibiotic therapy is not indicated for a localised odontogenic infection (see p.81); however, if
dental treatment is not likely to be received within 24 hours, start antibiotic therapy as for spreading
odontogenic infection without severe or systemic features (see p.83)
Dental treatment
endodontic treatment (root canal) or extraction is needed
Likely cause: fractured or cracked tooth (see p.225) or localised odontogenic infection (see p.81)
Initial management by medical practitioners
advise the patient to see a dentist urgently; it is difficult for medical practitioners to differentiate a
fractured tooth from a localised odontogenic infection (even with imaging) without a visible abscess or
pus to indicate infection
offer analgesics— NSAIDs are preferred if the patient can use them (see p.137)
antibiotic therapy is only indicated if a localised odontogenic infection is confirmed and dental
treatment is not likely to be received within 24 hours—see p.83 for a suggested regimen
Dental treatment
restoration, endodontic treatment (root canal) or extraction is needed
continued next page
w Therapeutic Guidelines: Oral and Dental
Table 12. A guide to differentiating and managing acute dental pain (cont.)
Description of pain and
associated features
facial swelling and pain following a toothache
without any of the following:
significant facial swelling and pain, trismus,
neck swelling, difficulty swallowing, difficulty
breathing, airway compromise or systemic
features of infection
swelling and pain following a toothache with any
of the following:
significant facial swelling and pain, trismus,
neck swelling, difficulty swallowing, difficulty
breathing, airway compromise or systemic
features of infection
Table 12. A guide to differentiating and managing acute dental pain (cont.)
Description of pain and
associated features
dental pain worsening 1to 4 days after tooth
extraction
acute onset of severe pain throughout the
mouth associated with gingival bleeding and
necrosis or ulcers of the interdental papillae
halitosis is usually present
oo
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Orofacial pain
-
SB
Likely cause and suggested management
Likely cause: spreading odontogenic infection without severe or systemic features (see p.82)
Initial management by medical practitioners
offer analgesics—NSAIDs are preferred if the patient can use them (see p. 137)
if dental treatment is not likely to be received within 24 hours, start antibiotic therapy (see p.83);
otherwise antibiotic therapy is not indicated
advise the patient to see a dentist urgently
Dental treatment
endodontic treatment (root canal) or extraction is needed
Likely cause: spreading odontogenic infection with severe or systemic features (see p.84)
Initial management by medical practitioners
provide appropriate support of airway, breathing and circulation
arrange urgent transfer to a hospital with an oral and maxillofacial surgeon or other appropriate expert
Dental treatment
surgical intervention and intravenous antibiotic therapy is needed—see p.85
continued next page
Likely cause and suggested management
Likely cause: alveolar osteitis (dry socket; see p.222)
Initial management by medical practitioners
flush the socket with warm sterile saline until all debris is removed from the socket
offer analgesics—NSAIDs are preferred if the patient can use them (see p.137)
advise the patient to see the practitioner who performed the extraction urgently
antibiotic therapy is not indicated
Dental treatment
further socket irrigation and analgesia may be needed
an obtundent dressing may relieve pain
Likely cause: necrotising gingivitis (previously known as acute necrotising ulcerative gingivitis)
Initial management by medical practitioners
offer analgesics (to select an appropriate analgesic regimen for acute dental pain, see p.137)
chlorhexidine mouthwash or hydrogen peroxide solution may be used if pain limits the patient’s ability
to mechanically clean their teeth
advise the patient to see a dentist urgently
for further management advice, see p.73
Dental treatment
thorough local debridement of the gingiva, local irrigation and antibiotic therapy are needed
continued next page
M
 Choice of analgesic for acute dental pain
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 Analgesic regimens for mild to moderate
acute dental pain in adults
For factors that affect the choice of analgesic regimen, see p.137.
Nonopioid analgesics (NSAIDs and paracetamol) should be taken regularly,
rather than as required, to achieve continuous pain relief.
Analgesic regimens for severe acute dental
pain in adults
For factors that affect the choice of analgesic regimen, see p.137.
Nonopioid analgesics (NSAIDs and paracetamol) should be taken regularly,
rather than as required, to achieve continuous pain relief.

If adjunctive analgesia is required for mild to moderate acute nociceptive For severe acute nociceptive dental pain (eg after dental surgery) in
dental pain (for indications, see p.131), use:
patients who can use NSAIDs, as a three- drug regimen, consider:

ibuprofen 400 mg orally, 6- to 8- hourly for the shortest duration

ibuprofen 400 mg orally, 6- to 8- hourly for the shortest duration
possible and no more than 5 days without review
possible and no more than 5 days without review

PLUS OR (if a C0X- 2-selective NSAID is preferred based on the

patient’s risk factors— see pp.44-9)
paracetamol 1000 mg orally, 4- to 6-hourly (to a maximum of 4 g
in 24 hours) for the shortest duration possible. celecoxib 100 mg orally, twice daily for the shortest duration
possible and no more than 5 days without review

Avoid fixed- dose combination products because they do not allow the daily PLUS
dose of each drug to be maximised. As the tissue heals, stop ibuprofen
paracetamol 1000 mg orally, 4- to 6- hourly (to a maximum of 4 g
and use paracetamol as a single drug.
in 24 hours) for the shortest duration possible
If a C0X- 2-selective NSAID is preferred based on the patient’s risk factors
( see pp. 44-9), use: PLUS
oxycodone immediate- release 5 mg orally, every 4 to 6 hours as
celecoxib 100 mg orally, twice daily for the shortest duration
necessary, for the shortest duration possible and no more than
possible and no more than 5 days without review
3 days. Use a lower dose in elderly or frail patients because they
PLUS are particularly vulnerable to adverse effects. Prescribe small
75
M quantities to avoid inappropriate use in the community.
0 paracetamol 1000 mg orally, 4- to 6- hourly (to a maximum of 4 g
Q in 24 hours) for the shortest duration possible. In patients who cannot use NSAIDs, use paracetamol plus oxycodone.
o
c
cu Always consider the benefits, harms and regulatory requirements of pre-
As the tissue heals, stop celecoxib and use paracetamol as a single drug.
75 scribing an opioid ( see pp.50 4) . Prescribe the lowest effective dose, and
If NSAIDs are contraindicated (see Box 8; p. 46) , use:
-

O advise patients to take a dose only when necessary. Ensure the patient
i
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0
paracetamol 1000 mg orally, 4- to 6- hourly (to a maximum of 4 g
£o in 24 hours) for the shortest duration possible.
the opioid or return for review (eg if pain persists for longer than expected).
This is of particular importance because long-term opioid use often starts
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If analgesics are used after a surgical procedure that causes postoperative patient requires less analgesia, use a stepwise approach to tapering
Q .
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pain, inform the patient of the usual course of pain (eg pain is worst 48 to and stopping analgesics. First, stop oxycodone, then stop ibuprofen or 75
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72 hours after surgery, then improves). Advise the patient to return to the celecoxib, and lastly, stop paracetamol.
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dentist for review if pain persists.
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Ensure patients understand the intended duration of opioid use.

138 139
 For patients currently taking opioids for another indication, consult their
medical practitioner to determine an appropriate analgesic regimen;
specialist pain management advice may be required if the patient is
opioid- dependent.
If opioids have not been required in hospital or pain can be successfully
managed with nonopioid analgesia, do not prescribe opioids on discharge.
Do not use modified-release opioids for acute dental pain.
Administering local anaesthetics by infiltration or regional block is an alter-
native or additional strategy for the management of severe acute dental
pain, provided the clinician is competent in these methods (for information
on local anaesthetic use in dentistry, see pp.201-9) .
If analgesics are used after a surgical procedure that causes postoperative
pain, inform the patient of the usual course of pain (eg pain is worst 48 to
72 hours after surgery, then improves) . Advise the patient to return to the
dentist for review if pain persists.
If postoperative pain persists for longer than expected, advise
patients to return to the dentist for review.
Particular care is required for dose selection in children at extremes of
weight or height:
• For children who are not obese, calculate the dose of analgesic
using the child ’s actual body weight, even if they are significantly
underweight. If the child’s weight cannot be determined, use the age-
based dose in Table 13 (p.142) for ibuprofen or Table 14 ( p.143) for
paracetamol; however, age- based dosing is imprecise for children at
extremes of weight or height.
• For children who are obese, calculate the dose using ideal body
weight; because of changes in drug pharmacokinetics in obesity, using
the child ’s actual body weight will result in an excessive dose. If the
child’s height is known, estimate their ideal body weight using the
corresponding weight for the height percentile on the growth chart
(eg < www.cdc.gov/growthcharts> ). If the child ’s height cannot be
determined, use the age-based dose in Table 13 (p.142) for ibuprofen
or Table 14 ( p.143) for paracetamol; however, age- based dosing is
imprecise for obese children at extremes of height.

Analgesic regimens for acute dental pain in

children
For factors that affect the choice of analgesic regimen, see p.137. Do not
use aspirin in people younger than 16 years because of the risk of Reye
syndrome. Do not use opioids for acute dental pain in children outside the
75 specialist setting.
0
o For acute dental pain in children 3 months or older, use ibuprofen or par-
~o acetamol; ibuprofen and paracetamol can be combined for enhanced pain
c
03 management. Give doses regularly, rather than as required, to achieve con-
75 tinuous pain relief. Use:
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to 400 mg orally, 3 times daily, at 6- to 8-hour intervals. See
0

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0 shortest duration possible and no more than 3 days without review
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140 141
E Therapeutic Guidelines: Oral and Dental

Table 13. Weight- based dose and approximate volumes of IBUPROFEN liquid for children [NB1]
Age (years) Average body Dose of ibuprofen Approximate volume of Approximate volume of
weight (kg) [ NB2] 100 mg/5 mL liquid [ NB3] 200 mg/5 mL liquid [ NB3]
1 9 45 to 90 mg 2.5 to 4.5 mL 1.5 to 2 mL

2 12 60 to 120 mg 3 to 6 mL 1.5 to 3 mL

3 14 70 to 140 mg 3.5 to 7 mL 2 to 3.5 mL

4 16 80 to 160 mg 4 to 8 mL 2 to 4 mL
5 18 90 to 180 mg 4.5 to 9 mL 2.5 to 4.5 mL

6 21 105 to 210 mg 5.5 to 10.5 mL 3 to 5 mL

7 23 115 to 230 mg 6 to 11.5 mL 3 to 5.5 mL

8 25 125 to 250 mg 6.5 to 12.5 mL 3.5 to 6 mL

9 29 145 to 290 mg 7.5 to 14.5 mL 4 to 7 mL

10 33 165 to 330 mg 8.5 to 16.5 mL 4.5 to 8 mL

11 36.5 182.5 to 365 mg 9.5 to 18 mL 5 to 9 mL

12 41 205 to 400 mg 10.5 to 20.5 mL 5.5 to 10 mL

NB1: Particular care is required for dose selection in children at extremes of weight or height. To determine whether to use the child's age or weight to select an
appropriate dose, see the discussion on p.141.
NB2: The average body weight- for-age values were derived from the World Health Organization (WHO) growth charts for children 5 years or younger ( < www.who.int/
childgrowth/standards/weight_for_age/en/ > ) and the Centers for Disease Control and Prevention (CDC) growth charts for children older than 5 years ( < www.cdc.
gov/growthcharts > ).
NB3: For practicality, volumes have been specified to the nearest 0.5 mL that achieves a dose no less than 5 mg kg or more than 10 m kg.
' ^

Table 14. Weight- based dose and approximate volumes of PARACETAMOL liquid for children [ NB1]
Age (years) Average body Dose of paracetamol Approximate volume of Approximate volume of
weight (kg) [NB2] 120 mg/5 mL liquid [ NB3] 240 mg/5 mL liquid [ NB3 ]
1 9 135 mg 5.5 mL 3 mL

2 12 180 mg 7.5 mL 4 mL

3 14 210 mg 9 mL 4.5 mL

4 16 240 mg 10 mL 5 mL

5 18 270 mg 11.5 mL 5.5 mL

6 21 315 mg 13 mL 6.5 mL

5:
7 23 345 mg 14.5 mL 7 mL

8 25 375 mg 15.5 mL 8 mL

9 29 435 mg 18 mL 9 mL

10 33 495 mg 20.5 mL 10.5 mL

11 36.5 547.5 mg 23 mL 11.5 mL

12 41 615 mg 25.5 mL 13 mL

NB1: Particular care is required for dose selection in children at extremes of weight or height. To determine whether to use the child’s age or weight to select an
appropriate dose, see the discussion on p.141.
NB2: The average body weight- for-age values were derived from the World Health Organization (WHO) growth charts for children 5 years or younger ( < www.who.int/
childgrowth/standards/weight_for_age/en/ > ) and the Centers for Disease Control and Prevention (CDC) growth charts for children older than 5 years ( < www.cdc.
gov/growthcharts>) .
NB3: For practicality, volumes have been specified to the nearest 0.5 mL.

H-

CO Orofacial pain
 Chronic temporomandibular disorders are often associated with psycho-
Temporomandibular disorders logical disorders.
Temporomandibular disorders (TMD) is a collective term for a number of
clinical problems that involve the masticatory muscles, or the temporo- Management of temporomandibular disorders
mandibular joints (TMJ) and associated structures. They can be classified
The aim of temporomandibular disorder management is to control the
into subtypes such as temporomandibular joint disorders and masticatory
patient’s symptoms rather than achieve a cure. Treatment goals should
muscle disorders.
be tailored to the specific diagnosis, and may include reducing pain and
Accurate diagnosis of a temporomandibular disorder requires appropriate adverse loading, restoring mandibular function and resuming normal daily
history, examination and imaging. Table 15 (below) outlines signs and activities.
symptoms of temporomandibular disorders.
Management strategies are conservative and can include:
Table 15. Signs and symptoms of temporomandibular • patient education and reassurance
disorders • jaw rest, using strategies such as dietary modification to minimise
chewing (eg eating only soft foods)
Common pain and restriction with mandibular function
pain in and around the ears and masticatory muscles
• avoidance of extreme jaw movements (eg yawning, chewing gum,
symptoms
singing)
headache
neck pain
• massage and application of warm packs to the temporomandibular
joints and cheeks several times per day. Cold packs can be useful in
limited jaw opening
the presence of redness and swelling ^
joint sounds
clenching of teeth (bruxism; see p.149) • behavioural modification (eg identifying and managing sources of
stress, which may be facilitated by individual or group counselling)
reduced hearing
Uncommon • regular treatment (gentle muscle stretching and massaging) by a
symptoms changes in occlusion
physiotherapist familiar in the management of temporomandibular
toothache
disorders
altered sensation in the face (eg paraesthesia, a feeling of swelling)
• use of custom - made full- coverage intraoral occlusal splints* to reduce
76 Signs tenderness of the temporomandibular joints and masticatory muscles joint loading, muscle activity and pain—splints are generally worn
during movement
0 at night and protect teeth from the effects of bruxism. They should
o temporomandibular joint sounds (clicking, clunking or crepitus) during
constitute only one part of a broader management approach
o repetitive opening and closing of the mouth, as well as lateral and
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TO
protrusive movements [NB1] • short-term use of drugs—discourage patients from relying on drugs
76 deviation on opening of the jaw alone (particularly drugs of dependence) to treat the symptoms
O-
i
NBl: Temporomandibular joint sounds are not an indication for treatment, unless associated of temporomandibular disorders because of their chronic nature.
in with pain or dysfunction. Analgesics, muscle relaxants, anxiolytics, anticonvulsants,
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corticosteroids and antidepressants have been used with variable
1
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Risk factors for temporomandibular disorders include direct trauma or
2
=3 indirect trauma (eg acceleration-deceleration injury) and parafunctional =TO
O An acute exacerbation of chronic temporomandibular disorder can be
activities (eg tooth grinding or clenching teeth). Psychosocial issues (eg CL
-—
.49»
stress, anxiety) may also contribute to the development of temporoman-
treated with ibuprofen and/or paracetamol (to select an appropriate anal- 76
CD
dibular disorders. Malocclusion has not been shown to be a risk factor for
gesic regimen, see p.137) . o
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sz fingernails, chewing gum and smoking can perpetuate an existing temporo- * To avoid any permanent effect on the position of the teeth, it is essential that splints are O
custom-made and full- coverage. The fit of the splint should be reviewed regularly and
mandibular disorder.
adjusted when required. 145
144
 If conservative measures are inadequate and pain and dysfunction become morning and increases in intensity as the day progresses; this presentation
severe or chronic, refer the patient to an oral medicine specialist or oral has the best prognosis.
and maxillofacial surgeon.
Other signs and symptoms associated with burning mouth syndrome
There is some evidence for the use of botulinum toxin to manage the symp- include:
toms of temporomandibular disorders when conservative measures are • parafunctional habits (eg unconsciously rubbing the tongue against
inadequate. Ensure patients understand that botulinum toxin is not a cure the adjacent teeth and the hard palate, which can cause traumatic
for temporomandibular disorders, but may be used as part of the overall abrasion of the filiform papillae on its dorsal surface)
management strategy. The use of botulinum toxin for temporomandibular
• dry mouth
disorders is off- label. Dentists require additional training to administer
botulinum toxin.* If the recommended doses and protocols are adhered
• halitosis
to, the incidence of adverse effects is low. Local complications include • dysgeusia (most commonly a metallic taste).
stinging during injections, bruising at the site of injection and excessive
muscle weakness. Adverse effects associated with inadvertent injection of Diagnosis and management of burning mouth
botulinum toxin into nontarget tissues are rare, but can include alteration syndrome
in smile and temporary dry mouth. Systemic adverse effects include an
influenza -like syndrome that is transient and hypersensitivity reactions. If burning mouth syndrome is suspected, the initial work - up is extensive
Surgery for temporomandibular disorders is rarely required. Only consider and requires a detailed clinical history, including a dental, medical and
medication history. Because burning mouth syndrome is a diagnosis of
referring the patient for a surgical assessment if symptoms have not
responded to conservative management and there is definitive evidence of
exclusion, other causes of the patient’s symptoms must be ruled out, such
internal joint derangement or other joint pathology on imaging.
as:
• local causes (eg mucocutaneous conditions, fungal infections, rough
dental surfaces)
Burning mouth syndrome • systemic causes
• hypersensitivity in patients who feel the problem is prosthesis- related
Burning mouth syndrome is an oral sensory disorder without a detect- ( hypersensitivity can be identified with skin patch testing, but this is
TO able cause; it is diagnosed when other conditions that can cause an oral rarely required)
burning sensation have been excluded. Burning mouth syndrome is more • drugs (eg drugs that cause sensory neuropathy, taste aberrations or
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o than 70 years. The onset of burning mouth syndrome may be sudden
E Some practitioners use questionnaires to assess the impact of symptoms
TO following a specific event (eg dental treatment, a significant increase in
personal stressors) or gradual and unrelated to any obvious event. Burning
on the patient’s mood and quality of life.
o-
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mouth syndrome is often poorly diagnosed and managed. The management of burning mouth syndrome is complex. The most impor-
CO tant component of management is helping the patient to understand the
Although symptoms of burning mouth syndrome vary, the characteristic
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condition ( ie that burning mouth syndrome is a chronic neuropathic pain
symptom is a burning sensation of the tongue and, less frequently, the
syndrome, irrespective of the likely initial triggers) . Some patients may
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=
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cause minor inconvenience or, in severe cases, prevent patients from

improve with discussion and counselling alone. £
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TO
suicidal tendencies. Most commonly, the burning sensation is mild in the
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£
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* For more information on the training required for botulinum toxin administration, see the syndrome is helping the patient to understand the condition. O
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JZ Australian Dental Association Policy Statement 6.30: Neurotoxins and Dermal Fillers in
Dentistry and the Dental Board of Australia Fact Sheet: The Use of Botulinum Toxin and
Dermal Fillers by Dentists .
146 147
 Other management strategies for burning mouth syndrome include:
• lifestyle changes to modify a patient’s response to external stressors
(eg relaxation therapy, time management, exercise, community group
participation)
• pharmacological management—topical or systemic use of
psychotropic drugs (eg tricyclic antidepressants, antiepileptic drugs,
Bruxism
clonazepam).

Pharmacological management is the treatment chosen by most patients Bruxism is repetitive teeth clenching, teeth grinding, or bracing or thrusting
and requires specialist referral. of the mandible. It can occur during sleep or when awake.
The aetiology of sleep bruxism is complex and multifactorial but is not
fully understood. There is no evidence that occlusal factors cause sleep
bruxism. In sleep bruxism, rhythmic masticatory muscle activity peaks in
the minutes before rapid eye movement (REM) sleep, suggesting that its
onset is related to sleep- stage transitions.
Tooth grinding during sleep, which is usually noted by a sleep partner, is
common. However, in the sleep laboratory, approximately 50% of people
with a history of tooth grinding have low frequencies of jaw muscle con-
tractions and tooth grinding. It remains to be clarified when tooth grinding
becomes a disorder associated with negative consequences such as tooth
damage and pain.
Bruxism may rarely be a sign of orofacial dyskinesia, or occur following a
head injury. Acute oromandibular dystonia or tardive dyskinesia caused by
dopamine antagonist antiemetic drugs (eg metoclopramide, prochlorpera -
zine) or antipsychotic drugs may be mistaken for bruxism.
15
Box 17 ( p.150) lists common triggers of bruxism.
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Management of bruxism
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o- Identify the cause and address any triggers of bruxism ( see Box 17;
x

p.150), if possible, which may require a multidisciplinary approach.

(0
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niques, hypnotherapy, biofeedback, cognitive behavioural therapy (CBT)
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0 and stress management. There is no evidence for hypnotherapy, biofeed- E
2 back or cognitive behavioural therapy for awake bruxism. .2X
0 3
JZ There is insufficient evidence to support the use of drugs in the manage-
ment of awake or sleep bruxism.
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148 149
 Box 17. Common triggers of bruxism
• caffeine and other stimulants, including herbal stimulants
• alcohol
• smoking Trismus
• snoring
• obstructive sleep apnoea
• stress and anxiety Trismus is a reduced ability to open the jaws. There are a large number of
• antidepressants potential causes, some of which are serious and warrant urgent treatment.
Common causes of trismus are:
- selective serotonin reuptake inhibitors (SSRIs)
- serotonin and noradrenaline reuptake inhibitors ( SNRIs)
• acute and chronic temporomandibular disorders (see p.144)
• antipsychotics • temporomandibular joint derangement
• amfetamines • oral infections, such as:
- pericoronitis (associated with partially erupted wisdom teeth)
- dexamfetamine
- spreading odontogenic infection ( see pp.82-6)
- lisdexamfetamine
- peritonsillar abscess (a potential complication of tonsillitis)
- metamfetamine
• surgery (eg wisdom teeth removal)
- MDMA (ecstasy)
• haematoma following dental injection
• cocaine
• tetanus
• acute dystonic reactions (eg drug-related)
Full-coverage intraoral occlusal appliances (splints or dental guards) can be
• oral submucous fibrosis (common in parts of the world where areca
used to protect the teeth from attrition during sleep bruxism. They should
nut [ betel quid] chewing is frequent)
be custom- made by a dentist with appropriate expertise or an oral medi-
cine specialist, regularly reviewed and adjusted as required. In addition • head and neck radiotherapy.
to preventing tooth damage, intraoral occlusal appliances reduce muscle
15 Accurately determining the cause of trismus requires a thorough history,
examination and, sometimes, imaging. Promptly initiating management
strain and loading of the temporomandibular joints; however, they do not
cure bruxism. Partial coverage splints should not be used because of the
can improve outcomes. Management is tailored to the cause, and may
0)
o
include dental treatment, physiotherapy or the use of passive range-of-
potential for significant occlusal changes and the risk of aspiration.
T3
C
cu motion devices .
15
o Patients with ongoing trismus require prompt specialist referral to
investigate less common causes (eg malignancies involving the temporo-
mandibular joint or masticatory muscles, scleroderma).
i/>
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151
150
Dental management
of patients with
medical conditions
Patients attending a general dental practice can have medical conditions or
be taking medications that affect their dental management. It is important
to obtain a complete medical and medication history (p.2 outlines history-
taking in dental practice).

For patients with a medical condition, consider the potential effect of

dental treatment on their condition. If the patient can only tolerate short
periods of dental treatment or their medical condition is easily destabilised,
modify dental treatment accordingly. For patients with complex medical
conditions, schedule appointments in the morning so that any potential
sequelae can be resolved during the day.
If the patient’s life expectancy is short or if they have severe disease, con-
sider whether dental treatment will improve the patient’s quality of life and
level of pain. Consult the patient’s medical practitioner, specialist or multi-
disciplinary team to determine an appropriate treatment plan for acute oral
and dental conditions.
The following topics outline common medical conditions and medications,
and the dental issues associated with them. They are not a substitute for M
c
formal training or detailed texts. Medical emergencies can arise during .2
dental treatment—call 000 and administer first aid (see pp.233-59 for TO
Q
-
.i2
first-aid management of medical emergencies occurring in dental practice) . o
+•»

Antithrombotic drugs « §
g -°cu
*OJ0

Antithrombotic drugs include: ro .E

• oral anticoagulant drugs (egapixaban, dabigatran, rivaroxaban, E?
warfarin) Tz E
• injectable anticoagulant drugs (eg enoxaparin, heparin) g
|
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• antiplatelet drugs (eg aspirin, clopidogrel, prasugrel, ticagrelor,
dipyridamole) .
153
 Patients taking antithrombotic drugs are at increased risk of prolonged
bleeding associated with an oral or dental procedure. Before any oral or
dental procedure, take a comprehensive medical and medication history,
including doses and indications. Particularly note the use of anticoagu-
lant or antiplatelet drugs (including nonprescribed aspirin) and any other
drugs with antithrombotic effects (eg nonsteroidal anti- inflammatory drugs
[ NSAIDs ], complementary medicines).
When planning an oral or dental procedure in a patient taking an
antithrombotic drug, weigh the potential harm of continuing a drug that
may increase the risk of prolonged bleeding against the risk that stopping
the drug could cause a thromboembolic event (for risk assessment, see
below). Many common dental procedures have a low risk of bleeding, and
the consequences of a thromboembolic event are usually more significant
than the consequences of bleeding. However, bleeding can be unexpected
and potentially life threatening.
In dental practice, the consequences of a thromboembolic event
are usually more significant than the consequences of bleeding.
Temporary interruption of antithrombotic therapy is sometimes necessary
to reduce the risk of prolonged bleeding ( see pp.156 63 for further infor-
- The non-vitamin K antagonist oral anticoagulants (NOACs) include direct
mation on when to consider temporary interruption). Temporary interruption
of antithrombotic therapy should only be done in consultation with the cli-
nician managing the drug.
Risk assessment for patients taking
antithrombotic drugs and undergoing an oral
O
0
or dental procedure
O
c Box 18 (p.156) outlines important patient-related factors that increase
03 Risk assessment for a patient taking antithrombotic therapy before an oral
75 or dental procedure includes consideration of:
o-
J
Clinical judgment is required from both the dentist and the clinician man-
aging the antithrombotic drug to determine if temporary interruption is
necessary. See pp.156-63 for the approach to managing patients taking
antithrombotic therapy undergoing an oral or dental procedure.
Antithrombotic drugs
Antiplatelet drugs include P2Y12 inhibitors (eg clopidogrel, prasugrel,
ticagrelor) , aspirin and dipyridamole. Some patients take nonprescribed
aspirin. Dual antiplatelet therapy (aspirin plus a P2Y12 inhibitor) is usually
prescribed for a specific duration; early interruption of dual antiplatelet
therapy increases the risk of ischaemic events and thrombosis.
Warfarin is an oral anticoagulant that inhibits the production of vitamin
K-dependent coagulation factors. The international normalised ratio (INR)
indicates the extent of anticoagulation in patients taking warfarin; the
target INR varies depending on the indication for therapy. The INR should
not be relied on solely to determine the bleeding risk in patients taking
warfarin; other determinants of bleeding include concurrent drug therapy
and other patient factors.
thrombin inhibitors (eg dabigatran) and factor Xa inhibitors (eg apixaban,
rivaroxaban). Unlike the INR in warfarin therapy, there is no test to indicate
the extent of anticoagulation in patients taking NOACs.
Injectable anticoagulants include heparin and low molecular weight hep-
arins (eg enoxaparin). They are usually prescribed for a short duration.
Patient- related bleeding risk factors
2
c
&
the risk of prolonged bleeding from an oral or dental procedure in patients
00
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taking antithrombotic drugs; this list is not exhaustive. Patients with mul-
**— <£>

• the properties of the antithrombotic drug(s) (see p.155)

a • patient- related bleeding risk factors ( see p.155)
tiple risk factors have an additive risk of prolonged bleeding.
21
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ECD • procedure-related bleeding risk (see pp.156-7)
If possible, address modifiable patient- related risk factors before pro- Si
2 ceeding with elective oral or dental procedures. O o
• the likely clinical effect of bleeding or thrombosis, should it occur.
3
CD
To assess periprocedural bleeding risk, dentists need to obtain an accurate
Many complementary medicines can affect haemostasis, either directly or g 75
.2 through drug interactions, so consider stopping the complementary medi -
medical and medication history, which may require consultation with the
cine before the procedure.

n
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CL patient’s medical practitioner. Risk assessment also includes an assess- 75 E
2 ment of the patient’s overall capacity to provide an accurate medical
CD
JC
history, understand and consent to the procedure, and understand and
adhere to postprocedural care requirements.
154 155
 Box 18. Important patient- related factors that increase the Table 16. Risk of prolonged bleeding following oral and
risk of prolonged bleeding from an oral or dental dental procedures [ NB1]
procedure in patients taking antithrombotic drugs Oral and dental procedures that are unlikely to cause prolonged bleeding
Patients with multiple risk factors have an additive risk of prolonged bleeding. Risk examination and diagnostic procedures (eg periodontal examination, impressions)
factors include: restorative treatments (eg restorations, root canal therapy)
• elevated blood pressure orthodontic treatment
• abnormal kidney or liver function Oral and dental procedures that are likely to cause prolonged bleeding
• prior stroke Lower risk of prolonged bleeding
• history of bleeding (particularly if this occurred with a similar procedure) extraction of a small number of teeth (eg 1to 3 teeth) that are not adjacent
• pre -existing bleeding disorder periodontal procedures (eg subgingival debridement)
• poor anticoagulant control (eg labile INR) incision and drainage of swellings
• older age or frailty limited or small soft tissue biopsies

• other drugs that predispose to bleeding [NB1], including NSAIDs (eg Higher risk of prolonged bleeding [ NB 2 ]
nonprescribed NSAIDs, low -dose aspirin) extraction of a large number of teeth (eg 4 or more teeth) or extraction of adjacent teeth
that creates a large wound
• hazardous alcohol consumption.
any procedure where a mucoperiosteal flap is used (eg surgical extractions, implant
INR = international normalised ratio; NSAIDs = nonsteroidal anti-inflammatory drugs placement, periapical surgery, periodontal surgery)
NB1: Many other prescription, over-the-counter and complementary medicines can affect
extensive soft tissue biopsies
haemostasis, either directly or through drug interactions.
hard tissue biopsies

Procedure-related bleeding risk NBl: The bleeding risk associated with these procedures is based on the consensus opinion
of the Oral and Dental Expert Group. Risk assessment requires clinical judgment of the
individual procedure- , patient- and drug- related risks of bleeding, and the practitioner 's
Table 16 (p.157) classifies oral and dental procedures by their risk of pro- competency to manage prolonged bleeding, should it occur.
longed bleeding. NB2: Consider specialist referral for procedures with a higher risk of prolonged bleeding in
patients taking antithrombotic drugs.

15
-M Management of patients taking
o
o antithrombotic drugs undergoing an oral or For specific advice on whether to continue or interrupt antithrombotic
therapy, see: <J)
o
c dental procedure • ‘Patients taking triple antithrombotic therapy’ on p.159
c
TO
15
o-
i
The management of a patient taking antithrombotic therapy depends on
the patient- (see p.155) and procedure-related (see Table 16; p.157)
• ‘Patients taking an oral anticoagulant plus an antiplatelet drug’ on
p.159 _ >
u
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bleeding risk, and the type or combination of antithrombotic therapy. • ‘Patients taking a single anticoagulant or dual antiplatelet therapy’ on Zi
a§
CO
CD
ECD Clinical judgment is required from both the dentist and the clinician p.161
managing the antithrombotic drug to assess the risks associated with
interrupting or continuing antithrombotic therapy. Involve the patient in the
• ‘Patients taking a single antiplatelet drug’ on p.162 i
§) 0
3
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decision.
§ If antithrombotic therapy has been prescribed for a specific period (eg dual E -8
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antiplatelet therapy for 12 months following an acute coronary syndrome 15 E
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or implantation of a drug-eluting stent) , delay elective oral or dental proce-
jC dures until after this period, if possible. o

156 157
 Consider specialist referral (eg oral and maxillofacial surgeon, periodontist)
for patients with patient- related bleeding risk factors (see Box 18; p.156) ,
or procedures with a higher risk of prolonged bleeding (see Table 16;
p.157). For procedures of a long duration, consider limiting the extent of
surgery performed in one sitting or referring to a specialist.
Paracetamol is the preferred analgesic for postoperative pain in patients
taking antithrombotic drugs—concomitant use of nonsteroidal anti-
inflammatory drugs (NSAIDs) and antithrombotic drugs increases the risk
of postoperative bleeding (to select an appropriate analgesic regimen for
acute dental pain, see p.137).

Consider specialist referral for patients with patient -related NSAIDs increase the risk of bleeding in patients taking
bleeding risk factors or for procedures with a higher risk of antithrombotic drugs.
prolonged bleeding.
Arrange a review dental appointment for 2 days after the procedure
Box 19 (below) outlines local haemostatic measures for oral and dental
to check for bleeding, pain, delayed healing or infection, and treat as
procedures in patients taking antithrombotic drugs.
necessary.
Box 19. Local haemostatic measures for oral and dental
procedures in patients taking antithrombotic drugs Patients taking triple antithrombotic therapy
• Apply pressure to the wounds—pressure is the most important factor in undergoing an oral or dental procedure
achieving haemostasis.
For patients taking triple antithrombotic therapy (eg dual antiplatelet
• Minimise tissue trauma.
therapy plus one anticoagulant) , consult the clinician managing the
• Place cellulose and collagen, if indicated. antithrombotic therapy before performing any oral or dental procedure.
• Place sutures to ensure closure of the wounds, if indicated. Consider specialist referral for the procedure.
• Consider using tranexamic acid 4.8% mouthwash as an adjunctive measure
for patients taking warfarin—tranexamic acid mouthwash can stabilise a blood
clot in patients taking warfarin. There is no evidence on the use of tranexamic Patients taking an oral anticoagulant plus an
acid mouthwash in patients taking NOACs. Apply tranexamic acid mouthwash antiplatelet drug undergoing an oral or dental
.
topically just before surgery After the procedure, give the patient tranexamic
procedure
acid 4.8% mouthwash with instructions for use (10 ml. rinsed in mouth for
TO 2 minutes then spat out, 4 times daily for 2 days) [NB1].
This advice applies to patients taking one anticoagulant (eg apixaban,
NOAC = non-vitamin K antagonist oral anticoagulant
0) dabigatran, rivaroxaban, warfarin) plus one antiplatelet drug (eg aspirin,
O NB1: Tranexamic acid 4.8% mouthwash can be compounded by a pharmacy. If it is not
clopidogrel, prasugrel, ticagrelor, dipyridamole). These patients have a high
o available, a suitable alternative solution can be made by crushing a 500 mg tablet and c
c dispersing it in 10 mL of water immediately before administration. risk of prolonged bleeding because of the combination of antithrombotic .2
CD
drugs used. Therefore, there is a lower threshold for considering tempo-
75
—
It is essential to provide the patient with written information on postproce- rary interruption of antithrombotic therapy (in consultation with the medical Q./
o <>
dural care, including contact information in an emergency. Advise patients practitioner) or referring the patient to a specialist for the procedure. If the *
</ 5
0 to seek urgent medical attention if there is persistent ooze or bleeding, patient has any patient-related bleeding risk factors (see Box 18; p.156) ,
Mo bleeding that restarts, or any bleeding of concern. Advise patients that they

= may have extensive bruising.

this further increases the risk of prolonged bleeding.
i§
If antithrombotic therapy has been prescribed for a specific duration, delay <2 -CD
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elective oral or dental procedures until after this period if possible. S .2
§ Advise patients to seek urgent medical attention if there is
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158 159
 For patients taking an oral anticoagulant plus an antiplatelet drug, tempo-
rary interruption of antithrombotic therapy is not required for the following
oral and dental procedures:
• procedures that are unlikely to cause prolonged bleeding (see
Table 16; p.157).*
Consult the clinician managing the antithrombotic therapy to determine if
temporary interruption or specialist referral is required for the following oral
and dental procedures:
• procedures with a lower risk of prolonged bleeding (see Table 16;
.
p 157)
• procedures with a higher risk of prolonged bleeding ( see Table 16;
p.157).
If temporary interruption is required, follow the advice from the medical
practitioner.
If temporary interruption is not required, for patients taking warfarin, also
consider the current international normalised ratio (INR) and stability of the
INR. Recheck the INR within 24 hours before the procedure. Provided the
INR is 3.5 or less, perform the procedure. Do not perform the procedure
if the INR is more than 3.5; refer the patient for medical assessment and
stabilisation of the INR .
Use local haemostatic measures when performing an oral or
dental procedure in a patient taking antithrombotic therapy.
TM5 For procedures performed in patients taking an oral anticoagulant plus an
Q) antiplatelet drug, use local haemostatic measures (see Box 19; p.158)
Q
and follow the general management advice (pp.156-9) to minimise
Patients taking a single oral anticoagulant or
dual antiplatelet therapy undergoing an oral
or dental procedure
This advice applies to patients taking either:
• a single oral anticoagulant (egapixaban, dabigatran, rivaroxaban,
warfarin)
• dual antiplatelet therapy (eg aspirin plus clopidogrel).
If antithrombotic therapy has been prescribed for a specific duration, delay
elective oral or dental procedures until after this period if possible.
For patients taking a single oral anticoagulant or dual antiplatelet therapy,
temporary interruption of antithrombotic therapy is not required for the fol-
lowing oral and dental procedures*:
• procedures that are unlikely to cause prolonged bleeding (see
Table 16; p.157)
• procedures with a lower risk of prolonged bleeding (see Table 16;
p.157) in patients without patient- related bleeding risk factors ( see
Box 18; p.156) .
Consult the clinician managing the antithrombotic therapy to determine if
temporary interruption or specialist referral is required for the following oral
and dental procedures:
• procedures with a lower risk of prolonged bleeding ( see Table 16;
p.157) in patients with patient-related bleeding risk factors ( see
Box 18; p.156)
• procedures with a higher risk of prolonged bleeding (see Table 16;
p.157). <S)

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c bleeding risk. Advise patients that they may have extensive bruising, and c
CO If temporary interruption is required, follow the advice from the medical &
to seek urgent medical attention if there is persistent ooze or bleeding,
To practitioner. CO
bleeding that restarts, or any bleeding of concern.
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If temporary interruption is not required, for patients taking warfarin, also
consider the current international normalised ratio (INR) and stability of the
21
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INR. Recheck the INR within 24 hours before the procedure. Provided the
1]
2
3 INR is 3.5 or less, perform the procedure. Do not perform the procedure i§
CD if the INR is more than 3.5; refer the patient for medical assessment and (0

.9 stabilisation of the INR. S .2

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* Evidence to inform the risk of bleeding in patients taking non-vitamin K antagonist * Evidence to inform the risk of bleeding in patients taking non-vitamin K antagonist o
oral anticoagulants (NOACs) undergoing oral and dental procedures is limited, so this oral anticoagulants (NOACs) undergoing oral and dental procedures is limited, so this
recommendation is based on the consensus view of the Oral and Dental Expert Group. recommendation is based on the consensus view of the Oral and Dental Expert Group.
160 161

JJ
 For procedures performed in patients taking a single oral anticoagulant or
dual antiplatelet therapy, use local haemostatic measures ( see Box 19;
p.158) and follow the general management advice (pp.156-9) to minimise
bleeding risk. Advise patients that they may have extensive bruising, and
to seek urgent medical attention if there is persistent ooze or bleeding,
bleeding that restarts, or any bleeding of concern.
Patients using an injectable anticoagulant
undergoing an oral or dental procedure
For patients using an injectable anticoagulant, delay elective procedures
until after the anticoagulant therapy has stopped. Refer patients to hospital
for emergency or semi - elective procedures.

Use local haemostatic measures when performing an oral or

dental procedure in a patient taking antithrombotic therapy. Corticosteroids
Corticosteroids are used at replacement doses for adrenal insufficiency
Patients taking a single antiplatelet drug disorders. They are also used at therapeutic doses in the management
undergoing an oral or dental procedure of inflammatory and immune disorders (eg rheumatoid arthritis, severe
dermatological conditions, asthma) —at therapeutic doses, corticosteroids
This advice applies to patients taking a single antiplatelet drug (eg clopi-
can cause immunosuppression (for advice on the dental management of
dogrel, prasugrel, ticagrelor, aspirin, dipyridamole) and not taking an
immunocompromised patients, see p.181).
anticoagulant.
The long-term use of therapeutic doses of corticosteroids can cause
Temporary interruption of single antiplatelet therapy is not required for the
adrenocortical suppression and subsequent dependence on exogenous
following oral and dental procedures:
corticosteroid therapy. The dose and duration of treatment likely to cause
• procedures that are unlikely to cause prolonged bleeding ( see clinically relevant adrenocortical suppression is not clear and varies
Table 16; p.157)
significantly between patients. Oral prednisolone at a dose of 10 mg or
• procedures with a lower risk of prolonged bleeding (see Table 16; more daily (or the equivalent dose of another corticosteroid) for more than
p.157). 3 weeks could be expected to cause adrenocortical suppression. A high
dose of an inhaled, topical or intra-articular corticosteroid can also cause
Consult the clinician managing the antiplatelet drug to determine if tempo-
adrenocortical suppression.
rary interruption of single antiplatelet therapy is required for the following
w oral and dental procedures: Patients with adrenocortical suppression or adrenal insufficiency are at risk
<1)
• procedures with a higher risk of prolonged bleeding (see Table 16; of glucocorticoid deficiency during periods of physiological stress (eg sig-
Q p.157). nificant systemic illness or surgery) , since the usual response of increased
*U
adrenal cortisol production will not occur. This can precipitate adrenal crisis M
c
n
c
For procedures performed in patients taking a single antiplatelet drug, use ( also known as acute adrenal insufficiency or Addisonian crisis). The pri- .2
(5 local haemostatic measures (see Box 19; p.158) and follow the general mary manifestations of adrenal crisis are gastrointestinal symptoms and 15Q.
o-
si
i

management advice (pp.156-9) to minimise bleeding risk. Advise patients symptoms of acute circulatory failure (eg hypotension, confusion).

Ss—
U)
o that they may have extensive bruising, and to seek urgent medical atten-
Patients undergoing a dental procedure may require an increased dose
+*.
Eo tion if there is persistent ooze or bleeding, bleeding that restarts, or any
of corticosteroid—see p.164 for the recommended approach for different
2 bleeding of concern.
types of oral and dental procedures. Perform dental treatment in the
gi
§
Z3
C3
Use local haemostatic measures when performing an oral or morning~so that if an adrenal crisis occurs, symptoms present while the
0
°
.9
dental procedure in a patient taking an antiplatelet drug. patient is awake. After dental treatment, ensure the patient remains in the S .2
care of a responsible adult for the rest of the day, and the carer remains EU
<D

Si
CD
Q _ Iz E
Co in contact with the patient for the following 2 to 3 days. Advise the patient
CD
SZ and the carer to seek urgent medical attention if the patient experiences
symptoms of adrenal insufficiency.
Q 2?

162 163
 Corticosteroid dose adjustment for oral or
dental procedures
The following recommendations are based on the consensus view of
the Oral and Dental Expert Group. There is limited evidence to inform
the approach to corticosteroid dose adjustment for dental procedures in
patients at risk of adrenocortical suppression.
For noninvasive dental procedures (eg dental check, impressions, X- rays) ,
the dose of corticosteroid does not need to be increased in patients at risk
of adrenocortical suppression. Advise patients to take their usual dose on
the day of treatment.
For invasive dental procedures of less than 1 hour in an outpatient set-
ting (eg professional teeth cleaning, restorative treatment, tooth extraction,
periodontal treatment, implant placement) , patients at risk of adreno -
cortical suppression require an increased dose of corticosteroid. These
patients may have a dosing strategy ( action plan) for periods of stress. If
the patient does not have a dosing strategy in place already, consult their
medical practitioner. The increased dose is usually started on the morning
of the procedure.
For invasive dental procedures that are longer than 1 hour or dental
procedures requiring sedation, general anaesthesia or fasting in patients
at risk of adrenocortical suppression, seek specialist advice.
Osteonecrosis of the jaw is an uncommon adverse effect of antiresorp-
tive drugs. Severe cases have mainly occurred in patients who had dental
surgery during treatment with a high-dose intravenous bisphosphonate for
.
multiple myeloma or metastatic cancer Current data in oncology popula -
tions suggests that the incidence of medication - related osteonecrosis of
the jaw is up to 12 222 per 100 000 patient-years for bisphosphonates,
and up to 2316 per 100 000 patient-years for denosumab.* The incidence
of medication- related osteonecrosis of the jaw in patients treated with
antiresorptive drugs for osteoporosis is significantly lower than oncology
populations. Based on limited data, the incidence of medication - related
osteonecrosis of the jaw in patients taking antiresorptive drugs for osteo-
porosis may be up to 150 per 100 000 patient-years, which is only slightly
higher than in the general population.
Although medication - related osteonecrosis of the jaw has significant
consequences for the patient and can be difficult to treat, the benefits of
antiresorptive therapy outweigh the risk of harm in most patients.
Table 17. Stages of osteonecrosis of the jaw
Stage of osteonecrosis Features
of the jaw
Stage 0 [NB1] symptomatic (eg pain)
radiographic changes
no exposed bone
Stage 1INB1] asymptomatic

75
Medication-related osteonecrosis of the exposed bone

0
jaw no inflammation or infection

O Stage 2 symptomatic (eg pain)

V)
TJ Medication -related osteonecrosis of the jaw (MRONJ) is an area of exposed exposed bone c
c
(0 bone in the jaw persisting for more than 8 weeks in a patient currently or adjacent soft tissue inflammation or secondary infection £
75 previously treated with an antiresorptive or antiangiogenic drug, who has toQ.
o-
symptomatic (eg pain)
— <2
J Stage 3
not received radiation therapy to the craniofacial region. Antiresorptive full thickness bone involvement
M

(/)
0
drugs include bisphosphonates and denosumab. Antiangiogenic drugs ( eg pathological fracture
E0 bevacizumab, sunitinib) interfere with the formation of new blood vessels,
i§
extensive soft tissue infection and fistulae
IS and are used in the treatment of some malignancies.
0
CD For information on osteonecrosis occurring in a patient who has received
NB1: Stage 0 and stage 1require follow up and monitoring, but no treatment. •OX)
<2 75 °
radiation therapy (osteoradionecrosis) , see p.175. S .2
4
^
0
Table 17 ( p.165) outlines the stages of osteonecrosis of the jaw. 75 E
if
0
0
£
* Patient-years are used to express incidence, which is the number of new cases observed O £
during a specified period. For example, an incidence of 150 per 100 000 patient - years
means that 150 new cases occur for every 100 000 patients taking the drug for 1year. 165
164

M
 Risk assessment for medication-related osteonecrosis of the jaw will not occur. Furthermore, the serum C-terminal
osteonecrosis of the jaw telopeptide concentration is affected by many variables, including patient
age, gender, medical conditions (eg bone disease) , menopausal status,
Bone- invasive dental procedures (eg tooth extractions, difficult surgical drugs (eg oral contraceptives, hormone replacement therapy, antiresorp-
extractions, implant placement, periapical or radicular surgery, periodontal tive drugs) , and the assay method used. It is therefore difficult to use a
flap surgery) can trigger medication- related osteonecrosis of the jaw. patient’s C -terminal telopeptide test result to assess the risk of medica -
However, medication-related osteonecrosis of the jaw can occur in patients tion- related osteonecrosis of the jaw.
who have not had a bone- invasive dental procedure, such as patients
with poorly fitting dentures or exostoses (eg tori, mylohyoid ridges). Box 20. History taking to assess the risk of medication-
Osteonecrosis that is not related to medication use can also occur at these
sites spontaneously.
related osteonecrosis of the jaw
N
Establish whether a patient is currently receiving or has previously received Has the patient ever received treatment for any bone or calcium
an antiresorptive or antiangiogenic drug ( see Box 20; p.167). Figure 6 disorders or malignancy?
(p.168) summarises how to assess a patient’s risk of medication-related Conditions that are treated with antiresorptive drugs include:
osteonecrosis of the jaw. A thorough medical, medication and dental his- • osteoporosis
tory informs risk assessment for medication- related osteonecrosis of the • Paget disease of the bone
jaw; consider consulting the patient’s medical practitioner. • cancer with spread to the bone (eg breast, prostate, liver, lung, kidney)
The risk of medication-related osteonecrosis of the jaw is higher for long • multiple myeloma.
durations and high doses of antiresorptive therapy, and may be higher
when antiresorptive and antiangiogenic drugs are used concomitantly. Is the patient currently receiving or have they previously received
treatment with an antiresorptive drug?
Additional risk factors for medication- related osteonecrosis of the jaw are Antiresorptive drugs can be taken orally, either daily, once weekly or once monthly,
inconsistently reported in international guidelines.* Commonly listed risk or can be administered intravenously and given less frequently (eg once or twice
factors for medication-related osteonecrosis of the jaw are included in yearly). Antiresorptive drugs available in Australia are:
Figure 6 ( p.168). Female gender and increasing age (older than 65 years) • alendronate
have been associated with medication- related osteonecrosis of the jaw;
75 • denosumab
M however, this may be a reflection of the population who are likely to be
0) using antiresorptive drugs for osteoporosis. • ibandronic acid
o • pamidronate
a C -terminal telopeptide (CTX) is a breakdown product of bone resorption. +2
c • risedronate c
03 The serum C-terminal telopeptide concentration has been proposed as a
• zoledronic acid.
.2
75 way of estimating a patient’s risk of medication-related osteonecrosis of the 03
a.
o jaw. However, there is insufficient evidence to support a threshold serum </>
21
Has the patient received an antiangiogenic drug for the management
to
CD
C-terminal telopeptide concentration beyond which medication-related of cancer?
CD
* Ruggiero SL, Dodson TB, Fantasia J, Goodday R, Aghaloo T, Mehrotra B, et al. American Antiangiogenicdrugs are used as targeted therapies for specific cancers. At the
Association of Oral and Maxillofacial Surgeons position paper on medication-related time of writing, some antiangiogenic drugs (sunitinib [a tyrosine kinase inhibitor ] O O
=3 osteonecrosis of the jaw-2014 update. J Oral Maxillofac Surg 2014;72(10):1938 - 56.
and bevacizumab [a monoclonal antibody-targeting VEGF]) have been associated
CD
.2 .
Hellstein JW, Adler RA Edwards B, Jacobsen PL, Kalmar JR, Koka S, et al. Managing with an increased risk of medication- related osteonecrosis of the jaw; the risk may
§ 75
the care of patients receiving antiresorptive therapy for prevention and treatment of also be increased with other drugs that have a similar mechanism of action.

if
CD osteoporosis: executive summary of recommendations from the American Dental
CD Association Council on Scientific Affairs. J Am Dent Assoc 2011;142(11):1243 - 51. If the patient has received any of the treatments above, see Figure 6
75 E
(p.168) for further risk assessment.
CD
C Khan AA, Morrison A, Hanley DA, Felsenberg D, McCauley LK, O’Ryan F, et al. Diagnosis
|
and management of osteonecrosis of the jaw: a systematic review and international o£
consensus. J Bone Miner Res 2015;30(l):3- 23.
VEGF = vascular endothelial growth factor
166 167
g Therapeutic Guidelines: Oral and Dental

Figure 6. Assessing the risk of medication- related osteonecrosis of the jaw before a bone- invasive
dental procedure in a patient treated with an antiresorptive or antiangiogenic drug [NB1]

Has the patient been diagnosed with medication-related

osteonecrosis of the jaw in the past? YES

1
NO

1
Has the patient received antiresorptive or antiangiogenic
drugs for the management of cancer? - YES

I
NO

1
Is the patient currently receiving or have they previously
received a bisphosphonate for a noncancer indication? [NB2]

1
f 1
NO YES

Is the patient currently receiving or have they previously What is or was the duration of bisphosphonate therapy?
received denosumab /tor a noncancer indication?

! [
i
)
YES less than 4 years 4 years or more

I 1
Does the patient have additional risk factors for medication-related
osteonecrosis of the jaw, such as immune compromise, diabetes, anaemia,
hyperthyroidism, renal dialysis, glucocorticoid therapy, tobacco use,
periodontal disease, denture use, or local suppuration?

I
[ I
NO YES

I 1
Patient at low risk of medication- related osteonecrosis of the jaw [NB3] Patient at high risk of medication- related
osteonecrosis of the jaw
The dentist can proceed with the bone -invasive procedure (see management
advice for patients at risk of medication-related osteonecrosis of the jaw who The dentist should seek expert advice and refer
are undergoing bone-invasive dental procedure in Box 21, p.171) . the patient to an appropriate surgical specialist.

5
Dental management of patients
with medical conditions
 Figure 6. Assessing the risk of medication- related Precautions for patients undergoing bone -
osteonecrosis of the jaw before a bone- invasive invasive dental procedures
dental procedure in a patient treated with an
antiresorptive or antiangiogenic drug (footnotes) Bone- invasive dental procedures (eg tooth extractions, difficult surgical
NBl: This risk assessment tool is based on limited data and cannot definitively classify a extractions, implant placement, periapical or radicular surgery, periodontal
patient's risk of medication-related osteonecrosis of the jaw. flap surgery) require careful consideration in patients at risk of medication-
NB2: Patients who have taken bisphosphonates in the past may still have an increased risk related osteonecrosis of the jaw.
of medication- related osteonecrosis of the jaw because the half-life of bisphosphonates
in the bone is long; it is not known how fast and to what extent the risk diminishes after Assess the risks and benefits of the dental procedure and the patient’s
stopping bisphosphonates.
risk of medication- related osteonecrosis of the jaw (for risk assessment,
see p.166) —this requires a thorough medical history (see Box 20; p.167).
NB3: Patients classified as ‘low risk' still have a risk of medication-related osteonecrosis of the
jaw that is higher than the general population.
Determine the patient’s risk of medication-related osteonecrosis of the
jaw using Figure 6 (p.168). For patients at high risk of medication- related
Prevention of medication-related osteonecrosis of the jaw, the dentist should seek expert advice and refer
osteonecrosis of the jaw the patient to an appropriate surgical specialist. Patients at low risk of
medication- related osteonecrosis of the jaw can undergo bone-invasive
dental procedures in a general dental practice—see Box 21 (below) for
Maintaining optimal oral health
management advice.
Ensuring optimal oral health by implementing early dental assessment and
initiation of appropriate dental care reduces the incidence of medication- Antibiotic prophylaxis is not recommended to reduce the risk of
related osteonecrosis of the jaw. medication-related osteonecrosis of the jaw.

If a medical practitioner refers a patient for dental assessment before or

shortly after starting an antiresorptive drug, the dentist should undertake a
Box 21. Management advice for patients at risk of
comprehensive oral examination including pulp tests and radiographs. The
medication- related osteonecrosis of the jaw
dentist should ensure that the patient is dentally fit and unlikely to require
extractions in the foreseeable future. The dentist should eliminate dental undergoing a bone-invasive dental procedure
15 caries (eg extractions, restorations) , establish a healthy periodontium (eg • Inform the patient of the risk of medication-related osteonecrosis of the jaw and
debridement, extractions), and encourage good oral hygiene. obtain consent for the procedure .
0
Q • See advice on drug holidays and scheduling of procedures (p.172).
-o If possible, any necessary dental treatment should be completed before <J )
• Do not use antibiotic prophylaxis to reduce the risk of medication-related c
c or shortly after starting antiresorptive therapy for osteoporosis (eg within .2
(0
osteonecrosis of the jaw—there is insufficient evidence to support this practice.
6 months) —the risk of medication- related osteonecrosis of the jaw in toQ.
15 However, an active infection should be treated.
o- patients with osteoporosis remains low in the early stage of treatment.
58
i

Patients with cancer who are prescribed high doses of antiresorptive drugs • Ensure optimal oral hygiene before and after the procedure.

*3 3g
c/5
0 are at greater risk of medication-related osteonecrosis of the jaw, so ideally • Reduce the plaque load with mechanical debridement and pre- and post-
E0 dental procedures should be completed before starting treatment. procedural chlorhexidine mouthwash.
E
5 <D O
• Minimise trauma-andperiosteum stripping, and close any mucosal flaps that
>«
0 Regular dental review is essential to monitor oral health (eg clinical oral
C5 are raised with sutures. gi
examinations, radiographs) , particularly if the patient has a history of perio-
4
-
.2»
dontal disease. Advise patients to seek early management of oral or dental
• Monitor the oral wound until it heals—healing may be slow.
c "o
E o
0
Q. symptoms and, if worn, ensure optimal fit for dentures. • Do not debride nonhealing wounds. 15 E
2 • Refer to a specialist if bone is still visible at 8 weeks.
0 Effective communication between treating dentists and medical practi-
JZ
o £
tioners is essential. Inform and involve the patient in treatment decisions.
170 171
 Drug holidays and scheduling of procedures For patients with cancer, the decision to alter antiresorptive therapy lies
with the specialist managing the cancer.
If a bone- invasive dental procedure cannot be avoided but is not urgent,
temporary discontinuation of antiresorptive therapy (a ‘drug holiday ’) , or
timing the procedure to coincide with a low serum drug concentration,
have been suggested to reduce the risk of medication-related osteone- Bleeding disorders
crosis of the jaw. These practices are based on extrapolation of the drug
Acquired or congenital bleeding disorders include haemophilia, von
pharmacokinetics in the serum and on bone physiology; however, outcome
Willebrand disease, other factor deficiencies and thrombocytopenia. Some
evidence to support them is not available.
systemic conditions interfere with haemostasis, such as kidney, liver and
There is no evidence that drug holidays reduce the risk of bone marrow disorders.
medication - related osteonecrosis of the jaw.
Patients with bleeding disorders should be managed in a specialist setting,
with appropriate consultation with the patient’s specialist or multidiscipli-
Recommendations in international guidelines are inconsistent, and vary
nary team.
depending on the indication for antiresorptive drugs, the duration of
therapy and the presence of additional risk factors. * Clinical judgment of
treating doctors and dentists is required to determine the appropriate man-
agement of each patient. The decision to alter antiresorptive therapy lies Bone and metabolic disorders
with the practitioner responsible for managing the antiresorptive drug.
Osteoporosis
Clinical judgment of treating doctors and dentists is required to
determine the appropriate management of each patient. For the dental management of patients taking antiresorptive drugs (bispho-
sphonates or denosumab) , see pp.164-73.
For patients receiving antiresorptive drugs for osteoporosis, the benefits
of continued therapy outweigh the low risk of medication-related osteone-
crosis of the jaw. Although stopping bisphosphonates for a short period
Adrenal disorders
is unlikely to cause harm in a patient at low risk of fracture, there is no Patients with adrenocortical suppression or adrenal insufficiency are at risk
evidence that this approach reduces the risk of medication- related oste- of glucocorticoid deficiency during periods of physiological stress (eg sig-
75 onecrosis of the jaw. nificant systemic illness or surgery), since the usual response of increased
Q) adrenal cortisol production will not occur. See p.163 for the management
o Denosumab is a reversible antiresorptive administered every 6 months for
of patients with adrenocortical suppression or adrenal insufficiency under-
osteoporosis. If it is possible to delay a bone- invasive dental procedure in a M

going dental procedures.

TS C
c
n patient taking denosumab for osteoporosis, ideally schedule the procedure .2
75
o-
i
just before the next dose of denosumab. It is never appropriate to interrupt
or delay the dose of denosumab; withdrawal of denosumab has been asso- Thyroid disorders
_.
n
Q

21
u CO

i/ 5
o ciated with an increased risk of spontaneous vertebral fractures.
Patients with a stable medication-controlled thyroid disorder do not usu-
5?
o
=3
* Ruggiero SL, Dodson TB, Fantasia J, Goodday R, Aghaloo T, Mehrotra B, et al. American
Association of Oral and Maxillofacial Surgeons position paper on medication-related
osteonecrosis of the jaw-2014 update. J Oral Maxillofac Surg 2014;72(10):1938- 56.
ally have difficulties with dental treatment. Although adrenaline-containing
local anaesthetic solutions are contraindicated in patients with unstable i§
O hyperthyroidism, they can be safely used in patients with stable thyroid c 75
.9 Hellstein JW, Adler RA, Edwards B, Jacobsen PL, Kalmar JR, Koka S, et al. Managing disorders.
§ .2
* the care of patients receiving antiresorptive therapy for prevention and treatment of
o
CL osteoporosis: executive summary of recommendations from the American Dental Defer dental treatment in patients known to have an unstable thyroid 75 E
ro Association Council on Scientific Affairs. J Am Dent Assoc 2011;142 (11):1243- 51.
0 disorder.
.0
Khan AA , Morrison A, Hanley DA, Felsenberg D, McCauley LK, O’Ryan F, et al. Diagnosis o
and management of osteonecrosis of the jaw: a systematic review and international
consensus. J Bone Miner Res 2015;30l ( ):3-23.
172 173

Cancer
Dentists have an important role in the initial recognition and diagnosis of
oral cancer. If a patient who has had head and neck cancer treatment has
a suspicious oral lesion, refer for investigation to exclude cancer recurrence
or a new primary cancer. Metastatic cancers to the oral soft tissues and
jawbones commonly originate from primary malignancies in the breast,
prostate, kidneys and lungs. Leukaemias and lymphomas may also pre-
sent in the oral cavity. For further information on assessing an oral mucosal
lesion, see p.93.
For more information on the dental management of patients with head and
neck cancer and the oropharyngeal adverse effects of cancer treatments,
see the eviQ website < www.eviq.org.au > .
Chemotherapy
Ideally, patients should be dentally fit before starting chemotherapy, par-
ticularly if the chemotherapy used can cause severe mucositis and reduced
salivary flow. For the management of these complications, see p.120 for
mucositis and p.121 for dry mouth.
Some types of chemotherapy cause immune suppression, and increase
the risk of oral infections such as oral candidiasis (see p.114), herpes sim-
plex virus infection (see p.110) and postoperative infection (see p.87).
Head and neck radiotherapy
Patients who require head and neck radiotherapy should be reviewed by a
dentist experienced in cancer management, as part of a multidisciplinary
team. Radiotherapy can cause oral pain, mucositis (see p.120) , reduced
salivary flow (see p.121), oral infection, trismus and altered taste. Reduced
salivary flow can increase the risk of periodontal disease and dental caries.
Good oral hygiene can reduce the incidence, severity and duration of
adverse effects associated with radiotherapy. Ensure optimal oral health;
if possible, any necessary dental treatment should be completed before
starting radiotherapy. If extractions are performed, allow adequate time for
wound healing (usually 10 days to 3 weeks) before starting radiotherapy, if
possible.
Patients who have had head and neck radiotherapy are at increased risk of
osteoradionecrosis. Encourage regular dental review and seek advice from
the patient's multidisciplinary team before performing tooth extractions that
are within the field of radiotherapy. If possible, choose conservative dental
treatment options (eg periodontal treatment, restorations, endodontic
treatment [ root canal ], fluoride application). Neutral fluoride products are
better tolerated than acidulated products. Management of osteoradione-
crosis is difficult and requires specialist management.
Do not extract teeth from a patient who has had head and neck
radiotherapy without consulting the patient’s multidisciplinary
team.

For more information on the dental management of patients undergoing

Develop dental treatment plans in consultation with the patient’s
75 head and neck radiotherapy, see the eviQ website < www.eviq.org.au > .
treating specialist or multidisciplinary team.
<D
O in
Develop dental treatment plans in consultation with the patient’s treating c
O
c specialist or multidisciplinary team. Some types of chemotherapy cause Cardiovascular conditions .2
_
75Q.
03
significant neutropenia and thrombocytopenia, particularly with treatments
15
o- for leukaemia and lymphoma. Patients with neutropenia or thrombocyto- Elevated blood pressure
=>
i U C/
o
</>
CD
penia require specialist management for dental treatment. Perform dental
procedures when the neutrophil and platelet counts are adequate; seek
Patients treated for elevated blood pressure can undergo general dental -4»

3
treatment if their blood pressure is controlled and stable.
ECD expert advice for emergency dental procedures. For further information on
the dental management of patients with immune compromise, see p.181. Although local anaesthetics containing adrenaline (epinephrine) theoreti-
!§
=5
CD cally elevate blood pressure, they do not have a clinically significant effect c 75
Tooth extraction sockets heal well in most patients undergoing chemo-
§ therapy. However, patients taking antiresorptive or antiangiogenic drugs are
(for more information on adding vasoconstrictors to local anaesthetics, see c D
<
p. 202). 15 E
at risk of medication- related osteonecrosis of the jaw (see pp.164-73) —
CD

IS
Q-

seek specialist advice. Avoid nonsteroidal anti-inflammatory drugs (NSAIDs) in patients taking a
Oj

CD
diuretic plus an angiotensin converting enzyme inhibitor (eg perindopril) o
175
174

or an angiotensin II receptor blocker (eg candesartan). Combining these
three drug classes can cause kidney failure. Alternate analgesics (eg par-
acetamol) are recommended (to select an appropriate analgesic regimen
for acute dental pain, see p.137).
Calcium channel blockers (eg amlodipine) can cause gingival enlargement
(gingival hyperplasia ). Gingival enlargement can be minimised with good
oral hygiene; however, extensive gingival hyperplasia requires specialist
management.
Coronary ischaemic syndromes
In dental practice, first-aid management of angina or an acute coronary
syndrome is outlined on p.242.
Check if the patient is taking antithrombotic drugs—for patients taking
an antithrombotic drug and undergoing an oral or dental procedure, see
pp.153-63 for management advice.
In the 12 months after myocardial infarction, stent placement or coronary
artery bypass surgery, patients are at increased risk of a major adverse
cardiac event (eg sudden death). Defer elective dental treatment for
6 months after myocardial infarction, stent placement or coronary artery
bypass surgery. If dental pain or infection occurs within the 6- month period
following the event, provide adequate emergency treatment in order to
defer definitive treatment, and consider seeking specialist advice.
Defer elective dental treatment for 6 months after myocardial
75 infarction, stent placement or coronary artery bypass surgery.
0)
o Patients with a history of a coronary ischaemic syndrome can undergo
O
c dental treatment as long as their condition is stable and they are following
cu
their preventive or rehabilitation program.
75
o-
The presence of a pre-existing coronary stent is not an indication for sur-
i
c/5 gical antibiotic prophylaxis for dental procedures ( indications for surgical
CD
antibiotic prophylaxis for dental procedures are outlined on p.189) .
£CD
Instruct patients with angina to bring their medication (eg glyceryl trini-
Z3
CD trate spray or tablets) when attending for dental treatment, and have it
in a readily accessible place. Limit the duration of dental procedures. Use
relaxation techniques and consider anxiolysis (for advice on anxiolysis [min-
CD
CL
CD imal sedation] for dental procedures, see pp.211-20) . Ensure effective
CD
176
I
analgesia during dental procedures using a local anaesthetic —the use of
a vasoconstrictor with local anaesthetic is not contraindicated in these
patients (for advice on local anaesthetics in dentistry, see pp.201-9) .
Heart failure
Do not undertake dental treatment unless the patient’s heart failure is
stable. Limit the duration of dental procedures. Patients with heart failure
may not tolerate being placed in a horizontal position—position the dental
chair so the head is higher than the heart, at a similar angle to how the
patient can comfortably sleep.
Patients with severe heart failure are at increased risk of adverse outcomes
from sedation and general anaesthesia. Dental procedures requiring seda-
tion or general anaesthesia should be undertaken in a hospital with an
anaesthetist present.
Avoid nonsteroidal anti-inflammatory drugs (NSAIDs) in patients with heart
failure ( see pp.44-9 for further information).
Cardiac implanted electronic devices
Cardiac implanted electronic devices include implantable cardioverter
defibrillators and permanent pacemakers. Patients with cardiac implanted
electronic devices can undergo most general dental treatment.
Surgical diathermy can interfere with some cardiac implanted electronic
devices. With modern cardiac implanted electronic devices, interference
from most other dental electronic and ultrasonic devices is usually not clin-
ically significant. However, if in doubt, consult the cardiologist responsible
for the management of the cardiac implanted electronic device or seek V)
expert advice before a dental procedure.* c
.2
_.
The presence of a cardiac implanted electronic device is not a specific indi-
D
cation for surgical antibiotic prophylaxis ( indications for surgical antibiotic u </>
oc
prophylaxis for dental procedures are outlined on p.189). +*
§
1
Cardiac implanted electronic devices should not be confused with pros-
thetic cardiac valves. The presence of a cardiac implanted electronic device So
i
is not a specific indication for infective endocarditis prophylaxis (indications °
2 75
for endocarditis prophylaxis are outlined on p.194).
c "o
E
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if
75 E
* For further information, see the American Dental Association Center for Scientific Q
Information topic on cardiac implanted electronic devices and interference from electronic
dental instruments.
177
 infective dental conditions. If unsure whether dental treatment can safely
Diabetes proceed, consult the patient’s medical practitioner.

In dental practice, first-aid management of hypoglycaemia is outlined on
p.244.
For patients with diabetes, take a thorough medical history and determine
if their diabetes is well controlled and stable. Consult the patient’s medical
practitioner if needed. A glycated haemoglobin (HbAlc) above the patient’s
target is an indicator of poor glycaemic control. Glycaemic targets are indi-
vidualised; a common glycated haemoglobin target is 53 mmol/mol ( 7%)
or less.
Poorly controlled diabetes is associated with postprocedural complications
such as infection and poor wound healing. Although the risk of postop-
erative infection can be higher in patients with poorly controlled diabetes,
antibiotic prophylaxis is not indicated (indications for surgical antibiotic
prophylaxis for dental procedures are outlined on p.189). Patients with
poorly controlled diabetes are at increased risk of periodontal disease.
Diabetes may be associated with sialadenosis, which can cause impaired
salivary gland function.
For all patients with diabetes, provide regular dental care, including instruc-
tions in oral hygiene and denture maintenance.
Consider the possibility of undiagnosed diabetes in patients with sudden
onset or progression of periodontal disease, poor response to periodontal
treatment, poor wound healing, or recurrent or persistent bacterial or
fungal oral infections—refer the patient to a medical practitioner.
75
0
Q Dental procedures in patients with diabetes
Sodium - glucose co-transporter 2 (SGLT2) inhibitors may need to be
stopped temporarily before a dental procedure—see below for more
information.
If preprocedural fasting is required (eg for general anaesthesia or intra-
venous sedation) for a patient with diabetes, an anaesthetist or other
appropriate medical practitioner must supervise the dental procedure.
Dental procedures in patients taking sodium-
glucose co -transporter 2 (SGLT2) inhibitors
Sodium-glucose co-transporter 2 (SGLT2) inhibitors (eg dapagliflozin,
empagliflozin, ertugliflozin) have been associated with the development of
euglycaemic diabetic ketoacidosis (DKA) in patients with type 1 or type 2
diabetes. The risk of diabetic ketoacidosis is increased in patients taking
SGLT2 inhibitors who:
• have been fasting or have a very restricted dietary intake
• have undergone a surgical procedure
• are dehydrated
• have an active infection.
SGLT2 inhibitors may need to be stopped before a dental
procedure—consult the medical practitioner .
For prolonged dental procedures, or procedures in which fasting or dehydra-
tion is likely either before or after the procedure, consider stopping SGLT2
inhibitors preprocedurally. This must only be done in consultation with the V)

.8
O
patient’s medical practitioner. Alerts highlighting the periprocedural risk of c
c Use clinical judgment to decide whether a patient with diabetes can be
cs
75
o-
i
safely treated with outpatient dental treatment, or if they require dental
treatment in hospital. Most patients with diabetes have a routine of
diabetic ketoacidosis in patients taking an SGLT2 inhibitor have been issued
by the Australian Diabetes Society < www.diabetessociety.com.au/position- u
_
<Q0.
C/5
statements. asp > and the Australian Therapeutic Goods Administration o
medications, diet, activity and blood glucose monitoring that maintains
.—
C
In
blood glucose concentration within safe limits. Provided this routine is < www.tga.gov.au/alert/sodium -glucose-co-transporter-2-inhibitors> .
M
CJ
Eo
2
not interrupted, most dental treatment can proceed in an outpatient set-
ting. Box 22 (p.180) outlines the approach to outpatient dental treatment i0
So
§
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.9 hypoglycaemia.
c 0
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Optimal glycaemic control periprocedurally improves outcomes in patients

If
Q.
2 with diabetes. If possible, postpone elective dental procedures until gly-
CD
jC caemic control is optimised; however, do not delay treatment of acute or

178 179
 Box 22. Management of a patient with stable diabetes HIV infection
undergoing a dental procedure in an outpatient
setting Antiretroviral drugs interact with many commonly prescribed drugs—consult
an HIV expert before prescribing any drug in a patient taking antiretroviral
Before the procedure drugs. Unusual and rare adverse reactions (eg perioral paraesthesia) can
• Determine the patient’s usual routine (eg medications, diet, activity, blood occur with antiretroviral drugs.
glucose monitoring).
• Determine whether any type of activity destabilises the patient’s blood glucose With currently available antiretroviral therapy, many patients with HIV are
control. well managed and stable. However, patients with HIV infection, particu-
larly smokers, are at increased risk of oral diseases, such as opportunistic
• For patients taking SGLT2 inhibitors, see additional advice on p.179.
infections, periodontal disease ( see pp.71-6) , necrotising periodontitis
• Determine the extent and type of dental treatment required. ( see p.73) , oral hairy leukoplakia and oral squamous cell carcinoma (see
• Ask patients to bring their glucose monitor on the day of the procedure if they p.95). HIV- related salivary gland hypofunction can occur, and increases the
use one. risk of oral candidiasis (for management of oral candidiasis, see p.114) .
Other oral manifestations of HIV include recurrent aphthous stomatitis,
Scheduling the procedure
intramucosal haemorrhages and hyperpigmentation of the oral mucosa.
• Schedule the procedure for the morning, so that any potential sequelae can be
resolved during the day.
Some conditions are particularly related to late- stage HIV, such as Kaposi
sarcoma and oral hairy leukoplakia.
• Consider the patient’s usual meal times and medication regimen; aim to
minimise interruption to their routine. Oral diseases and opportunistic infections in patients with HIV infection
• Avoid extensive treatments and long appointments. should be managed in conjunction with an HIV expert. Referral to an oral
medicine specialist may also be appropriate.
Day of the procedure
• Check that the patient has followed their usual meal times and medication For patients with HIV, manage oral diseases and opportunistic
regimen and is feeling well. infections in conjunction with an HIV expert.
• If the patient has missed a meal, if possible, ask them to eat and start
treatment 30 minutes later; otherwise reschedule the appointment.
75 • Do not give patients glucose or a sweetened drink ‘just in case’; this is
Immune compromise
Q) ineffective and can destabilise their diabetes management.
Q Patients with immune compromise are at increased risk of infection. The
• If a patient feels ill during the procedure, stop treatment. Assess their blood
dental management of an immunocompromised patient requires a multi- 2
c
c
“O
glucose concentration if a blood glucose monitor is available. If unsure of
03 disciplinary approach.
the cause of their symptoms, call 000. For the first -aid management of
75
o-
i hypoglycaemia occurring in a dental practice, see Box 35 (p.244). Conditions that can cause profound immune compromise include: _.
Q

21
U (/)

• Do not allow the patient to leave your care if they are unwell or confused. • end- stage kidney disease
0
• end- stage liver disease
After the procedure
• Advise patients to maintain their usual caloric intake, activity level and • malignancies §§
§0
CD medications, even if their mouth is sore. • untreated or end- stage human immunodeficiency virus (HIV) infection <2 75 °
• malnutrition. § .2
-
.9
4 »
• Provide dietary advice on preparation of soft foods if they are likely to have
.
difficulty eating =o
E
0
CL
CO SGLT2 = sodium -glucose co- transporter 2
75 E
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180 181
 Conditions that can be treated with immunosuppressive therapies include:
• autoimmune and inflammatory conditions (eg rheumatoid arthritis,
psoriasis, inflammatory bowel disease, systemic lupus erythematosus,
vasculitides)
• organ transplantation
• malignancies (also see the advice for patients taking chemotherapy on
p.174).
The degree of immune compromise affects treatment decisions and the
use of surgical antibiotic prophylaxis. For example, poorly controlled dia-
betes can compromise the immune system but is not an indication for
surgical antibiotic prophylaxis. Conversely, profoundly immunocompro-
mised patients (eg patients taking high doses of immunosuppressive
therapy) may require surgical antibiotic prophylaxis. Consult the patient’s
medical practitioner, specialist or multidisciplinary team to determine an
appropriate treatment plan and the need for surgical antibiotic prophylaxis
(for further discussion of antibiotic prophylaxis for dental procedures, see
pp.189-99).
Chronic musculoskeletal disorders
Pain and restricted mobility are common symptoms of musculoskeletal
disorders. Chronic musculoskeletal disorders encompass a range of condi-
tions affecting:
• muscles (eg sarcopenia )
15 • joints (eg osteoarthritis, rheumatoid arthritis)
Q) • bones (eg osteoporosis, traumatic fractures)
O implant- borne prosthesis—the patient must be sufficiently healthy to
• spine (eg back and neck pain)
c
O
cu • multiple body systems and locations (eg widespread and regional
15 pain disorders, inflammatory connective tissue diseases, systemic
o vasculitides, fibromyalgia) .
</ >
o In dental practice, first-aid management of a seizure is outlined on p.247.
Patients with pain and restricted mobility due to a musculoskeletal disorder
may find extended dental treatment uncomfortable. Modify treatment to
0
minimise the time spent in the dental chair, and consider changing the
0
chair configuration or using filler pillows to support the neck, hips or knees.
Patients with chronic musculoskeletal disorders may be prescribed
0
Q- immunomodulatory drugs, which can cause immunosuppression ( see
0
2 p.181). If corticosteroids are used, also see p.163.
C
| generalised seizure occurs during treatment .
182
Some patients with chronic musculoskeletal disorders take large doses of
over-the-counter or prescription analgesics, including opioids. Opioids can
cause dry mouth and consequently dental decay and periodontal disease,
particularly if taken with other drugs that can cause dry mouth (for the
management of dry mouth, see p.121). Consult the patient’s medical
practitioner if pain management is required for a dental indication.
Patients with chronic musculoskeletal disorders may have prosthetic joints;
this is not a specific indication for surgical antibiotic prophylaxis before
dental procedures (for further information, see p.191).
Neurological conditions
Stroke
In dental practice, first- aid management of stroke is outlined on p.246.
Patients who have had a stroke may be taking antithrombotic therapy—see
pp.153-63.
Patients who have had a stroke may have a physical impairment that
affects their ability to carry out usual oral hygiene practices. Patients with
a residual neurological deficit of the arm can have difficulty cleaning their
teeth. Large- handled or powered toothbrushes can improve the effective-
ness of oral hygiene.
Patients with seventh cranial (facial) nerve weakness accumulate food
debris on the affected side and can have difficulty with denture fitting.
Modifications to denture design include a thickened flange. Consider an
2
undergo the surgical procedure and be able to maintain good oral hygiene. +
c
.s
CQ
Epilepsy .
— «2
Q
M
For patients with epilepsy, assess the stability of their condition, including
how frequently seizures occur and what triggers them. At each appoint- £j §
g!«5
ment, check that the patient has taken their usual medication because
omission of doses can cause seizures. c5
n
Avoid stressful extended procedures. Consider the use of a mouth prop to 15 E
prevent the patient from biting the operator’s fingers or instruments if a
o £
183
 Some antiepileptic drugs ( phenytoin, sodium valproate, carbamazepine
and barbiturates) can cause gingival enlargement (gingival hyperplasia) .
Gingival enlargement can be minimised with good oral hygiene; however,
extensive gingival enlargement requires specialist management.
Trigeminal neuralgia
Patients with trigeminal neuralgia may mistake their symptoms for tooth-
ache. Dental pain, particularly pulpitis, is qualitatively similar to trigeminal
neuralgia, so careful evaluation of the teeth is required. If the findings from
an oral examination and tests (eg pulp tests, radiographs) do not suggest
a dental pathology, or if initial dental treatment does not reduce the pain,
consider the possibility of trigeminal neuralgia. Do not undertake further
dental treatment or perform invasive or irreversible procedures unless a
dental pathology is confirmed. If facial pain is not dental in origin, refer the
patient for medical assessment.
Trigeminal neuralgia can mimic dental pain.
In patients with unstable trigeminal neuralgia, dental treatment can exacer-
bate pain, even if performed at other sites in the mouth. Treating the area
afflicted by trigeminal neuralgia with a local anaesthetic block can reduce
the degree of exacerbation.
Psychological and psychiatric disorders
75
The psychological status of patients can affect dental treatment plans and
outcomes. Determine the psychological status of patients by taking a thor-
0
Q practitioner.
T3 ough medical and medication history, noting the use of, and indication for,
C
(0 any psychoactive drugs.
o—
75
Patients with psychiatric and psychological disorders may have barriers to
3
adhering to dental treatment, maintaining daily oral hygiene and attending
regular dental reviews.
(/)
0
ECD
2
3
Psychotropic drugs such as antidepressants, antipsychotics and psycho-
stimulants can cause dry mouth (for the management of dry mouth, see
CD
p.121) . Selective serotonin reuptake inhibitors (SSRIs) , serotonin and
—
.49«
noradrenaline reuptake inhibitors (SNRIs) , antipsychotics and amfeta -
0
CL mines can trigger bruxism (for the management of bruxism, see p.149) .
CD
CD Psychotropic drugs are associated with many other adverse effects on
oral and dental health—consult the patient’s medical practitioner if a
-C
psychotropic drug is suspected to be causing an oral adverse effect.
184
Patients with a history of sedative drug use (eg analgesics, anxiolytics, illicit
drugs) or hazardous alcohol consumption may have a tolerance to sedative
drugs. If procedural anxiolysis or sedation is required for a patient tolerant
to sedatives, seek expert advice or refer for specialist management.
Substance use disorder and illicit drug use
Illicit drug use can have adverse effects on oral health. Many illicit drugs
cause dry mouth, and, combined with a cariogenic diet and a lack of
oral hygiene, can result in dental caries ( see pp.63-70), oral candidiasis
(see p.114) and other oral infections. Intake of drugs through smoking
increases the risk of oral cancer ( see p.95) . Bruxism, jaw clenching and
resultant tooth damage is common in users of amfetamines and cocaine
(for the management of bruxism, see p.149).
If a substance use disorder is identified, it is important to investigate the
use of other substances, because multiple drug use is common.
Patients with a previous or current substance use disorder are at particular
risk of developing benzodiazepine dependence—consider the risks and
benefits of using benzodiazepines for anxiolysis for a dental procedure
( for discussion of anxiolysis [ minimal sedation ] for dental procedures, see
pp.211-20).
Drug- dependent and drug- seeking patients may present to a dental prac -
tice. Be circumspect if a patient demands analgesic drugs and exhibits a
good level of knowledge or a preference for a specific opioid. Be aware
of legislative requirements for prescribing drugs of dependence to a drug-
dependent patient (for information on legislation about prescriptions
and prescribing, see p.9); advise the patient to consult their medical
C
.2
Respiratory conditions Q .
Si
Asthma S
In dental practice, first-aid management of acute asthma is outlined on i§
p.255. £ 75
Advise patients with asthma to bring their reliever inhaler and spacer to E
c 0
nz
dental appointments. 75 E
Patients with severe asthma are at increased risk of adverse outcomes
a
from sedation and general anaesthesia. Dental procedures requiring
185
 sedation or general anaesthesia in a patient with severe asthma should be
undertaken in a hospital with an anaesthetist present.
Nonselective nonsteroidal anti- inflammatory drugs (NSAIDs) (eg aspirin,
ibuprofen, naproxen) can cause bronchoconstriction in patients with
NSAID - exacerbated respiratory disease. Cyclo - oxygenase- 2 (C0X- 2)-selec -
tive NSAIDs (eg celecoxib) do not cause bronchospasm in patients with
NSAID- exacerbated respiratory disease. If analgesia is required in asth-
matic patients with known NSAID -exacerbated respiratory disease, use a
C0X-2-selective NSAID or paracetamol (to select an appropriate analgesic
regimen for acute dental pain, see p.137).
Patients with asthma can develop oral candidiasis secondary to the use
of inhaled corticosteroids. For the management of oral candidiasis, see
p.114; to prevent recurrence, advise patients to rinse their mouth and
throat with water and spit out after inhalation.
Patients are sometimes prescribed a short course of systemic corticoster-
oids following an asthma exacerbation—consider delaying elective dental
treatment until the course is complete.
Chronic obstructive pulmonary disease
Dental treatment for patients with COPD may need to be modified
according to the patient's condition. Patients with severe COPD do not tol-
erate being placed in a horizontal position.
Patients with severe COPD are at increased risk of adverse outcomes from
15 sedation and general anaesthesia. Dental procedures requiring sedation or
-M
general anaesthesia in a patient with severe COPD should be undertaken
in a hospital with an anaesthetist present.
(1)
Q The most relevant hepatitis viruses to dental practice are the blood-borne
o viruses that cause chronic liver disease and cirrhosis: hepatitis B and C.
c Patients with COPD are sometimes prescribed a short course of systemic
03
15
corticosteroids following an exacerbation of COPD—consider delaying elec -
- tive dental treatment until the course is complete.
s
O planus ( see p.101) , dental caries (see pp.63-70) and periodontal disease
Patients with COPD can develop oral candidiasis secondary to the use
(0
of inhaled corticosteroids. For the management of oral candidiasis, see
CD
E0
)
p.114; to prevent recurrence, advise patients to rinse their mouth and
(3
3 throat with water and spit out after inhalation.
.9
In some patients with COPD, supplemental oxygen is contraindicated—
consult the patient’s COPD action plan.
CD
CL
CD
sz
CD
186
Obstructive sleep apnoea
Dentists have an important role in the multidisciplinary management of
obstructive sleep apnoea, including the diagnosis of facial skeletal retru -
sion (eg retrognathia) and the construction of mandibular advancement
splints. Some patients with obstructive sleep apnoea can be effectively
treated with a mandibular advancement splint, but this must be done in
association with a multidisciplinary team led by a specialist respiratory
physician. The use of oral appliances for management of obstructive sleep
apnoea are reviewed in detail in the American Academy of Sleep Medicine
and the American Academy of Dental Sleep Medicine guidelines.*
Snoring may or may not be a sign of obstructive sleep apnoea. It is not
possible to diagnose the cause of snoring without a medical examination
and sleep laboratory investigation. Use of oral devices to treat snoring
without such investigations is not appropriate. If obstructive sleep apnoea
is suspected, refer the patient for medical assessment.
Use of oral devices to treat snoring without medical examination
and investigation is not appropriate.
Patients with obstructive sleep apnoea are at increased risk of respiratory
.
arrest from sedation and general anaesthesia Dental procedures requiring
sedation or general anaesthesia in a patient with obstructive sleep apnoea
should be undertaken in a hospital with an anaesthetist present .
Viral hepatitis
on
c
£
Most cases of hepatitis C can now be cured with antiviral therapy. Patients s.
with chronic or untreated hepatitis C have a higher incidence of oral lichen Q
S§
.2
(see pp.71-6) . Periodontal health, in particular, is markedly poorer and
M
salivary flow is reduced in patients with hepatitis C—whether this is a direct
§§
viral effect or due to other causes is unknown. Preventive dental care and
management is particularly important for patients with hepatitis C because g!5
the outcomes of major restorative treatment may be poor. c5 £
n
15 E
* Ramar K, Dort LC, Katz SG, Lettieri CJ, Harrod CG, Thomas SM, et al. Clinical Practice Q
Guideline for the Treatment of Obstructive Sleep Apnea and Snoring with Oral Appliance
Therapy: An Update for 2015. J Clin Sleep Med 2015;ll(7):773 -827.
187
 Before proceeding with an invasive dental procedure in a patient with
chronic viral hepatitis, consider the potential coagulopathy and immune
compromise associated with end- stage liver disease. Consult the patient’s
treating specialist or multidisciplinary team to determine an appropriate
treatment plan, including antibiotic prophylaxis (for further discussion of
antibiotic prophylaxis for dental procedures, see pp.189-99) .
Avoid sedatives and nonsteroidal anti-inflammatory drugs (NSAIDs)
in patients with viral hepatitis, because they can cause liver toxicity.
Paracetamol can be used at normal therapeutic doses. However, it is
particularly important to ensure that the maximum dose of paracetamol is
not exceeded because patients with viral hepatitis are at increased risk of
liver damage at supratherapeutic doses. To select an appropriate analgesic
regimen for acute dental pain, see p.137.
75
Antibiotic prophylaxis
for dental procedures
Overview of antibiotic use for dental
procedures
Only use antibiotics before a dental procedure if there is a clear indication
for their use.
• Surgical antibiotic prophylaxis (use of antibiotics to prevent surgical
site infection) is rarely indicated—see pp.189-92.
• Infective endocarditis prophylaxis ( use of antibiotics to prevent
infective endocarditis) is needed for patients with specific cardiac
conditions ( see Box 24; p.194) undergoing specific dental procedures
( see Box 25; p.195), even if surgical antibiotic prophylaxis is not
indicated—see pp.192-9.
• Antibiotics to treat acute odontogenic infection may be required,
even if surgical antibiotic prophylaxis and infective endocarditis
prophylaxis are not indicated—see pp.79-87.

Q)
Q
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Surgical antibiotic prophylaxis in dentistry <5
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75
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Indications for surgical antibiotic prophylaxis £
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Surgical antibiotic prophylaxis is rarely indicated for dental procedures—
15
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19
3
see Table 18 (p.190). The recommendations to use surgical antibiotic -CQ-
O
prophylaxis are informed, when possible, by evidence that prophylaxis is
a.
(D
.9 beneficial for the relevant procedure and patient group. Furthermore, the «2
0
C3
potential benefits of preventing postoperative infection with surgical anti- -
+» 3
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2 biotic prophylaxis is balanced against the potential harms of antimicrobial IS
0
-0 use (eg diarrhoea, rash, bacterial resistance; see also p.19-21). J Q2.
<
188 189
 The role of surgical antibiotic prophylaxis for patients with profound
immune compromise (for guidance on assessing a patient’s degree of
immune compromise, see p.181) who are undergoing an invasive dental
procedure is uncertain. Discuss the need for surgical antibiotic prophylaxis
with the treating specialist or multidisciplinary team.
Surgical antibiotic prophylaxis is rarely indicated for dental
procedures .
Even if surgical antibiotic prophylaxis is not indicated, consider the need
for treatment of acute odontogenic infection (see pp.79 87) or infective -
endocarditis prophylaxis (see pp.192-9).
For the role of surgical antibiotic prophylaxis before dental procedures in
patients with a prosthetic joint or a breast implant, see p.191.
Do not use prophylactic antibiotics to prevent alveolar osteitis (dry socket) ,
which is a post- extraction complication caused by premature clot lysis
rather than infection. For further discussion of alveolar osteitis, see p.222.
Prophylactic antibiotics do not prevent alveolar osteitis.
If prophylaxis is indicated, follow the principles for appropriate prescribing
of surgical antibiotic prophylaxis in Box 23 (p.191).
Table 18. Dental procedures and their requirement for
surgical antibiotic prophylaxis
w Procedures Is surgical antibiotic
-M prophylaxis indicated?
0)
Q tooth extractions NO [NB1]
o
c third molar surgery
Box 23. Principles for appropriate prescribing of surgical
antibiotic prophylaxis in dentistry
• Do not use surgical antibiotic prophylaxis unless there is a clear indication for
its use—see Table 18 (p.190).
• The choice of antibiotic is determined by the susceptibilities of the organism(s)
most likely to cause postoperative infection. Antibiotic choice may need to be
modified in certain circumstances—see p.191.
• If prophylaxis is indicated, a single preoperative dose of antibiotic(s) is usually
sufficient—postoperative doses are not required.
• Surgical antibiotic prophylaxis must be administered before surgical incision. For
short - acting antibiotics, such as amoxicillin, the dose should be administered no
more than 60 minutes before incision.
Surgical antibiotic prophylaxis for patients
with a pre- existing joint prosthesis
Although surgical procedures can result in incidental bacteraemia, there
is a low risk of seeding of the joint prosthesis and subsequent infection.
Accumulated evidence supports the same approach to surgical antibiotic
prophylaxis for patients with and without a pre-existing joint prosthesis;
neither the indication for prophylaxis nor the choice of antibiotic regimen
is altered by the presence of a joint prosthesis. This is true even for proce-
dures that commonly cause bacteraemia (eg tooth extractions, periodontal
procedures). The potential adverse effects outweigh the potential benefits
of prophylaxis.*
Only give surgical antibiotic prophylaxis to patients with a
pre- existing joint prosthesis or breast implant if prophylaxis is
indicated for the procedure. To
-
M

n procedures involving insertion of dental implants 0

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15 Surgical antibiotic prophylaxis for patients
o-
i periodontal surgery
periapical surgery with a pre- existing breast implant
CO &
CD soft and hard tissue removal X
Neither the indication for prophylaxis nor the choice of antibiotic regimen is 3
oral maxillofacial procedures see ‘Surgical prophylaxis for
CD
oral maxillofacial surgery' in
altered by the presence of a breast implant; therefore, the same approach -CCL
ID eTG complete to surgical antibiotic prophylaxis should be taken for patients with and o
o .
.9
without a pre-existing breast implant. Q (0
dental procedures not listed above NO
oS
CD
CL
CD
NB1: For patients with profound immune compromise (for guidance on assessing a patient’s
degree of immune compromise, see p.181), discuss the need for surgical antibiotic
M

58
3
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prophylaxis with the multidisciplinary team or treating specialists. * For a detailed discussion of prevention of prosthetic joint infection in patients undergoing
CD
dental procedures, see the American Dental Association Council on Scientific Affairs E Q2.
jC publication Management of Patients with Prosthetic Joints Undergoing Dental Procedures
<
Clinical Practice Guideline .
190 191
 Antibiotic choice for surgical prophylaxis in Endocarditis- related bacteraemia is more likely to result from daily oral
hygiene activities than from specific procedures, and is strongly associated
dentistry with poor oral hygiene and gingival disease. Therefore, the maintenance of
Surgical antibiotic prophylaxis is rarely indicated for dental procedures— good oral health and hygiene is more important than the use of antibiotic
see Table 18 ( p.190) . If prophylaxis is indicated (eg after discussion with prophylaxis. Oral hygiene is important for the general population but par-
their specialist, for a profoundly immunocompromised patient undergoing ticularly for patients with a cardiac condition listed in Box 24 ( p.194); for
an invasive procedure [ for guidance on assessing a patient’s degree of general measures to prevent endocarditis, see p.195.
immune compromise, see p.181]) , a single preoperative dose of a narrow- Endocarditis can occur after hospitalisation, especially in older, sicker
to moderate-spectrum penicillin (eg amoxicillin, benzylpenicillin) is usually patients with diabetes or chronic kidney disease. This does not appear
appropriate. Clindamycin is a suitable alternative for patients hypersensitive to be a sequel to a particular procedure but rather to problems such as
to penicillins. intravascular catheter infections. This emphasises the need for infection
Consider the principles for appropriate prescribing of surgical antibiotic prevention and control strategies in hospitals.
prophylaxis (see Box 23; p.191). No randomised controlled trial has been performed to determine the
The choice of antibiotic for surgical prophylaxis may not need to be altered role of antibiotic prophylaxis, and there are no human studies showing
in patients who have recently received antibiotic therapy. that it can prevent infective endocarditis. Consequently, guidelines rely
• For patients who have taken a short course of antibiotics for an on expert consensus. Since 2002, many international guidelines* have
unrelated illness within the preceding 4 weeks, there is no need to significantly reduced the number of indications for endocarditis prophy-
modify antibiotic choice. laxis. The National Institute for Health and Care Excellence (NICE) in the
United Kingdom (UK) went even further in 2008, recommending that anti-
• For patients who have recently received surgical antibiotic prophylaxis
( eg patients for whom a dental procedure is completed over multiple
biotic prophylaxis was not required for any person before dental or other
procedures.
sessions) , there is no need to modify antibiotic choice even if using
the same antibiotic each time. Studies examining the impact of the changes in guidelines have yielded
• For patients currently taking long-term antibiotics for another indication conflicting results. Some studies indicate the incidence of infective endo-
( eg rheumatic heart disease), it may be necessary to modify antibiotic carditis has not increased with restricted or no prophylaxis, but other
choice—seek expert advice to determine an appropriate antibiotic studies suggest that infective endocarditis cases have increased after the
75 regimen. adoption of new guidelines. In response to these data, NICE modified their
CD recommendations in 2016 to state that endocarditis prophylaxis is not
Q ‘routinely’ required. This update allows for clinical judgment to decide if 75
Prevention of infective endocarditis endocarditis prophylaxis is required.
TJ M
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75 In the absence of high-quality evidence, the Antibiotic Expert Groups con-
o- Rationale for endocarditis prophylaxis £
i
tinue to recommend antibiotic prophylaxis against infective endocarditis for
</ > a restricted group of patients—for indications for endocarditis prophylaxis, .<X2
CD Infective endocarditis is a relatively uncommon illness with high morbidity see p.194. J2
0 and mortality. The incidence in Australia is approximately five cases per .cCL
5
3
100 000 person-years, and the in- hospital mortality is 15 to 20%. o
CD
For many years, antibiotic prophylaxis was routinely given before dental a. (/)
.9
and other procedures to patients with cardiac conditions that have a high M 3
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lifetime risk of infective endocarditis. However, endocarditis after these pro-
Cl
2 cedures is rare, so prophylaxis prevents very few cases.
£ 8
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* International guidelines on the prevention of infective endocarditis are listed on p.199.
192 193
Indications for endocarditis prophylaxis
Antibiotic prophylaxis against infective endocarditis is recommended only
for patients who meet both of the following criteria:
• have a cardiac condition associated with an increased risk of
developing infective endocarditis and the highest risk of adverse
outcomes from endocarditis ( see Box 24, below)
• are undergoing a dental procedure associated with a high risk of a
bacteraemia that is associated with endocarditis ( see Box 25; p.195).
Endocarditis prophylaxis is not recommended for situations other than
those covered in this topic.
Box 24. Cardiac conditions for which endocarditis
prophylaxis is recommended for patients
undergoing a procedure listed in Box 25
Endocarditis prophylaxis is recommended only for patients with the following
cardiac conditions (that are associated with an increased risk of developing
infective endocarditis and the highest risk of adverse outcomes from
endocarditis) who are undergoing a procedure listed in Box 25 (p.195) [NBl]
[NB2]:
• prosthetic cardiac valve, including transcatheter- implanted prosthesis or
homograft
• prosthetic material used for cardiac valve repair, such as annuloplasty rings and
chords
• previous infective endocarditis
• congenital heart disease but only if it involves:
- unrepaired cyanotic defects, including palliative shunts and conduits
- repaired defects with residual defects at or adjacent to the site of a
prosthetic patch or device ( which inhibit endothelialisation)
• rheumatic heart disease in high -risk patients [NB3 ].
Box 25. Dental procedures for which endocarditis
prophylaxis is recommended for patients with a
cardiac condition listed in Box 24 [NB1] [NB2]
Endocarditis prophylaxis is recommended only for patients with a cardiac
condition listed in Box 24 (p.194) who are undergoing one of the following
procedures associated with a high risk of a bacteraemia that is associated with
infective endocarditis:
• only dental procedures involving manipulation of the gingival or periapical tissue
or perforation of the oral mucosa (eg extraction, implant placement, biopsy,
removal of soft tissue or bone, subgingival scaling and root planing, replanting
avulsed teeth) .
NBl: Endocarditis prophylaxis is not recommended for procedures other than those covered in
this topic. However, surgical prophylaxis may be indicated even if endocarditis prophylaxis is
not— for surgical antibiotic prophylaxis for dental procedures, see pp.189-92.
NB2: For nondental procedures, see ‘Prevention of infective endocarditis’ in eTG complete.
It is thought that Aboriginal and Torres Strait Islander people with rheu-
matic heart disease are at higher risk of developing infective endocarditis
and adverse outcomes from the disease. However, it has been argued that
the higher risk, and poorer outcomes, are associated with socioeconomic
disadvantage rather than ethnicity. New Zealand guidelines recommend
prophylaxis for all patients with rheumatic heart disease, specifically
including Maori and Pacific Islander people. It is the consensus view of the
Antibiotic Expert Groups that antibiotic prophylaxis should be administered
to all Aboriginal and Torres Strait Islander people with rheumatic heart dis-
ease who are undergoing certain procedures ( see Box 25 above) . Other
patients with rheumatic heart disease who are at significant socioeconomic
disadvantage should also be considered for antibiotic prophylaxis.
75
General measures to prevent infective -
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endocarditis o
Data to support antibiotic prophylaxis are limited, and many cases of
£
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infective endocarditis are not preceded by a procedure. Therefore, general x
preventive strategies and early recognition and treatment of infective endo-
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carditis are important. .
JC
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All people, but particularly those with cardiac abnormalities, should prac - .
Q (/)
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tise good oral hygiene and have regular dental check-ups, with preventive
dental and periodontal treatment to ensure optimal oral health.
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195
 For people with a cardiac condition listed in Box 24 (p.194) or any form of mucosa (eg extraction, implant placement, biopsy, removal of soft tissue or
native valve disease, the following preventive strategies are recommended: bone, subgingival scaling and root planing, replanting avulsed teeth).
• twice-yearly dental examination and scaling Other dental procedures do not require endocarditis prophylaxis. Surgical
• timely treatment of all bacterial infections, particularly those caused by antibiotic prophylaxis may be indicated even if endocarditis prophylaxis is
Staphylococcus aureus or streptococci not—for surgical antibiotic prophylaxis in dentistry, see pp.189-92.
• avoidance of intravascular catheters and invasive procedures, unless
necessary
• strict adherence to protocols for managing central and peripheral
Endocarditis prophylaxis regimens for dental
intravenous devices (eg ‘care bundles’) procedures
• active discouragement of tattooing, piercing (particularly tongue
piercing) and intravenous drug use. Antibiotic prophylaxis regimens
If, after careful evaluation of both the cardiac condition (see Box 24;
An unexplained fever should be investigated in patients with a cardiac
p.194) and the dental procedure (see Box 25; p.195) , antibiotic prophy-
condition listed in Box 24 (p.194) , because it could be a sign of infective
laxis is considered necessary, give a single dose of antibiotic before the
endocarditis—refer the patient to their medical practitioner.
procedure. There is no proven value to giving a dose after the procedure.
If a patient is having more than one procedure requiring antibiotic prophy-
Approach to endocarditis prophylaxis for
laxis, the dentist should plan the treatment so that all procedures can be
dental procedures completed in a single sitting, or at most two sittings, to avoid/ the need for
multiple antibiotic doses.
Bacteraemia associated with dental procedures usually involves viridans
group streptococci, which are known to cause infective endocarditis. For endocarditis prophylaxis, use:
Traditionally, the presence of ‘significant bleeding’ associated with a dental
procedure was assumed to be an indication of bacteraemia and hence a amoxicillin 2 g (child: 50 mg/kg up to 2 g) orally, 60 minutes
need for prophylaxis; however, studies show that bleeding is a poor indi- before the procedure.
cator of bacteraemia from dental procedures.
If oral administration is not possible, use:
75 Self- performed oral hygiene (eg toothbrushing, flossing, use of oral irriga -
0 tors) can produce a similar incidence of bacteraemia to that caused by I amoxicillin 2 g (child: 50 mg/kg up to 2 g) intramuscularly,
o most dental procedures (excluding extractions) . As these activities are per- 30 minutes before the procedure 75
c
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formed more frequently than dental procedures, they have the potential to OR
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75
produce regular episodes of bacteraemia. Bacteraemia from self- performed -0O
o- oral hygiene is strongly associated with poor oral hygiene and gingival dis-
'
amoxicillin 2 g (child: 50 mg kg up to 2 g) intravenously, within the
i 1
ease; therefore, the maintenance of good oral health and hygiene is likely 60 minutes before the procedure
£
«05 .2X
to be more important than the use of antibiotic prophylaxis—for general
:§ OR J2
0 measures to prevent infective endocarditis, see p.195. Dental procedures
-CQ.
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5 are generally of longer duration than self-performed oral hygiene, so l ampicillin 2 g (child: 50 mg kg up to 2 g) intramuscularly,
expose patients to a longer duration of bacteraemia. Antibiotic prophylaxis
0
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.2 Q CD.
is therefore warranted for some dental procedures for high- risk patients.
0
Cl Endocarditis prophylaxis is recommended only for patients with a cardiac
OR
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condition listed in Box 24 (p.194) who are undergoing procedures involving
I
'
ampicillin 2 g (child: 50 mg kg up to 2 g) intravenously, within the 58
0
manipulation of the gingival or periapical tissue or perforation of the oral 60 minutes before the procedure. J Q2.
<
196 197
 For patients with delayed nonsevere hypersensitivity to penicillins ( see
pp.31-5), cefalexin can be used in most cases.* Use:
cefalexin 2 g (child: 50 mg/kg up to 2 g) orally, 60 minutes before
the procedure.
If oral administration is not possible, use:
i cefazolin 2 g (child: 30 mg/kg up to 2 g) intramuscularly,
30 minutes before the procedure
OR
1 cefazolin 2 g (child: 30 mg/kg up to 2 g) intravenously, within the
60 minutes before the procedure.
For patients with immediate ( severe or nonsevere) or delayed severe
hypersensitivity to penicillins ( see pp.31-5) , use:
Considerations for patients recently or currently
taking beta lactams
In patients taking long-term benzathine benzylpenicillin for prevention of
recurrent rheumatic fever, evidence suggests that the amoxicillin suscep-
tibility of viridans streptococci in the oral flora is not significantly affected
by the benzathine benzylpenicillin prophylaxis. The consensus view of the
Antibiotic Expert Groups is that amoxicillin is appropriate for endocarditis
prophylaxis in this setting.
In contrast, in patients currently taking or who have recently taken a course
of beta- lactam therapy (except for the situation described above) , evidence
suggests that the amoxicillin susceptibility of viridans streptococci may be
affected. Therefore, a non-beta-lactam antibiotic, such as clindamycin,
may be considered for prophylaxis in this setting.
Further reading

'^
clindamycin 600 mg (child: 20 mg kg up to 600 mg) orally, 60 to International guidelines on the prevention of infective endocarditis
120 minutes before the procedure. American Heart Association. Prevention of infective endocarditis guidelines
( 2007) < www.ncbi.nlm.nih.gov/pubmed/17446442 >
If oral administration is not possible, use:
American College of Cardiology/American Heart Association. Focused Update
of the 2014 AHA/ACC Guideline for the Management of Patients With Valvular
'
clindamycin 600 mg (child: 20 mg kg up to 600 mg)
intravenously, within the 120 minutes before the procedure. Heart Disease ( 2017) < www.ncbi.nlm.nih.gov/pubmed/28315732 >

British Society for Antimicrobial Chemotherapy. Guidelines for the prevention of

7u There is some evidence that moxifloxacin may be used as an alternative to endocarditis ( 2006) < www.ncbi.nlm.nih.gov/pubmed/16624872 >
clindamycin for patients with immediate (severe or nonsevere) or delayed
0) European Society of Cardiology. Guidelines for the management of infective
severe hypersensitivity to penicillins, but this has not been validated.
endocarditis ( 2015) < www.ncbi.nlm.nih.gov/pubmed/26320109 >
Q
o 75
c
CD National Heart Foundation of New Zealand. Guideline for prevention of infective <D
75 endocarditis associated with dental and other medical interventions ( 2008) .
T3

o- a
k
i

<http://assets.heartfoundation.org.nz/resources/prevention-of- infective-
CO
CD
endocarditis > .<x2
ECD National Institute for Health and Care Excellence (NICE). Prophylaxis against
J2
.9 infective endocarditis (2008 [updated July 2016]) < www.nice.org.uk/guidance/
"

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CD
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* It is safe to use cefalexin in patients who had a delayed nonsevere reaction to a penicillin cg64 > Q ./()

in the distant past. It is also safe to use cefalexin in patients who have had a delayed o|
4-> 3
nonsevere reaction recently, unless the reaction involved amoxicillin or ampicillin, because o -o
18
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CL cross-reactivity between these drugs is possible. For patients who have had a recent

«< 2.
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0 delayed nonsevere reaction to amoxicillin or ampicillin, use the drug recommended for
-£ = patients with immediate (nonsevere or severe) or delayed severe hypersensitivity, Q
t An oral liquid formulation of clindamycin is not commercially available but can be
prepared, if required, by dispersing a capsule in liquid; see p. 41 for instructions.
198 199
Local anaesthetics in dentistry
Local anaesthetics are commonly used in dentistry. They provide effec -
tive pain control (analgesia ) , and have a low incidence of adverse effects.
However, before administering a local anaesthetic clinicians must have an
understanding of the local and systemic complications (see pp.202-4) that
can arise from their use.
In dentistry, the most common methods of administration are:
• infiltration—local anaesthetic is injected adjacent to the site where
analgesia is required. Infiltration is sufficient for most teeth, except the
lower molars
• regional block— local anaesthetic is injected adjacent to the nerve,
proximal to the site where analgesia is required. A regional block aims
to prevent pain being experienced in the area of nerve distribution
distal to the site of injection (eg mandibular [ inferior alveolar nerve ]
blocks are required for procedures of the lower molars).

Topical administration of a locaLanaesthetic * is indicated for minor painful

procedures (eg band removal, crown placement, mucosal incision). It may
also be used to facilitate injection of local anaesthetic in anxious or needle-
phobic patients by eliminating pain on the mucosal surface; however,
patients may experience discomfort upon injection of local anaesthetic into
the deeper tissues.
The onset of effect depends on the method used; analgesia occurs ts
approximately 2 to 3 minutes after an infiltration injection, 4 to 5 minutes +5
c
after a block injection, and 3 minutes after topical administration. Pulp Q>
o
analgesia takes longer than analgesia of the soft tissues. The duration of
.£
effects depends on the local anaesthetic used, the dose and the method </)
of administration. Advise patients of the likely duration of effects and that
they should seek advice if they have not recovered after this time. «
£
Medical practitioners who are experienced in the use of local anaesthetic </>
0
0
via infiltration or regional block may use these techniques for temporary C
relief of acute severe dental pain (eg irreversible pulpitis). Some local fl
15
o
o
* Topical local anaesthetic formulations intended for use on the skin can be used off-label in
the mouth; ensure any excess is spat out.
201
 anaesthetics are available in single- use dental cartridges, which may be
easier to use.
Adding vasoconstrictors to local
anaesthetics
Local anaesthetics may be used in combination with a vasoconstrictor to
prolong local anaesthetic effects. Vasoconstriction reduces the rate of local
anaesthetic loss to the circulation and reduces bleeding, both during and
after the procedure.
Adrenaline (epinephrine) is a commonly used vasoconstrictor in dental
practice. Avoid adrenaline-containing solutions in patients with known
sensitivity to sulfites*, because metabisulfites are used as a preservative.
If adrenaline cannot be used, local anaesthetic solutions containing fely-
pressin or solutions without a vasoconstrictor are alternatives.
Felypressin is an alternative vasoconstrictor to adrenaline (epinephrine)
because it has minimal effects on the myocardium at the concentra-
tion used in dental cartridges (0.03 international units/mL) . Felypressin
is safe for dental use in pregnant patients, although previously this was
contraindicated.
Adverse effects of local anaesthetics
75
Adverse effects of local anaesthetics include local complications (see
a> P - 203) and systemic toxicity (see p.204) . The incidence of adverse effects
o is low, and differs between individual local anaesthetics. Although local
•a
c
n
anaesthetic adverse effects are rare, clinicians should be familiar with their
diagnosis and management. Resuscitation drugs and equipment, including
75
i
O
- oxygen, should be available for the immediate management of systemic
toxicity. If adverse effects occur (or are suspected) , stop administration
In)
a of the local anaesthetic and provide appropriate management. Acute
ECD emergencies can arise with administration of local anaesthetics—for the
first-aid management of medical emergencies occurring in dental practice,
Z3
0 see pp.233-59.
.y
CD
Cl
2 75
CD
* There is no cross-reactivity between sulfite preservatives and sulfonamide antibiotics,
sulfur or sulfates, although people can have multiple allergies.
202
Problems with the injection technique or injection into the incorrect site
(due to interindividual anatomical variation) can result in:
• complete or partial failure of local anaesthetic effect—if this occurs,
reassess the patient’s anatomy and review the injection technique.
A repeat injection may be tried, provided the maximum dose (see
Table 20; p.208) is not exceeded
• trauma to the nerves and surrounding tissues—for further information
on local complications, see below
• profound systemic effects (see p.204) if injected into a blood vessel
(particularly if combined with a vasoconstrictor) —to mitigate the risk of
intravascular injection, aspirate to exclude the presence of blood, then
inject slowly and monitor the patient’s response.
For more information on adverse effects of local anaesthetics, including in
combination with vasoconstrictors, consult a comprehensive source of drug
information (for resources, see p.61) .
Local complications
Local neurological complications include paraesthesia, dysaesthesia,
temporary facial nerve paralysis (eg paralysis of the periocular muscles; for
first-aid management, see p.248) and/prolonged anaesthesia. Most cases
of prolonged anaesthesia resolve spontaneously; permanent anaesthesia
is rare. Nerve injuries are rare and can be caused by direct nerve trauma ,
indirect nerve trauma (from bleeding within the nerve sheath), or localised
neurotoxicity. The risk of nerve damage is increased with repeat injections
into a partially anaesthetised site or administration of higher concentration
local anaesthetic solutions.
Trauma to the tissues (eg haematoma) can occur during injection of local
anaesthetic. Accidental intramuscular injection of local anaesthetic can to
cause trismus, either as a direct effect of the drug or due to bleeding within P
c
the muscle. If trismus occurs, promptly seek specialist advice or refer to an -0o
oral medicine or oral surgical specialist, because early management can .£
improve outcomes. >
</
.a
Rarely, local complications can arise from equipment failure (eg cartridge 0
explosion). £
Cf )
0
03
C
03
o
O
203
 Systemic toxicity
Systemic toxicity can follow inadvertent intravascular injection of local
anaesthetic, excessive dose administration, impaired drug clearance or,
rarely, rapid systemic absorption.
Adverse systemic effects are usually seen in a continuum as plasma con-
centration increases, so use the lowest effective dose and do not exceed
the maximum recommended dose (for further discussion of doses of local
anaesthetics, see p.206) .
Choosing a local anaesthetic in dentistry
Table 19 (below) outlines properties of local anaesthetic preparations for
infiltration or regional block in dentistry. Consult a source of drug infor-
mation for precautions, contraindications, drug interactions and adverse
effects (for resources, see p.61) .
Table 19. Local anaesthetics for infiltration or regional
block in dentistry

Systemic toxicity of local anaesthetics is more likely at higher Local anaesthetic Comments
plasma concentrations, so do not exceed the maximum Short - to intermediate -acting preparations
recommended dose . shorter acting—use in dentistry may be limited
lidocaine
The clinical presentation of systemic toxicity is variable and can include lidocaine with adrenaline intermediate acting
neurological, psychiatric, cardiovascular and respiratory effects, allergic (epinephrine) [ NB1] first line for routine dental procedures
reactions and, rarely, methaemoglobinaemia.* Minor central nervous
prilocaine [NB1] shorter acting—use in dentistry may be limited
system (CNS) effects (eg restlessness, anxiety, tinnitus, dizziness, blurred
vision, tremors, CNS depression, drowsiness) are early indicators of sys- prilocaine with adrenaline intermediate acting
temic toxicity. However, cardiovascular effects may occur before CNS (epinephrine) [NB1]

effects if a longer-acting local anaesthetic is used (particularly bupiv- prilocaine with felypressin [NB1] intermediate acting
acaine). Serious systemic effects include seizures and cardiovascular first line for routine dental procedures when
toxicity. adrenaline (epinephrine) is contraindicated
mepivacaine [NB1] shorter acting—use in dentistry may be limited
Allergic reactions may be caused by the local anaesthetic or another com -
do not use in children younger than 3 years
ponent in the solution.
mepivacaine with adrenaline intermediate acting
Methaemoglobinaemia is mainly associated with prilocaine (particularly at (epinephrine) [ NB1] do not use in children younger than 3 years
15 doses over 600 mg) and benzocaine, but is occasionally reported with lido-
0 caine, articaine and tetracaine. Slate- grey skin discolouration and cyanosis articaine with adrenaline risk of prolonged or permanent anaesthesia
Q
are the most distinct features. Methaemoglobinaemia can be life threat-
(epinephrine) [NB1] for infiltration only—do not use for regional blocks
TJ (injection close to inferior alveolar, lingual and
c ening and requires emergency referral to hospital—see p.246 for first-aid mental nerves)
TO
management in the dental practice. do not use in children younger than 4 years C
15 0
o If signs of systemic toxicity occur (or are suspected) , stop administra - continued next page
T5
.E
o tion of the local anaesthetic and provide appropriate management (see if )

Eo pp.233-59 for first-aid management of medical emergencies) . .2

0
=5 If systemic adverse effects of local anaesthetics occur, stop £/)
CD <
administration of the local anaesthetic and provide appropriate 0
.9 05
management. C
05
0
CL
15
CO
o
0 o
-0
* For further information on local anaesthetic systemic toxicities, see the Therapeutic Goods
Administration safety update (Volume 9, Number 3). 205
204

1L
 Table 19. Local anaesthetics for infiltration or regional
block in dentistry (cont.)
Local anaesthetic
Long-acting preparations
ropivacaine
bupivacaine
bupivacaine with adrenaline
(epinephrine)
NBl: Available in dental cartridges.
Doses of local anaesthetics in dentistry
Use the lowest dose of local anaesthetic necessary to prevent the patient
from experiencing dental pain.
Comments
useful for situations in which prolonged analgesia
(eg 12 to 18 hours) is required, postoperative
pain, and refractory acute dental pain
concentrations up to 0.5% can be used in children
similar indications to ropivacaine
more cardiotoxic than ropivacaine
cardiac toxicity may manifest before neurological
toxicity
do not use in children younger than 12 years
similar indications to ropivacaine
more cardiotoxic than ropivacaine
cardiac toxicity may manifest before neurological
toxicity
do not use in children younger than 12 years
The dose required for an individual patient will depend on the area to be
anaesthetised, the vascularity of the tissues, whether infiltration or regional
block is used, and the age and physical condition of the patient. Overdose
can occur relatively easily in children, particularly young children. Elderly
patients may require a lower dose because of age- related physiological
changes.
Before administering local anaesthetic, always calculate the maximum safe
single dose. Box 26 (below) shows a worked example of a dose calculation.
Multiple repeated doses within a short time period can result in accumula -
tion of local anaesthetic, and potentially lead to systemic toxicity. In case of
incomplete or failure of local anaesthetic injection, a repeat dose may be
tried, provided the total dose administered to the patient does not exceed
the maximum single dose ( see Table 20; p.208).
Box 26. A worked example of calculating the maximum
volume of a safe single dose of local anaesthetic
A 70 kg patient requires a local anaesthetic for a dental procedure. Lidocaine 2%
^
(20 m mL) with adrenaline (epinephrine) 1:80 000 (12.5 micrograms/mL) will be
used [NB1].
Calculate the maximum dose in milligrams based on the patient’s weight
maximum safe single dose of lidocaine with adrenaline is 7 mg/kg
7 mg/kg x 70 kg = 490 mg
Use the concentration of solution (mg/mL) to convert the calculated dose to
volume

Table 20 (p.208) gives the maximum safe single doses of local anaesthetics '
<D 490 mg + 20 mg mL = 24.5 mL
O
T3 available in dental cartridges. For maximum safe single doses of local Convert the calculated volume to number of 2.2 mL dental cartridges [ NB2 ]
C
anaesthetics available in other presentations, see the Analgesic topics in V
=
03 )
24.5 mL + 2.2 mL/cartridge = 11 cartridges ‘4
5 eTG complete. The dose required to prevent the patient from experiencing c
o dental pain is usually much lower than the maximum dose, provided the Therefore, the total volume administered must not exceed 24.5 mL or 11 -OCD
CO method of administration is appropriate for the indication, and the local cartridges containing 2.2 mL each. £
CD
£CD anaesthetic is injected into the correct site. The product information may NBl: To convert a percentage concentration to mg/mL, multiply by 10 (eg 2% = 20 mg/mL). </>
£
provide a guide to the usual dose. NB2: Dental cartridges are available in a variety of volumes (eg 1.7 mL, 1.8 mL, 2.2 mL).
£
"
5
=
o
J
£CO
£ Use the lowest dose necessary to prevent the patient from CD
cu
experiencing dental pain—do not exceed the maximum dose. c
CD
CL
cu
2 (Q
o
CD
C o
|

206 207
 Table 20. Maximum safe single doses of local anaesthetics
available in dental cartridges in Australia [NB1]
Local anaesthetic
preparation [ NB2 ]
lidocaine 2% (20 mg/mL)
with adrenaline (epinephrine)
1:80 000 (12.5 micrograms/mL)
mepivacaine 2% (20 mg/mL)
with adrenaline (epinephrine)
1:100 000 (10 micrograms/mL)
mepivacaine 3% (30 mg mL)
' • child 6 to 14 years—maximum 2.7 mL
'
prilocaine 3% (30 mg mL) with
felypressin 0.03 international
units/mL (0.54 micrograms/mL)
prilocaine 3% (30 mg/mL)
with adrenaline (epinephrine)
1:300 000 (3.3 micrograms/mL)
prilocaine 4% ( 40 mg/mL)
Some clinicians combine local anaesthetics to take advantage of the
properties of each drug. If combining local anaesthetics, exercise caution
because the effects and toxicities are additive, and there are few data to
Maximum Approximate maximum
support this practice. There is a lack of consensus on the optimal method
mg/kg dose of volume [NB 4]
local anaesthetic of determining the maximum doses of the individual drugs; the method
[ NB3 ] 70 kg adult 20 kg child described below provides a pragmatic way to determine the total maximum
dose. However, be mindful that the dose required may be much lower than
7 mg/kg 24.5 mL 7 mL
this calculated maximum; always use the lowest effective dose.
If combining local anaesthetics, calculate the maximum volume of each
a maximum mg/kg dose is not specified in the of the anaesthetics to be used (noting that maximum volumes are con-
centration dependent) (for a worked example, see Box 26; p.207). From
Australian product information [NB5], The Australian
product information specifies:
• child 3 to 6 years—maximum 1.8 mL these calculated maximums, identify the lowest maximum volume, and
ensure the combined volume of the anaesthetics to be used (ie the sum
• adolescent 14 to 17 years—maximum 4.4 mL of the volumes of each anaesthetic) does not exceed this. For example,
• adult—maximum 6.6 mL if combining lidocaine 2% with adrenaline (epinephrine) 1:80000 and
ropivacaine 3% for use in a 70 kg patient, calculate the maximum volume
of each drug. For this patient, the maximum volumes of safe single doses
9 mg/kg 21 mL 6 mL are 24.5 ml_ of lidocaine 2% with adrenaline (epinephrine) 1:80000 and
28 mL of ropivacaine 3%. The lowest of these two maximum volumes is
24.5 mL, so the combined volume of lidocaine and ropivacaine must not
exceed 24.5 mL.
6 mg/kg 10.5 mL 3 mL

'
articaine 4% ( 40 mg mL)
with adrenaline (epinephrine)
1:100 000 (10 micrograms/mL)
7 mg/kg 12.25 mL 3.5 mL
articaine 4% ( 40 mg/mL)
15 with adrenaline (epinephrine)
1:200 000 ( 5 micrograms/mL)
Q
o NB1: Dental cartridges are available in a variety of volumes (eg 1.7 mL, 1.8 mL, 2.2 mL).
T3 NB2: For preparations containing different concentrations of vasoconstrictor, the maximum
C
cu doses in this table may not apply — consult the product information. ts5
NB3: Maximum doses are expressed in terms of the local anaesthetic, not the vasoconstrictor.
<c
15 These doses are a guide only —the dose required for dental indications is usually much <~D
O o
lower, and varies depending on area to be anaesthetised, the vascularity of the tissues,
CO whether infiltration or regional block is used, and the age and physical condition of the £
o patient. Use the lowest dose necessary. d)
Eo NB4: The approximate maximum volumes in this table are provided to assist clinicians to
£
£ evaluate their dose calculations.
NB5: The maximum dose for mepivacaine without a vasoconstrictor is 5 to 7 mg/kg in the £</
CD >
Australian Medicines Handbook . 0
£ 0
c
0 0
C0
2 15
o
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208 209
Anxiolysis (minimal sedation)
for dental procedures
Anxiolysis refers to a range of pharmacological and nonpharmacological
methods used to alleviate fear and anxiety. This topic focuses on the phar-
macological methods used for anxiolysis (minimal sedation) in patients
undergoing dental procedures. Safe and effective use requires careful
patient assessment (see p.212), appropriate choice of drug (see p.213)
and effective management of patients (see p.215) .
Anxiolysis should only result in minimal sedation. Patients respond nor-
mally to verbal commands. Cognitive function and coordination may be
impaired, but no interventions are required to maintain a patent airway,
spontaneous ventilation or cardiovascular function. The transition from
consciousness to loss of consciousness is a continuum. There is significant
interpatient variability in the effects of drugs used for anxiolysis—loss of
consciousness can occur rapidly and unexpectedly. Therefore, practitioners
involved in the administration and monitoring of patients receiving anxi-
olysis must be prepared to manage the associated risks, including:
• oversedation or loss of consciousness
• airway obstruction or respiratory depression
• cardiovascular depression
• drug interactions, adverse reactions or anaphylaxis. a
Conscious sedation refers to a drug- induced depressed conscious state;
patients respond purposefully to verbal commands, with or without light
.2
CB
tactile stimulation. In exceptional circumstances, interventions to maintain TJ
Q)
a patent airway, spontaneous ventilation or cardiovascular function may be </>
required. The Dental Board of Australia provides a standard for the use of w
conscious sedation in dental practice.* IS
Deeper sedation (including intravenous sedation) and general anaes- I!^O
thesia are characterised by a greater depression or loss of consciousness, 2.
.2/ Q
and are restricted to appropriately trained practitioners practicing in <>
15
X C
< -O
c 0

* The Dental Board of Australia Registration Standard: Endorsement for Conscious Sedation .
2 ±±
 accredited facilities. Fatalities have occurred due to incorrectly adminis-
Box 27. Patient groups at increased risk of adverse
tered intravenous sedation in dental practice. Guidelines on intravenous
outcomes with anxiolysis (minimal sedation)
sedation are under constant review to improve its safety and those appli-
cable to dental practice were updated in 2014.* • children younger than 2 years
• elderly or frail patients
Fatalities have occurred due to incorrectly administered • patients with severely limiting heart, cerebrovascular, lung, liver or kidney
intravenous sedation in dental practice. disease
• obese patients
Conscious sedation, deeper sedation and general anaesthesia are beyond
• patients with significant obstructive sleep apnoea
the scope of this topic (for the management of procedural-related pain,
see the Analgesic topics in eTG complete ) . • patients with a known or suspected impediment to endotracheal intubation
• patients with a history of acute gastrointestinal bleeding, particularly if
associated with cardiovascular compromise or shock
Patient assessment for anxiolysis • patients with severe anaemia

(minimal sedation) in dentistry • patients at risk of aspiration ( which may necessitate endotracheal intubation)
[NB1]

Careful patient assessment is essential for the safe and effective use of • patients who have had previous adverse events due to anxiolysis, sedation,
anxiolysis (minimal sedation). The assessment determines the patient 's
analgesia or anaesthesia
suitability for anxiolysis as part of planned dental treatment. NBl: Use clinical judgment to assess the risk of aspiration for each patient.
Source: Australian and New Zealand College of Anaesthetists. Guidelines on sedation and/
To determine the suitability of anxiolysis, assess: or analgesia for diagnostic and interventional medical, dental or surgical procedures [ PS09].
Melbourne: ANZCA; 2014.
• the nature of the patient’s anxiety
• the patient’s medical, surgical, dental and medication histories,
including allergies
• the patient ’s cardiovascular, respiratory and airway status Choosing a drug for anxiolysis (minimal
15
• the patient’s exercise tolerance or functional status sedation) in dentistry
• the patient’s social circumstances, including intake of alcohol and
<D
Q
other psychoactive substances. Oral benzodiazepines (see p.216) and inhaled nitrous oxide (see p.219) .
h

-cO are the most commonly used drugs for anxiolysis (minimal sedation) in a £
CO If in doubt about the suitability of anxiolysis for a patient, seek .
general dental practice Administer a single drug. The choice between an
medical advice . oral benzodiazepine or nitrous oxide depends on patient factors (eg con- .2
i

O
- traindications, potential drug interactions, preference) , the clinical setting VQ
T3
CO Box 27 ( p.213) outlines patient groups at increased risk of adverse out- and the dentist’s expertise— see Table 21 (p.214). CD
<r>

II
0
E0 comes. If in doubt about the suitability of anxiolysis for a patient, seek Administer a single drug for anxiolysis for a dental procedure.
medical advice.
0
CD
§
s §
<jjj
/)
|.
Q

II
0
0

1«
0
JZ * Australian and New Zealand College of Anaesthetists. Guidelines on sedation and/or
analgesia for diagnostic and interventional medical, dental or surgical procedures [ PS09 J.
Melbourne: ANZCA; 2014.
212 213
 Table 21. Advantages and disadvantages of oral Management of patients having anxiolysis
benzodiazepines and inhaled nitrous oxide for
anxiolysis in dentistry (minimal sedation) in dentistry
Drug Advantages Disadvantages Advise patients of the effects of anxiolysis (minimal sedation) , including
oral well accepted by patients slow onset and long duration of possible adverse effects. The patient must consent to having anxiolysis, as
benzodiazepine easy to administer action well as the dental procedure. For further information about consent, see
cannot be titrated to rapidly the Australian Dental Association website < www.ada.org.au > .
lighten or deepen the level of
sedation Provide patients with written instructions—Box 28 ( p.216) gives example
not suitable for use in children instructions for patients having an oral benzodiazepine or inhaled nitrous
or adolescents outside the
specialist setting
oxide for anxiolysis for a dental procedure.

inhaled nitrous rapid onset and offset of action
oxide easy to administer
can be titrated to rapidly lighten
or deepen the level of sedation
suitable for use in children and
adolescents
requires training and specialised
equipment
Patients must be clinically monitored during the procedure and until fully
recovered, before being discharged with a responsible adult who will super-
vise them for 24 hours.
Patients receiving anxiolysis must be clinically monitored during
the procedure and until recovered.

Correct positioning of the patient is essential to protect their airway. The

Methoxyflurane is an analgesic used to facilitate painful surgical pro-
semireclined position is preferred because it reduces the risk of airway con-
cedures and for the emergency relief of acute pain; however, it is not
tamination with blood, saliva, filling materials or teeth, passive reflux and
recommended for use as an anxiolytic for dental procedures because of aspiration. Do not lie the patient flat or head-down. The dental chair must
inadequate evidence. The use of methoxyflurane is further limited by its
be able to be rapidly positioned horizontally to perform cardiopulmonary
short duration of action and the need for oral inhalation, which restricts
resuscitation. Use a rubber dam where possible, to protect the airway. For
access to the mouth. Repeated use can pose an occupational risk to staff,
preventive measures to minimise the risk of inhaled or swallowed objects
particularly during pregnancy.
during dental treatment, see Box 47 ( p.258).

a
0 Methoxyflurane is not recommended for anxiolysis for dental
Q
procedures.
T3
c
03
Other sedative drugs ( eg sedating antihistamines) are not recommended .2
O—
75
i
for anxiolysis for dental procedures.
cS
~o
0
</)

li
If ) Intravenous administration of sedative drugs (intravenous sedation)
0
requires specialised postgraduate training. Further, intravenous sedation

!!
0
must be administered in an accredited facility, with appropriately trained
staff present.
CD ^O

§ .2 2

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0
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0 c 0
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< T3
214 215
 Box 28. Instructions for patients having anxiolysis (minimal
sedation) for a dental procedure
Before the appointment
You can have a light meal on the day of your appointment, but do not have
anything to eat or drink within 2 hours of your appointment.
Do not drink alcohol or use illicit or recreational drugs on the day of your
appointment.
the appropriateness of benzodiazepine use, consider the patient’s previous
sedative use, medication history, alcohol intake and illicit drug use because
sedation is increased by concomitant administration of sedative drugs. Also
consider the legislation about prescribing drugs of dependence (for infor-
mation on legislation about prescriptions and prescribing, see p.9).
Do not use benzodiazepines for anxiolysis in children and
adolescents outside the specialist setting.

If you are taking other medicines, take them at the usual times unless otherwise The factors that influence the appropriateness of benzodiazepine use also
advised. influence the required dose; sedative- naive patients usually respond to a
If you are having an oral medicine for anxiolysis, it will need to be taken at the low dose and are more sensitive to the adverse effects of benzodiazepines,
dental clinic approximately 1hour before your treatment starts. whereas patients who have a tolerance to sedating drugs (eg hypnotics,
Wear loose - fitting clothes, and do not wear jewellery. Remove contact lenses. opioids, alcohol, cannabis) may require higher doses—seek expert advice.
The response to oral benzodiazepines is widely variable. Use the lowest
dose possible and do not use more than one benzodiazepine concurrently.
Let your dentist know if you are unwell on the day of your appointment, because it
may affect your treatment .
After the appointment Use the lowest dose of benzodiazepine possible and do not use
more than one benzodiazepine concurrently.
Stay at the clinic until you have recovered.
You must be escorted home by a responsible adult and supervised for 24 hours. Most benzodiazepines are considered equally effective at equivalent doses;
differences are explained by their pharmacokinetic properties (see Table 22,
Rest and do not undertake strenuous activities for the remainder of the day.
below). Benzodiazepines, particularly those with a longer duration of action
If you are hungry, you can have a light meal. Avoid hot food and drinks because ( eg diazepam) , may cause prolonged drowsiness, which can persist the day
your mouth will be numb from the local anaesthetic. after administration. Benzodiazepines with a shorter duration of action are
Do not drive or operate machinery for 24 hours after the appointment. preferred; however, midazolam and alprazolam are not recommended for
Do not drink alcohol, return to work, make important decisions or sign important
dental procedures.
TO
+• documents until the day after your appointment.
a>
q Table 22. Pharmacokinetic properties of benzodiazepines V.
-a used in dentistry £
c
cu Elimination half- life
Oral benzodiazepines for anxiolysis Drug Time to peak plasma
concentration after oral .2
<5
TO
o (minimal sedation) in dentistry administration [NB1] T3
0
< /) diazepam 30 to 90 minutes 1to 5 days [NB2 ] <J )
o
Low- dose oral benzodiazepines can be given preprocedurally to reduce TO ( j)

.12
lorazepam 120 minutes 10 to 20 hours
72 anxiety before and during dental treatment. Their advantages and disad-
C 3
=3
(3
vantages are shown in Table 21 (p.214) . Adverse effects are described on
oxazepam 120 to 180 minutes 4 to 15 hours
£ 0
p.218. temazepam 30 to 120 minutes 8 to 15 hours ^ o
4
^ NB1: Benzodiazepines are generally fully absorbed after oral administration.
.2 2
</) Q.
CD Do not use benzodiazepines for anxiolysis in children or adolescents outside
NB2: Diazepam has an elimination half-life of 1to 2 days; its active metabolite has an
is
CL
CD the specialist setting. In adults, carefully consider the appropriateness of elimination half- life of 2 to 5 days. X c
QJ
benzodiazepines for anxiolysis (minimal sedation) —see Box 27 (p.213) for c 0
jC < T3
a list of patients at increased risk of adverse outcomes. When determining
216 217
 For adults not at increased risk of adverse outcomes (see Box 27; p.213) ,
typical regimens for anxiolysis (minimal sedation) using short-acting benzo-
diazepines are:
I lorazepam 1mg orally, 1to 2 hours before the procedure,
administered at the dental practice
OR
l oxazepam 7.5 mg orally, 1to 2 hours before the procedure,
administered at the dental practice
OR
I temazepam 10 mg orally, 1hour before the procedure,
administered at the dental practice.
If a longer duration of anxiolysis is required for adults not at increased risk
of adverse outcomes ( see Box 27; p.213), use:
diazepam 5 mg orally, 1hour before the procedure, administered
at the dental practice.
For adults at increased risk of adverse outcomes (see Box 27; p.213),
consider using a lower dose or reconsider the appropriateness of adminis-
tering benzodiazepines for anxiolysis.
Adverse effects of benzodiazepines include impaired psychomotor perfor-
mance, impaired memory function, delirium, dry mouth and blurred vision.
15 Elderly or frail patients are particularly susceptible to ataxia ( with conse-
quent falls and injury), confusion, memory dysfunction ( both retrograde
0
Q
"O
and anterograde amnesia ) and cognitive impairment.
C
(0 Warn patients that the adverse effects of benzodiazepines can affect their
15 behaviour, coordination and ability to drive or operate machinery safely.
o-
i
All benzodiazepines can produce discontinuation symptoms; these can be
to
physiological or psychological, and are related to the dose and duration of
0
Nitrous oxide for anxiolysis (minimal
sedation) in dentistry
Nitrous oxide (combined with oxygen and administered via a nasal mask)
is an established, safe and effective technique for anxiolysis (minimal
sedation) in dentistry. The use of nitrous oxide for anxiolysis was previously
known as relative analgesia. Nitrous oxide can be used for apprehensive
patients, and to facilitate treatment in patients who could not otherwise be
managed in a general dental practice. Nitrous oxide is the preferred agent
to facilitate dental treatment in anxious or uncooperative children. Nitrous
oxide also reduces the gag reflex. Table 21 (p.214) lists the advantages and
disadvantages of nitrous oxide. Adverse effects are described on p.220.
Nitrous oxide is the preferred agent to facilitate dental treatment
in anxious or uncooperative children.
Carefully consider the appropriateness of nitrous oxide for anxiolysis—see
Box 27 (p.213) for a list of patients at increased risk of adverse outcomes.
Nitrous oxide is contraindicated in patients with a condition where air is
trapped within a body cavity (eg pneumothorax, bowel obstruction, recent
middle ear surgery) because nitrous oxide may increase the pressure or
volume within such spaces.
Effective delivery of nitrous oxide depends on good flow through the nasal
passages, so confirm there is no nasal congestion or obstruction before
administration.
Nitrous oxide is administered starting at a low concentration, and then
titrated to clinical effect. It is commonly administered at a concentration of
50% for anxiolysis for dental procedures. In most purpose-built equipment,
a
there is an inbuilt safety feature that does not allow more than 70% nitrous .2
oxide to be delivered to the patient. 15
~o
Nitrous oxide has a rapid onset of action. Response varies between o
<0
individuals; at a concentration of 50% nitrous oxide, peak effect would
is

1 use. Rebound anxiety can occur after a single dose of a short-acting ben- be expected in a 70 kg adult within 3 to 5 minutes. Monitor the patient
zodiazepine, particularly alprazolam or midazolam. Because of the potential clinically at all times, preferably with pulse oximetry. Resuscitation equip-
=3
CD for tolerance and dependence with continued use, only a single dose of ment must be available. Use nitrous oxide in a well-ventilated area with Eo
^ o
.9 benzodiazepine should be prescribed. an appropriate scavenging device to minimise room air contamination and 2.
is
CO Q
0 staff exposure. Repeated nitrous oxide exposure may be associated with
o
spontaneous first-term miscarriage in staff; inform staff of this risk.
.

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X c
0
J0 5 0
< T3
Resuscitation equipment must be available.

218 219
 When nitrous oxide administration is stopped, recovery is rapid because
the drug is rapidly removed from the body. If nitrous oxide has been
administered for 10 minutes or longer, it is common practice to administer

Complications after
supplemental oxygen for 3 to 5 minutes after nitrous oxide is stopped , to
prevent an abrupt decrease in oxygen saturation of arterial blood. Monitor
the patient’s clinical response and recovery.
The main adverse effects of nitrous oxide relate to the development of
oral surgery
hypoxia. Even with the commonly used concentration of 50%, nitrous oxide
is capable of occasionally producing loss of consciousness, and impaired
cough and gag reflexes. Some children have a paradoxical reaction to
nitrous oxide. Other adverse effects are rare and include nausea, vomiting,
hypotension and respiratory effects.
Pain and swelling after oral surgery
Pain and swelling follow most oral surgical procedures, usually due to
inflammation from trauma, rather than infection. Even after difficult third
molar (wisdom teeth) extractions, the incidence of infection is low ( 2 to
5%) . Swelling normally increases in the first 48 hours after oral surgery and
may take up to 3 days to reach its maximum.

Swelling normally increases in the first 48 hours after oral surgery

and may take up to 3 days to reach its maximum.

Management of pain and swelling includes:

• reassurance
• local measures (eg external application of a cold compress
intermittently for up to 20 minutes at a time during the first 24 hours,
75 followed by mouth rinsing with warm saline)
0 • nonopioid analgesics (to select an appropriate analgesic regimen for
Q acute dental pain, see p.137)
•0 0
c • communication with the practitioner who performed the oral surgery jo
03 3
75 • monitoring the patient’s condition. (/)

o- 75
J

Pain increasing in severity 1 to 4 days after a tooth extraction may be o

alveolar osteitis ( dry socket; see p.222) .
0
0 0
cns
0 Medical practitioners should refer patients with suspected infection to the
2 </)
0 practitioner who performed the oral surgery. Most infections following oral c
CD 2
surgery can be managed with dental treatment; however, antibiotic therapy
.9
may be necessary in cases of spreading infection (for the management of <5
2
infection following dentoalveolar surgery, see p.87). o.
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220 221

Alveolar osteitis (dry socket)
Alveolar osteitis ( dry socket) is a localised painful osteitis of an extraction
socket following premature lysis of the blood clot. It complicates approxi-
mately 5% of tooth extractions. The condition presents as postoperative
pain in and around an extraction socket that increases in severity between
1 and 4 days after the extraction. A disintegrated blood clot within the
socket, with or without halitosis, is diagnostic. Although alveolar osteitis
is caused by a failure of healing, it is commonly misdiagnosed as an
infection. Antibiotic therapy has no place in the management of alveolar
osteitis.
Although alveolar osteitis usually resolves spontaneously over 2 to
3 weeks, initiate interventions to reduce pain early because symptoms are
severe. Initial management strategies include:
• socket irrigation with warm sterile saline until there is no more debris
present
• nonopioid analgesics (to select an appropriate analgesic regimen for
acute dental pain, see p.137)
• an obtundent dressing.
For patients who have had multiple tooth extractions, if the bleeding occurs
from one extraction site, it is likely to be a local cause. Conversely, if the
bleeding occurs from multiple extraction sites, consider systemic causes.
If bleeding occurs after oral surgery, apply firm pressure at the surgical
wound and consider using an absorbable haemostatic pack. This is
sufficient to stop the bleeding in most instances, even in patients taking
antiplatelet or anticoagulant therapy. Table 23 (p.224) gives a suggested
management protocol.
If bleeding persists despite initial management, assess the area to deter-
mine the site of the bleed ( see Figure 7, below) and perform the local
haemostatic procedure ( see Table 23; p.224) . Common sites of persistent
bleeding after tooth extraction include the mucosa ( near the floor of the
mouth or the tongue) or the gingiva at the alveolar crest. Uncommon sites
of persistent bleeding after tooth extraction include the side or base of the
tooth socket.
Figure 7. Possible sites of persistent bleeding after tooth
extraction

Use of antibiotics for alveolar osteitis (dry socket) is of no benefit.

tongue nucosa
If pain persists for more than 3 weeks or if there are signs outside the tooth
socket, review the diagnosis. Differential diagnoses include osteomyelitis,
medication-related osteonecrosis of the jaws ( see p.164) , alveolar squa-
TO
mous cell carcinoma, and localised odontogenic infection with retained
a> tooth fragments ( see p.81).
Q
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Bleeding after oral surgery

TO
3
.
TO </)
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TO
A postoperative bleeding complication requires prompt assessment floor of mouth
0 O
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1. mucosa near the floor of the mouth—very common bleeding site
Consider the patient’s use of drugs that can affect haemostasis (eg antico- £
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agulants, antiplatelet drugs, complementary medicines) —for management —
2. subgingival region common bleeding site TO
0 3. socket wall—uncommon bleeding site C/)
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oral or dental procedure, see pp.153-63. Bleeding can occur when vaso-
constriction induced by a local anaesthetic preparation subsides. Consider
TO
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stasis (eg von Willebrand disease) . o
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222 223
 Table 23. Management of bleeding after oral surgery
Initial screen and management (can be conducted by phone)

Dental and maxillofacial

Check the patient’s medical and medication history.
Reassure the patient—in most cases, the following approach stops the bleeding.
Advise the patient to:
• sit upright
• place a small gauze square or small clean cloth directly and firmly over the surgical
trauma
wound
• apply pressure—bite hard or press a finger firmly over the wound for 15 minutes, then
check if the bleeding has stopped.
Common mistakes that result in inadequate pressure at the site of bleeding include:
• placing gauze over the adjacent teeth, rather than at the site of bleeding A broken tooth or filling, or a lost filling
• using excessive amounts of gauze.
Advise the patient not to: Teeth, fillings and other forms of restoration (eg crowns, veneers)
• keep rinsing or spitting may break for various reasons. Damage to the tooth or restoration can
• use paper tissues or cotton wool occur during normal functioning (eg while eating) or following trauma.
• remove the gauze or cloth too soon to look at the bleeding site. Restorations can also be lost due to further decay in the tooth that under-
Contact the practitioner who performed the oral surgery. mines the restoration, leaving it unsupported.
Pain associated with tooth damage indicates that the dentine or pulp has
If bleeding does not resolve with initial management
been exposed.
Use suction and a good light to examine the patient’s mouth to identify the bleeding site
(see Figure 7; p.223). Exposure of the dentine causes an intermittent pain (reversible pulpitis)
Check for active bleeding. Brisk bleeding is usually from torn soft tissues rather than the that occurs only when the tooth is exposed to a stimulus (eg hot, cold
socket. or sweet food or drinks) . If the patient presents to a medical practitioner,
Ensure adequate pressure is applied to the site of bleeding. advise the patient to see a dentist as soon as possible—analgesics and
antibiotics are not indicated in the interim.
15 Local haemostatic procedure after applying appropriate pressure at the
surgical wound Antibiotic therapy is not required for reversible or irreversible
Q
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pulpitis associated with a broken tooth . 05
Infiltrate the bleeding site with a local anaesthetic containing a vasoconstrictor.
o E
c Use an absorbable haemostatic agent to pack the surgical wound. Ribbon gauze is an 3
Exposure of the pulp causes more severe pain that persists as a dull
alternative if a haemostatic agent is not available.
-5
03
15 throbbing ache even after removal of the stimulus ( irreversible pulpitis).
M
Tranexamic acid applied as a topical solution can be considered as an additional 15
o haemostatic method if pressure is insufficient to stop the bleeding. Tranexamic acid Red soft tissue seen in the area of fracture or within a cavity indicates o
</ j
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stabilises an existing blood clot. Either rinse the bleeding site with tranexamic acid that the pulp has been exposed. Typically, this tissue is very sensitive to a£
—
solution or use a gauze pad soaked in tranexamic acid solution to dress the bleeding site.
touch and the patient may be avoiding any contact of this tooth with the
1 tongue, food, drink or cold air. The exposed pulp may bleed or have a blood X
03
3 Emergency department transfer
clot over it. Tooth damage with pulp exposure requires urgent dental treat- E
CD
If the local haemostatic procedure cannot be performed or is unsuccessful in controlling ment (preferably within 24 hours) to prevent further damage or infection o
§ the bleeding, arrange urgent transfer to an emergency department.
of the tooth. If a delay in dental treatment is expected, pain relief with
C
03
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oral analgesics (to select an appropriate analgesic regimen for acute dental 15
pain, see p.137) or local anaesthetics (for advice on the use of local
03
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anaesthetics for dental indications, see p.201) is indicated in the interim. O

224 225
 Placement of a covering material (eg calcium - based dental cements, tem- Assessment of tooth avulsion
porary filling materials) over the tooth fracture or exposed pulp requires
dental expertise and should not be attempted by medical practitioners. Avulsion of a tooth is the complete disarticulation of the tooth from its
bone socket. In most cases, the tooth is knocked out of the mouth com-
Tooth damage with pulp exposure requires urgent dental treatment pletely, but occasionally it may remain in the mouth.
to prevent further damage or infection of the tooth. Prognosis is Assess all patients with trauma to their teeth for other injuries, especially
worse the longer the delay in treatment.
head and neck injuries.
Antibiotic therapy is only indicated for a broken tooth if there is an associ- Assess if the tooth has been avulsed—it may have been intruded (pushed
ated spreading infection (for management of odontogenic infections, see into the alveolar bone) or the tooth root may have fractured so that only
pp.79-87). the crown has been lost. Refer the patient urgently to a dentist for X- ray,
assessment and management of an intruded or fractured tooth.
If a tooth appears to be missing and is not found at the site of the acci-
Tooth avulsion (knocked-out tooth) dent, consider if the patient has inhaled or swallowed the tooth.
Box 29 ( below) summarises the initial assessment and management of an If the avulsed tooth has been retrieved, determine if it is a primary ( baby)
avulsed tooth. or secondary (adult) tooth. Children older than 5 years may have a mix-
ture of primary and secondary teeth, and it may be difficult to distinguish
Box 29. Initial assessment and management of an avulsed between avulsed teeth. In general, primary teeth are much smaller in
tooth all dimensions and lighter in colour than secondary teeth; however, sec -
• Check for other injuries, especially head and neck injuries. ondary teeth in 5- to 8-year- old children have short roots with large crowns
because the roots have not yet fully developed. Additionally, the roots of a
• Do not replant primary (baby) teeth.
primary tooth resorb when they are nearing the time they would naturally
• Do not scrape or handle the root of the tooth. fall out, so appear blunted or shorter. See Photo 17 (below) for images of
• Rinse the tooth with dairy milk or saline if it is dirty—do not use water. avulsed primary and secondary teeth. Figure 9 and Figure 10 (pp.268-9)
• Replant secondary (adult) teeth as soon as possible. give an indication of the average ages at which primary tooth exfoliation
• Use a temporary splint to hold the replanted tooth in place until the patient can and secondary tooth eruption occurs.
15
see a dentist.
a> Check the patient’s tetanus immunisation status.
Q • Ensure that tetanus immunisation is up -to- date. CS
"O
c • Prescribe antibiotic therapy. Photo 17. Avulsed primary and secondary teeth E
3
cu Refer to a dentist urgently.
• 5
15
o- 15
i
If the tooth cannot be replanted immediately:
• Do not let the tooth dry out. =O o
< /5
0 = CO £
E0 • Store the tooth in dairy milk; if milk is not available, store the tooth in saline, £
—x
£
saliva or plastic wrap—do not use water. =O
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primary tooth on the right and the primary tooth on the right O

226 227
 Replanting and splinting an avulsed tooth be appropriate to bond the replanted tooth to the adjacent teeth. The tem-
porary splint needs to be easily removed by the dentist without damaging
Do not replant or reposition a primary tooth because this will damage the
the adjacent teeth.
secondary tooth that is developing in the bone.

Primary ( baby) teeth should not be replanted or repositioned. Management of an avulsed tooth after
replanting and splinting
Hold an avulsed secondary tooth carefully by the crown so the root is not
For all patients with tooth avulsion, ensure that tetanus immunisation is
damaged—do not hold the root. Survival of the cells of the periodontal
up- to - date.
ligament, which is attached to the root, is essential for healing of the liga -
ment following replantation. If the ligament heals, the tooth has a reduced Antibiotic therapy is indicated after replanting the tooth; however, there is
risk of replacement root resorption and can remain in the mouth for many limited evidence that it reduces healing complications (eg inflammatory
years. root resorption, which is associated with the presence of bacteria in the
root canal system). Doxycycline is preferred because of widespread clinical
If the tooth is dirty, rinse it briefly with milk or saline—do not scrub or rub
experience with its use in this setting, and there is some evidence that it
the tooth. Replant an avulsed secondary tooth into its socket as soon as
has direct antiresorptive activity; use:
possible. Teeth replanted within 15 minutes are more likely to heal without
complications. doxycycline orally, once daily for 7 days
adult: 100 mg
If the tooth cannot be replanted immediately, arrange urgent
transfer to a dentist or emergency department. Prognosis is worse child 8 years or older and less than 26 kg: 50 mg
the longer the delay in treatment child 8 years or older and 26 to 35 kg: 75 mg
child 8 years or older and more than 35 kg: 100 mg
If the tooth cannot be replanted immediately, arrange urgent transfer to
a dentist or emergency department. Submerge the tooth in cool or room If doxycycline is contraindicated (eg children younger than 8 years) ; use:
temperature dairy milk until it can be replanted. The cells of the periodontal
ligament can survive in milk for up to 6 hours. All first- aid kits, especially amoxicillin 500 mg (child: 15 mg/kg up to 500 mg) orally, 8- hourly
those for sporting clubs and schools, should stock a small container of for 7 days.
75
long-life milk.
<D Recommend the use of chlorhexidine mouthwash after replantation while
o If milk is not available, saliva, saline or plastic wrap can be used, but the
cs
-o the tooth is splinted; use: E
C periodontal ligament cells will survive for up to 1hour at most under these 3
03
conditions. If plastic wrap is used, ask the patient to spit some saliva into 2
75 I chlorhexidine 0.2% mouthwash 10 mL rinsed in the mouth for -
+*

o- the plastic before wrapping the tooth. Avoid using water for cleaning or 1minute, 8- to 12 - hourly* 75
i

storing an avulsed tooth because the osmotic effect of water causes cell o
(/ >
death in the periodontal ligament. OR 4E
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£0 I chlorhexidine 0.12% mouthwash 15 mL rinsed in the mouth for
—X
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3 Do not use water to rinse or store the avulsed tooth. 1minute, 8- to 12-hourly.* E
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After replanting the tooth, place a temporary splint to hold the tooth in c
03
position. Use a small piece of aluminium foil or malleable material (eg Blu
0
CL 75
0 Tack), then ask the patient to bite down to hold it in position. Refer the
0 patient to a dentist urgently for further treatment and splinting. If a delay in Q
0

dental treatment is expected, skin glue or another adhesive material may * When used for more than a few days, chlorhexidine may cause a superficial discolouration
of the teeth and fillings (see p.59 for more information).
228 229
 Antibiotic prophylaxis is not required for closed or open facial fractures
Maxillofacial trauma that do not require surgical management. Facial fractures requiring sur-
gical management may require surgical antibiotic prophylaxis, given within
Arrange urgent transfer to an emergency department for a patient with any
120 minutes of the procedure (see ‘Surgical prophylaxis for oral maxillo-
of the following:
facial surgery’ in eTG complete ) ; antibiotic prophylaxis between injury and
• loss of consciousness
the perioperative period is usually not necessary. For management of open
• airway compromise facial fractures, see ‘Open fractures’ in eTG complete.
• uncontrolled bleeding
Refer all patients with significant maxillofacial trauma to a specialist as
• significant eye injury (eg orbital swelling, proptosis, vision loss).
soon as possible for further review and management.
See Figure 8 ( p.235) for the basic life support flowchart.
Although some patients with minor injuries to the mandible ( lower jaw),
zygomatic complex (cheekbone) and nose may look reasonably well at
presentation, all patients require thorough assessment. Patients presenting
with significant maxillofacial trauma should undergo a formal primary and
secondary trauma survey in hospital.
For all patients with maxillofacial trauma, ensure that tetanus immunisa -
tion is up-to- date.
Account for all dental fragments, dentures or other restorations.
Debride any soft tissue injuries. Soft tissue injuries that require operative
care by an appropriate specialist include:
• significant lacerations of the gums
• significant lacerations of the lip or vermillion border
• degloving injuries (where the bone has been exposed) .
75 To ensure there are no dental fragments or foreign bodies in the soft tis-
0 sues, imaging may be considered. Plain X- rays of the facial skeleton (eg
Q
orthopantomogram, postero-anterior skull or occipito-mental views) are co
T3 E
C usually sufficient for the assessment of uncomplicated trauma (eg iso- 3
CO
lated mandibular fractures) . Computed tomography (CT) is required for 2
+»
co
o- significant injuries (eg multiple facial injuries, middle third facial injuries, 75
i

associated head injury). o

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0 45
£o Presumptive antibiotic therapy may be required for wounds at high risk of
infection or significantly contaminated wounds (see ‘Acute wound infec-
—
£
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Antibiotic prophylaxis is not required for closed or open facial co
fractures that do not require surgical management.
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230 231
Medical emergencies
in dental practice
The Therapeutic Guidelines series (see < www.tg.org.au > ) and the
Australian Resuscitation Council guidelines (see < www.resus.org.au > )
form the basis of the information in this topic.
Potential medical emergencies range from transient problems that resolve
spontaneously (eg syncope) , to serious emergencies that require transfer
of the patient to hospital (eg severe asthma attack), to life-threatening
emergencies that require on- site resuscitation (eg cardiac arrest).
Medications have the potential to cause adverse effects, some of which
are life threatening (eg anaphylaxis) .
Medical emergencies in dental practice can be minimised by careful
assessment of the patient; this includes obtaining a detailed medical and
medication history. When emergencies occur, prompt diagnosis and man-
agement improve outcomes.

Dentists and staff have a professional obligation to maintain competency

in emergency management and basic life support. If dental assistants have
not been through a formal training program, they should have, at least, a
basic - level first-aid certificate.
Dentists must ensure that their practice:
15
• has an established medical emergency plan, which considers the M

usual emergency services response time 0

~o
• prominently displays the emergency phone number (000) £
• prominently displays the nearest medical facility phone number. <J )
.o2
The level of staff training and the emergency drugs and equipment required c
0
by the dental practice are determined by the patient population, the prac - OJD
tice type and the emergency services response time. 0
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0
15 8
.o2 .o2
The longer the time before assistance can reasonably be expected
to arrive, the greater the need for staff training and equipment.
0 TO
2 a.

233
 Drugs and equipment for medical Basic life support flow chart
emergencies Use the basic life support flow chart (Figure 8, below) to assess and
respond to a medical emergency.
Drugs and equipment that may be used for the management of medical
emergencies occurring in a dental practice include:
Figure 8. Basic life support flow chart
• an easily transportable source of oxygen—the simplest and safest way
of administering oxygen to a patient who is breathing is via a mask
( supplemented with oxygen at 6 to 8 IVminute) or nasal prongs (with Basic Life Support
oxygen at 2 IVminute) . For a patient who is not breathing, use a bag-
valve mask or start mouth-to- mask resuscitation
• disposable plastic airways to secure the oral airway, and facilitate Dangers?
mouth- to-mouth resuscitation or ventilation with oxygen
• adrenaline (epinephrine) for the management of anaphylaxis,
in sufficient quantity to give 2 doses. Adrenaline (epinephrine) is Responsive?
available in preloaded autoinjectors and ampoules. A preloaded
autoinjector is preferred, since an ampoule requires dose calculation
and has to be drawn up into a syringe
• pulse oximeter for measuring arterial oxygen saturation
Send for help
• glucose for the management of hypoglycaemia, as either a readily
available glucose-containing food (eg fruit juice, honey) or pure
glucose (eg glucose gel or tablets) Open Airway
• glyceryl trinitrate spray for the management of angina or an acute
coronary syndrome. Glyceryl trinitrate spray has a longer shelf life than
tablets Normal Breathing?
75 • short-acting bronchodilator inhaler (eg salbutamol) and spacer for
Start CPR
the management of an acute asthma attack
0
Q • aspirin for the management of a suspected acute myocardial 30 compressions : 2 breaths
~o
infarction 75
c
03
• blood pressure monitor for the assessment of patients with 0
a Attach Defibrillator ( AED)
T3

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i cardiovascular symptoms and collapsed patients
as soon as available, follow prompts
.£
• blood glucose monitor for the assessment of patients with diabetes cr
.2o
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In
0 • automated external defibrillator for the management of cardiac
CD arrest. Continue CPR until responsiveness or C
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5 normal breathing return Qfi
3 Regularly check drugs and equipment, and replace expired or damaged 0
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75 .8
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2 0 jo
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31
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<resus org.au/guidelines/flowcharts-3/>

234 235
 Allergies
Allergies can occur to drugs, food, insect bites, or environmental sub-
stances (eg pollen) . Patients may have multiple allergies or have an allergic
response to something they have been previously exposed to without inci-
dent. After exposure to an allergen, the onset of an allergic reaction can be
immediate or delayed.
Always check for a history of allergy before starting dental treatment.
Instruct a patient with a known anaphylactic allergy to bring their adrena-
line (epinephrine) autoinjector when attending for dental treatment.
Although they occur rarely, the most common allergies encountered
in dental practice are to antimicrobials (also see Antimicrobial hyper-
sensitivity’ on pp.25-37) , local anaesthetics and latex. Document any
suspected allergic reaction and consider referring the patient for confirma-
tion of the allergy.
Common contact allergies in dental practice
Allergy to rubber gloves or a rubber dam commonly presents as a delayed
hypersensitivity contact dermatitis beginning hours to days after exposure.
This is usually associated with allergy to rubber components other than the
latex protein (eg accelerants and vulcanising chemicals used in the manu-
facturing process) . However, if contact dermatitis occurs in areas exposed
to rubber materials following dental treatment, consider the possibility of
latex allergy.
15
Allergy to latex is rare and usually presents as a localised contact urticaria
<D
O or dermatitis starting minutes to hours after exposure. For management
u
•
c
of urticaria, see Box 30 (p.238) . Occasionally allergy to latex can cause
03 anaphylaxis (for management, see Box 31; p.239) . If a patient, dentist
15 or staff member reports immediate hypersensitivity to latex, refer them for
o- medical assessment. In patients with a confirmed latex allergy, perform
V
Urticaria and angioedema
Urticaria is characterised by transient erythematous lesions that vary in
size; they are often filled with fluid. Urticarial lesions persist for a few min-
utes to 24 hours and tend to be itchy.
Acute angioedema ( oedema of the subcutaneous tissue) can coexist with
urticaria, as single or multiple lesions. Angioedema can be painful or cause
a burning sensation, but the lesions are usually not itchy. They can occur
anywhere on the body, but often affect the face, periorbital region, lips,
tongue, glottis, dorsa of feet and hands, and genitals. Angioedema usually
resolves over several hours to days.
Acute urticaria or angioedema may be associated with anaphylaxis.
If laryngeal swelling occurs, or there are other signs of anaphylaxis
(bronchospasm, upper airway obstruction and hypotension), treat as ana-
phylaxis— see Box 31 (p.239) .
Consider drug causation, particularly in cases of acute reactions. However,
delayed drug- associated reactions can occur after more than one dose of a
drug—onset may be days after starting the drug. Urticaria may not immedi-
ately resolve when the drug is stopped.
Occasionally, urticaria can be caused by contact with a substance (con-
tact urticaria ). Advise the patient to avoid contact with the cause (eg latex
rubber gloves) in the future .
For management of patients with urticaria and angioedema, see Box 30
(p.238) .
15
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o
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dental treatment in a latex-free environment.
£o Allergy to acrylates usually presents as contact dermatitis. Acrylates
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13
and methacrylates (eg methyl methacrylate, 2- hydroxyethylmethacrylate)
CD are plastic materials that are widely used in dentistry (eg dental bonding 0)
E
-
.491 agents, materials in dentures). Acrylate contact allergy is more common
in people who are frequently exposed, such as dental personnel, and may
o
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o B
is .2
Q.
2 occur despite the use of protective gloves. O
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CD 0) 5
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For the management of contact dermatitis, refer patients to a medical 2 .
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practitioner.
236 237
 Box 30. Management of urticaria and angioedema Box 31. Management of anaphylaxis [NB1]
For mild urticaria or angioedema: If anaphylaxis occurs:
• Stop dental treatment . • Stop dental treatment.
• Remove or stop administration of the allergen. • Remove or stop administration of the allergen.
• Recommend an oral antihistamine. • Lie the patient flat.
For extensive urticaria or angioedema, or swelling involving eyelids, lips or • Give an intramuscular injection of adrenaline (epinephrine):
tongue:
l adrenaline (epinephrine) intramuscularly, via preloaded autoinjector, into
• Stop dental treatment. the anterolateral thigh [NB2]
• Remove or stop administration of the allergen. adult or child more than 20 kg: 300 micrograms
• Refer for urgent medical attention; systemic corticosteroids may be indicated. child 10 to 20 kg: 150 micrograms
For urticaria or angioedema with associated hypotension and evidence of OR
anaphylaxis: 2 adrenaline (epinephrine) (adult and child) 10 micrograms/kg up to
• Stop dental treatment. 500 micrograms (0.5 mL of 1:1000 solution) intramuscularly, into the
• Remove or stop administration of the allergen. anterolateral thigh .
• Call 000. • Call 000—the patient must be taken to an emergency department.
• Give intramuscular injection of adrenaline (epinephrine) (see Box 31; p.239). • Start supplemental oxygen and airway support if needed.
• Be prepared to start CPR (for ‘Basic life support flow chart ’, see Figure 8;
p.235).
Anaphylaxis
• Repeat adrenaline (epinephrine) every 5 minutes until the patient responds, or
Anaphylaxis is a severe, immediate-type, generalised hypersensitivity reac - assistance arrives.
tion affecting multiple organ systems—it has a rapid onset and can be
Follow up:
fatal. Anaphylaxis is characterised at its most severe by bronchospasm,
• Update records with details about the suspected allergen and the patient’s
upper airway obstruction and hypotension. Severe gastrointestinal symp-
response.
75 toms may also occur.
• Request a copy of the medical report of the allergic reaction.
0 Anaphylaxis can occur within minutes of parenteral or mucosal exposure to CPR = cardiopulmonary resuscitation
-uc
O
a drug, and approximately 30 minutes to hours after drug ingestion. NB1: A widely available and more detailed wall chart on the recognition and initial emergency 75
management of anaphylactic reactions is available from Australian Prescriber.
cc Instruct patients with a history of anaphylaxis to bring their adrenaline (epi - NB2: Preloaded autoinjectors contain 300 micrograms in 0.3 mL (for use in an adult or child 0
75 nephrine) autoinjector when attending for dental treatment. more than 20 kg) and 150 micrograms in 0.3 mL ( for use in a child 10 to 20 kg).
TJ
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Box 31 (p.239) outlines the management of patients with anaphylaxis. c/)
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238 239
 Cardiovascular emergencies Box 32. Management of syncope
If the patient feels faint:
Syncope • Stop dental treatment .
Syncope is an acute hypotensive episode, resulting in transient global cer- • If the patient is in the dental chair, tilt the chair back to a horizontal position.
ebral hypoperfusion and loss of consciousness, which usually leads to loss If the patient is not in the dental chair, ask the patient to lie down. The seated
of postural tone and falling. Brief periods of twitching or convulsive move- position is not adequate for patients with syncope.
ments can sometimes accompany syncope but should not be confused • Raise the patient’s legs.
with epilepsy. Secondary injury (following a fall) can result in significant • Measure the patient’s heart rate.
harm. The onset is almost always rapid; recovery is usually rapid, sponta- • Assess consciousness by talking to the patient.
neous and complete.
If the patient loses consciousness:
Presyncope is a condition in which the patient feels as though syncope is • Stop dental treatment.
imminent; signs and symptoms include light-headedness, nausea, anxiety,
• Raise the patient’s legs and try to achieve a position where the head is lower
pallor, sweating and tinnitus. than the heart. If the patient is in the dental chair, tilt the chair back to a
Syncopal episodes are common at all ages. Important causes of syncope horizontal position.
include neurally mediated syndromes (vasovagal syncope), volume deple- • Measure the patient’s blood pressure and heart rate.
tion and heart arrhythmias. Common causes of syncope in dental practice Consciousness usually returns rapidly. Allow patients to recover slowly under
are: supervision; do not discharge them prematurely from care, particularly if they
• vasovagal syncope—can occur either as a reaction to pain, or to will be driving. If possible, check standing blood pressure. Check the patient can
anxiety and fear before, during or after a dental procedure stand unassisted without recurrence of symptoms. Consider referring for medical
• orthostatic hypotension—can occur when standing up after sitting or evaluation if the patient is elderly, recovers slowly or has repeated episodes of
syncope without obvious triggers.
lying down for an extended period of time in the dental chair.
If the patient does not regain consciousness, consider other causes of
For management of patients with syncope, see Box 32 ( p.241). syncope or collapse and:
• Call 000.
75
• Start basic life support (for ‘Basic life support flow chart’, see Figure 8; p.235) .
0
O • Place the patient on their side.
o • Maintain treatment until the patient regains consciousness or assistance 75
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240 241
 Coronary ischaemic syndromes Box 33. Management of angina or an acute coronary
Coronary ischaemic syndromes include stable angina and acute coronary syndrome (cont.)
syndromes (eg ST elevation myocardial infarction, non-ST elevation acute
If chest pain is severe or new:
coronary syndrome) .
• Call 000.
Typical symptoms of an acute coronary syndrome include crushing or heavy • For patients with a history of angina, give glyceryl trinitrate as above.
central chest pain that may radiate to the arms, neck, back and jaw, short-
• For all patients, give:
ness of breath, nausea and sweating. However, atypical presentations are
aspirin 300 mg orally, chewed or dissolved before swallowing.
also common. Some patients, particularly elderly patients or patients with
diabetes, have no pain. • Measure blood pressure, heart rate and pulse oximetry.
Patients with stable angina experience episodic retrosternal chest discom- • Start supplemental oxygen if Sa02 is less than 90%, and titrate to Sa02
fort (pain or tightness) that lasts 10 minutes or less and subsides promptly 90 to 96% if possible .
with rest. It is commonly triggered by physical activity or emotional stress. • Provide reassurance until assistance arrives.
However, new or increasing symptoms indicate an acute coronary syn- • If the patient loses consciousness, start basic life support (for ‘Basic life support
drome, which is a medical emergency. flow chart’, see Figure 8; p.235. Use an automated external defibrillator if
For management of patients with angina or an acute coronary syndrome,
available .
see Box 33 (below) . Sa02 = oxygen saturation

Box 33. Management of angina or an acute coronary

syndrome
Cardiac arrest
In cardiac arrest, the patient suddenly loses consciousness, has no pulse
Ensure that patients with a history of angina bring their medication (eg glyceryl
and is not breathing.
trinitrate spray or tablets) when presenting for dental treatment, and have it in a
readily accessible place. For management of patients with cardiac arrest, see Box 34 (below) .
If chest pain occurs in a patient with a history of angina:
• Stop dental treatment . Box 34. Management of cardiac arrest
75
• Measure blood pressure, heart rate and pulse oximetry. If cardiac arrest occurs:
0
a • Assess consciousness by talking to the patient. • Stop dental treatment.
~a 75
c • To relieve symptoms, use glyceryl trinitrate. Ask the patient to sit down (because • Call 000. M
cu
of the possibility of hypotension) , then give: 0
75 • Start basic life support, including CPR (for ‘Basic life support flow chart’, see o
o- Figure 8; p.235). Use an automated external defibrillator if available. .£
i
1 glyceryl trinitrate spray 400 micrograms sublingually, repeat every
5 minutes if pain persists, up to a total of 3 doses if tolerated • Maintain treatment until the patient regains consciousness or assistance </>
< /> £o
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ECD OR c
CPR = cardiopulmonary resuscitation 0
3
1 glyceryl trinitrate tablet 300 to 600 micrograms sublingually, repeat every tip
o 5 minutes if pain persists, up to a total of 3 doses if tolerated. 0
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^ If pain persists for more than 10 minutes despite taking 2 doses of glyceryl
8
4

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below).
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242 continued next page 243
 Symptoms of hypoglycaemia can be classified as:
Endocrine emergencies • adrenergic (autonomic) —eg pale skin, sweating, shaking, palpitations,
feeling anxious
Hypoglycaemia • neuroglycopenic (due to altered brain function) —eg hunger, difficulty
Hypoglycaemia is defined as a blood glucose concentration below concentrating, confusion and inappropriate behaviour, loss of
4 mmol/L; however, symptoms of hypoglycaemia may occur at a higher consciousness, seizures.
blood glucose concentration. Hypoglycaemia can also occur without symp-
Factors that increase the risk of hypoglycaemia in diabetic patients include:
toms and signs, particularly in patients who have had diabetes for more
than 10 years. • inappropriately high doses of insulin or sulfonylureas
• forgotten or delayed meals
Box 35. Management of hypoglycaemia • insufficient carbohydrate intake (especially if the patient is taking
rapid- acting insulins or sulfonylureas)
• rigorous or prolonged exercise (which can have a delayed effect) .
If the patient is conscious and cooperative:
• Stop dental treatment.
• Give glucose if available: If hypoglycaemia occurs or is suspected, see Box 35 (p.244) for manage-
ment. Obtain a blood glucose measurement to confirm hypoglycaemia if
- adult: 15 g
possible. If a blood glucose monitor is not available, start management of
- child 5 years or younger, or up to 25 kg: 5 g hypoglycaemia based on clinical signs or symptoms.
- child 6 years or older, or more than 25 kg: 10 g
• If glucose is not available, give a fast- acting glucose- containing food or drink
[NB1].
Hyperglycaemia
• If after 15 minutes the blood glucose concentration has not returned to normal Hyperglycaemia in the absence of symptoms is rarely a medical emergency.
or the symptoms have not improved, repeat the dose of glucose. Advise patients to take their usual medications for diabetes and to seek
• If three or more portions of glucose are needed to restore the blood glucose medical review if their blood glucose concentration remains high. Patients
concentration to normal, seek medical advice. with associated symptoms such as abdominal pain, nausea, vomiting,
• If symptoms have improved, the patient should eat a longer- acting carbohydrate fatigue, shortness of breath or an altered conscious state may have dia -
(eg sandwich, dried fruit, yoghurt) to prevent recurrence of hypoglycaemia . betic ketoacidosis (DKA) or hyperglycaemic hyperosmolar state (HHS) ; the
• Keep the patient under observation until recovered. Do not allow them to drive onset is usually over a number of hours. If a patient with known diabetes
0
a home. Strongly advise medical review. appears unwell, seek medical advice, call 000 or start basic life support as
TJ
C
appropriate (for ‘Basic life support flow chart’, see Figure 8; p.235). To
CO If the patient is drowsy, uncooperative or unconscious:
• Stop dental treatment. Patients taking a sodium -glucose co-transporter 2 (SGLT2) inhibitor (eg 0
To
o—
O
i
dapagliflozin, empagliflozin, ertugliflozin) may develop diabetic ketoacidosis .E
• Call 000.
with a normal blood glucose concentration—call 000 if they develop any tn
«)
CD • If the patient is unconscious, start basic life support (for ‘Basic life support flow symptoms of diabetic ketoacidosis. .o2
£O chart’, see Figure 8; p.235). c
0
2 NBl: Examples of food and drink containing 15 g of glucose include: 15 g of easily absorbed «0
CD carbohydrate (eg 6 to 7 regular glucose jelly beans, 4 large glucose jelly beans): three 0
2
teaspoons of sugar or honey: 125 ml.of fruit juice (approximately one glass or a small £
popper or box) ; 150 ml_ of soft drink (not ‘diet’); 100 mL of oral glucose solution (eg 0
0
CL
Lucozade). 75
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244 245
 • Face—check the face. Has the mouth drooped?
Methaemoglobinaemia • Arms—can the patient lift both arms?
Methaemoglobinaemia occurs when haemoglobin oxidises to meth- • Speech—is speech slurred? Does the patient understand you?
aemoglobin, resulting in a reduced oxygen-carrying capacity of blood • Time—time is critical. If you see any of these signs, call 000
cells, functional anaemia and impaired delivery of oxygen to the tissues. immediately.
Methaemoglobinaemia can occur after exposure to oxidants, and is a rare For management of patients with stroke, see Box 37 (below).
adverse effect of local anaesthetics. Onset can occur within minutes or be
delayed. Slate-grey skin discolouration and cyanosis are the most distinct Box 37. Management of stroke
features; other signs and symptoms include headache, light- headedness,
shortness of breath, fatigue and tachycardia. Blood may appear to be dark If a stroke occurs:
red or brown in colour, and can remain so even after administering oxygen. • Stop dental treatment .
Methaemoglobinaemia can be life threatening and requires emergency • Call 000.
referral to hospital. For management of patients with methaemoglobi- • Measure blood pressure, heart rate and pulse oximetry .
naemia, see Box 36 (below). • Start supplemental oxygen if Sa02 is less than 90%, and titrate to Sa02
90 to 96% where possible.
Box 36. Management of methaemoglobinaemia • Maintain airway.
If methaemoglobinaemia occurs: • Monitor vital signs until assistance arrives and start basic life support if required
(for 'Basic life support flow chart', see Figure 8; p.235).
• Stop dental treatment .
• Call 000. Do not give aspirin because it is difficult to identify if the stroke is haemorrhagic
or ischaemic.
• Start supplemental oxygen and airway support if needed.
Sa02 = oxygen saturation
• Monitor blood pressure, heart rate and pulse oximetry until assistance arrives.
• Start basic life support if required (for 'Basic life support flow chart', see
Figure 8; p.235). Seizures
Seizures can be caused by epilepsy, syncope (see p.240), hypoglycaemia
(see p.244) , stroke (see p.246) and cerebral hypoxia from other causes. In
Q
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Neurological emergencies young children, fever can cause seizures.
~o
Seizures can involve a sudden spasm of muscles (producing rigidity such
Stroke that the patient falls) , jerky movements of the head, arms and legs, and
03

2 loss of consciousness. Seizures may affect all or part of the body. The
O
o
patient may have warning symptoms before the seizure (aura).
A stroke is a medical emergency. Recognising the signs of stroke early .E
to and starting emergency treatment reduce the risk of brain damage, and 0
CO

.
tu
improve the chance of survival Status epilepticus refers to continuous seizure activity or repeated seizures o
=0
5 Facial weakness, unilateral weakness and difficulty with speech are the
without full recovery of consciousness between attacks. Status epilepticus
is a medical emergency—call 000 for immediate transfer to hospital.
i
5
CD most common symptoms and signs of stroke. The F.A.S.T. test is an easy
8 way to recognise the most common signs of a stroke. The F.A.S.T. test For management of patients with seizures, see Box 38 (p 248). . E
0
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246 247
 Photo 18. Patient with right- sided facial palsy
Box 38. Management of seizures
If a seizure occurs:
• Stop dental treatment .
• Ensure the patient is not in danger in the dental chair—protect the patient from
falling from the chair, or lift them onto the floor.
• If possible, turn the patient on their side to reduce the risk of aspiration.
• Avoid restraining the patient during the seizure, unless it is essential to avoid
injury.
• Wait until the seizure stops.
• Assess consciousness by talking to the patient.
• Maintain airway.
• If there is vomit in the mouth or pharynx, remove it with high-volume suction
once the seizure has stopped. Do not place anything in the patient's mouth
during the seizure.
See further management advice for seizures known to be caused by syncope
. . .
244) or stroke (p 246).
(p 240), hypoglycaemia (p

For seizures of unknown cause or in patients with known epilepsy, if the patient the maxillary molars. Note
This patient had a right posterior superior infiltration for restoration of
.
recovers completely, keep under observation for at least a further 30 minutes . the inability to close the right eye and right side of the lips. The left
.
side is functioning normally
Do not allow the patient to drive home. Advise the patient to seek urgent medical Patient permission was obtained for use of this image
review and provide a written summary of events of the seizure directly to the
medical practitioner.
Box 39. Management of temporary paralysis of the
If the seizure or loss of consciousness lasts for more than a few minutes, or if
repeated seizures occur without recovery of consciousness between attacks (ie
periocular muscles
status epilepticus):
If temporary paralysis of the periocular muscles occurs:
• Call 000.
• Stop the local anaesthetic injection and dental treatment.
• Maintain airway. is
• Explain what has happened and reassure the patient that the paralysis
• Monitor the patient until assistance arrives. temporary. 75
• Advise the patient not to rub the eyes. s
Temporary paralysis of the periocular • Close the eye and cover with two eye patches—fold the first patch in
half and
folded
T5
.£
muscles place over the eye, then tape the second patch over the top of the (0

patch. 0)

If a local anaesthetic is inadvertently injected into the parotid gland (eg a • Keep the patient under observation until the ability to blink starts to return
This . o
of the o
misdirected mandibular block or posterior maxillary infiltration), it will dif- usually happens within the hour, depending on the dose and strength op
fuse to the branches of the seventh cranial (facial) nerve. This may cause local anaesthetic. 0)

temporary paralysis of the periocular muscles. • The patient should not drive that day and should be escorted home . E
<u
.
.a -M8
Photo 18 (p.249) shows a patient with right-sided facial palsy. • Check on the patient by phone later that day If the patient has not
fully 75
recovered within 12 hours, medical review is required .
For management of patients with temporary paralysis of the periocular
muscles, see Box 39 (p.249).
5 a.
249
 Ocular emergencies Box 40. Management of chemical eye injuries
If a chemical injury to the eye occurs:
Patients’ eyes are vulnerable to injury during dental treatment. Injuries can
also happen to members of the dental team. • Stop dental treatment .
• Immediately irrigate the eye with water.
Eye injuries can be caused by:
• Hold the eyelid open.
• chemicals (eg endodontic irrigating solutions), particularly alkaline
• Remove contact lens if present.
solutions—see below
• Continue irrigation with water, poured from a cup or beaker or from a tap, for at
• foreign bodies (eg calculus, fragments of fillings)—see p.251 least 15 minutes.
• penetrating objects (eg drills and endodontic instruments)—see p.252. • Do not use an eyecup because a continuous flow of water over the eye is
The risk of injury is minimised by wearing eye protection during oral exami- required.
nation and treatment, and is essential at all times for both patients and • If weak chemical injury and minor eye irritation have occurred, organise medical
staff. Do not pass chemicals and instruments over the patient's face. review for the same day.
• If caustic chemical injury or a marked inflammatory response has occurred, call
000 and continue irrigation until assistance arrives.
Rapid emergency treatment can minimise the extent of injury and the risk
of blindness.
• Inform the medical team which chemical caused the injury .
For an extensive resource with illustrations of various conditions, see
the Eye Emergency Manual <www.aci.health.nsw.gov.au/networks/
ophthalmology/about/eem > . Foreign bodies lodged on the surface of the
eye
Chemical eye injuries
Foreign bodies can lodge on the surface of the eye. For management of
Caustic solutions used in dental treatments can cause severe chemical eye patients with nonpenetrating foreign bodies lodged on the surface of the
injuries. In particular, alkaline solutions cause liquefactive necrosis because eye, see Box 41 (below).
they burn the ocular tissues. For management of patients with chemical
75 eye injuries, see Box 40 (p.251). Box 41. Management of foreign bodies lodged on the
5 surface of the eye
-
O
o If a foreign body becomes lodged on the surface of the eye: 75
. g
4
<u • Stop dental treatment o
2 • Immediately irrigate the eye.
o £
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• Hold the eyelid open. (A

• Do not touch the eye surface.

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=5
• Do not attempt to remove the foreign body.
12
If the foreign body does not dislodge following a short attempt at irrigation,
of)
5 •
transfer the patient to an emergency department . a)
s
•
• If the patient has any ongoing symptoms despite apparent removal of the
E)
9
5a. foreign body, organise prompt medical review . 75 8
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250 251
 Penetrating eye injuries Box 43. Management of unilateral blindness following
Sharp objects can penetrate the unprotected eye. For management of injection of local anaesthetic containing a
patients with penetrating eye injuries, see Box 42 (below). vasoconstrictor
Box 42. Management of penetrating eye injuries If unilateral blindness occurs following injection of local anaesthetic containing
a vasoconstrictor:
If a penetrating eye injury occurs: • Stop dental treatment.
• Stop dental treatment. • Call 000—the patient must be taken to an emergency department urgently.
• Call 000—the patient must be taken to an emergency department urgently . • If the patient is unconscious, start basic life support (for ‘Basic life support flow
• Do not attempt to remove the penetrating object from the eye. chart ’, see Figure 8; p.235).
• Do not irrigate the eye.
• Prevent the patient from rubbing the eye. Unilateral blindness following injection of dermal
• Cover the eye with an eye shield, or use the base of a polystyrene cup and tape fillers
it on so it rests on the bony rim of the eye socket.
• Keep the patient calm until assistance arrives. Accidental intravascular injection of dermal fillers (eg hyaluronic acid) can
cause unilateral blindness by occluding the ophthalmic artery. Vision loss
• Describe the object that penetrated the eye to the medical team (or show them
may be permanent.
a similar instrument).
For management of patients with unilateral blindness following injection of
dermal fillers, see Box 44 ( below).
Unilateral blindness
Unilateral blindness can occur following accidental intra - arterial injection Box 44. Management of unilateral blindness following
of a local anaesthetic containing a vasoconstrictor, or following accidental injection of dermal fillers
intravascular injection of dermal fillers in the face.
If unilateral blindness occurs following injection of dermal fillers:
• Stop treatment.
Unilateral blindness following injection of local • Call 000—the patient must be transferred to an emergency department
0 anaesthetic containing a vasoconstrictor urgently .
o • Note the time of onset of blindness.
~o
c Accidental intra - arterial injection of a vasoconstrictor causes spasm of the
• As long as this does not delay transfer to an emergency department:
(3
03 ophthalmic artery and related blood vessels. Loss of consciousness may
assess the visual deficit 0
is occur. Patients usually have spontaneous full recovery of their vision. -

o-
u
.£
i
- assess the presence of any symptoms of stroke (eg facial weakness,
in For management of patients with unilateral blindness following injection of unilateral weakness, difficulty with speech) if)
0 local anaesthetic containing a vasoconstrictor, see Box 43 ( p.253) .
assess the presence of any cutaneous symptoms or signs (eg pain,
.o2
E0
.
-
blanching of the skin)
c
0
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• If hyaluronic acid was used as the dermal filler, inject hyaluronidase if
gP
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E
0
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2 .2
NBl: Hyaluronidase is essential for the management of serious adverse effects associated
0
with hyaluronic acid; practitioners using hyaluronic acid must be familiar with the use of W S
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252 253
 Respiratory emergencies Acute asthma
Acute asthma attacks can be fatal. Ask patients with asthma to bring
Hyperventilation syndrome their reliever inhaler with them when attending for dental treatment. Many
patients with asthma have an asthma action plan, or, at least, a good
Hyperventilation syndrome can occur when a patient hyperventilates understanding of how to manage their asthma.
(overbreathes) . It is common, and is often associated with anxiety or
panic attacks. For signs and symptoms of hyperventilation syndrome, see Patients with severe asthma may not wheeze. Cyanosis indicates
Table 24 (below) ; signs and symptoms may be similar to syncope (see life-threatening asthma.
p.240), asthma attack (see p.255), anaphylaxis (see p.238), or a myocar-
dial infarction (see p. 242). If an acute asthma attack occurs, perform a rapid physical examination to
evaluate the severity of the attack (see Table 25, below) . Wheezing is an
Table 24. Signs and symptoms of hyperventilation unreliable indicator of the severity of an asthma attack and may be absent
syndrome in a severe attack. Cyanosis indicates life-threatening asthma —patients
require urgent transfer to hospital.
Symptoms Signs
An acute asthma attack is initially treated with a short-acting bronchodi-
light -headedness
lator (eg salbutamol, terbutaline) —see Box 46 ( p.256) .
rapid breathing
dizziness occasional deep sighing breaths
shortness of breath rapid heart rate Table 25. Initial assessment of the severity of an acute
feeling of panic and impending death altered consciousness asthma attack in adults and children
blurred vision involuntary contraction of the hands and
fingers Mild or moderate can walk and can speak whole sentences in one breath
tingling in the fingers, toes and lips
for young children: can move around and can speak in phrases
feeling of detachment
oxygen saturation greater than 94% [NB1]

Observe patients after the administration of a local anaesthetic, because Severe

any of these findings:
hyperventilation syndrome commonly occurs at that time. use of accessory muscles of neck or intercostal muscles during
inspiration
For management of patients with hyperventilation syndrome, see Box 45 ‘tracheal tug’ during inspiration
(below).
0 subcostal recession (‘abdominal breathing’)
O unable to complete sentences in one breath because of
O
c
Box 45. Management of hyperventilation syndrome dyspnoea <5
(Q
obvious respiratory distress
T5 If hyperventilation syndrome occurs:
oxygen saturation 90 to 94% [ NB1] -0o
o
i
- • Stop dental treatment . .E
any of these findings:
>
(/ • Encourage the patient to slow their breathing, and to breathe in through their Life- threatening (A
0
nose and out through their mouth. reduced consciousness or collapse .o2
exhaustion c
P
.
0
• Reassure the patient, explain the cause of the symptoms, and have them talk 0
0 to you. cyanosis SO
O 0
oxygen saturation less than 90% [NB1]
.9 • Re-breathing into a bag is not recommended. E
poor respiratory effort, soft or absent breath sounds 0
. a8
.o2 ."S2
0 If the patient does not rapidly recover, review the diagnosis
CL NBl: If oxygen therapy has already been started, it is not necessary to stop oxygen to measure
2 If acute symptoms persist for more than 5 to 10 minutes: .
pulse oximetry Oxygen saturation levels are a guide only and are not definitive: clinical
o rc
:> o.
0 judgment should be applied.
jC • Call 000.
Source: Adapted from National Asthma Council Australia. Australian asthma handbook Version
• Monitor the patient until assistance arrives. 2.0 [ online]. Melbourne: National Asthma Council Australia: 2019: Accessed April 2019.
254 255
Using a spacer device with a pressurised metered dose inhaler enables
better drug penetration into the lungs, and is easier to use effectively
than an inhaler alone. Spacers are essential for management of a severe
asthma attack, because these patients cannot inhale the drug effectively.
However, salbutamol should never be withheld on the grounds that a
spacer is not available.
Spacers are essential for management of a severe asthma attack.
If the patient recovers swiftly after an acute asthma attack:
• Temporise the dental state.
• Make another appointment to complete the dental treatment (if
needed).
• When the patient is breathing easily, discharge from care.
• Advise the patient to take their asthma medication as prescribed and
seek medical review.

Inhaled or swallowed objects

Box 46. Management of an acute asthma attack
An inhaled or swallowed object can present a significant risk to the patient.
Stop dental treatment. Sit the patient upright.
Use preventive measures to minimise the risk of an object being inhaled or
If the asthma attack is mild or moderate: swallowed during dental treatment ( see Box 47; p.258).
• Give 4 puffs of salbutamol inhaler via a spacer, 1puff at a time. Shake the
inhaler before each puff. Although swallowed objects usually pass through the gastrointestinal tract
without causing harm, occasionally they require removal.
• Ask the patient to take 4 breaths in and out of the spacer after each puff [NB1J.
• Wait 4 minutes. Foreign objects in the airways and lungs ( inhaled objects) must be removed
• If there is little or no improvement, give another 4 puffs using the technique urgently. Partial or complete airway obstruction can occur following inha-
above. lation of a foreign body. If the patient can breathe, speak, cry or cough,
Assess the patient ’s status. If there is little or no improvement, manage as for a
some movement of air is occurring, and the obstruction is partial. See
•
severe attack (see below). Table 26 ( below) for signs of partial and complete airway obstruction.
For management of patients who have inhaled or swallowed an object, see
Box 48 (p.259).

Table 26. Signs of airway obstruction

Signs of partial airway obstruction Signs of complete
airway obstruction

breathing is laboured there may be attempts to breathe 75

M

breathing may be noisy no breathing sounds 0

~o
some movement of air can be felt from air does not emit from nose or mouth
the mouth .E
c/ )
Source: Australian and New Zealand Committee on Resuscitation ( ANZCOR). ANZCOR Guideline .2o
4: Airway. East Melbourne: ANZCOR: 2016. c
0
gy
CD
E
0
75 8
.52 .2
$
2 .
Q

257
 Box 47. Preventive measures to minimise the risk of
Box 48. Management of an inhaled or swallowed object
inhaled or swallowed objects [NB1]
If possible, use a rubber dam for procedures with a high risk of inhaling
or In the event that an object appears to have fallen down the oropharynx:
swallowing a foreign object . • Stop dental treatment .
If the procedure precludes the use of a rubber dam, other precautions
include: • Check whether the object is present in the patient's mouth or clothes and, if so,
• ensuring a careful and unrushed approach remove it .
• having the patient reclined rather than supine • If the object is not found, put the patient into an upright position.
• having instruments and facilities available that can be used to retrieve an object • Although the majority of ingested foreign bodies will pass through the
from the oropharynx gastrointestinal tract without incident, refer the patient for further medical
• tying dental floss to any object that can be dropped (if appropriate) assessment and management. If the patient is stable and asymptomatic, it may
• placing gauze across the back of the tongue to trap small items (eg crowns) be appropriate to complete dental treatment before doing so.
that may be dropped
If the patient is conscious with signs of airway obstruction (see Table 26;
• rotating the patient's head so that a dropped object will fall to the side
of the p.257):
mouth • Call 000.
• using high- volume suction. • Reassure the patient and encourage them to relax, breathe deeply and try to
dislodge the object by coughing.
• If coughing is ineffective, give up to 5 back blows between the shoulder blades
using the heel of the hand (checking for effectiveness between each blow) .
• If back blows are unsuccessful, give up to 5 chest thrusts delivered at the same
compression point as for CPR (checking for effectiveness between each chest
thrust).
• Continue to alternate between back blows and chest thrusts until the
obstruction is relieved or assistance arrives.

If the patient with airway obstruction becomes unconscious:

75
• Call 000.
o .
a • Inspect the back of the throat for the foreign object and remove it if possible
• Start CPR (for 'Basic life support flow chart', see Figure 8; p.235).
•
D
CO 5
• Clinicians with appropriate expertise and equipment should consider performing
g cricothyroidotomy . -o<5
o .E
• Abdominal thrusts, such as those described in the Heimlich manoeuvre, can
cause internal organ damage so are not recommended . </>
0)
1 CPR = cardiopulmonary resuscitation
o
NB1: A flow chart for the management of choking can be downloaded from the Australian 5
o . .
Resuscitation Council website <resus.org au/guidelines/flowcharts-3/>
a)

5Cl
i
«8
II
Os
a?

258 259
Guidance for medical
practitioners managing
oral and dental issues

Triaging dental presentations for medical

practitioners
Patients with dental problems commonly present initially to a medical prac -
titioner. The medical practitioner should usually redirect these patients to a
dentist, particularly if the presentation relates to previous dental treatment
( eg complications after tooth extraction). However, medical practitioners
often provide acute care for dental problems, particularly in the rural or
remote setting— see Table 27 ( pp.262-5).

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75
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261
g Therapeutic Guidelines: Oral and Dental
Table 27. Common dental problems encountered by medical practitioners
Presenting problem
Acute dental pain
acute dental pain (see pp.136-43) with
or without facial swelling
Conditions presenting after an oral or dental procedure
bleeding after oral surgery (eg tooth
extraction) (see pp.222-4)
pain and swelling after oral surgery (eg
tooth extraction) (see p.221)
prolonged numbness (anaesthesia)
or altered sensation in the mouth
(paraesthesia) after a dental procedure
Table 27. Common dental problems encountered by medical practitioners (cont.)
Presenting problem
Dental and maxillofacial trauma
broken tooth or filling, or lost filling (or
other restoration) (see p.225)
tooth avulsion (knocked-out tooth) (see
-
P 226)
maxillofacial trauma (see p.230) ,
deranged occlusion (teeth not biting
together normally)
Conditions affecting the jaw
jaw clicking or locking with acute
unilateral or bilateral pre -auricular pain
restricted mouth opening (trismus; see
p.151)
ro
G)
w Medical practitioners managing
oral and dental issues
Comments
antibiotics are rarely indicated
analgesics may be indicated
for a guide to differentiating acute dental pain, see Table 12
(pp.132-6)
check anticoagulant status
manage with direct pressure and local haemostatic
measures
pain and swelling usually peaks 48 to 72 hours after
surgery, before it starts to resolve
antibiotics are rarely indicated
can be caused by nerve trauma or local anaesthetic
neurotoxicity
Comments
assess whether dentine or pulp has been exposed
antibiotics are not indicated
requires urgent assessment
primary teeth (baby teeth) must not be replanted
address any life-threatening complications immediately
all patients require thorough assessment
jaw clicking without pain, discomfort or trismus is normal-
referral is not needed
consider temporomandibular disorders (see p.144)
consider tetanus and dystonic reactions, including drug-
related dystonic reactions (eg metoclopramide)
oral and dental causes include infection (for odontogenic
infections, see pp. 79-87) , procedural complications
(eg haematoma) , partially erupted wisdom tooth or
temporomandibular disorders (see p 144).
Urgency and referral
urgency and referral are dependent on the
diagnosis
if bleeding is not controlled, emergency
referral to hospital or oral surgeon
referral to or consultation with practitioner who
performed the oral surgery (within 24 hours)
referral to or consultation with practitioner who
performed the procedure (within 24 hours)
continued next page
Urgency and referral
without pain, nonurgent referral to dentist
(within a few days)
with pain, urgent referral to dentist (within
24 hours)
for a secondary tooth, urgent referral to
dentist
for a primary tooth, nonurgent referral to
dentist
for patients with significant trauma,
emergency referral to hospital
referral to oral medicine specialist or oral and
maxillofacial surgeon (urgency dependent on
severity)
if medical causes excluded, urgent referral to
dentist ( within 24 hours)
continued next page
g Therapeutic Guidelines: Oral and Dental
Table 27 . Common dental problems encountered by medical practitioners (cont.)
Presenting problem
Conditions affecting the gums
bleeding gums caused by minor trauma
(eg eating, cleaning teeth)
spontaneously bleeding gums
swollen, puffy or enlarged gums (gingival
hyperplasia), with or without bleeding
swollen, painful or bleeding gums around
a dental implant, or a loose or broken
implant
Table 27. Common dental problems encountered by medical practitioners (cont. )
Presenting problem
Conditions affecting the gums (cont ) .
sore areas beneath dentures
Other oral presentations
oral malodour (halitosis; see p.125)
acute onset of numbness (anaesthesia) ,
altered sensation (paraesthesia) or
weakness in the mouth
NJ
o
cn Medical practitioners managing
oral and dental issues
Comments Urgency and referral
in children, commonly due to exfoliating teeth (see p.267) for adults, referral to dentist or periodontist
in adults, commonly due to gingivitis (see p.71) or (urgency dependent on severity)
.
periodontitis (see p 72)
with pain, halitosis, necrosis or ulceration of the interdental necrotising gingivitis requires urgent referral
papillae, the likely cause is necrotising gingivitis (see p.73) to dentist
consider drugs that affect haemostasis, acquired or
congenital bleeding disorders, or other haematological
disorders
consider adverse effects of drug (eg calcium channel nonurgent referral to dentist if review required
blockers, phenytoin, ciclosporin); encourage improved oral
hygiene (see pp.273-5)
in the absence of drug causation, consider possible
malignancy
for further information on peri-implant diseases, see p.76 referral to dentist who placed the implant
(urgency dependent on severity)
continued next page
Comments Urgency and referral
remove denture and examine the mouth and denture; nonurgent referral to dentist (within a few
consider denture hygiene (see p.275) weeks) if dental review required
consider trauma from an ill-fitting denture—it may need
adjustment
consider oral candidiasis or denture -associated
erythematous stomatitis (see Table 11; pp.115-7)
consider possible malignancy—any suspicious lesions or
pigmentation require investigation (for assessment of an
oral mucosal lesion, see p.93)
commonly caused by oral conditions, but may be a if medical causes excluded, referral to dentist
symptom of systemic disease (urgency dependent on likely intraoral cause)
consider malignancy, multiple sclerosis urgent referral for medical investigation
 Oral and dental issues in older people
Medical practitioners have an important role to play in promoting oral
health in older people, who may rarely see a dentist. Encourage older
people to have regular dental reviews.
Medical practitioners have an important role to play in promoting
oral health in older people, who may rarely see a dentist.
Poor oral hygiene is common in older people, particularly in residen-
tial aged-care facilities. Maintaining oral hygiene is often hampered by
cognitive or physical impairment (eg dementia, poor manual dexterity,
blindness) . Promote oral hygiene ( see pp.273-5) the use of a powered
— extractions under general anaesthesia; encourage regular dental
toothbrush and alcohol- free mouthwash are effective strategies to prevent
dental caries and periodontal disease.
Undiagnosed or poorly managed dental conditions that cause pain can
contribute to behavioural issues in patients with dementia. Older people,
particularly those in residential aged-care facilities, often have complex
oral health issues. Dry mouth (see p.121) and falls are common in older
people, particularly in people taking multiple medications. Falls have the
potential to cause oral trauma (eg a broken tooth, tooth avulsion, maxil-
lofacial trauma; see pp.225-31).
Denture use is associated with traumatic ulcers (see p.106), denture-
associated erythematous stomatitis ( see p.117), oral candidiasis ( see
p.115) and angular cheilitis (see p.116). Ask about denture fitting and
75 check denture hygiene is correct and effective ( see p.275). Flowever, den-
M- ture use is declining with older people increasingly retaining their teeth;
Q
<D
this is contributing to a significant increase in the incidence of dental caries
TJ and periodontal disease.
C
cu
Dental caries ( see pp.63-70) in older people is exacerbated by dry mouth,
75
poor oral hygiene and changes in diet. The stages of dental caries are
o-
i
depicted in Figure 4 (p.63) and Photo 1 (p.64). While awaiting dental
in
review, consider the use of toothpaste containing 5000 ppm of fluoride.
0
ECD Reassure patients that, in some cases, dental caries can be managed with
2 professionally applied topical treatments (eg fluoride varnish, silver fluoride
13
CD formulations) that do not require tooth extraction or fillings.
.9
Periodontal disease ( see pp.71-6) is common in older people. There is
CD
Cl growing evidence that poor periodontal health is associated with many sys-
CD
temic diseases, including aspiration pneumonia, cerebrovascular events,
CD
XI
atherosclerosis, diabetes, autoimmune diseases (eg rheumatoid arthritis)
and other chronic diseases.
266
For patients presenting with lesions in the mouth, have a high index of
suspicion for oral cancer—oral cancer (see p.95) is more common in older
people and can mimic many oral mucosal diseases (for assessment of an
oral mucosal lesion, see p.93).
Oral and dental issues in children
Medical practitioners may encounter oral and dental issues in children.
Common presentations are outlined below:
• tooth eruption and teething pain (see below)
• dental caries (see pp.63-70) —can lead to hospital admission for
review and good oral hygiene (see pp.273-5)
• tooth avulsion (knocked-out tooth; see p.226) —a primary (baby) tooth
should not be replanted.
Painful intraoral lesions in children may be caused by oral infection with
herpes simplex virus (see p.110) . This may resemble necrotising gingivitis
(p.73) , which is rarely, if ever, seen in children.
Periodontitis in children is rare and usually associated with systemic dis-
ease (eg leukaemia, type 1diabetes, cyclic neutropenia) (see p.72).
Tooth eruption and teething pain
Tooth eruption (teething) in infants is often accompanied by local pain and
swelling, drooling, irritability and occasionally a mild fever. Rubbing the
gums with a clean finger, teething rings and cold compresses can provide
symptomatic relief of teething pain. Teething rings should be cold but not tUD
.•£OJO
frozen. Systemic analgesics (eg paracetamol) can be used. 03
c
Teething gels should not be used because of the lack of evidence of effi-
03
lo *<
cacy and the potential for harm. Some teething gels contain salicylates
and excessive doses or prolonged use can cause systemic toxicity. Teething
tO p
3
P
gels containing local anaesthetic should not be used for teething pain in
infants and children due to the risk of serious adverse effects (eg seizures, s 75
cardiac effects, death). Amber teething necklaces are ineffective and dan-
gerous because they are a choking and strangulation hazard. 2 ®
Teething gels should not be used because of the lack of evidence 751
« <o
of efficacy and the potential for harm.
0
S o
2
average ages
Figure 9 and Figure 10 (pp.268-9) give an indication of the
at which tooth eruption occurs . 267
gg Therapeutic Guidelines: Oral and Dental

Figure 9. Primary teeth eruption and exfoliation pattern

Upper Teeth Erupt Exfoliate

central incisor 8 to 12 months 6 to 7 years

lateral incisor 9 to 13 months 7 to 8 years
canine (cuspid) 16 to 22 months 10 to 12 years
)- • first molar 13 to 19 months 9 to 11 years
second molar 25 to 33 months
$
10 to 12 years

*
Lower Teeth Erupt Exfoliate

i second molar 23 to 31 months 10 to 12 years

h first molar 14 to 18 months 9 to 11 years

•
canine (cuspid) 17 to 23 months 9 to 12 years
• lateral incisor 10 to 16 months 7 to 8 years
|
central incisor 6 to 10 months 6 to 7 years

Figure 10. Secondary teeth eruption pattern

Upper Teeth Erupt
central incisor 7 to 8 years
lateral incisor 8 to 9 years
canine ( cuspid) 11 to 12 years
first premolar ( first bicuspid) 10 to 11 years
second premolar (second bicuspid) 10 to 12 years
first molar 6 to 7 years
second molar 12 to 13 years
third molar ( wisdom tooth) 17 to 21 years

Lower Teeth Erupt

third molar (wisdom tooth) 17 to 21 years
second molar 11 to 13 years
first molar 6 to 7 years

second premolar (second bicuspid) 11 to 12 years

first premolar ( first bicuspid) 10 to 12 years

canine (cuspid) 9 to 10 years
i
lateral incisor 7 to 8 years
central incisor 6 to 7 years

•o
O
Medical practitioners managing
oral and dental issues
 Dental anatomy and terminology Dental numbering system
Figure 11. Anatomy of the tooth and surrounding tissues There are numerous dental numbering systems to identify teeth and their
maturity. The most commonly used system in Australia is the Federation
Dentaire Internationale (FDI) system ( see Figure 12; p.272). When com-
municating with a dentist, identify which numbering system is being used.

The FDI numbering system divides the mouth into quadrants. The first
number indicates the quadrant and whether it is a primary or secondary
tooth. The second number indicates the tooth; tooth numbering begins at
the central incisor and counts backward to the molars.
Using the FDI numbering system, for adults, the quadrants are numbered
as:
• patient’s upper right is quadrant 1
• patient’s upper left is quadrant 2
• patient’s lower left is quadrant 3
• patient ’s lower right is quadrant 4.
For primary teeth in children, the quadrants are numbered as:
• patient’s upper right is quadrant 5
• patient’s upper left is quadrant 6
l Enamel The hard, calcified substance that is the surface of a crown of a • patient’s lower left is quadrant 7
tooth.
• patient’s lower right is quadrant 8.
2 Dentine The calcified tissue that forms the major part of a tooth. In the
crown of the tooth, the dentine is covered by enamel. The pulp
chamber of the tooth is enclosed by dentine.
75
3 Pulp The organ at the centre of a tooth containing blood vessels,
0 connective and neural tissue, and cells that produce dentine.
Q Blood vessels and neural tissue enter the tooth from the apex of OD
-o the root. .•E
c OJO
0 03
4 Gingiva The marginal part of the gum that surrounds the tooth where it c
75 emerges from the deeper, supporting tissues. 0
o-
i

5 Periodontal The ligament that connects a tooth, by its root, to the supporting
ligament bone. £o
0
Ea
) 6 Cementum The calcified tissue on the surface of the root of a tooth, which o -
provides attachment for the periodontal ligament. Sg
3
CD
.2
7 Fissure A naturally occurring crevice in the enamel. 1 =
1-8
8 Crown The part of the tooth that is visible and is above the gingival
0 margin.
CL « <c
0
9 Root The part of the tooth below the gingival margin; it is connected
0
through cementum on its surface and the fibres of the
.0
periodontal ligament to the supporting bone.
5o

270 271
 Oral hygiene
Regular oral hygiene by mechanical brushing and cleaning between the
teeth removes soft dental plaque. When dental plaque becomes mineral-
ised (calculus), it must be removed by a dental practitioner. Dental plaque
and calculus can cause periodontal disease ( see pp.71-6) and dental
caries (see pp.63-70) .
Frequent exposure to dietary sugar and carbohydrates leads to an increase
in the risk of dental caries. Avoid sucrose in sticky forms and limit other
sugars (eg acidic drinks) and carbohydrates as snacks between meals.
m
H
%
O
Avoid drinks other than water at bedtime after brushing teeth (including
milk, formula and expressed breastmilk) —saliva flow diminishes during
sleep and the sugar from the drink remains on the teeth overnight. This is
a common cause of dental caries in children and the elderly.

Interdental cleaning
Interdental cleaning using floss or interdental brushes is recommended
once each day before brushing the teeth.* Brushing teeth with a tooth-
brush does not remove plaque from between the teeth or below the gum
line.
Dental floss can be used to wipe the interdental tooth surface to remove
plaque (back and forth, then up and down several times on each tooth
surface) . Manual dental floss, floss- holding devices or automated flossing
devices are available—the choice is based on personal preference or level
of dexterity.
Interdental brushes are as effective as dental floss in plaque removal, and
.EJO
"OJO

often more effective for debris removal. They require less dexterity than 0
dental floss. Interdental brushes are particularly useful in patients with gum CD
C
recession or disease, where the spaces between the teeth are larger. n

:
Interdental wood sticks can remove food particles, but do not effectively
remove plaque.
gs
2 </)
o
o -!2
Water jets do not effectively remove plaque. Ere

73
.752w eoC

§ 75
* Further information on oral hygiene techniques can be found in: 2o
Daly C. Prescribing good oral hygiene for adults. Australian Prescriber 2009;32( 3):72 - 5.
273
Tooth and tongue cleaning
Soft- bristle toothbrushes are recommended; hard-bristle toothbrushes are
not more effective and can damage the gums and the softer root surface.
Children younger than 6 years should use a children’s toothbrush. Powered
toothbrushes with a rotation oscillation action are slightly more effective at
plaque removal than manual brushes. Powered toothbrushes are useful for
people with dexterity or disability problems, and for carers. Toothbrushes
should be replaced once damaged or when the bristles become deformed.
Advise patients to use a fluoride-containing toothpaste; for recommended
concentrations of fluoride in toothpaste, see Table 7 (p.67). Toothpastes
that do not contain fluoride provide little protection against dental caries.
Toothpastes also contain other additives (eg abrasives, detergents, anti-
bacterials, bleaches, remineralising agents).
Toothpastes that do not contain fluoride provide little protection
against dental caries.
Advise patients to brush teeth for 2 minutes, twice each day with fluoride
toothpaste. Toothpaste should be spat out and not swallowed to minimise
fluoride ingestion; the mouth should not be rinsed to allow increased
uptake of fluoride from the saliva.
Advise patients to brush or gently scrape the tongue, but not to brush or
massage the gums.*
Mouthwash
Mouthwash is usually not required as part of a standard oral hygiene rou -
tine, provided mechanical cleaning (toothbrushing, interdental cleaning)
is performed properly. Mouthwash should not be used as substitute for
proper mechanical teeth cleaning.
Fluoride-containing mouthwashes can be used as an additional source of
fluoride for people at high risk of dental caries on the recommendation of a
dentist (for further information on topical fluoride applications, see Table 8;
p.68) .
Mouthwash that inhibits plaque formation (eg chlorhexidine) can be used
for a short duration in addition to mechanical tooth cleaning, usually when
pain associated with periodontal disease restricts mechanical cleaning.
For more information, see the topics on gingivitis (p.71) and necrotising
gingivitis ( p.73).
Alcohol-containing mouthwashes may be associated with oral cancer and
are not recommended—see p.58 for further information on mouthwashes.
Specialised oral hygiene
People with dental implants, bridges, crowns that are joined together,
and orthodontic brackets should follow the oral hygiene advice from their
dentist.
Denture hygiene
Dentures should be regularly cleaned twice a day to remove food parti-
cles and plaque. Advise patients to remove dentures from the mouth and
clean them with warm water, mild soap and a toothbrush, denture brush or
soft nail brush. Avoid cleaning dentures with hot water, toothpaste, kitchen
detergents, laundry bleaches, methylated spirits, antiseptics or abrasives
(unless instructed to by a dental practitioner) . Patients should clean their
gums and remaining teeth with a soft toothbrush and toothpaste.
Advise patients to place dentures in a dry environment overnight after
cleaning them. Traditionally, it was recommended that dentures were kept
in liquid overnight. However, allowing the cleaned denture to dry out at
night is more effective for reducing yeast colonisation and plaque accumu-
lation, compared with both denture cleansers and water. Although repeated
cycles of hydration and dehydration can change the shape of the denture,
these changes are small and not clinically significant.
•OJD
Dentures should be cleaned then placed in a dry environment at .OX£)
night. 03
c
03
If there is a build- up of hard deposits (tartar, calculus) , dentures can be
soaked overnight in a solution of white vinegar (diluted 1:4) , then cleaned
as usual. Advise patients to see their dentist for professional cleaning if
hard deposits cannot be removed.
P-
0 2
is T5
Denture-associated erythematous stomatitis is prevented by regular 1=
!§
cleaning of the dentures and storing them in a dry environment overnight.
Advise patients with denture-associated erythematous stomatitis to opti- re ?
re
mise denture hygiene—it can take 1month for symptoms to improve; see
re re
p.117 for further information. 5 o
275
Appendix 1.
Drug use in pregnancy and
breastfeeding

Drug use in pregnancy

A drug can have more than one harmful effect on the fetus. Individual
effects depend on the time of fetal exposure to the drug.
During the first 2 weeks after fertilisation and before full implantation, the
embryo is thought to be resistant to any teratogenic effects of drugs. This
is because there is no direct communication between maternal and embry-
onic tissue until after the placenta starts to form.
The critical period for teratogenic effects is during organogenesis. This
starts at about 17 days after conception and is complete by 60 to 70 days.
Exposure to certain drugs during this period (17 to 70 days) can cause
major birth defects. •OJO

Some drugs can interfere with functional development of organ systems .-o£
0
(eg central nervous system, integumentary system, cardiovascular system) 0
in the second and third trimesters and produce serious consequences. if )
0
A woman may not be aware of her pregnancy until after the early stages of 0

organogenesis. For this reason, drugs in the most severe category of risk (X -
Q

in the Australian categorisation of drugs in pregnancy; see p.281) should

T3
C
0
not be prescribed to a woman of childbearing potential, unless a pregnancy
test is negative and she is using an effective method of contraception. o
c
c
0
However, there are several conditions in which long-term medication will be "OD
necessary in a woman of childbearing potential despite known harms of the 0

drugs. At the time of initial prescribing in any such situation, the prescriber
Q .
should discuss the desirability of reviewing medication requirements well
.£
0
before conception. For some disorders, it may be possible to change to a </)
different category of drug. If a woman conceives while on medication and
3
uo
3
there has been no opportunity for earlier discussion with the prescriber, her
D
medication should be reviewed as soon as possible.
277
 The following checklist may assist in deciding whether to prescribe a par- • overdose
ticular drug during pregnancy: • occupational exposure
• Nonpharmacological treatment: Is such a treatment available and • other situations in which the recommended therapeutic dose has been
likely to be successful? Would such treatment be reasonable at least exceeded.
until the first trimester is complete? Most pregnant women strongly
favour this type of treatment and concordance is likely to be high. The Australian categorisation system is not hierarchical.
• Harm-benefit analysis: For the particular drug under consideration,
follow a
what are the potential harms and benefits to the woman and harms to The categorisation of medicines for use in pregnancy does not
the fetus of prescribing? What are the harms and benefits (for each) of hierarchical structure.
not prescribing? • Human data are lacking or inadequate for drugs in the Bl, B2 and B3
• Incidence of spontaneous congenital abnormality: When drugs categories .
cannot be avoided, it may be appropriate to discuss the incidence • Subcategorisation of the B category is based on animal data.
of non-drug-related spontaneous abnormalities. This is often • The allocation of a B category does not imply greater safety than a C
.
underestimated The incidence in Australia of significant congenital category.
abnormality is 2 to 4% of live births, and minor abnormalities are
• Medicines in category D are not absolutely contraindicated during
recognised in approximately 15% of newborns.
• Education, documentation and communication: Has the education
pregnancy .
have, in
of the woman and, with her permission, her significant others Because of legal considerations in Australia, sponsor companies
, applied a more restrictive category than can be justified on
(eg partner, family, friends) regarding harms and benefits been some cases
properly documented in the patient’s notes? Have those health
.
the basis of the available data
professionals involved in obstetric management been informed? For pharmaceutical products containing two or more active ingredients
, the
It may be appropriate to discuss the use of, and limitations of, categorisation of the combination is based on the active ingredient with the
available antenatal screening to detect abnormalities in the fetus. The most restrictive pregnancy categorisation.
woman, with or without her significant others, will need to give some
consideration to the consequences of an abnormal result. The TGA pregnancy category should not be the sole basis of decision-
making in the use of a drug during pregnancy, because it does not
provide .E
aj Routine review later in the pregnancy includes consideration of whether information about the balance of harms and benefits for a particular
e . <g
s woman and fetus Furthermore, the category does not indicate the stage s
dose alteration is indicated during delivery to avoid neonatal problems such ( )
as respiratory depression. of fetal development that might be affected by drug exposure and may not g
pregnancy. £
reflect the most up-to-date information about the drug’s use in
D
A
| Australian categorisation of drugs in O

o pregnancy Category A CD
><
« women and
£ .
Table 28 (p 282) lists the pregnancy category assigned by the Australian Drugs which have been taken by a large number of pregnant S£
of childbearing age without any proven increase in the frequency of
§ Therapeutic Goods Administration (TGA) for individual drugs used in women
g*
’
.
having
malformations or other direct or indirect harmful effects on the fetus
o.
5
•
the management of oral and dental conditions in pregnant women.
<3 The TGA pregnancy categorisation is from the Prescribing medi- been observed.
.£
S .
cines in pregnancy database at the TGA website <www tga.gov.au/
s
•

(D prescribing-medicines-pregnancy-database>. Category Bl 3
CD
<5 The pregnancy categorisation system only applies to recommended thera- Drugs which have been taken by only a limited number of pregnant
women |?
j£ peutic doses. It cannot be assumed that the classifications assigned to frequency of O
and women of childbearing age, without an increase in the
individual medicines are valid in situations such as:
279
 malformation or other direct or indirect harmful effects on the human fetus Category X
having been observed.
Drugs which have such a high risk of causing permanent damage to the
Studies in animals have not shown evidence of an increased occurrence of
fetus that they should not be used in pregnancy or when there is a
pos-
fetal damage . sibility of pregnancy.

Category B2
Drugs which have been taken by only a limited number of pregnant women
Drug use in breastfeeding
and women of childbearing age, without an increase in the frequency
of
malformation or other direct or indirect harmful effects on the human fetus
.
Table 28 (p 282) provides advice on the safety of individual drugs used in
.
the management of oral and dental conditions in breastfeeding women
having been observed .
The benefits of breastfeeding are sufficiently important to recommend that
Studies in animals are inadequate or may be lacking, but available data
it should not be discontinued or discouraged unless there is substantial
show no evidence of an increased occurrence of fetal damage.
evidence that the drug taken by the woman will be harmful to the infant
,
and no alternative treatment can be found .
Category B3
Unless there is significant risk to the infant from necessary
medication, breastfeeding should be continued.
Drugs which have been taken by only a limited number of pregnant women
and women of childbearing age, without an increase in the frequency of
Most drugs are excreted only to a minimal extent in breast milk, and in
malformation or other direct or indirect harmful effects on the human fetus
having been observed . most cases the dosage to which the infant is ultimately exposed is
very low
Studies in animals have shown evidence of an increased occurrence of and well below the therapeutic concentration for infants. For this reason,
fetal damage, the significance of which is considered uncertain in humans. few drugs are totally contraindicated while breastfeeding.
In most situations, drugs cross the placenta more efficiently than into
Category C* breast milk.
=5
I
s Drugs which, owing to their pharmacological effects, have caused or may When considering prescribing drugs (particularly longer-term) during breast-
I
0

be suspected of causing harmful effects on the human fetus or neo- feeding, the following checklist may assist in guiding the decision:
• Woman’s desire to breastfeed.
Q i/)
nate without causing malformations. These effects may be
reversible.
CD
o
(U Specialised texts should be consulted for further details . • Availability of nonpharmacological treatment . 2
-Q
I • Potential for the drug to cause harm, weighed against the benefits o
o Category D of breastfeeding: For the infant, breastfeeding has multiple benefits,
to
>»
including improved immunocompetence (eg decreased rates of otitis
8 Drugs which have caused, are suspected to have caused or may I
be media) and enhanced cognitive development (eg increased IQ in the
I expected to cause an increased incidence of human fetal
malformations or
irreversible damage. These drugs may also have adverse pharmacological
.
older child) For the woman, breastfeeding provides psychological 5
£
)

benefits (eg enhanced maternal-infant attachment) and physiological n.

o .
effects Specialised texts should be consulted for further details. benefits (eg better uterine involution, decreased risk of breast and =
B ovarian cancers). S3
&
5) Document the discussion with the woman in the patient’s notes Inform . toll
* Category C in the Australian and Swedish categorisations of
1 risk is a pharmacological other health professionals involved in postnatal management of medication
(
C
| effect category and differs from the US Food and Drug Administration (FDA) categorisation
(where category C indicates greater likelihood of risk changes. a
than B on the basis of adverse effects
of any type in animal studies).
280 281
The main consideration overall is that unless there is significan
the infant from necessary maternal medication, breastfeeding
t risk to Table 28. Drugs used in the management of oral and
continued . should be dental conditions in pregnancy and breastfeeding
(cont.)
Drug TGA pregnancy Compatibility with
Drugs used in the management of oral category [NB1] breastfeeding [ NB 2 ]

and dental conditions in pregnancy and casein phosphopeptide-

amorphous calcium phosphate
unlisted compatible

breastfeeding cefalexin A compatible; may cause

diarrhoea in infant
Table 28 is intended to support the practical implementation compatible; may cause
of the drug cefazolin B1
recommendations in these guidelines, so only includes advice on diarrhoea in infant
those
drugs recommended in these guidelines. compatible [NB4]
celecoxib B3 [ NB3]
compatible
Table 28. Drugs used in the management of oral and chlorhexidine A

dental conditions in pregnancy and breastfeeding clindamycin A compatible; may cause

diarrhoea in infant
Drug TGA pregnancy Compatibility with
clobetasol propionate unlisted compatible, remove excess
category [NB1] breastfeeding [NB2] from nipple area before
aciclovir feeding
B3 compatible
compatible
 .
is u£d useu in ine management of oral and Table 28. Drugs used in the management of oral and
dental conditions in pregnancy and breastfeeding dental conditions in pregnancy and breastfeeding
(cont.) (cont.)
TGA pregnancy Compatibility with Drug TGA pregnancy Compatibility with
category [NB1] breastfeeding [NB2] category [ NB1] breastfeeding [NB2]
hydrogen peroxide unlisted C compatible; monitor infant for
compatible temazepam
ibuprofen drowsiness
C [NB3] compatible [ NB4J
tranexamic acid B1 compatible
lidocaine A compatible
lincomycin triamcinolone acetonide A compatible
A compatible; may cause
diarrhoea in infant trimethoprim + sulfamethoxazole C compatible if infant is healthy
lorazepam and older than 1month;
C compatible; caution with avoid if infant has glucose -
chronic use, monitor infant 6-phosphate dehydrogenase
for drowsiness (G6PD) deficiency, is
mepivacaine A younger than 1month or has
use with caution hyperbilirubinaemia
methylprednisolone aceponate C compatible compatible; may cause
vancomycin B2
metronidazole B2 compatible; may cause some diarrhoea in infant
bitterness in breast milk
NB1: Therapeutic Goods Administration (TGA) pregnancy categorisation is from the
Prescribing medicines in pregnancy database at the TGA website < www.tga.gov.au/
and may cause diarrhoea in
infant. Consider withholding
prescribing- medicines- pregnancy- database>. See also Australian categorisation of drugs
breastfeeding for 12 to
in pregnancy’ (p.278) for explanation of the categories.
24 hours after high single-
dose (2 g) treatment NB2: Definitions for compatibility with breastfeeding:
miconazole • compatible—there are sufficient data to demonstrate:
A compatible
- an acceptably low relative infant dose and/or
mometasone furoate B3 compatible - no significant plasma concentration in breastfed infants and/or cuo
naproxen C [NB3] - no adverse effects in breastfed infants. ."E
O
compatible [ NB4]
• use with caution—minor adverse effects in the breastfed infant have been 0
0
compatible reported, or there are insufficient data to demonstrate:
- an acceptably low relative infant dose and/or (/)

compatible 0
- no significant plasma concentration in breastfed infants and/or 0
compatible; monitor infant for - no adverse effects in breastfed infants. -o
Q
drowsiness However, the characteristics of the drug suggest significant adverse effects are unlikely.
Consider monitoring the infant for adverse effects.
c
0
use with caution; monitor
• avoid, insufficient data—the characteristics of the drug suggest significant
infant for drowsiness o
adverse effects are possible and there are insufficient data to demonstrate: E
compatible - an acceptably low relative infant dose and/or 0
c
- no significant plasma concentration in breastfed infants and/or •0JO
compatible; may cause
- no adverse effects in breastfed infants.
0
diarrhoea in infant
• avoid—there are sufficient data to demonstrate:
Q.
compatible - an unacceptably high relative infant dose and/or .E
0
- significant plasma concentration in breastfed infants and/or (/
>
compatible - significant adverse effects in breastfed infants. 3
to
3
compatible continued next page
a
continued next page
285
 Table 28. Drugs used in the management of oral and
dental conditions in pregnancy and breastfeeding Index
(cont.)
NB3: For discussion of nonsteroidal anti- inflammatory drug (NSAID)
use for musculoskeletal
conditions in women who are pregnant , see 'NSAIDs and reproductive
health in women' in
eTG complete .
NB4: If an NSAID is required in a breastfeeding patient, diclofenac
.
or ibuprofen is preferred
NB5: Tetracyclines are safe for use during the first 18 weeks of pregnancy (
16 weeks
postconception) after which they may affect the formation of
the baby's teeth and cause
discolouration.
A
abscess, dental see odontogenic amoxicillin
infections clinical pharmacology 40
aciclovir endocarditis prophylaxis 197
clinical pharmacology 43 odontogenic infection 83
herpes simplex 112 peri-implantitis 77
pregnancy & breastfeeding ( table) 282 pregnancy & breastfeedin g (table 282
)
see also antimicrobial drugs tooth avulsion 229
acrylate allergy 236 see also antimicrobial drugs
Acts (legislation) amoxicillin+ clavulanate
prescriptions 10 clinical pharmacology 40
acute coronary syndromes pregnancy & breastfeeding (table) 282
dental management of patients spreading odontogenic infection
with acute coronary syndromes 176 without severe or systemic
emergency management (box) 242 features 83
acute necrotising ulcerative with severe or systemic features 86
gingivitis 73 see also antimicrobial drugs
acute pain see pain amphotericin B
acute ulcerative gingivitis 73 candidiasis, oral 118
Addisonian crisis 163 clinical pharmacology 43
adrenal disorders pregnancy & breastfeedi ng table 282
( )
lz corticosteroid therapy 163 see also antimicrobial drugs
dental management of patients with173 ampicillin
0) adrenaline clinical pharmacology 40
O anaphylaxis (box) 239 endocarditis prophylaxis 197
u
•
drug for medical emergencies 234 pregnancy & breastfeedi ng table 282
( )
C
<u local anaesthesia 202 see also antimicrobial drugs
Tz pregnancy & breastfeeding (table) 282 anaesthetics, general 211
O airway, disposable 234 anaesthetics, local 201-9
airway obstruction addition of vasoconstrictors 202
CD emergency management 257 adverse effects 202
signs (table) 257 bleeding after oral surgery (table) 224
0 alcohol in mouthwash 58 choice of local anaesthetic (table) 205-6
.2 alendronate see medication- related dosing 206-9
3
CD osteonecrosis of the jaw maximum doses (table) 208
.2 allergy 236-9 example calculation (box) 207
^ antimicrobial allergy see antimicrobial pain, severe acute (adults) 140
4

0
Q
0
. common contact allergies
hypersensitivity
236
anaesthetics, topical
herpes, primary oral X
-oC1
( )
0 emergency management 237-9 mucocutaneous Ill
0 = alveolar osteitis 222 painful procedures 201
amalgam tattoo 104 ulcers , aphthous 109
286 appearance (photo) 105 ulcers, traumatic 106
287
 analgesic drugs antimicrobial hypersensitivity (cont. ) bicarbonate mouthwash
aspirin (cont. )
clinical pharmacology 43-53 misconceptions (box) 26 pregnancy & breastfeeding (table) 282 dry mouth 124
see also nonsteroidal antimicrobial resistance 2 :1 see also antithrombotic drugs hairy tongue 105
anti-inflammatory drugs, opioids antimicrobial stewardship 22 biopsy
asthma
and paracetamol strategies for dental practice ( table) 24 255 antibiotic prophylaxis
assessment of severity (table)
anaphylaxis 238 antiplatelet drugs see antithrombotic infective endocarditis (box) 195
dental management of patients
emergency management (box) 239 drugs, dental management with asthma 185 surgical (table) 190
angina antiresorptive drugs see 157
emergency management 255-7 bleeding risk (table)
dental management of patients medication-related box 256 see also procedures, oral or dental
with angina 176 osteonecrosis of the jaw AUG ( acute ulcerative gingivitis) 73 bisphosphonates see medication-related
emergency management (box) 242 antiseptic mouthwash 58-60 autoimmune conditions, dental osteonecrosis of the jaw
angioedema 237 antithrombotic drugs management of patients with 182 bleeding disorders
emergency management (box) 238 dental treatment of patients avulsed tooth see tooth avulsion dental management of patients
angular cheilitis 116 taking an antithrombotic drug 153-63 with a bleeding disorder 173
awake bruxism see bruxism
antifungal therapy 119 bleeding risk, patient-related (box) 156 bleeding gums
angular stomatitis see angular cheilitis bleeding risk, procedure -related triage & management by
antiangiogenic drugs see (table) 157 B medical practitioner (table) 264
medication- related local haemostatic measures (box) 158 back pain
bleeding, postoperative 222
osteonecrosis of the jaw antiviral drugs dental management of patients
182 sites of persistent bleeding (figure) 223
antibacterial drugs clinical pharmacology 43 with back pain
management (table) 224
clinical pharmacology 38-42 see also antimicrobial drugs basic life support flow chart (figure) 235
blindness, unilateral
see also antimicrobial drugs ANUG (acute necrotising ulcerative benzodiazepines
adverse effect of vasoconstrictor 252
antibiotic prophylaxis 189 99 gingivitis) 73 anxiolysis for dental procedures 216
-
emergency management (box) 253
surgical 189-92 anxiolysis 211-20 pharmacokinetic properties (table) 217
adverse effect of dermal fillers 253
indications (table) 190 drug choice 213 benzydamine
emergency management (box) 253
principles (box) 191 comparative table 214 clinical pharmacology 60
block anaesthesia (regional) 201
infective endocarditis 192 9 patient assessment 212 mucositis, oral 120
blood glucose monitor
-

indications: cardiac conditions patient instructions (box) 216 pregnancy & breastfeeding (table) 282
equipment for medical
(box) 194 patient management 215 primary oral mucocutaneous
emergencies 234
indications: procedures (box) 195 patients at increased risk of herpes 111
blood pressure monitor
antibiotics see antibacterial drugs adverse outcomes (box) 213 ulcers
equipment for medical
anticoagulant drugs see antithrombotic anxiolytic drugs see anxiolysis aphthous 109
emergencies 234
drugs, dental management aphthous ulcerative disease, traumatic 106
BMS (burning mouth syndrome) 146
75 antifungal drugs recurrent 107 benzylpenicillin
bone & metabolic disorders
M
clinical pharmacology 42-3 appearance (photo) 108 clinical pharmacology 39
dental management of patients
CD see also antimicrobial drugs apical periodontitis 81 pregnancy & breastfeeding (table) 282
O with bone & metabolic disorders 173
antimicrobial drugs location (figure) 81 spreading odontogenic infection
o botulinum toxin
c adverse effects 19-21 apixaban see antithrombotic drugs, with severe or systemic features 85
temporomandibular disorders 146
n explaining harms (box) 20 dental management see also antimicrobial drugs
breastfeeding
75 drug shortages 23 ARONJ see medication-related beta-lactam antibiotics
O
-
i
duration of therapy (box) 19 osteonecrosis of the jaw hypersensitivity (allergy) 31-4 dental treatment in a
breastfeeding woman 7
hypersensitivity (allergy) 25-37 arthritis, dental management of see also antimicrobial drugs,
c/j drug use (appendix) 281
o intravenous to oral switch (box) 18 patients with 182 cephalosporins and penicillins
breast implant
oral bioavailability (box) 17 articaine betamethasone dipropionate
=5 101 prevention of infection 191
patient resources 24 maximum dose (table) 208 lichen planus, oral
P broken filling 225
principles of use 15-24 pregnancy & breastfeeding (table) 282 pregnancy & breastfeeding (table) 282
3 broken tooth 225
see also antibacterial drugs, use in dentistry (table) 205 properties & potency (table) 55
bronchodilator, short-acting
P antifungal drugs and antiviral drugs see also anaesthetics, local see also corticosteroids, topical drug for medical emergencies 234
antimicrobial hypersensitivity 25-37 artificial saliva betamethasone valerate
<D BRONJ see medication-related
assessment (box) 29 dry mouth pregnancy & breastfeeding (table) 282
beta -lactam structure &
123
properties & potency (table) 55
osteonecrosis of the jaw x
2 mucositis, oral 120 bruxism 149
o
JZ side-chain (figure) 36 aspirin see also corticosteroids, topical triggers (box) 150
management of patients reporting drug for medical emergencies 234 bevacizumab see medication -related C
bupivacaine
penicillin hypersensitivity (figure) 32 chest pain 243 osteonecrosis of the jaw pregnancy & breastfeeding (table) 282
288 289
 bupivacaine (cont ) . cavity (dental) see caries, dental choking cotrimoxazole see
use in dentistry (table) 206 cefalexin emergency management (box) 259 trimethoprim -r- sulfamethoxazole
see also anaesthetics, local acute suppurative sialadenitis 92 chronic obstructive pulmonary disease CPP- ACP see casein
burning mouth syndrome 146 clinical pharmacology 38 ( COPD) , dental management of phosphopeptide-amorphous
burns, chemical endocarditis prophylaxis 198 patients with 186 calcium phosphate
ocular (emergency management) 250 pregnancy & breastfeeding (table) 283 chronic pain 130 CPR (cardiopulmonary resuscitation)
oral (causing traumatic ulcer) 106 see also antimicrobial drugs clavulanate see amoxicillin + clavulanate basic life support flow chart (figure) 235
cefazolin clindamycin cracked tooth 225
c acute suppurative sialadenitis 91 acute suppurative sialadenitis
91
crown
definition 270
cancer clinical pharmacology 38 initial intravenous therapy
dental management of patients endocarditis prophylaxis 198 oral continuation therapy 92 restorations see restorations, dental
with cancer pregnancy & breastfeeding (table) 283 clinical pharmacology 41 C -terminal telopeptide (CTX)
174
oral spreading odontogenic infection endocarditis prophylaxis 198 concentration 166
95-7
appearance (photo) 96-7 with severe or systemic features 86 pregnancy & breastfeeding (table) 283
with spread to bone see see also antimicrobial drugs spreading odontogenic infection D
medication-related celecoxib without severe or systemic dabigatran see antithrombotic drugs
osteonecrosis of the jaw acute dental pain in adults features 83
DAES see denture-associated
candidiasis, oral 114-9 mild to moderate pain 138 with severe or systemic features 86 erythematous stomatitis
angular cheilitis (angular stomatitis) 116 severe pain 139 see also antimicrobial drugs dapagliflozin, dental management of
antifungal therapy 118 pregnancy & breastfeeding (table) 283 clinical records 7
patients taking 179
denture- associated erythematous see also nonsteroidal clobetasol propionate deeper sedation 211
stomatitis (denture stomatitis) 117 anti-inflammatory drugs pregnancy & breastfeeding (table) 283 defibrillator, automated external
erythematous candidiasis cementum ( definition) 270 properties & potency (table) 55
115 equipment for medical
hyperplastic candidiasis 116 cephalexin see cefalexin see also corticosteroids, topical emergencies 234
median rhomboid glossitis 117 cephalosporins clopidogrel see antithrombotic drugs defibrillator (implantable) see cardiac
overview (table & photos) 115-7 clinical pharmacology 38 clotrimazole implanted electronic devices
pseudomembranous candidiasis 115 hypersensitivity (allergy) 31-5 clinical pharmacology 42 demeclocycline 57
risk factors (table) cephazolin see cefazolin angular cheilitis 119 denosumab see medication - related
114
candidosis see candidiasis, oral cetylpyridinium chloride 60 pregnancy & breastfeeding (table) 283 osteonecrosis of the jaw
carcinoma, squamous cell 95 cheilitis, angular 116 see also antimicrobial drugs dental abscess see odontogenic
cardiac arrest antifungal therapy 119 codeine infections
emergency management (box) chemical eye injuries 250 role in dentistry (table) 54 dental caries see caries, dental
243
cardiac implanted electronic devices chemotherapy, dental management of cold sores 112 dental cavity see caries, dental
75 patients having 174 conscious sedation 211
-
M dental management of patients with 177
chest pain COPD, dental management of
dental extractions see tooth extractions
0 cardiopulmonary resuscitation dental implants see implants
O basic life support flow chart (figure) 235 emergency management (box) 242 patients with 186 dental infections see odontogenic
o cardiovascular conditions chlorhexidine coronary artery bypass surgery, dental infections
e dental management of patients with caries, dental 70 management of patients with 176 dental floss 273
03
clinical pharmacology 59 coronary artery stents, dental

—
a cardiovascular condition 175-7 dental fracture 225
75
5 emergency management 240-3 gingivitis 72 management of patients with 176 dental numbering system 271
O caries, dental 63-70 hairy tongue (cause of) 105 coronary ischaemic syndromes Federation Dentaire Internationale
c /> diagnosis 63 mucositis, oral 121 dental management of patients with a ( figure) 272
CD
fluoride applications, elevated risk necrotising gingivitis 75 coronary ischaemic syndrome 176 dental pain see pain
ECD of caries (table) 68 odontogenic infection, localised emergency management 2 42 dental problems in medical
fluoride toothpaste (table) pericoronal infection 82 corticosteroids practice (table) 262-5
67
management 65 medication-related osteonecrosis dental management of patients dental procedures see procedures,
CD of the jaw, precautions for taking corticosteroids 163
pathology 63 oral or dental
.9 risk assessment patients at risk of (box) 171 dose adjustment for oral or see restorations,
64 dental restorations
CD stages ( figure & photo) 63, 64 pregnancy & breastfeeding (table) 283 dental procedures 164 dental
CL tooth avulsion 229 intradental 56 225 X
-oC<D
CD
casein phosphopeptide-amorphous dental trauma
CD calcium phosphate (CPP- ACP) chlorhexidine + fluoride systemic 57 dentine (definition) 270
£ caries, dental 69 caries, dental 70 topical 55-6 denture- associated erythematous
clinical pharmacology 61 pregnancy & breastfeeding application instructions (box) 56 stomatitis 117
pregnancy & breastfeeding (table) 283 (table) 283 properties & potency (table) 55 prevention 275
290 291
 denture E felypressin H
hygiene 275 local anaesthesia 202 haemostasis
elevated blood pressure, dental
sore areas beneath pregnancy & breastfeeding (table) 283 bleeding after oral surgery ( table) 224
management of patients with 175
triage & management by medical fibromyalgia, dental management of local measures for oral & dental
emergencies, medical see medical
practitioner ( table) 265 patients with 182 procedures (box) 158
emergencies
stomatitis 117 empagliflozin, dental management filling, dental see restorations, dental hairy leukoplakia, oral 181
diabetes of patients taking fissure (definition) 270 hairy tongue 105
dental management of patients 179
enamel (definition) 270 floss, dental 273 appearance (photo) 106
with diabetes 178 80 flucloxacillin halitosis 125-7
endocarditis prophylaxis see antibiotic
-

box 180 acute suppurative sialadenitis common causes (box) 125-6

prophylaxis, infective endocarditis
hyperglycaemia 245 initial intravenous therapy 90 head and neck radiotherapy, dental
endocrine conditions
hypoglycaemia 244 oral continuation therapy 91 management of patients
dental management of patients with
ketoacidosis an endocrine condition 173, 178 clinical pharmacology 39 undergoing 175
prevention in patients taking pregnancy & breastfeeding (table) 283 heart disease see cardiovascular
emergency management 244-5
SGLT2 inhibitors 179 enoxaparin see antithrombotic drugs see also antimicrobial drugs conditions
emergency management 245 fluoride heart failure, dental management
diagnosis, principles of °1 epilepsy
applications, elevated risk of caries of patients with 177
dental management of patients with
diagnostic tests, principles of 3 ( table) 68 heparin see antithrombotic drugs
epilepsy 183
diazepam clinical pharmacology 60 hepatitis (viral), dental management
emergency management 247
anxiolysis for dental procedures 218 box caries, dental 66-9 of patients with 187
pharmacokinetic properties (table) 248
217 epinephrine see adrenaline concentration in toothpaste (table) 67 herpes labialis see herpes simplex,
pregnancy & breastfeeding (table) 283 equipment for medical emergencies 234 pregnancy & breastfeeding (table) 283 oral mucocutaneous
see also benzodiazepines ertugliflozin, dental management of fluorosis, dental 66 herpes simplex, oral
dicloxacillin patients taking fractures mucocutaneous 110-2
179
acute suppurative sialadenitis 91 erythema migrans 103 restoration, dental 225 appearance ( photo) 110
clinical pharmacology 29 erythematous candidiasis, oral 115 tooth 225 primary 110
pregnancy & breastfeeding (table) 283 erythroplakia, oral 99 recurrent 112
see also antimicrobial drugs herpetic gingivostomatitis see herpes
dipyridamole see antithrombotic drugs
appearance (photo) 99 G
euglycaemic diabetic ketoacidosis see general anaesthesia 211 simplex, oral mucocutaneous
direct oral anticoagulant see herpetiform aphthous ulcers 108
diabetes, ketoacidosis geographic tongue 103
antithrombotic drugs examination, principles of 104 history-taking
DKA (diabetic ketoacidosis) 3 appearance (photo)
see extractions, tooth see tooth extractions gingiva (definition) 270 principles 2
diabetes, ketoacidosis eye injuries MRONJ risk assessment (box) 167
DOAC see antithrombotic drugs 250-2 gingival bleeding
TO
chemical 250 triage & management by medical HIV infection, dental management
doxycycline of patients with 181
emergency management (box) 251 practitioner (table) 264
9
O
clinical pharmacology 42 foreign body on surface 251 gingival hyperplasia HPV-related lesions, oral 100
pregnancy & breastfeeding (table) 283 emergency management (box) appearance (photo) 100
T3 251 triage & management by medical
c tooth avulsion 229 penetrating object 252 practitioner (table) 264 HSV see herpes simplex,
TO see also antimicrobial drugs oral mucocutaneous
drug use (principles)
emergency management (box) 252 gingivitis 71
TO
location (figure) 81 human papilloma virus see HPV-related
O drugs of dependence 9 lesions, oral
F necrotising 73
off-label prescribing 5
co facial nerve palsy gingivostomatitis, herpetic 110 hydrocortisone
o role in dentistry 4g
_
angular cheilitis 119
sporting authorities g emergency management 248 glossitis, median rhomboid 117
aphthous ulcers 109
o drug holidays (bisphosphonates) 172 facial nerve weakness, dental glucose
pregnancy & breastfeeding (table) 283
3
CD
drug information
resources
15 61 -01 management of patients with 183
famciclovir
drug for medical emergencies
pregnancy & breastfeeding (table) 283
234
properties & potency (table) 55
244 see also corticosteroids, topical
I drugs for medical emergencies clinical pharmacology 55 hypoglycaemia
234 hydrogen peroxide
dry mouth pregnancy & breastfeeding (table) 283 glyceryl trinitrate
121-4 242, 243 clinical pharmacology 59
0
drugs associated with (box) herpes simplex 112 chest pain

^
ci 122 pregnancy & breastfeeding ( table) 283 necrotising gingivitis 74
. X
TO practical advice for patients (box) 124 see also antimicrobial drugs pregnancy & breastfeeding (table) 284
0 dry socket Federation Dentaire Internationale drug for medical emergencies 234
-TO 222 gums, bleeding see gingival bleeding hyperplastic candidiasis, oral 116 c
dental numbering system 271 hyperglycaemia
figure 272 gums, enlarged see gingival hyperplasia
emergency management 245
292 293
 hypersensitivity
hypertension
see allergy
see elevated blood
inhaled objects (cont.)
prevention (box)
-
liver disease (end stage), dental
management of patients with 181, 187
methylprednisolone aceponate
pregnancy & breastfeeding (table) 284
258
pressure signs (table) 257 local anaesthetics see anaesthetics, local properties & potency (table) 55
hyperthyroidism see thyroid disorders interdental cleaning local analgesia see anaesthetics, local see also corticosteroids, topical
273
hyperventilation syndrome metronidazole
254 intravenous sedation 211 lorazepam
emergency management (box) 254 ischaemic heart disease see coronary anxiolysis for dental procedures 218 clinical pharmacology 42
signs and symptoms (table) 254 ischaemic syndromes pharmacokinetic properties (table) 217 necrotising gingivitis 74
hypoglycaemia 244 pregnancy & breastfeeding (table) 284 odontogenic infections, spreading
emergency management (box) 244 see also benzodiazepines without severe or systemic features 83
hypothyroidism see thyroid disorders J 225 with severe or systemic features 85
jaw clicking, locking, pain lost filling
lubricants, topical peri-implantitis 77
triage & management by medical
I dry mouth 123 pregnancy & breastfeeding (table) 284
practitioner (table) 263
ibandronic acid see medication- related mucositis, oral 120 see also antimicrobial drugs
joint prosthesis
osteonecrosis of the jaw Ludwig angina 84 miconazole
prevention of infection 191 119
ibuprofen angular cheilitis
acute dental pain ,
^uiididiasis oral
118
K M clinical pharmacology 42
adults: mild to moderate pain 138 malignancies
adults: severe pain kidney disease (end-stage), dental pregnancy & breastfeeding (table) 284
139
management of patients with 181 dental management of patients with 174 see also antimicrobial drugs
children 140 oral cancer 95
children s doses table)
’ ( knocked- out tooth see tooth avulsion minimal sedation see anxiolysis
142 malnutrition, dental management mometasone furoate
pregnancy & breastfeeding (table) 284 of patients with 181
temporomandibular disorders L pregnancy & breastfeeding (table) 284
145 malodour, oral see halitosis 55
see also nonsteroidal latex allergy properties & potency (table)
236 management, principles of 1
anti - inflammatory drugs legislation 1 see also corticosteroids, topical
box mouth ulcers see ulcers, oral
illicit drugs, dental management of prescriptions 9 masticatory muscle disorders see
patients using mouthwash 58
185 leukoplakia, oral 98 temporomandibular disorders oral hygiene 274
immune compromise appearance (photo) 98 maxillofacial procedures see oral
dental management of leukoplakia, oral hairy MRONJ see medication-related
181 maxillofacial procedures osteonecrosis of the jaw
immunocompromised patients 181 lichenoid lesion, oral 103 maxillofacial trauma 230
immunosuppressive therapy, dental mucoperiosteal flap
appearance (photo) 102 median rhomboid glossitis 117
bleeding risk (table) 157
management of patients taking 182 lichen planus, oral 101 medical conditions, dental
implanted cardiac device, dental see also procedures, oral or dental
appearance (photo) 102 management of patients with 153-88 mucosal disease, oral 93 124
-
15
management of patients with 177 lidocaine medical emergencies 93
implants, dental pregnancy & breastfeeding (table) 284 assessment
drugs & equipment 234 94
antibiotic prophylaxis for insertion ‘red flag’ features (box)
<D solution for injection management in dental practice 233-59 mucositis
O infective endocarditis (box) 195 maximum dose ( table) medication-related osteonecrosis
surgical (table)
208 oral 120
o 190 use in dentistry (table) 205 of the jaw (MRONJ) 164-73
c peri-implant 76
cu bleeding risk with insertion ( table) 157 viscous solution prevention 170-3
broken or loose mucous membrane pemphigoid 113
15 mucositis, oral 120 management advice (box) 171
appearance (photo) 113
triage & management by medical primary oral mucocutaneous risk assessment 166-70
O multiple myeloma see
practitioner (table) 264 herpes 111 figure 168 medication related
-
(ft medication-related osteonecrosis aphthous ulcers 109 history-taking (box) 167
0
of the jaw osteonecrosis of the jaw
166, 171 see also anaesthetics, local 165
M0 peri-implant diseases 76 life support flow chart (figure) 235
stages (table)
mepivacaine
musculoskeletal disorders (chronic) ,
5 swelling, pain or bleeding around lignocaine 208
dental management of patients
see lidocaine maximum dose (table) 182
0 triage & management by medical lincomycin with
C3 pregnancy & breastfeeding (table) 284 myeloma (multiple) see
practitioner (table) 264 acute suppurative sialadenitis 91 use in dentistry (table) 205
.2 see also procedures, oral or dental medication-related
clinical pharmacology 41 see also anaesthetics, local
infiltration anaesthesia pregnancy & breastfeeding (table) 284 osteonecrosis of the jaw
0 201 metastases to the bone see
o inflammatory conditions, dental myocardial infarction X
spreading odontogenic infection medication-related <D
.

ro
management of patients with 182 with severe or systemic features 86 dental management of patients with
osteonecrosis of the jaw “O
c
0
JZ inhaled objects see also antimicrobial drugs a history of myocardial infarction 176
methaemoglobinaemia emergency management (box) 242
emergency management 257 emergency management (box) 246
box 259 methoxyflurane 214
294 295
 N nystatin oral maxillofacial procedures .
pain (cont )
narcotics candidiasis, oral antibiotic prophylaxis adults 138
see opioids 118-9
naproxen clinical pharmacology infective endocarditis (box) 195 children 140
43
pregnancy & breastfeeding (table) 284 pregnancy & breastfeeding (table) 284 surgical (table) 190 differential diagnoses (table) 132-6
see also nonsteroidal see also antimicrobial drugs bleeding risk (table) 157 drug choice (box) 137
anti-inflammatory drugs see also procedures, oral or dental definitions 129-30
neck cancer, dental management of oral or dental procedures see teething 267
0 procedures, oral or dental see also bruxism, burning mouth
patients with 174 obstruction of the airway see airway see pain syndrome and temporomandibular
neck pain, dental management of oral pain
patients with
obstruction organ transplant, dental management disorders
182 obstructive sleep apnoea, dental
necrotising periodontal disease 73-5 of patients with 182 pamidronate see medication -related
management of patients with 187 osteonecrosis of the jaw
necrotising gingivitis 73-5 orofacial pain see pain
ocular emergencies paracetamol
necrotising periodontitis 74 orthodontic treatment
emergency management 250-3 157 acute dental pain
necrotising stomatitis 74 bleeding risk (table)
odontogenic infections 79 87
-
see obstructive sleep apnoea adults: mild to moderate pain 138
nerve injuries features & management overview
OSA
local anaesthetic complication osteitis, alveolar see alveolar osteitis adults: severe pain 139
203 (table) 80 140
neurological conditions osteoarthritis, dental management children
localised 81-2 182 children’s doses (table) 143
dental management of patients of patients with
anatomical location ( figure) 81 see clinical pharmacology 49
with a neurological condition 183-4 osteonecrosis of the jaw
dental treatment options (box) 82 medication - related pregnancy & breastfeeding (table) 284
emergency management 246-9 postoperative 87
neuropathic pain osteonecrosis of the jaw temporomandibular disorders 145
129 spreading 82-6
neurotoxicity osteoporosis, dental management paraesthesia
Ludwig angina 84 173 triage & management by
local anaesthetic complication 203 of patients with
without severe or systemic 175 medical practitioner (table) 262, 265
nitrous oxide osteoradionecrosis
features 32
oxazepam paralysis of periocular muscles 248
anxiolysis for dental procedures
(

219 with severe or systemic features 84

pregnancy & breastfeeding (table) 284 anxiolysis for dental procedures 218 emergency management (box) 249
off-label prescribing 5 right-sided facial palsy (photo) 249
nociceptive pain 129 pharmacokinetic properties (table) 217
opioids 50-3 parotitis 89-92
nociplastic pain 129 pregnancy & breastfeeding (table) 284

drugs
-
nonsteroidal anti inflammatory
acute dental pain (adults)
drug choice
137, 139
53
see also benzodiazepines
oximetry see pulse oximeter
pemphigoid, mucous membrane 113
pemphigus vulgaris see eTG complete
44-9 advantages & disadvantages of
acute dental pain oxycodone penciclovir 43
137-41 commonly used opioids
adverse effects 45 pregnancy & breastfeeding (table) 284 Penicillin G see benzylpenicillin
( table) 54
cardiovascular toxicity 46 role in dentistry (table) 54 Penicillin V see phenoxymethylpenicillin
75 harms 51 severe acute dental pain in adults 139 penicillins
gastrointestinal toxicity 47 adverse effects (table) 52 clinical pharmacology 38-40
in elderly people 47 see also individual drugs see also opioids
0)
in pregnancy & breastfeeding 47-8 oxygen hypersensitivity (allergy) 31-7
o oral cancer see cancer, oral 256 see also antimicrobial drugs
o renal toxicity 46 oral candidiasis acute asthma
c
see candidiasis, oral anaphylaxis 239 periapical abscess 81
table 44 oral erythroplakia see erythroplakia, oral
TO
clinical pharmacology chest pain 243 dental treatment options (box) 82
44 oral hairy leukoplakia 181
75 drugs commonly used (table) drugs & equipment for medical location ( figure) 81
-
i 44 oral hygiene 273-5 emergencies 234 periapical inflammation see apical
O contraindications (box) 46 oral HPV-related lesions see periodontitis
drug choice 48 methaemoglobinaemia 246
HPV-related lesions, oral 247 periapical surgery
0 see also individual drugs oral leukoplakia see leukoplakia, oral
stroke
E NOAC see antithrombotic drugs use with nitrous oxide 220 antibiotic prophylaxis
oral lichenoid lesion see lichenoid 195
CD
non-vitamin K antagonist oral infective endocarditis (box)
5 lesion, oral surgical (table) 190
3 anticoagulants see antithrombotic oral lichen planus see lichen planus, oral P
C3 bleeding risk ( table) 157
drugs oral malodour P2Y12 inhibitors see antithrombotic
.2 NSAIDs see nonsteroidal
see halitosis
oral mucocutaneous herpes simplex see drugs
see also procedures, oral or dental
anti-inflammatory drugs pericoronal abscess 81
0 herpes simplex, pacemaker see cardiac implanted 82 x
a numbering system, dental 271 dental treatment options (box)
oral mucocutaneous electronic devices 81 CD
2 numbness, oral location ( figure)
0 oral mucosal disease see mucosal Paget disease see medication-related pericoronal infection 81 O
a triage & management by osteonecrosis of the jaw C
disease, oral dental treatment options (box) 82
medical practitioner (table) 262, 265 oral mucositis see mucositis, oral pain
location ( figure) 81
acute dental 130-43 297
296
 peri -implant diseases 76-7 prilocaine rheumatoid arthritis, dental (SGLT2) inhibitors, dental
peri- implant mucositis 76 see also anaesthetics, local management of patients with 182 management of patients taking 179
peri- implantitis 77 risedronate see medication-related spacer devices
periodontal abscess 75 procedures, oral or dental osteonecrosis of the jaw acute asthma 256
location (figure) 81 antibiotic prophylaxis 189-99 rivaroxaban see antithrombotic drugs equipment for medical
periodontal diseases 71-6 infective endocarditis (box) root of tooth (definition) 270 emergencies 234
195
periodontal ligament ( definition) 270 surgical ( table) root canal system infection see splints
190
periodontal procedures anxiolysis 211-20 odontogenic infections bruxism 150
antibiotic prophylaxis bleeding risk (table) root canal therapy obstructive sleep apnoea 187
157
infective endocarditis (box) 195 complications bleeding risk (table) 157 temporomandibular disorders 145
221-4
surgical (table) 190 alveolar osteitis (dry socket) see also procedures, oral or dental sporting authorities & drug use 6
222
bleeding risk (table) 157 bleeding ropivacaine spreading odontogenic infection see
222-4
see also procedures, oral or dental pain & swelling 221 use in dentistry (table) 206 odontogenic infection, spreading
periodontal surgery local anaesthesia 201-9 pregnancy & breastfeeding (table) 284 squamous cell carcinoma see cancer,
antibiotic prophylaxis pain, post -procedural 137-43 see also anaesthetics, local oral
infective endocarditis (box) 195 sedation, minimal 211-20 rubber allergy 236 stents (coronary artery), dental
surgical (table) 190 prophylactic antibiotic therapy see management of patients with 176
bleeding risk (table)
see also procedures, oral or dental
157
prosthetic joint
antibiotic prophylaxis s stomatitis
angular 116
periodontitis salbutamol denture-associated erythematous 117
72 prevention of infection 191 256
aggressive (early-onset) acute asthma mucositis 120
72 pseudomembranous candidiasis 115 234
location figure)
( drugs for medical emergencies necrotising 74
81 psychiatric disorders, dental
phenoxymethylpenicillin pregnancy & breastfeeding (table) 284 stroke
management of patients with 184
clinical pharmacology saline dental management of patients
39 psychological disorders, dental 222
pregnancy & breastfeeding (table) 284 alveolar osteitis with a history of stroke 183
management of patients with 184 228
spreading odontogenic infection avulsed tooth emergency management 246
pulp, dental (definition) 270 82
without severe or systemic features 83 pericoronal infection, localised box 247
pulse oximeter 76
see also antimicrobial drugs periodontal abscess substance use disorder, dental
equipment for medical emergencies 234
plaque, dental pain & swelling after oral surgery 221 management of patients with 185
caries saliva, artificial see artificial saliva
sulfonamide hypersensitivity 35
63 121
halitosis 126
R salivary gland hypofunction sunitinib see medication-related
oral hygiene radiographs (intraoral) & pregnancy 7 salivary gland infection 89-92 osteonecrosis of the jaw
273
gingivitis radiotherapy (head and neck) , salivary gland swelling surgery, oral see procedures,
71 90
dental management of patients potential causes (box)
75 Poisons Standard 10
undergoing sedation
oral or dental
povidone-iodine 60 175 surgical prophylaxis see antibiotic
0) prasugrel see antithrombotic drugs records, clinical 7 intravenous 211 prophylaxis, surgical
a prednisolone see corticosteroids, recurrent aphthous ulcerative disease 107 minimal see anxiolysis
surgical extractions see tooth extractions
D referral 6 conscious 211
c dental management of patients taking and procedures, oral or dental
03 prednisone see corticosteroids, dental regional block anaesthesia 201 deeper 211 surgical removal of soft or hard tissue,
Regulations (legislation) seizures
75 management of patients taking or bone
i
O
- pregnancy prescriptions 10 emergency management 247
antibiotic prophylaxis
relative analgesia see nitrous oxide box 248 195
dental treatment 7 infective endocarditis (box)
( /)
drug use (appendix) remineralising agents see also epilepsy surgical (table) 190
CD 277
caries, dental SGLT2 inhibitors, dental management
Eo table 282
clinical pharmacology
66-9
60-1 of patients taking 179
bleeding risk (table) 157
radiographs, intraoral 7 see also procedures, oral or dental
resistance to antimicrobials 21-2 sialadenitis, acute suppurative 89-92
=
CD
5 prescriptions & prescription writing 9-14
Acts & regulations 10
respiratory conditions Sjogren syndrome 121 surgical site infections
prevention see antibiotic
dental management of patients sleep bruxism see bruxism
.2 example format ( figure) 14 prophylaxis, surgical
legislation with a respiratory condition 185-7 snoring
treatment 87
9
CD
patient information emergency management 254-9 dental management of patients swallowed objects x
Q. 13
2 restorations, dental who snore 187 CD
CD
prilocaine
maximum dose ( table) bleeding risk (table) 157 sodium bicarbonate mouthwash see
emergency management 257
259
-o
208 box £
jC pregnancy & breastfeeding (table) 284 fracture 225 bicarbonate mouthwash
prevention (box) 258
loss 225 sodium chloride see saline 221
use in dentistry (table) 205 swelling, post -procedural
298 see also procedures, oral or dental sodium-glucose co-transporter 2 299
 syncope 240 tramadol vasoconstrictors
emergency management ( box) 241 role in dentistry ( table) 54 bleeding after oral surgery
see also opioids (management) 224
T tranexamic acid local anaesthesia 202
tapentadol bleeding after oral surgery (table) 224 unilateral blindness (adverse
role in dentistry (table) local haemostatic measures (box) 158 effect) 252
54
see also opioids pregnancy & breastfeeding (table) 285 veneers, dental see restorations, dental
teeth cleaning see oral hygiene transplant (organ), dental Vincent disease see gingivitis,
management of patients with 182 necrotising
teething 267
temazepam traumatic oral ulcers 106 vinegar
anxiolysis for dental procedures persistent ulcer (photo) 107 denture hygiene 275
218
pharmacokinetic properties (table) 217 trauma vision loss see blindness, unilateral
pregnancy & breastfeeding (table) 285 dental 225-9 viral hepatitis, dental management
see also benzodiazepines maxillofacial 230 of patients with 187
temporomandibular disorders trench mouth see gingivitis, necrotising
triamcinolone acetonide
(TMD) 144-6
pregnancy & breastfeeding (table) 285 W
signs & symptoms ( table) 144 water jets 273
terminology, dental ( figure) properties & potency (table) 55
270 warfarin see antithrombotic drugs
third molar surgery see also corticosteroids, intradental see third
and corticosteroids, topical wisdom tooth removal
antibiotic prophylaxis molar surgery
infective endocarditis (box) triclosan 60 273
195 wood sticks, interdental
surgical (table) 190 trigeminal neuralgia, dental
bleeding risk (table) management of patients with 184
157
see also procedures, oral or dental trimethoprim + sulfamethoxazole X
acute suppurative sialadenitis 92 xerostomia 121-4
thrush, oral see candidiasis, oral
thyroid disorders, dental management clinical pharmacology 40
of patients with 173 hypersensitivity (allergy)
pregnancy & breastfeeding (table) 285
35 z
ticagrelor see antithrombotic drugs zoledronic acid see medication-related
TMD see temporomandibular disorders see also antimicrobial drugs osteonecrosis of the jaw
tongue cleaning 274 trismus 151
tooth avulsion 226-9
avulsed teeth (photos) 227 U
endocarditis prophylaxis (box) 195 ulcers, oral
75 initial assessment & management erythema multiforme see eTG complete
(box) 226 mucous membrane pemphigoid 113
®
O toothbrushes 274 pemphigus vulgaris see eTG complete
o tooth cleaning see oral hygiene recurrent aphthous ulcerative

75
O
^-
i
tooth decay
tooth eruption
primary teeth ( figure)
see caries, dental
267
268
disease
traumatic
viral
107
106
see herpes simplex, oral
secondary teeth (figure) 269 mucocutaneous
c/j tooth extractions unilateral blindness see blindness,
2: antibiotic prophylaxis unilateral

^ infective endocarditis (box)

surgical (table)
195
190
urticaria
emergency management (box)
237
238

^g
bleeding risk (table) 157
see also procedures, oral or dental
0
tooth fracture
V
- 225
vancomycin
<D tooth infection see odontogenic infection x
acute suppurative sialadenitis 90
toothpaste
clinical pharmacology 41 <1)
fluoride concentration (table) 67 T3
d3 pregnancy & breastfeeding (table) 285 C
see also oral hygiene
topical anaesthetics see anaesthetics,
see also antimicrobial drugs
topical 301
300
 r

Oral and Dental 3 includes:

Principles of diagnosis and management in dental practice
• Dental prescriptions and prescription- writing
• Practical information on using drugs in dentistry
• Dental caries
• Periodontal and peri-implant diseases
• Acute odontogenic infections
• Salivary gland infections
• Oral mucosal disease
• Halitosis
• Orofacial pain
•
Bruxism
• Trismus
•
Dental management of patients with medical conditions
• Antibiotic prophylaxis for dental procedures
• Local anaesthetics in dentistry
Anxiolysis (minimal sedation) for dental procedures
• Complications after oral surgery
• Dental and maxillofacial trauma
• Medical emergencies in dental practice
• Guidance for medical practitioners managing oral and
dental issues

Provided by

CIATION