Oral and Dental

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2012
Management Guidelines: Developmental Disability
VERSION 2

Therapeutic Guidelines Limited , Melbourne

Tnerapeutic
Guidelines
Copyright 2012 Therapeutic Guidelines Lim ited
All rights reserved. Apart from any fa ir dealing for the purpose of private Contents
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Tables, boxes, figures and photos ......... ............. .. ... .. ... .. .. .. ......... ... ..... vii
Suggested citation:
Oral and Dental Expert Group .............. .. .. ........................................... xi
Oral and Dental Expert Group. Therapeutic guidelines: oral and dental.
Infective Endocarditis Prophylaxis Expert Group (July 2008) .......... xiii
Version 2. Melbourne: Therapeutic Guidelines Limited; 2012.
Acknowledgments ........ ............... .......................... ... ..... ................... . xiv

First published 2007 Endorsements ....... .................. .. .... ..................................................... xvii

Reprinted 2008 About Therapeuti c Guidelines Limited ............................................. xix
Reprinted 2009
Reprinted 20 10 Board of directors ofTGL .. ................. ................. .. ......... ................ xxvi
Version 2 20 12
Reprinted 2013 Chapters
Principles of diagnosis and prescribing ....... ... ... ..... .. ............................ 1
Prescriptions and prescription-writing ........ ....... .. ... ................... ......... .. 5
Getting to know yo ur drugs ................ ........ .......................... ...... ........ 13
Dental caries............ ......... ......... ................... .... ..... ................ .............. 47
Periodontal disease ............................. .. ........................ ................ ....... 55
Acute odontogenic and sali vary gland infections ............ ........ ........... 61
Publisher and distributor:
Therapeutic Guidelines Limited Oral mucosal disease ........... ................... .. ........... ................................ 71
Ground Floor, 473 Victoria Street Orofacial pain ............ ... ... ... ...... ........................ ... ............ .... .. ......... ..... 91
West Melbourne, Victoria 3003
Australia Halitosis ... .... .................. ..... .......... ... ...... ..... ................. .................. ..... 97

Telephone: (03) 9329 1566 Antibiotic prophylaxis ....... ...... ..... .. ............ ........... ... ......... .. ....... .. .. .. 101
Facsimile: (03) 9326 5632 Local anaesthesia ................................. .. .... .............. .......................... Ill
Freecall : 1800 061 260
Emai l: sales@tg.org.au Anxiolysis and sedation for dental procedures .. ..... ........ ....... ... .. ...... 121
Website: <www.tg.org.au> Post-treatment pain management .................... ................................. . 127
I >e ntal management of patients with medical conditions ........... ...... 137
ISBN : 978-0-9808253- 1-2
Medi cal emergencies in dental practice ........................................ .... 167
J;j MIX
Paper from
responsible sources Mii nagement of dental problems for medical practitioners .............. 191
Printed in Australia by McPherson's Printing Group FSC
www.bc.org FSC C001695
v
 Appendices
Appendix I. Drugs and sport .. ....... ....... ..... ........ ...... ....... ...... ... ... ...... 203
Appendix 2. Dental pro.cedures and drugs during pregnancy and
breastfeedmg ............. ... ... .. ... ... .. ..... ... ... .............. ...... .... 20S
Abbreviations and acronyms .. .... .... .. ..... ...... .. ...... .... ...... ... ..... ........... 2IS
Glossary ................................ ... ... ........................................ ........ ...... 217
Index .. ....... .. ................. ... ....................... .................. .. ............ ..... ...... 223
Request for comment on guidelines .................................................. 239
vi
Tables, boxes, figures and
photos
Tables
Table I. Common antimicrobial drugs used in dentistry .... .......... .... .. 17
Table 2. Adverse effects of nonsteroidal anti-inflammatory drugs ..... 29
Table 3. Adverse effects of opioids ..................................................... 33
Table 4. Properties of topical corticosteroids used on the
oral mucosa ........................................................................... 36
Table 5. Examples of topical applications and how they can be
used to reduce caries in patients at high risk of caries .......... 52
Table 6. Predisposing factors in oral candidosis ................................. 83
Table 7. Oral preparations for the management of oral mucositis
and dry mouth ................ .. .... ........ ...... .. .......... .............. .. .. ..... 87
Table 8. Denta l procedures and their requirement for endocarditis
prophy laxis in patients with cardiac conditions listed in
Box 10 ........... ... .... .... ...... .......... ... ......... .......... ............ ......... 104
Table 9. Maximum safe doses oflocal anaesthetics available
in dental cartridges in Australia .............. .... .. .. .................... 118
Table 10. Advantages and disadvantages of oral anxio lytics
and sedatives ..................................................................... 122
Table 11. Mean body weight for age in children .............................. 136
Table 12. Interpretation offasted morning serum C-terminal
telopeptide (CTX) concentration .... .. ........ ...... .......... .. ...... 155
Table 13. Drugs commonly used in psychiatric disorders .... ...... ...... 165
Table 14. Signs and symptoms of hyperventilation syndrome ......... 171
Table 15. Initial assessment of the severity of an acute asthma
attack in adults and children .............................................. 172
Table 16. Signs of airway obstruction ............ ............. ....... ... ............ 175
Table 17. Symptoms ofhypoglycaemia ............ ..... ... .... ........... ..... .... l79
vi i
 Table 18. A guide to diagnosing acute dental pain and suggestions
for initial management by medical practitioners .............. . 192
Table 19. The ' dos and don 'ts' ofmanaging an avulsed tooth ....... .. 197
Table 20. Management of the bleeding tooth socket .. ...................... 200
Table 21. Common dental problems for which patients may
present to their medical practitioner.. ................................ 201
Table 22. Drug use in pregnancy and breastfeeding ......................... 210
Boxes
Box I. General principles of managing oral and dental conditions ...... 1
Box 2. Aspects of the examination and diagnosis that should be
included in clinical records ............................ ...... .... ................ .. 3
Box 3. General principles of antimicrobial use .................................. 15
Box 4. The antimicrobial creed ............................................ .. ............. 16
Box 5. Risk factors for NSAID-i nduced upper gastrointestinal
bleeding or perforation ............................................................ 29
Box 6. Poi~ts to co~sider when prescribing topical intraoral
corticosterOids ....................... .......................... ................... ...... 38
Box 7. !reat~ent options for acute localised odontogenic
mfectwns ....................................................................... ...... .... 63
Box 8. Practical advice for patients with dry mouth ........................... 89
Box 9. Some common causes of halitosis ........................................... 98
Box 10. Cardiac conditions associated with the highest risk of
adverse outcomes from endocarditis .......... ........ ................. 102
Box 11. Instructions for patients having oral anxiolysis or
sedation, or inhalational sedation ........................................ 123
Box 12. How the recommendations for pain management
were derived ............................... ......................................... 131
Box 13. Combining ibuprofen with paracetamol (or
paracetamol+codeine) for enhanced pain management
in adults .... .. ............................. .................... ........................ 134
Box 14. Management of patients taking warfarin who require
minor oral surgery .............................................................. . 141
viii
Box 15. Approach to general dental treatment for a patient
with stable diabetes ............................................................. 149
Box 16. History-taking relating to bisphosphonates ......................... 155
Box 17. Management of syncope ......................................... ...... .. 168
Box 18. Management of angina or an acute coronary syndrome ..... 170
Box 19. Management of cardiac arrest ..... ..... ................ ...... ....... 170
Box 20. Management of hyperventilation syndrome ........................ 171
Box 21. Management of an acute asthma attack .............................. 173
Box 22. Management of an inhaled or swallowed object .................... \75
Box 23. Management of acute stroke ................... ............. ... ............ 177
Box 24. Management of seizures ...................................................... 178
Box 25. Management of hypo glycaemia ...................... .. ...... ... ......... 179
Box 26. Management of urticaria ............................. ............ ............ 181
Box 27. Management of anaphylactic and anaphylactoid
reactions ... ......... .. ....... .. .......................................... ......... 182
Box 28. Management of chemical eye injuries .......................... ....... 184
Box 29. Management of foreign bodies lodged on the surface
ofthe eye .. .................................... ............. ............ .............. 185
Box 30. Management of penetrating eye injuries ............................. 185
Box 31. Management of temporary paralysis of the periocular
muscles ............................ ......................... ... ........................ 187
Box 32. Management of unilateral blindness ................................... 187
Figures
Figure 1. Example of the format required for a legal prescription
written by a dentist... ....................... ... .......... .. .. .. .. .. ................ 9
Figure 2. Schematic diagram of localised odontogenic infections
and the stages of dental caries ............................................. 62
Figure 3. Schematic representation of pain relief with different
analgesics using the ' third molar model' .. .. ......... .............. 131
Figure 4. Example of instructions for a patient taking ibu~rofen
plus paracetamol following dental treatment (usmg a
ix
timeline) .................. ....... ... ......... .......... ... ..... ..... ... .. 13 5
 Figure 5. Basic life support flow chart ............ .................. ........... .. ... 183
Oral and Dental Expert Group
Figure 6. Schematic diagram of the tooth socket and possible
sites of persistent bleeding after tooth extraction ......... ..... 199

Photos
Professor Robert Moulds (chairman)
Photo 1. Leukoplakia of the ventral surface of the tongue and Medical Advisor, Therapeutic Guidelines Limited, Melbourne, Victoria
floor of mouth .............. ...... ..... .. .. .... .......... .. ....... ............... .... 73
Winthrop Professor Paul Abbott
Photo 2. Squamous cell carcinoma of the left ventral surface Winthrop Professor of Clinical Dentistry, Program Director
of the tongue ...................................................... ... ................ 73 (Endodontics), Director of Postgraduate Studies and Research,
and Deputy Head of School, School of Dentistry, The University
Photo 3. Oral lichen planus of the left buccal mucosa showing
of Western Australia, Nedlands, Western Australia
characteristic white striations .... .. .................. ....................... 74
Associate Professor Christopher Daly
Photo 4. Oral hairy leukoplakia of the right lateral margin of
Discipline of Periodontics, Faculty of Dentistry, The University of
the tongue ....... ....... ... ................................... ........ ............ ..... 76
Sydney, Sydney, New South Wales
Photo 5. Longstanding traumatic ulcer of the right posterior
Dr John Dowden
lateral margin of the tongue .. ... ....... ........ .. .... .. ............ ... ..... .. 77
Editor, Australian Prescriber, Deakin, Australian Capital Territory
Photo 6. Patient with right-sided facial palsy ............... ....... ............. 186
Professor A lastair Goss
Professor of Oral and Maxillofacial Surgery, School of Dentistry,
The University of Adelaide, and Emeritus Consultant Surgeon,
Royal Adelaide Hospital, Adelaide, South Australia
Ms Melanie Jeyasingham
Editor, Therapeutic Guidelines Limited, Melbourne, Victoria
Dr Angus Kingon
Oral Surgeon, Pymble, New South Wales
Professor Michael McCullough
Oral Medicine, Melbourne Dental School, The University of
Melbourne, Carlton, Victoria
Dr Jo-Anne Manski-Nankervis
General Medical Practitioner, Dianella Community Health,
Broadmeadows, and Academic Registrar and Lecturer, General
Practice and Primary Health Care Academic Centre, The University
of Melbourne, Carlton, Victoria
Dr John Matthews
General Dentist, Essendon, Victoria
continued next page

X xi
 Associa.te Professor Neil Savage
Reader .m 0I:a1 Medicine and Oral Pathology, School of Dentistry,
The Uni~erslty of Queensland, and Consultant Oral Pathologist
Royal Bnsban~ and Women 's Hospital and Queensland Medicai
Laboratory, Bnsbane, Queensland
Dr Leanne Teoh
Pharmacist, Ringwood, and General Dentist, Bundoora, Victoria
~embers ofth~ exp~rt g~oup ~av.e stated that they have complied
With Ther~peutJc ~UJdehnes LJmJted policy on conflict of interest.
For more mformatwn, see <www.tg.org.au/conflict_of_interest>.
xii
Infective Endocarditis
Prophylaxis Expert
Group (July 2008)
Professor Robert Moulds (chairman)
Professor of Medicine, Fiji School of Medicine, Suva, Fiji
Professor Bart Curri e
Head, Infectious Diseases Program, Menzies School of Health
Research and Royal Darwin Hospital, Casuarin a, Northern Territory
Associate Professor Cluistopher Daly
Associate Professo r of Peri odontol ogy, Facu lty of Dentistry, The
Un iversity of Sydney, Sydney, New South Wales
Professor A lasta ir Goss
Professor of Oral and Maxillofacial Surgery, The University of
Adelaide, and Director of Oral and Maxillofacial Surgery, Adelaide
Dental Hospital and Royal Adelaide Hospital, Adelaide, South
Australia
Ms Melanie Jeyasingham
Editor, Therapeutic Guidelines Limited, Melbourne, Victoria
Professor Julian Smith
Professor of Surgery, Monash Univers ity, and Head, Card iothoracic
Surgery Unit, Monas h Medical Centre, Clayton, Victoria
Associate Professor Nei l Strathmore
Associate Professor, The Uni versity of Melbourne, and Cardi ologist,
The Royal Melbourne Hospital, Melbourne, Victori a
Dr Alan Street
Deputy Director, Victorian Infectious Diseases Service, The Royal
Melbourne Hos pital, Melbourne, Victoria
Members of the expert gro up have stated that they have compi ied
with Therapeutic Guidelines Limited policy on conflict of interest.
For more information, see <www.tg.org.au/conflict_of_ interest>.
xii i
 Acknowledgments
The expert groups thank colleagues who have contributed
to this manuscript by review, advice and other assistance. We would
especially like to thank the following:
Associate Professor Roger Allan
Cardiac Services Clinical Stream Director, South Eastern Sydney
Illawarra Health, Sydney, New South Wales
Clinical Associate Professor Ramesh Balasubramaniam
Specialist in Oral Medicine, School of Dentistry, The University of
Western Australia, and Pe1ih Oral Medicine & Dental Sleep Centre,
Subiaco, Western Australia
Professor Peter Collignon
Director of Microbiology and Infectious Diseases, Canberra Hospital,
and Professor, Australian National University Medical School,
Canberra, Australian Capital Territory
Ms Judy Cmrie
Senior Registered N urse, Oral & Maxillofacial Surgery Unit, Royal
Adelaide Hospital, Adelaide, South Australia
Associate Professor Ivan Darby
Head of Periodontics Unit and Director of Graduate Studies,
Melbourne Dental School, The University of Melbourne, Carlton,
Victoria
Associate Professor Paul Desmond
Director, Department of Gastroenterology and Director of Medical
Services, Aged and Community Care, St Vincent's Hospital, Fitzroy,
Victoria
Associate Professor Steven Doherty
Director, University Department of Rural Health, The University of
Newcastle, and Emergency Physician, Tamworth, New South Wales
Professor Peter Ebeling
Professor of Medicine and Chair of the North West Academic Centre,
Western Section (Assistant Dean), The University of Melbourne, and
Head of Endocrinology, Western Health, Melbourne, Victoria
xiv
Dr John Fahey
Managing Director, Cynergex Group Pty Ltd, Sydney, New South
Wales
Adjunct Associate Professor John Highfield
Discipline of Periodontics, Faculty ofDentistry, The University of
Sydney, Sydney, New South Wales
Emeritus Professor Ken Ilett
Pharmacology and Anaesthesiology Unit, School of Medicine and
Pharmacology, The University of Western Australia, Crawley,
Western Australia
Dr Jennifer Johns
Cardiologist, Medical Director, Specialty Services CSU, Austin
Health, Heidelberg, Victoria
Ms Benafsha Khariwala
Editor, Therapeutic Guidelines Limited, Melbourne, Victoria
Ms Judith Kristensen
Senior Pharmacist, King Edward Memorial Hospital, Subiaco,
Western Australia
Associate Professor Richard Logan
Head of Oral Pathology, School of Dentistry, The University of
Adelaide, Adelaide, South Australia
Professor Peter McCluskey
Director, Save Sight Institute, and Professor of Clinical
Ophthalmology & Eye Health, Sydney Medical School, The
University of Sydney, Sydney, New South Wales
Professor David Manton
Elsdon Storey Chair of Child Dental Health, Melbourne Dental
School, The University of Melbourne, Carlton, Victoria
Dr Anita Nolan
Faculty of Dentistry, University of Otago, Dunedin, New Zealand
Professor Eric Reynolds AO
Head of the Melbourne Dental School, Melbourne Laureate Professor
and CEO of the Oral Health CRC, The University of Melbourne,
Carlton, Victoria.
Dr Susie Rogers
Editor, Therapeutic Guidelines Limited, Melbourne, Victoria
 Associate Professor Louis Roller Endorsements
Faculty ofPham1acy and Pharmaceutical Sciences, Monash
University, Parkville, Victoria
Professor Richard Ruffin AM
Emeritus Professor, Discipline of Medicine, The University of
Australasian Society for Infectious Diseases (prevention of
Adelaide, Adelaide, South Australia
endocarditis)
Dr Margaret Stacey
Australian College of Rural and Remote Medicine (prevention of
Senior Lecturer, Melbourne Dental School, The University of
Melbourne, Carlton, Victoria endocarditis)

Dr Alan Street Australian Dental Association Inc.*

Deputy Director, Victorian Infectious Diseases Service, The Royal Australian Society for Antimicrobials (prevention of endocarditis)
Melbourne Hospital, and Visiting Physician, Infectious Diseases Unit,
The Cardiac Society of Australia and New Zealand (prevention
The Alfred, Melbourne, Victoria
of endocarditis)
Mrs Alison Tandy
Heart Foundation (prevention of endocarditis)
First aid and cardiopulmonary resuscitation trainer, Adelaide, South
Australia National Prescribing Service Limited
Professor Martin Tyas AM Royal Australasian College of Dental Surgeons
Honorary Professorial Fellow, Melbourne Dental School The
The Royal Australian College of General Practitioners (prevention of
University of Melbourne, Carlton, Victoria '
endocarditis)
Professor Laurie Walsh
The Society of Hospital Pharmacists of Australia
Head of School of Dentistry, The University of Queensland, Brisbane,
Queensland
Mr David Wiesenfeld * The Australian Dental Association (ADA) congratulates Therapeutic
Oral and Maxillofacial Surgeon, The Roya l Melbourne Hospital and Guidelines Limited on the development of these guidelines, which will
Clinical Associate Professor, Melbourne Dental School The ' be a useful contribution to resources for both dental practitioners and
University of Melbourne, Carlton, Victoria ' general medical practitioners throughout Australia for the oral health care
of their patients. These guidelines have been developed by a group of
distinguished contributors and the ADA welcomes the publication of these
Version 1 of these guidelines form ed the bas is for this revised version.
guidelines as an aid to dental practice patient care.
The expert groups thank colleagues who worked on version I:
continued next page
Dr J Pope
Associate Professor L Roller
Associate Professor M Tennant
The expert groups thank the Therapeutic Guidelines evaluation
network of over 200 users who provided invaluable feedback on
the use of the guidelines in clinical practice, and also those who
have provided feedback to Therapeutic Guidelines eith er directly
or through the 'Request for comments' page at the end of the books. xvii
xvi
 Dentistry at James Cook Un iversity
Melbourne Dental School, The University of Melbourne
About Therapeutic Guidelines
School of Dentistry & Health Sciences, Charles Sturt Un iversity Limited
School of Dentistry, The University of Adelaide
Schoo l of Dentistry, The University of Queensland
School of Dentistry, The University of Western Australia
KEY INFORMATION ABOUT THESE GUIDELINES

Dosing regimens
The dosing regimens in the text apply to nonpregnant adu lts of
average size, unless otherwise specified. Higher or lower doses will be
appropriate for some patients.
Where alternative drug regimens are listed, the order of preference for
use of each drug is indicated by the number placed next to its regimen
( 1 for first preference, 2 for second preference, and so on). Drugs of
eq ual preference are marked with the same number and are generally
listed in alphabetical order.

Disclaimer
These guidelines form an acceptable basis for management of patients,
but there may be sound cli ni cal reasons for different therapy in
individual patients or in specific institutions. The comp lexity of clinical
practice requires that, in all cases, users understand the individual
clinical situation, and exercise independent professional judgment
when basing therapy on these guidelines . Paiiicularly in complicated
situations, these guidelines are not a substitute for seeking appropriate
advice.
These guidelines do not include comprehensive drug information, some
of which may be important; usually contra indications and precautions
for the recommended drugs are not included. Responsible use requires
that the prescriber is familiar with these matters.

HOW THERAPEUTIC GUIDELINES ARE PRODUCED

The aim of Therapeutic Guidelines Limited (TGL) is to provide clear,
practical, authoritative and succinct therapeutic information for busy
health practitioners, for the management of patients with specific
xviii
conditions. xix
 The guidelines are comprehensive in that they cover all common
disorders seen in clinical practice. The information is independent and
unbiased and is a disti llation of current evidence and opinion. Topics
and sections are arranged according to diagnostic entities. Each section
gives sufficient surrounding information to orient the reader, followed
by succinct and explicit recommendations for therapy.
The guidelines are not primarily meant to instruct, but rather to assist
prescribers ensure their patients receive optimum treatment.
The content of each topic is revised by an expert group every 3 to
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The essential principles underlying the process for guideline
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TGL having a strict policy on conilict of interest for directors, staff
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of interest (see <www.tg.org.au/conflict_of_interest>).
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a perception of possible problems in an area, arising from
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drug usage data
XX
a clear problem (eg size of health burden, co~t, variations i? .
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Factors taken into consideration in choosing members of the expert
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relevant expertise
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 The editor prepares the papers for each meeting, including minutes,
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their clinical expe1iise and the current evidence in the relevant area.
xxii
They are encouraged to also prepare a separate document summarising
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Basis of recommendations
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ness of any given treatment are fundamental to the development of
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about which treatment(s) to recommend. But, to make sure the advice
the relevant evidence, but also contextualise and tailor the information
to the likely clinical situations that will be faced by prescribers in the
everyday care of their patients. xxiii
 Decision-making in clinical practice is inherently complex and Postpublication evaluation
multifaceted. In addition to the evidence, other factors are considered The evaluation unit of TGL liaises with a netw~rk of approximately
to ensure the advice is relevant and useful. Examples of such factors 200 users (including general practitioners, jum_or hosp~t~l doctors,
include the adverse effects, availability and affordability of the health academics, pharmacists and students) to act1vely soltc1t feedback
treatment, risk factors, and patient characteristics and comorbidities. on the guidelines .
' Evidence-rich' areas are in the minority in clinical practice, so a large Participants in the network are provided with al.l ~herapeutic Guideline~
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in areas where there is little published evidence. In these 'evidence- twice each year to discuss and record the feedback.
poor' areas, recommendations for therapy may be based on the known
pathophysiology of the disease, the clinical experience of expert group Before a topic is revised, accrued feedback on the prev~ous ~ersion is
members, the adverse effect profile of the possible therapeutic options, collated and passed on to the expert group for their cons1derat1on when
long-term safety data, and cost. Using these criteria, older drugs that revising the text.
have been shown to have a reasonable adverse effect profile over a long Users are encouraged to comment about the content or format of
period are often recommended as first-line therapy rather than newer the guidelines by emailing comments to. feedba~k($tg.org.au or by
drugs that have a less certain adverse effect profile (pat1icularly in the completing the form at the back ofTGL pnnt publ1catwns .
long term), and are usually more expensive.
Because the totality of the evidence, and not just clinical trials, is
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All major sources of information on which recommendations are based
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this is kept to a minimum to ensure the readability of the text is not
impeded .
A summary of major recommendations and changes is accessible from
the home page of TGL's electronic products with each release, and as
an insert to the books.

Endorsement
Once the manuscript has been finalised and approved by the expe11group,
peak organisations are invited to endorse the text. These organisations
include The Royal Australian College of General Practitioners, The
Society of Hospital Pharmacists of Australia, Royal College ofl\ursing
Australia, National Prescribing Service and relevant specialty societies.

xxiv
 Board of directors of TGL

Principles of diagnosis and

Mr RS Kneebone (chairman)
Albe1i Park, Victoria prescribing
Dr JS Dowden
Yarralumla, Australian Capital Territory
There are several general principles that must be followed when
Professor PP Glasziou managing any condition (see Box 1, below).
Robina, Queensland
The process of making a diagnosis should be considered as an
Mr MJ Harvey ' information gathering exercise'. The necessary information can be
Sandringham, Victoria obtained by taking a thorough history, conducting a complete clinical
Professor MR Kidd examination and performing the appropriate diagnostic tests. Once
Potts Point, New South Wales the information has been gathered, the clinician should review it and
decide on the diagnosis. This requires a thorough working knowledge
Professor JE Marley of the various local disease processes that may affect the oral and dental
New Lambton Heights, New South Wales tissues and surrounding structures, plus a thorough knowledge of the
Dr CD Mitchell* various systemic diseases that may manifest in the mouth.
Ballina, New South Wales
Dr JG Primrose Box 1. General principles of managing oral and dental
Farrer, Australian Capital Territory conditions
Professor JWG Tiller"i" 1. Identify the disease and its cause-make a diagnosis.
Melbourne, Victoria 2. Remove the cause to prevent recurrence.
3. Remove the effect of the disease.
Chief executive officer ofTGL
4. Restore the tissues to their normal function.
Dr SM Phillips
5. Monitor the healing.
Williamstown, Victoria
6. Observe the stability of the area over time.
7. Prevent recurrence of the disease.

Nominees of the following organisations:
* The Royal Australian College of General Practitioners
xxvi
;Victorian Medical Postgraduate Foundation Inc.
HISTORY
The first stage of taking a history is to determine the patient's presenting
complaint or their reason for attending the dental surgery. This allows
the clinician to focus on the patient's particular problem so they can be
managed effectively and efficiently.
The medical history should then follow as this may provide information
essential to the diagnosis of the presenting problem or indicate that
changes to the patient's management are required. The medical history 1
 should include a medication hi story (including prescription medicines,
over-the-counter and complementary medicines, alcohol and illicit
drugs), and a history of allergies and adverse reactions to drugs. The
medical history should be checked periodically, as the patient's health
status and medications may change over time.
The dental history should include an overview of the patient's previous
dental problems and treatment, and a detai led history of the presenting
condition. While listening to the patient's outline of the presenting
problem, the clinician should begin to form a provisional diagnosis-
that is, the cl inician should think of several potential diagnoses (ie
differential diagnoses), and then ask specific questions to narrow the
possible range of diseases. ' Open-ended' questions should be asked
rather than ' leading' questions (eg the clinician should ask the patient
what particular things cause the pain, rather than asking if hot or cold
drinks cause the pain).
EXAMINATION AND DIAGNOSTIC TESTS
the first stage) of managi ng the disease. If the cause is not removed,
full or rap id recovery may not occur. The condition may merely be
converted from an acute and painful condition to a chronic state with
reduced or no symptoms, but with the disease still present and slowly
progressing. Risk factors for the disease should also be identified and
modified, where possible, as part of the overall management of the
patient.
Good clinical records should be kept with the diagnosis recorded. Box 2
(below) shows the aspects of the examination and diagnosis that should
be included in the records.
Box 2. Aspects of the examination and diagnosis that
should be included in clinical records
a description of the patient's presenting complaint
t he medical and dental histories (includi ng medications)
the clinical findings

The clinician should form a provisional diagnosis before starting the the results of all tests performed

clinical exam ination, so the examination and di agnostic tests can be a rad iograph ic report for all ra diographs taken
targeted towards confirming the diagnosis and identifying which tooth the diagnosis
or other tissues are involved. the cause
Ideally, for most diseases, there should be at least two signs or a management plan including specific treat ment to be provided
symptoms present to indicate the disease process. If there is any doubt, details of all discussions with the patient, including advice given to and consent
the clinician should either defer treatment until the diagnosis becomes from the patient.
clear (if the pain is not severe), or refer the patient to a specialis1.
It is not necessary to perform every possible diagnostic test; clinicians
MANAGEMENT
must choose tests that are relevant to the presenting complaint. Specific
tests may be required to provide futiher information as part of the There is a distinction between ' management' and ' treatment'. Treatment
"C
diagnostic process. Such tests should not be considered 'special tests', refers to a systematic course of medical or surgical care, whereas c
but routine or required tests for the specific condition being considered management is a broader term that refers to the overall handling of the ctl
(/)
(eg pulp sensibility tests and periapical radiographs are required for patient and their problems in a sensitive manner. Management includes u;
the diagnosis of pulp and periapical diseases; probing of periodontal skilful, careful and tactful treatment. Ideally, clinicians should ' manage' 0
c
pockets is essential for periodontal disease; blood tests may be required the patient and their problems rather than just ' treat' them. 'Q.O
ctl
for some mucosal diseases; a biopsy may be required for some lesions) . :g
Irreversi ble treatment or drug therapy should not be commenced until ....o'Q.O
The diagnosis of any disease is incomplete if the cause of the disease a definitive diagnosis has been established because the diagnosis C/lC
CI) ' -
has not been determined. The cause may be simple (eg dental caries as determines the treatment required . The approach of ' let's try this and -.C
Q.';:
a cause for pulp disease) or complex (ega systemic disease with oral see if it helps ' or 'j ust in case' should be avo ided as it may lead to
g(/)
-Col
manifestations); complex conditions may require other management in
addition to dental treatment. It is essential to identify the cause(s) of the
incorrect and/or inappropriate treatment, and may mask important signs
or symptoms that wo uld help establish a diagnosis.
....
- Cl)
Q.Q.
disease because removing the cause(s) is an integral part (and usually
2 3
 Drugs should not be prescribed as the sole means of managing most oral
and dental problems. Most conditions that cause a patient to visit their
dentist require some form of active dental (or oral) treatment, and such
treatment is usually the most effective and efficient means of managing
their condition. Drugs are usually only needed as an adjunct to this.
There is also a risk of adverse effects with every drug, and therefore
drugs should only be prescribed ifthey are likely to have a demonstrable
benefit. If a drug is not required, it should not be used.
When considering the management of all dental conditions (and most
oral conditions), the '3 Ds' principle should be applied:
Diagnosis- the disease and its cause must always be identified
first.
Dental treatment- once the diagnosis has been determined, the
appropriate dental treatment should be provided; this includes
removing the cause(s) of the disease.
Drugs- the final consideration is whether any drugs are required;
this decision is based on the severity of the problem and can often
be deferred until the response to the dental treatment has been
reviewed.
If these principles are followed, the drugs commonly used in dentist1y
(antimicrobials, analgesics and anti-inflammatory drugs) can often be
avoided (or at least their use can be minimised). If drugs are needed,
they are more likely to be effective since the cause of the disease has
been removed and the appropriate dental treatment has been initiated.
4 5
Prescriptions and
prescription-writing
Prescribers should have a clear understanding of both the impOiiance
of prescribing appropriately and the processes involved, so they can
prescribe rationally and independently. Inappropriate prescribii;Jg can
lead to ineffective and unsafe treatment, exacerbate or prolong illness,
distress or harm the patient, and be costly.
Treatment of any so1i needs to be effective, safe and affordable. Most
conditions that lead a patient to visit their dentist require some form
of active dental (or oral) treatment, and drugs are usually only needed
as an adjunct to this. The patient should be involved as a partner in
management decisions and the option of not using drug treatment should
always be considered . If drug therapy is required, the prescriber must
use up-to-date evidence-based knowledge to choose the best treatment
for the individual patient and their specific problem.
Recent data indicate that over 100000 Australians are hospitalised
annually because of adverse reactions to medicines.* Many more
people suffer adverse drug reactions without needing hospitalisation.
Prescribers should be aware of the potential benefits and harms of drug
therapy (eg the risk of infection from dental treatment in an established
joint prosthesis is approximately 0.03%, whereas the risk of an urticarial
adverse reaction to penicillin is around 3%'i} Many adverse reactions
can be prevented by clinicians taking an appropriate detailed history
and prescribing rationally.
THE PROCESS OF RATIONAL TREATMENT
The process of rational treatment involves:
defining the problem
*Australian Institute of Health and Welfare. Australia's health 2010: the twelfth biennial
health report of the Australian Institute of Health and Welfare. Canberra: AIHW; 2010.
< www.aihw.gov.au/publications/index.cfm/title/1137 4 >
i Scott JF, Morgan D, Avent M, Graves S, Goss AN. Patients with artificia l joints: do they
need antibiotic cover for dental t reatment? Aust Dent J 2005;50(4 Suppl 2):545-53.
 specifYing the therapeutic objective (eg pain relief, infection
prevention, treatment) presumed patient demands, and ratio~a! presc~ib!ng habits ~e~p
counter patient demands caused by adverttsmg, addtctwn or unreahsttc
choosing the treatment-in dentistry, drugs are usually an adjunct expectations. Always consider alterna~ives to dru? trea_tment ~nd gtve
to active dental treatment. If required, drug choice is based on: the patient the reasons why the alternattve may be m thetr best mterests.
efficacy
safety
OVERPRESCRIBING AND UNDERPRESCRIBING
suitability (eg adherence issues, patient comorbidities, drug
formulation) It is important that the dose, the duration of treatment and the quantity
- cost. of drugs prescribed are accurate.

Before commencing treatment, it is essential that a prescriber has a Overprescribing is wasteful, can cause unnecessary adverse ef!e~ts,
full medical and medication history of the patient, including: and increases the opportunity for overdose. Some drugs are addtcttve
if overused. Some drugs have a narrow therapeutic index (ie the
age and weight
therapeutic dose is very close to the toxic dose).
allergies
adverse drug reactions Underprescribing is also wasteful and potentially harmful. It can result
pregnancy and breastfeeding status in ineffective treatment, and the patient may need a different and more
expensive treatment later (often seen with antibiotic and analgesic
medical conditions
prescribing).
medications (including prescription medicines, over-the-counter
and complementary medicines, alcohol and illicit drugs).
THE PRESCRIPTION
Starting treatment involves:
A prescription is a legal document; it is a precise written instruction
giving the patient information about the condition and the reasons
from a prescriber to a pharmacist for preparing and dispensing a drug
for the treatment, and clear instructions about the treatment (see
for a patient. Who may write prescriptions and how. they sh~uld. be
'Prescription and the patient' , p.9)
written are outlined in the appropriate state and terntory legtslatwn
performing appropriate oral or dental treatment (Acts and Regulations) (see p.l2).
C6 if required, writing an appropriate and accurate prescription (see
....
c 'The prescription', p. 7) . The prescriber has a duty of care to provide a prescription tha~ is
Q) legible; this reduces the potential for errors in treatment. An tlleg1ble
Q
Monitoring progress involves: prescription can constitute professional negligence. Computer-
'C
c reviewing the patient generated prescriptions are generally t?ore legible tha~ ~hose that
co
deciding whether to stop, continue or change the treatment. are handwritten; however, errors can sttll occur. The prmctple to be
~ followed is one of constant checking. Care should be taken to ensure
0
Ui The above process is in line with the guidelines for quality use the instructions are not ambiguous.
([)
c of medicines in Australia's National Medicines Policy. For more
Q) information, see <www.health.gov.au/internet/main/publishing.nsf/ Essential information required for a legal prescription written by a
:2 Content/National+Medicines+Po !icy-2>. dentist may vary slightly between the states and territories, but generally
::J
0 comprises:
(.) Prescribers need to be confident in their ability to evaluate information prescriber's name, address, telephone number and qualifications
.;:::;
::J about drugs to determine their therapeutic value, and become familiar
([) patient's full name (given and family names), address and date of
0. with their use. New and expensive drugs should be critically evaluated
~ birth
([) before use instead of established treatments.
.c date the prescription is written
I-
Patients may demand particular drugs, or the prescriber may presume drug name in full (preferably generic or approved name)
they are requesting certain drugs. Good communication helps avoid drug strength (eg 250 mg, 500 mg)
6 7
 drug form (eg tablet, capsule or mixture) Figure 1. Example of the format required for a legal
quantity of drug to be supplied prescription written by a dentist
drug dose, route of administration, frequency, and duration of Dr J Smith BOSe
treatment (if necessary) Address
clear instructions for the patient (in English)- it is not appropriate Telephone number
to write 'take as directed' PBS prescribing number

any further instructions necessary for the pharmacist

the words 'for dental treatment only'
Patient's Medicare number
signature of the prescriber-handwritten.
Patient's name Ms Jane Citizen
Figure 1 (p.9) is an example ofthe format required for a legal prescription
Patient's address
written by a dentist. If the prescription is for an item included in the
Pharmaceutical Benefits Scheme (PBS), the dentist's unique prescriber Patient's date of birth

number must be on the prescription. PBS prescription pads are available

from Medicare Australia.
Points to note when writing a prescription are as follows:
Make the prescription as tamper-proof(unalterable) as possible Rx
and use indelible ink. Phenoxymethylpenicillin 500 mg capsules
Do not write prescriptions for more than one person on the same 20
form.
Take 1 capsule 4 times a day at 6-hourly intervals
Use standard language for instruction. for 5 days
Do not use abbreviations or Latin terms .
Avoid using decimal points if possible (eg write quantities less
than I gram as milligrams, and quantities less than I milligram as
micrograms).
(ij
....c Ifusing a decimal point, put a '0' in front ofthe point (eg '0.5',

"'"''""~
Q) not ' .5').
Q
Do not abbreviate microgram, nanogram , international or unit.
'C
c Limit the number of items on a prescription to two or, at the most,
(II
three. Date
~ Use computer-generated prescriptions (if possible).
0 For dental treatment only
Ui
Q)
If using brand or trade names, ensure that you know the approved
c or generic name as well.
(ij
:Q If any space is unused on the prescription, put a line across the THE PRESCRIPTION AND THE PATIENT
:::J
CJ
area to prevent the addition of items.
() Dentists may not order repeat prescriptions. When prescribing drugs, give the patient specific information about the
.;::;
:::J drug, including:
Q)
Q. Prescribers and pharmacists have complementary roles in ensuring the brand name and the approved name of the drug
~ optimum patient outcomes. This is enhanced by mutual respect for each
Q) the effects of the drug and why it is needed
..c other's skills.
r- possible adverse effects and what to do if they occur
instructions on how to take the drug 9
8
 warnings (eg possible interactions, maximum dose)
when to return for review
permission to ring you if concerned about any issues.
Patients often do not remember the details or instructions they are given
during a consultation, so it is desirable to give written instructions as
well. Consumer medicine information (CMI) leaflets are available for
the majority of medicines prescribed in Australia, and should be offered
every time a drug is dispensed. They are available from pharmacies and
some clinical software packages. Consumers can access CMis directly
via the NPS: Better choices, Better health website <www.nps.org.au>.
SOURCES OF DRUG INFORMATION
Recommended sources of drug information include the fo llowing
journals, books, electronic resources and websites:
Journals
Australian Dental Journal (ADJ)-see 'Medications in dentistry supplement' in
December 2005 ed ition (can be accessed via the Austra lian Dental Assoc iation
website <www.ada .org.au >)
Australian Prescriber <www.austra lianprescriber.com>
Books and electronic resources
Australian Medicines Handbook (AMH)- independently prepared source of
:sc evidence-based drug information; also includes a section on prescription-writing
and drug interactions (updated electronically biannually and in print annually)
Q)
0 Therapeutic Guidelines- Analgesic, Antibiotic, Cardiovascular, Dermatology,
'C
c Endocrinology, Gastrointestinal, Neurology, Psychotropic, Palliative Care ,
Websites
Pharmaceutical Benefits Scheme (PBS) website <www.pbs.gov.au >
Australian Dental Association website <www.ada.org.au >
Pharmacist-relevant website <http://auspharmacist.net.au/> , which has links
to a large number of sites with drug inform ation
NPS: Better Choices, Better Health website < www.nps.org.au>
LEGISLATION ABOUT PRESCRIPTIONS AND
PRESCRIBING
For legislation pertaining to prescriptions and prescribing in each of
the states and territories, see p.l2. Overall, there are no significant
differences in the requirements for what constitutes a legal prescription
between the states and territories, but there are some minor differences.
If dentists are in doubt, they should consult the appropriate legislation
for their state or territory.
A 'prescription-only ' drug is a drug that can only be obtained with a
prescription; it cannot be purchased over-the-counter. Dentists may
prescribe any prescription-only drug provided it is for the dental
treatment of a patient under their care.
Dentists may prescribe any drug
Additional caution should be
of dependence (in most states and
exercised when prescribing
territories) for a patient under their drugs of dependence.
care provided they do so in accord-
ance with legal requirements, and have taken all reasonable steps to
ascertain the identity of that person and to ensure that a therapeutic need I
c
exists, and the drug is required for dental treatment. Additional caution 0

~
Cll
Respiratory, Rheumatology, Toxicology & Wilderness, and Developmental should be exercised when prescribing drugs of dependence. a
;:
Disability management guideline. All print titles are avai labl e through the Dentists may not order repeat prescriptions. (,)
0 (/)
electronic products, eTG complete and miniTG ~
Ui
<!) Legislation regarding prescribing for the purpose of self-administration Q.
c MIMS-contains product information as provided by pharmaceutical companies 'C
Q) varies between the states and territories; however, generally, self- c
:Q
and approved by the Therapeutic Goods Administration (can be accessed via prescribing is not recommended. Cll
:::J the Australian Dental Association website <www.ada.org.au >) (/)
(.!) c
The Pharmaceutical Benefits Schedule includes a number of medicines 0
()
.;::;
:::J
<!)
Drug Interaction Facts (Tatro DS, editor. St Louis: Facts and comparisons)-this
is an exce llent resou rce on drug interactions (updated electronically quarterly
that are subsidised by the Pharmaceutical Benefits Scheme (PBS) if
prescribed by a dentist. For more information, see <www.pbs.gov.au>.
a
;: '0.0
0.
~ and in print annually) 1;l.!:
<!)
..c
......
Q).'!:
o..:=
I- Any recent textbook on cl inical pharmacology

10 11
 Relevant regulations
The fol lowing are the relevant Acts and Regu lations for each state and
territory. The Poisons Standard lists the classification of medicines and
chemi ca ls into schedules for inclusion in the relevant legislation. For
more inform ation, see <www.tga.gov.au/ industry/scheduling-poisons-
standarcl.htm#susmp>.
Getting to know your drugs
Auslralian Capital Territory
Dentists may prescribe any drug approved by the Therapeutic Goods
Drugs ofDependence Act 1989
Administration (TGA), provided the drug is prescribed as part of
Drugs of Dependence Regulation 2009
the dental treatment for a patient that the dentist has established (by
Medicines, Poisons and Therapeutics Goods Act 2008 examination) needs the drug. Most of the drugs discussed in this chapter
Medicines, Poisons and Therapeutics Goods Reg ulation 2008 are subsidised by the Pharmaceutical Benefits Scheme (PBS).
New South Wales Dentists must know the beneficial and the adverse effects of the drugs
Poisons and Therapeutic Goods Act 1966 they prescribe (see ' Sources of drug information', p.lO), as well
as the patient's medical history and current medications, including
Poisons and Therapeutic Goods Regulation 2008
prescription, over-the-counter and complementary medicines.
Notthern Territory
Poisons and Dangerous Drugs Act ANTIMICROBIALS
Poisons and Dangerous Drugs Regu lations
Therapeutic Goods and Cosmetics Act Principles of antimicrobial use
Queensland The problems posed by pathogenic organisms resistant to antimicrobial
Health Act 193 7 drugs are increasing globally. Adherence to the principles of
Health (Drugs and Poisons) Regu lation 1996 antimicrobial use outlined in Box 3 (p.l5) and summarised in the
antimicrobial creed (see Box 4, p.J6) is impotiant.
South Australia
It must first be determined if an antimicrobial drug is needed. The
Contro lled Substances Act 1984 majority of infections that present in the dental clinic require active
Controlled Substances (Poi sons) Regulations 20 II dental treatment to remove the source of infection, and this is usually
Tasmania the most effective method of treating the problem . It should also be
kept in mind that most viral and minor bacterial infections are self-
Poisons Act 1971 limiting and do not require an antimicrobial. Unnecessary prescription
Poisons Regulations 2008 of antimicrobials exposes patients to adverse drug effects, is costly, and
Victoria creates conditions that favour the proliferation of resistant organisms in
the patient and the community.
Drugs, Poisons and Controlled Substances Act 1981
Drugs, Poisons and Controlled Substances Regulations 2006 Only antimicrobials with an oral and dental indication are discussed in
this chapter. Refer to Therapeutic Guidelines: Antibiotic for information
Western Australia on other antimicrobials.
Poisons Act 1964
Poisons Regulations 1965

12 13
 Antimicrobial resistance
Antimicrobial drugs are different fiom other drugs in that their use
in one patient can influence their future effects in other patients. The
development and spread of bacterial resistance to antimicrobials is a
major problem wi thin hospitals and in the community. A lthough the
mechanisms are complex, resistance is essentially due to selective
pressure exerted by the widespread presence of antimicrobial drugs
in the biosphere, together with the fac ilitated transfer of organisms
between staff and pati e nts.
Ant imicrob ial resistance is increasing in many pathogens. As there are
only a limited number of new antim icrobial drugs becoming availab le,
they are a particularly va luab le reso urce. Restraint in prescribing and
adherence to the principles outlined in these guidelines are essential
to ensure that anti microbials remain effective in treating important
infections. Appropriate antimicrobial use delays the emergence of
resistance and minimises res istance prevalence after it has emerged
(see Box 3, p.lS). The Centers for Disease Control and Prevention
webs ite has usefu l information on
Restraint in the use of all
how to prevent antimicrobial resist-
antimicrobi als is the best way to
ance in health care settings- see
ensure their continuing efficacy.
< www. cdc .gov I drugres i stance/
healthcare/patients. htm>.
Prophylactic, empirical or directed antimicrobial therapy
Antimicrobial use can be prophylactic, empirical, or directed against a
known organism.
Prophylactic use aims to prevent infection in clinical situations where
there is significant risk of infection.
Empirical antimicrobials are used when the causative organism is
proven. This may occur if treatment must be commenced before
culture susceptibility results are avai lab le, the clinical situation is
serious eno ugh to warrant taking cu ltu res, or appropri ate material
culture cannot be obtained.
Directed use occurs when culture susceptibility results are used to guide
therapy.
In all three of these circumstances, the principles listed in Box 3 (p.!S)
and summarised in the antimicrobial creed (see Box 4, p.16) should be
closely adhered to.
Classes of antimicrobial drugs common ly used in dentistry and
14 examples of drugs from each class are shown in Table 1 (p.l7).
Box 3. General principles of antimicrobial use
Prophylactic therapy
Restrict use of prophylactic antimicrobial therapy to situations in which prophylaxis
has been shown to be effective or where the consequences of infection would be
disastrous.
Base choice of antimicrobial(s) on known or likely target pathogen (s).
For most surgical prophylaxis indications, use a single perioperative dose sufficient
to achieve therapeutic tissue concentrations at the time contamination is most
li kely. To maintain adequate tissue concentrations, a repeat dose is only requ ired
if a short half-life drug is used and the procedure is prolonged.
Empirical therapy
Use antimicrobials only where proven benefits are substantial. Avoid use in minor
or self-limiting ill ness- unnecessary use is a significant driver of antimicrobial
resistance.
Base t herapy on the most likely and/or important potential pathogen(s) and
their likely antim icrobial susceptibilities. In general, use the narrowest spectrum
antimicrobial to treat the likely pathogen(s).
Use a dose that is high enough to ensure efficacy and minim ise the risk of
resistance selection , and low enough to minimise the risk of dose-related toxicity.
Before commencing therapy, where appropriate, obtain specimens for blood
cu lture (at least two sets from clinically septic patients) and other cu ltures.
If possible, direct therapy from the start through antigen detection tests, nucleic
acid tests and/or Gram stain results .
Cease therapy if a noninfective diagnosis is confi rm ed.
In the absence of a proven causative organism at 48 hours, evaluate t he cl inical
and microbiological justification for continuing therapy.
Liaise regu larly with local pathology providers to obtain up-to-date information on
local antimicrobial resistance patterns for significant pathogens.
Directed therapy
not Critically evaluate culture and other microbiological results to distingu ish infection
the from colon isation or contamination that does not require specific antimicrobial
treatment. If necessary, obtain advice from an infectious diseases physician or a
not
cli nical microbiologist.
for
Based on a demonstrated microbial cause and its antimicrobial susceptibility,
direct antimicrobial therapy in accordance with recommendations using the most
effective, least toxic , narrowest spectrum drug available.
Use a single drug unless it has been proven that combination therapy is required to
ensure efficacy (ega proven mixed infection), for synergy, or to reduce the selection
of clinically significant resistance (eg treatment of tuberculosis, HIV infection).
Keep duration of therapy as short as possible. Do not exceed 7 days without a
proven indication for a longer duration (eg for treatment of endocarditis). For most
odontogenic infections 5 days of therapy with appropriate denta l treatment is
sufficient. 15
 Box 4. The antimicrobial creed Antibiotics may be used within the tooth (ie intradental therapy).
Commercial intradental antibiotic preparations usually also contain
M microbiology guides therapy wherever possible
a cot1icosteroid. These preparations are used to manage intracanal
indications should be evidence-based infections and apical periodontitis, and to reduce inflammatory root
N narrowest spectrum required
resorption.

D dosage appropriate to the site and type of infection

Table 1. Common antimicrobial drugs used in dentistry

Examples
M minimise duration of therapy
Antibacterial drugs
E ensure monotherapy in most situations
beta /actams

Route of administration penicillins

narrow-spectrum benzylpenicillin, phenoxymethylpenicillin

The oral route of administration is preferred, where possible, because
it is usually associated with less serious adverse effects, has a cheaper narrow-spectrum with dicloxacillin, flucloxac illin
antistaphylococcal activity
drug product cost and has lower administration costs than parenteral
therapy. Antimicrobials that have a high oral bioavailability (eg moderate-spectrum amoxycillin, ampicillin
clindamycin and metronidazole) can usually be given orally rather than broad-spectrum (beta-lactamase amoxycillin +clavulanate
intravenously. There is no basis to the common belief that injections are inhibitor combinations)
more 'powerful' than tablets.
cephalosporins
However, parenteral administration (usually intravenous) is required
moderate-spectrum cephalexin, cephazolin
in certain circumstances :
oral administration is not tolerated or is not possible (ega patient gtycopeptides teicoplanin, vancomycin
with swallowing difficulties)
lincosamides clindamycin, lincomycin
gastrointestinal absorption is likely to be significantly reduced (eg
vomiting, gastrointestinal pathology), or reduced absorption might macro/ides roxithromycin

accentuate already poor bioavailability nitroimidazotes metronidazole, tinidazole

an oral antimicrobial with a suitable spectrum of activity is not tetracyclines doxycycline
available
Antifungal drugs
higher doses than can conveniently be administered orally are
required to achieve effective concentrations at the site of infection azo/es fluconazole, itraconazole, miconazole
(eg spreading deep odontogenic infections) potyenes amphotericin, nystatin
urgent treatment is required because of severe and rapidly
Antiviral drugs
progressive infection (although rarely would the hour or two
required for oral absorption significantly alter the outcome). guanine analogues aciclovir, famciclovir, penciclovir,
valaciclovir
If parenteral administration is used, reassess the need daily and convert
to oral therapy as soon as possible.
To reduce the development of resistant organisms, topical therapy
should be restricted to proven indications (eg miconazole for oral
16 candidosis). 17
 Adverse effects of antimicrobials
All antimicrobials can cause adverse effects so the possibility of harm
must always be considered when deciding whether to prescribe an
antimicrobial. Usually the adverse effects are minor and/or self-limiting;
however, some can be more significant. For more information on
antimicrobial hypersensitivity and antibiotic-associated diarrhoea, see
discussion below and p.20.
Particular care should be taken in the elderly, who often have altered
pharmacokinetic or toxicodynamic profiles making them more likely to
suffer an adverse effect. In patients with renal or hepatic impairment,
dose and/or dose interval adjustment may be required to prevent
concentration-related adverse effects (toxicity).
A history of hypersensitivity or other
adverse response to the drug should Always check if the patient has a
history of hypersensitivity before
always be sought before prescribing
prescribing an antimicrobial.
an antimicrobial drug.
Antimicrobial hypersensitivity (allergy)
It is common for a patient to give a history of being 'allergic' to an
antimicrobial-usually penicillin-and this can present a dilemma. If
penicillin is administered to a highly allergic patient, fatal anaphylaxis
can occur. However, many patients who report a penicillin allergy have
a vague history and are not allergic at all. Also, it is important not to
deny patients treatment with an antimicrobialtmnecessarily, especially
if they have a serious infection for which that antimicrobial would be
the most effective treatment.
~ Types of hypersensitivity
lgE-mediated immediate hypersensitivity- while many reactions are
labelled as 'allergic', true IgE-mediated immediate hypersensitivity is
characterised by the development of u1iicaria, angioedema, broncho-
spasm or anaphylaxis (with objectively demonstrated hypotension,
hypoxia or tryptase elevation) within 1 to 2 hours of drug administration.
Anaphylaxis is mainly associated with parenteral rather than oral
administration. For penicillin, anaphylaxis occurs at an estimated
frequency of 1 to 4 cases per 10 000 courses, with 10% of these reactions
being fatal. Ifthere is a clear history of an IgE-mediated reaction, the
drug should not be administered again without appropriate precautions
(eg desensitisation).
18
IgE-independent reactions-mimicking conditions of'pseudoallergy'
(eg responses to vancomycin infusions such as 'red-man' syndrome)
involving the direct release of vasoactive mediators. These reactions
may be ameliorated by prophylactic antihistamines and slowing the
infusion rate.
Delayed reactions- macular, papular, or morbilliform rashes occurring
several days after commencement of treatment are more common than
immediate reactions, and may be caused by the infection or its treatment.
Such reactions are usually T-cell (not IgE) mediated. Skin testing often
proves negative, particularly when performed several months or years
after the event. Delayed reactions commonly occur in patients with
intercurrent Epstein-Barr virus or HIV infection and such reactions are
often not reproducible with deliberate challenge when the patient is
well. Delayed rashes due to penicillin, especially amoxy/ampicillin, are
not strongly predictive of future reactions and repeat exposure to beta
lactams is not necessarily contraindicated.
Patients with known hypersensitivity should be strongly advised to
wear an ale1i bracelet or necklace advising of their allergy.
~ Diagnosis of antimicrobial hypersensitivity
Antimicrobial hypersensitivity is usually diagnosed based on clinical
history (especially its timing after antimicrobial use). If the patient
reports an allergy, seek specific details about the nature of the
reaction, the timing and the outcome. For information on diagnosis of
antimicrobial hypersensitivity and protocols for desensitisation, see
Therapeutic Guidelines: Antibiotic.
~ Penicillin hypersensitivity
Patients with penicillin hypersensitivity are more likely also to be
hypersensitive to other structurally related drugs. However, the
exact prevalence and impmiance of cross-reactivity is not kn'own.
For example, in patients who report penicillin allergy, subsequent
administration of a cephalosporin has been reported to result in an
adverse reaction in 0.17% to 8.4% of patients. Cross-reactivity between
penicillins and meropenem (a carbapenem) appears to be low (0.9% in
one study*).
*Romano A, Viola M, Gueant-Roddiguez RM, Gaeta F. Valluzi R, Gueant JL. Brief
communication: tolerability of meropenem in patients with lgE-mediated hypersensitivity to
penicillins. Ann Intern Med 2007;146(4):266-0.
19
 A clear history of an lgE-mediated immediate hypersensitivity reaction
(m1icaria, angioedema, bronchospasm or anaphylaxis within 1 to
2 hours of drug administration) contraindicates further exposure to
penicillins, cephalosporins or carbapenems, unless desensitisation is
undertaken. For detailed information on the management of patients
reporting penicillin hypersensitivity, see Therapeutic Guidelines:
Antibiotic.
Antibiotic-associated diarrhoea
Diarrhoea is an adverse effect of many antib iotics. In most cases, no
pathogen is identified . If possible, cease treatment with any antibiotic
likely to be causing the symptoms.
Clostridium difficile is responsible for the most serious cases of
antibiotic-associated diarrhoea. Exposure to broad-spectrum antibiotics
such as cephalosporins, quinolones and lincosamides is an important
predisposing factor. For more information, see Therapeutic Guidelines:
Gastrointestinal.
Antimicrobial drug interactions
Some antimicrobials can interact with other drugs, which may affect the
dose or choice of antimicrobial. Antimicrobials commonly implicated in
drug interactions include rifampicin, linezolid, erythromycin, systemic
azoles and antiretrovirals.
Studies have failed to show a significant interaction between oral
contraceptives and common antimicrobials used in dentistry. Additional
contraceptive precautions are required in patients taking hormonal
contraceptives who are treated with antimicrobials that are enzyme
inducers (eg rifampicin, some antiretrovirals).*
A comprehensive listing of interactions between antimicrobials and
other drugs is beyond the scope of these guidelines, but re levant
interactions are referred to in the text when considered particularly
important. For more detailed information, see the product information
for individual drugs or an appropriate drug interactions reference (eg
Australian Medicines Handbook).
Faculty of Sexual and Reproductive Healthcare. Drug interactions with hormonal
contraception. London: Royal College of Obstetricians & Gynaecologists; 2011.
<www.ftprhc.org.ul</pdfs/CEUGuidanceDruglnteractionsHormonal.pdf>
20
Antibacterial drugs
Beta lactams
Penicillins
The most common adverse effects of the penicillins are nausea,
diarrhoea, rash, urticaria, pain and inflammation (at the injection
site), and superinfection (after prolonged treatment and/or with broad-
spectrum penicillins).
See also 'Antimicrobial hypersensitivity (allergy)' (p.l8) and
'Antibio tic-associated diarrhoea' (p.20).
~ Narrow-spectrum penicillins
Narrow-spectrum penicillins are active mainly against Gram-positive
organisms, and they are inactivated by beta-lactamases.
Phenoxymethylpenicillin (penici llin V) is acid-stable, so it can be given
orally, although food impairs absorption. lt is intrinsically less active
than benzylpenicillin. Phenoxymethylpenicillin is the drug of choice
in acute odontogenic infections due to its narrow (and appropri ate)
spectrum of activity, with 85% of oral bacteria susceptible. Although
susceptibi li ty to amoxyci llin is marginally higher (91 %), its use shou ld
be reserved to prevent the development of resistance in infections
caused by Streptococcus pneumoniae. Phenoxymethylpenicillin has
fewer gastrointestinal problems than amoxyc illin and is less likely to
cause a rash.
Benzylpenicillin (penicillin G) is administered parentera[y and is the
treatment of choice for susceptible infections if parenteral treatment is
warranted.
~ Narrow-spectrum penicillins with antistaphylococca l acti;ity
Dicloxacillin and flucloxacillin are stable to beta-lactamases produced
by staphy lococci. They are reliably absorbed by the oral roLte; however,
food reduces absorption and they are best taken half to one hour
before food. Ideally, they should be dosed at 6-hourly intervals, but
for practical purposes (eg in children) four-times-a-day dosing, evenly
spaced during waking hours, can be given. They are rarely indicated in
general dental practice.
F lucloxacillin is generally well tolerated but, rarely, is associated
w ith cholestatic jaundice, particularly in older patients on prolonged 21
 therapy. This may occur after oral or intravenous administration and up
to 6 weeks after treatment. It may last for months, can be irreversible
and, rarely, may be fatal. Dicloxacillin appears to cause less irreversible
hepatotoxicity but results in more infusion phlebitis and interstitial
nephritis. Dicloxacillin may be preferable to flucloxacillin for oral
therapy or in patients requiring prolonged therapy.
In these guidelines, di/fl ucloxacillin refers to dicloxacillin or
flucloxacillin.
~ Moderate-spectrum penicil lins
The aminopenicillins, amoxycillin and ampicillin, have greater activity
than benzylpenicillin against some Gram-negative organisms (eg
Escherichia coli, Haemophilus influenzae), but are destroyed by beta-
lactamase- producing strains. Amoxycillin is better absorbed orally than
ampicillin, is not affected significantly by food and requires fewer oral
doses per day, but when administered parenterally they are equivalent.
Amoxycillin and ampicillin can increase the likelihood of rash in
patients taking allopurinol (used in the prevention of gout).
In these guidelines, amoxy/ampicillin refers to amoxycillin or
ampicillin.
~ Broad-spectrum penicillins (beta-lactamase inhibitor combinations)
The beta-lactamase inhibitor clavulanate inhibits the enzymes produced
by Staphylococcus aureus, Bacteroides fragilis and H. influenzae, and
also most of the beta-lactamase enzymes found in E. coli and Klebsiella
species. Clavulanate possesses little
Amoxycillin + clavulanate
inherent antibacterial activity, but
should not be used as first-line
significantly extends the spectrum of
treatment for odontogenic
activity of amoxycillin when given infections.
with it. This combination should
be reserved for the treatment of beta-lactamase- producing organisms.
Additional anaerobic cover (eg metronidazole) is not required with
beta-lactamase inhibitor combinations .
Amoxycillin+clavulanate can cause dianhoea and hepatotoxicity,
which occur more frequently than with amoxycillin alone.
Cephalosporins
Cephalexin and cephazolin are moderate-spectrum cephalosporins
with a similar range of antimicrobial activity. They are active against
22
streptococci and staphylococci , including beta-lactamase-producing
staphylococci. Their Gram-negative spectrum includes E. coli and most
Klebsiella species, but they are inactive against many Gram-negative
aerobes (eg Serratia, Enterobacter and Pseudomonas species). They
are not useful against the Gram-negative anaerobe Bacteroides fi"agilis
and related species.
The common adverse effects are dianhoea, nausea, rash, eosinophilia,
drug fever, electrolyte disturbances, and pain and inflammation (at the
injection site). See also 'Antimicrobial hypersensitivity (allergy)' (p.18)
and 'Antibiotic-associated diarrhoea' (p.20).
Glycopeptides
Teicoplanin and vancomycin are active against a wide range of Gram-
positive organisms; Gram-negative organisms are not susceptible.
Glycopeptides are sometimes used to treat severe infection with
susceptible organisms in patients hypersensitive to penicillin.
Vancomycin or teicoplanin may be used for prophylaxis of endocarditis
in patients hypersensitive to penicillin.
Teicoplanin can be given by intramuscular injection, or slow intravenous
injection or infusion. Vancomycin is given by slow intravenous infusion
to avoid producing a histamine-release reaction, commonly known as
'red-man' syndrome.
Lincosamides
Clindamycin and lincomycin are active against Gram-positive aerobes
and most anaerobes. They are used as second-line therapy in those
intolerant to conventional therapy or where resistance is of concern.
Oral clindamycin and intravenous formulations of both clindamycin
and lincomycin are available. There is no oral liquid formulation of
clindamycin currently marketed in Australia; however, a 50 mg/mL
clindamycin solution can be made before each dose by dissolving the
contents of a 150 mg capsule in 2 mL of water. Draw this solution into
a syringe and make the volume up to 3 mL (if necessary) . The required
volume of solution should be mixed with juice or soft food to disguise
the taste before administration.
Clindamycin is well absorbed orally. Intravenous doses should be
administered slowly to avoid producing serious arrhythmias.
The most common adverse effects of lincosamides are diarrhoea
(see 'Antibiotic-associated diarrhoea', p.20), nausea, vomiting, 23
 abdominal cramps, abdominal pain, metallic taste (with intravenous
administration), itch and rash.
Macrolides
Macrolides are rarely indicated in dental practice, although
roxithromycin may be used to treat acute odontogenic infections in
patients with penicillin hypersensitivity. In vitro, roxithromycin has
reasonable activity against some oral organisms, such as viridans grqup
streptococci and Gram-positive anaerobes. However, its activity against
Gram-negative anaerobic organisms is more variable; Bacteroides
fragilis and Fusobacterium species are resistant.
Roxithromycin is preferred to erythromycin because it has a more
benign adverse effect profile, fewer drug interactions and better activity
against oral pathogens.
The most common adverse effects of macrolides are nausea, vomiting,
diarrhoea, abdominal pain, cramps, headache, dyspnoea, cough and
candida! infections.
Nitroimidazoles
Metronidazole and tinidazole have a spectrum of activity that
encompasses Gram-negative anaerobes such as Bacteroides fragilis,
Gram-positive anaerobes such as Clostridium species, and anaerobic
protozoa. Metronidazole is the drug of choice for spreading neck
infections and acute ulcerative gingivitis.
Metronidazole is available as an intravenous preparation; however,
excellent absorption means that tablets or suppositories can often be
used instead. In these guidelines, for the treatment of mixed aerobic
and anaerobic infection, metronidazole is recommended at a dose of
400 mg orally and 500 mg intravenously, with a 12-hourly dosing
schedule to increase patient adherence. This dosing regimen is based
on pharmacokinetic data and minimum inhibitory concentrations of the
pathogens involved, rather than formal clinical studies.
Tinidazole is available only as an oral preparation. It has a longer half-
life than metronidazole so it can be administered less frequently or as
a single dose.
The most common adverse effects of nitroimidazoles are nausea,
diarrhoea and a metallic taste. Nitroimidazoles can interact with alcohol
causing a disulfiram-like reaction (severe intestinal cramping, flushing,
tachycardia, nausea and vomiting). Patients should be counselled to
24
avoid alcohol during treatment, and for at least 24 hours after treatment
with metronidazole or 72 hours after treatment with tinidazole.
Metronidazole also inhibits the metabolism of warfarin, increasing
its concentration and the risk of bleeding, so patients taking warfarin
should have their international normalised ratio (INR) monitored.
Tetracyclines
Tetracyclines are usually bacteriostatic and have a broad spectrum of
activity, which includes Gram-positive and Gram-negative bacteria,
Chlamydia, Rickettsia, Mycoplasma, spirochaetes, some nontuberculous
mycobacteria and some protozoa. Tetracyclines are rarely indicated in
general dental practice, but may be used in the management of tooth
avulsion to help prevent root resorption.
Doxycycline is the preferred tetracycline in most situations, as once-
daily dosing enhances patient adherence and dosage adjustment is not
required in patients with renal impairment. Demeclocycline is available
in combination with triamcinolone acetonide as an intracanal paste (see
'Intradental corticosteroids', p.34).
Tetracyclines are contraindicated in children 8 years of age or less as
they chelate calcium ions and are incorporated into the hydroxyapatite
of the developing enamel and dentine, leading to tooth discolouration
and enamel dysplasia. They are also deposited in bone, causing
deformities and inhibiting bone growth. As dentine development may
continue beyond 8 years of age, some practitioners avoid tetracyclines
in children up to 12 years of age. 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.
There have been rare occurrences of hepatic necrosis in pregnant
women. Tetracyclines may be used for short courses (eg 7 to 10 days)
in breastfeeding women if there are no appropriate alternatives.
All tetracyclines cause some gastrointestinal symptoms. Oesophagitis
can occur with any tetracycline so they should be taken after food with a
full glass of water and the patient should be instructed to remain upright
for at least 30 minutes after oral administration. Photosensitivity
reactions can occur with any tetracycline, but are most likely with
doxycycline, and sun protection should be recommended. Candida]
overgrowth can also occur with any tetracycline.
There are several important interactions with tetracyclines. Antacids
decrease the absorption of tetracyclines, and oral doses of tetracyclines
and antacids should be separated by 2 hours. Some drugs (eg
25
 carbamazepine, phenytoin) reduce the plasma concentrations of
doxycycline. Tetracyclines can enhance the activity of warfarin so
patients taking warfarin should have their international normalised ratio
(INR) monitored.
Antifungal drugs
Miconazole
Miconazole is an imidazole derivative with broad antifungal activity.
It is available as a topical 2% oral gel, which is used to treat oral
candidosis.
Patients should be counselled to use the gel after food and retain the
gel in their mouth for as long as possible before swallowing. Treatment
should be continued for 7 days after symptoms disappear to prevent the
germination of remaining spores, which are invariably present.
Topical imidazole preparations can cause local irritation but
sensitisation is uncommon. Miconazole use on the oral mucosa may
cause a significant increase in the international normalised ratio (INR)
in patients taking warfarin.
Polyenes
Nystatin and amphotericin are highly effective against Candida
species. They can be used topically on the oral mucosa to treat candidosis,
as they are not absorbed through the mucosa or the gastrointestinal tract
to any significant extent.
Amphotericin is available as a lozenge-advise patients to suck the
lozenge after food to reduce the adverse effect of nausea. Nystatin is
available as oral drops- advise patients to take the drops after food and
to swish the medicine around the mouth for as long as possible before
swallowing.
Topical intraoral polyenes have few adverse effects. The most common
are mild gastrointestinal symptoms (eg nausea, vomiting, diarrhoea).
Antiviral drugs
Guanine analogues
Aciclovir, famciclovir and valaciclovir are active against herpes
26 simplex and varicella-zoster virus. Aciclovir is absorbed poorly and
erratically from the gut, and even less through the skin. Valaciclovir, a
prodrug of aciclovir, has improved oral bioavailability compared with
aciclovir. Famciclovir is well absorbed from the gut. Famciclovir and
valaciclovir require fewer oral doses per day than aciclovir. They are all
generally well tolerated.
Topical aciclovir and penciclovir are indicated for the treatment of
herpes simplex virus infection of the lips (herpes simplex labialis). For
best effect, they should be applied to the lesions or impending lesions
as early as possible, pm1icularly for treatment of recurrent episodes.
Common adverse effects include a transient stinging or burning
sensation. Application of topical aciclovir and penciclovir to mucous
membranes (eg in the mouth, eye or vagina) should be avoided as they
may be irritant.
ANALGESICS
Three broad groups of drugs are used as analgesics for oral and dental
pain- nonsteroidal anti-inflammatory drugs (NSAIDs), paracetmnol
and opioids.
Nonsteroidal anti-inflammatory drugs
General considerations
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most
commonly used drugs for pain relief. Many patients use NSAIDs for
self-management of common pain problems (eg headaches, muscular
aches, period pain, toothache).
NSAIDs relieve nociceptive pain associated with inflammation due
to tissue damage, as well as having a direct anti-inflammatory action.
They exert their main effect by inhibiting cyclo-oxygenase (COX),
which in turn reduces the synthesis of pro-inflammat01y mediators
(prostaglandins) from arachidonic acid. NSA!Ds act both at peripheral
sites in the body (ie where the tissue damage has occurred) and in the
central nervous system.
As the majority of dental pain is inflammatory in origin, NSAIDs are
the drug class of choice for the treatment of acute dental pain. They
are also effective in treating bone pain, which makes them very useful
for dental pain. NSAIDs can be used alone for mild to moderate pain;
however, severe pain usually requires the addition of another analgesic,
such as paracetamol.
27
 The analgesic and, particularly, anti-inflammatory actions of NSAIDs
are dose-related. Lower doses can provide pain relief, but higher
doses are required for effective anti-inflammatory action (ega single
dose of 200 mg of ibuprofen may relieve pain temporarily, but at least
400 mg is required to reduce the inflammatory response; 600 mg is
even more effective). However, adverse effects are also dose-related,
and the analgesic needs of the patient must be balanced against the risk
of adverse effects (see below for adverse effects). The dosing interval
is important to maintain therapeutic blood concentrations. These drugs
should be used as a 'course of treatment' with regular doses at specified
time intervals rather than when the patient feels pain or discomfort. It
is important to educate the patient about how to use NSAIDs properly.
Many different NSAIDs are available and they have similar efficacy.
Therefore, the choice of drug is largely based on safety, availability,
cost and the required route of administration. The pharmacokinetic
profiles of individual NSAIDs vary considerably. The most commonly
used NSAIDs for dental, oral and facial pain are ibuprofen and aspirin.
Ibuprofen produces greater analgesia than paracetamol+codeine
combinations.
Adverse effects, interactions and precautions
All NSAIDs have potential adverse effects and these should be
discussed with the patient (see Table 2, p.29). Older patients have a
higher risk ofNSAID-related adverse effects and their need for NSAID
therapy should be assessed carefully.
NSAIDs may cause gastric erosions and peptic ulcers (gastric and
duodenal) and increase the risk of upper gastrointestinal complications
(bleeds, perforation). These lesions may occur in the presence or
absence of symptoms. The relative risk of a serious gastrointestinal
adverse event varies between NSAIDs and is dose-related. The risk is
also related to patient-specific factors (see Box 5, p.29).
NSAIDs are typically contraindicated in patients with a definite history
ofNSAID allergy (particularly NSAID-induced asthma), active peptic
ulcer disease or gastrointestinal bleeding. Aspirin should not be used
for analgesia in children less than 16 years of age because of its rare
association with Reye syndrome.
NSAIDs interact with many drugs, including angiotensin convetiing
enzyme inhibitors, angiotensin II receptor blockers, inhibitors of some
cytochrome P450 enzymes, some diuretics, lithium and warfarin.
28
NSAIDs are available as over-the-counter medications and on
prescription; they are packaged in ditferent dosages for different markets.
It is impotiant that the correct dosage is prescribed and the potential
problems are explained to the patient. Some commercial formulations
combine NSAIDs with other drugs; a careful medication history needs
to be taken to determine the total daily dose of each component.
Table 2. Adverse effects of nonsteroidal anti-inflammatory
drugs
System Adverse effects
cardiovascular rise in blood pressure, fluid retention, myocardial infarction, stroke
neurological headaches, confusion , hallucinations, depersonalisation reactions,
depression, tremor, aseptic meningitis, tinnitus, vertigo, neuropathy,
toxic amblyopia, transient transparent corneal deposits
nausea, vomiting, dyspepsia, diarrhoea, constipation, gastri c mucosal
gastro i ntesti na I
irritation, superficial erosions, peptic ulceration, oesopha~tis and
strictures, faecal blood loss, major gastrointestinal haemorrhage,
penetrating ulcers, small bowel erosions
haematological anaemia, bone marrow depression, decreased platelet aggregation
hepatotoxicity, fulm inant hepatic failure
renal glomerulopathy, interstitial nephritis, changes in rena l blood flow
leading to a fall in glomerular filtration rate, alterations in tubular
function, reduction in diuretic-induced natriuresis, inhibition of renin
release, oedema
other precipitation of asthma in patients with nasal polyps, skin rashes
Box 5. Risk factors for NSAID-induced upper
gastrointestinal bleeding or perforation
older age
past history of upper gastrointesti nal bleeding
past history of peptic ulcer disease
Helicobacter pylori infection
concomitant drugs, including (in order of risk) anticoagulants, antiplatelet drugs,
SSRis and corticosteroids
significant comorbidity
smoking.
NSAID - nonsteroidal anti-inflammatory drug; SSRI = select1ve serotonin reuptake inhibitor
29
 Paracetamol
General considerations
Paracetamol (acetaminophen) has analgesic and antipyretic actions
through inhibition of prostaglandin synthesis in the central nervous
system. In therapeutic doses, inhibition of prostaglandin synthesis is
not significant in peripheral tissues, so paracetamol has minimal anti-
inflammatory action.
Paracetamol may be used to reduce the required daily dose of
nonsteroidal anti-inflammatory drugs (NSAIDs) or opioids, thus
reducing the risk of their adverse effects. Other indications include:
an alternative to NSAIDs, including when NSAIDs are
contraindicated (see 'NSAIDs: Adverse effects, interactions and
precautions', p.28)
mild procedural pain
management of fever.
Paracetamol is rapidly absorbed after oral administration, with peak
blood concentrations reached within 10 to 60 minutes; its half-life is
1 to 3 hours. It readily crosses into the cerebrospinal fluid and into the
brain where it has its major analgesic effect. It undergoes extensive first-
pass metabolism in the liver, and the kidneys excrete its metabolites.
The typical dose schedule for healthy adult patients is 0.5 to l g every
4 to 6 hours up to 4 g per day (less in the elderly and the frail). Some
oral preparations are modified for slow release and can be taken every
8 hours.
Formulations of paracetamol include immediate-release tablets and
capsules, modified-release tablets, chewable tablets, soluble and
effervescent tablets, oral solutions and suspensions, suppositories,
and an injectable formulation. Paracetamol may be combined with
other analgesics (eg NSAIDs, codeine), decongestants, antihistamines
and antiemetics. Some combination products are available without a
prescription. Clinicians should be familiar with the range of preparations
available so they can advise patients.
Adverse effects, interactions and precautions
Paracetamol is generally considered a safe analgesic with a low
incidence of adverse effects compared with other drugs. Rarely,
patients may experience urticarial or erythematous rashes, fever or
blood dyscrasias. Long-term use of paracetamol alone does not seem
30 to cause analgesic nephropathy and it can be used in patients with liver
metastases; however, paracetamol should be administered cautiously in
patients with renal or hepatic dysfunction. Tolerance and dependence to
paracetamol have not been reported.
Paracetamol doses of more than 3.5 g per week may interact with
warfarin to increase the international normalised ratio (INR) so patients
taking warfarin should have their INR monitored.
Inadvertent overdose is a possibility (see below). Due to the variety of
paracetamol-containing products available, patients should be advised
to consider the paracetamol content of all medications taken. A careful
medication history should be taken to determine the total daily dose of
paracetamol. Care is required when prescribing paracetamol and the
dose should be stated in grams or milligrams rather than as number of
tablets or volume of liquid.
Overdose
Acute paracetamol overdose (in adults with a single ingestion of more
than l 0 g and children with a single ingestion of more than 200 mg/kg)
is a potentially life-threatening event. Excessive metabolite production
in overdose may overwhelm the availability of hepatic glutathione to
detoxify the harmful metabolite, leading to severe toxicity with hepatic
necrosi s. Much lower doses of paracetamol may be toxic in patients
who already have reduced hepatic glutathione due to starvation, fasting
or other acute hepatic insult. A paracetamol overdose is a medical
emergency that requires recognition and prompt management (see
Therapeutic Guidelines: Toxicology & Wilderness for assessment and
management). Clinical signs of overdose may take several days to
develop so liver biochemistry, renal function tests and plasma
paracetamol concentration should be performed immediately and
monitored.
Opioids
General considerations
Opioids (narcotics) are generally used for severe pain (eg severe
postoperative pain, severe acute trauma, chronic cancer-related pain).
Opioids include codeine (the most commonly prescribed opioid in
dental practice) (see p.32), morphine, oxycodone and tramadol.
Opioids have many significant adverse effects in all major systems
of the body (see Table 3, p.33) and should be used with caution. Safe
use requires knowledge of the available opioids and their relative
31
 indications, formulations and routes of admi nistration, as well as
awareness of their potential adverse effects and how to manage these.
Opioids act on specific receptors at supraspinal, spinal and peripheral
sites. They can block all forms of pain, not just pain arising from tissue
damage and inftammat01y processes. The normal clinical doses used
also dampen the patient's emotional response to the pain, perhaps more
effectively than blocking the pain (ie pain may still be noted by patients
but they can tolerate it or cope with it better).
Adverse effects, interactions and precautions
The adverse effects of opioids are summarised in Table 3 (p.33).
Hypersensitivity may manifest as pruritus, urticaria, rash or broncho-
spasm. Opioid withdrawal syndrome includes body aches, diarrhoea,
'goose flesh', loss of appetite, nervousness or restlessness, runny nose,
sneezing, tremors or shivering, stomach cramps, nausea, sleeplessness,
diaphoresis, yawning, asthenia, tachycardia and unexplained fever.
Concomitant use of central nervous system depressant drugs (eg
sedatives, hypnotics, anti psychotics, antidepressants, anaesthetics,
alcohol) may increase the sedative and respiratory depressant effects
of opioids. Concomitant use of drugs with anticholinergic activity (eg
tricyclic antidepressants, atropine) may increase the risk of severe
constipation, urinary retention and delirium. Drugs that induce or
inhibit the hepatic cytochrome P450 system may affect the blood
concentrations of opioids, lead ing to either decreased effectiveness or
toxicity. Opioids affected include tramadol and codeine.
Optimal analgesia is difficult to achieve in an opioid-dependent person
and specialist advice may be needed.
Codeine
Codeine is metabolised to morphine, which is responsible for most of
codeine's analgesic action. Approximately 7% to 10% of Caucasians
and I% to 2% of Asians are poor metabolisers of codeine, and have no
detectable analgesic effect from codeine. In these individuals, there is
no benefit in increasing the dose, and it is potentially harmful because
codeine itself can cause constipation and drowsiness.
Codeine is available for oral use, and has a duration of action of 4 to
6 hours. For opioid adverse effects, interactions and precautions, see
above.
32
Table 3. Adverse effects of opioids
System Adverse effects
cardiovascular bradycardia due to stimulation of the vagal nucleus in the medulla
histamine rel ease by morphine and morphine analogues, which
may cause vasodilation and hypotension during intravenous
administration
postural hypotension from peripheral vasodilation and baroreflex
inhibition
dermatological sweating, flushing
urticaria and pruritus due to histamine release
gastrointestinal vomiting, anorexia, decreased gastric motility, increased antral tone,
delayed gastric emptying, slowed digestion, prolonged large bowel
transit time, increased anal sphincter tone, constipation (these
are caused by mu and delta receptor agonists acting locally and
centrally)
chest wall rigid ity (with fe ntanyl and fentanyl analogues), myoclonus
musculoskeletal
neuroendocrine hypothalamic effects (including inhibition of gonadotrophin-releasing
hormone and corticotrophin-releasing factor) leadi ng to decreased
gonadotroph ins, adrenocorticotrophic hormone, beta-endorphin,
testosterone and cortisol, and increased prolactin
antidiuretic hormone release is variably increased by mu receptor
agonists (leading to fluid retention or oedema), and inhibited by
kappa receptor agonists
neurological dose-dependent mental clouding, delirium, sedation, nausea and
vomiting, cough suppression, miosis, respiratory depression or
apnoea, excitatory phenomena with myoclonus with high doses
relative to renal function, reactivation of herpes simplex (with spinal
and epidural morphine)
following intraspinal use of morphine or hydromorphone, central
adverse effects may be considerably delayed (6 to 12 hours)
respiratory dose-related respiratory depression (which is more marked during
sleep or with concomitant sedatives, hypnotics, alcohol and general
anaesthetics)
bronchospasm due to histamine release
urinary urinary retention and difficulty with micturition , increased external
sphincter tone, decreased detrusor muscle tone, antidiuretic effect
33
 CORTICOSTEROIDS
Corticosteroids are useful drugs for the management of many dental and
oral mucosal inflammatory conditions. Their use must be prefaced by a
complete medical and medication history, and an accurate diagnosis of
the presenting condition.
In dentistry, cotiicosteroids can be used intradentally (within a tooth),
topically on the oral mucosa or systemically. The most effective route
of administration should be chosen. Intradental or topical intraoral
cmiicosteroids are preferred as the drug is placed at the site of action,
which generally results in a more rapid onset of action and less systemic
adverse effects.
lntradental corticosteroids
Cmiicosteroids have been combined with antibiotics for intradental
application in the management of pulp and periapical diseases. The
corticosteroid component is included as almost all pulp and periapical
diseases are inflammatory in nature. The antibiotic component is
included as these diseases are usually caused by the presence of bacteria
within the tooth, pulp or root canal system.
There are two forms of cotiicosteroid-antibiotic compounds commer-
cially available for intradental use- a water-soluble paste and a hard-
setting cement. The form used depends on the condition being treated
and where the material is to be placed .
The cotiicosteroid-antibiotic pastes are used as an intracanal medication
(within the root canal system of a tooth) during endodontic treatment.
The paste can be used as an initial medication for rapid and reliable
relief of pain associated with irreversible pulpitis. It is also used as
an intracanal medication to reduce the periapical inflammation (acute
or chronic apical periodontitis)- and hence the pain- that is often
associated with irreversible pulpitis and always associated with an
infected root canal system. The pastes are also used as an intracanal
medication to prevent and manage several forms of inflammatory
root resorption (eg internal inflammatory resorption, external apical
inflammatory resorption, external lateral inflammatory resorption).
An additional effect of intracanal corticosteroid pastes is a reduction
in external replacement resorption following tooth avulsion and
intrusive luxation injuries, as cotiicosteroids inhibit the action of
clastic cells. Commercial preparations of pastes include clindamycin or
demeclocycline with triamcinolone acetonide.
34
The corticosteroid-antibiotic cements are used within th e crown o l" a
tooth as part of a cavity lining or base, as an indirect pulp cap, as a direct
pulp cap, or as a pulpotomy agent before restoration of cavities in teeth
that have reversible pulpitis. Commercial preparations typically al so
contain various other substances (eg calcium hydroxide, zinc oxide,
eugenol). The cement is presented as a powder and liquid, which are
mixed to form a paste that is placed on the dentine or exposed pulp; it
then sets to form the hard cement.
Topical corticosteroids
General considerations
Topical corticosteroids have anti-inflammatory and immunosuppressant
effects that are useful in a number of skin, mucosal and mucocutaneous
diseases. Modifications of the naturally occwTing hydrocortisone
molecule have produced a range of drugs with vatying anti-inflammatory
potency for topical use (see Table 4, p.36). An understanding of this
potency is critical to their effective and safe clinical use. The potency
depends on the concentration used, the intrinsic activity ofthe compound,
and its ability to penetrate the banier of the epidermis or mucosa, which
may be influenced by the vehicle in which it is applied and the method of
application. The permeability of the oral mucosa varies at different sites.
Keratinised masticatory mucosa (palate, dorsum of tongue and gingivae)
is less permeable than nonkeratinised lining mucosa (floor of mouth
and ventral surface of tongue). The cumulative effect of cmiicosteroids
depends on the frequency and duration of application.
Topical corticosteroids should not be used unless a clinical diagnosis
that requires the use of corticosteroids has been made. It is important
that the pathogenesis of the condition is understood so an appropriate
regimen can be determined and, equally, the outcome of this regimen can
be defined and discussed with the patient. For example, the indications
and outcome with oral lichen planus are quite distinct from pemphigoid
and aphthous ulcerative disease.
Most mucosal lesions progress through several stages (eg an aphthous
ulcer may be prodromal, preulcerative, ulcerative, or show signs of
healing or advanced healing). The stage of the disease must be identified
to assist in determining the treatment. Consideration of the stage helps
establish if a corticosteroid is indicated and, if so, the appropriate potency,
the method of application, the frequency and duration of treatment, and
the expected treatment outcome.
continued p.37
35
 Table 4. Properties of topical corticosteroids used on the Most mucosal diseases respond best to a topical corticosteroid
oral mucosa when it is applied at the earliest stage (eg topical corticosteroids arc
most useful for aphthous ulcers when they are in the prodromal and
Drug Strength Form* Clinical Oral uses preulcerative stages, as this disease has a well established cell-mediated
potency immunopathogenesis).
on oral
mucosa t The topical cotiicosteroids that can be applied intraora lly and their
hydrocortisone
suggested uses are outlined in Table 4 (p.36). In the mouth, ointments
1% ointment mild minor mucosal
acetate
inflammation,
are preferred, as creams are less effective in enhancing contact time.
cheilitis (not Generally, twice-daily application is adequate and there is no additional
su itable for angular benefit from more frequent use. Most areas receive adequate coverage
cheilitis)
with frugal app lication and brief gentle rubbing without abrading
triamcinolone 0.02%
acetonide
ointment moderate inflammatory tissues. If prolonged application is indicated, for example in gingival
mucosal conditions erosive conditions, custom-made applicators can be worn by the patient.
betamethasone 0.02%, ointment moderate inflammatory
valerate 0.05% mucosal conditions
Clinicians should exercise caution with the entire range of
(eg aphthous corticosteroids, and avo id potent drugs unless familiar with their use
ulceration, lichen and there is a clear indication for this level of drug. The prolonged use
planus) (use with
caution)
of hi gh potency corticosteroids requires careful control. Often their use
betamethasone
indicates a lack of understanding of the disease mechanisms and an
0.1% ointment potent inflammatory
valerate unrealistic expectation of the treatment by the patient and clinician (ie
mucosal conditions
(eg aphthous expect cure/lesion resolution, as opposed to symptom reduction and
ulceration, lichen control).
planus) (use with
caution)
betamethasone 0.05% ointment potent inflammatory General principles of use
dipropionate
mucosal conditions
(eg aphthous Most topical corticosteroids available in Australia are marketed for
ulceration, lichen external use on the skin and packaging is marked accord ingly. Therefore,
planus, pemphigoid, it is important patients are made aware of the nature of the prescribed
pemphigus) (use
with caution) medication and are reassured that the medication is safe for intraoral
methylprednisolone 0.1%
application when used as instructed. Patients also benefit from written
ointment moderate inflammatory
aceponate
mucosal conditions
confirmation of verbal instructions separate from the prescription, as
(eg aphthous the dispensing pharmacist or attending medical practitioner may not be
ulceration, lichen familiar with the intraora l use of these drugs and may provide conflicting
planus) (use with
caution)
advice. (On occasion, the drug may not be dispensed on the basis that it
mometasone 0.1%
is 'for external use only'.) Points to consider when prescribing topical
ointment potent severe inflammatory
furoate intraoral cotiicosteroids are outlined in Box 6 (p.38).
mucosal conditions
(eg erosive lichen
Caution must be taken with corticosteroid use in patients with certain
planus) (use with
caution) conditions, and patients must be advised of potential adverse effects and
* In the mouth, ointments are preferred, as creams are less effective in enhancing contact time.
be reviewed regularl y (see p.38 for adverse effects).
t Potencies of corticosteroids when applied to the oral mucosa are not the same as when they The use of topical corticosteroids must be precise and controlled.
are applied to the skin .
Many commonly prescribed topical cotiicosteroids are medium to high
36 potency and this is not apprec iated by the patient and, on occasion, by
37
 the prescriber. A general guideline is to prescribe the lowest potency
clinically indicated, with a minimal amount applied as infrequently as
possible for the minimum time. Extending use outside of this guideline
requires specialist advice.
The goal of treatment should be defined and explained to the patient.
This may be:
o symptomatic relief only
o complete lesion resolution (eg for minor aphthous ulceration)
resolution but with residual visible tissue changes (eg for major
aphthous ulceration)
o clinical management of a chronic condition (eg for atrophic lichen
planus).
Box 6. Points to consider when prescribing topical intraoral
corticosteroids
o Corticosteroids are best applied with the pad of a washed finger. Applicators,
including cotton tips, are fibrous and may inadvertently damage the fragile
atrophic mucosa.
o Corticosteroids should be applied to wet mucosa. Drying the tissues before
application is a natural instinct, but tissue trauma must be balanced against
any benefit of drying (which is minimal).
o Prolonged avoidance of food and drink after topical corticosteroid application
seems logical, but is not req uired as corticosteroid absorption is reasonably
rapid.
A convenient time for application is after oral hygiene in the morning and at
night.
o Patients readily become frustrated when ointments do not adhere effectively.
This is overcome by frugal application, brief gentle rubbing with the finger pad,
and reassurance that this method of application is adequate.
o Patients using special methods of application (eg sprays, adhesives) require
additional written explanation.
Adverse effects, precautions and contraindications
Adverse effects of topical corticosteroids may be due to local effects on
the skin or mucosa at the site of application, or due to systemic effects
following absorption of the drug (see 'Systemic corticosteroids' for a
discussion of systemic adverse effects, p.40). The intensity of adverse
effects increases with the potency of the preparation. When topical
corticosteroids are used on the oral mucosa, systemic absorption is
generally limited; however, caution is required when potent topical
preparations are used.
38
I ntraorally, adverse effects are somewhat hidden, but they are noticeable
on the face and the vermilion of the lips. Penetration of corticosteroid
into the dermis is greater on the face and only mild cot1icosteroids (eg
hydrocortisone) should be used on this site. In cet1ain circumstances,
more potent corticosteroids (eg methylprednisolone aceponate) may
be used intermittently for up to 2 weeks. If improvement does not
occur after 2 weeks, do not persevere with treatment-reconsider the
diagnosis and seek specialist advice.
Potential local skin effects include:
o loss of dermal collagen, leading to skin atrophy, formation of
striae, fragility and easy bruising
o telangiectasia (development of prominent blood vessels)
o promotion of infection
o idiosyncratic reactions (eg allergic contact dermatitis, perioral
dermatitis).
The most common adverse reactions to topical intraoral corticosteroids
are secondary oral candidosis, nausea, intolerab ility (eg because of
unpleasant taste), refractory response, mucosal atrophy and delayed
healing. Secondary oral candidosis imposes a treatment interruption
and delays effective management. In many cases, it can be anticipated,
and preventive and interceptive strategies can be used concurrently.
For example, patients with salivary gland hypofunction or atrophic
candidosis under prostheses, or patients who are using corticosteroid
inhalers or have hyperkeratotic lesions (Candida is keratinophilic) are
more likely to develop candidosis.
A number of oral mucosal diseases cause tissue atrophy, particularly
on the tongue (eg lichen planus), which can persist even with lesion
resolution or entry into a quiescent phase. Long-term use of topical
corticosteroids compounds the disease-related atrophy. Monitor patient
use and adherence, and regulate use against the level of tissue and
sensory morbidity experienced by the patient.
With greater potency, there is also an increased risk of rebound on
withdrawal. Many conditions benefit from a tapered dose red uction to
complete cessation or, on occasion, a maintenance level.
Topical cot1icosteroids should not be used in the presence of infection
without appropriate antimicrobial cover. Generally, infections
or a predisposition to develop an infection should be managed
initially before commencing topical corticosteroids. Avoid topical
corticosteroids if a viral disease is suspected as they prevent cytotoxic
T lymphocytes attaching to virally infected cells and do not control
39
 the local inflammatory component of conditions such as herpes zoster.
Systemic contraindications, including the possibility of reactivation
of tuberculosis, should be considered when using methods likely to
enhance contact time and systemic absorption. These include occlusive
devices, such as custom applicators, and cotiicosteroid mouthwashes.
Caution is also required in patients with hypertension or diabetes.
Systemic corticosteroids
Systemic cotiicosteroids are usually inappropriate for general dental
practice. They represent a highly potent class of medication, and
while adverse events are uncommon and of short duration, they are
significant. Wherever possible, the topical cotiicosteroids are preferred
because their immunosuppressive effects are much less (see ' Topical
corticosteroids', p.35).
Some oral inflammatory mucosal conditions, however, do require
systemic corticosteroids. Systemic corticosteroids should on ly be used
in patients who have been assessed as suitable for treatment (eg there
are no contraindications to their use) and in whom they are the treatment
of choice. Systemic corticosteroids may be useful in the management
of severe postoperative swelling, severe trauma, and periapical nerve
sprouting and acute apical periodontitis following removal of acutely
inflamed pulp. All of these conditions usually require specialist
management.
The major limiting factor in the use of systemic cotiicosteroids is the
development of adverse effects, which may be extensive and are largely
dose-related. Treatment with prednisolone or prednisone at doses greater
than I 0 mg daily for more than 3 weeks may be sufficient to cause
adrenal suppression. A patient taking corticosteroids should have their
dose increased before surgery. Addisonian (adrenal) crisis can present
6 to 12 hours after surgical stress in a patient taking corticosteroids
who has not had the dose increased before the surgery (see 'Adrenal
disorders: Dental issues ', p.l51) .
LOCAL ANAESTHETICS
See the 'Local anaesthesia' chapter (pp.lll - 19) for detailed information.
ANXIOLYTIC AND SEDATIVE DRUGS
Depending on the dose administered, drugs classified as anxiolytics and
sedative-hypnotics have the ability to calm a patient and relieve anxiety
40
(;mxiolytic effect), promote drowsiness (sedat i v~ effect) and induce
sleep (hypnotic effect). All anxiolytic and sedattve drugs are centra l
nervous system (CNS) depressants. The most common!y us~d dru gs
lor oral anxiolysis and sedation in dentistry are benzodtazepmes (see
below).
The development of substance dependence, tolerance and withdrawal
can be a major concern to both patients and prescribers. For more
information, see p.42.
Benzodiazepines
General considerations
Benzodiazepines are the most commonly prescribed anxiolytic and
sedative drugs because of their efficiency and relatively low incidence
of adverse effects. They act by potentiating the action of gamma-
aminobutyric acid (GABA) at the GABAAreceptor resulting in neuronal
inhibition.
Benzodiazepines are generally rapidly and fu lly absorbed after oral
ingestion with peak plasma concentrations occurring from 0.5 to
2 hours after administration. They There is little basis for the use of
are metabolised by glucuronidation, more than one benzodiazepine
which inactivates them, and by o_x i- concurrently in any patient.
dation which may produce acttve
metab~lites. Most differences between benzodiazepines are exp licable
in terms of different pharmacokinetic properties. There is little basis for
the use of more than one benzodiazepine concurrently in any patient.
Adverse effects, interactions and precautions
Drowsiness is a common initial reaction to benzodiazepines. Psycho-
motor performance may be impaired, as may some memory functions.
Older people are patiicularly vulnerable to the adverse effects of
ataxia (with conseq uent fa lls and injury), confusio~, _memory loss and
cognitive impairment. Benzodiazepines can prectpttate deltnum. ~n
younger patients, ataxia, nystagmus, muscle wea~_e ss and dysar!hna
are repotied less often. Dry mouth and blurred vtstOn are somettmes
troublesome.
Sedation may persist the following day after benzodiazepine dosing
(even with short-acting drugs) and the effects of a l co~ol and othe_r CNS
depressants (eg opioids) can be potentiated. Warn pattents that thts may
affect their abi lity to drive and operate machinery safely. 41
 The potential for developing tolerance, dependence and withdrawal
symptoms is an important consideration (see below). Dependence
develops rarely in patients taking therapeutic doses of benzodiazepines
for short periods (eg 1 to 2 weeks). All benzodiazepines can produce
withdrawal symptoms; these can be physical and psychological and are
related to the dose and duration of use. Tolerance occurs more with
the sedative and hypnotic effects of benzodiazepines than with other
effects; the degree of tolerance differs between patients. Patients with
a history of dependence on alcohol and other drugs are more likely to
become dependent or intentionally misuse benzodiazepines.
Avoid benzodiazepines in patients with myasthenia gravis, severe
respiratory impairment or severe hepatic impairment.
Diazepam and temazepam
Diazepam and temazepam are widely used as anxiolytics and sedatives.
Diazepam is also used as a muscle relaxant and as an antiepileptic.
Diazepam is available as tablets, an oral liquid and an injection. It
is reliably absorbed from the gut and its optimum clinical effect is
reached after I hour. Diazepam's half-life is between 14 and 70 hours;
its primary metabolite, nordiazepam, retains significant CNS depressant
activity. Temazepam also has a rapid onset of action, but has a relatively
short half-life (3 to 25 hours) and no active metabolites. Temazepam is
only available as tablets.
For benzodiazepine adverse effects, interactions and precautions, see
(6 p.41.
....c:
Q)
Q be beneficial (eg for short-term use in patients with gingivitis when
"C
Dependence, tolerance and withdrawal
c:
~ Tolerance is a physical state whereby, after repeated administration, a
~ given dose of drug produces a decreased effect, or increasingly larger
0 doses must be taken to obtain the effects observed with the original dose.
Physiological dependence occurs when repeated administration of the
drug is necessary to prevent a characteristic withdrawal syndrome.
Substance dependence is a behavioural syndrome in which individuals
have an overwhelming drive to use a substance, often despite medical
or social consequences, and they behave as if the effects of the drug
are needed for continued wellbeing. The term ' addiction' is best used
synonymously with dependence. Tolerance and withdrawal represent
only 2 of the 7 criteria for substance dependence in the most commonly
used diagnostic criteria of DSM-IV-TR (see Therapeutic Guidelines:
42
Psychotropic for more information). Some drug classes (eg se lective
serotonin reuptake inhibitors) are associated with a withdrawal
syndrome, but patients taking these drugs do not show development of
dependence.
Patients with a substance use disorder, particularly alcohol- or opioid-
related, or a history of such a disorder, are at particular risk of developing
benzodiazepine dependence. If a drug use problem is identified, it is
imp011ant to investigate the use of other substances as multiple drug use
is very common. A range of psychiatric disorders also occurs with greater
frequency among patients with problem drug use. The most common
are depression, anxiety disorders (pa11icularly social phobias) and
personality disorders. It should also be recognised that many psychiatric
patients use drugs such as alcohol, cannabis and amphetamines.
See also 'Legislation about prescriptions and prescribing' (p.ll) for
prescribing drugs of dependence.
MOUTHWASHES
A mouthwash may be recommended as:
an antiseptic to decrease the number of microorganisms in the oral
cavity (eg for periodontal disease, halitosis, dental caries)
fluoride treatment for dental caries
an anti-inflammatory (eg for oral mucosal di sease)
an analgesic (eg for oral mucositis).
The use of antiseptic mouthwashes in periodontal disease is
controversial; however, there are specific instances where they can
inflammation restricts normal toothbrushing). These mouthwashes
are only effective against supragingival plaque, and are not effective
beyond the gingival crevice or periodontal pocket. Therefore, they
are not appropriate as the sole treatment for periodontal disease.
Patients should be informed that the principal treatment for chronic
periodontal disease is professional intervention with root planing of
involved teeth and meticulous oral hygiene (see 'Gingivitis ', p .55, and
' Periodontitis', p.56).
The use of mouthwash alone for oral hygiene is not recommended.
Oral hygiene must be, principally, toothbrushing and dental flossing.
Nevertheless, the use of mouthwashes containing fluoride has significant
benefits in patients at high risk of caries (see 'F luoride' , p.50).
43
 Although anti-inflammatory mouthwashes can provide symptomatic
relief of oral inflammatory mucosal disease, the use of topical
corticosteroids is often the most effective treatment; this is discussed
in the 'Oral mucosal disease' chapter (pp.71-90) and in the ' Topical
corticosteroids' monograph (p.35).
Use of alcohol in mouthwashes
Alcohol causes profound drying of the oral mucosa. Advise patients
with oral mucosal disease and dry mouth to avoid alcohol-containing
mouthwashes, as they will exacerbate their condition.
There is currently controversy surrounding a possible link between
alcohol-containing mouthwashes and oral cancer. Until this is resolved,
it is recommended that alcohol-containing mouthwashes be used
with care.
Antiseptic mouthwashes
Chlorhexidine
Chlorhexidine, an antiseptic commonly used in mouthwashes, is
bactericidal and effective against fungi (including yeasts). Chlorhexidine
adsorbs onto oral surfaces so it is effective over a prolonged period. By
these mechanisms, it prevents plaque formation on a clean tooth surface,
but does not reduce pre-existing plaque. Therefore, where possible,
chlorhexidine should not be recommended without mechanical oral
hygiene measures.
In a mouthwash, it is available as chlorhexidine gluconate in
concentrations of 0.12% and 0.2%. It is also used in sprays, creams,
gels, solutions, dressings and powders. A slow-release formulation is
available for local delivery into periodontal pockets.
Chlorhexidine salts can cause skin reactions, irritate mucosal surfaces
and interrupt wound healing. Chlorhexidine mouthwash and intraoral
gel can discolour teeth, margins of restorations, the tongue and buccal
cavity; this extrinsic staining is not permanent and can be professionally
removed. Chlorhexidine can also cause a burning sensation, altered
taste and increased calculus formation . For these reasons, particularly
to prevent the adverse effect of staining, chlorhexidine is usually
recommended for short periods of up to 2 weeks.
44
Povidone-iodine
Povidone-iodine is an iodine complex that has antibacterial, antifungal
and antiviral properties. It is used in mouthwashes and gargles. It is also
used in skin cleansers; antiseptic creams, ointments, powders, solutions
and paints; and in some antiseptic swabs and wound dressings.
Povidone-iodine can cause irritation of skin and mucous membranes.
It is absorbed through damaged skin so application over a large broken
skin surface is not recommended.
Povidone-iodine should not be used during pregnancy or lactation as it
has the potential to cause hypothyroidism in the neonate.
Triclosan
Triclosan is a broad-spectrum antibacterial used in mouthwashes
and toothpastes. It effectively inhibits plaque build-up. It also has
anti-inflammatory properties, which futiher helps to reduce gingival
inflammation. Triclosan is also used in medicated soaps and topical skin
preparations. Allergic contact dermatitis has been reported.
Fluoride mouthwashes
Mouthwashes containing fluoride are discussed on p.SO.
Benzydamine
Benzydamine is a nonsteroidal anti-inflammatory drug (NSAID) and
therefore has anti-inflammatory and analgesic properties. It can be used
for the temporary relief of painful inflamed oral mucosal conditions.
It is available in mouthwashes, mouth gels and sprays, sometimes in
combination with chlorhexidine, in concentrations of 0.15% to 1%.
Local adverse reactions of benzydamine, such as numbness, burning,
erythema and rash, have been occasionally reported. Systemic adverse
reactions are uncommon and not serious.
Further reading
Sources of drug information are given on p.10.
45
Dental caries
Dental caries (tooth decay) is a pathological process resulting in localised
destruction of tooth tissue. The disease begins with demineralisation of
the hard tissue of the tooth by organic acids. Bacteria resident in dental
plaque produce these acids by fermenting carbohydrates in food. See
Figure 2 (p.62) for a schematic diagram of the stages of dental caries.
The incidence of dental caries has declined in most developed countries
over the last three decades, largely due to the use of fluorides. However,
the incidence has now plateaued, and there are some indications that
the rate of caries may be increasing in children. Therefore, although
preventable, dental caries remains a major worldwide public health
problem.

PATHOLOGY
Dental plaque must be present for caries to develop. Dental plaque
is a complex biofilm that builds up on teeth. It includes a mixed
community of bacteria and their by-products. These bacteria have
variable capacities to produce organic acids (eg acetic, lactic and formic
acids) from fetmentable carbohydrates (particularly dietary sugars).
Frequent exposure to fermentable carbohydrates leads to an increase
in the population of cariogenic bacteria (eg Streptococcus mutans and
Lactobacillus species) in the biofilm. These bacteria survive readily
in an acidic environment and, when exposed to sugars, are prolific
producers of organic acids, particularly lactic acid . This causes the
pH of the biofilm to fall below the critical pH for maintaining enamel
mineral content (carbonated hydroxyapatite) and results in enamel
demineralisation.
Frequent exposure to fermentable carbohydrates maintains the plaque
rn
pH below the critical pH for extended periods, leading to net subsurface Q)
;:
enamel demineralisation and the formation of 'white spot' carious
lesions. These lesions have a relatively intact surface, but continued ~
subsurface demineralisation can progress to cavitation. If untreated,
larger and deeper cavities form. Once cavitation occurs within dentine,
s
c:
Q)

caries gradually progresses towards the dental pulp, leading to pulpitis.

c
47
 Once pulpitis is established, pain is experienced with various stimuli.
Eventually, if the caries is still untreated, pulpitis will be followed by
pulp necrosis and infection of the root canal system, which progresses
to inflammation of the periapical tissues (known as apical periodontitis).
Infection of the root canal system can also give rise to periapical
abscess (see 'Localised odontogenic infections', p.61) and spreading
odontogenic infection (see p.63).
The ability of plaque bacteria to demineralise the tooth surface can be
modified by several factors, including:
diet- patterns of consumption (frequency) and type of diet (eg
high sugar content)
plaque amount and composition- the level of cariogenic bacteria
in plaque and their capacity to produce a sustained low-pH
environment
saliva composition and characteristi cs (eg flow; buffering capacity;
antimicrobial factors; calcium, phosphate, hydroxide and fluoride
ion concentrations; the effect of drug therapy-see ' Dry mouth' ,
p.87)
tooth resistance (eg exposure to remineralising agents such as
topical fluoride, p.SO, and casein phosphopeptide-amorphous
calcium phosphate [CPP-ACP], p.Sl).
MANAGEMENT
Individual caries risk assessment
Changing perceptions on management favour treating dental caries
as an infectious disease, with an emphasis on individual caries risk
assessment, preventive strategies and minimal intervention.
Individual caries risk assessment involves quantification of risk factors
such as saliva quality and quantity, plaque characteristics, diet, oral
hygiene habits and the use of fluoridated products.* Early modification
of these factors is part of the primary preventive strategy (see 'General
considerations' , p.49).
Minimal intervention involves early diagnosis and interception of
carious lesions (including chemical treatment of lesions), minimally
destructive methods of removing infected tooth structure after cavitation
has occurred, and restoration of cavities with adhesive dental materials
that do not require removal of sound tooth tissue for their retention in
the prepared cavity.
48 * Fontana M, Zero DT. Assessing patients' ca ri es ri sk. J Am Dent Assoc 2006;137(9):1231-9.
Early ' white spot' lesions can be accurately detected and quantified
by traditional methods (eg visual and radiographic techniques) as well
as newer technologies involving laser and light-inducecj fluorescence .
This allows an assessment of the effect of preventive interventions over
time. It is now recognised that carious lesions can be identified before
a 'white spot' can be seen, through careful drying of the enamel or by
using enhanced visual methods. Early recognition of carious lesions
in enamel maximises the opportunities for their arrest and reversal.
Similar considerations apply to lesions that develop on exposed root
surfaces, which undergo softening over a broad front.
General considerations
In the early stages of caries, before a cavity forms, several strategies can
be used to arrest further decay and promote remineralisation:
plaque reduction by cleaning of teeth:
- brushing at least twice a day with a toothpaste containing
fluoride (see p.SO)
- flossing, preferably immediately before brushing
using other interdental cleaning aids
dietary modification, particularly avoiding sucrose in sticky
forms or as snacks between meals, and limiting the intake of acidic
drinks containing sucrose and other fermentable carbohydrates
between meals
plaque modification, to reduce the level of cariogenic bacteria,
by using antimicrobial products ( eg chlorhexidine gel, p.51 ),
or topical fluoride at high concentrations and in an acidulated
form, which has an antimicrobial effect
tooth surface modification by the application ofremineralising
agents such as fluoride and casein phosphopeptide-amorphous
calcium phosphate (CPP-ACP) (p.51), and by the placement of
fissure sealants and other adhesive materials that cover and protect
the tooth surface
increased salivary flow and buffering capacity by using low-acid,
sugar-free chewing gum or lozenges, or nonacidic coarse foods
( eg carrots).
Table 5 (p.52) shows examples of topical applications and how they can
be used to reduce caries in patients at high risk of caries.
After cavitation has occurred, the infected tooth structure must be
removed and the cavity restored. Following restoration of the tooth,
strategies must still be used to decrease caries risk and prevent further
decay. 49
 Fluoride
In randomised controlled clinical trials, the use of toothpastes and
mouthwashes containing fluoride significantly reduced the incidence of
caries. The efficacy of these products has been attributed to their ability
to incorporate fluoride ions into plaque-several studies have shown
an inverse relationship between plaque fluoride concentrations and
caries. Once plaque fluid or the incipient carious lesion fluid becomes
supersaturated with fluoride, the fluoride ions immediately promote
enamel remineralisation through the formation of fluoride-containing
apatites (eg fluorhydroxyapatite and/or fluorapatite), which are more
resistant to future acid challenge than the carbonated hydroxyapatites
of normal tooth enamel.
Fluoride ions have an antimicrobial effect at ve1y high concentrations.
Formulations with low pH (eg acidulated phosphate fluoride) also have
some antimicrobial activity.
Toothpastes and other topical applications containing fluoride should
be used with care in children less than 6 years of age to minimise
the ingestion of fluoride. Excessive ingestion of fluoride during the
tooth-forming years damages the enamel-forming cells resulting in
an irreversible mineralisation disorder of the teeth known as dental
fluorosi s. In patients with dental fluorosis, the porosity of the subsurface
enamel is increased and the teeth may have white spots, various
discolourations and/or mottling of the enamel.
Children less than 18 months of age frequently swallow toothpaste so
they should have their teeth cleaned with a child-sized soft toothbrush
but with no toothpaste, unless they are at high risk of caries and
toothpaste is used on the prescription of a dentist (see below).
Adults and children more than 18 months of age can benefit from using a
toothpaste containing fluoride twice daily. After brushing, the toothpaste
should be spat out and not swallowed; the mouth should not be rinsed:
children 18 months to less than 6 years- toothpaste containing
fluoride 400 to 550 ppm (0.4 to 0.55 mglg), a small pea-sized
amount applied to a child-sized soft toothbrush, twice daily if risk
of caries is low
adults and children 6 years or more- toothpaste containing
fluoride 1000 ppm (1 mglg) twice daily.
Children less than 6 years at high risk of caries may require the use of
adult-strength toothpaste under parental supervision, as prescribed by
their dentist. Parents should be advised of the risk of dental fluorosis.
50
Table 5 (p.52) shows examples of topical fluoride applications and how
they can be used to reduce caries in patients at high risk of caries. Fluoride
supplements in the form of drops or tablets are no longer recommended
because of the risk of dental fluorosis and limited efficacy.
Community water fluoridation is supported by scientific evidence as an
effective, inexpensive and safe community health measure to prevent
dental caries.
Chlorhexidine
Chlorhexidine has a role in caries-susceptible children and adults. It
does not reduce established plaque, but helps prevent plaque formation
on a cleaned tooth surface. The anionic detergent sodium Iaury! sulfate
used in standard toothpaste inactivates chlorhexidine, so chlorhexidine
should not be used immediately before or after using standard toothpaste.
Chlorhexidine gel is preferred for caries control as it has fewer adverse
effects than the mouthwash and can be used weekly. Table 5 (p.52)
shows how chlorhexidine gel can be used to reduce caries in patients at
high risk of caries.
For more information about chlorhexidine, see p.44 .
Casein phosphopeptide-amorphous calcium
phosphate
Calcium and phosphate ions are required with hydroxide and fluoride
ions for the formation offluorhydroxyapatite, or with fluoride ions for
the formation of fluorapatite. In the healthy mouth, the low concen-
trations of calcium and phosphate ions can limit the remineralising
action of fluoride, and this calcium limitation is exacerbated in a dry
mouth (hyposalivation). The intraoral persistence of calcium and
phosphate ions is limited as they combine rapidly into insoluble and
nonbioavailable forms.
Casein phosphopeptide-amorphous calcium phosphate (CPP-ACP)
contains high concentrations of calcium and phosphate ions stabilised
Ill
in a bioavailable form using phosphopeptides from the milk protein Q)
;:
casein. This form of bioavailable calcium phosphate can help slow C'O
(,)
the progression of caries and promote regression in the early stages of
the disease. CPP-ACP is available in a sugar-free chewing gum and in
ii
....
c
creams (see Table 5, p.52). Q)
0
CPP-ACP should be avoided in patients with allergies to milk proteins.
51
 Table 5. Examples of topical applications and how they Further reading
can be used to reduce caries in patients at high Austra lia n Researc h Ce ntre for Population Ora l Hea lth . The use of fluori des in
risk of caries Au st ra lia: gui delines . Aust De nt J 2006;51(2): 195 -9.
Application Example of how application can be used Fej e rskov 0 , Kidd E, editors. Dent al cari es: the disease and its c lin ica l
in patients at high risk of caries * ma nagement. 2 n d e d . Oxford: Blackwell M u nksgaard ; 2 0 08.

fluoride
fluoride varn ish 22 600 ppm
(22.6 mgtm L)
acidulated phosphate
fluoride gel or foam
1500 to 12 300 ppm
(1.5 to 12.3 mgtg)
Kidd E. Esse nt ials of dent al cari es : the d isease and its management. 3 rd ed .
Apply in the dental surgery to all at-risk dent al surfaces at Oxford : Oxford Univers ity Press; 2 005 .
the clinician's discretion, usually twice a year depend ing on
caries risk.
Can be used by adults and children aged 10 years or more.
Apply in the dental surgery for 4 minutes using trays-
evacuate excess, and spit out residual gel after tray
removal. Adults can use the gel daily at home by brushing
on the teeth, or apply it usi ng customised t rays. While the
use of gels is sti ll relatively common, they have largely
been replaced by concentrated fluoride varnishes in denta l
surgeries. Concentrated fluoride toothpastes and other
remineralising pastes are preferred for home use.
Acidulated gel or foam is preferred as it has better enamel
uptake; however, it is better to use neutral gel or foam
in patients with ceramic crown and bridgework, direct
restorations containing glass particles, or poor sa livary
flow (eg those undergoing head and/or neck irradiation).

fluoride mouthwash
200 ppm (0.2 mgtmL)
neutral fluoride mouthwash
220 ppm (0.22 mgtmL)
:sc neutral fluoride mouthwash
900 ppm (0.9 mgtml)
QJ
c spat out and not swallowed.
'C neutral fluoride toothpaste
c
ca 5000 ppm (5 mgtg)
Can be used daily by adults and children aged 6 years or
more. After rinsing, the mouthwash should be spat out and
not swallowed.
Can be used daily by adults and children aged 6 years or
more. After rinsing, the mouthwash should be spat out and
not swa llowed .
Can be used weekly or daily by adults and children aged
6 years or more. After rinsing, the mouthwash should be
Can be used daily by adults and children aged 10 years
or more.

~ chlorhexidine
0
Ui chlorhexidine 0.2% gel Can be used weekly or daily by brushing on the teeth
Q) (pea-sized amount on a soft t oothbrush) for 7 to 14 days.
c
Q) casein phosphopeptide-amorphous calcium phosphat e (CPP-ACP)
:9 1/)
:::J QJ
(.!J CPP-ACP sugar-free gum Can be used 4 times daily, preferably after meals and after
;:
() cleaning teeth with a toothpaste containing fl uoride. ca
.;:::; (,)
:::J CPP-ACP cream Apply in the denta l surgery after denta l procedures and
Q)
0..
~
after topical fluoride applications. Adults can apply the
cream nightly to teeth after tooth-cleaning and not rinse out.
:sc
QJ
Q)
.c The decision is based on clinical judgment and requ ires a complete assessment of the patient
c
f-
(eg age, other medications, disease risk).
53
52
Periodontal disease

Periodontal disease is usually chronic inflammation of the gingivae

and the supporting structures of the teeth-the periodontal ligament,
the cementum and the alveolar bone. There are two major forms of
chronic periodontal disease- plaque-induced gingivitis (see below)
and periodontitis (see p.56). Periodontitis has two major variations-
chronic and aggressive.
Periodontal disease is caused by dental plaque-a complex biofilm
of mixed bacteria and their by-products that builds up on the teeth.
Plaque can calcifY to become calculus. The accumulation of plaque and
calculus is associated with poor oral hygiene; that is, the teeth have not
been cleaned thoroughly and/or often enough.
In the early stage of periodontal disease, bacteria in plaque cause
inflammation of the gingivae- gingivitis. Gingivitis can usually be
treated successfully by removal of the plaque and calculus followed
by thorough and regular oral hygiene practices. In some patients,
untreated gingivitis progresses to a more advanced stage of periodontal
disease called periodontitis, which may result in loss of the bone and
the tissues that support the teeth. As gingival inflammation progresses,
periodontal pockets are formed and the gingivae may recede. As a result
of damage to the supporting structures, the teeth can become loose and
may eventually require extraction. For locations of infections around
the tooth, see Figure 2, p.62.
Acute forms of periodontal disease can occw- if bacteria from the
biofilm invade the tissues. These include acute ulcerative gingivitis (see
p.57) and periodontal abscess (see p.59).

GINGIVITIS
Gingivitis is the most common form of periodontal disease. It is defined
as inflammation restricted to the gingival tissues, which become red
and swollen, and bleed easily. There is no destruction of the periodontal
ligament or alveolar bone. Gingivitis is rarely painful and, with the
correct dental treatment, is reversible.

55
 Gingivitis develops because of the presence of an undisturbed bacterial alveolar bone destruction, and familial aggregation. Secondary featu res
biofilm (plaque) in the gingival crevices and adjacent to the gingival include amounts of microbial deposits inconsistent with the severity
margins. Bacterial antigenic products from the biofilm diffuse into the of periodontal destruction, elevated proportions of Aggregatibacter
adjacent gingival tissue causing a nonspecific inflammatory response. actinomycetemcomitans and/or Porphyromonas gingiva/is, and
localised immunological abnormalities.
Management Periodontitis is rarely seen in children. Children require urgent
specialist review because periodontitis in children is almost invariably
Gingivitis should be managed by a dentist or dental hygienist under the
associated with systemic disease (eg leukaemia, type 1 diabetes, cyclic
prescription of a dentist. The aim oftreatment is to remove plaque and
neutropenia).
calculus (by thorough dental cleaning), and smooth any irregularities on
the teeth (eg rough edges of fillings) that allow plaque to accumulate.
Calculus deposits are removed by dental scaling (eg ultrasonic cleaning Management
and/or hand scaling). Complete resolution of the inflammation can be
The management of periodontitis
expected within 1 week. Dental treatment should be combined with Antibiotic therapy is rarely
requires debridement to break up the
patient education about oral hygiene. required and is not effective
bacterial biofilm (plaque). Systemic
without concomitant
Antibiotics are not indicated in the management of gingivitis. The short- antibiotics are rarely required, and debridement.
term use of a chlorhexidine mouthwash to inhibit supragingival plaque are not effective without local
formation may be useful when inflammation restricts normal brushing: debridement (scaling and root planing) as they cannot penetrate the
biofilm.
chlorhexidine 0.2% mouthwash 10 mL rinsed in the mouth for
1 minute, 8- to 12-hourly for 5 to 10 days* " Management includes:
or chlorhexidine 0.12% mouthwash 15 mL rinsed in the mouth for thorough toothbrushing and interdental cleaning
1 minute, 8- to 12-hourly for 5 to 10 days.* patient education about oral hygiene and habit management,
particularly smoking cessation (see Therapeutic Guidelines:
Cardiovascular for information on assessment and treatment of
PERIODONTITIS smoking)
Periodontitis is inflammation affecting the periodontal ligament, removal of plaque and calculus with dental scaling (eg ultrasonic
gingivae, cementum and alveolar bone, resulting in loss of tooth support cleaning and/or hand scaling)
with progress ive bone loss and, ultimately, tooth loss. It is characterised root planing, which involves removal of plaque and calculus
by pocket formation and/or gingival recession. It is often associated from deeper pockets, together with planing of the roots. This is
with halitosis (see p.97) and bad taste. In advanced cases, the teeth may often done under local anaesthetic and is usually accompanied by
become loose and may also drift, allowing spaces to develop between polishing, reshaping, or replacement of defective fillings
the teeth. in advanced periodontitis, periodontal surgery, which involves
Cll
Major risk factors for the development and progression of periodontitis raising a mucoperiosteal flap to assist root planing, may be en
necessary and is sometimes associated with bone recontouring.
ca
include smoking and poorly controlled diabetes. Cll
en
Usually the disease presents in a chronic slowly progressing form Unresponsive periodontitis or periodontitis in an immunocompromised
:c
(with brief acute episodes). However, a relatively aggressive form patient requires specialist management. !c
(previously known as early onset periodontitis) may present in 0
"C
systemically healthy patients; this requires specialist management. 0
;:
Primary features of aggressive disease are rapid attachment loss and
ACUTE ULCERATIVE GINGIVITIS
~
Acute ulcerative gingivitis (previously known as acute necrotising
*With prolonged use (more than a few days), chlorhexidine may cause a superficial
ulcerati ve gingivitis [ANUG], trench mouth, and Vincent's disease) is an 57
56 discolouration of the teeth and fi ll ings (see p.44 for more information).
 extremely painful infection of the periodontal tissues. It is characterised chlorhexidine 0.2% mouthwash I 0 mL rinsed in the mouth for
by punched-out interdental papillae, ulcers (often covered with a I minute, 8- to 12-hourly until pain has abated*
greyish membrane) and, usually, a fetid odour. It can be associated with or chlorhexidine 0.12% mouthwash 15 mL rinsed in the mouth for
systemic signs and symptoms. I minute, 8- to 12-hourly until pain has abated.*

Acute ulcerative gingivitis is most common ly seen in young adult The addition of an oxygenating mouthwas h may be considered.
smokers. It is rarely, if ever, seen in children. In children, acute herpetic
Metronidazole is often given as an 8-hourly regimen; however, in these
gingivostomatitis (see p.79) is sometimes misdiagnosed as acute
guidelines it is recommended as a 12-hourly regimen, which is thought
ulcerative gingivitis.
to increase patient adherence to treatment.
Immediate management involves:
In immunocompromised, unresponsive or very severe cases, prompt
gentle removal of as much plaque and necrotic debris as possible specialist referral is indicated. ln the interim, use:
local irrigation with chlorhexidine 0.2% mouthwash or hydrogen
peroxide 3% solution metronidazole 400 mg orally, 12-hourly for 5 days
smoking cessation counselling (see Therapeutic Guidelines: PLUS EITHER
Cardiovascular for information on assessment and treatment of
smoking) 1 phenoxymethylpenicillin 500 mg orally, 6-hourly for 5 days
antibiotic therapy with metronidazole or tinidazole (see dosage OR
recommendations below)
2 amOJ..ycillin 500 mg orally, 8-hourly for 5 days.
analgesics (see p.l3 2 for pain management strategies).
For patients hypersensitive to penicillin (see p. \9), use metronidazole
The patient will not be able to mechanically clean teeth adjacent to
as above and substitute for phenoxymethylpenicillin or amoxycillin:
necrotic gingivae due to discomfort and they should be advised to
rinse with chlorhexidine 0.2% or 0.12% mouthwash until the pain has clindamycin 300 mg orally, 8-hourly for 5 days.
abated (see p.59). The patient should be reviewed in 48 to 72 hours
For patients hypersensitive to penicillin who are unable to swallow
for oral hygiene instruction and periodontal examination. Treatment
clindamycin capsu les, see 'Lincosamides' (p.23) for instructions on
of periodontal disease, especiall y thorough local debridement (scaling
m
....!: and root planing), is required to
preparation of an oral so lution.
Antibiotic therapy alone, without
Cl) prevent recurrence. This should be In patients with HIV infection, acute ulcerative gingivitis can spread to
Q debridement and improvement
provided once the acute stage has in oral hygiene, invariably leads
involve the underlying bone (necrotising ulcerative periodontitis) and
"C
!: resolved; however, where possible, to recurrence. requires specialist management.
ca
scaling could be attempted at the
~ first consultation (under local anaesthesia if necessary). Antibiotic
0 PERIODONTAL ABSCESS
therapy alone, without debridement and improvement in oral hygiene,
invariab ly leads to recutTence. A periodontal abscess is seen almost exclusively in patients with
existing periodontal disease and/or uncontrolled diabetes. The
For antibiotic therapy, use:
discomfort associated with the swelling is usually not enough to keep
1 metronidazole 400 mg orally, I2-hourly for 5 days the patient awake at night. Pain is often difficult to localise. The flora
associated with periodontal abscesses is more mixed than with most
OR (ifpatient adherence is a concern)
other periodontal infections.
1 tinidazole 2 g (four 500 mg tablets) orally, as a single dose
PLUS IN ALL PATIENTS
*With prolonged use (more than a few days), chlorhexidine may cause a superficial
discolouration of the teeth and fillings (see p.44 for more information) .
58 59
 Treatment requires drainage of pus. Un der local anaesthesia, this may be
done by lanc ing the externa l surface of the g ing iva l swelling or through
the peri odontal pocket beneath the swelling. T horough debridement to
remove plaque and calculus deposits should be performed at this time
plus irrigation w ith water, saline solution or local anaesthetic solution.
In advanced cases where the tooth cann ot be retained, drainage of pus
sho uld be obtained by extraction of the tooth and, if required, thorough
irri gation and curettage of the socket should be undertaken. If systemic
signs and symptom s are present, the pat ient is not responding to local
treatment (see ' Periodontitis: Management', p.57), or the pat ient is
immunocompromised, co nside r antimicrobial therapy:
1 phenoxymethylpenicillin 500 mg (child: 12.5 mg/kg up to 500 mg)
orally, 6-hourly for 5 days
OR
2 amoxycillin 500 mg (child: 12.5 mg/kg up to 500 mg) orally,
8-hourly for 5 days.
For patients hypersens itive to penicillin (see p.l9), use:
clindamycin 300 mg (child: 7.5 mg/kg up to 300 mg) orally,
8-hourly for 5 days.
For patients hypersensi ti ve to penicillin who are unab le to swallow
c lindamycin capsules, see 'Lincosam ides' (p .23) for instructions on
preparation of an oral solution. Alternatively, roxithromycin can be
used at a dosage of 300 mg orally, daily (child : 4 mg/kg up to 150 mg
ora ll y, 12-hourly) for 5 days.
Patients who are not responding to treatment and w ish to retain their
teeth require specialist management.
Further reading
An update in contemporary periodontics. Aust Dent J 2009;54(3 Suppl 1).
(can be accessed via the Austral ian Dental Association website
<www.ada .org.au >)
Daly C. Prescribing good oral hygiene for adults. Austral ian Prescriber
2009;32 (3): 72-5. < http://www.austra lianprescriber.com/magazine/32/3/72/5 >
Lindhe J, Lang N, Karring T. Clinical periodontology and implant dentistry. 5th
ed. Oxford: Blackwell Mun ksgaard; 2008.
60
Acute odontogenic and
salivary gland infections
ACUTE ODONTOGENIC INFECTIONS
Acute odontogenic (or tooth-related) infections are common. They can
arise from the dental pulp (secondary to restoration breakdown, caries,
or loss of tooth structure fro m trauma), the peri odonta l tissues (most
commonly due to advanced periodontitis), or the pericoronal tissues
(most commonly from partially impacted mandibular third molars). The
infection usually consists of mi xed anaerobic and aerob ic oral bacteria.
The process of odontogenic infection always com mences in the vicinity
of the tooth. lf ignored or inappropriately treated, it progresses to a
locali sed abscess, then spreads beyond the confines of the jaws to the
facial or neck soft tissues. Occasionally it becomes L udw ig's angina or
spreads to the brain or mediastinum. The medical status of the patient is
very impmiant, pa1iicularly if the patient is immunocom promised.
An acute odontogenic infection is an emergency and requires immediate
management. First-line management should be active dental treatment,
with drugs sometimes used as adjunctive therapy. If patients seek
treatment from medical practitioners,
they shou ld be promptly directed to Treatment with antibiotics alone,
without active dental treatment,
a dentist. However, patients often
ca n lead to more severe
seek (or are given) anti biotic-only episodes of acute odontogenic
treatment, obtain initial symptomatic infection with risk of airway
relief, and then avoi d seeking dental compromise.
treatment. This leads to increasingly
severe episodes of ac ute odontogenic infection with risk of airway
compromise and increased antibiotic resistance.
Localised odontogenic infections
The vario us types of localised odontogenic infections are presented in
Figure 2 (p.62). A localised dental abscess is a collecti on of pus that can
be periapical, pericoronal or periodontal in origin.
61
 Figure 2. Schematic diagram of localised odontogenic
replacement). Antibiotics should not be used for dental pain, pulpitis or
infections and the stages of dental caries infection localised to the teeth, or to delay providing dental treatment.
Tooth A: Localised odontogenic infections Tooth B: Stages of dental caries If referral to a dentist is not immediately possible, see 'Acute dental
pain' (p.l91).

Box 7. Treatment options for acute localised odontogenic

infections
Periapical abscess
endodontic (root canal) treatment
extraction

Periodontal abscess (see also p.59)

periodontal t reatment (scaling, root planing)
extraction

Pericoronal infection
local treatment
Diagram showing pericoronal disease and periodontal disease on tooth A, and caries and its - remove or recontou r the opposing tooth if it is impinging on the operculum
sequelae on tooth B:
1. pericoronal infection - irrigate with steri le solution
2. pericoronal abscess - warm saline or chlorhexidine mouthwashes
3. gi ngivitis (see p.55)
extraction
4. periodontitis (bone loss) (see p.56)
5. periodontal abscess (see p.59)
6. ca ries (see p.47)
Spreading odontogenic infections
- a. 'white spot'
- b. in itial cavity The consequence of untreated localised odontogenic infection is that
- c. la rge cavity involving the pulp it may spread into the surrounding tissues. Spreading odontogenic
7. periapical inflammation (apical periodontitis) or abscess infections may be superficial (involving the canine or buccal spaces) or
deep (involving the upper neck). ~

Management Treatment of spreading odontogenic infection-regardless of whether -~

10f/)
Odontogenic infections require active dental treatment to drain any pus the infection is an abscess (a collection of pus) or cellulitis (an infected
"C
and remove the source of the infection. Removal of the infection source inflammatory swelling)-is by: c
ca
can be via extraction, endodontic (root canal) treatment or periodontal draining any pus (,)

treatment (see Box 7, p.63). removing the cause (via endodontic or periodontal treatment, or c: f/)
Q)c
extraction) 'Qilo
Antibiotics should be considered .S:;::;
only when the infection has spread Antibiotics should not be used supporting the patient with analgesia and rehydration C(,)
OQ)
for dental pain, pulpitis or considering antibiotics. "C""'
beyond the jaws and has produced infection localised to the teeth, 0,5
facial swelling, or when there are or to delay providing dental Sedation (see p.l21) or general anaesthesia of the patient may be Q)"C
... c
systemic symptoms and fever (see treatment. required to facilitate dental treatment. Active dental treatment should :lea
'Spreading odontogenic infections', not be delayed on the basis that local anaesthetics will not be effective ~'So
62 p.63). Antibiotic use is then an adjunct to active dental treatment (not a until antibiotics are given. 63
 Superficial infections
Most superficial infections can be treated with local surgical or dental
treatment alone.
In patients who have severe superficial infections with swelling and
systemic signs and symptoms, use antibiotic therapy in addition to local
surgical or dental treatment:
1 phenoxymethylpenicillin 500 mg (child: 12.5 mg/kg up to 500 mg)
orally, 6-hourly for 5 days
OR
2 amoxycillin 500 mg (child: 12.5 mg/kg up to 500 mg) orally,
8-hourly for 5 days.
For pat ients hyperse nsiti ve to penicillin (see p.l9), use :
clindamycin 300 mg (child: 7.5 mg/kg up to 300 mg) orally,
8-hourly fo r 5 days.
For patients hypersensitive to penicillin who are unable to swal low
clindamycin capsules, see 'L incosamides' (p.23) for instructions on
preparation of an oral so luti on. Alternatively, rox ithromyci n can be
used at a dosage of300 mg orally, daily (child : 4 mg/kg up to ISO mg
orally, 12-hourly) for 5 days.
If superficial infections are inadequatel y treated, they may spread-
canine fossa infections may spread intracrani ally via the orbital veins;
buccal space infections may spread to the neck and become deep
infections. Both can lead to life-threatening situations.
Advise the patient to contact their
All patients with infection
dentist fo r prompt review if their shou ld be reviewed within
condition deteri orates. All patients 48 to 72 hou rs of co mmencing
with infection should be reviewed treatment.
within 48 to 72 hours of commencing
treatment. If the infection has not resolved within 5 days, do not just
' repeat the antibiotic'. Check that any pus has been drained, the cause
has been removed, the appropri ate antibiotic is being used for the
particular microbial susceptibility, and the patient's general condition
and medical situation are being managed .
64
For unresponsive infections, use:
1 metronidazole 400 mg (child: 10 mglkg up to 400 mg) orally,
12-hourly for 5 days
PLUS EITHER
1 phenoxymethylpenicillin 500 mg (ch ild: 12.5 mg/kg up to
500 mg) orally, 6-hourly for 5 days
OR
2 amoxycillin 500 mg (child: 12.5 mglkg up to 500 mg) orally,
8-hourly for 5 days
OR (as a single drug)
2 amoxycillin+clavulanate 875+125 mg (child: 22.5+3.2 mg/kg up
to 875+ 125 mg) orally, 12-hourly for 5 days.
For patients hypersensitive to penicillin (seep. 19), as a single drug, use:
clindamycin 300 mg (child: 7.5 mglkg up to 300 mg) orally,
8-hourly for 5 days.
For patients hypersensitive to penicillin who are unable to swallow
clindamycin capsules, see 'Lincosamides' (p.23) for instructions on
preparation of an oral solution.
If a patient presents with recurrent infection after inappropriate
antibiotic-only treatment, the appropriate dental or hospital referral
must be made and followed through.
Deep infections
Odontogenic infections that spread to the submandibular and pharyngeal
spaces in the upper neck are potentially life-threatening, as there is a risk
of airway obstruction. Any patient who has trismus and cannot open
their mouth more than 2 em (interincisal) must be assessed for signs
of airway compromise. Signs and symptoms of airway compromise
include stridor (noisy breathing), dyspnoea (difficult breathing),
dysphagia (difficulty in swallowing), and elevation and firmness of
the tongue.
65
 Patients with deep infections and a compromised airway must be
assessed urgently by an oral and - - - - - - - - - - -
maxillofacial surgeon, or other sur- Patients with trismus and
gical or anaesthetic specialist with breathing or swallowing diffic ulty
require urgent referral to an
training in the management of such appropriate specialist or hospital
patients. Prescription of antibiotics emergency department.
without active dental treatment and
referral is not appropriate.
Patients with systemic symptoms of pain and dehydration usually need
to be managed in hospital, particularly if the infection is extensive.
Management involves drainage, removal of the tooth, culture and
susceptibilities of causative organisms, and treatment with intravenous
fluid therapy and antibiotics.
In conjunction with active dental treatment, while awaiting the results
of susceptibility testing, use:
metronidazole 500 mg (child: 12.5 mg/kg up to 500 mg) IV,
12-hourly
PLUS EITHER
1 benzylpenicillin 1.2 g (child: 30 mg/kg up to 1.2 g) IV, 6-hourly
OR
2 amoxylampicillin 2 g (child: 50 mg/kg up to 2 g) IV, 6-hourly.
For patients hypersensitive to penicillin (excluding immediate
hypersensitivity, see p.19), use metronidazole as above and substitute
for benzylpenicillin or amoxy/ampicillin:
cephazolin 2 g (child: 50 mglkg up to 2 g) IV, 8-hourly.
For patients with immediate penicillin hypersensitivity (see p.l9), use
metronidazole as above and substitute for benzylpenicillin or amoxy/
ampicillin:
1 clindamycin 450 mg (child. 10 mglkg up to 450 mg) IV, 8-hourly
OR
1 lincomycin 600 mg (child: 15 mglkg up to 600 mg) IV, 8-hourly.
Ongoing therapy should be guided by susceptibility results. Continue
the intravenous regimen until the drains cease being productive, or
swelling and trismus cease (and the patient can swallow), then change to
an oral regimen (see 'Superficial infections', p.64) for a further 5 days.
66
Ludwig's angina
Classically, Ludwig's angina is a severe bilateral cellulitis involving
all of the neck spaces from the mandible to the thoracic inlet. Patients
are severely ill and have a significant risk of death, usually from
airway obstruction. Older medically compromised patients may die of
multiorgan failure secondary to septicaemia.
It has become common to call all severe deep neck infections 'Ludwig's
angina', which is technically incorrect. However, inadequately treated
deep neck infections can progress to Ludwig's angina. The condition
requires special attention to the complex airway problems, as well
as treatment for the deep space
infections (see p.65). Patients with Patients with Ludwig's angina
require urgent referral to an
Ludwig's angina require urgent
appropriate specialist or hospital
referral to an appropriate specialist
emergency department.
or hospital emergency department.
Once the airway has been secured, imaging to determine the extent
of infection should be performed. Wide incision and drainage of all
infected spaces in the mouth and neck are required.
Dentoalveolar surgical infections
Infection following dentoalveolar surgery is uncommon (2% to 5%)
and the incidence is similar regardless of whether or not prophylactic
antibiotics have been given. It is often confused with postsurgical
inflammation or alveolar osteitis (dry socket) (see p.69) . The specific
signs of dentoalveolar surgical infection are:
cellulitis (ie a hot tense swelling)
fluctuation
purulent discharge from the extraction or other surgical site for
more than 72 hours after surgery
pain and swelling that either worsens or fails to improve 48 hours
after surgery
persistent hyperpyrexia (more than 39 C at 48 hours or more after
surgery).
Full blood count, erythrocyte sedimentation rate (ESR) and C-reactive
protein (CRP) can also be used to identify evidence of infection. A
radiograph should be taken to exclude the presence of residual roots or
bony sequestra.
67
 Management
Management must include drainage of any pus. Hourly wound irrigation
(eg with warm saline or chlorhexidine 0.2% solution) is helpful.
If there are systemic signs or the patient is medically compromised,
consider using antibiotics:
1 phenoxymethylpenicillin 500 mg (child: I2.5 mg/kg up to 500 mg)
orally, 6-hourly for 5 days
OR
2 amoxycillin 500 mg (child: I 2.5 mglkg up to 500 mg) orally,
8-hourly for 5 days.
For patients hypersensitive to penicillin (see p.l9), use:
clindamycin 300 mg (child: 7.5 mglkg up to 300 mg) orally,
8-hourly for 5 days.
For patients hypersensitive to penicillin who are unable to swallow
clindamycin capsules, see 'Lincosamides' (p .23) for instructions on
preparation of an oral solution. Alternatively, roxithromycin can be
used at a dosage of300 mg orally, daily (child: 4 mg/kg up to 150 mg
orally, 12-hourly) for 5 days.
In more severe or unresponsive cases, use:
metronidazole 400 mg (child: I 0 mglkg up to 400 mg) orally,
12-hourly for 5 days
~Q)
PLUS EITHER
c 1 phenoxymethylpenicillin 500 mg (child: I2.5 mg/kg up to 500 mg)
"C
c orally, 6-hourly for 5 days
ctl
For pain, use a nonsteroidal anti-inflammatory drug (NSAID) or
paracetamol (see p.l32 for pain management strategies).
Severe postsurgical infections that have spread beyond the confines of
the jaws are clinically similar to spreading infections and should be
managed similarly (see p.63).
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
approximately 5% of tooth extractions and is due to a failure of healing,
but is commonly misdiagnosed as an infection. The condition presents
as postoperative pain in and around an extraction socket that increases
in severity between 1 and 4 days after the extraction. It is accompanied
by a disintegrated blood clot within the socket, with or without halitosis.
Alveolar osteitis should resolve spontaneously in 2 to 3 weeks; however,
it is recommended that the patient returns to a dentist for treatment of
the socket (with obtundent dressings) and other symptomatic measures
(eg analgesics and mouthwashes). Treatment with antibiotics is of no
benefit. lfthe pain persists for more than 3 weeks or if there are signs
beyond the socket, the diagnosis needs to be reviewed. Differential
diagnoses include osteomyelitis, bisphosphonate-related osteonecrosis
of the jaws (see p.l52) and alveolar squamous cell carcinoma.
SALIVARY GLAND INFECTIONS
Swellings of the large major salivary glands (parotid, submandibular
and sublingual glands) are common presentations and, in many cases,
do not represent infection. Detailed clinical and imaging investigations
(eg ultrasound or computerised tomography scan) should be carried

0
..
(ij OR out to differentiate between inflammatory, immunologic and neoplastic
causes of gland enlargement. Benign masseteric hype1irophy, lymph-
Ui 2 amoxycillin 500 mg (child: I 2. 5 mglkg up to 500 mg) orally, adenopathy and acute spreading odontogenic infections (see p.63) may
(j)
c 8-hourly for 5 days. also masquerade as glandular enlargement.
Qj
:'Q For patients hypersensitive to penicillin (see p.19), as a single drug, use: Acute suppurative sialadenitis (including parotitis) is usually due to
:::J
<.!J infection with Staphylococcus aureus in neonates and adults, although
(.) clindamycin 300 mg (child: 7.5 mglkg up to 300 mg) orally,
.;:::;
8-hourly for 5 days.
it may occasionally be polymicrobial in adults. The glands are enlarged,
:::J
(j) often hot and tense, and pus may be expressed from the gland duct. Th '
0.
~ For patients hypersensitive to penicillin who are unable to swallow patient is usually ill and may be dehydrated.
(j)
.r::: clindamycin capsules, see 'Lincosamides' (p.23) for instructions on
r- preparation of an oral solution.
68 69
 Management of acute suppurative sialadeniti s includes surgical rev iew,
intraductal or surgical drainage if fluctu ant, rehydration and antibiotics.
For antibiotic therapy, use :
1 di/flucloxacillin 2 g (child: 50 mglkg up to 2 g) IV, 6-hourly
then di/flucloxacillin 500 mg (child: 12.5 mg/kg up to 500 mg) Oral mucosal disease
orally, 6-hourly fo r a total of 10 days
OR
Oral mucosal lesions are com mon. They can be due to local disease, a
2 clindamycin 450 mg (child: 10 mg/kg up to 450 mg) IV or orally, manifestation of cutaneous or gastroi ntestinal disease, an adverse dru g
8-hourly for a total of 10 days reaction or a sign of systemic disease.
OR Diagnosis of oral mucosal lesions is made with a full history
(including a medication hi story), a thorough oral examination and,
2 lincomycin 600 mg (child: 15 mglkg up to 600 mg) I V, 8-hourly
often, cytological, haematological/serological and histopathological
then clindamycin 450 mg (child: 10 mg!kg up to 450 mg) orally,
investigations. It is also important to examine the skin of patients
8-hourly for a total of 10 days.
presenting with oral mucosal disease as many cutaneous diseases
can involve the oral mucosa. The oral les ions may be the presenting
complaint ( eg pemphigus vu lgaris) or the most persistent complaint ( eg
lichen planus) of the cutaneous disease. Some cutaneous conditions (eg
perioral dermatitis) can also be caused by topical intraora l drugs.
Mucosal diseases can be divided clinically into three broad groups-
mucosal discolourations (see below), ulcerative conditions (see p.77)
and fun gal infections (see p.82). Oral mucositis (see p. 85) and dry mouth
(see p.87) are also discussed in this section.
The management of oral mucosal disease is principally with topical
s c
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intraoral drugs, of which many are antiseptic/anaesthetic proprietary
preparations. Symptomatic relief with these preparations is important,
Q but does not alter the un derlying disease process and the use of them
"C alone in most cases represents a significant undertreatment of a usually
c
(1)
readily manageable condition. Topical corticosteroids usuall y address
~ the immune mechanisms responsible for the condition and, with
0 appropriate titration to an individual patient's needs and response, these
Ui drugs can minimise the often significant functional morbidity associated
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Changes in the oral mucosa can result in a range of discolourations :s
Q. and textural changes . The most common are white patches, wh ich can E
~
be manifestations of physiological (norma l) or pathological states.
<lJ
..c ~
r- Physiological manifestations include Fordyce's spots (ectopic sebaceous 0
glands) and leukoedema. Pathological states include keratos is (eg
70 7:J
 idiopathic or reactive keratosis, including fr ictional keratotic pl aques, Photo 1. Leukoplakia of the ventral surface of the tongue
or smoker's keratosis), epithelial dysplas ia, carcinoma and dermatoses and floor of mouth
(eg lichen planus).

Oral leukoplakia
' Leukopl akia' refers to a wh ite patch or plaque that cannot be removed
and cannot be characterised clinically or histologically as any other
pathological condition (see Photo 1, p.73).
Homogenous leukoplakias are smooth white plaques without surface
or textural variation; they have a reported long-term malignant
transform ation rate of about 3%. Nonhomogenous leukoplakias
(including speckled leukopl akias) present as white patches on a red
background and have a higher risk of malignant change- reported to
be 7 times that of homogenous leukopl akias.* Any leukop lakia with
surface irregu larity or textural variation is co nsidered non homogenous.
The site of oral leukoplakias is important- leukoplakias on the flo or of
the mouth an d the ve ntral surface of the tongue have higher rates of
malignant transformation. The size of leukop lakias is not significant,
with small and large lesions equ all y likely to transform. Other features Photo 2. Squamous cell carcinoma of the left ventral surface
relating to ma lignant transformation are longer duration of the lesion of the tongue
and the use of alcohol and tobacco.
If there is doubt about the diagnos is
A persistent undiagnosed oral
of an oral white patch, speciali st
white patch must be biopsied
referra l is required to in vesti gate to exc lude epithelia l dysplasia,
the possibility of squamous cell ca rcinoma in situ and squamous
carcinoma (see Photo 2, p.73) . cell carcinoma.
Biopsy of any persistent undi agnosed
oral wh ite patch is essential to exclude ep itheli al dysplasia, carcinoma
in situ and sq uamous cell carcinoma. However, biopsy results onl y
represent an instant in time and cannot be extrapolated to the future
CJ)
behaviour of the lesion.
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72
* HolmstrupP, Vedtofte P, Reibel J, Stoltze K. Long-term treatment outcome of oral
premalignant lesions. Oral Oncol2006;42(5):461-74.
.,
 Oral lichen planus Management
Lichen planus is an immunologically mediated disease that may affect If biopsy-proven oral lichen planus becomes symptomati c, it ca n be
the skin, hair, nails, and oral and genital mucosae. Oral lesions oflichen treated with:
planus typically occur on the buccal mucosa, tongue and gingivae (see
betamethasone dipropionate 0.05% ointment topically to the
Photo 3, below). In the non-erosive form of the disease, the lesions
lesions, twice daily after meals.
consist of a characteristic reticular pattern of white striations or plaques.
Erosive oral lichen planus presents as erythematous, ulcerated or eroded A general guideline is to minimise the
areas of mucosa, which are often painful. frequency, amount and duration of Topical corticosteroids should
not be used continuously for
topical corticosteroid use; however,
Oral lesions can be persistent, difficult to treat, and frequently occur in more t han 3 weeks without
the patient should be encouraged to
the absence of cutaneous lesions. There is a slightly elevated risk of oral specialist advice.
use the topical corticosteroid oint-
squamous cell carcinoma, particularly in erosive forms of lichen planus.
ment if symptomatic.
Advise patients to cease smoking, and avoid regular use of alcohol-
containing preparations and consumption of alcoholic beverages. If the lesions have not resolved after 3 weeks, or have an appearance
Periodic review is strongly recommended. other than that of classic reticular lichen planus, seek specialist advice.
Most cases of oral lichen planus are idiopathic, but lichenoid changes of
the mucosa can be induced by a wide range of drugs. Dental amalgam Geographic tongue
restorations have been implicated in cases of persistent lichenoid
Geographic tongue (erythema migrans) is a benign condition affecting
lesions where there is direct contact between a lichenoid plaque and
up to 5% of the general population. It manifests as migratory areas of
an amalgam restoration. In this case, only the implicated amalgam
erythema usually involving the dorsal surface of the tongue, but it may
restoration should be replaced; removal of all amalgam restorations is
extend to ectopic sites such as the floor of the mouth and buccal mucosa.
not recommended.
The erythematous areas represent a central atrophic and depapillated
Photo 3. Oral lichen planus of the left buccal mucosa
zone which, in the most frequently seen pattern, is surrounded by
elevated white or cream margins. Occasionally the central erythematous
showing characteristic white striations
areas are sensitive. Although the cause of geographic tongue is unknown,
C6 there may be a family history of the condition and some patients have
....
c atopic allergies or can relate the lesions to particular foods or stress. It
Cl)
c is occasionally seen in patients with psoriasis and, histologically, the
"C
c lesions are psoriasiform. However, it is not associated with any specific
ell condition, including psoriasis.
~ Management of geographic tongue is generally not required other than
0
correct diagnosis and reassurance. Ifthere is pain or burning, it may be
a symptom of burning mouth syndrome (see p.91) and specialist advi ce
is required.

Hairy tongue
Hairy tongue (usually black, but may be other colours) occurs when
excessively long and hyperkeratinised filiform papillae of the tongul,)
become stained by an accumulation of epithelial cells, exoge nous
material and, perhaps, chromogenic microorganisms. It occurs 1110Hl
74
 commonly with the use of chlorhexidine mouthwash or after a course
of antibiotics. It is also seen in patients who have limited oral intake (eg
with percutaneous endoscopic gastrostomy [PEG] feeding).
Management primarily involves identifying and eliminating causative
factors. In addition, improving oral hygiene, brushing the tongue gently
with a toothbrush and using oxygenating mouthwashes (eg sodium
bicarbonate) can help.
Oral hairy leukoplakia
Oral hairy leukoplakia (see Photo 4, below) usually presents as a white
'corrugated' lesion on the lateral border of the tongue. It can extend
onto the dorsal and ventral surfaces of the tongue and to the buccal
mucosa. The lesion is associated with Epstein-Barr virus and develops
in immunosuppressed patients, particularly patients with HIV infection.
Generally, oral hairy leukoplakia is asymptomatic. Specific treatment
is not required, but management must address the underlying
immunosuppression. Some patients complain of a burning sensation,
which is often due to secondary infection with Candida. In this case,
treatment with appropriate antifungal drugs usually resolves the
symptoms (see 'Oral candidosis: Management' , p.84).
ULCERATIVE CONDITIONS
Mouth ulcers can be classified into several broad groups- llaumul i ~.:
(see Photo 5, below), infective (usually viral , p.79, occasionall y
bacterial or fungal), dermatological (eg lichen planus, p.74; mucous
membrane pemphigoid, p.81 ; pemphigus vu lgaris, p. 8 1), neoplastic,
and other (including recurrent aphthous ulcerative disease, p. 78).
Mouth ulceration most commonly occurs due to trauma from eating
rough, sharp or hot foods, or from sharp broken teeth or dental
restorations. Therefore, initial management of mouth ulcers must
address possible causes of trauma. This may include changing oral
hygiene practices, smoothing sharp edges of teeth or restorations,
adjusting prostheses, or placing wax on orthodontic appliances.
Ulcers persisting for longer than 3 weeks are potentially neoplastic;
patients with such ulcers require speciali st input into their management
and biopsy should be considered.
Photo 5. Longstanding traumatic ulcer of the right posterior
lateral margin of the tongue

Photo 4. Oral hairy leukoplakia of the right lateral margin of

the tongue

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76 77
 Recurrent aphthous ulcerative disease
Recurrent aphthous ulcerative disease is the most common cause
of nontraumatic lesions of the oral mucosa. The disease has an
immunopathogenesis and is characterised by the periodic eruption of
painful solitary or multiple ulcerations of the oral mucosa. These may
commence spontaneously or transform from traumatic ulceration in
a genetically predisposed patient. The disease prevalence is between
5% and 25% in the general population. Its onset is usually during
adolescence, with peak onset between 10 and 19 years of age. The
eruptions tend to diminish in frequency and severity with age. Aphthous
ulcers can occur acutely with smoking cessation, but these usually
resolve with time.
Eruptions generally occur on the non-attached and nonkeratinised
lining mucosa (eg of the cheek, lip and the floor of the mouth), rather
than the keratinised masticatory mucosa of the gingivae and hard palate.
Tluee forms are recognised:
Minor aphthous ulceration, the most common fonn , presents as
smaller lesions that are usually 2 to 4 mm in diameter, occur a
few at a time and heal within 7 to I 0 days.
Major aphthous ulceration, a less common form, presents as
larger lesions of 10 mm or more that can persist for up to 6 weeks
(and occasionally months) and heal with submucosal scarring.
Herpetiform aphthous ulceration presents as recurrent crops of
nonvesicular small ulcers, 1 to 2 mm in diameter, that coalesce to
form larger ulcers, which heal within 1 to 2 weeks. Herpetiform
!c aphthous ulcers are not caused by the herpes virus, so they do not
GJ have a cluster pattern.
c
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c
Assessment of aphthous ulcers involves exclusion of underlying causes
(II by history, examination and, when required, relevant blood tests for
ca... deficiencies (full blood count, iron studies, and serum vitamin B 12 and
0 folate). Deficiencies should be treated only on laboratory confirmation
Ui
and not empirically.
Q)
c often occurs in childhood with fever, toxicity and oral ulceration
Qj Aphthous ulcers can be associated with coeliac disease or ulcerative
:Q colitis. They are not associated with Crohn 's disease, where ulcerative
::J
(!) lesions are persistent and linear, usually in the reflection of the
u 0
.;:::; mucobuccal folds, and are associated with tissue tags. Aphthous
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0.
in children, PFAPA (periodic fever, aphthous stomatitis, pharyngitis,
~ ca...
Q)
..c cervical adenitis) syndrome.
I-
78
Management
Management of minor trauma (eg from toothbrushing or orthodonti c
appliances) is important as it can be a trigger for aphthous ulcers (set:
p. 77 for management of minor trauma).
For patients with minor aphthous ulcers, topical anaesthetics may be
effective for symptomatic relief (eg lignocaine 2% gel, with or without
0.05% chlorhexidine, every 3 hours-use with caution in patients with
cardiac, hepatic or renal disease).
Specific treatment directed at immunocompetent cells in the oral mucosa
can produce rapid healing, particularly if applied in the prodromal or
preulcerative stage. The aim of treatment is to control the disease rather
than cure it. Use:
betamethason e dipropionate 0. 05% ointment topically to the
lesions, twice daily after meals.
Management of patients with major aphthous ulceration or
immunocompromised patients with neutropenic ulceration requires
specialist advice.
Viral ulcers
Herpes simplex virus is the most common cause of viral oral
ulceration (see below). Other causes include varicella-zoster virus,
coxsackie viruses (herpangina, and hand, foot and mouth disease), and
cytomegalovirus in HIV-infected patients (see Therapeutic Guidelines:
Antibiotic for more information).
Oral mucocutaneous herpes simplex
Oral mucocutaneous herpes simplex virus infection is very common in
children and adults. Over 90% of adults have positive serology from
virus exposure. The primary episode (herpetic gingivostomatitis) GJ
(J)
(II
GJ
associated with lymphadenopathy. The intraoral distribution is usually (J)
typical and diagnostic. Healing occurs within several days for infants, :s
but can be up to 2 weeks in older children. During this time it may ca
(J)
be difficult for the child to eat and drink and hospitalisation may be (,)
:I
required. In adults, although rare, herpetic gingivostomatitis can be
very debilitating with severe dehydration and malnutrition.
E
Recurrent episodes are due to latent virus reactivation. They usually 0
occur on the lips (herpes simplex labialis or cold sores), but if the
7
 primary infection has been on the skin, recurrences can occur on that
area of skin. The lesions are usually preceded by pain, burning, tingling
or itching for several hours to days (prodromal stage). The lesions
begin as macules, rapidly become papular, with vesicles appearing
within 48 hours and scabs appearing within 3 to 4 days; healing occurs
without scarring. Recurrences are usually mild and infrequent, but are
occasionally very frequent and disabling. Sun protection is important in
preventing recurrences.
In children with atopic dermatitis and in immunocompromised patients
(including those with autoimmune skin conditions such as pemphigus),
herpes simplex virus may disseminate, causing a generalised
eruption requiring hospitalisation for intravenous antiviral therapy. In
immunocompromised patients, including those with HIV infection,
herpes simplex infection may also become chronic with recalcitrant
crusted lesions and ulceration. Herpes simplex infection may be
complicated by erythema multiforme (see p.82), which is often more
disabling than the infection itself.
Confirmation of the diagnosis of herpes simplex, if in doubt
clinically, can be made by polymerase chain reaction (PCR) or rapid
immunofluorescence.
Minor episodes
Minor episodes of viral oral ulceration should always receive supportive
treatment with attention to fluid balance and alimentation, pyrexia, if
-
Cii
c
c
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present, and analgesia. Lesions can be treated symptomatically with
systemic analgesics and topical anaesthetics (eg lignocaine 2% gel,
with or without 0.05% chlorhexidine, every 3 hours- use with caution
c in patients with cardiac, hepatic or renal disease). Chlorhexidine
co mouthwash may act as an adjunct to oral hygiene. Use:
~ chlorhexidine 0.2% mouthwash 10 mL rinsed in the mouth for
0 as an extensive erosive disease or as small clear flmd-filled veste!es
I minute, 3 times daily while the ulcers are present.*
Chlorhexidine mouthwash is also available in combination with
benzydamine, a topical analgesic. Topical corticosteroids are
contraindicated as they prevent attachment of white blood cells to
virally infected epithelial cells, and therefore prevent virus destruction
as well as aiding local spread.
Aciclovir or penciclovir cream may be effective in reducing the duration
of a recurrence if applied at the first sign of a lesion (preferably during
*With prolonged use (more than a few days) , chlorhexidine may cause a superficial
80 discolouration of the teeth and fillings (see p.44 for more information) .
the prodromal stage), but there is no benefit in continued application
beyond the recommended duration. Use:
1 aciclovir 5% cream topically, 5 times per day (eve1y 4 hours while
awake) for 4 days at the first sign of recurrence
OR
1 penciclovir (adult and child 12 years or more) 1% cream topically,
at least 6 times per day (every 2 hours while awake) for 4 days at
the .first sign of recurrence.
Severe episodes
Severe herpes simplex virus infections (particularly th.e primary e~isode,
severe recurrent episodes, or if the patient has difficulty eatmg or
swallowing) generally require systemic antiviral therapy. For systemtc
antiviral recommendations, see Th erapeutic Guidelines: Dermatology.
Mucous membrane pemphigoid and pemphigus
vulgaris
Mucous membrane pemphigoid and pemphigus vulgaris are uncommon
autoimmune vesiculobullous disorders that affect stratified squamous
epithelium. Mucous membrane pemphigoid is confined to the n:ucous
membranes, whereas pemphigus vulgaris can affect all epit~ehal
surfaces. Both conditions can present as large, painful and persistent
erosions in the mouth. Their onset is usually in older patients and, like
most autoimmune diseases, they are more common in women than
in men.
In pemphigus vulgaris, the oral ulceration typically precedes the
development of cutaneous lesions by 6 or more months . It may present
appearing on the oral mucosa, including th~ gingivae. The vesicles
and bullae are thin roofed so they rupture easily, leavmg large erosive
mucosal lesions with tiny white tissue shreds around the periphery.
Mucous membrane pemphigoid is characterised by subepithelial
splitting, with bulla or vesicle formation occ~rring predominantl y
on the gingivae and palate. These heal with vanable amounts of scar
formation.
Diagnosis and management require specialist advice. In ad? ili on,,
referral to an ophthalmologist is required because of the .nsk o l
blindness. Definitive diagnosis requires a biopsy of ti ssue, and 1 ~ bus d
 on histological features as well as immunofluorescence studies offresh
tissue. Management of both conditions is inevitably protracted and
usually requires oral immunosuppressive therapy with corticosteroids,
azathioprine or cyclosporin, alone or in combination with topical
immunosuppressants.
Erythema multiforme
Hyperplastic candidosis presents as a fixed lesion on the oral mucosa ;
it is usually white. It sometimes clinically resembles oral cancer, and
therefore biopsy is important to confinn the diagnosis. Speciali st
management is required. This condition is frequently associated with
dysplasia and, irrespective of the initial histopathology report, the area
must remain under review with early re-biopsy if resolution is not
achieved.

Erythema multi forme is an acute, sometimes recurrent, hypersensitivity

Table 6. Predisposing factors in oral candidosis
reaction, with the oral mucosa involved alone or in association with
generalised skin lesions. It can present with a wide spectrum of Local factors Systemic factors
severity. Orally, it is characterised by blood-crusted lips and severe and
th e wearing of dentures immunosu ppression (eg HIV infection,
widespread ulceration. Erythema multiforme occurs mainly in young leukaemia)
adults, more commonly in males. A wide variety of factors can trigger salivary gland hypofunction
the use of some drugs (eg inhaled and
the reaction. Herpes simplex virus has been implicated in up to 70% of incorrect use of corticosteroid inhalers
systemic corticosteroids, antibiotics)
patients. Drugs are usually implicated in older patients. poor oral hygiene

Healing can be slow (up to 3 to 6 weeks) and no specific treatment is

available. Urgent specialist referral is advised for all patients due to Denture hygiene
the rapid onset of severe sequelae in many cases, some of which are
potentially life-threatening. Regular nocturnal denture use should be avoided and, traditionally,
it has been recommended that dentures be kept in a liquid overnight.
For management of erythema multi forme, see Therapeutic Guidelines: However, it has been shown that allowing the denture to dry out at
Dermatology. night is much more effective in reducing yeast colonisation and plaque
reaccumulation compared with either denture cleansers or water.
FUNGAL INFECTIONS Dimensional changes in the denture can occur during repeated cycles of
hydration and dehydration; however,
co.... these changes are very small and are Dentures shou ld be placed in a
c
Q)
Oral candidosis not clinically significant. Therefore,
dry environment at night when
they are not worn.
0 advise patients to take their dentures
"C Oral candidosis (candidiasis) has many clinical presentations and is
c an opportunistic infection- it is uncommon in healthy individuals and out at night, clean them, and place them in a dry environment.
10
is sometimes termed the 'disease of the diseased' (see Table 6, p.83, Mechanical cleaning with a toothbrush and soap on a regular (at
~ for predisposing factors). Oral candidosis must be evident on clinical
0 least twice daily) basis is the most effective way of removing the
Ui appearance before commencing antifungal therapy. biofilm from the denture material. It is not only recommended for
Q)
c preventing disease, but also as first-line treatment of denture-associated
Qj
The creamy white plaques of thrush (pseudomembranous candidosis),
which are not fixed to the oral mucosa, are easily recognisable. Once erythematous candidosis (can take 1 month before improvement is
:Q
::J
removed, these plaques leave a red inflamed mucosa. Some plaques are seen). To aid mechanical cleaning, twice weekly soaking of dentures
(.!)
() tenacious and can only be removed with difficulty and some discomfort. for 15 to 30 minutes in white vinegar (diluted 1:20), 0.1% hypochlorite
_;:::;
::J Other presentations of candidosis, such as erythematous candidosis solution (diluted Milton's solution) or chlorhexidine solution should
Q)
0. (eg tender red mucosa after antibiotics or steroids, or associated with be encouraged. Long-term use of chlorhexidine solution can cause
~ discolouration of the denture.
Q) ill-fitting dentures), are often overdiagnosed. Red inflamed mucosa in
.c
1- contact with the fitting surface of dentures is common and not always
associated with candidosis.
82
 Management Angular cheilitis
Effective management reli es on a Angular cheilitis presents as an erythematous skin plaqu e usuall y w ith
Antifungals shou ld not be
correct diagnosis and identification format ion of fissuring (rhagades) at one or both corners of the mouth . It
used unless oral candidosis is
of underlying predisposing factors confirmed.
is often assoc iated w ith intraoral candida! ca rriage or cli nically obvious
(see Table 6, p .83), especia lly in infect ion. The condition is usually a mixed infection with Candida
recwTent cases of oral candidos is. Local precipitating factors, such as coexisting sy nergistically with staphylococci and streptococci . Facia l
ill-fitting dentures, incorrect use of corticosteroid inhalers (see' Asthma: skin folds and wrinkl ing at the corners of the mouth and along the
Dental issues', p.144) and poor oral hygiene, should be addressed first. naso labial fo ld leads to a chronically moist environment that predisposes
Patients with denture-associated erythematous candidosis should be to angular cheilitis.
managed with denture hygiene (see p. 83) alone and do not require
The angul ar fo ld becomes more pronounced in edentulous patients,
antifunga l therapy.
especially if dentures are not worn. Sali va can accu mulate in this
Further clinical assessment is required to determine the anticipated fold, producing maceration and eventually chei litis. New dentures can
outcome of treatment and the li ke lihood of recurrence. For example, sometimes help correct th is excessive foldin g, and therefore a dental
a patient with prostheses and sali vary g land hypofunction as well as review is recomm ended.
anatomica l skin folds at the commissures can reasonably be expected to
Other factors that can cause angular cheilitis are atopic and sebo rrhoeic
require periodic re-treatment.
dermatitis, and iron, vitamin 8 12 or folate deficiency. If suspected,
If antifungal th erapy is indicated, use: deficiencies should be confim1ed by laboratory investigation s before
commencing supplements. D iabetes has been implicated, but angular
1 amphotericin (adult and child) 10 mg lozenge sucked (th en
cheilitis and oral candidosis have not been shown to occur at increased
swallowed), 4 times daily, after food, for 7 to 14 days*
frequency in patients with diabetes, irrespective of the level of control
OR of their diabetes.

2 miconazole 2% gel2.5 mL (ch ild 6 months to 2 years: 1. 25 mL) Treat oral candidosis if present (see 'O ral candidos is: Management' ,
topically (then swallowed), 4 times daily, after food,for 7 to p.84) . In addition , use:
14 days (measuring spoon supplied with pack). Place directly in 1 miconazo/e 2% cream or gel topically to the angles of the mouth,
(6 the mouth and on the tongue!"
....c 4 times daily for a! least 14 days*
Q) OR
c OR
-c 3 nystatin (adult and child) 100 000 units/mL suspension 1 mL
c 1 nystatin 100 000 units/g cream topically to the angles of the
ro topically (then swallowed), 4 times daily, after food,for 7 to
(6 mouth, 2 to 3 times daily for a/least 14 days.
0
... 14 days. Place under the tongue or in the buccal cavity.
Management of persistent angular cheilitis requ ires specialist advice,
U)
Continue treatment for several days after sym ptoms resolve. Adv ise
Q)
c as treatment for mixed infection may be required or there may be an
denture wearers to app ly the antifunga l to the cleaned fitting surface of
Q) underlying condition, such as Crolm's disease or granul omatous disease.
TI the dentures before inserting them.
::l
(!)
Management of disease in immunocompromised patients requires
u ORAL MUCOSITIS
+=' speciali st advice. Systemic antifunga l drugs, such as flucon azole
::l
Q) or itraconazo le, may be indicated and long-tetm treatment may be Oral mucositis is conventionally defined as erythema and ulceration
0..
~ required. For more information, see Therapeutic Guidelines: Antibiotic. of the oral mucosal surfaces due to cancer treatment modalities such
Q)
.s:::. as radiotherapy and/or chemotherapy. Stomatitis conventional ly
1- Do not use amphotericin lozenges in patients with severe dry mouth, as the action of
sucking lozenges can cause further trauma and irritation to the oral mucosa.
refers to any infl ammatory condition of the oral tissues and inc lud es
84 i" Miconazole can potentiate th e effect of warfarin. * Miconazole can potentiate the effect of warfarin.
 oral mucositis. Other causes of stomatitis include salivary gland Table 7. Oral preparations for the management of oral
hypofunction (see 'Dry mouth' , p. 87) and vitamin deficiencies. In most
mucositis and dry mouth
instances, a history, careful examination, and investigations clarify the
underlying cause.
Preparation Method of use Purpose
Oral mucositis can lead to significant functional problems with Antiplaque/antibacterial preparations
eating, drinking and adherence to medi cations. In addition, patients
chlorhexidine 0.2% dilute 5 ml can be used by people having
undergoing cancer treatment who develop mucositis have an increased mouthwash alcohol- mouthwash wi th 5 ml concurrent chemotherapy and by
risk of systemic infection. They require longer hospital admissions free water, rinse twice daily people with chemotherapy-induced
and sometimes treatment modification or cessation because of their mucositis
mucositis. li mits exposure to water-borne
pathogens
Patients should be dentally fit before commencing radiotherapy to may assist with cleansing of mucositis
the head and neck region or chemotherapy, particularly if th e cancer and shifting of mucous plaques on
mucosal surfaces
treatment will result in severe mucositis and reduced salivary flow.
oral hygiene adjunct
Warn patients of the probability of mucositis (and its nature and likely
duration) before they begin cancer treatment. For more information on chlorhexidine 0.2% apply when needed to ora l hygiene adjunct
gel alcohol-free all mucosal surfaces
the dental management of patients receiving chemotherapy, see p.l62, provides lu brication
and gingival margins
or head and neck radiotherapy, see p.l61. eases discomfort

For information on oral mucositis in patients receiving palliative care, Anti-inflammatory and pain-relief preparations
see Therapeutic Guidelines: Palliative Care. benzydamine rinse 10 to 15 ml provides some pain relief
hyd rochloride 0.15% and spit out, 4 to
solution 6 times daily
Management
lignocaine 2% rinse 10 to 15 ml and provides some pain relief
The underly ing cause of oral mucositis must be known and ad dressed; viscous spit out, 4-hourly

however, management is essentially symptomatic, often requiring Lubrication preparations

anaesthetic or anti-inflammatory mouthwashes to reduce pain, relieve lip balm with apply as necessary useful fo r lip mucositis
inflammation and allow some oral dietary intake. Initial and regular chlorhexidine
ongoing assessment of oral pain is essential.
artificial saliva apply as necessary transient relief of oral dryness
Patients with profound mucositis are unable to undertake normal oral
hygiene measures effectively, although this should be encouraged as
much as is physically possible. Preparations containing chlorhexidine DRY MOUTH
can assist in maintaining oral hygiene in patients unable to brush their The subjective complaint of dry mouth (xerostomia) is a relatively
teeth adeq uately because of oral di scomfort. Preventive oral care common condition, and may or may not occur in the context of reduced
regimens, and initial and ongoing assessment of the oral cavity are salivary flow. The correct term for objective dry mouth is 'sal ivary
required.
gland hypofunction'; however, in practice 'xerostomia' is com~only
There is currently no widely available treatment for oral mucositis. used to describe both subjective and objective dry mouth. Sahvmy
Table 7 (p.87) lists some available oral preparations for the management gland hypofunction may involve a reduction in both th: quantity and
of oral mucositis. the quality of saliva. Many physiological and pathological conditions
can result in salivary gland hypofunction ; these may be developmental ,
infiammat01y or neoplastic.
~
0
Dry mouth most commonly occurs as an adverse effect of dru~s~ the ~ost
86 frequently implicated drugs are tricyclic antidepressants, antihistammes 87
 and anticholinergics. Warn patients if dry mouth is a possible adverse Atiificial saliva can be considered, but the effects are often too lra n ~ i nt
effect of any drug prescribed. This is particularly important for patients to be of significant benefit. A range of products (eg throat lozenges <II ICI
with chronic conditions, who may be taking medications for a long chewing gum) that stimulate salivary flow may give temporary relic!'
time. Dry mouth is also a common adverse effect of some illicit drugs from oral dryness in some patients. However, many of these products
(eg marijuana, heroin) and is implicated in the profound deterioration are very acidic or have high sugar content, which can fwiher increase
of the teeth observed in people with drug dependencies. Injecting drug demineralisation of teeth. Oral preparations that are used for oral
users have a higher prevalence of hepatiti s C infection than the general mucositis may be useful in the symptomatic management of dry mouth
community, and a common extrahepatic manifestation of hepatitis C (see Table 7, p.87). Nonpharmacological advice for patients with dry
infection is dry mouth (see also 'Viral hepatitis: Dental issues', p.l60). mouth is given in Box 8 (below). These recommendations are based on
practical experience and general principles rather than clinical trials.
Dry mouth can be associated with primary Sjogren syndrome, which
occurs predominantly in postmenopausal women. It can also be Tooth extractions require careful consideration, as patients with dry
associated with autoimmune connective tissue disorders that result in mouth may be unable to cope with dentures. Thus, good oral hygiene,
secondary Sjogren syndrome. Dry mouth may also be a direct effect of regular dental examinations, dental treatments as necessary, and topical
head and neck radiotherapy, with the degree of salivary flow reduction remineralising agents are of paramount importance in patients with
dependent on the dose and region of the radiation (see also 'Head and long-term dry mouth.
neck cancer: Dental issues' , p.162).
Prolonged dry mouth can have a profound effect on the oral environment Box 8. Practical advice for patients with dry mouth
and teeth. A decrease in the quantity and/or the quality of saliva can
Managing dry mouth
cause extensive and recurrent smooth smface dental decay resulting
Ensure adequate hydration.
in a marked increase in caries. It can also cause significant worsening
of periodontal disease and any underlying mucosal disease, increased - Dri nk (rather than sip) adequate amounts of fluid, particularly tap water.
risk of oral candidosis, and significant difficulty with the retention of Eat chewy foods to stimulate saliva flow and chew food thoroughly before
dentures. There may also be difficulty with mastication, swallowing swallowing.
and speech. The end result of long-term dry mouth is dental pain and - Chew sugarless gum or suck sugarless sweets (avoid fruit flavours).
loss of teeth. Prevention of these dental diseases may be possible, but - Chew celery.
...
C6
c
only if preventive measures are instituted early and continued (see
'Management', below).
- Choose some foods at meal times that require chewing (especially at
breakfast).
Q)
c For further infmmation on dry mouth in patients receiving palliative Limit caffeine and alcohol intake, and avoid cigarettes.
"C
c care, see Therapeutic Guidelines: Palliative Care. Avoid astringent foods and drinks (eg black tea and coffee).
ca
..
C6
0 Management
Avoid alcohol-containing mouthwashes.
Use bicarbonate mouthwashes.
Ui - A bicarbonate mouthwash can be made up by adding approximately half
(l)
c Before patients commence medications that can cause dry mouth, they
a teaspoon of bicarbonate powder to a glass of warm water. Rinse with
Q) should have a detailed dental check-up followed by treatment of any
:Q mouthwash on waking and at any time during the day.
:::J
active disease. Topical fluoride can be used to reduce deminera;isation
<!l and to promote remineralisation. Other agents that promote remineral- Preventing oral and dental complications (eg dental caries)
()
'.P isation of the teeth may also be used, such as casein phosphopeptide- Ensure good oral hygiene and regular dental examinations.
:::J
(l) amorphous calcium phosphate (CPP-ACP) cream or gum (see Table 5, Avoid acidic beverages (eg wine, fruit juices, soft drinks, sports drinks) and, if
Cl.
~ p.52 , for topical applications used for caries reduction). Anecdotal must have, limit consumption to meal times.
(l)
.c repotis indicate that these also diminish the feeling of oral dryness. Li mit sugar intake and avoid sugary snacks .
f-
The patient should be given oral hygiene instruction, and review
appointments should be at 3- to 6-monthly intervals. 89
88
 Further reading
eTG complete [CD-ROM or online]. Melbourne: Therapeutic Guidelines Limited
[regularly updated ] .

Medications in dentistry supplement. Aust Dent J 2005;50(4 Suppl 2):51-81.

(can be accessed via the Australian Dental Association website
Orofacial pain
<www.ada.org.au > )

The pathophysiology of pain and the management of acute oral and dental
pain are discussed in the 'Post-treatment pain management' chapter (see
pp.l27- 36). In this chapter, two aspects of chronic orofacial pain are
discussed-burning mouth syndrome (BMS) (see below), which is
the most common form of oral dysaesthesia, and temporomandibular
disorders (TMD) (see p.95). Due to their association with TMD, trismus
(see p.93) and bruxism (see p.93) are also discussed.

BURNING MOUTH SYNDROME

Burning mouth syndrome (BMS) is defined as an oral sensory disorder
that presents in the absence of a detectable cause. This stringent
definition effectively excludes all other conditions that might cause an
oral burning sensation. The onset of BMS may be sudden and often
follows a specific event, such as dental treatment or a significant
increase in personal stressors . However, the condition may also have a
gradual onset unrelated to any obvious event. BMS was only recently
recognised as a discrete pain syndrome and is often poorly diagnosed
and managed . Diagnosis requires an accurate and detailed clinical
history and examination, often with laboratory investigations, to
exclude the many conditions that might resemble BMS (see 'Diagnosis
and management', p.92) .
The level and type of presenting symptoms vary; however, the
characteristic symptom of BMS is a burning sensation that typicall y
involves the tongue (usually anterior dorsum) and, less frequently, th e
coincident hard palate and mucosal aspect of the lips. In most patients,
the burning sensation is relatively constant and varies in intensity from
mild with minor inconvenience to profound with patients unab le to
conduct normal daily activities and, on occasion, exhibiting sui cidal c
'(ij
tendencies. In the most common presentation, the burning sensation c.
commences in the morning, with little awareness on wak ing, and 'iii
'(3
increases in intensity as the day progresses. This presentat ion has the
best response to management. Patients may exhibit parafunctional
habits secondary to BMS , such as unconsciously rubbin g th eir tongue 0
~
against the adjacent teeth and hard palate, which can cause traumatic
90 91
abrasion of the filiform papillae on the dorsum.
 The dysaesthesia of BMS is often accompanied by a range of other The general categories of management are:
signs and symptoms, which can include salivary gland hypofunction, discussion with the patient- required in all patients
halitosis and dysgeusia (most commonly a metallic taste). The lifestyle changes designed to modify a patient's response to
dysgeusia and, to a lesser extent, the subjective complaint of dry mouth external stressors (eg relaxation therapy, time management,
(xerostomia) are helpful in assessing clinical progress as they are often exercise, community group participation)
the first symptoms to improve with treatment. They can be used by pharmacological management (eg topical or systemic use
practitioners to reinforce the diagnosis and to indicate to patients that of psychotropic medications, usually one of the tricyclic
they are improving even if the dysaesthesia persists. antidepressants, or antiepileptic drugs such as clonazepam).
Pharmacological management is the path chosen by most patients and
Diagnosis and management requires specialist referral.
The initial work -up of potential BMS patients is extensive and consists
of:
TRISMUS
a detailed clinical history
exclusion of local organic causes (eg mucocutaneous conditions, Trismus can be defined as the inability to open the mouth as wide as is
fungal infections and rough dental surfaces) usual for that person. There are a large number of potential causes for
trismus; the most common causes are:
exclusion of systemic causes with medical history and laboratory
investigations (full blood count, iron studies, serum vitamin B 12 pericoronitis
and folate) inflammation of the masticatory muscles (eg following dental
exclusion of hypersensitivity (impo1iant in patients who feel the injection)
problem is prosthesis related) . A 24- to 48-hour skin patch test can spreading odontogenic infection (see p.63)
be a valuable and supportive adjunct to the discussion, particularly peritonsillar abscess (a potential complication of tonsillitis)
in patients who may be sceptical of the diagnosis temporomandibular disorders (see p.95)
review of medications that may cause sensory neuropathy, taste oral submucous fibrosis (very common in parts of the world where
aberrations or salivary gland hypofunction. betel nut chewing is frequent).
:ss::::
Some practitioners use questionnaires to assess the patient's An accurate aetiology for trismus requires appropriate history,
examination and imaging. Management of the underlying cause may
<I> psychological and pain status. However, interpretation of these
c questionnaires requires specialist psychological or psychiatric input. include dental treatments, physiotherapy, and passive range of motion
"C
s:::: devices. Additionally, symptoms may be controlled with analgesics (see
C'Cl The management of BMS is complex and involves local, systemic p.l32 for pain management strategies) and warm compresses.
~ and psychological elements. Management must always be prefaced by
0 a correct diagnosis and open discussion with the patient so they have Patients with ongoing trismus or in whom an underlying cause has
Ui an understanding of the condition. not been identified require urgent specialist referral to investigate
Q)
c Some patients may improve with The most important aspects of less common causes of trismus, such as malignancies involving the
Q) management are discussion masticatory muscles and scleroderma.
"0 discussion and counselling alone.
with the patient and an
::::l
C.?
It is critical patients appreciate that
understanding of the condition
u BMS is a chronic neuropathic pain by the patient. BRUXISM
..:::;
::::l syndrome, irrespective of the likely
Q)
0.. initial triggers and associated personality type. Patients also appreciate Bruxism is defined as a parafunctional activity that includes clenching,
~ an explanation of the cause of their tongue discomf01i. bracing, gnashing and grinding of teeth. It can occur while people arc
Q)
_c
I- awake or asleep. Awake bruxism is defined as the awareness of jaw 0
clenching, usually as a reaction to stress, and is present in about 20% f'
92
 adults. Sleep bruxism, a sleep-related movement disorder, is a rhythmic
motor activity unrelated to the presence of food and associated with the
unconscious co-contraction ofjaw-closing and -opening muscles. Tooth
grinding during sleep (as noted by sleep partner or family members) has
been reported by 8% of adults. There is no evidence to support the role
of occlusal factors in the cause of sleep bruxism. Rhythmic masticatory
muscle activity in sleep bruxism peaks in the minutes before rapid eye
movement sleep. This suggests the onset of sleep bruxism is facilitated
by a mechanism related to sleep stage transitions.
About 50% of people with a history of tooth grinding have low
frequencies of jaw muscle contractions and tooth-grinding events in
the sleep laboratory. This may be related to the natural variability in
the occurrence of sleep bruxism over time. It remains to be clarified
when bruxism, as a behaviour found in healthy people, becomes a
disorder associated with negative consequences such as tooth damage
and pain. Bruxism may rarely be a sign orofacial dyskinesia, or occur
following a head injury or as an adverse effect of drugs that stimulate
the sympathetic nervous system (eg amphetamines).
Intraoral occlusal appliances (splints or dental guards) can be
constructed to protect the teeth from abrasion during sleep bruxism.
They have been shown to reduce muscle strain, decrease loading of
the temporomandibular joints and prevent tooth damage, but will not
cure bruxism. The use ofwell-fitted and adjusted full -coverage intraoral
occlusal splints can be essential during and after the rehabilitative phase
of restorative treatment to protect the dentition in patients with sleep
bruxism.
Over the past decade, splints have been used that are thought to act by
a nociceptive trigeminal inhibition tension suppression system (NTI-
TSS) . NTI-TSS splints are constructed to only fit the most anterior teeth
on the maxilla and translate the bite force in such a way as to result in
an undesirable sensation. This should automatically and subconsciously
reduce the clenching force as the nociceptor senses and responds to
pressure. Unfortunately for patients who do not subconsciously clench
less while using NTI-TSS splints, severe damage and tooth movement
from clenching can occur. Cases of device aspiration during sleep have
also been reported. Thus, these splints should be recommended with
caution, and patients who are treated with NTI-TSS splints should be
reviewed on an ongoing basis.
94
TEMPOROMANDIBULAR DISORDERS
Temporomandibular disorders (TMD) is a collective term embracing a
nwnber of clinical problems that involve the masticatory muscu lature,
the temporomandibular joints (TMJs) and associated structures, or
both. TMD usually arises in early adulthood, but can be present in
children and the elderly. It has been estimated between 40% and 75% of
people will exhibit one sign ofTMD during their lifetime, but usually
this is subclinical with only 5% of sufferers seeking treatment. Risk
factors for TMD include direct trauma or indirect trauma (acceleration-
deceleration injury), parafunctional habits and psychosocial factors.
Malocclusion as a risk factor for TMD is not supported by the literature.
Patients with TMD often report trismus (see p.93), joint sounds, pain
and asymmetry with mandibular function as well as persistent pain in
and around the ears and masticatory muscles, headache (particularly on
waking) and neck pain. They occasionally describe reduced hearing,
changes in occlusion, clenching of teeth (see 'Bruxism', p.93) and
sometimes toothache. Tenderness of the TMJs and masticatory muscles
dming movement is often reported on palpation. TMJ sounds, described
as clicking, clunking or crepitus, are most easily detected by palpation
during repetitive opening and closing movements as well as lateral and
protrusive movements. Isolated TMJ sounds are not an indication for
treatment unless associated with pain or dysfunction.
TMD is commonly misdiagnosed or undiagnosed, and frequently patients
are subjected to inappropriate diagnostic and therapeutic procedures .
This often leads to considerable patient concern. An accurate diagnosis
of TMD requires appropriate history, examination and imaging.
Diagnostic categories of TMD include TMJ articular disorders and
masticatory muscle disorders. Articular disorders encompass congenital
disorders, disk derangement disorders, dislocations, inflammatory
conditions, arthritis, ankylosis and fractmes. Muscle disorders include
myofascial pain, myositis, myospasm, local myalgia and myofibrotic
contractures. Chronic TMD is often associated with and perpetuated by
psychosocial factors, particularly anxiety, depression and somatisation.
Rarely is TMD a consequence of psychological disorders.
Management
Management of TMD requires clear treatment goals based on the
established diagnosis, with the aim of controlling the symptoms rather
than achieving a cure. These goals should include decreasing pain and
adverse loading, restoring mandibular function, resuming norm al dail y
activities and eliminating contributing factors.
 General management strategies include patient education and self-care
with modification of diet to minimise chewing (eg eating only soft foods),
avoidance of extreme jaw movements such as yawning and chewing,
and application of warm packs to the TMJs and cheeks several times
per day. Behavioural modification can be achieved through individual
or group counselling to identify and manage sources of stress. Gentle
muscle stretching and appropriate massaging of the jaw muscles by an
experienced physiotherapist can be extremely helpful and, if carried out
on a regular basis, play an important role in the management ofTMD.
Intraoral occlusal splints may be required to alter the mandibular vetiical
dimension, thereby reducing joint loading, muscle activity and pain,
and to protect the teeth from bruxing habits. They are usually worn only
at night, and should be meticulously adjusted and regularly monitored
over several months. They should not have any permanent effect on
the position of the dentition, and should be seen as a management tool
rather than a 'one-stop cure'. Splints do not re-establish horizo ntal or
vertical jaw relationships and should be described to patients as an
'oromandibular crutch' similar to a back brace or ankle support.
A vast array of medications has been used to treat TMD with varying
levels of success. These include analgesics, muscle relaxants,
anx iolytics, corticosteroids and antidepressants. However, due to
the long-term nature of this condition, patients should be generally
discouraged from rely ing on med ication alone to treat the symptoms
ofTMD.
If simple conservative measures fa il and the patient's pain and
"ai
....
c dysfunction become severe and chronic, spec iali st referral for further
Cl) management is appropriate. Surgery is rarely required, and should
c only be contemplated if symptoms do not respond to conservative
'C
c management and there is definitive evidence of internal joint
(tl
Halitosis
Halitosis (oral malodour) is common on waking, usually due to low
salivary flow and lack of oral cleansing during sleep. This is rarely
significant, and can be readily rectified by eating, tongue-brushing and
rinsing the mouth with fresh water. Halitosis occurring at other times
usually results from eating cetiain foods (eg garlic, onion, spices), or
from habits such as smoking or drinking alcohol. The cause is therefore
often obvious, and hali tosis can be prevented by avo iding these
substances and habits.
Infections are a common cause of oral malodour, such as periodontal
infections and pericoronitis. Improvement of oral hygiene and
prevention or treatment of infection, sometimes with antimicrobials,
can usually manage this type of halitosis . Mucosal ulcerative conditions
(eg recurrent aphthous stomatitis, oral lichen planus) can also cause oral
mal odour.
Common causes of halitosis are summarised in Box 9 (p.98).
Studies have shown that halitosis is associated with an increase in
specific oral bacteria (Veillonella, Actinomyces and Prevotella species)
that are the predominant producers of hydrogen sulfide (H 2S). A recent
study on the bacterial composition of saliva in patients complaining
of oral mal odour found that both the amount of bacteria and the type
of bacteria in the mouth are critical in detetmining the severity of

..
"ai
0
derangement or other joint pathology on imaging. malodour.*
The dorsal surface of the tongue is thought to be the location of the
(;j microbial population causing halitosis. Thus, dental plaque and food
ClJ
.~ debris associated with poor oral hygiene or a poorly designed denture
a:; or bridge only add to the level of halitosis.
'"0
::J
<.!J
()
.;:;
::J
ClJ
0.
~
ClJ

1-
*Takeshita T, Suzuki N, Nakano Y, Shimazaki Y. Yoneda M, Hirofuji T, et al. Relation ship
between oral ma lodor and t he global composition of indigenous bacteri al populntl onn In
96 saliva. Appl Envi ron Microbiol 2010;76(9):2806- 14.
 Box 9. Some common causes of halitosis come from the sinuses or nasal passages. Similar odour equall y sensed
from both the nose and the mouth can indicate one of the many systemi c
Transient causes causes of halitosis.
odour-causing foods (eg garlic, onions)
A Halimeter is a specific apparatus for objectively measuring th e
smoking and alcohol
responsible volatile sulfur compounds; however, measurements given
dry mouth by this device are variable and the results are difficult to interpret.
Definitive diagnosis of halitosis is often difficult, with studies showing
Intraoral causes
only a weak correlation between self-rep01ied halitosis and either
intraoral bacteria
organoleptic or direct measurements of volatile sulfur compounds.
- tongue colonisation
- caries
Initial management of halitosis requires identify ing and addressing its
cause (see Box 9, p.98), and assessing the severity of the malodour.
- chronic periodontitis
Examination of the nose, tonsils, mucosal surfaces of the pharynx and
acute infections within the mouth including: oral cavity, and dentition is required. Confirm the patient's subjective
- dental abscess halitosis (ie as noted by family/friends and clinician).
- oral candidosis
In vitro studies modelling bacterial colonisation of the tongue have
- acute ulcerative gingivitis shown that, although the number of H 2S-producing organisms is low
poor oral hygiene (eg putrescent food particles between the teeth, on the (at about 2.5% of all tongue flora organisms), a reduction in these
tongue and around the gu ms) organisms decreases the amount of volatile sulfur compounds. A
mouthwash containing chlorhexidine may be effective in the short-term
Extraoral causes management of halitosis caused by oral conditions:
hepatic encephalopathy
diabetic acidosis
chlorhexidine 0.2% mouthwash 10 mL rinsed in the mouth for
1 minute, 8- to 12-hourly. *
uraemia
trimethylaminuria Limited studies have shown that lozenges containing low concentrations
of zinc may reduce the amount of vo latile sulfur compounds. Other
iii
.... infectious or neoplastic disease of the respiratory tract (eg nasal sepsis,
I: postnasal drip, sinusitis) or gastrointestinal tract (eg oesophageal reflux, pyloric
studies have shown that triclosan, a lipid-soluble antibacterial agent,
Q)
c stenosis, oral or gastric cancer) may reduce the amount of volatile sulfur compounds in a dose-
"C lung abscess
dependent fashion. However, neither of these agents has been studied
I:
ctl in patients with halitosis. A recent trial of a mouthwash containing
starvation
chlorine dioxide reported its effectiveness in reducing volatile sulfur
~ compounds and morning halitosis in the small number of participants;,
0 Psychogenic causes
halitophobia but further evidence is required before its use can be recommended.
An occasional clinical dilemma is the complaint of halitosis by patients
who do not have it but imagine it. Objective testing is difficult and
DIAGNOSIS AND MANAGEMENT often unreliable, and the halitosis may then be attributable to a form
of delusion or monosymptomatic hypochondriasis (ie psyc hoge ni c
~iagno~is of halitosis is usually subjective, by simply smelling exhaled
air commg _from the patient's mouth and nose and comparing the two *With prolonged use (more than a few days) , chlorhexidine may cause a superficial
(organoleptic assessment). Odour originating in the mouth, but not discolouration of the teeth and fil lings (see p.44 for more information).
detectabl~ ~-o,~ th~ nose, is likely to be of oral or pharyngeal origin. ; Shinada K, Ueno M, Konishi C, Takehara S, Yokoyama S, Zaitsu T, et al. Effects of a
mouthwash with chlorine dioxide on oral malodor and saliva!)' bacteria: a randoml7ocl
Odour ongmatmg m the nose, but not detectable from the mouth, may placebo-controlled 7-day trial. Trials 2010;11:14.
98
 halitosis). Other people's behaviour, or perceived behaviour, such as
covering the nose or averting the face, is typically misinterpreted by
these patients as an indication their breath is offensive. Such patients
may have latent psychosomatic illness. They present a diagnostic and
treatment challenge, and despite reassurance may require psychiatric
consultation.
Antibiotic prophylaxis
For patients with persistent or recurrent halitosis, a full assessment of
oral and dental health by a dentist is advised. If this proves unhelpful, Antibiotic prophylaxis is the administration of an antibiotic before a
specialist referral is needed. This may include referral to an oral dental procedure to minimise the risk of bacterial infection. It is only
medicine specialist; an otorhinolaryngologist to rule out the presence given when the risk of infection is high. Infection can occur at:
of chronic tonsillitis or chronic sinusitis; a physician to rule out gastric, a distant site through the haematogenous route, usually the heart
hepatic, endocrine, pulmonary, metabolic or renal disease; and/or a (eg endocarditis, see below)
psychologist or psychiatrist.
an oral surgical site (eg following dentoalveolar surgery, see
Further reading p.l07) .

Hughes FJ, McNab R. Oral malodour-a review. Arch Oral Bioi 2008;53 Suppl There is a very small risk of infection at a prosthetic joint site through
1:51-7. the haematogenous route. Therefore antibiotic prophylaxis is not
recommended before dental procedures in patients with prosthetic
joints (see p.l06).
If required, antibiotic prophylaxis
Antibiotic prophylaxis shou ld
should be given just before the
be given just before the
procedure. The aim is to achieve high procedure-there is no benefit
plasma and tissue concentrations in giving prophylactic doses after
at the time contamination is most the procedure .
likely. Prescribing antibiotics after
the procedure is of no prophylactic value.

PREVENTION OF ENDOCARDITIS

General considerations
Infective endocarditis is an uncommon illness with a high morbidity
and mortality. For many years antibiotic prophylaxis has been given
routinely before dental and other procedures to patients with cardiac
conditions that carry a high lifetime risk of infective endocarditis.
However, the evidence suggests that endocarditis after dental or other
procedures is infrequent and hence prophylaxis prevents very few
cases. Infective endocarditis is more likely to result from bacteraemias
associated with daily activities, so the maintenance of good oral hea lth
and hygiene is more important than periprocedural antibiotics.

100 101
 No randomised controlled trial has been performed to decide the role
of antibiotic prophylaxis and there are no human studies showing that
it can prevent endocarditis. Guidelines produced in di fferent parts of
the world rely on expert consensus and consequently can differ in
their recommendations. These Australian guidelines follow the lead
of the American Heart Association*, continuing a trend to reduce the
categories of patients fo r whom prophylaxis is recommended while still
specifying procedures for which prophylaxis is required.
Antibiotic prophylaxis is now recommended only for patients with
cardiac conditions associated with the highest risk of adverse outcomes
from endocarditis (see Box 10, below) if und ergoing a specified dental
(see Table 8, p.l04) or other procedure (see Therapeutic Guidelines:
Antibiotic). This list of cardiac conditions is short and all of these
patients have had significant cardiovascular diseases or interventions.
Prophylaxis is no longer recommended for patients with other forms
of valvular or structural heart disease, including mitral valve prolapse.
Box 10. Cardiac conditions associated with the highest
risk of adverse outcomes from endocarditis
Antibiotic prophylaxis is recommended in patients with the following cardiac
conditions if undergoing a specified dental (see Table 8, p.104) or other
procedure (see Therapeutic Guidelines: Antibiotic):
prosthetic ca rdiac valve or prosthetic material used for card iac va lve repair
previous infective endocarditis
congenital heart disease but only if it involves:
!c - unrepaired cyanotic defects, includi ng palliative shu nts and condu its
Q)
c - completely repaired defects with prosthetic materi al or devices, whether
"C placed by su rgery or catheter intervention , during the first 6 months after
c
(II the procedure (after which the prosthetic material is likely to have been
0
...
"iii endothelialised)
- repaired defects with residual defects at or adj acent to the site of a
Ui prosthetic patch or device (which inhibit endothelial isation)
(])
c cardiac transplantation with the subsequent development of card iac
(ij
:"Q valvulopathy
:::l
0 rheumatic heart disease in Indigenous Australians on ly.
()
.;:::;
:::l
(])
a. *Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM , Levison M, et al. Prevention
~ of infective endocarditis: gu idel ines from the American Heart Association: a guidelrne from
(])
.c the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease
t- Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical
Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and
102 Outcomes Research Interdisciplinary Working Group . Circulation 200 7; 116(15):1736-54.
It is recognised that the change in recommendations, while justifi ed and
in progression from past guidelines, may appear to be controversial. In
certain individual circumstances, medical practitioners and denti sts may
consider giving antibiotics to patients not covered by these gu idelines.
These include patients who have received prophylactic antibiotics over
their lifet ime and are unwi lling to change this practice.
In addition, Indigenous Australian patients with rheumatic heati di sease
may be a special population at high risk fo r infective endocarditis or for
adverse outcomes from endocarditi s. Accordingly, this group has also
been included in the list of patients w ith cardi ac conditions requiring
prophy laxis (see Box 10, p.l02).
All patients with cardiac abno rm aliti es should be reminded to practise
good oral hygiene and have regular dental evaluation. In particular,
dental examination is recommended twice yearly for patients with
cardiac conditions involving the end ocardium, especially those listed
in Box 10. Doctors should be alert to investigate an unexplained fever
that could be a sign of endocarditis, and take blood cultures before
ad ministering any oral or intravenous antibiotics.
The National Prescribing Service has developed a patient information
reso urce to help practitioners explain the changes to the guidelines on
prevention of endocarditis (see <www. nps.org.au/health _professionals/
patient_resources/patient_ leaflets> and choose ' Infective endocarditis
and antibiotic prophylaxis' ).
Dental procedures and antibiotic
recommendations
Bacteraemia associated with dental procedures predominantly involves
viridans group streptococci, organ isms known to cause infective endo-
carditi s. Traditionally, the presence of 's ignificant bleeding' associated
w ith a dental procedure has been taken as an indication of bacteraemia
and hence need fo r prophylaxis; however, bleeding has been shown to
be a poor indicator ofbacteraem ia from dental procedures.
The key parameters of a bacteraemia are its incidence, magn itude and
duration. The magnitude and duration of the bacteraemia are dependent
on the state of periodontal health, the vigour of the dentogingiva l or (J
apical manipulation and the duration of the procedure. Some procedure.
!1'1
,0
may or may not require prophylaxis depending on these factors.
1
 :r~phylax i s is always required for those procedures with a high Patient-performed oral hygiene act1 vtt1 es, such as toothbrushing,
mc1dence of ~acteraemia (may occur in 70% or more patients). Dental flossing or use of oral irrigators, can produce similar incidences of
procedures w1th a moderate incidence of bacteraemia (may occur in bacteraemia as th at caused by most denta l procedu res (excluding
30% or ~ore patients) should be considered for prophylax is depending extractions and subgingival scaling/root plani ng). As th ese activities
on the Circumstances of the procedure and the periodontal condition are performed more frequently, they have th e 1 otential to produ ce
(~ee Ta ble 8, below). Thus, for example, periodontal probing on a regular episodes of bacteraemia, part icularl y in pa ti ents with gingiva l
smgle healthy tooth would not justi fy antibiotic prophylaxis whereas inflammation. It is considered that the cumul ati ve c l"fcct o l" repea ted
full-mouth periodontal probing on a patient with periodontitis would. episodes ofbacteraemia caused by oral hyg ie ne ac ti vities is ve ry likely
to be a more important risk factor for infecti ve end oca rditi s th a n isolated
Prophylaxis is not required for procedures with a low incidence of
bacteraemia. episodes of bacterae mia occurring durin g dental visils, espec iall y in
patients with poor oral health and hyg iene.
Table 8. Dental procedures and their requirement for If after careful evaluation of both th e card iac co ndition (sec Box I 0,
endocarditis prophylaxis in patients with cardiac p.l02) and th e dental procedure (see Table 8, p. 104) anti bioti c
conditions listed in Box 10 prophylax is is considered necessary, a single dose of antibi oti c sho uld
be given before the procedure; there is no proven va lue to giving a
Prophylaxis Prophylaxis required in Prophylaxis not required foll ow-up dose 6 hours later.
always required some circumstances
extraction
If a patient is hav ing more than one procedure requiring antibiotic
Consider prophylaxis for oral examination
the following procedures if prophylax is, dentists should carefully consider th eir treatment plan and
periodontal infiltration and block local
procedures including
multiple procedures are being modify it as necessary so all of the procedures can be completed in
conducted, the procedure anaestheti c injection
surgery, subgingival a single or at most two sittings, thus avoiding the need for multiple
is prolonged or periodontal restorative dentistry
scaling and root antibiotic doses.
disease is present:
plan ing
fu ll periodontal probi ng for su pragingiva l rubber dam
replanting avulsed patients wit h peri odontitis clamping and placement For standard prophy laxis, use:
teeth of rubber dam
intraligamentary and amoxycillin 2 g (child: 50 mg/kg up to 2 g) orally, 1 hour before
other surgica l intraosseous local intracanal endodontic
procedures (eg procedures
the procedure
anaesthetic injection
implant placement, or amoxy/ampicillin 2 g (child: 50 mg/kg up to 2 g) I V, just before
supragingival calculus removal of sutures
apicectomy) the procedure
removal/c leaning impressions and
or amoxy/ampicillin 2 g (child: 50 mg/kg up to 2 g) IM, 30 minutes
rubber dam placement construction of dentures
with clamps (where risk of
before the procedure.
orth odontic bracket
damaging gingiva) placement and adjustment Patients hypersensitive to penicillin (see p. l9), and those on long-term
restorative matrix band/ of fixed appl iances
penicillin therapy or who have taken penicillin or a related beta-lactam
strip placement applicati on of gels
(f) antibiotic more th an once in the previous month, can use:
Q) endodontics beyond t he intraoral radiographs
c apical foramen 1 clindamycin 600 mg (child: 15 mglkg up to 600 mg) orally, 1 hour
(ij supragingival plaque
:Q placement of orthodont ic removal
before the procedure
:::J bands or clindamycin 600 mg (child: 15 mg/kg up to 600 mg) I V over at
(!)
(.)
.;::; placement of interdental least 20 minutes, j ust before the p rocedure
:::J wedges
Q)
a. subgingival placement of
OR
~ retraction cords, antibiotic
Q)
_c fib res or antibiotic strips
1 lincomycin 600 mg (child: 15 mg/kg up to 600 mg) I V over at least
1- 1 how; just before the procedure

104 OR 'IOh
 2 vancomycin 25 mg/kg up to 1.5 g (child less than 12 years:
30 mglkg up to 1.5 g) IV, ending the infusionjust before the
procedure (slow irifusion required- in adults and children 12 y ears
or more, infuse at a rate not exceeding 10 mg/ min; in children less
than 12 years, infuse over 2 hours)
OR
3 teicoplanin 400 mg (child: 10 mg/kg up to 400 mg) IV, just before
the procedure
or teicoplanin 400 mg (child: 10 mglkg up to 400 mg) IM,
30 minutes before the procedure.
For patients who are unable to swallow clindamycin capsules, see
'Lincosamides' (p.23) for instructions on preparation of an oral
solution . An alternative for patients who are hypersensitive to penicillin
(excluding immediate hypersensitivity, see p.l9), is:
cephalexin 2 g (child: 50 mglkg up to 2 g) orally, 1 hour bef ore the
procedure.
Cephalexin is not suitable for those who have been on long-term
penicillin or have taken a related beta-lactam antibiotic more than once
in the previous month.
PREVENTION OF INFECTION IN JOINT
PROSTHESES
Before placement of joint prostheses
Patients should be referred to a dentist for a comprehensive dental
examination (including radiographs) before placement of a joint
prosthesis. Dental treatments should be performed as required to make
the patient orally and dentally fit- the dentist may be requested to give
a written opinion on the patient's oral and dental health. Arrangements
should be made for regular dental review after placement of the
prosthesis.
After placement of joint prostheses
All patients with a joint prosthesis have a very small risk of infection
at the prosthetic site by the haematogenous route. Even in procedures
in which bacteraemia is likely to occur (eg tooth extractions and
periodontal procedures), the value of antibiotic prophylaxis has not been
106
demonstrated. Therefore, prophylaxis before dental procedures is not.
recommended as the risk of adverse effects outweighs the likelihood o l
benefit from prophylaxis. Early recognition and treatment of infecti on
at any site is important to prevent seeding of the prosthesis.
PREVENTION OF DENTOALVEOLAR SURGICAL SITE
INFECTIONS
General considerations
It is essential that dentists and medical practitioners understand the
general principle of antibiotic prophylaxis for surgety. :Vhen antibi?t.ics
first became readily available, they were widely used m both medtcme
and dentistry as a 'protective cover' against surgical site inf~ctions .
However the low risk of wound infection must be balanced agamst the
risk of adverse effects and the risk of developing resistant organisms
from antibiotic use. Antibiotic prophylaxis must be restricted to
situations in which it has been shown to be effective. For most
dentoalveolar procedures in fit immunocompetent patients, antibiotic
prophylaxis is not required or recommended.
Antibiotic prophylaxis should be considered for:
surgical removal of a bone-impacted t~oth or periapi~al sur~ery
in a patient with a history of recunent mfecttons (pat tents With
evidence of active infection in the area of planned surgery do
not have a prophylactic indication but may have a therapeutic
indication for antibiotics)
dentoalveolar surgery in immunocompromised patients (including
those with rheumatoid atihritis or poorly controlled diabetes, those
taking immunosuppressive treatment for organ tran.splants or.
malignancy, and those taking systemic COliicosteroids [eg pattents
with severe asthma, dermatological problems]).
Asplenic patients may be on long-term prophylaxis to prevent
pneumococcal sepsis and this should be continued (~e~ Therapeuttc
Guidelines: Antibiotic). Surgical antibiotic prophylaxts ts not recom-
mended in asplenic patients, other than as indicated above.
The critical period for successful prophy laxis is the .4 hours follow~ng
entry of organisms into a wound. In general, a smgle preoper~ti ve
dose of antibiotic is sufficient. Postoperative doses are not advi sed.
Established infection should of course be treated (see p.67).
 If antibiotic prophylaxis is required, give: Implants
1 phenoxymethylpenicillin 2 g (child: 40 mg/kg up to 2 g) orally, D~.:ntal implants involve the elective surgi.cal placement or forci gi~
1 hour before the p rocedure bod ies into the jaw. Strict attention to sur~Ical. asepsiS and techniql;~.:
IS essential. The incidence of wound infectiOn IS very low and mai n y
OR relates to technique issues.
2 amoxycillin 2 g (child: 50 mg/kg up to 2 g) orally, 1 hour before ( 'ontrolled studies for mandibular third molar su~g~r~ and placement ol;
the procedure dental implants show little or no benefit f~om ~ntibiOtic prophylaxis anc
or amoxy/ampicillin 2 g (child: 50 mg/kg up to 2 g) IV, just before !here is a risk of adverse effects from antibiotiCS.
the procedure
or amoxy!ampicillin 2 g (child: 50 mglkg up to 2 g) IM, 30 minutes Further reading
before the procedure
eTG complete [CD-ROM or online]. Melbourne: Therapeutic Guidelines Limited
OR [regularly updated] .

2 benzylpenicillin 1.2 g (child: 30 mglkg up to 1.2 g) IV, just before Medications in dentistry suppleme nt. Aust Dent J 2005;50(4 Suppl 2):51- 81.
the procedure. (can be accessed via the Australian Dental AssociatiOn website
< www.ada.org.au>)
For patients hypersensitive to penicillin (see p.l9), use:
1 clindamycin 600 mg (child: 15 mg/kg up to 600 mg) orally, 1 hour
before the procedure
or clindamycin 600 mg (child: 15 mg/kg up to 600 mg) IV over at
least 20 minutes, just before the procedure
OR
1 lincomycin 600 mg (child: 15 mg/kg up to 600 mg) IV over at least
1 hour, just before the procedure.
:s
c For patients hypersensitive to penicillin who are unable to swallow
e8 clindamycin capsules, see 'Lincosamides' (p.23) for instructions on
-g preparation of an oral solution.
l1l

Tooth extractions
The incidence of wound infection following simple extractions is
negligible. The incidence following the removal of bone-impacted
wisdom teeth in fit healthy patients is low (2% to 5%). An infection is
usually, but not always, confined to the socket and of such low incidence
that, generally, antibiotic prophylaxis is not required or recommended.
Alveolar osteitis (dry socket) (see p.69) is not a bacterial infection but
a wound-healing problem so prophylactic antibiotics are of no value.

l t:l
108
Local anaesthesia

Local anaesthetics are commonly used in dentistry to achieve local

analgesia. They provide a safe and effective method of pain control, and
have a very low incidence of significant adverse effects. However, it is
still important that clinicians have an understanding of the complications
that can arise from local anaesthetic use.
In dentistry, local anaesthetics are usually given by injection. The
technique used depends on many factors. The two most common
injection techniques are:
o infiltration- the injection is given adjacent to the site where
analgesia is required
o regional block- the injection is given adjacent to the nerve, but

at a distance proximal to the site where analgesia is required. The

aim is to prevent pain sensation for the entire nerve distribution
distal to the site of injection.
The onset of action is related to the injection technique, and is approxi-
mately 2 to 3 minutes for an infiltration injection and 4 to 5 minutes
for a block injection. Pulp analgesia takes longer than analgesia of
the soft tissues. The duration of action is variable depending on the
local anaesthetic used, the dose and the injection technique. Advise
patients ofthe likely duration of anaesthesia (usually a few hours) and
recommend seeking advice if they have not recovered after this time.
Topical local anaesthetics are used by some practitioners and requested
by some patients before local anaesthetic injections. They can also be
used for minor procedures where injections are avoided, such as band
removal, crown placement and mucosal incision. Topical anaesthetics
only affect the mucosal surface so they do not prevent the painful
feeling of pressure when fluid is injected into deeper tissue. They also
widely diffuse around the mouth and some patients do not tolerate this.
Topical anaesthetics have a very low risk of adverse reactions, but
should be avoided in patients with a confirmed allergy. Some examples
oftopical anaesthetics are lignocaine plus prilocaine (eutectic mixture)
5% cream and lignocaine 10% adhesive ointment. They should be
applied to the area at least 3 minutes before the procedure or local
anaesthetic injection. 111
 PHARMACOLOGY
Local anaesthetics inhibit the generation of electrical impulses and
their conduction along the neuronal axon membrane by reversible
blockade of sodium ion channels. Recent research has shown that
calcium, potassium and G-protein regulated channels are also blocked.
The progression of local anaesthesia relates to nerve fibre diameter,
myelination, and conduction velocity. In general, loss of nerve function
occurs in the sequence of autonomic activity, followed by pain sensation,
other sensory functions and finally motor activity.
A local anaesthetic molecule comprises a lipophilic head, a hydrophilic
tail and a linking intermediate chain. The intermediate chain may be an
aminoester group or an am inoamide group. All local anaesthetics used
in dentistry are aminoamides (eg lignocaine, prilocaine, mepivacaine,
articaine). Aminoamides are primarily metabolised by the liver and are
less water soluble than aminoesters.
ADDITION OF VASOCONSTRICTORS
Local anaesthetics currently in use do not cause vasoconstriction so a
separate vasoconstrictor is commonly added. Vasoconstrictors prolong
the working time of local anaesthetic solutions by reducing their rate
of loss to the general circulation. Therefore, a lower dose of local
anaesthetic is required to achieve effective analgesia. Vasoconstrictors
also reduce bleeding, which improves the operator's vision of the
procedural site and therefore the quality of patient care.
!c If a local anaesthetic is used without a vasoconstrictor, it is more likely
Cl) that the patient will experience pain and, as a result, produce substantial
c amounts of endogenous ad rena line.
"C
c
ca Adrenaline (see below) and felypressin (see p.113) are the most
~ commonly used vasoconstrictors in current practice. Noradrenaline
0 was previously used, but is not recommended due to significant adverse
effects, particularly increased blood pressure.
Adrenaline
The concentration of adrenaline in most dental cartridges is 1:80 000 or
1:100 000, although more dilute solutions are available in vials.
Adrenaline is affected by heat and light so dental cartridges should
be stored in a cool dark place in accordance with the manufacturer's
instructions.
112
Adrenaline is not contraindicated with antihype11ensives, sympatho-
mimetic drugs, cardiac glycosides, and antidepressants other than
monoamine oxidase inhibitors (MAOis). MAOis inhibit the metabolism
of adrenaline, so local anaesthetic preparations containing adrenaline
should not be used in patients taking these drugs .
Some patients report an allergy to adrenaline but, while there are
isolated cases, true allergy is extremely rare. In most cases of repm1ed
allergy, patients describe a physiological response to adrenaline (eg
tachycardia) when questioned closely. If allergy is confirmed, local
anaesthetic solutions with felypressin or plain solutions (ie without a
vasoconstrictor) may be used.
Felypressin
Felypressin is a vasoconstrictor based on the p1tmtary hormone
oxytocin. It is used in a concentration of 0.03 international units/mL,
and at this concentration has minimal myocardial effects. At higher
doses, felypressin may cause some coronary a11ery constriction. Its lack
of effect on the central nervous system makes it useful when adrenaline
is contraindicated (which is rare).
Although similar in structure to oxytocin (the hormone responsible
for causing contraction of the uterus during labour), felypressin is not
contraindicated in pregnancy.
ADVERSE EFFECTS
Relative to the number of local anaesthetic injections given, the rate
of complications (especially major complications) is exceedingly low.
The most common complications of local anaesthetic injections
are associated with anatomical or technique problems. Difficulty
in identifying anatomical landmarks (most commonly with inferior
alveolar nerve blocks) can result in incomplete or failure of local
anaesthetic effect. This is often associated with poor technique or
anatomical variation. Injecting local anaesthetic solution (particularly
if it contains a vasoconstrictor) directly into a blood vessel can cause
significant systemic effects and increase the risk of adverse outcomes.
The adverse effects of local anaesthetics include:
local complications (see p.ll4)
systemic toxicity (see also p.l15)
central nervous system (CNS) effects-light-headcdnes ,
nervousness, apprehension, euphoria, confusion , di zzinc s,
113
 CNS effects (cont.)
drowsiness, blurred or double vision, twitching, tremors,
convulsions and unconsciousness, difficulty swallowing,
slurred speech, sensations of heat or cold
respiratory effects- respiratory depression, respiratory arrest
cardiovascular effects-bradycardia, hypotension, and
cardiovascular collapse which may lead to cardiovascular
arrest
allergic responses (usually due to the ester group of
local anaesthetics)- cutaneous lesions, urticaria, oedema,
anaphylactoid reactions
methaemoglobinaemia (prilocaine and articaine, dose-
dependent)- excessive amounts of methaemoglobin (formed
by the oxidation of haemoglobin) in the blood, which results in
reduced blood oxygen-carrying capacity.
Different local anaesthetics have a different incidence of complications.
For more information on adverse effects of local anaesthetics, see
'Further reading' (p.ll8). For adverse effects of vasoconstrictors, see
'Addition of vasoconstrictors' (p.ll2).
local complications
Although local complications are generally not as significant as
systemic complications, they can result in the patient needing to return
for treatment, as well as loss of confidence in the operator.
There is a wide variety of potential local complications associated
with local anaesthetic injections. These include equipment failure (eg
cat1ridge explosion), anatomical issues (eg nerve trauma, paraesthesia,
facial nerve paralysis), and tissue trauma- either operator- or patient-
induced (eg trismus, haematoma, infection).
Nerve injuries resulting in paraesthesia or dysaesthesia are often
considered a consequence of direct nerve trauma; however, there are
data to suggest that local anaesthetics have varying potential to cause
neurotoxicity. The literature is still limited in this area, but nerve injuries
can be caused by direct nerve trauma, indirect nerve trauma from
bleeding within the nerve sheath, or nemotoxicity. The risk of nerve
damage is greater if repeated injections are given into a previously
pat1ially anaesthetised site or if higher concentration local anaesthetic
solutions are administered.
Trismus (see p.93) can occur as a result of intramuscular injection of
114 local anaesthetic, either as a direct effect of the drug or due to bleeding
within the muscle. If prolonged anaesthesia or trismus occurs, prompt
specialist advice is indicated.
Systemic toxicity
Clinicians using local anaesthetics should be familiar with the diagnosis
and management of drug-related toxicity. Acute emergencies can arise
with nerve blocks. Resuscitation drugs and equipment, including
oxygen, should always be available for the immediate management
of adverse reactions (see p.188 for drugs and equipment required by
dentists for emergencies).
Systemic toxicity may arise after inadvet1ent intravascular injection
of local anaesthetic, rapid systemic absorption, excessive dose
administration or impaired drug clearance. Adverse systemic effects
are usually seen in a continuum as plasma concentration increases.
Local anaesthetics can cause circumoral and tongue numbness, light-
headedness, visual and auditory disturbances, generalised muscular
twitching, loss of consciousness, tonic-clonic seizures, coma,
respiratory arrest and cardiovascular collapse. Minor CNS effects are
usually seen before seizures or cardiovascular toxicity, and may act as a
warning sign for serious events.
Longer-acting local anaesthetics, notably bupivacaine, can cause
cardiovascular effects before any observed CNS effect. Changes in
cardiac conduction, excitability, refractoriness, contractil ity and per-
ipheral vascular resistance can occur at therapeutic blood concentrations.
Higher concentrations lead to life-threatening atrioventricular block,
ventricular arrhythmias and depressed cardiac contractility.
The recommended maximum doses of local anaesthetics are very
important (see p.117). Signs and symptoms of overdose range from
excitability, sweating, vomiting, nervousness, numbness, disorientation
and loss of consciousness through to respiratory and/or cardiac depression.
Allergic reactions to local anaesthetics are very rare, although they
have been reported. Patients may experience an allergic reaction to Cll
components in the local anaesthetic solution; however, this now occurs 'iii
Cll
infrequently because stabilisers have been removed from the anaestheti c .s::.
solution. There is a theoretical risk of an allergic reaction to th e latex ol'
tiCll
Cll
the bung in a cat1ridge, but this has not been repmied clinically. Pos itive s::::
Cll
skin testing to one local anaesthetic does not provide inform ati on about
other drugs. <au
s
115
 If a patient reports an allergy to a local anaesthetic, their previous
history must be discussed carefully with them. There are rare cases of
true allergy to local anaesthetics; patients show either an urticarial or
eczematous response, or an anaphylactic reaction. If an allergy to local
anaesthetic is suspected, the patient should be referred to a specialist
immunologist or anaesthetist with training in drug reactions to check
the nature of the response. True allergic reactions should be treated as
for urticaria (see Box 26, p.l81) or anaphylaxis (see Box 27, p.l82) .
CHOOSING A LOCAL ANAESTHETIC
Safety and efficacy are the main factors that determine the most
appropriate local anaesthetic to use. Effectiveness is determined by the
concentration at the site of action. The addition of a vasoconstrictor
prolongs the duration of action (see p.ll2).
Lignocaine and prilocaine are probably the most widely used local
anaesthetics and have an excellent safety record. They are also very
effective when used for routine dental procedures. Allergy to lignocaine
is rare. The dose may need to be reduced in those with impaired renal
function or liver disease. Lignocaine without a vasoconstrictor is very
short acting and has limited applications in dentistry.
Prilocaine is equipotent to lignocaine without adrenaline, but is less
toxic and has a slightly longer duration of action. For dental use,
prilocaine is often combined with the vasoconstrictor felypressin.
Prilocaine is metabolised to Oliho-toluidine Co-toluidine), which can
s
c
Q)
oxidise haemoglobin to methaemoglobin- therefore it should be
avoided in patients susceptible to methaemoglobinaemia. Doses of
0 prilocaine greater than 600 mg can lead to methaemoglobinaemia and
"C cyanosis, often with delayed onset. Prilocaine should be used cautiously
c reached. It is very unlikely that an overdose will occur in adults.
l in infants less than 3 months of age due to their lower concentrations of
~ methaemoglobin reductase compared to adults.
0 in younger children, so extra care is required to calculate the maximum
Ui
Articaine has been claimed to be more effective, but there are reports
Q)
c of an increased risk of neurotox icity, presenting as prolonged numbness
Q) in the area of distribution, often with pain. This may be due to the
:g
:J
high concentration of the solution rather than the anaesthetic itself.*
(!) Consequently, it is recommended that articaine should not be used for
()
.;:; regional blocks (eg inferior alveolar). Methaemoglobinaemia can occur
:J
Q) with large doses of articaine in susceptible patients. All preparations of
0..
articaine contain adrenaline. Articaine is not recommended in children
~ to confirm it is the correct drug
Q)
..c less than 4 years of age.
r-
*For more information, see Kingan A, Sam brook P, Goss A. Higher concentration local
anaesthetics causing prolonged anaesthesia. Do th ey? A literature review and case
116
reports. Aust Dent J 2011;56(4) :348-51.
Mepivacaine (short acting) and bupivacaine (long acting) appear safe
and effective for use as the clinical situation demands. Mepivacaine
without adrenaline is useful for routine dental procedures of a short
duration where the use of vasoconstrictors is contraindicated. It has an
extremely low incidence of allergy. Mepivacaine is not recommended
in children less than 3 years of age.
Bupivacaine with adrenaline is used for long surgical procedures where
prolonged analgesia is required. It is also used for management of
postoperative pain or acute pain that has been difficult to relieve (eg an
acute irreversible pulpitis that has led to sleep deprivation). The onset
time is relatively long (approximately 5 minutes) . It is not recommended
in children less than 12 years of age. Ropivacaine is an alternative to
bupivacaine. It is less cardiotoxic, and concentrations up to 0.5% may
be used in children. Neither bupivacai ne nor ropivacaine are available
in dental cartridges in Australia.
Table 9 (p.ll8) gives the maximum safe doses of local anaesthetics
available in dental catiridges in Australia. For adverse effects of local
anaesthetics, see p.ll 3.
DOSES OF LOCAL ANAESTHETICS
The maximum safe doses of local anaesthetics available in dental
cartridges in Australia are summarised in Table 9 (p.\18) based on the
manufacturer 's recommendations. If more than one local anaesthetic
is used, the total dose used must be less than the maximum dose of the
drug with the lower maximum dose.
It is essential that the maximum dose is not exceeded. Provided the
injection technique is appropriate, maxi mum doses should not be
However, overdose in children can occur relatively easily, particularly
dose for children .
In dental practice, local anaesthetics are generally administered from l
2.2 mL single-use cartridges (known as dental cartridges). It is 'iii
Q)
recommended that dental cartridges be used at room temperature. It is .c
tiQ)
essential to check that the correct drug is being given before inj ection
l
(ie check the label on the cartridge), c
Check the label on the cartridge l
and that the local anaesthetic solution
ii
is not expired. When giving a dental u
before injection.
injection, aspirate first and inject .9
slowly watching the patient's response carefully.
117
 Table 9. Maximum safe doses of local anaesthetics Medications in dentistry supplement. Aust Dent J 2005;50(4 Suppl 2):S1- 81.
available in dental cartridges in Australia (ca n be accessed via t he Australian Dental Association website
<www.ada.org.au >)
Drug Maximum Example
Sambrook P, Goss A. Severe adverse reactions to dental loca l anaesthetics:
mgtkg
Approximate Approximate prolonged mand ibula r and lingual nerve anaest hesia. Aust Dent J
dose*
maximum maximum 2011;56(2):154-9.
number number
Sambrook P, Smith W, Elijah J, Goss A. Severe adverse reactions to dental loca l
of 2.2 ml of 2.2 ml
anaesthetics : systemic reactions. Aust Dent J 2011;56(2):148-53.
cartridges that cartridges that
can be used in can be used in
a 70 kg adult a 20 kg child
lignocaine 2% (20 mgtmL) 7 mgtkg 11 3
with adrenaline 1:80 0 00
(12.5 micrograms/mL)

mepivacaine 2% (20 mgtmL) a maximum mgtkg dose is not specifi ed in the

with adrenaline 1:100 000
(10 micrograms/mL)
mepivaca ine 3% (30 mgtmL)
Australian product information (PI).t The Australian PI
specifies:
adults- generally do not exceed 3 cartridges
children 3 to 6 years of age-maximum of 1.8 ml
children 6 to 14 yea rs of age-maximum of 2 . 7 mL

priloca ine 3% (30 mgtmL) 9 mgtkg 9 2

with felypressin
0.03 international units/mL

prilocaine 3% (30 mgtmL) 9 mgtkg 9 2

with adrenaline 1:300 000
(3.3 microgram s/mL)

s
c:
Q)
priloca ine 4% (40 mgtmL)

articaine 4% (40 mgtmL)

6 mgtkg

7 mgtkg
4

5
1

1
c with adrenaline 1:100000
'C (10 micrograms/mL)
c:
(II * Maximum doses are expressed in terms of the local anaesthetic, not the vasoconstrictor. They

~
are variable, dependent upon injection technique, medical history and many other factors.
Maximum doses are unlikely to be reached in most adults for most dental procedures. This
0 might not be so in children and the elderly. As with all drugs, it is recommended that the
Ui clinician confirm the dosages with the relevant data provided through the manufacturer.
<lJ
c 1 Maximum mgikg dose in the US PI is 6.6 mgikg up to 400 mg in adults.
Qj
:"Q
::l
(!)
Further reading
(.)
. p Blanton PL, Jeske AH. Avoiding complications in local anest hesia induction:
::l
<lJ anatomica l considerations. J Am Dent Assoc 2003; 134(7):888-93.
D..
~ Kingon A, Sambrook P, Goss A. Higher concentration local anaesthetics causing
<lJ
..c: prolonged anaesthesia. Do t hey? A literature review and case reports. Aust
1-
Dent J 20 11;56(4):348-51.
118 ~ I
Anxiolysis and sedation for
dental procedures

Anxiolytic and sedative drugs can be used in patients undergoing dental

procedures to alleviate pain, fear and anxiety. This is often termed
'premedication' .
Anxiolysis refers to a drug-induced state during which patients respond
normally to verbal commands. Cognitive function and coordination
may be impaired but spontaneous ventilation and cardiovascular
functions are unaffected. No interventions are required to maintain a
patent airway, spontaneous ventilation or cardiovascular function.
Conscious sedation refers to a drug-induced depression of conscious-
ness during which patients respond purposefully to verbal commands,
either alone or accompanied by light tactile stimulation. No interventions
are required to maintain a patent airway and spontaneous ventilation
is adequate. Cardiovascular function is usually maintained .* Sedation
administered in a general dental practice setting must be effected as
conscious sedation to ensure there is no compromise to the protective
reflexes and the technique is safe.
The oral route is the most commonly used route for drug administration ;
it is also the safest, most convenient and most economical. Oral
anxiol ytics and sedatives can be used effectively to reduce stress
before and during dental treatment, and to manage preoperative
and postoperative pain. They can be given the night before dental
treatment to ensure restful sleep, or preoperatively to produce a Iight
level of sedation that lowers preoperative anxiety. The advantages and
disadvantages of oral anxiolytics and sedatives are shown in Table I0
(p.l22).

For further information, see the registration standard and guideline on conscious sedation
area of pra ctice endorsement at < W\\M.dentalboard. gov.au/Registration/Consciou s-
Sedation .aspx> . 121
 Table 10. Advantages and disadvantages of oral Box 11. Instructions for patients having oral anxiolysis or
anxiolytics and sedatives sedation, or inhalational sedation

Advantages Disadvantages Before appointment

almost universal acceptability reliance on patient adherence You can have a light meal 2 hours before the appointment, but do not have
anything to eat or drink after that. Do not drink alcohol on the day of the
ease of adm inistration long latent period appointment.
low cost erratic and incomplete absorption
If you are taking any medicines, take them at the usual times unless otherwise
decreased incidence and severity inability to titrate advised.
of adverse effects compared with
intravenous sedation inability to readily lighten or deepen the If you are having an oral anxiolytic or sedative, it witt be given to you on arrival
level of sedation
no need for needles, syringes, at your appointment and your treatment witt commence approximately 1 hour
equipment long duration of action afterwards.
no need for specialised training Wear loose-fitting clothes, and no jewellery. Remove any contact lenses.
You must be accompanied by a responsible adult, who must remain in the waiting
room throughout your appointment, escort you home afterwards, and arrange for
ASSESSMENT AND PREPARATION OF PATIENTS you to be looked after for the following 24 hours.
FOR ANXIOLYSIS OR SEDATION Report any illness occurring before the appointment immediately, as it might affect
your treatment.
Careful patient assessment helps optimise the safety and effectiveness
of anxiolysis and sedation, and is an essential prerequisite to the success After appointment
of the subsequent dental treatment. The assessment is used to determine
Remain at the clinic for at least 1 hour after your treatment has finished.
the patient's suitability for anxiolysis or sedation, and dental treatment.
Your escort must take you home by means other than public transport.
Patient assessment must include details of the nature of the patient's
fears and anxieties; the patient's medical, medication and dental Rest and do not undertake strenuous activities for the rest of the day.
histori es; and information about the patient's social circumstances, If you are hungry, you can have a tight meat, but at lukewarm temperatures only.
including alcohol intake. Determine if the patient is fit for anxiolysis or Do not drive any vehicle, operate any machinery or use any domestic appliance for
sedation. 24 hours after the appointment.
Advise patients of the effects of Alcohol should not be taken with Do not drink alcohol, return to work, make any important decisions or sign any
the drugs used for anxiolysis and any sedative. important documents for 24 hours after the appointment.
sedation, including the possible
adverse effects. The patient must consent to any procedures to be done
under anxiolysis or sedation. For further information about consent, see MANAGEMENT OF THE ANXIOLYSED OR SEDATED
the Australian Dental Association webs ite <www.ada.org.au>. PATIENT
Box II (p.123) gives instructions for patients having oral anxiolysis or The semireclined (rather than fully reclined) position has less risk of
sedation, or inhalational sedation. airway contamination with blood, saliva, filling materials and teeth, and
from passive reflux and aspiration. The patient should not be ly ing flat
or head-down. The dental chair must be able to be placed rapidly into
the horizontal position for cardiopulmonary resuscitation. Use a rubber
dam during all restorative dental procedures to protect th e airway. For
management of inhaled or swallowed objects, see p.l74.

122 123
 A pulse oximeter is a simple instrument that can be used to monitor
the patient's pulse and arterial oxygen saturation during and following
the procedure. Patients should be
observed by appropriately trained Appropriately trained staff
should observe the patient
staff during the procedure and for
during the procedure and for at
1 hour after the procedure, or longer least 1 hour after the procedure.
if they have not fully recovered,
before being discharged with their escort.
ORAL ANXIOLYSIS OR SEDATION
The response to oral anxiolytics and sedatives is widely variable. When
determining the dose, consider the patient's previous sedative use,
medication history and alcohol intake. Sedatives should be used with
caution in the elderly and lower doses should be considered.
Typical regimens for anxiolysis or sedation in adults are:
1 temazepam 10 to 20 mg orally, 1 hour before the procedure
OR
1 diazepam 5 to 10 mg orally, 1 hour before the procedure.
INHALATIONAL SEDATION
Nitrous oxide {relative analgesia)
Combined nitrous oxide and oxygen is a long-standing, safe and
effective technique for inhalational sedation and is administered via
a nasal mask. It is helpful in apprehensive, but cooperative, patients
and allows many people to tolerate office-based dental treatment who
would not otherwise be ab le to do so. Nitrous oxide has the added
benefit of reducing the gag reAex in patients who have sensitive palates.
For particularly anxious patients, an oral sedative can be taken the night
before the procedure.
In most purpose-built equipment, there is an inbuilt safety feature that
does not allow more than 70% nitrous oxide to be delivered to the
patient. Nitrous oxide has an onset of action of 20 seconds and the peak
effect is achieved within 3 to 5 minutes. Confirm there is no airway
compromise preoperatively (eg the patient does not have a cold), as
effectiveness depends on good flow of both nitrous oxide and oxygen.
124
The patient should be monitored clinically at all times, and pulse
oximetry is desirable. Resuscitative equipment should be avai lable.
There must be an appropriate gas scavenging system to minimise room
air contamination so personnel working in th e environment are not at
any occupational risk.
At the conclusion of administration of nitrous ox ide lor I0 or more
minutes, administer 100% oxygen for 3 to 5 minutes to 1 rcvent an
abrupt decrease in oxygen saturation of arterial blood (term ed ' d ifTu sion
hypoxaemia'). Recovery is quick as nitrous oxide is rapidly removed
from the body when 100% oxygen is admin istered.
The main complications of nitrous oxide rel ate to the developm ent
of hypoxia. Even in the common ly used concentration of 50%, it is
capable of occasionally producing loss of consciousness and impaired
cough and gag reflexes. It is contraindicated if there is an impaired
level of consciousness or in patients with severe chronic obstructive
pulmonary disease. Nitrous oxide expands gas-containing cavities
within the body so it is contraindicated in patients with undrained
pneumothorax and large lung cysts and in patients who have had recent
middle ear surgery. Other adverse effects can rarely occur, including
hypotension, respiratory effects, and nausea and vomiting.
Methoxyflurane
Methoxyflurane has been available for nearly 50 years and is widely
used by ambu lance services throughout Australia as a first-line
analgesic while patients are being transpotted to hospital. It must be
noted that these patients are under the care of trained paramedics and
will be admitted to hospital under the ongoing care of trained medical
practitioners and nursing staff.
In recent years, methoxyflurane has been marketed for use in dentistry.
While it appears to be effective and appropriate for ambu lance use,
there is inadequate evidence regarding its use and safety in a general
dental setting. Therefore, its use cannot be recommended in this setting
until controlled evaluation is undertaken.
INTRAVENOUS SEDATION
Intravenous sedation is a highly effective technique, but requires
postgraduate training in a course approved by the Dental Board or
Australia. Intravenous sedation must be administered in an acc redit ed
facility. There have been sporadic fatalities over the years due to
125
 intravenous sedation administered in a dental practice, most of which
were avoidable. Guidelines on intravenous sedation are under constant
review to improve its safety and those applicable to dental practice were
updated in 2010- see 'Further reading' (below).
Further reading
Australian and New Zealand College of Anaesthetists, et al. Guidelines on
sedation and/or analgesia for diagnostic and interventional medical, dental or
surgical procedures [PS91 . Melbourne: ANZCA; 2010.
< http://www.anzca .ed u .au/resources/professiona 1-docu ments/pdf/PS9- 2010.
pdf>
~<I>
c Pain is a subjective phenomenon that is difficult to measure. It depends
'C
c on the patient's perception of pain, their coping strategies, and their
C'a
~ in the clinician's ability to diagnose and manage their problem may also
0 play a role.
126
Post-treatment pain
management
Acute oral and dental pain is largely inflammatory in origin; however,
there can be various causes of the inflammation. An accurate diagnosis
of the presenting condition must be formulated and the appropriate
active dental treatment should be
Dental treatment is the most
provided before considering the use
predictable means of reducing
of any adjunctive drugs, since dental
pain of dental origin .
treatment is the most predictable
means of reducing a patient's level of pain.
An accurate diagnosis also helps to determine what type of adjunctive
drugs, if required, may be effective (eg pain caused by infection may
require an antibiotic in conjunction with appropriate dental treatment;
pain caused by inflammation may require an anti-inflammatory drug in
conjunction with appropriate dental treatment). Sometimes analgesics
may be appropriate- either alone or in conjunction with other required
drugs.
UNDERSTANDING PAIN
previous experiences with pain and pain relief. The patient's confidence
If analgesics are deemed necessary, both the level and the type of pain
should be assessed. The level of pain is usually described as mi ld,
moderate or severe and the type of pain can be classified as nociceptive
or neuropathic.
Nociceptive ('physiological') pain arises from stimulation or supc: r
ficial or deep tissue receptors ( nociceptors) by exogenous stimuli ( '!J,
heat or cold) or endogenous stimuli (eg chemical mediators rclcas 'cl n,
part of the in:flammatmy response to tissue injury) .
1 r
 N ~uropathic pain arises from a disturbance of neural pathways at any
pomt from the afferent conducting system to receptive centres in the
central nervous system. It can be due to compression, inflammation
trauma, metabolic insult or degenerative disease. Neuropathic pain i~
not uncommon among dental patients, but it can be difficult to diagnose.
Pain can also be classified as acute or chronic.
Acute pain is nociceptive in origin and is the most common type
of ~am managed by ~ent1sts. Acute oral and dental pain is relatively
straightforward to diagnose, provided the clinician follows the
re~ommended di~gnostic processes (see p.l ). In most patients, acute
pam resolves rapidly once the appropriate dental treatment is started
however, some patients require adjunctive analgesic therapy for th~
fir~t 24 to 48 hours (or for slightly longer if they have very severe
~a1~. or have had extensive surgery). Generally, acute pain is self-
hmJtmg, serves a protective biological function and results in few or no
psychological symptoms.
Ch~onic_ pain is pred~minantly neuropathic in origin, but may be
nocteeptJv~. It c~n be d1fficult to diagnose accurately as there may not
be any obv10us stgns or symptoms. Chronic pain is often more difficult
t~ resolve than ~cute pain. It is not self-limiting, serves no protective
b10logtcal functwn, and may result in anxiety, fear, depression, loss of
sleep a_nd impairment _of social functioning. Treatment with analgesics
a_lone t.s rarei_Y su~c1ent, and other more appropriate management
~mcludi_ng adjunctt;e drugs and behavioural/psychosocial therapies)
IS reqUJre?. In patients with chronic oral neuropathic pain, dental
treatment IS usually counterproductive and should be discontinued (see
'Orofaci~l pa!n', pp.91-6). For fmiher information on the management
of chrome pam, see Therapeutic Guidelines: Analgesic.
USE OF ANALGESICS IN DENTISTRY
General considerations
Most acute painful oral and dental problems are due to inflammation
ofthe_oral, dental or associated tissues. This inflammation may be due
to vanous factors (eg infection, trauma, a surgical procedure). Hence,
a~sessment of the cause of the pain is essential as this will dictate
management.
Analgesi~s do not ~ddress the cause of the pain-they essentially act
by blockmg the pam sensatiOn. Analgesics should only be used when
128
the patient's pain cannot be removed, reduced or controll ed a I quately
by the appropriate dental treatment and other required drug lo r the
presenting condition. They may also be required followin g surgicul
procedures that cause postoperative pain. Analgesics should be
considered only as an adjunct to the appropriate dental treatment and
other required drugs.
When analgesics are definitely required, an appropriate regimen
should be established for each patient, taking into account any contra-
indications and precautions to drug use and potential adverse effects
(see 'Analgesics', pp.27- 33). Nonsteroidal anti-inflammatmy drugs
(NSAIDs) (eg aspirin, ibuprofen) are preferred as they have analgesic
and anti-inflammatory actions. The combined action is generally
more effective because there is some reduction in inflammation at
the site of the pain in addition to the analgesic effect. If NSAIDs are
contraindicated, the choice is essentially limited to paracetamol or
paracetamol+codeine in adequate doses. Opioids other than codeine are
rarely indicated in dentistry.
Often the dental treatment and other drugs are effective in reducing the
pain, and analgesics are usually only indicated for a shOJi time. However,
flexible pain management strategies should be adopted where the drug
and dosage are matched to the expected level of pain. Inadequate pain
control during or after treatment can lead to chronic pain.
Examples of dental pain and appropriate management:
If pain is caused by infection, the infection should be
managed by operative procedures and drainage, with
appropriate antimicrobial drugs if adjunctive drug therapy is
deemed necessary. Analgesics are given only if pain relief is
inadequate following the above measures.
If pain is caused by inflammation, the irritating factors should
be removed and an NSAID should be used as an adjunct
to help reduce the inflammation more rapidly and more
predictably. Paracetamol (with or without codeine) is given
only if the pain relief is inadequate with an NSAID alone.
Dosing
Analgesics should be used at the lowest effective dose and for as short
a time as possible to minimise the development of adverse effects <tnd
the risk of drug interactions.
I ll
 Many practitioners have traditionally prescribed analgesics on a 'take
as required for pain' basis rather than as a 'course of medication'. This
approach results in suboptimal pain management because the blood
concentrations of analgesic drugs can fluctuate considerably from high
to very low, depending on the timing of analgesic use. The associated
pain management can range from excellent or good pain control to
recurrence of pain. A cycle between pain and pain relief occurs, with the
patient often suffering more than is necessary and the overall condition
taking longer to resolve.
Ideally, analgesics should be taken on a regularly scheduled basis
(ie similar to a course of medication) for a specified duration so the
blood concentrations of the drug are maintained above the threshold
concentration for effective pain relief. Using analgesics regularly
generally means that a shorter comse of treatment is required,
particularly for drugs with both analgesic and anti-inflammatory
properties. The dosing interval depends on the pharmacokinetic
propet1ies of the drug used (eg its half-life), the drug formulation (eg
immediate-release or modified-release preparation), patient factors
(eg renal and liver function) and possible drug interactions. Most
immediate-release analgesics need to be taken every 4 to 6 hours.
The 'third molar model' has been used in many studies to compare
the effectiveness of various analgesics. The results of the studies are
outlined in Box 12 (p.l31 ). The recommendations for post-treatment
pain management in adults (see p.132) are based on findings from these
studies.
Analgesics can also be administered by the parenteral (injecti ons) and
rectal (suppositories) routes. Suppositories can be very effective and
can be self-administered, while injections require administration by an
appropriate health professional.
Box 12. How the recommendations for pain management
were derived
The 'third molar model' refers to wisdom teeth extraction (a dental procedure
that causes a predictable amount of pain). It has been used in many studies to
compare the effectiveness of various analgesics.
These studies have consistently shown that codeine is not a very effective
analgesic when used alone, but pain relief is increased when it is combined with
paracetamol or aspirin. Increasing the dose of codeine and paracetamol increases
the effectiveness of pain relief for this combination of drugs. Ibuprofen has been
shown to be an even better analgesic, particularly as the dose increases (see
Figure 3 below).
In adults, at least 30 mg of codeine is required for analgesia, but it is more
effective if 60 mg is taken (which is generally required for severe pain). Codeine
can be prescribed alone or in combination with paracetamol (or other drugs).
There are a variety of over-the-counter (with low amounts of codeine) and
prescription-only combination preparations of paracetamol+codeine. However,
combination preparations with low amounts of codeine are usually inadequate.
Figure 3. Schematic representation of pain relief with different analgesics
using the 'third molar model' (note there is wide variation in the
effectiveness of analgesics between individual patients)

s
c
(j) Route of administration ibuprofen 400 mg
Q
-c Most patients attending a dental practice for the management of oral paracetamol+codeine 1000+60 mg
c
m or dental pain can use oral analgesic preparations in the form of
~ tablets, capsules or liquids. However, patients may not tolerate oral
0 administration if: codeine 60 mg
Ui they have swallowing difficulties (eg because of physical or
Cl) placebo
c psychological problems)
Cl)
0 1 2
~ gastrointestinal absorption is likely to be significantly reduced (eg time (hours)
::J
<.!J due to nausea, vomiting, or gastrointestinal pathology). This may
u occur if the patient has been taking multiple medications (either This figure is a schematic diagram of the results of studies using the third molar
.p
::J prescribed or self-initiated, or both) in an attempt to manage their model. All the drugs are effective for about 4 hours; however, there is a 'lag
Cl)
Cl. time' while each tablet is absorbed , and then a 'tapering off' effect as the blood
pain.
~ concentration drops after reaching its peak.
Cl)
..c
1-
1' 1
130

PAIN MANAGEMENT STRATEGIES
Principles
Effective pain management begins with an accurate diagnosis and an
appropriate treatment plan using the principle of the '3 Ds'- Diagnosis,
Dental treatment and then Drugs (see ' Principles of diagnosis and
prescribing: Management', p.3).
If analgesics are required for post-treatment pain, five questions should
be answered before prescribing medications:
Is the pain nociceptive in origin? If not, further investigations and
other management approaches are required.
Is the pain mild, moderate or severe? This estimation includes the
patient's perception of the pain, and the clinician's assessment of
the severity of the problem causing the pain.
Has the appropriate dental treatment been provided? If not, it
should be arranged immediately.
Can the patient use nonsteroidal anti-inflammatOty drugs
(NSAIDs) (eg aspirin, ibuprofen)? If not, use paracetamol, with or
without codeine. Typical contraindications to the use ofNSAIDs
are a definite history ofNSAID allergy (particularly NSAID-
induced asthma), active peptic ulcer disease or gastrointestinal
bleeding (see also 'NSAIDs: Adverse effects, interactions and
precautions', p.28).
Can the patient take medications via the oral route? If not,
consider suppositories or injections (see p.l30) .
Post-treatment pain management in adults
The clinical situation indicates if analgesics are required to help manage
a patient's pain or expected pain following dental treatment. The
management strategies used depend on the level of pain.
For mild pain, use:
1 ibuprofen 400 mg orally, every 4 hours (to a maximum of
2400 mg/24 hours)
OR
2 aspirin 600 to 900 mg orally, every 4 hours (to a maximum of
3600 mg/24 hours)
OR (ifNSA!Ds are contraindicated)
132
3 paracetamo/500 to 1000 mg orally, every 4 hours (to a maxirnum
of 4 g/24 hours).
For moderate pain, use:
1 ibuprofen 400 to 600 mg orally, every 4 hours (to a maximum of
2400 mg/24 hours)
PLUS
paracetamol 1000 mg orally, every 4 hours (to a maximum of
4 g/24 hours)
OR (ifNSA!Ds are contraindicated)
2 paracetamol+codeine 1000+60 mg orally, every 4 hours (to a
maximum paracetamol dose of 4 g/24 hours).
For severe pain, use:
1 ibuprofen 400 to 600 mg orally, every 4 hours (to a maximum of
2400 mg/24 hours)
PLUS
paracetamol+codeine 1000+60 mg orally, every 4 hours (to a
maximum paracetamol dose of4 g/24 hours)
OR (ifNSA!Ds are contraindicated)
2 paracetamol+codeine 1000+60 mg orally, every 4 hours (to a
maximum paracetamol dose of4 g/24 hours).
The potential benefits of NSAIDs should be balanced against their
potential harms, particularly in high-risk patients (see 'NSAIDs:
Adverse effects, interactions and precautions', p.28). Overdose with
paracetamol is a concern (see ' Paracetamol: Overdose' , p.31 ). For
adverse effects of codeine, see p.32.
If patients need to take ibuprofen plus paracetamol (or ibuprofen plus
paracetamol+codeine), the analgesic effect may be more continuous if
the drugs are taken 2 hours apart, with each drug taken every 4 hours.
The paracetamol (or paracetamol+codeine) can usually be stopped after
24 hours (or even the morning after the dental treatment is perform ed),
but ibuprofen is useful for its anti-inflammatory effect for a furth er 2 to
3 days until the pain has completely resolved (see Box 13, pp.\ 34- 5,
for a detailed explanation).
Doxylamine is an antihistamine present in some co mm ~ r i d
preparations with paracetamol+codeine. It acts as a ' calmati ve' , whi ~ h 1 ,~ .1
 may help patients cope with the pain, at doses not exceeding 10 mg Box 13. (cont.)
ora ll y, 4-hourly. However, patients must be warned that doxylamine
Figure 4. Example of instructions for a patient taking ibuprofen plus
can cause drowsiness. Most commercial preparations combining
paracetamol following dental treatment (using a timeline)
doxylam ine with paracetamol+codeine contain inadequate amounts of
codeine for effective pain relief.
p p
Advise patients to return to their
If the patient has inadequate
treating clinician if they have
pain relief or severe persistent
inadequate pain relief or severe pain, review the diagnosis and 2 pm 4pm 6pm 8 pm 10 pm during night,
persistent pain (ie for more than consider specialist referral.
end of provided it is
5 days) for reconsideration of the
treatment after 2 am
diagnosis-consider specialist referral.
I = ibuprofen 400 mg
Box 13. Combining ibuprofen with paracetamol (or P = paracetamol 1000 mg
paracetamol+codeine) for enhanced pain The paracetamol (or paracetamol+codeine) can usually be stopped after
management in adults 24 hours or even t he next morning, but the ibuprofen should be continued for
As the main action of ibuprofen is local (ie at the site of inflammation) and a furth er 2 to 3 days since its anti-inflammatory effect helps further resolve the
paracetamol and codeine work within the central nervous system, they are inflammation that caused t he pain.
complementary. If ibuprofen is taken first, and immediately after the dental
treatment, it can provide effective pain relief as the local anaesthetic effect wears Post-treatment pain management in children
off. It also begins its anti-inflammatory action (which further helps to minimise
pain, or prevents it enti rely, by reducing the inflammation in the affected tissues). Pain management in children is usually much simpler than in adults
Analgesia can be improved if ibuprofen and paracetamol (or
because of the lack of psychological overlay that usually modifies adults'
paracetamol+codeine) are taken 2 hours apart, with each drug taken every responses to pain. However, the parent's response to their child being in
4 hours. After the initial absorption time, the blood concentration of ibuprofen pain needs to be considered, as the parent must provide the medication.
rises above its threshold concentration for effective pain relief. After some
The paediatric patient is no different from the adult patient in requiring
time, the concentration falls below the threshold concentration and it becomes
ineffective as an analgesic. However, if paracetamol (or paracetamol+codeine) is
an accurate diagnosis of the cause of the pain and appropriate dental
taken 2 hours after the ibuprofen, the ibuprofen concentration will still be above treatment. Common procedures in children that can cause post-treatment
its threshold concentration for effective analgesia while the paracetamol (or pain are dental restorations, simple extractions and surgical extractions.
paracetamol+codeine) is absorbed. The paracetamol and codeine concentrations
To limit post-treatment discomfort, it is important that pain control
wi ll then reach their threshold concentrations for pain relief before the ibuprofen
concentration falls below its effective threshold.
during the procedure is adequate. Use of a local anaesthetic and inhal-
ational sedation (eg relative analgesia with nitrous oxide), or a general
It is not essential to use the above approach , and patients can sti ll have effective anaesthetic to limit emotional overlay is the initial step in pain control.
pain relief if ibuprofen and paracetamol (or paracetamol+codeine) are taken at
the same time every 4 hours. However, there may be a reduction in pain control Analgesia with paracetamol or an NSAID (eg ibuprofen) is genera ll y
towards the end of each 4-hour period and before full absorption of the next dose the cornerstone of post-treatment pain management in children. Aspirin
of each drug (30 to 60 minutes). The alternating approach may also reduce gastric should not be used for analgesia in children less than 16 years of age
irritation as the stomach is not subjected to multiple drugs at the same time. because of its rare association with Reye syndrome.
The alternating approach relies on patient adherence so the rationale for taking
Paediatric prescribing generally involves calculating drug doses based
the drugs at different times should be explained to the patient. The patient can
be provided with a written set of instructions outlining the specific times to take
on body weight. In children who are significantly obese, cal culut
each drug (rather than telling the patient 'every 2 hours') . A simple timeline, such the dose according to the mean body weight for the chi ld's age rath er
as that shown in Figure 4 (p.135), can be given to the patient with the times and than their actual body weight, as the latter may result in overd ose (s
drugs adjusted for the patient's particular needs. Table 11 , p.l36, for mean body weight for age in ch ildren).
134
 Table 11. Mean body weight for age in children
Age (years) Mean body weight (kg)

1 9
3 14 Dental management of
5 18
patients with medical
7 23
10 32 conditions
12 39
Source: Paediatric Formulary Committee. BNF for Children 2010- 2011. London: BMJ Publishing
Group, Pharmaceutical Press, and RCPCH Publications; 2010 Patients presenting to a general dental practice may have medical
problems or be taking medications that can affect their dental
For post-treatment pain in children, use: management. This chapter outlines some common and significant
medical conditions and the dental issues associated with them, but
1 ibuprofen 5 to 10 mg/kg orally, 6- to 8-hourly (to a maximum of it is not a substitute for f01mal training or detailed texts. Medical
2400 mg/24 hours) emergencies may arise during dental treatment and these are discussed
OR in the 'Medical emergencies in dental practice' chapter (pp.l67- 89).

1 paracetamo/15 mg/kg orally or rectally, 4- to 6-hourly (to a

A detailed list of current medications, including prescription, over-
the-counter and complementary medicines, is an important part of the
maximum of 4 g/24 hours).
patient's medical history (see p.l for a discussion on history-taking).
As the main action of ibuprofen is local (ie at the site of inflammation) If the patient is not sure what medications they are taking, ask them
and paracetamol works within the central nervous system, . they are to bring in a list of their medications or obtain a current list from their
complementary and can be combined. If post-treatment pam IS severe, medical practitioner or pharmacist. Crosscheck the medications with the
opioids such as codeine may be required in addition to the other drugs. medical history that the patient has provided, as there may be conditions
iii
.... the patient has forgotten to mention or has not disclosed because they
c: It is important that post-treatment analgesics are given regularly and may have underestimated the significance of the condition.
Q)
c in adequate doses. If pain persists after 24 hours, the patient should be
Before commencing dental treatment, carefully consider the effect
"0 reassessed.
c: of the treatment on the patient's underlying medical condition. If the
Cll
patient can only tolerate short periods of dental treatment, their medical
0
...
iii Further reading
condition is easily destabilised or their life expectancy is short, modify
Ui
Dionne RA, Phero JC, Becker DE. Management of pain and anxiety in the dental dental treatment accordingly.
Ql
c office. Philadelphia: WB Saunders Co.; 2002.
Qj
:g eTG complete [CD-ROM or online]. Melbourne: Therapeutic Guidelines Limited CARDIOVASCULAR CONDITIONS
:J [regularly updated] .
(!)
Cardiovascular conditions are common, particularly with increased
u Hargreaves K, Byrne E, Keiser K. Analgesics in endodontics. In: Cohen S,
'+" age. For information on cardiovascular conditions, see Therapeutic
:J Hargreaves K, editors. Pathways of t he pulp. 9th ed. St Louis: Mosby Elsevier;
Ql Guidelines: Cardiovascular. Dentists should reinforce strategies (eg
0.. 2006.
~ smoking cessation) to reduce cardiovascular disease risk.
Ql
.c Holstein A, Hargreaves KM, Niederman R. Evaluation of NSAIDs for treating
I- post-endodontic pain. Endod Topics 2002;3:3-13. The main dental issues relating to cardiovascular cond itions are
prevention of endocarditis (see p.lOI) and potential problems with
136 137
 anticoagulant and anti platelet drugs in patients undergoing dentoalveolar
surgery (see below). Patients may also have a history of hypertension
(see p.140), coronary heart disease (see p.142) or heart failure (see
p.143), which can affect dental treatment.
Potential problems with anticoagulant and
antiplatelet drugs in patients undergoing
dentoalveolar surgery (including extractions)
Many patients with a cardiovascular disorder, including coronary heart
disease, cerebrovascular disease, atrial fibrillation and venous thrombo-
embolic disease, take anti platelet and/or anticoagulant drugs.
The key issue with patients taking Stroke is a catastroph ic event,
an anticoagulant or antiplatelet drug whereas bleeding from the
is the balance between the increased mouth can be managed by local
risk of bleeding from a wound if the measures.
drug is not stopped before surgery
and the risk of a thromboembolic event if the drug is stopped before
surgery. The emphasis in the past has been on minimising bleeding;
however, a thromboembolic event is potentially much more serious
(ega stroke is a catastrophic event, whereas bleeding from the mouth,
although messy and troublesome, can be easily managed by local
measures).
It is essential to ascertain if the patient is taking any anticoagulant or
iii antiplatelet drugs and, if so, which drug(s) they are taking, the current
..... dosage and the indication. Also check if the patient is taking any other
c
C1)
Q medications.
'C
c The most commonly used anticoagulant drug is warfarin (see p.139).
ctl
Commonly used anti platelet drugs are aspirin (see below), clopidogrel
0
...
iii
(see p.139) and prasugrel (see p.l39). Some complementary medicines,
including fish oil, ginkgo biloba and glucosamine, have a weak
anti platelet effect, but this is usually not clinically significant.
Aspirin
Antiplatelet therapy with aspmn does not usually cause ~ignificant
bleeding from extraction wounds. For dentoalveolar surgery (including
extractions), there is no indication to temporarily cease a patient's
prescribed regular aspirin. Warn patients that they have a slightly
higher chance of bruising if aspirin is not ceased, but the risk is minor
compared with the risk of embolism if aspirin is ceased. Local measures
138
can be undertaken to help achieve haemostasis, including innltratio n
of an adrenaline-containing local anaesthetic, insertion of a resorbabl
pack, and suturing. See also 'Complications after tooth ex trac ti on:
Bleeding', p.198.
If aspirin is to be ceased (eg for an extensive soft tissue procedure), it
should be stopped at least 7 days before the procedure and restarted
2 days after the procedure. Stopping aspirin for only a few days before
the procedure is of no benefit.
Clopidogrel and prasugrel
Clopidogrel or prasugrel is commonly used with aspirin to prevent stent
thrombosis for up to 1 year after coronary stent placement. They are
also used in patients who have had ischaemic events despite treatment
with aspirin or who cannot tolerate aspirin.
Premature discontinuation of dual anti platelet therapy after placement
of a coronary stent markedly increases the risk of stent thrombosis,
which frequently leads to myocardial infarction or death.* Detailed
studies indicate the risk can be up
to 15%. Clopidogrel or prasugrel Do not stop clopidogrel or
prasugrel without expert advice.
should not be stopped prematurely
without expert advice.
Advise patients who are taking clopidogrel or prasugrel and require
dentoalveolar surgery (including extractions) not to cease the
medication. Use local haemostatic measures and counsel patients that
they may have extensive bruising.
Warfarin
It is important that both the patient and their medical practitioner
understand how the patient's warfarin treatment should be managed in
relation to tooth extraction. It is not uncommon for patients to reduce
their warfarin dose without consultation or, alternatively, to consult
with their medical practitioner who may (unnecessarily) suggest the
traditional course of ceasing anticoagulants for minor surgery.
See Box 14 (p.141) for management of patients taking warfarin who
require minor oral surgery. For more information about management oi'
* Grines CL,Bonow RO, Casey DE, Jr., Gardner TJ, Lockhart PB, Molitemo DJ, et al.
Prevention of premature discontinuation of dual antiplatelet therapy in patients wi th
coronary artery stents: a science advisory from the American Heart Association, Am orlonrl
College of Cardiology, Society for Cardiovascular Angiography and Intervention , Arnorl 1111
College of Surgeons, and American Dental Association, with rep resentation lror n ll1n
I i!J
American College of Physicians. Circulation 2007 ;115(6):8138.
 tooth extractions for patients taking warfarin, see the Australian Dental
Journal* where this issue has been comprehensively rev iewed.
Other anticoagulant or antiplatelet drugs
Several other anticoagulant and antiplatelet drugs are available (eg
dipyridamole, dabigatran, enoxaparin, ri varoxaban). Dabigatran and
rivaroxaban are increasingly used oral anticoagulants but, unlike
warfarin, there is currently no laboratory test to guide treatment and
they do not have a specific antidote.
If a patient is taking an anticoagulant or antiplatelet drug other than
aspirin (see p.l38), clopidogrel (see p.l39), prasugrel (see p.l39) and
warfarin (see p.l 39), do not cease it. Consult the patient's medical
practitioner before undertaking dentoalveolar surgery (including
extractions). In all cases, use local measures to help achieve haemostasis.
If there is spontaneous bleedin g, urgent medical attention is required.
Hypertension
Hypertension is common with increasing age. Many drugs are ava ilab le
for the management of hypertension and they are commonl y used in
combination. For more information on hypertension, see Therapeutic
Guidelines: Cardiovascular.
Dental issues
Hypertension that is controlled and stable is usually not a problem
dming dental treatment. Check if th e patient is also taking antiplatelet
or anticoagulant drugs-see ' Potential problems with anti coagul ant
and antiplatelet dru gs in patients undergo ing dentoalveolar surgery
(including extractions)', p.l38.
Severe longstanding dental pain can increase hypertension, so
appropriate dental treatment should be instituted promptly. Severe
anx iety assoc iated with dental phobia may increase blood pressure. In
this circumstance, sedatives shoul d be considered (see 'Anxiolys is and
sedation for dental procedures', p.l21 ).
Theoretically, local anaesthetics containing adrenaline may elevate
blood pressure; however, clinically, they have no significan t hypertensive
effects (see ' Local anaesthesia: Addition of vasoconstrictors', p.ll2).
continued p.142
Carter G, Goss AN, Lloyd J, Tocchetti R. Current concepts of the management of dental
extractions for patients taking warfarin. Aust Dent J 2003;48(2):8996; quiz 138.
140
Box 14. Management of patients taking warfarin who
require minor oral surgery
Before surgery (for all patients)
Take a detai led medical history including:
- warfarin dose regimen
- stability of INR
- underlyi ng medical conditions and other medications
- need for anti bioti c prophylaxis (see pp .101- 9).
Organise blood t est for INR within 24 hours before surgery:
- If INR is less than 2 .2 and there are no contraindications, proceed with
surgery; tranexamic acid mouthwash is not required.
- If INR is 2.2 to 4 .0 , proceed with surgery using the tranexamic acid
mouthwash protocol below.
- If INR is more than 4.0, do not proceed with surgery and refer patient to
their medical practitioner.
DO NOT CEASE WARFAR IN.
Tranexamic acid mouthwash protocol (for patients with INR 2.2
to 4.0)
Day of surgery
Check INR (INR must be 2.2 to 4 .0) .
Administer antibiotic prophylaxis if indicated.
Obtain a bottle of 4.8% tranexamic acid mouthwash*
During surgery (for extraction of teeth only)
After teeth have been extracted, irrigate sockets with tranexamic acid
mouthwash using a disposable syringe.
Fill the socket with loosely packed haemostatic agent.
Place one suture per socket.
Ask the patient to bite on a gauze pack soaked in tranexamic acid nouthwash.
After surgery
Give the patient tranexam ic acid mouthwash with instructions on use (10 ml
rinsed in mouth for 2 m inutes, 4 times daily for 2 to 5 days).
Arrange review denta l appointment for 2 days afte r the proced ure.
Review appointment (2 days after the procedure)
Check for bleeding, pain, delayed healing or infection, and treat as 1ecessary.
Review the patient again in 1 to 2 weeks to check healing has occurred.
11 a 4.8% tranexamic acid mouthwash is not available, a 5% solution can be maj lly ru 1111lA
a 500 mg tablet and dispersing it in 10 ml of water immediately before adminiWotlon,
INR = international normalised ratio lrl l
 Nonsteroidal anti-inflammatory drugs (NSAIDs) should be used
with caution in patients with hypertension as they can cmuse renal
impairment. The risk of renal impairment is increased if a patient is
taking an NSATD in combination with a diuretic plus an angiotensin
converting enzyme inhibitor (eg perindopril) or an angiotensin II
receptor blocker (eg candesartan); the end resu lt of concurrent use of
these three drug classes may be renal failure.
Coronary heart disease
For more information on coronary heart disease, see Therapeutic
Guidelines: Cardiovascular.
Dental issues
Apart from the potential problems
Defer elective dental treatment
with a11tip latelet and anticoagulant
for 3 months after myocardial
drugs it1 patients undergoing dento- infarction, stent placement or
alveolar surgery (see p.l38), the coronary artery bypass surgery.
key issue with dental treatment for
patients with a history of coronary heart disease is to ensure that their
current condition is stable and they are following their preventive ancl/
or rehabilitation program. Defer elective dental treatment for 3 months
after myocardial infarction, stent placement or coronary artery bypass
surgery. If dental pain or infection occurs within the 3-month period
following infarction, treat it as simply and expediently as possible.
'iii
....s:: Antibiotic prophylaxis for dental procedures is not required in patients
Q) with coronary stents, unless otherwise indicated (see p.lOl). Patients
c with pacemakers and other implantable cardiac devices (eg implantable
whether periodontal disease and cardiovascular di seas;c arc COil 'UI'I'cnt
manifestations of vascular disease, or whether treatmc:nt or periodontal
disease results in improved cardiovascular status. Flllrther studies are
needed but, regardless of this, improving periodontal he:alth is important.
For more information, see 'The American Journad of Catdiology
and Journal of Periodontology editors ' consensus: periodontitis and
atherosclerotic cardiovascular disease ' .*
Management of angina or an acute coronary syndrome in the dental
surgery is discussed in the 'Medical emergencies in dental practice'
chapter (see p.l69).
Heart failure
Heart failure is usually a condition of the elderly. It can be predom-
inantly left ventricular with pulmonary congestion1 and dyspnoea,
or predominantly right ventricular with elevated venous pressure,
peripheral oedema and hepatic congestion. Usually both coexist in
the classical syndrome of congestive or biventricular heart failure.
For more information on heart failure, see Therapeutic Guidelines:
Cardiovascular.
Dental issues
Dental treatment should only be undertaken if the patient's heart failure
is stable and should be performed in short appointments. Patients with
heart failure usually do not tolerate being placed in a horizontal position
and should be placed with their head higher than thei.r heart. A useful
guide is to determine the extent to which the patient needs to be propped
up in bed at night; if they can only comfortably sleep with the aid of ....s::
1/)

"C
s:: cardioverter-defibrillators) do not present a problem during general multiple pillows, they may not tolerate the dental chair being placed Q)
ca dental treatment. Interference from dental electronics does not occur horizontally. :;;
ca
0
...
'iii with modern implantable devices, and endocarditis is not a risk as the
Nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided in
c.
...,Ill
device is implanted within the muscle. os::
Ui patients with heart failure as they can worsen heart failure. .....2
(1) S::;t:
c A patient who is known to have episodes of angina should be instructed 4l"C
Q)
to bring their medication (eg glyceryl trinitrate spray or tablets) when
Es::
D RESPIRATORY CONDITIONS Q)O
'0.0(,)
::::J presenting for dental treatment. Dental treatment should be undertaken in ca-
<.!}
short appointments. Use relaxation techniques and consider sedation (see The most common and significant respiratory disorder affecting eca
() ca.!:!
.;:::;
::::J 'Anxiolysis and sedation for dental procedures', p.l21 ). Ensure effective dental management is asthma (see p.l44). Other important respiratory e-cQ)
(1)
0. local anaesthesia-the use of vasoconstrictors with local anaesthetics is conditions are chronic obstructive pulmonary disease (see p.l45) and mE
....
~ indicated in these patients (see 'Local anaesthesia', p.lll). s::.s::
(1) Q);t:
..c * Friedewald VE, Kornman KS, Beck JD, Genco R, Goldfine A, Libby P, et al. The American c:::
f- Epidemiological studies have implicated periodontal disease as a risk Journal of Cardiology and Journal of Periodontology editors' consensus: periodontitis and
factor for cardiovascular disease. However, it has not been proven atheroscl erotic cardiovascular disease . J Periodontal 2009;80(7):102132.
142 143
 obstructive sleep apnoea (see p.l46). For more information on these and
other respiratory conditions, see Therapeutic Guidelines: Respiratory.
Asthma
Asthma is a chronic inflammatory disorder of the airways associated
With airway hyper-responsiveness that leads to recurrent episodes of
wheezmg, breathlessness, chest tightness and coughing. The episodes
are usually associated with widespread, but variable, airflow obstruction
that is often reversible either spontaneously or with treatment. Many
of the symptoms of asthma overlap with other diseases (eg chronic
obstructive pulmonary disease).
Abo ut 10% of adults (16 years and over) and II% of children in
Australia have asthma. Asthma frequently presents in childhood but
can occur for the first time at any age. '
Medications used to control asthma include inhaled corticosteroids
(eg fluticasone), long-acting beta2 agonists (eg salmeterol), oral pred-
msolone, montelukast and sodium cromoglycate-these medications
are often referred to as 'preventers'. Acute asthma attacks are treated
with short-acting beta 2 agonists (eg salbutamol, terbutaline)- these
medicatiOns are often referred to as 'rel ievers'.
For more information on asthma, see Therapeutic Guidelines:
Respirat01y.
(ij Dental issues
....
s:::
Q) The most important consideration in the dental treatment of patients
c tolerate being placed in a horizontal position. Patients taking systemic
'C With asthma IS to avoid triggering an asthma attack during treatment.
s::: Patients who regularly use inhalers should be advised to bring them
(tl
(ij ~o dental appomtments so they can self-medicate if necessary. If
0 mtravenous sedatiOn or general anaesthesia is required for a dental
(f) procedure in a patient with asthma, it should be administered in a
Q)
c hospital by a specialist anaestheti st.
Q)
~ Patients taking systemic corticosteroids require an increased dose
::J
(.? of their corticostero id before dental treatment if they have adrenal
(.) suppressiOn (see 'Adrenal disorders: Dental issues ', p.l51).
.,:::;
::J
Q)
Several drugs ( eg aspirin and other nonsteroidal anti -inflammatory drugs
0.
[10l [NSAIDs]) can cause bronchoconstriction in susceptible patients with
Q)
.s::::. asthma and these should be avoided or used cautiously. Paracetamol is
f-
the analgesic and antipyretic of first choice because adverse reactions
are rare and tend to be milder than reactions to NSAIDs.
144
Patients may develop oral candidosis secondary to the use of inhaled
corticosteroids. To reduce the risk of oral candidosis and systemic
absorption of coiiicosteroids, advise patients to rinse their mouth and
throat with water and spit out after inhalation. Patients using a metered
dose inhaler have the additional risk of dysphonia and should be advised
to use a spacer.
Management of acute asthma in the dental surgery is discussed in the
'Medical emergencies in dental practice ' chapter (see p.l72).
Chronic obstructive pulmonary disease
Chronic obstructive pulmonary disease (COPD) is characterised by
airflow obstruction that is not fully reversible. The airfl ow limi tation
is usually progressive and associated with an abnorma l inflammatory
response of the lungs to noxious particles or gases, most common ly
cigarette smoke. COPD is usually a combination of emphysema (where
the lung parenchyma is structurall y damaged) and airway damage
(with wall thickening and narrowing of the airway). Typically, COPD
involves middle-aged or older people, and cigarette smoking is the
major causative factor.
For more information on COPD, see Therapeutic Guidelines:
Respiratory.
Dental issues
Dental treatment for patients with COPD needs to be modified
according to the patient's condition. Patients with severe COPD do not
corticosteroids requ ire an increased dose of the ir corticosteroid before
dental treatment if they have adrenal suppression (see ' Adrenal
disorders: Dental issues ', p.l51).
Smoking cessation is the only intervention that has been shown to
improve the natural history of COPD. All health professionals should
be actively involved in encouraging patients to stop smoking. Advice
about smoking cessation is discussed in Therapeutic Guidelines:
Cardiovascular and on the QUIT Victoria website <www.quit.org.au>.
Patients may develop oral candidosis secondary to the use of inhaled
corticosteroids. To reduce the risk of oral candidosis and systemic
absorption of corticosteroids, advise patients to rinse their mouth and
throat with water and spit out after inhalation. Patients using a metered
dose inhaler have the additional risk of dysphonia and should be advised
to use a spacer. 145
 Obstructive sleep apnoea
Obstructive sleep apnoea (OSA) affects approximately 4% of males
and 2% of females. It is characterised by repetiti ve obstruction of
the pharyngeal airway, leading to episodes of apnoea (cessation of
breathing) or hypopnoea (partial obstruction) during sleep. If OSA
is not diagnosed and treated appropriately, it may lead to premature
cardiovascular or accidental death. OSA has been reviewed in detail
in the Australian Dental Journal* and in the Journal of Clinical Sleep
Medic in e . "~
Major risk factors in OSA are obesity and facial skeletal retrusion (eg
retrognathia).
Management of OSA includes weight reduction, smoking cessation,
avoidance of alcohol and drugs that affect sleep, treatment of nasal
congestion, tonsillectomy, changing sleeping position, continuous
positive airway pressure (CPAP), mandibular advancement splints, and
surgery. CPAP pneumaticall y splints the upper airway, preventing its
closure during sleep. It is achieved by a machine specifically designed
to blow air via a flexibl e hose into a close-fitting nasal mask worn
during sleep. A mandibular advancement spl int is usually made from
acry li c and worn on the teeth to hold the mandibular teeth in a protruded
position to keep the airway open.
Dental issues
Denti sts have an important role in the multidisciplinaty management
of OSA , including the diagnosis of fac ial skeletal retrusion and th e
constru ction of mandibul ar advancement spl ints.H Some patients with
OSA can be effectively treated with a mandibular advancement splint;
this must be don e in assoc iati o n with a multidisciplinary team led by a
specialist respiratory physician.
Sherring D, Vowles N, Antic R, Kri shnan S, Goss AN. Obstructive sleep apnoea: a review of
the orofacial implications. Aust Dent J 2001;46(3): 154-65.
i Epstein U , Krista D, Strollo PJ, Jr., Friedman N, Mall1otra A, Patil SP, et al. Clinical
guideline for the evaluation, managemen t and long-term care of obstructive sleep apnea in
adults. J Clin Sleep Med 2009;5(3):263-76.
tvowles N, Goss AN . Mandibular advancement splints. ENT and Audiology News
2010;19(3) :58-60.
Kush ida CA, Morgenthaler Tl , Littner MR , Alessi CA, Bailey D, Coleman J, Jr. , et al. Practice
parameters fo r th e treat ment of snorin g and obstructive sleep apnea with oral appliances:
an update for 2005. Sleep 2006;29(2):240-3.
146
Snoring can occur in isolation or can
Use of oral devices to treat
be a sign of OSA. It is not possible to
snori ng without medical
diagnose the cause of snoring without exa mination and investigation is
a medical examination and sleep not appropriate.
laboratory investigation. Use of oral
devices to treat snoring without such investi gati ons is not appropriate.
Patients with OSA have an increased risk of respiratory arrest under
sedation or general anaesthesia. Any dental procedure requiring
sedation or anaesthesia should be undertaken in a hospital with a
specialist anaesthetist present.
ENDOCRINE CONDITIONS
Endocrine conditions of specific importance to dental treatment include
diabetes (see below), thyroid disord ers (see p.l50), adrenal disorders
(see p. l51 ), and bisphosphonate-treated bone and calcium disorders
(see p.152). For more infonnation on these conditions, see Therapeutic
Guidelines: Endocrinology.
Diabetes
Type 1 diab etes accounts for 10% of all di abetes in adu lt populations
of European origin. It is primarily caused by the immune-mediated
destruction of insulin-producing beta cells. Type 2 diabetes is
multifactorial in origin; risk factors include impaired glucose tolerance
or impaired fastin g glucose, previous gestational di abetes, age, obesity,
first-degree relative with type 2 diabetes, hypertension, ethnic origin,
and clinical cardiovascular disease (see Therapeutic Guidelines:
Endocrinology for more infonnation).
All patients with type I diabetes require therapy with insulin, whereas
diet and regular exerci se can often achieve good control of type 2
diabetes initially. If diet and exerc ise are not effective, therapy with one
or more oral antidiabetic drugs (eg sulfonylureas, metformin) may be
prescribed. Most people with type 2 diabetes eventuall y require insulin,
even after many years of successfu l oral th erapy.
Haemoglobin Ale (HbA ! c or glycated haemoglobin) measurement
indicates th e average blood glucose concentration over th e previous 2 to
3 months. It has a useful role in monitoring long-term glycaemiccontrol in
patients with diabetes and predicting diabetes-specific complications. A
common HbAl c target in patients with diabetes is 7.0% (53 mmol/mol)
or less. If a patient's HbA!c is more than 8.0% (64 mmol/mol), they
147
 may have delayed soft tissue healing- the dentist should liaise w ith the medical emergency (see p.l78 for management of hypogl ycaemia
patient's medical practitioner. in the dental surgery)
if a patient on insulin presents with an oral infection and is
For more information on diabetes, see Therapeutic Guidelines: confused, consider the possibility of diabetic ketoacidosis (DKA).
Endocrinology.
Essentially, a decision needs to be made as to whether an individual
Dental issues patient can be safely treated in the general dental setting or if they
require dental treatment in hospital. The approach to general dental
Dentists should ascertain how wel l the patient's diabetes is managed by treatment for patients with stable diabetes is shown in Box 15 (below).
takmg a thorough medical history and assessing the patient's adherence Patients with type I or complex type 2 diabetes who require dental
to and understanding of their treatment. treatment under general anaesthesia or intravenous sedation need
Patients with poorly controll ed diabetes have an increased risk of specialist medical supervision for preoperative fasting and peri operative
perio?ontal disease. The~ may also have impaired salivary gland management.
function from s1aladenosis. They should have regular dental care
including instruction in oral hygiene and denture maintenance. ' Box 15. Approach to general dental treatment for a patient
with stable diabetes
Consider the possibility of undiagnosed diabetes in patients with a
sudden onset of periodontal disease or delayed soft tissue healing, and Initial appointment
111 patients w1th recurrent or persistent bacterial or fungal oral infections. Determine the patient's usual routine and what type of activity destabilises their
diabetic control.
Determine the extent and type of denta l treatment required.
Destabilisation of diabetic control
Ask the patient to bring their glucose monitor with them (if they use one) .
Most patients with diabetes have a routine of medications, diet, acti vity,
and blood glucose momtonng that keeps them feeling well and their Timing of treatment appointments
blood glucose concentrations within safe limits. Provided this routine is Make treatment appointments for midmorning or early afternoon.
not interrupted, most general dental treatment can proceed uneventfully. Remind the patient to maintai n their usual meals and med ications.
Ho~ever~ some s1tuatwns can cause instability that, particularly in a
(ij Avoid extensive treatments and long appointments.
....1:: patient w 1th unstable type I diabetes, can lead to loss of diabetic contro l
C1) and need for hospitalisation.
c Treatment
"C Patients on insulin require regular blood glucose monitoring. Patients When the patient attends for treatment, check that they have followed their
1::
ctl often have the1r own blood g lucose monitor and thus are aware of their normal medication regimen. If they have missed a meal or scheduled snack,
(ij current blood glucose concentrations. In this situation: either reschedule the appointment, or send them to eat and commence
0 if the random blood glucose concentration is between 3.5 and
treatment 30 minutes later.
Ui
Q) 12 mmol/L, it is reasonable to proceed with the required dental Do not give the patient glucose or a sweetened drink 'just in case'; this routine
c is usually ineffective and destabilises the patient's diabetes management.
Qj treatment (a nom1al random blood g lucose concentration range for
:Q a person without diabetes is 3 to 8 mmol!L) If the patient feels ill during treatment, cease treatment. Assess the patient's
:::s blood glucose concentration if a blood glucose monitor is available . For the
(!) if the random blood glucose concentration is more than
(.)
emergency management of hypoglycaemia , see Box 25 (p.179) .
:;:::; 12 mmol!L, the patient's diabetic medication needs to be adjusted
:::s by their medical practitioner Do not allow the patient to leave your care if they are unwell or confused.
Q)
0.
~ if the random blood glucose concentration is less than
Q)
3.5 mmol/L or the patient exhibits symptoms or signs of Dentists can inadvertently induce fasting by makin g the patient's
.!::
f-
hypoglycaemia, administer glucose and treat the patient as a mouth sore. Patients with diabetes must be adv ised that even if their
mouth is sore, they must maintain their caloric intake, activity level
148 149
 and medications. They should be given advice on how to prepare food
to a softer consistency if they are likely to have difficulty with eating.
Management ofhypoglycaemia in the dental surgery is discussed in the
'Medical emergencies in dental practice' chapter (see p.l78).
Problems with healing
In patients with poorly controlled diabetes, healing can be delayed and
the risk of infection can be increased. Although there are no detailed
studies showing clear benefit from antibiotic prophylaxis, consider
prophylaxis for dentoalveolar surgery in patients with poorly controlled
diabetes (see 'Prevention of dentoalveolar surgical site infections' for
drug and dosage recommendations, p.l 07).
Thyroid disorders
Hypothyroid ism
Hypothyroidism is a common condition-particularly in females over
55 years, in whom the prevalence may approach 2%. It is generally
managed with oral thyroxine.
For more information on hypothyroidism, see Therapeutic Guidelines:
Endocrinology.
Hyperthyroidism
Important symptoms of hyperthyroidism include weight loss, heat
intolerance, tremor, muscle weakness and palpitations. The diagnosis
may be obvious if there is associated tachycardia and goitre, but
presentations of hyperthyroidism are often atypical, particularly in
elderly people. Treatment includes drug therapy, radioactive iodine and
surgery.
For more infonnation on hyperthyroidism, see Therapeutic Guidelines:
Endocrinology.
Dental issues
Patients with a stable medication-controlled thyroid disorder do not
usually have difficulties with dental treatment.
Patients with an unstable thyroid disorder (particularly unstable
hyperthyroidism) must have dental treatment deferred until their thyroid
150 condition has been stabilised. Adrenaline-containing local anaesthetics
are not contraindicated in patients with stable thyroid disorder, but they
should be avoided in patients with unstable hypetihyroidism as there is
a risk of thyroid storm (crisis).
Adrenal disorders
The adrenal glands produce steroid hormones from the cortex and
catecholamines from the medulla. When both adrenal glands have been
destroyed or removed (primary adrenal insufficiency), replacement
of steroid hormones, particularly the glucocorticoids, is essential.
Replacement of catecholamines is not needed. Removal of one adrenal
gland does not usually require steroid replacement therapy.
The therapeutic use of cotiicosteroids is the most common cause of
adrenal suppression. Cmiicosteroids are used in the management of
some inflammatory and immune disorders (eg rheumatoid arthritis,
severe dermatological conditions, severe asthma). Treatment with
prednisolone or prednisone at doses greater than I 0 mg daily for more
than 3 weeks can be sufficient to cause adrenal suppression.
Dental issues
It is important to ascertain if a patient is taking cmiicosteroids and, if
so, their underlying condition and current drug regimen. Also check if
they are taking bisphosphonates to treat steroid-induced osteoporosis
(see ' Dental issues: bisphosphonate-related osteonecrosis of the jaws',
p.l52). If a patient requires long-term treatment with corticosteroids,
they generally have a serious underlying condition. Consultation
with the patient's medical practitioner is usually appropriate before
proceeding with dental treatment or making any temporary alterations
to the patient's corticosteroid dose.
Dental treatment may be physiologically stressful, particularly tooth
extractions, root planing and extended restorative treatment. If a patient
with adrenal insufficiency or suppression cannot produce sufficient
steroid hormones (patiicularly glucocmiicoids) following such stress,
Addisonian (adrenal) crisis may occur. This presents as a progressive
hypotension occurring 6 to 12 hours after the dental treatment. The
patient may initially feel faint, become confused and collapse.
If a patient has adrenal insufficiency and is taking replacement therapy,
their dose of replacement steroid should be increased on the day before
and the day of dental treatment to simulate the normal increase in
glucocmiicoid secretion that occurs in response to stress. lf a patient
has been taking corticosteroids sufficient to cause adrenal suppression, 151
 the dose may need to be doubled. If the treatment is more extensive (eg
full dental clearance), or if the patient has been fasting or vomiting, the
dose may need to be trebled or quadrupled.
Stressful dental treatment should be performed in the morning so that
if an Addisonian crisis occurs, symptoms present while the patient is
awake. If treatment is performed in the afternoon, the condition may
manifest at night and progress while the patient is asleep; this can
result in death. After dental treatment, the patient should remain in the
presence of a responsible adult for the rest of the day. If symptoms
occur, the patient's medical practitioner must be contacted.
Bone and calcium disorders (including
osteoporosis)
Osteoporosis is a common health problem. It is characterised by low
bone mass and deterioration in the microarchitecture of the bone (bone
quality), leading to increased bone fragility and a consequent increase
in fracture risk. About 50% of women can expect to sustain fractures
in their lifetime. Low-trauma fractures can occur in 30% of older men
and one-third of all hip fractures in the community occur in men. Drug
therapy is aimed at improving bone strength by preventing further bone
loss and/or increasing bone mass.
Osteopenia refers to a bone mass that is lower than normal, but not
low enough to be classified as osteoporosis. Other bone and calcium
disorders include Paget's disease of bone, malignancy involving bone,
'1ii
....
c
and hypercalcaemia .
Cl)
c The bisphosphonates are one of the drug classes used to treat bone and
'C calcium disorders; however, they have been related to osteonecrosis of
c
(tl the jaws (see below) .
0
...
'1ii
For more information on bone and calcium disorders, see Therapeutic
Guidelines: Endocrinology.
Dental issues: bisphosphonate-related osteonecrosis of
the jaws
Bisphosphonate-related osteonecrosis of the jaws (BRONJ) is an area
of exposed bone in the jaws persisting for more than 8 weeks in a patient
treated with a bisphosphonate. It is usually painful, and sometimes
there is a draining sinus with extensive undermining of the surrounding
mucosa overlying the necrotic bone. The most common complication
1152 ol" BRONJ is soft tissue infection, which may be extensive. Other
pathologies should be excluded, particularly malignancy at the site and
a history of head and neck radiotherapy where the condition is correctly
described as osteoradionecrosis of the jaws (see 'Head and neck cancer:
Dental issues', p.l62).
BRONJ is thought to be caused by bisphosphonate inhibition of
osteoclastic bone resorption, leading to reduced bone turnover. The
severity of BRONJ can be classified in stages, ranging from stage 0
with bone pain but no exposed bone to stage III with full thickness bone
involvement, pathologic fracture, and extensive soft tissue infection
and fistulae.
BRONJ most commonly follows tooth extractions, but may be
associated with poorly fitting dentures. There have also been cases of
BRONJ without evident bone-invasive procedures; these commonly
occurred over exostoses, such as tori or mylohyoid ridges.
Initial reports based on pharmaceutical data described the incidence of
BRONJ in patients treated with oral bisphosphonates as I in I 0 000 to
I in I 00 000. Independent investigations in Australia and North America
show an incidence in the order of I in 500 to I in 1500 patients .*i"
The incidence is much higher in patients treated with intravenous
bisphosphonates, usually for malignancy, where BRONJ can occur in
I in 10 to 1 in 15 patients following tooth extractions.*
Denosumab is a new monoclonal antibody for osteoporosis and,
similarly to the bispbosphonates, acts by inhibiting bone resorption.
Cases of osteonecrosis of the jaws have been rep01ied in patients taking
denosumab, which supports the view that osteonecrosis of the jaws is
caused by suppression of normal bone turnover. The approach to dental
management for patients treated with denosumab should be the same as
for patients treated with bisphosphonates.
Dental procedures in patients treated with
bisphosphonates
Before commencing long-tetm oral or intravenous bispbosphonates in
any patient, the medical practitioner should refer the patient to a dentist
to undet1ake a comprehensive oral examination, including pulp tests
and radiographs, to ensure that they are dentally fit and unlikely to
* Mavrokokki A, Cheng A, Stein B, Goss A. The nature and frequency of bisphosphonate
associated osteonecrosis of the jaws in Australia. J Oral Maxillofac Surg
2007;65(3):415-23.
; Lo JC, O' Ryan FS, Gordon NP, Ya ng J, Hu i RL, Martin D, et al. Prevalence of osteonecrosis
of the jaw in patients with oral bisphosphonate exposure. J Oral Maxil lofac Surg
2010;68(2):243-53. 153
 require extractions in the foreseeable
future.* The dentist should eliminate All patients should be referred
to a dentist before commencing
caries (eg extractions, restorations),
long-term oral or intravenous
establish a healthy periodontium (eg bisphosphonate therapy.
scaling, extractions), and advise the
medical practitioner when the patient is dentally fit. Patients should be
informed of the potential benefits and harms ofbisphosphonate therapy,
including the risk of developing BRONJ.
After commencement of a bisphosphonate, the dentist should monitor
the patient's oral health regularly (eg clinical dental examinations,
radiographs), undertake dental treatment as required and, if worn,
ensure dentures fit well. Patients with dental implants need to have their
implants monitored as loss of osseointegration and BRONJ may occur.
Do not undertake extractions or bone surgery in any patient until it
is known if they are being treated with a bisphosphonate and, if so,
until their risk ofBRONJ has been assessed (see Box 16, p.155 , for
questions to ask when taking a medical history). The risk of BRONJ
is related to the potency of the bisphosphonate (nitrogen-containing
bisphosphonates are more potent than non-nitrogen-containing
bisphosphonates), the total dose, and the dmation of bisphosphonate
therapy. The patient's underlying bone condition, age and comorbidities
are also factors. Bisphosphonates enter the bone matrix where they
remain for at least l year, and possibly up to I 0 years. Clinically,
however, the risk ofBRONJ decreases I year after therapy is ceased.
C-terminal telopeptide (CTX) is a breakdown product of bone
resorption and therefore its serum concentration provides an estimate
of bone turnover. The normal serum CTX concentration is between
400 and 500 pg/mL. Measurement of the fasted morning serum CTX
concentration may be considered to assess the risk of BRONJ (see
Table 12, p.155).
If the CTX concentration is 150 pg/mL or more, bone invasive
procedures can safely proceed. If the CTX concentration is less than
150 pg/mL, patients are at risk of developing BRONJ and consideration
should be given to a 'drug holiday' , where the bisphosphonate is ceased
temporarily. Temporary cessation
of bisphosphonate therapy should Bisphosphonate therapy
be decided by the patient's medical should not be ceased without
consulting the patient's medical
practitioner after consultation with
practitioner.
the dentist. The CTX concentration
'See the joint position statement by Osteoporosis Australia and the Australian Dental
Association on bisphosphonates and osteonecrosis of the jaw. Ava ilable at
154 < www.ada.org.au> (sea rch on 'osteonecrosis of the jaw').
usually increases by 25 pg/mL each month after the bisphosphonale is
ceased. This can be used to estimate when bone invasive procedures
can be safely undertaken and the length of the drug holiday. A repeat
CTX test should be performed to confirm the concentration before
undertaking any bone invasive procedures. Generally, bisphosphonate
therapy can be restarted 10 days after an extraction.
continued next page
Box 16. History-taking relating to bisphosphonates
It is highly recommended that dentists check the following points with their
patients or in the patient's medical history:
1. Have you received treatment for any bone or calcium disorders?
Conditions that may be treated with a bisphosphonate include:
osteoporosis
Paget's disease of bone
cancer with spread to bone (eg breast, prostate, liver, lung, kidney)
multiple myeloma.
2. Are you taking any bisphosphonate medications?
Bisphosphonates are usually taken orally, either daily or once weekly. However,
they are sometimes administered intravenously and given less frequently (eg once
yearly). Bisphosphonates available in Australia are:
nitrogen-containing bisphosphonates (alendronate, risedronate, pamidronate,
zoledronic acid, ibandronate)
non-nitrogen-containing bisphosphonates (et idronate, clod ronate, tiludronate).
If the answer to either of the questions is 'yes', the patient is at risk of
bisphosphonate-related osteonecrosis-do not proceed with extractions or
bone surgery without careful establishment of the facts regarding the bone or
calcium disorder and the medication history. Specialist advice may be needed.
Table 12. Interpretation of fasted morning serum
C-terminal telopeptide (CTX) concentration
Fasted morning serum Risk of bisphosphonate-related
CTX concentration osteonecrosis of the jaws (BRONJ)
less than 70 pg'ml high risk of BRONJ
70 to 150 pg'm l mode rate risk of BRONJ
150 pg'ml or more negl igi ble risk of BRONJ
155
 All procedures involving bone ( eg implant placement, orthodontic tooth
movement, periapical or radicular surgery, periodontal flap surgety)
require careful consideration and informed consent from the patient
before proceeding.*
If an extraction is unavoidable, it should be performed with the minimum
of trauma and with closure of the socket by suturing. Medically well
patients can usually be managed in a general dental practice. Severely
medically compromised patients on intravenous bisphosphonates for
malignancy are best managed by a dental specialist associated with the
oncology team. If the patient is medically compromised (particularly
if they have diabetes or are taking corticosteroids), consider antibiotic
prophylaxis (see 'Prevention of dentoalveolar surgical site infections'
for drug and dosage recommendations, p.l 07).
Monitor the extraction wound until it heal s. Healing may be slow. If
bone is still clinically visible at 8 weeks, BRONJ has occurred and
urgent specialist referral is required. Do not curette nonhealing sockets.
Dental issues
Dental treatment for patients who have had a stroke may need to be
modified depending on their medical status and prognosis.
Patients with residual motor defects of the arm may have difficulty
cleaning their teeth. Large-handled or powered toothbrushes may
improve the effectiveness of oral hygiene.
Patients with seventh cranial (facial) nerve weakness accumulate food
debris on the affected side and may have difficulty with dentures.
Design modifications to dentures include a thickened flange. An
implant-borne prosthesis may be of benefit, but the patient must be
able to cope with the additional treatment load and be able to maintain
effective oral hygiene.
Anticoagulant and antiplatelet drugs should not be ceased for
dentoalveolar procedures (see 'Potential problems with anticoagulant
and antiplatelet drugs in patients undergoing dentoalveolar smgery
(including extractions)', p.\38, for more information).

NEUROLOGICAL CONDITIONS
A wide range of neurological conditions may affect dental treatment
(eg dementia can lead to diagnostic problems and lack of understanding
of treatment progress). However, this section only discusses the dental
issues associated with stroke, epilepsy and trigeminal neuralgia.
Management of neurological conditions are discussed in Therapeutic
Guidelines: Neurology. For management of dementia, see Therapeutic
sc
(I)
Guidelines: Psychotropic.
Management of stroke in the dental surgery is discussed in the 'Medical
emergencies in dental practice' chapter (see p.\76).
Epilepsy
The epilepsies are a group of chronic neurological conditions
characterised by recurrent unprovoked epileptic seizures. Epilepsy may
be the primary problem, or it may be a secondary symptom of another
brain disorder. Epileptic seizures may be partial or generalised.

c The aim of pharmacotherapy is to maximise the patient's quality of life

"C Stroke by preventing seizure recurrence, with minimal adverse drug effects.
c Nonadherence to treatment or lifestyle advice is a common cause of
ca
Stroke is the leading cause of long-term adult disability in Western therapy failure.
~ countries and the third most common cause of death .
0 For more information on epilepsy, see Therapeutic Guidelines:
Ui Primary prevention of stroke involves management of risk factors in
(j)
c
Neurology.
individuals who have not experienced cerebral vascular symptoms.
Qi
:9 Modifiable risk factors include atrial fibrillation, hypertension, smoking,
::::l
<.!)
diabetes, cardiovascular disease and hypercholesterolaemia. Secondary Dental issues
() prevention of ischaemic stroke mainly involves antiplatelet therapy. The stability ofthe patient's epilepsy
.;:::; A person with stable epilepsy
::::l Patients with atrial fibrillation may be taking warfarin. must be assessed- this includes
(j) who has not taken their
Cl.
For more information on stroke, see Therapeutic Guidelines: Neurology. how frequently seizures occur and medication in the last 48 hours
~
(j)
.c what triggers them. Before each is at risk of a seizure .
I- For more information , see the joint position statement by Osteoporosis Austra lia and the appointment, check that the patient
Australian Dental Association on bisphosphonates and osteonecrosis of the jaw. Available
157
156 at <www.ada.org.au > (search on 'osteonecrosis of the jaw') .
 has taken their medication that day. A person with stable epilepsy who
has not taken their medication in the previous 48 hours is at risk of
a seizure.
Avoid stressful extended procedures as they may trigger seizures.
Consider the use of a mouth prop so the operator's fingers and
instruments can be retrieved if the patient suffers a generalised seizme
during treatment.
Some patients develop gingival hyperplasia secondary to antiepilepsy
medication . This can be minimised with good oral hygiene. Extensive
hyperplasia requires specialist management.
The management of a seizure in the dental surgery is discussed in the
'Medical emergencies in dental practice' chapter (see p.l77).
Trigeminal neuralgia
Trigeminal neuralgia is characterised by sudden, brief and very severe
paroxysms of pain on one side of the face, in the distribution of one or
more branches of the fifth cranial (trigeminal) nerve. Because of the
very brief nature of the pain, it is sometimes described as stabbing, or
compared to an electric shock. There is no sensory loss in the painful
area. Attacks are triggered by trivial sensory stimulation (eg touching
the face, cold air blowing on the face, or activities such as talking,
chewing or toothbrushing). A specific trigger point can sometimes be
identified on the gingivae. The pain usually does not awaken the patient
from sleep; indeed sleep is a period of relief. There may be a residual
(ij
....c ache after the shock-like pain has subsided. Attacks may remit for
Q) weeks or months, but then return.
Q
'C If pain persists at full intensity for more than a few minutes, or if the
c change, they may be helped by drugs such as carbamazepine. If such
Cl:l pain is predominantly in the forehead rather than the cheek or jaw, other
" diagnoses (eg paroxysmal hemicrania, cluster headache or atypical
0 facial pain) should be considered. Trigeminal neuralgia should be
Ui
<ll
c
distinguished from postherpetic neuralgia (where there is a history of
herpes zoster eruption). Trigeminal neuralgia in a young person (under
Qj
:2 40 years) may be due to multiple sclerosis.
::J
(!)
Trigeminal neuralgia is primarily managed by pharmacotherapy with
(.)
.;::; carbamazepine. In intractable cases, other drugs (alone or in combination
::J
<ll
a. with carbamazepine) or neurosurgery is appropriate. Other drugs that
may be effective are baclofen, clonazepam, gabapentin, lamotrigine,
~
<ll
oxcarbazepine, phenytoin and sodium valproate.
..c
1-
For more infonnation on trigeminal neuralgia, see Therapeutic
158 Guidelines: Neurology.
Dental issues
Many patients with trigeminal neuralgia think they have toothache.
Dental pain, pm1icularly pulpitis, is very similar to trigeminal neuralgia,
so careful evaluation of the teeth is required. If the findings from an oral
examination and tests (eg pulp tests and radiographs) are inconsistent
with the patient's symptoms, do not commence invasive or irreversible
procedures. If initial dental treatment does not reduce the pain, consider
the possibility of trigeminal neuralgia before undertaking fm1her dental
treatment.
Questions that assist in making a diagnosis include- Is the pain
consistent with the condition of the teeth? Can it be stimulated by soft
tissue contact? Does it interfere with sleep? What are the effects of
diagnostic nerve blocks?
Nerve blocks with long-acting local anaesthetics (eg bupivacaine with
adrenaline) not only give diagnostic information and provide tempormy
relief so the patient can eat, but also decrease pain for up to 14 days.
Response to carbamazepine is not diagnostic of trigeminal neuralgia
as carbamazepine also relieves toothache. If there is uncertainty about
the diagnosis, specialist referral is required before commencing dental
treatment.
In patients with unstable trigeminal neuralgia, dental treatment may
exacerbate the pain, even if performed on other sites in the mouth. If this
occurs, it may help to block the area afflicted by trigeminal neuralgia
with a local anaesthetic while treating the other areas; this reduces the
degree of exacerbation.
If patients with a tri geminal nerve injury fi-om either a local anaesthetic
injection or a tooth extraction have a painful dysaesthetic sensory nerve
injuries are more than transitory, specialist referral is recommended.
VIRAL DISEASES
Viral hepatitis
There are five known hepatitis viruses-Hepatitis A, B, C, D and E.
Those most relevant to dental practice are hepatitis B and C, both
of which are blood-borne viruses. Most people with hepatitis B or
C in Australia are living with chronic infection requiring long-term
management and support. Hepatitis B can be controlled with drug
therapy, while cure is possible for hepatitis C. For fm1her information
159
 on viral hepatitis, see Therapeutic Guidelines: Gastrointestinal
and guidelines from the Gastroenterological Society of Australia
<www.gesa.org.au>.
Dental issues
Any patient's blood and bodily fluids must be treated as potentially
infectious, with standard infection control/precautions exercised at all
times. There are two main principles to prevent transmission:
All members of the dental team should be vaccinated against
hepatitis B.
Standard precautions must be followed with all patients as there
is no legal obligation for a patient to disclose their blood-borne
virus status and the current situation may not be known.
Sharps injuries, including needlestick injuries, are an uncommon cause
of blood-borne virus transmission. There is no evidence that 'double
gloving' adds any extra protection from a sharps injury. This practice
is stigmatising and may lead to patients not revealing their full medical
history. Individual hospitals and health districts have their own infection
control policies to deal with sharps injuries. The principles of these
policies are discussed in Therapeutic Guidelines: Antibiotic.
Patients with hepatitis C have a higher incidence of dental caries and
periodontal disease. Periodontal health, in particular, is markedly
poorer and salivary flow is reduced; however, whether this is a direct
viral effect or due to other causes requires fUiiher research. Dental
management of patients with hepatitis C should have a heavy emphasis
on preventive care- well-planned preventive care and management is
most appropriate, as the response to extensive dental rehabilitation may
be poor.
If a patient has advanced hepatitis C (approximately 7% of patients
who have had hepatitis C for more than 20 years) or is taking antiviral
drugs, consider antibiotic prophylaxis for high-risk dental procedures
(extraction, periodontal procedures including surgery and root p laning,
replanting avulsed teeth, other surgical procedures [eg implant
placement, apicectomy]). For antibiotic prophylaxis regimens, see
'Prevention of dentoalveolar surgical site infections' (p. 107).
In general, sedatives and nonsteroidal anti-inflammatory drugs
(NSAIDs) should be avoided in patients with viral hepatitis, as they
may be hepatotoxic. Paracetamol can be used sparingly. Patients may
also have issues with excessive alcohol consumption or intravenous
160 drug use that may affect adherence to dental treatment.
Human immunodeficiency virus
All patients with symptomatic human immunodeficiency virus (HIV)
infection require antiretroviral therapy. The need for antiretroviral
therapy in patients with asymptomatic HIV infection depends on the
patient's CD4 cell count, viral load and comorbidities. Antiretroviral
drugs may significantly delay disease progression.
There are several groups of antiretroviral drugs-nucleoside/nucleotide
reverse transcriptase inhibitors (eg emtricitabine ), non-nucleoside
reverse transcriptase inhibitors ( eg nevirapine ), protease inhibitors
(eg atazanavir), HIV entry inhibitors (eg enfuvirtide) and integrase
inhibitors (eg raltegravir). All have significant drug interactions and
potential adverse reactions, but their benefits include prolonged life
with improved quality.
For more information on HIV infection, see Therapeutic Guidelines:
Antibiotic and the Australasian Society for HIV Medicine website
<www.ashm.org.au>.
Dental issues
Consultation with an HIV expe1i is strongly recommended before
starting any new medication in patients taking antiretroviral drugs.
Antiretroviral drugs can interact with many commonly prescribed drugs
(eg erythromycin, codeine, itraconazole, diazepam), so patients requ ire
close monitoring and may need alteration of drug dosage or timing of
administration.
Unusual and rare adverse reactions (eg perioral paraesthesia) can occur
with antiretroviral drugs.
Patients with HIV infection, particularly smokers, have an increased risk
of oral diseases, such as periodontal disease, oral hairy leukoplakia and
oral squamous cell carcinoma. Therefore, thorough dental examination,
treatment and monitoring are required.
See also the discussion on sharps injuries in 'Viral hepatiti s: Dental
issues' (p.160).
HEAD AND NECK CANCER
The morbidity and m01iality from head and neck cancer is high.
Treatment is mainly by surgery and/or radiotherapy, sometimes with
chemotherapy.
161
 A patient with head or neck cancer may be in a weakened state from
the effects of the disease and its treatment. The effects of radiotherapy
are localised to the treatment area, whereas chemotherapy affects the
whole body.
Dental issues
Dentists have a responsibility in the initial recognition and diagnosis
of oral cancer. Specialist dentists are an essential part of the head and
neck cancer team.
Patients who require head and neck radiotherapy should be reviewed by
a dentist experienced in cancer management to ensure they are dentally
fit and able to maintain their teeth through the oral pain, mucositis and
reduced salivary flow that occur with irradiation . If the patient will not
be able to maintain their teeth, the teeth are best extracted. Radiotherapy
can start 7 to I 0 days after extractions are completed.
Mandibular extractions after head and neck radiotherapy can cause
osteoradionecrosis, a painful and debilitating condition. Maxillary
extractions are generally uncomplicated. If possible, dental treatment
should be conservative (eg restorations, endodontic [root canal]
treatment and fluoride application). If
mandibular extractions are required, Do not extract teeth from a
the risk of osteoradionecrosis can be patie nt who has had head
and neck radiotherapy without
minimised by the use of prophylactic specialist advice.
hyperbaric oxygen. Antibiotic prophy-
laxis alone (without hyperbaric oxygen) may be insufficient to prevent
~c osteoradionecrosis. Specialist advice is recommended before proceeding
Q)
c
'C
with any extraction in a patient who has had head and neck radiotherapy.
c Management of osteoradionecrosis is difficult and requires specialist
ca
input. Treatment usually involves hyperbaric oxygen in combination
~ with surgical resection of the necrotic bone.
0 cessation and physical activity. Pharmacological management may
The possibility of cancer recurrence
Consider the possibility of
or a new primary cancer must be cancer recurrence or a new
considered and excluded in patients primary cancer in patients who
who have had head and neck cancer have had head and neck cancer
treatment. treatment.
CHEMOTHERAPY
Chemotherapy with cytotoxic drugs is widely used in the management
of patients with malignancy. There is a great variety of drugs used as
162
monotherapy or in combination (sometimes with corticosteroids). For
information on chemotherapy use in palliative care, see Therapeuttc
Guidelines: Palliative Care.
Chemotherapy can cause mucositis of the entire gastrointestinal tract.
This is commonly the dose-limiting factor of treatment.
Dental issues
Patients should be dentally fit before starting chemotherapy, particularly
if the drug regimen will result in severe mucositis and reduced salivary
flow. Warn patients of the probability of mucositis (and its nature and
likely duration) before they begin chemotherapy. For management of
oral mucositis, see p.85.
Modify dental treatment to suit the patient's needs and circumstances.
Dental treatment should be performed between chemotherapy
treatments. Tooth extraction sockets generall y heal well in patients
undergoing chemotherapy; however, caution is required in p~tients
taking bisphosphonates- seek specialist advice (see 'Dental Issues:
bisphosphonate-related osteonecrosis of the jaws', p.l52).
CHRONIC MUSCULOSKELETAL DISORDERS
Rheumatological diseases encompass arthropathies, myopathies,
systemic vasculitis syndromes, and musculoskeletal and connect~ve
tissue disorders. Many of these conditions are chronic and progressive
and have a degenerative, inflammatory or autoimmune basis.
Chronic pain problems include chronic back or neck pain, osteoarthritis,
rheumatoid arthritis, fibrom yal gia, and complex regional pain syndromes . ...c
1/)
Q)
The management of chroni c musculoskeletal di sorders is complex, and
~Q.
includes advice on lifesty le factors, diet and weight control, smokmg
..,_II)
oc
include the use of analgesics (eg paracetamol, nonsteroidal anti- ....9
C:t::
inflammatory drugs [N SA IDs], opioids), corticosteroids, disease- Q)"C
EC
modifying antirheumatic drugs, immunosuppressants, specific drugs Q)O
'Q.O(,)
for specific conditions (eg allopurinol for gout) and complementary ca-
eca
medicines. ca.!:!
E"Q)
For more information on chronic musc uloskeletal disorders, see 'i6E
Therapeutic Guidelines: Rheumatology. 'l:.s
Q),_
c:=
163
 Dental issues
Table 13. Drugs commonly used in psychiatric disorders
Dental patients with musculoskeletal problems may find extended Drug group Drug class Examples
dental treatment uncomfortable, and it may exacerbate their medical
antidepressants selective serotonin reuptake citalopram, escitalopram,
condition. Modify treatment to minimise the time spent in the dental
inhibitors (SSRis) fluoxetine, fluvoxamine,
chair, and consider changing the chair configuration and using filler paroxetine, sertra line
pillows to support the neck, hips or knees.
t ricyclic anti depressants (TCAs) amitriptyline, doth iepin ,
Some patients have prosthetic joints. There is a very small risk of doxepin

infection at a prosthetic joint site through the haematogenous route, and monoamine oxidase inhibit ors moclobemide, phenelzine
antibiotic prophylaxis before dental procedures is not recommended (MAOis)
(see also discussion in 'Prevention of infection in joint prostheses', serotonin and noradrenaline venlafaxine, duloxetin e
p.l06). reu ptake inhibit ors (SNRi s)

Some patients may be taking significant doses of a corticosteroid. The others mirtazapine, reboxetine

problems with dental treatment in patients taking corticosteroids are

mood stabilisers carbamazepine, lamotrigine,
discussed in ' Adrenal disorders: Dental issues ' (see p.l51). (used in bipolar lithium, sodium valproate
disorder)
Some patients may be taking large doses of analgesics, including opioids
(either medically prescribed or self-initiated in combination with antipsychotic first-generation antipsychotics chlorpromazine, drop eridol,
drugs flupenthixol , fluph enazine,
complementary medicines or illicit drugs). Some of these may result haloperidol, peri cyazine,
in dry mouth and consequently extensive dental decay and periodontal t rifluoperazine, zuclopenthixol
disease, particularly if they are taken with tricyclic antidepressants. For
second-generation anti psychotics amisulpride, aripi prazole,
management of dry mouth, see p.87. clozapine, olanzapine ,
queti apine, risperidone

PSYCHOLOGICAL AND PSYCHIATRIC DISORDERS psychostimulants dexampheta mine ,

methylphenidate, modafinil
Approximately 15% of the population have a significant psychological benzodiazepines diazepam, temazepam
anxiolytics and
disorder and approximately 2% have a major psychiatric disorder. If hypnotics
these are not managed, they can have serious individual and societal
others zolpidem, zopiclon e
consequences. Pharmacological treatment is often used in the
management of psychological and psychiatric disorders. For psychiatric drugs used in buprenorphine, methadone,
conditions and their management, see Therapeutic Guidelines: substance use na ltrexone
Psychotropic. disorders

drugs used in cholineste rase inh ibitors donepezil, galantamine,

Table 13 (p.l65) lists classes of drugs commonly used in psychiatric dementia rivastigmine
disorders with some examples of drugs in each class.
others memantine

Dental issues
Drugs commonly used in dentistry rarely have significant interactions
with psychotropic drugs. Local anaesthetics containing adrenaline are
not contraindicated with tricyclic antidepressants (TCAs) or selective
serotonin reuptake inhibitors (SSRis), but should be avoided in patients
taking monoamine oxidase inhibitors (MAOis).
164
Dentists and their staff should be aware of the psychological status of
their patients as this can affect the dental treatment plan and outcon:es.
Psychological status should be determined by taking a th~rough medt.cal
history. The patient's medication list may be helpful 111 determmmg
their underlying mental health condition.
165
 Examples:
A patient who is taking lithium has a serious underlying
psychiatric disorder. This knowledge can help define an
appropriate dental treatment plan.
A patient who has body dysmorphic disorder (characterised
by a preoccupation with imagined or slight defects in physical
appearance) may at first seem suitable for an aesthetic dental
procedure. However, no matter how much the appearance of
their teeth and j aws improve, they will never be satisfied .
A patient who is markedly thin with marked erosion ofthe
enamel surface of the teeth may have an eating disorder (see
Therapeutic Guidelines: Psychotropic for more information).
Patients with anxiety or phobic states can be difficult to manage. Many
do not present to the dentist for routine treatment and seek treatment
only when a painful emergency occurs. Routine sedatives may be
ineffective as these patients may have developed a tolerance to them.
General anaesthesia or specialist referral may be required.
Drug-dependent and drug-seeking Drug-dependent and drug-
patients may present to a dental seeking patients are common in
practice. Be suspicious of any patient general dental practice.
who demands analgesic drugs and
exhibits a good level of knowledge or a preference for a specific opioid.
Do not initiate treatment in the absence of demonstrable disease. At
most, offer a smal l amount of analgesic and advise the patient to consult
their medical practitioner.
Further reading
eTG complete [CD-ROM or onli ne]. Melbourne: Therapeutic Guidelines Limited
[regularly updated].
Little JW, Fa lace DA, Miller CS, Rhodus NL. Dental rnanagernent of the
medically compromised patient. 7th ed. St Louis: Mosby; 2008 .
166
Medical emergencies in
dental practice
The best way to avoid a medical emergency in dent~! practice is. by
careful assessment of the patient; this includes obtammg a deta!led
medical and medication history.
Occasionally unavoidable emergencies occur. Dentists and their staff
must be trained and have a plan for emergency management. Prompt
diagnosis and primary managerr~ent Afai led attempt at resuscitation
can improve the outcome. A failed is always better than failing to
attempt at resuscitation is always attempt resusc itation.
better than fai Iing to attempt resus-
citation.
Medical emergencies range from transient ~roblems th~t resolve
spontaneously (eg syncope), to serious emergencieS that reqmre tran~fer
of the patient to medical faciliti~s ~eg sev~re asthJ?a attac~), to life-
threatening emergencies that reqmre immedtate on-site resuscitatiOn (eg
cardiac arrest). All drugs have the potential to cause ?dverse outcomes,
some of which can be life -threatening (eg anaphylaxis) .
The information and guidelines in this section are not a s~bstitute for
formal training and regular updates. Va luable sources of mformatJOn
include the following:
The Therapeutic Guidelines series has information on medical
and medication-related problems.
The Australian Resuscitation Counc il has pol~cy stat~m~nts
and advice on resuscitation. Figure 5 (p. I 83) IS a bas1c life .
support flow chart that can be downloaded from the Australian
Resuscitation Council website
<www.resus.org.au/public/arc_basic _life _support. pdf>
The Therapeutic Guidelines series and the Au.stra~ian Res~scitation
Council information form the basis of the followmg mformat1on.
'I 7
 CARDIOVASCULAR EMERGENCIES
Syncope
Syncope is a transient self-limiting loss of consciousness, usually
leading to loss of postural tone and falling. The onset is almost always
rapid and the recovery is usually rapid, spontaneous and complete.
The underlying mechanism for syncope is a transient global cerebral
hypoperfusion. Presyncope refers to a condition in which the patient
feels as though syncope is imminent; the patient feels light-headed,
may be nauseated and anxious, and may appear pale. Symptoms of
presyncope tend to overlap premonitory symptoms of true syncope.
Syncopal episodes are common. The prevalence of syncope increases
with age and it can cause significant morbidity in the elderly.
Important causes of syncope include neurally mediated syndromes
(including paroxys mal orthostatic tachycardia syndrome [vasovagal/
vasodepressor syncope, carotid sinus syncope]), volume depletion and
cardiac arrhythmias. Vasovagal syncope is the most common type of
syncope and is usually a reaction to anxiety and fear before, during or
after a dental procedure.
For management of patients with syncope, see Box 17 (below and
p.169).
Box 17. Management of syncope
:sc If the patient feels faint:
Cease dental treatment.
Q)
c If the patient is in the dental cha ir, t ilt the chair back to a horizontal position
't:l (the patient should not be placed in a 'head lower than heart' position). If the
c syndrome. Rapid identification and decisive action in referring the
Ia patient is not in the dental chair, ask the patient to lie down.
~ Raise the patient's legs sl ightly.
0 Assess consciousness by ta lking to the patient.
If the patient is unconscious:
Cease denta l treatment.
If the patient is in the dental chair, tilt the chair back to a horizontal position
(the patient should not be placed in a 'head lower than heart' position).
Measure the patient's blood pressure and pulse rate.
Place the patient on their side (if they are pregnant, they should be turned to
their left side).
Stimulate and cool the patient by placing a cold compress on their forehead.
continued next page
168
Box 17. Management of syncope (cont.)
If the patient has a vasovagal-type syncope, they should rapidly return to
consciousness. Allow the patient to recover slowly under supervision; do not
discharge them premat urely from care, particularly if they will be driving. Refer the
patient for medical evaluation , particularly if the patient is elderly, recovery is slow
or the patient has had repeated events of syncope without obvious triggers.
If the patient does not regain consciousness, consider other causes of
syncope or collapse and:
Call 000.
Institute basic life support (for 'Basic life support flow chart', see Figure 5,
p.183).
Maintain treatment until the patient regains consciousness or assistance arrives.
Coronary heart disease
Coronary heart disease can cause myocardial ischaemia secondary
to coronary obstruction. Not all patients with myocardial ischaemia
experience typical retrosternal cardiac chest pain, which is constricting
and radiates to the neck, jaw or arm. Some patients experience atypical
pain, shortness of breath or light-headedness. Others, especially elderly
patients or patients with diabetes, may have no symptoms.
Patients with cluonic symptoms are classified as having stable angina.
The pain associated with stable angina bears a predictable relationship to
walking and other activities involving physical effmi or stress. The pain
is typically transient (lasting less than 10 minutes) and subsides promptly
with rest. Patients with new or increasing symptoms are considered to
have an acute coronary syndrome, which can be a medical emergency.
A patient in the dental surgery may develop angina or an acute coronary
patient to appropriate care are essential to a good outcome. Instruct
patients with a history of angina to bring their medication (eg glyceryl
trinitrate spray or tablets) when presenting for dental treatment.
For management of patients with angina or an acute coronaty syndrome,
see Box 18 (p.170).
Cardiac arrest
Cardiac arrest is generally due to ventricular tachycardia, ventricular
fibrillation, asystole or electromechanical dissociation. The pati ent
suddenly loses consciousness; there is no pulse and no respiration.
For management of patients with cardiac anest, see Box 19 (p.170). 169
 Box 18. Management of angina or an acute coronary RESPIRATORY EMERGENCIES
syndrome
Hyperventilation syndrome
Ensure that any patient with a history of angina brings their medication (eg glyceryl
trinitrate spray or tablets) when presenting for dental treatment. Hyperventilation syndrome may occur when a patient hyperventilates
(overbreathes) . It is common, and often occurs in patients suffering anx-
If chest pain occurs in a patient with a history of angina:
iety or an acute panic attack. For signs and symptoms ofhyperventilation
Cease dental treatment.
syndrome, see Tab le 14 (below). Symptoms of hyperventilation
Measure the patient's blood pressure and pulse rate, and assess consciousness syndrome are commonly confused with syncope; patients may also be
by talking to the patient.
in the early phase of an acute asthma attack or a myocardial infarction.
To shorten the attack, use*:
Table 14. Signs and symptoms of hyperventilation syndrome
g/yceryl trinitrate spray 400 micrograms sublingually, repeat every 5 minutes
if pain persists, up to a maximum of 1200 micrograms
Symptoms Signs
or gtycery/ trinitrate tablet 600 micrograms sub/ingually, repeat every
5 minutes if pain persists, up to a maximum of 1800 micrograms. light-headednesS/dizziness rapid breathing
Ask the patient to sit or lie down, particularly when first using glyceryl trinitrate, shortness of breath occasional deep sighing breaths
because of the possibility of hypotension. feeling of panic and impending death rapid pulse
If the patient recovers, do not proceed with dental treatment; the patient should blurred vision altered consciousness
be med ically evaluated even if apparently well.
tingling in the fingers, toes and lips carpopedal spasm of the hands and
If pain persists for more than 10 minutes despite taking 2 doses, give a third dose fingers
feeling of detachment
and manage as for chest pain that is severe and new (see below) .
If chest pain is severe and new: Hyperventilation sy ndrome is best prevented by observing the
Call 000. patient, especiall y after the administration of a local anaesthetic as
Give oxygen. hyperventilation syndrome commonly occurs at that time. If the
patient is taking fast but shallow breaths, encourage them to slow their
Give (provided aspirin has not already been taken):
breathing and to breathe in through their nose and out tluough their
aspirin 300 mg chewed or dissolved before swallowing. mouth. Firm ly reassure them, give them an explanation of the cause of
Monitor the patient's vital signs and reassure them until assistance arrives. the symptoms and have them talk to you.
If the patient loses consciousness, institute basic life support-cardiopulmonary For management of patients with hyperventilation syndrome, see
resuscitation (CPR) (for 'Basic life support fl ow chart', see Figure 5 , p.183). Use Box 20 (below).
an automated external defibrillator if available.

* Nitrates should not be administered within 3 to 5 days of tadalafil, or within 24 hours of Box 20. Management of hyperventilation syndrome
sildenafil or vardenafil, as these drugs greatly potentiate the hypotensive effects of nitrates.
Cease dental treatment.
Encourage the patient to slow t heir breathing.
Box 19. Management of cardiac arrest Ask the patient to rebreathe their expired air by cupping their hands close over,
Cease dental treatment. but not obstructing, their mouth and nose.
Call 000. Do not give oxygen (as this prolongs the symptoms) .

Institute basic life support-cardiopu lmonary resuscitation (CPR) (for 'Basic
life support flow chart', see Figure 5, p.183). Use an automated external
defibrillator if available.
Maintain treatment until the patient regains consciousness or assistance arrives.
170
If the patient does not rapidly recover, review the diagnosis. Differential diagnoses
include acute asthma (see p.172) , heart failure and anaphylaxis (see p.182).
If acute symptoms persist for more than 5 to 10 minutes, or if carpopedal spasm
is extensive (and particularly if it spreads to involve the legs):
Call 000. 171
 Acute asthma Box 21. Management of an acute asthma attack
;\cute asthma attacks can be fatal. Instruct patients with asthma to bring Ensure that any patient with asthma brings the bronchodilator inhaler medication
the bronchodilator inhaler medication they use to relieve attacks when they use to relieve attacks when presenting for dental treatment. Many patients
with asthma have an action plan, or at least a good understanding of how to
presenting for dental treatment.
manage their asthma, and this should be encouraged.
lf an acute asthma attack occurs, a The initial management of an acute asthma attack is determined by the severity
Patients with severe asthma
rapid physical examination should of the attack (see Table 15, p.172), and the patient's background asthma pattern
may have no wheeze. Cyanosis
be performed to evaluate the severity indicates life-threatening and severity. In all cases, cease dental treatment. Sit the patient comfortably
of the attack (see Table 15, below). asthma. upright, and be calm and reassuring.
Wheezing is an unreliable indicator
If the attack of asthma is mild:
of the severity of an asthma attack and may be absent in a severe attack. Give 4 puffs of a short-acting bronchodilator (eg salbutamol) inhaler via a
Cyanosis is an indicator of life-threatening asthma and patients require spacer-give 1 puff at a time and ask the patient to take 4 breaths in and out
prompt hospitalisation. of the spacer after each puff.
For management of patients with an acute asthma attack, see Box 21 If a spacer is not available, give 4 puffs of the inhaler alone-give 1 puff at
(p.173). a time and ask the patient to hold their breath for 4 seconds or as long as is
comfortable after each puff, then breathe out slowly away from inhaler.
Table 15. Initial assessment of the severity of an acute Wait 4 minutes.
asthma attack in adults and children If there is no improvement, give another 4 puffs using the technique above.

Clinical features Mild Moderate Severe Assess patient's status. If there is little or no improvement, manage as for a
and life- moderate or severe attack (see below). If the patient recovers swiftly:
threatening * Temporise the dental state.

physical exhaustion I altered no no yes Make another appointment to complete the dental treatment (if needed).
conscious state When the patient is breathing easily, discharge from care .
altered consciousness no no yes Recommend that the patient takes their asthma medications strictly as
(in children) prescribed and has an urgent medical review.
increased accessory muscle no some marked If the attack of asthma is moderate or severe:
use (in children)
Call 000.
talks in sentences phrases words
Give oxygen by mask at a flow rate of 6 Umin.
pulse ratet less than 100/ adults: 100 to adults: greater Give 4 puffs of a short-acting bronchodilator (eg salbutamol) inhaler v~ a
minute 120/minute than 120/minute
children: 100 to children: greater spacer- give 1 puff at a time and ask the patient to take 4 breaths in and out
200/minute than 200/m inute of the spacer after each puff.*
hospital admission needed no probably, yes, high If a spacer is not available, give 4 puffs of the inhaler alone- give 1 puff at
especially if poor dependency or a time and ask the patient to hold their breath for 4 seconds or as long as is
initial treatment intensive care comfortable after each puff, then breathe out slowly away from inhale.*
response unit
Wait 4 minutes.
* Any of these features indicates that the episode is severe. The absence of any feature does
not exclude a severe attack. Continue giving 4 puffs every 4 minutes, using the technique above, Lntil
t Bradycardia (slow pulse rate) may be seen when respirat01y arrest is imminent. assistance arrives.
Source: National Asthma Council Australia. Asthma management handbook 2006. Melbourne: Monitor the patient until assistance arrives.
National Asthma Council Australia Ltd; 2006. (p.39 and p.44)
* If the attack is severe and if available, instead of an inhaler, consider giving salbutamol 5 mg
by nebuliser driven by oxygen. If there is no response to the initial dose, repeat immediately,
then every 15 to 30 minutes until assistance arrives.
172
 Inhaled or swallowed objects Table 16. Signs of airway obstruction
The re is always a risk of objects being inhaled or swallowed during Signs of partial airway obstruction Signs of complete airway obstruction
dental treatment. An inhaled or swallowed object may present a
wheeze inability to breath, speak, cry or cough
significant risk to the patient. Foreign objects in the lungs (inhaled
stridor (noisy inspiration) agitation, gripping of the throat
objects) must be removed as a matter of urgency. Swallowed objects
may have an uneventful passage through the gastrointestinal tract; laboured breathing cyanosis
occasionally they may need to be removed. There may be medicolegal coughing spasms bulging of the neck veins
implications for the practitioner in the event of an object becoming cyanosis (indicates a severe lack of rapid development of respiratory failure
lodged in the lungs or the gastrointestinal tract. oxygen) (followed by ca rdiac failure)
loss of consciousness

Prevention
All steps must be taken to minimise the risk of inhaling or swallowing Box 22. Management of an inhaled or swallowed object*
a foreign object: In the event that an object appears to have fallen down the oropharynx:
When practicable, use a rubber dam for procedures where the risk Cease dental treatment.
of inhalation or swallowing is high.
Check whether the object is present in the patient's mouth or clothes and, if so,
If procedures preclude the use of a rubber dam, precautions to remove it.
take include: If the object is not found , put the patient into an upright position.
ensuring a careful and unrushed approach Check the patient's vital signs .
having the patient reclined rather than supine
Do not allow the patient to drink.
having instruments and facilities available that can be used to
Arrange for a chest radiograph (a swallowed object will remain in the upper
retrieve an object from the oropharynx gastrointestinal tract for some time so a chest radiograph done within 1 hour
tying dental flo ss to any object that can be dropped (if wi ll show any radiopaque object that has been inhaled or swa llowed; if the
appropriate) time interval is longer, a swal lowed object will have passed through the upper
placing gauze across the back of the tongue to trap small items gastrointestinal tract).
ii
.... (eg crowns) that may be dropped All objects in the lungs should be removed by bronchoscopy or thoracotomy.
c
Q) rotating the patient's head so that a dropped object will fall to Patients who have swa llowed sharp objects, such as needles, burs or
Q
-o the side of the mouth endodontic files, require urgent medical referral if they develop abdominal
c
Ctl using high-volume suction. pain . An abdominal radiograph may be considered in asymptomatic patients !c
after 7 days to confirm the object has cleared. If it has not cleared, the patient Q)
ii may require medical referral for consideration of remova l of the object by -o
0 Obstruction of the airway gastroscopy, colonoscopy or laparotomy. .5
(t) II)
Q)
<ll
c It is imp011ant to differentiate between pat1ial and complete airway If partial airway obstruction (see Table 16, above) is present:
'(j
<ll obstruction following inhalation of a foreign body. If the patient can Call 000 . c
~
"0
s breathe, speak, cry or cough, some movement of air is occurring, and Reassure the patient and encourage them to relax, breathe deeply and try to
(.!J the obstruction is pat1ial. See Table 16 (p.l 75) for signs of partial and dislodge the object by coughing. Look at all spit and expectorant for the object.
Q)
0
complete airway obstruction. E
Q)
~ If the patient is unable to cough up the object, give up to 5 back blows between
<ll
0. Fo r management of patients with an inhaled or swallowed object, see the shoulder blades using the heel of the hand (checking for effectiveness ii~
[1:1 between each blow). .~:;:;
<ll
Box 22 (pp. 175- 6). -oc.>
Q)nl
~ continued next page :?!a
174 175
 Box 22. Management of an inhaled or swallowed object*
(cont.)
If complete airway obstruction (see Table 16, p.175) is present:
Call 000 .
Turn patient to their side.
Attempt to clear and open the airway by manually removing the obstruction .
Check for signs of breathing. If no signs of breathing:
Give up to 5 back blows between the shoulder blades using the heel of the
hand (checking for effectiveness between each blow).
Check for signs of breathing. If no signs of breathing:
Give up to 5 chest thrusts (checking for effectiveness between each thrust)
(chest thrusts are identical to cardiac compressions but sharper and harder).
headac he, usually severe and of abrupt onset, or unexplai ned
change in the pattern of headaches
difficulty swallowing.
The F.A.S.T. test is an easy way to recognise the most common signs of
a stroke. The F.A.S.T. test stands for:
Face- check their face. Has their mouth drooped?
Arms-can they lift both arms?
Speech- is their speech slurred? Do they understand you?
Time-is critical. If you see any of these signs, call 000 straight
away.
For management of patients with acute stroke, see Box 23 (below).

If complete obstruction continues : Box 23. Management of acute stroke

Cricothyroidotomy is indicated Cease dental treatment.
- Extend the head back to stretch the neck. Call 000.
- Palpate the cricothyroid ligament. Give oxygen.
- Incise through t he skin and ligament. Maintain airway.
- Maintain airway unti l assistance arrives. Monitor the patient's vital signs until assistance arrives.

(Note: The Heim lich manoeuvre, a technique where abdomi nal thrust is applied to It is difficult to identify if the stroke is haemorrhagic or ischaemic; therefore, aspirin
expel an airway foreign body, is not recommended by the Austra lian Resuscitat ion should not be given.
Council. This is on the basis that it can damage internal organs [pa rticu larly the
liver, spleen and stomach]. may precipitate regurgitation of stomach contents, and
is dangerous for pregnant women.) Seizures
~---------------------------
iii
....c A flow chart for the management of choking can be downloaded from the Australian
Resuscitation Council website <www.resus.org.au/publiC/arc choking.pdf>.
Patients with epilepsy can have seizures during dental treatment or
Q) while in the dentist's office. Not all fitting is epileptic; patients suffering
Q
'tl
syncope (see p.l68), hypoglycaemia (see p.l78), stroke (see p.l 76)
c and cerebral hypoxia from other causes can also present with seizures.
C'il NEUROLOGICAL EMERGENCIES
Young children with fever can have seizures.
~
0 Stroke Seizures can be generalised or partial. There may be warning symptoms
i.Jj
(aura). Seizures can involve a sudden spasm of muscles (producing
c
Q)
The signs of.str~ke and trans ient ischaemic attack (TIA) may be any
rigidity such that the patient falls); jerky movements of the head, arms
Cii one, or combmat10n, of the acute onset of the following :
:Q and legs; or loss of consciousness (which may be associated with noisy
:::J weakness, numbness or paralysis of the face, arm or leg on one or breathing, salivation and urinary incontinence).
<.!J both sides of the body
()
..:::;
difficulty speaking or understanding In status epilepticus, recurrent seizures occur without recovery of
:::J
Q)
0. di zziness, loss of balance or an unexp lained fall consciousness between attacks. This is a medical emergency and the
~ patient should be swiftly transferred to hospital.
Q) loss of vision, or sudden blurred or decreased vision in one or both
~ eyes For management of patients with seizures, see Box 24 (p.l78).

176 177
 Box 24. Management of seizures Table 17. Symptoms of hypoglycaemia
The first priority in the management of a patient having a seizure is to ensure the Adrenergic symptoms Neuroglycopenic symptoms
patient is not in danger in the denta l chai r. (mediated by the sympathetic (due to altered brain function)
If a seizure occurs: nervous system)
Cease dental treatment. pale skin hunger
Protect the patient from falling from the chair and injuri ng themselves on sweating suboptimal intellectual function
surrounding equ ipment, or lift them onto the floor.
shaki ng confusion and inappropriate behaviour
Avoid restraining the patient during the seizure unless it is essential to avoid
palpitations coma
injury.
feel ing of anxiety seizures
Wait until obvious fitting has subsided.
Assess consciousness by tal ki ng to the patient. If possi ble, confirm hypoglycaemia by a blood glucose measurement.
Maintain airway. If a blood glucose monitor is not available, commence management fo r
If there is vomitus, remove it from the mouth and pharynx by high-volume hypoglycaemia. For management of patients with hypoglycaemia, see
suction. Box 25 (below) .
If the patient recovers completely, keep them under observation for at least a
further 30 minutes. Do not allow them to drive themselves home and advise them Box 25. Management of hypoglycaemia
to seek urgent medical review.
If the patient is conscious and cooperative:
If the seizure or loss of consciousness lasts for more than a few minutes, or if Cease dental treatment.
recurrent seizures occur without recovery of consciousness between attacks:
Give 20 to 25 g of glucose to adults or, if not available, a fast-acting glucose-
Call 000.
containing food or drink (eg fruit juice, lemonade , jelly beans, honey). This must
Maintain airway. be followed by a lower glycaem ic load carbohydrate meal (eg sandwich , dri ed
Monitor the patient until assistance arrives. fruit).

ENDOCRINE EMERGENCIES
Endocrine problems can cause a wide range of medical emergencies.
Generally, in the dental setting, an endocrine emergency occurs only in
a patient with a known hi story of an endocrine disorder.
Hypoglycaemia
Hypoglycaemia occurs in patients with diabetes who are treated with
insulin or insulin secretagogues when their blood glucose concentrations
fall below 3.5 rrunoi/L or are low eno ugh to cause symptoms and signs
(see Table 17, p.l79).
Hypoglycaemia can occur at any time of the day or night. Factors that
increase the risk ofhypoglycaemia include inappropriately high doses of
insulin or insulin secretogogue, forgotten or delayed meals, insufficient
carbohydrate (especially if the patient is taking rapid-acting insulins or
insuli n secretogogues), excessive alcohol intake, and unaccustomed or
178 unpl an ned exercise (including delayed effects of exercise).
Keep the patient under observation until they feel recovered. Do not allow them to
drive themselves home and strongly advise they seek medical review.
If the patient is drowsy, uncooperative or unconscious:
Cease dental treatment.
Call 000. ...c
"i
If the patient is unconsci ous, institute basic life support (for 'Basic life support 41
"CI
flow chart', see Figure 5, p.183).
.E
ALLERGIES
Allergies can occur to drugs, food, insect bites, or components of
the environment (eg pollen). Often patients have multiple allergies.
The most common allergies affecting dental management are to
antimicrobials (see p.l8), local anaesthetics (see p.l15) and latex (see
p.180). Always check for a history of allergy before commencing dental
treatment.
Although food allergy is relatively rare, a significant number of
individuals suffer from allergies to food (including fish, nuts, eggs 179
 ~ nd. dairy [in children]) and food substances (eg preservatives). Such
mdtvtduals may present at dental surgeries after exposure en route. and occasionally seen following subcutaneous or intramuscu lar admin-
istration.
Instruct a patient with a known allergy to bring their medication when
If a drug is suspected or established as the cause of urticaria, stopping the
presenting for dental treatment.
drug may be the solution. However, even when this is done, the urticaria
may not immediately cease. Occasionally, external contact with cetiain
Latex allergy substances causes utiicaria (contact urticaria) and removing contact
with the cause (eg latex rubber gloves) may resolve the problem.
Allergy to rubber gloves or rubber dam commonly presents as a delayed
hypersens iti vity contact dermatitis beginning hours to days after Treatment of acute urticaria depends on the severity. For management
exposure. This is associated with allergy to rubber components other of patients with urticaria, see Box 26 (below).
than latex protein (eg accelerants and vulcanising chemicals used in the
manufacturing process). However, if contact dermatitis occurs on the Angioedema
patient's face following dental treatment, the possibility of latex allergy
Acute oedema of the subcutaneous tissue, either as single or multiple
must be considered.
lesions, is typical of angioedema. Lesions are not itchy and may occur
Allergy to latex is rare and usually presents as a localised contact anywhere, but frequently affect the face, periorbital region, lips, tongue,
u1iicaria or dermatitis staJii ng minutes to hours after exposure. For glottis, dorsa offeet and hands, and genitalia. Individual lesions resolve
management of urticaria, see Box 26 (p.l81 ). Occasionally allergy to over hours to several days. Angioedema can be painful or burning, and
latex may present as a life-threatening systemic reaction. If there is a is paJiicularly dramatic when it causes swelling of the lips, eyelids or
severe reaction, treat as for anaphylaxis (see Box 27, p.l82). tongue. Laryngeal involvement can cause airway obstruction.
If a patient, dentist or staff member repmis an immediate hypersensitivity Angioedematous lesions are common in acute and chronic forms of
to latex, they should be referred to a clinical immunologist to confirm urticaria. Drug causation should be considered, particularly in cases of
their cond iti on. In patients with a confirmed allergy, dental treatment acute utiicaria and angioedema. Management is the same as for urticaria
shou ld be performed only in a latex-free environment. An affected (see Box 26, below). Systemic corticosteroids may be indicated if the
person shou ld be encouraged to wear an alert bracelet or necklace and angioedema is not controlled by antihistamines.
if th ere is a significant risk of exposure, to carry adrenaline in case of~
sc
Qj
severe anaphy lactic reaction.
Box 26. Management of urticaria
c For mild urticaria:
"C
c Types of allergic reactions Cease dental treatment.
ctl
Remove and/or cease administration of allergen.
~ Urticaria
0 Give an oral antihistamine. Use a less-sedating antihistamine during the day
Ui (eg cetirizine, desloratadine, fexofenadine, loratadine). If response is poor, add
<lJ Urticaria is characteri sed by transient erythematous and/or oedematous
c a sedating antihistamine at night (eg cyproheptadine, dexchlorpheniramine,
swell in~ of the dermi s or subcutaneous tissues (angioedema, see p.l81 ). promethazine).
Qi
:2 The leswns are always transient, persisting from a few minutes to
:::J
CD 24 hours. S~perficial.swellin gs tend to be itchy, while deeper swellings Refer patients with extensive urticaria, or severe urticaria involving eyelids and lips
(.) ma~ be pamful. It 1s rarely poss ible to establish the diagnosis or for urgent medical attention.
<=>
:::J aetwlogy based solely on the appea rance of the lesions. If there is associated hypotension and evidence of anaphylaxis:
<lJ
0.. Cease dental treatment.
~ Many drug-associated utiicarial eruptions begin towards the end of
<lJ Remove and/or cease administration of allergen .
..c an antibiotic course (day 4 to 10 after sta rting therapy). Some may be
1-
acute and associated with anaphyla xis (see p.l82). Acute itch and/or Call 000.

180 urticaria occurring alone is more often seen after oral administration Give intramuscular injection of adrenaline (see Box 27, p.182).
181
 Box 27. Management of anaphylactic and anaphylactoid is defined simply as 'a serious allergic reaction that is rapid in onset and
reactions may cause death '.*
Cease dental treatment. For management of patients with an anaphylactic or anaphylactoid
Remove and/or cease administration of allergen. reaction, see Box 27 (p.l82).
Assess severity of reaction .
Call 000. Figure 5. Basic life support flow chart
Give intramuscular injection of adrenaline:

adrenaline (adult and child) 0.01 mgJkg up to 0.5 mg (= 0.5 mL of

1:1000 solution) IM into the anterolateral thigh, tongue or floor of mouth

OR Dangers?
adrenaline 300 micrograms (child 10 to 20 kg: 150 micrograms) IM, via
preloaded autoinjector, into the anterolateral thigh.*

Lay the patient flat. Responsive?

Give high-flow oxygen.
Be prepared to commence cardiopu lmonary resuscitation (CPR) (for 'Basic life
support flow chart', see Figure 5, p.183). Send for help
Repeat adrena line every 3 to 5 minutes until response or assistance arrives.
The patient must be taken to an emergency department.

All records must be correctly annotated as to the allergen and response. Request
Open Airway
a copy of the follow-up opinion of the specialist allergist before continuing dental
treatment. Advise the patient to wear appropriate medical identification (eg Medic
Alert). Normal Breathing?
* Preloaded autoinjectors contain 300 micrograms in 0.3 ml (for use in an adult) and
150 micrograms 1n 0.3 ml (for use in a child 10 to 20 kg).
A widely available and more detailed wall chart on the recognition and initial emergency Start CPR
management of anaphylactic reactions is available from the Australian Prescriber website 30 compressions . 2 breaths
1! umvi/Jmg /~;nable to perform resc1 e hren/11s { onf1r1ue clwsl compressions
<www.australianprescriber.com/magazine/34/4/artid/1210>.
~
Anaphylactic and anaphylactoid reactions
Anaphylactic (lgE-mediated) and anaphylactoid (pseudoallergic)
reactions have overlapping clinical features. Anaphylactic and
m Attach Defibrillator (AED)
as soon as available and follow its prompts
4)
'C

=
C/)
4)

anaphylactoid reactions usuall y appear within minutes of parenteral or

Continue CPR until responsiveness or '<:)
c
mucosal exposure to a drug, and around 30 minutes to hours after drug
ingestion.
normal breathing return ~
4)
E
4)
Anaphylaxis is a severe, immediate-type, generalised hypersensitivity The flow chart can be downloaded from the Australian Resuscitation Council website

reaction affecting multiple organ systems, characterised at its most <www.resus.org.au/public/arc _basic _life_support. pdf> . i6~
.5:!:;::;
severe by bronchospasm, upper airway obstruction and hypotension. It *Sampson HA, Munoz-Furlong A, Campbell RL, Adkinson NF, Jr. , Bock SA, Branum A, et al.
'g(,)
Q)I'CI
Second symposium on the definition and management of anaphylaxis: summary report-
Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis
:!:li
Network symposium. J Al lergy Clin lmmunol2006;117(2):391-7.
182 183
 OCULAR EMERGENCIES
Patients' eyes are vulnerable to injury during dental treatment. Injuries
may also occur to members of the dental team.
Prevention of injury by wearing special protective glasses, particularly
during the use of chemicals and rotary instruments, is essential for both
patients and members of the dental team. Chemicals and instruments of
any form should not be passed over the patient's face.
Eye injuries may be from:
chemicals (eg endodontic irrigating solutions), particularly alkali
solutions
foreign bodies (eg calculus, fragments offillings)
penetrating objects (eg drills and endodontic instruments).
Swift and appropriate emergency treatment can minimise the extent of
injury, pain and suffering, and the risk of blindness.
An extensive resource with illustrations of the various conditions is
the Eye Emergency Manual, published by the NSW Department of
Health. It is available at <www.health.nsw.gov.au/resources/gmct/
ophthalmology/eye_ manual_ pdf.asp>.
Chemical eye injuries
Caustic solutions used in dental treatments can cause severe chemical
eye injuries. In particular, alkali solutions cause liquefactive necrosis
as they keep burning the sensitive ocular tissues. For management of
patients with chemical eye injuries, see Box 28 (below) .
Box 28. Management of chemical eye injuries
Cease dental treatment.
Immediately irrigate the eye with copious amounts of water.
Hold the eyelids open.
Remove contact lens if present.
Continue irrigation with water, poured from a cup or beaker or from a tap, for at
least 15 minutes.
Do not use an eyecup as a continuous flow of water over the eye is required.
If weak chemical injury and minor eye irritation are present, organise medical
review for that day.
If caustic chemical injury and/or a marked inflammatory response are present,
dial 000 and continue irrigation until assistance arrives.
Keep the chemicals to show to the medical team.
184
Foreign bodies lodged on the surface of the eye
Foreign bodies may lodge on the surface of the eye and be irritating. For
management of patients with foreign bodies lodged on the surface of the
eye, see Box 29 (below).
Box 29. Management of foreign bodies lodged on the
surface of the eye
Cease dental treatment.
Immediately irrigate the eye with copious amounts of water.
Hold the eyelids open.
Do not touch the eye surface.
Do not attempt to remove the foreign body except by irrigating with water.
Check after 5 minutes to see if the foreign body is gone; if not, continue
irrigation for up to 15 minutes.
If the foreign body is gone, organise prompt medical review.
If the foreign body is still present, transfer the patient to an emergency
department.
Penetrating eye injuries
Sharp objects may either be dropped or be spun off into the unprotected
eye. For management of patients with penetrating eye injuries, see
Box 30 (below).
Box 30. Management of penetrating eye injuries
Cease dental treatment.
Dial 000.
Do not attempt to pull out the penetrating object from the eye.
Do not irrigate the eye.
Prevent the patient from rubbing the eye.
Cover the eye with an eye shield, or use the base of a polystyrene cup and tape
it on so it rests on the bony rim of the orbit.
Keep the patient and yourself calm until assistance arrives.
Keep the broken part (or similar instrument) to show the medical team.
The patient must be taken to an emergency department.
185
 Temporary paralysis of the periocular muscles
The eye is normally protected by the blink reflex, which provides
lubrication. Temporary paralysis of the periocular muscles may occur
if a local anaesthetic from a misdirected mandibular block or posterior
maxillary infiltration enters the parotid gland. It will then diffuse to and
paralyse the branches of the seventh cranial (facial) nerve .
Photo 6 (below) shows a patient with right-sided facial palsy.
For management of patients with temporary paralysis of the periocular
muscles, see Box 31 (p.l87).
Photo 6. Patient with right-sided facial palsy
Box 31. Management of temporary paralysis of the
periocular muscles
Cease the injection and any dental treatment.
Recognise the problem by asking the patient to close their eyelids.
Explain what has happened to the patient and reassure them that this will soon
resolve.
Tell the patient not to rub their eyes.
Cover the eye with an eye patch.
Keep the patient under observation until there is some return of blinkirg. This
usually occurs within the hour, depending on the dose and strength of the local
anaesthetic used.
The patient should not drive that day and shou ld be escorted home by a
responsible adult.
Check on the patient by phone later t hat day. If the patient has not fu l~
recovered within 12 hours, medical review is required.

Box 32. Management of unilateral blindness

Cease dental treatment.
Dial 000.
If the patient is unconscious, institute basic life support (for 'Basic life support
flow chart', see Figure 5, p.183).
The patient must be taken to an emergency department.

EMERGENCY DRUGS AND EQUIPMENT

The patient had a right posterior superior infiltration for restoration of the maxillary There is conflicting advice from various organisations and texts as to
molars. Note the inability to close the right eye and right-side lips. The left side is the extent of emergency equipment and drugs that a dentist should have
functioning normally. Parental permission was obtained for use of this image. available to assist in the management of medical emergencies in the
dental practice . It can range from virtually no equipment to a full
emergency doctor 's bag. One of the difficulties is that, usually and
Unilateral blindness hopefully, medical emergencies in dental surgeries are uncommon and
Rare cases of unilateral blindness have been reported following there is a risk that drugs will expire before use. Expired drugs can be
posterior local anaesthetic injections that contain a vasoconstrictor. The easily overlooked and can be expensive to replace.
mechanism for this is intra-arteria l injection of the vasoconstrictor with All dentists have a professional
spasm of the optic artery and rel ated blood vessels. The patient may lose obligation to ensure that they are
Generally, the longer the
consciousness. Patients usually spontaneously fully recover their vision. time before assistance can
properly trained and are up to date reasonably be expected to
For management of patients with unilateral blindness, see Box 32 with emergency management. They arrive, the greater the need for
(p.l87). should also ensure that all staff staff training and equipment.
are correctly trained in emergency
management and have maintained their competence. If dental assistants 187
186
 have not been through a formal training program, they should have, at
least, a basic level first aid certificate.
There should be an established plan for obtaining medical assistance.
The emergency phone number (000) for paramedical services should
be prominently placed as well as the phone number of the nearest
available medical facility. The reasonable time it takes for medical
assistance to anive must be known. For example, a dental clinic that is
part of a wider health clinic with medical practitioners and nurses could
reasonably expect assistance within a matter of minutes whereas an
isolated suburban or rural practice could reasonably expe~t a response
time of more than 30 minutes.
Drugs and equipment required by dentists for
emergencies
Dentists should carefully consider their emergency equipment needs
and staff training, relevant to their location, patient population and
practice type.
The minimum requirements for emergencies in the dental surgery are
oxygen, a disposable airway and adrenaline:
Oxygen: All surgeries should have an oxygen so urce that can
be easil y transported to the patient. The simplest and safest way
of administering oxygen to a patient is via a bag/mask/valve
supplemented with oxygen at 6 to 8 Llminute. Oxygen-powered
resuscitators are not recommended, as there is a risk of gaseous
'15
....
c extension of the stomach resulting in regurgitation. Rel ative
Cl)
analgesia machines with the oxygen override are not an efficient
c
means of administering oxygen, and do not allow ventilation of a
"C
c '15
l1l patient who is not breathing.
~ Airway: Simple disposable plastic airways secure the oral airway,
0 and facilitate mouth-to-mouth resuscitation or ventilation with
oxygen.
Adrenaline: There must be a sufficient quantity of adrenaline in Further reading
the surgery to give 2 doses for the management of anaphylaxis.
Adrenaline is available in ampoules (1:1000 and 1:10000)
and pre loaded auto injectors (1: 1000 and 1:2000). A pre loaded
auto injector is preferred to a vial, since the latter needs to be
drawn up into a syringe.
188
Drugs considered desirable in the dental surgery are:
Glucose: Patients exhibiting signs of hypoglycaemia require a
readily available glucose-containing food (eg fruit juice, honey)
or pure glucose (eg glucose gel or tablets).
Glyceryl trinitrate spray: Patients with a history of angina
usuall y have their glyceryl trinitrate tablets or spray with them.
However, the dental emergency kit could include glyceryl
trinitrate spray (which has a much longer shelflife than the
tablets), in case the patient does not have their glyceryl trinitrate.
Short-acting bronchodilator (eg salbutamol) inhaler and spacer:
Patients with asthma usually have their inhaler with them ; however,
the dentist could have a short-acting bronchodilator inhaler
available for a patient who has not brought their own inhaler.
Aspirin: Aspirin may be required for a patient with suspected
acute myocardial infarction.
Medical equipment items considered desirable in the dental surgery,
depending on the nature of the practice, are:
A blood pressure monitor for assessment of cardiovascular
patients and collapsed patients.
A blood glucose monitor for assessment of patients with
diabetes.
A pulse oximeter for measuring oxyhaemoglobin saturation;
essential for procedures performed under intravenous sedation
and desirable for procedures performed under oral or inhalational
sedation.
Laryngeal airways for airway protection and to minimise the
risk of gastric insufflation. They also make ventilating the patient
easier, allowing any member of staff to assist in intermittent
....
positive pressure ventilation. c
Cl)
An automated external defibrillator for management of patients
"C
with cardiac arrest. .5
VI
Cl)
'()
c
Guidelines at The Australian Resuscitation Council Online ~
Cl)
< http://www.resus.org.au/>.
E
Cl)
'15~
.s::;::;
"CCJ
Cl)t1l
~li
189
Management of dental
problems for medical
practitioners

Patients with dental problems commonly present first to a medical

practitioner and should be redirected to a dentist, pa11icularly if
the presentation relates to issues arising from dental treatment ( eg
complications after tooth extraction).
This topic covers the initial management of common dental problems
primarily for medical practitioners working in rural or remote areas,
where access to timely dental care may be difficult. This is not an
issue in metropolitan centres where appropriate general and specialist
emergency dental services are available.
Problems of access to dental care, or lack of contactability of a dentist
after-hours, in rural or remote areas should be addressed directly or, if
there are difficulties, via the appropriate professional organisations.*

ACUTE DENTAL PAIN

Acute pain in the orofacial region can originate from many sources,
only some of which are dental. The nature of the dental pain is often
a clue to the diagnosis (see Table 18, pp.l92- 3). In all instances, the
sooner a dental opinion is sought, the better. If a dental opinion is not
immediately available, a panoramic radiograph (commonly known as
an orthopantomogram [OPG]) can be helpful to exclude some serious
pathologies (eg gross caries, jaw fractures, and jaw lesions such as
cysts).
If there is facial swelling and the patient looks unwell, hospital
admission for intravenous antibiotic therapy may be needed. This is one
of the few instances when a dental condition can be life-threatening due
to airway compromise.
continued p.194

* McCullough M. Dental antibiotics [author comment on letter to the editor] . Australian

Prescriber 2010;33(6): 1689. <www.australianprescriber.com/ magazine/33/6/ 167/ 170 >
191

~ Therapeutic Guidelines: Oral and Dental
Table 18. A guide to diagnosing acute dental pain and suggestions for initial management by medical
practitioners
Nature of pain
short and sharp pain , disappears
on removal of the stimulus,
sensitive to hot/cold/ sweet sti muli
sharp and severe pain, becoming
a dull throbbing ache that persists
after removal of the stimulu s,
sensitive to hot/cold/sweet stimuli
dull ache, throbbing, may be
sore to bite on, but not sensitive
to hot/cold/sweet stimuli
Table 18. A guide to diagnosing acute dental pain and suggestions for initial management by medical
practitioners (cont.)
tender to pressure and biting
tender/painful swelling in the
region of recent toothache
pain worsens when the
head is ti lted forwards
pain worsening 1 to 4 days
after tooth extraction
Adapted from Kingan A. Solving dental problems in general practice. Aust Fam Physician 2009;38(4):211-6. 2011 Australian Family Physician. Reprodu ced with
permission from The Royal Australian College of General Practitioners. Text and images are copyright of Australian Family Physician . Permission to reproduce must be
sought from the publisher, The Roya l Australian College of General Practitioners.
p
c.o
w Management of dental problems
for medical practitioners
Ukely cause Suggestions for initial management
of pain by medical practitioners
reversible pulpitis advise patient to avoid foods that provoke pain
analgesics are NOT indicated
antibiotics are NOT indicated
cover any obvious cavity with an inert material
(eg chewing gum)
irreversible pulpitis advise patient to avoid foods that provoke pain
analgesics are indicated, especially
nonsteroidal anti-inflamm atory drugs (NSAIDs)
if the patient can use them
antibiotics are NOT indicated
cover any obvious cavity with an inert material
(eg chewing gum )
infiltrat e a local anaesthetic into the soft ti ssue
adjacent to the root apex of t he affected tooth
fo r temporary re lief if symptoms are severe
infected root canal analgesics are indicated, especial ly NSAIDs if
system with acute the patient can use them
apical periodontitis
antibiotics are NOT indicated
early dental abscess antibiotics may be indicated (see 'Acute
odontogenic infections', p.61)
dental abscess analgesics are indicated, especially NSAIDs if
the patient can use them
antibiotics may be indicated (see 'Acute
odontogenic infections', p.61)
if swelling causing dysphagia or dyspnoea
is present, admit to hospital for intravenous
antibiotic therapy and appropriate surgical
management
pain originating from antibiotics, inhalations and nasal sprays or
maxillary sinus {pus,! solutions are usually effective fo r maxi llary
exudate moves in sinusitis (see Therapeutic Guidelines:
sinus) Respiratory for more information)
alveolar osteitis (dry antibiotics are NOT indicated
socket) (see p.69)
flush socket with warm sterile saline until all
debris is removed and no debris is produced
from the socket
insert dressi ng, if available
"
Ongoing dental care
advi se patient to see a dentist as
soon as possible
simple restoration is usual ly
sufficient
advise pat ient to see a dentist as
soon as possible
either endodontic (root canal)
treatment or extraction is usually
needed
advise patient t o see a dentist
urgently
either endodontic (root canal)
treatment or extraction is needed
continued next page
advise patient t o see a dentist
urgently
either endodontic (root canal)
treatment or extraction is needed
advise patient to see a dentist
urgently
either endodontic (root canal)
treatment or extraction is needed
close monitoring of the airway is
needed-if cellulitis develops, it
can be life-threatening
advise patient to see the dentist
or oral surgeon who performed
the extraction urgently
socket irrigation and dressing are
needed
 Severe pain occurring a few days after a tooth extraction may be
alveolar osteitis (dry socket) (see p.69) and, once recognised, it is easily
managed with local meas ures . Alveolar osteitis is not an infection and
does not require antibiotic therapy.
Vertically cracked or fractured teeth can be extremely difficult to
diagnose, especially as sym ptoms may be intermittent and very acute
and imag ing is often unhelpful.
Dental pain can mimic trigeminal neuralgia and vice versa (see
'Trigeminal neuralgia', p. l5 8).
A BROKEN TOOTH OR FILLING, OR A LOST FILLING
Teeth, fillings and other fo rms of restorations (eg crowns, veneers)
may break for various reasons, with trauma the most common cause.
The trauma may be loca li sed to the affected tooth or restoration, and
may occur during normal functioning (eg while eating) or followin g an
accident. Restorations may be lost due to trauma, or furth er decay in the
tooth that undermines the restoration leaving it unsupported.
A broken tooth or restoration, or a lost restoration, are rarely urgent
problems so the simplest manage ment fo r a medical practitioner is to
refer the patient to a dentist. If the patient is experiencing pain, advise
them to see a dentist as soon as possible. In most cases, the pain is due to
reversible pulpiti s (see Ta ble J 8, p.192) as a result of exposed dentine.
Dental treatment is required to prevent the prob lem progressing to the
more serious conditions of irreversible pulpitis, an infected root canal
system or an abscess- all of which require more comprehensive and
urgent management.
If the tooth fracture or lost restoration has resulted in exposure of the
dental pulp, the patient should be seen by a dentist as soon as possible
(preferably within 24 hours). To assess if the pulp has been exposed,
visuall y exam ine the tooth. If red soft tissue can be seen in the area of
fracture or within a cavity, the pulp has been exposed. Typically, this
tissue is very sensitive to touch and the patient may be avo iding any
contact of this tooth with the tongue, food, drink and even cold air.
The exposed tissue may bleed or have a blood clot over it indicating
previous bl eeding.
TOOTH AVULSION (KNOCKED-OUT TOOTH)
Avulsion of a tooth is defined as the complete disarticulation of the
tooth from its bone socket. In most cases, the tooth is knocked
194
completely out of th e mouth, but occasionally it may sti ll be in the
mouth . Trauma is the most common cause of avulsed teeth, es pecially
due to phys ical violence, fa lls or sporting injuries.
Initial management of all patients with trauma to their teeth should
include an assessment for other injuries (primary trauma screen),
especially head and neck inj uri es if the patient lost consciousness
following the acc ident.
It is impmiant to assess if the tooth has been av ulsed or if it is just
not easily visible. Some teeth may have been intruded (pushed into the
alveolar bone) or the tooth root may have fractured so that only the
crown has been lost. These problems must be assessed via radiographs
so referral to a dentist is essential.
If a tooth appears to be missing (via visual examination ofthe mouth)
and has not been found at the site of the accident, it is essential to assess
if the patient has inhaled the tooth-this requires chest imaging. For
management of an inhaled or swallowed object, see p.l74.
If the av ul sed tooth has been retrieved, it should be replanted into its
socket as soon as possible. Teeth replanted within 15 minutes have the
best chance of healing without complications. However, many people
are reluctant to replant teeth or do not
Time is of the utmost
know how to do it. In such situations,
importance when managing
the best approach is to fully submerge avu lsed teeth.
the tooth in milk until it can be - - - - - - - - - - -
replanted. Any type of mil k is suitab le as long as it is not warmer than
37 C. The tooth should be hand led very carefully-it is best to hold the
tooth by the crown so as not to damage the root. Do not scrub or rub the
tooth at all. Milk is useful as the cells of the periodontal ligament, which
is attached to the root, can survive in milk fo r up to 6 hours. Survival of
these cells is essential for healing of the ligament following replantation.
If they survive, the tooth has a reduced chance of undergoing replacement
root resorption and can remain in the mouth for many years. It is
recommended that all first aid kits, especially those for spmiing clubs
and schools, contain a small container of long-life milk.
If milk is not available, saliva, saline
Do not use water to rinse or
or plastic wrap can be used, but the store the avulsed tooth.
periodontal ligament cells typically
last for only an hour at most under these conditions. If plastic wrap
is used, ask the patient to spit some saliva (which may contain blood
as we ll, which is desirable) into the plastic before wrapping the tooth.
Water shou ld be avoided at all times when managing an avulsed tooth as
the osmotic effect of water causes cell death in the periodontal ligament. 195
 After replanting the tooth, splinting is important to hold it in a stable
position- referral to a dentist should be arranged urgently. A small
piece of aluminium foil can be cut and shaped over the teeth to help
hold the avulsed tooth in its pos ition in the mouth until the patie nt can
see a dentist for splinting.
Assess the patient's tetanus immunisation status and g ive a booster
if there is any doubt about their status (see Therapeutic Guidelines:
Antibiotic for more information). Antibiotics are also recommended
as they can help reduce healing complications, such as inflammatory
root resorption, which is associated with th e presence of bacteria in the
root canal system. Tetracyclines are preferred as they also have some
Table 19 (below) summarises the initial management of an av ulsed
tooth.
Table 19. The 'dos and don'ts' of managing an avulsed tooth
Do
Check for other injuries, especially head and neck injuries if loss of consciousness has
occurred .
Only ri nse the tooth under milk or sal ine if it is dirty.
Replant secondary (adult) teeth as soon as possible.
Refer to a dentist urgently.

direct antiresorptive acti vity. Alternatively, amoxyc illin can be given if
tetracyclines are contraindicated, such as in children 8 years of age or
less. Use:
1 doxycycline 200 mg (child more than 8 years: 5 mg/kg up to
200 mg) orally, for the firs t dose, then 100 mg (child more than
Use a temporary splint (eg aluminium foi l) to hold th e replanted tooth in place until
the patient can see a dentist.
Store the tooth in milk if it cannot be replanted immed iately.
Store the t ooth in saline, saliva or plastic wrap if milk is not availa ble.
Check the patient's tetanus imm unisation status and give a booster if required.

8 years: 2.5 mgl kg up to 100 mg) orally, daily for 7 days Prescribe antibiotics.

OR Do not

2 amoxycillin 1 g (child: 25 mg/kg up to 1 g) orally,for the.first Do not scrape or handle th e root of th e tooth.
dose, then 500 mg (ch ild: 12.5 mglkg up to 500 mg) orally, Do not replant primary (baby) teet h.
8-hourly for 7 days. Do not delay seeking dental treatment.

Do not let tooth dry out.

Chlorhexidine mouthwashes are recommended after replantation while
Do not rinse or store the tooth in water.
the tooth is sp linted. Use :
i5
.... chlorhexidine 0.2% mouthwash 10 mL rinsed in the mouth for
c
(!) 1 minute, 8- to 12-hourly* MAXILLOFACIAL TRAUMA
c or chlorhexidine 0.12% mouthwash 15 mL rinsed in the mouth for
'C
c 1 minute, 8- to 12-hourly. * Solitary injuries to the mandible and zygomatic complex are relatively
(1)
common, and often patients present to a medical practice looking
~ Primary (baby) teeth should not be
Primary (baby) teeth should not reasonably we ll following an injury. To exclude other injuries, all
0 replanted or repositioned, as this be replanted or repositioned.
Ui patients should have a primary trauma screen on presentation and a
is likel y to damage th e secondary
<J.)
c secondary trauma screen in hospital. It is important to confirm there
(adu lt) tooth that is de ve loping in the bone. Do not repl ant teeth in
Qj has been no loss of consciousness, however transient, to exclude the
~
children less than 5 years of age, and be careful to assess avu lsed
possibility of a head injury. If a patient is not conscious and there is
:J teeth in those aged 5 yea rs or more to determine if they are primary
<.9 evidence of maxillofacial trauma, ensure a patent airway by pulling the
() or secondary teeth. In general, primary teeth are much smaller in all
.;:::; mandible forward. This is crucial as patients have died from airway
:J dimensions than secondary teeth, but secondary teeth in 5- to 8-year-
<J.) compromise.
0.. old children have shoti roots w ith large crowns as the roots have not
~ yet full y developed. Generally, preliminary measures include commencing intravenous
<J.)
..c fluid therapy and ben zy lpenicillin, and confirming the patient's
1-
*With prolonged use (more than a few days) , chlorhexidine may cause a superficial tetanus immunisation status is up-to-date (see Therapeutic Guidelines:
196 discolouration of the teeth and fillings (see p.44 for more information). Antibiotic for more information). If the teeth occlude norm ally after 197
 InJury, surgical intervention may not be necessary but management Figure 6. Schematic diagram of the tooth socket and
of facial trauma always requires specialist referral at the earliest possible sites of persistent bleeding after tooth
opportunity. extraction

COMPLICATIONS AFTER TOOTH EXTRACTION

The person responsible for the management of complications after
tongue
a tooth extraction is the dentist or oral surgeon who performed the
extraction. Patients should have been provided with their after-hours
contact details. As a first step, advise the patient to contact the dentist or
oral surgeon. If necessary, this can be done by the medical staff.

Bleeding
The patient's medical and medication history should be checked.
Antiplatelet therapy (eg aspirin, clopidogrel) and warfarin in patients
with an international normalised ratio (INR) of less than 4 should fioor of mouth
not be ceased before a tooth extraction. For more information, see 1. mucosa nea r the floor of the mouth-very common bleeding site
'Potential problems with anticoagulant and antiplatelet drugs in patients 2. subgingival region-com mon bleed ing site
undergoin g dentoalveo lar surgery (including extractions)' (p.138). 3. socket wall-uncommon bleedi ng site
4. apica l region-u ncommon bleeding site
If bleeding does occur after the extraction, apply firm pressure at the
site ofthe bleed. This is sufficient to stop the bleeding in most instances,
Swelling normally worsens in the first 48 hours after extraction and
even in patients taking antiplatelet therapy or warfarin. A suggested
may take up to 3 days to reach its maximum. Antibiotics are usuall y
management protocol is shown in Table 20 (p.200). It is often assumed
not required unless there is clearly demonstrable pus and spreading
that persistent bleeding occurs from the base and side of the tooth socket.
infection. Management is with local measures (eg external application
Howeve r, it is more commonly caused by laceration to the mucosa near
of a cold compress intermittently for up to 20 minutes at a time during the
:Br:: the floor of the mouth or the tongue, or it can occur from the gingiva
first 24 hours, followed by mouth rinsing with warm saline), analgesics
Q) at the alveolar crest (see Figure 6, p.l99). These locations should be
0 (see p.132) and reass urance. The dentist or oral surgeon who performed (/)
assessed so treatment can be directed to th e site of the bleeding. E
"C
r:: the extraction should be contacted for advice on management. The Q)
ra There are rare cases when previously undiagnosed blood dyscrasias, possibility of a compromised airway must always be considered, but ::c
'i
... such as von Willebrand disease, have become evident following a close monitoring is usually all that is needed. e
Q.~
0 surgical procedure, and thi s possibility should always be kept in mind . -Q)
C'ilr::
Ui ~0
<lJ
c MISCELLANEOUS OROFACIAL SYMPTOMS Q):.;:i
Qj Pain and swelling "C:.;:i
,._Q
:2 There are a number of dental problems for which patients may present
0~
:::J Pain and swelling are to be expected after most oral surgical procedures, to their medical practitioner (see Table 21, p.201). Some of these may +'Q.
0
u
.;:::;
and are usuall y due to infl am mation from trauma, rather than infection. indicate a more serious underlying disease. A dental opinion should be ~'i
:::J Eve n after difficult third molar (wisdom teeth) extractions, infection obtained as soon as possible. E.!:)
<lJ ~"C
a. is uncommon and has an incidence of 2% to 5%. Pain increasing in raQl
~ severity 1 to 4 days after a tooth extraction may be alveolar osteitis (dry r::E
<lJ C'ii '-
.c socket) (see p.69). :2:.E!
t-

198 199
 Table 20. Management of the bleeding tooth socket Table 21. Common dental problems for which patients may
present to their medical practitioner
Initial screen and management (can be conducted by phone)
Check if the dentist or oral surgeon who performed the extraction has been Presenting Comments
contacted . If not, this should be done.
problem
Advise the patient to:
apprehensive the medical practitioner must liaise and work with the
- sit calm ly and upright patients-the dentist
'dental phobic'
- place a small gauze square or small clean handkerchief over the socket and bite
hard for 15 min utes. bleeding gums (may by far the most cornrnon cause is periodonta l disease (see
Advise the patient not to: be spontaneous) p.55)

- keep rinsi ng or spitting leukaernias and other malignant conditions are possible
but unusual
- use paper tissues as these can fragment
some drugs can alter the appearance of the gingivae (eg
- take the gauze out to look at t he bleeding site. phenytoin, cyclosporin)
Reassure the patient-in most cases, this regimen stops any bleed ing. consultation with the patient's dentist and/or periodontist
is required
Examination if bleeding does not resolve with initial management
sore areas beneath examine the sore area to assess the possibility of
Check the patient's medical and medication history for bleeding tendencies. dentures malignancy
Evaluate the need for sedation if the patient is agitated (see p.121). the denture may need simple adjustment; refer to a dentist
Evaluate if the patient is actively bleeding, or if there is just excessive bloodstained annua l oral exam ination needed (wherever possible by a
saliva. dentist)
If th e patient is actively bleeding, estimate blood loss from the number of gauze paraesthesia simple causes are rare if no recent dental or su rgical
squares used (saturated 10 em x 10 em gauze square = 5 ml of blood loss). If procedure has been done
more than 50 to 100 ml of blood has been lost, undertake the local haemostatic
procedure below. causes include malignancy, multiple sclerosis

diagnosis may be difficult

Local haemostatic procedure
temporom andibular symptoms include jaw clicking, pain and locking
Use a good light to examine the patient's mouth to identify the bleeding site (see disorders
Figure 6, p.199). If there is brisk bleeding, this is usually from torn soft tissues rather more common in females
than the socket. management is usually conservative; refer to a dentist (see (/)

Infi ltrate a loca l anaesthetic containing a vasoconstrictor as close as possible to the also Temporomandibular disorders' , p.95) E
Q)
bleeding site.
almost pathognomonic of a jaw fracture (see 'Maxillofacial :c
Pack the socket with a haemostatic agent and sutu re at the bleed ing point.
deranged occlusion
(teeth not biting trauma ', p.197) e
o.~e
together normally) -G)
If this procedure cannot be undertaken, or the patient has extensive laceration or give antibiotics, assess tetanus immunisation status ('tis:;
bleeding, arrange transport to an emergency department.
refer to a specialist 'l:o
Gl :P
Adapted from Kingon A. Solving dental problems in general practice. Aust Fam Physician "Cti
2009;38(4):211- 6. 2011 Australian Family Physician. Reproduced with permission from The '0~
Royal Australian College of General Practitioners. Text and images are copyright of Australian +'0.

j
Family Physician. Permission to reproduce must be sought from the publisher, The Royal
Australian College of General Practitioners.

200 2 1
Appendix 1.
Drugs and sport
Sporting authorities prohibit the use of certain drugs by competitors in
sporting events. Some of the drugs prohibited in sport may be prescribed
or administered by dentists for dental treatment. If drugs are required
to treat an elite athlete, care must be taken regarding which drugs are
used or prescribed. Most elite athletes are aware of the requirements for
their particular sport.
Each national sporting federation or association has an antidoping
policy, which includes a list of prohibited substances. Most sporting
bodies reference the World Anti-Doping Code's prohibited list (see
<www. wad a -am a. org/ en/Science-Medicine/Prohibited-List/>),
which is maintained by the World Anti-Doping Agency (WADA).
The prohibited list includes categories and specific substances that
are prohibited in sport. A substance that is not specifically listed may
nonetheless be banned, as it may belong to a category on the list, or it
may contain a derivative of a prohibited substance. The list is reviewed
and updated annually. The list is divided into substances and methods
that are prohibited at all times (in and out of competitions), and those
that are prohibited during competitions only.
Drug groups on the prohibited list for all sports include:
anabolic agents (eg testosterone)
peptide hormones, growth factors and related substances (eg
growth hormone)
beta2 agonists (except salbutamol, eformoterol and salmeterol
when taken by inhalation in accordance with the manufacturers'
recommended therapeutic regimen)
hormone antagonists and modulators (eg tamoxifen) ~
0
diuretics and other masking agents (eg frusemide, thiazides, Q.
Ill
probenecid) 'C
c(ll
stimulants (eg amphetamines)
~
narcotics (eg morphine, oxycodone)
cannabinoids (eg marijuana) .
::s
Q
glucocorticoids (eg prednisolone).
203
 Inf~rmation 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 WADA,
<www.wada-ama.org/en>. '
Appendix 2.
Dental procedures and
drugs 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 '0.0
(ie the fourth, fifth and sixth months) of pregnancy. Elective procedures c
requiring general anaesthesia or intravenous sedation should be deferred
:s
Cl)

until after the baby is born and, preferably, until after breastfeeding has ~1/)
ceased. If the patient is unsure if she is pregnant, the decision about
whether to proceed with the procedure should be deferred until this is
known.
..
Cll
Cl)
.Q
'tl
c
If intraoral radiographs are necessary for assessment or diagnosis of Cll
>.
infection or trawna, or for treatment of these conditions, there is no u
c
reason, on radiation protection grounds, to defer them. The Australian Cll
c
Radiation Protection and Nuclear Safety Agency (ARPANSA)
guidelines* state that there are no contraindications to taking intraoral ..
~
c.
radiographs during pregnancy; however, provision of a leaded drape is '0.0
recommended when the X-ray beam is directed downwards towards the c
.:::
:I
patient's trunk (eg when taking occlusal views of the maxilla). 'tl

~
PREGNANCY AND THE USE OF DRUGS ..
:I
'tl
'tl
A drug can have more than one harmful effect on the fetus. Individual c
Cll
effects depend on the time offetal exposure to the drug.
During the first 2 weeks after fe1iilisation and before full implantation, .1/)
Cl)
:I
'tl
the embryo is thought to be resistant to any teratogenic effects of drugs. Ql
This is because there is no direct communication between maternal and
e
embryonic tissue until after the placenta starts to form .
The critical period for teratogenic effects is during organogene is.
This stmis at about 17 days after conception and is complete by 60 lo
-~
c.

~
204 Radiation protection in dentistry: Rad iation protection series No. 10. Au stra lian Racll li n
Protection and Nuclear Safety Agency; December 2005. ?0
 70 days. Exposure to certain drugs during this period (17 to 70 days)
can cause major birth defects .
Some drugs can interfere with functional development of organ systems
~eg central nervous system,integumentary system, cardiovascular system)
m the second and third trimesters and produce serious consequences.
A woman may not be aware of her pregnancy until after the early stages
o.f orga~ogenesis. For this reason, drugs in the most severe category of
nsk (X m the Australian categorisation, p.208) should not be prescribed
to a woman of childbearing potential, unless a pregnancy test is negative
and she is using an effective method of contraception.
There are several conditions, however, in which long-term medication
may be necessary in a woman of childbearing potential despite known
h.arm~ of the drugs. At the time of initial prescribing in any such
sJtu~tiO~, the pr~scriber should discuss the desirability of reviewing
medicatiOn reqmrements well before conception. For some disorders
it may be possible to change to a different categ01y of drug. If a patient
conceives while on medication and there has been no opportunity
for earlier discussion with the prescriber, her medication should be
reviewed as soon as possible.
The following checklist may assist in deciding whether to prescribe a
particular drug during pregnancy:
Non pharmacological treatment: Is such a treatment available
and likely to be successful? Would such a treatment be reasonable
at least until the first trimester is complete? Most pregnant women
strongly favour this type of treatment and adherence is likely to
be high .
Harm-benefit analysis: For the particular drug under
consideration, what are the potential harms and benefits to the
mother and harms to the fetus of prescribing? What are the harms
and benefits (for each) of not prescribing?
Incidence of spontaneous congenital abnormality: When
drugs cannot be avoided, it may be appropriate to discuss the
incidence of non- drug-related, spontaneous abnormalities. This
is often underestimated. In Australia, the incidence of significant
congenital abnormality is 2% to 4% of live bitihs, and minor
abnormalities are recognised in approximately 15% of newborns.
Education, documentation and communication: Has the
education of the woman and her partner regarding harms and
benefits been properly documented in the patient's notes? Have
those health professionals involved in obstetric manaaement been
informed? "'
206
Routine review later in the pregnancy includes consideration of whether
dose alteration is indicated during delivery to avoid neonatal problems
such as respiratory depression.
Australian categorisation of drugs in pregnancy*
Table 22 (pp.210- 13) lists the Australian pregnancy category assigned
by the Therapeutic Goods Administration for individual drugs used in
the management of oral and dental conditions.
The Australian categorisation of drugs in pregnancy applies only to
recommended therapeutic doses in women in the reproductive age
group . In situations such as overdose, occupational exposure and other
situations when the recommended therapeutic dose is exceeded, it
cannot be assumed that the classifications assigned to individual drugs
are valid.
For drugs in the Bl, B2 and B3 categories, human data are Jacking
or inadequate and subcategorisation is therefore based on available
animal data. The allocation of a B category does NOT imply greater
safety than the C category. Drugs in the category D are not absolutely
contraindicated in pregnancy. Moreover, in some cases the D category
has been assigned on the basis of suspicion.
Category A
Drugs which have been taken by a large number of pregnant women
and women of childbearing age without any proven increase in the
frequency of malformations or other direct or indirect harmful effects
on the fetus having been observed.
Category 81
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 malformation or other direct or indirect harmful effects on
the human fetus having been observed .
Studies in animals have not shown evidence of an increased occurrence
of fetal damage.
'Therapeutic Goods Administration (TGA) pregnancy categorisation is from the TGA
Prescribing medicines in pregnancy dat abase at <www.tga.gov. au/hp/ medicines-
pregnancy. htm >. 207
 Category 82
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 malformation or other direct or indirect harmful effects on
the human fetus having been observed.
Studies in animals are inadequate or may be lacking, but available data
show no evidence of an increased occurrence of fetal damage.
Category 83
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 malformation or other direct or indirect harmful effects on
the human fetus having been observed.
Studies in animals have shown evidence of an increased occurrence
of fetal damage, the significance of which is considered uncertain in
humans.
Category C*
Drugs which, owing to their pharmacological effects, have caused
or may be suspected of causing, harmful effects on the human fetus
or neonate without causing malformations. These effects may be
reversible. Accompanying texts should be consulted for further details.
Category D
Drugs which have caused, are suspected to have caused or may be
expected to cause, an increased incidence of human fetal malformations
or irreversible damage. These drugs may also have adverse
pharmacological effects. Accompanying texts should be consulted for
further details.
Category X
Drugs which have such a high risk of causing permanent damage to
the fetus that they should not be used in pregnancy or when there is a
possibility of pregnancy.
Category C in the Australian and Swedish Categorisations of Risk is a pharmacological
effect category and differs from that in the US Food and Drug Administration (FDA)
Categorisation (where category C indicates greater likelihood of risk than in B on the basis
208 of adverse effects of any type in animal studies).
BREASTFEEDING AND THE USE OF DRUGS
The benefits of breastfeeding are Unless there is significant risk
sufficiently important to recommend to the infant from necessary
that it should not be discontinued maternal medication,
or discouraged unless there is breastfeeding should be
substantial evidence that the drug continued.
taken by the mother will be harmful
to the infant, and no alternative treatment can be found.
Most drugs are excreted only to a minimal extent in breast milk, and
in most cases the dosage to which the infant is ultimately exposed is
very low and well below the therapeutic dose level for infants. For this
reason, few drugs are totally contraindicated whi le breastfeeding.
In most situations, drugs cross the placenta more efficiently than into
breast milk.
When considering prescribing drugs (particularly longer-term) during
breastfeeding, the following checklist may assist in guiding the decision:
Woman's preference for breastfeeding: Most women have a
strong preference for breastfeeding. Inability to breastfeed can
lead to a sense of fa ilure as a mother, which may predispose to
subsequent postnatal depression.
N onpharmacological treatment: If such a treatment is available
and likely to be successful, it may allow the woman to breastfeed,
at least until the period of maximum benefit to the infant has
passed.
Harm-benefit analysis: For the infant, there are demonstrable
increases in immunocompetence (eg decreased rates of otitis
media), and neurodevelopmental advantage (eg possible increased
IQ in the older child). For the woman, physiological benefits of
breastfeeding include better uterine involution, more delayed
ovulation and decreased risk of breast cancer.
Education, documentation and communication: The
discussion regarding harm/benefit with the mother and her partner
should be properly documented in the patient's notes. Other
health professionals involved in postnatal management should be
informed of medication changes.
Table 22 (pp.21 0-13) provides advice on the safety of individual drugs
used in the management of oral and dental conditions in breastfeeding
women.
209
 Table 22. Drug use in pregnancy and breastfeeding Table 22. Drug use in pregnancy and breastfeeding (cont.)

Drug TGA Drug TGA Compatibility with

Compatibility with
pregnancy breastfeedingt pregnancy breastfeedingt
category* category*

aciclovir B3 compatible diazepam c compatible; caution with chronic

use and monitor infant for
adrena line A compatible drowsiness

amoxycillin A compatible; may cause diarrhoea dicloxacillin B2 compatible; may cause diarrhoea
in infa nt in infant

amoxycl llin+clavu lanate Bl compatible; may cause diarrhoea doxycycline o compatible for short courses (eg
in infant 10 days) if alternative drug not
appropriate; may cause diarrhoea
amphotericin (oral) B3 compatible in infant

ampicill in A compatible ; may cause diarrhoea doxylamine A caution , insufficient data; monitor
in infant infant for irritability and sleep '0.0
c
articaine B3 caution, insufficient data
disturbances
:cQ)
Bl caution, insufficient data
aspirin c compatible in occasional doses;
famc iclovir
~1/)
avoid long-term therapy, if see prilocaine (with or without felypressin)
fe lypressin ca
possible, particularly in the
neonatal period* fl ucloxacillin Bl compatible; may cause diarrhoea ...
Q)
.&J
in infant
"'C
benzydamine (topical) B2 compatible c
fluconazole D compatible ca
benzylpenicilli n A compatible; may cause diarrhoea >-
(,)
in infant fluoride unlisted compatible
c
ca
betamethasone A compatible hydrocortisone A compatible c
'0.0
bupivacaine A compatible hydrogen peroxi de unlisted compatible ...
Q)
Q.
iV casein phosphopeptide- unlisted compatible ibuprofen c compatiblet '0.0
~
c c
Q)
amorphous calcium phosphate ;:
Q it raconazole B3 caution, insufficient data ::s
cephalexin A compatible; may cause diarrhoea "'C
"'C in infant lignocaine A compatible 1/)
c '0.0
ca A caution, insufficient data; may ...::s
cephazolin Bl compatible; may cause diarrhoea lincomycin

0
...
iV in infant
cause diarrhoea in infant "'C
"'C
rnepivacaine A caution, insufficient data c
Vi ch lorhexidine A compatible ca
(lJ 1/)
c
c
Q)
chlorine dioxide unlisted compatible methylprednisolone aceponate compatible
...::s
Q)

B2 compatible; may cause diarrhoea

:Q
:::J
CJ
clindamycin A compatible; rnay cause dia rrhoea
in infant
metronidazole (systemic)
in infant. Avoid high single-dose
therapy
a:g
()
:p codeine A compat ible in occasional doses; ...g,
:::J miconazole A compati ble
avoid repeated doses
(lJ
Q_
B3 compatible
J
~ continued next page mometasone furoate c
(lJ
.s::::
1-
continued next page ~
?1 1
210
 Table 22. Drug use in pregnancy and breastfeeding (cont.) Table 22. Drug use in pregnancy and breastfeeding (cont.)
* Therapeutic Goods Administrat ion (TGA) pregnancy categori sation is from the TGA Prescribing
Drug TGA Compatibility with medicines in pregnancy database at <www.tga.gov.au/hp/medicines-pregnancy.htm > .
pregnancy breastfeedingt t Definitions for compatibility with breastfeeding:
category* compatible- there are sufficient data available to demonstrate an acceptably low relative
infant dose and/or no significant plasma concentrations and/or no adverse effects in breastfed
nitrous oxide A compatible
infants
nystatin A compatible caution- there are insufficient data showing low relative infant dose and/or no significant
plasma concentrations and/or no adverse effects in breastfed infants
paracetamol A compatible avoid, insufficient data-there are no data on transfer into milk, or on plasma concentrations
or adverse effects in the breastfed infant
penciclovir B1 caution, insufficient data
avoid- significant plasma concentrations in exposed infants, or adverse effects in breastfed
phenoxymethylpenicillin A compatible ; may cause diarrhoea infants reported or predictable from the properties of the molecule.
in infant llf an NSAID is required in a breastfeeding patient, ibuprofen is preferred.
Tetracyclines are safe for use during the first 18 weeks of pregnancy (16 weeks postconception)
povidone-iodine unlisted (not avoid; may interfere with infant after which they may affect the formation of the baby's teeth and cause discoloura~on .
recommended) t hyroid function

prednisolone A compatible

prednisone A compatible

prilocaine (with or without A compatible

felypressin)

rop ivaca ine B1 compatible

roxithromyci n B1 compatible; may cause diarrhoea

in infant

teicoplan in B3 caution, insufficient data; may

cause diarrhoea in infant

temazepam c compatible; caution with ch ronic

m
.....
use and monitor infant for
drowsiness
c
Cll tinidazole B3 caution , insufficient data; may
Q
cause diarrhoea in infant
"C
c
m tranexamic acid B1 compatible

~ triamci nolone acetonide A compatible

0 (topica l)
u;
Q) triclosan unlisted caution, insufficient data
c
Qi valaciclovir B3 compatible
:2
::J
0
() va ncomycin B2 compatible; may cause diarrt10ea
".;:J
::J
in infant
Q)
c. zinc lozenges unlisted compatible
~
Q)
continued next page
..c
f-

213
212
Abbreviations and acronyms

ADA Australian Dental Association

amoxy/ampicillin amoxycillin or ampicillin

BMS burning mouth syndrome

BRONJ bisphosphonate-related osteonecrosis of the j aws

CMI consumer medicine information

CNS central neNous system

COPD chronic obstructive pulmonary disease

cox cyclo-oxygenase

CPAP continuous positive airway pressure

CPP-ACP casein phosphopeptide-amorphous calcium phosphate

CPR cardiopulmonary resuscitation

CRP C-reactive protein

di/flucloxacillin dicloxacillin or flucloxacillin

HbAlc haemoglobin Ale (glycated haemoglobin)

HIV human immunodeficiency virus

lgE immunoglobulin E

IM intramuscular(ly)

INR international normalised ratio (/)

IV intravenous(ly)
E
~
MAO Is monoamine oxidase inhibitors e
(,)
('Q
NSAIDs nonsteroidal anti-inflammatory drugs
"0
NTI-TSS nociceptive trigeminal inhibition tension suppression system 1:
('Q
(/)
OSA obstructive sleep apnoea 1:
0
PBS Pharmaceutical Benefits Scheme :;;
('Q
ppm parts per million
~
continued next page .c
.c
<
215
 SSRis selective serotonin reuptake inhibitors

TCAs tricyclic antidepressants

TGA Therapeutic Goods Administrati on

TGL

TMD
Therapeutic Guidelines Limited

temporomand ibular disorders

Glossary
The following definitions refer to the terms used in Therapeutic
Guidelines: Oral and Dental. They may differ from definitions used in
other publications.

alveolar bone part of the upper or lower jaw bone that supports the roots of the
teeth; forms the tooth socket

amalgam an alloy of mercury with silver and other metals; used in dental
restorations

anaesthesia loss of sensation (including pain) in a part or all of the body

analgesia removal of pai n sensation

angiotensin group of drugs used to t reat card iovascu lar disease; examples
converting enzyme are captopril , enalapril, fosinopril, lisinopril, perin dopri l, quinapril,
inhibitors (ACEis) ramipril and trandolapril

angiotensin 11 group of drugs used to treat cardiovascular disease; examples

receptor blockers are candesartan, eprosartan, irbesartan, losartan, olmesartan,
(ARBs) telmisartan and valsartan

anticholinergics drugs that inhibit the action of acetylcholine and t herefore block
the passage of impulses through the parasympathetic nervous
system. Adverse effects of anticholinergic drugs include dry
mouth, thirst, increased pulse rate, blurred vision, increased
intraocular pressure, constipation and urinary retention

antihistamines drugs that inhibit the action of histamine in the body by blocking
histamine H1receptors. Stimulation of H1 receptors contributes
to the signs and symptoms of lgE-mediated im mediate
hypersensitivity reactions such as hay fever and urticaria.
Antihistamines are practically divided into sedating and less
sedating groups

apical periodontitis inflammation of the periodontal ligament and bone surrounding

the apex or end of a tooth root

apicectomy resection of t he apex of a tooth root (usually performed in

conj unction wit h a curettage of the periapical tissues and the
placement of a retrograde root filling)

asthenia weakness or loss of strength

216 217
 beta2 agonists drugs that stimulate beta2 receptors on airway smooth muscle, fluorhydroxyapatite Ca 10 (P0 4) 6 (0H) F-a crystal formed when fluoride is incorporated
which relaxes the muscle resulting in bronchodilatation. They are into tooth enamel during formation of the tooth
used 1n asthma and other respiratory conditions. Examples are
salbutamol and terbutaline (short-acting), and eformoterol and gingiva commonly known as the gum tissue, this soft tissue encircles the
salmeterol (long-acting) necks of erupted teeth and covers the crowns of unerupted teeth
biofilm a community of microorganisms and their by-products adhering Gram stain a method of staini ng for the purpose of differentiating bacteria
1n a th1n layer to a surface. The community has a collective into two large groups (Gram-positive and Gram-negative) based
physiology and works together on the structure of their cell walls
bridge (dental) a dental prosthesis used to replace one or more missing teeth half-life (of a drug) the time required for half the quantity of a drug to be metabolised
and which is cemented on to the adjacent teeth or eliminated by normal processes
calculus (dental) hard deposit of mineralised material that forms on the teeth hydroxyapatite Ca 10 (P04 ) 6 (0H) 2-the crystalline component of tooth enamel
through calcification of dental plaque
immunoglobulin one of the five major classes of immunoglobulins that function as
cementum hard connective tissue covering the dentine of the tooth root; E (lgE) antibodies; other classes are lgt\ , lgD, lgG and lgM
seNes as an attachment structure for the periodontal ligament
impacted tooth an unerupted or partially erupted tooth that is positioned against
clastic general term used to describe cells that resorb hard tissue such another structure so that complete eruption is unlikely
as bone, cementum and dentine
implant (den tal) a device designed to be placed surgically into the oral tissues
coronal pertaining to the clinical crown of a tooth to provide a base for a dental prosthesis; it is usually made of
titanium
crepitus crackling sound or grating feeling produced by bone rubbing
on bone or roughened cartilage, detected on movement of an incidence the number of new cases of disease occurring in a population
arthritic joint within a specific time period
cytochrome P450 group of enzymes involved in the metabolism of many intraligamentouS/ a technique where the local anaesthetic solution is injected under
(CYP) enzymes endogenous substances and drugs intraligamentary pressure into the periodontal ligament of the tooth to be treated
local anaesthetic
dentine hard tissue that forms the bulk of the tooth beneath the enamel injection
and cementum and surrounding the pulp
intraosseous a technique where a small opening is made through the cortical
denture a removable dental prosthesis used to replace one or more local anaesthetic plate of the bone near the tooth to be treated, and the local
missing teeth, and carried on some type of plate or frame injection anaesthetic solution is injected directly into the underlying
diaphoresis sweating cancellous bone
iii
....
c diuretics keratosis a horny overgrowth of the skin or mucosa
drugs that increase the excretion of urine
Q)
Q dysaesthesia (oral) ketoacidosis acidosis with an accumulation of ketone bodies. Diabetic
abnormal, sometimes painful, sensation in the mouth
"Q ketoacidosis (DKA) occurs primarily in patients with type 1
c dysarthria speech disorder in wh ich the pronunciation is unclear, although diabetes and is characterised by hyperglycaemia, polyuria,
< polydipsia, hypeiVentilation and dehydration. Stresses such as
the language content and meaning are normal

0
...
iii
dysgeusia peiVersion of the sense of taste
infection, inappropriate withdrawal of insulin, acute myocardial
infarction and trauma are the most common precipitants of DKA
Ui
Q)
dysphonia disturbance of normal functioning in the production of sound luxation displacement of a tooth fro m its normal position in the alveolar
.S enamel (tooth) socket, usually due to a traumatic accident. Luxat ion can be
hard calcified tissue covering the dentine of the crown of a tooth extrusive, intrusive or lateral. Extrusive luxation is when the
03
3:! endodontics root canal treatment; a process where the dental pulp and/ tooth is displaced out of its socket in an axial direction; intrusive
:::J luxation is when the tooth is displaced into the soc l~et in an axial
<.!J I endodontic or Infected debris is removed from the tooth and its root canal
treatment direction; lateral luxation is when the tooth is displaced in any
u system, which is then cleaned, disinfected and filled
:,::; direction other than axially
:::J eugenol a liquid phenoi-C 10H1,02- contained in certain essential oils
Q)
Cl. (eg clove oil), used in some dental materials to reduce pulp nucleic acid tests tests that use molecular biology techniques to detect and identify ~
<
~ 1nflammat1on and to arrest dental caries microorganisms on the basis of their nucleic acids; includes II)
Q) polymerase chain rea ction (PCR) tests II)
..c fl uorapatite 0
I- Ca, 0 (P0, )6 F2- a crystal formed when fluoride is incorporated into
tooth enamel during formation of the tooth occlusion (dental) the way the teeth bite together <:;
218
219
 tooth-related rubber dam a sheet of rubber that is placed over the teeth to isolate the
odontogenic
operating field while procedures are performed on th e teeth
operculum loose flap of gingival tissue overlying the crown of a partially
eru pted tooth scaling (dental) a procedure to remove plaque and calculus from teeth

osseointegration the process by which certain materials, such as titanium, may somatisation conversion of psychological distress into physical symptoms
be introduced into living bone without producing a foreign-body group of lymphocytes primarily responsible for cell-m diated
reaction . This allows a very tight and strong joint between the two T cells
immunity
structures
temporise to place a temporary restoration in a tooth
parenteral admin istered by any way other than through the gastrointestinal
tract (eg subcutaneous, intramuscular, intravenous, intradental or zygomatic complex pai r of bones that form the prominent part of the cheeiiS and
intra-arti cular injection) contribute to the orbit s, commonly called t he cheekbones

pericoronitis soft tissue infection associated with a partia lly erupted tooth

periodontal ligament the fibrous connective tissue surrounding the root of a tooth,
attaching it to the bone

pH a means of expressing acidity and alkalinity. The pH scale ranges

from 0 to 14, with 7 being neutral; numbers increase with
increasing alkalinity, and decrease with increasing acidity

prevalence the proportion of a population with a particular disease at a

specified time

psychosomatic re lating to or involving both the mind and body; used to describe
il lnesses that are caused by an interaction of mental and physical
factors

pulp (dental) the mass of connective tissue in the pu lp cavity at the centre of a
tooth. It contains arteri es, veins, and lymphatic and nerve tissue

pulpitis inflammation of the dental pulp; this inflammation may be acute

or chronic, reversible or irreversible

pulpotomy endodontic treatment consisting of partial remova l of the dental

pulp
!c radicular pertaining to the root
Q)
c resorption loss of substance through physiological or pathological means
'C
c restoration (dental) commonly known as a filling or a crown; when a dental material
(II
is used to restore, rebuild or replace lost tooth structure; various
~ materials ca n be used, including meta l alloys, resins, glass
ionomers and porcelains
0
retrognathia abnorma lity of craniofacial anatomy, with posterior positioning of
the jaw relative to the facial skeleton

Reye syndrome a rare, serious, potentially fata l condition of the hepatic and
central nervous system that affects children; it most often occurs
following a viral infection

root canal treatment see 'endodontics I endodontic treatment' ~

(II
1/)
root planing a procedure to remove microbial ftora, plaque, bacterial toxins, 1/)
calculus and affected cementum or dentine on the root surface 0
and in a periodontal pocket a
221
220
Index

A
abbreviations 215-16 airway obstruction
abscess (dental) 61 emergency management 174
initial management by medical signs (table) 175
practitioners (table) 193 alcohol in mouthwashes 44
locat ions (schematic diagram) 62 alendronate
periodonta l abscess 59 adverse effects
acetaminophen see paracetamol osteonecrosis of the jaws 152
aciclovir pre cautions
clinical pharmacology 26 dental procedures 153
pregnancy & breastfeeding (table) 210 allergic reactions 179
therapeutic use causes
oral mucocutaneous herpes 80 adrenal ine 112
acronyms 215- 16 antimi crobi als 18
Actinomyces species latex 180
halitosis 97 loca l anaest heti cs 115
Acts (legislation) types
prescriptio ns 11 anaphylaxis and anaphylactoid
acute coronary syndromes reactions 182
dental management issues 142 angioedema 181
emergency management 169 urticaria 180
acute necrotising ulcerative alveolar bone (definition) 217
gingivitis 57 alveolar osteitis 69
acute pain see pain initial management by medical
acute ulcerative gingivitis 57 practitioners (table) 193
addiction (drug) 42 amalgam restorations
dental management issues 164 as a cause of oral lichen planus 74
Addison 's disease definition 217
dental management issues 151 amoxicillin see amoxy/ampicilli n
Addisonian crisis amoxy/a mpicillin
dental management issues 151 adverse effects 21
adrenal crisis see Addisonian crisis clinical pharmacology 22
adrenal disorders pregnancy & breastfeeding (table) 210
dental management issues 151 therapeutic use
adrenaline acute ulcerative gi ngivitis 59
clinical pharmacology 112 dentoalveolar surgical infections 68
precautions endocard itis prophylaxis 105
hyperthyroidism 150 odontogenic infections
monoamine oxidase inhibitors 164 {spreading) 64, 65, 66
pregnancy & breastfeeding (table) 210 periodonta l abscess 60
therapeutic use surgical prophylaxis 108
anaphylaxis and anaphylactoid tooth avu lsion 196
reactions (box) 182 amoxycillin see amoxy/a mpicillin
emergencies (required drug) 188 amoxycillin+clavulanat e
haemostasis in surgery 139 adverse effects 21 ><
Q)
local anaesthesia (table) 118 cli nical pha rm acology 22 'C
urticaria (box) 181 pregnancy & breastfeeding (table) 210 1:
airway (disposable) therapeutic use
emergencies (required equipment) 188 odontogenic infections (superficial
223
spreading) 65
 amphotericin antihistamines aspirin benzylpenicillin (cont.)
clinical pharmacology 26 adverse effects adverse effects 28 therapeutic use
pregnancy & breastfeeding (table) 210 dry mouth 87 clinical pharmacology 27 odontogenic infections (dee:>
therapeutic use definition 217 interactions 28 spreading) 66
candidosis (oral) 84 therapeutic use preca utions 28 su rgi cal prophylaxis 108
ampicillin see amoxy/ampici llin urticari a (box) 181 dentoa lveolar surgery 138 beta lactams
anaesthesia antimicrobial creed (box) 16 heart failure 143 clinical pharmacology 21
definition 217 antimicrobials hypertension 142 hypersensitivity (a llergy) 18
loca l see local anaesthesia adverse effects 18 risk factors for upper gastrointestinal beta-lactamase inhibitors 22
anaesthetics (local) see local cli nical pharmacology 21 bleeding or perforation (box) 29 bet a 2 agonists (definition) 218
anaesthesia common drugs used in dentistry viral hepatiti s 160 betamethasone
analgesia (table) 17 pregnancy & breastfeeding (ta ble) 210 adverse effects 38
definition 217 principles of use 13 therapeutic use clinical pharmacology 35
local anaesthesia 111-19 resistance 14 acute coronary synd rome (box) 170 potency (table) 36
post-treatment pain 127-36 antiplatelet drugs dental pain (post-treatment) 132 contraind ications 38
ana lgesics dental management issues 138 emergencies (desired drug) 189 precautions 38
clinical pharmacology 27 antiseptic mouthwashes 44 asthenia (definition) 217 pregnancy & breastfeeding (table) 210
principles of use 128 antithrombotic drugs asthma principles of use 37
anaphylactoid reactions 182 dental management issues 138 assessment of severity (table) 172 prescribing considerations (box) 38
anaphylaxis 182 antiviral drugs dental ma nagement issues 144 therapeutic use
angina clinical pharmacology 26 emergency management 172 lichen planus (oral) 75
dental management issues 142 common drugs used in dentistry AUG (acute ulcerative gingivitis) 57 recu rrent aphthous ulcerative
emergency management 169 (table) 17 avulsed tooth 194 disease 79
angioedema 181 principles of use 13 azathioprine biofilm (definition) 218
angiotensin converting enzyme ANUG (acute necrotising ulcerative therapeutic use bisphosphonate-related
inhibitors (definition) 217 gingivitis) 57 mucous membrane pemphigoid 82 osteonecrosis of the jaws 152
angiotensin II receptor blockers anxiety disorders pemph igus vu lgaris 82 bisphosphonates
(definition) 217 dental management issues 164 azole antifungal drugs adverse effects
angular cheilitis 85 anxiolysis 121-4 common drugs used in dentistry osteonecrosis of the jaws 152
antibacterial drugs assessment and preparation 122 (table) 17 precautions
adverse effects 18 instructions for patients (box) 123 dental procedures 153
antimicrobial resistance 14 management of the patient 123 B black hairy tongue 75
clinical pharmacology 21 oral 124 back pain
bleeding gums
(ij common drugs used in dentistry anxiolytic drugs 40 dental problems seen in medical
....s:: (table) 17 drug dependence 42
dental management issues
basic life support flow chart
163
practice (table) 201
Q) pri nciples of use 13 aphthous ulcerative disease (figure) 183 bleeding tooth socket 198
0 antibiotic prophylaxis 101-9 (recurrent) 78 blindness (unilateral) 186
"C benzodiazepines
s:: endocardi tis 101 apical periodontitis
adverse effects 41 blood glucose monitor
(II prin ciples 14 definition 217 cli nical pharmacology 41 emergencies (desired equipment) 189
(ij
,_ prosthetic joint infections 106 initial management by medical
interacti ons 41 blood pressure monitor
0 su rgica l site infections 107 practitioners (table) 192 precauti ons 41 emergencies (desired eq uipment) 189
(f)
antibiotics see antibacterial drugs location (schematic diagram) 62 benzydamine
BMS (burning mouth syndrome) 91
Cll anticholinergics apicectomy (definition) 217 cli nica l pharmacology 45 body dysmorphic disorder
c adverse effects articai ne dental management issues 164
Q) pregnancy & breastfeeding (table) 210
"0
dry mouth 87 adverse effects 113 therapeutic use
bone and calcium disorders
3 definition 217 clinical pharmacology 112 dry mouth (table) 87 dental management issues 152
<.!) anticoagulant drugs dosing 117 oral mucocutaneous herpes 80 breastfeeding (drug use in) 209
()
. p dental management issues 138 pregna ncy & breastfeeding (table) 210 oral mucositis (table) 87 compatibility (table) 210- 13
:::J antifungal drugs therapeutic use
benzylpenicillin
bridge (dental) (definition) 218
Cll 26
Q. cl inical pharmacology dental procedu res 116 adverse effects 21 broken filling 194 ><
Cl)
~ common drugs used in dentistry artificial joint infections see prosthetic
clinical pharmacology 21 broken tooth 194
Cll (table) 17 joint infections BRONJ (b isphosphonate- related "C
r.
f- prin ciples of use 13 artificial saliva
pregnancy & breastfeeding (table) 210
osteonecrosis of the jaws) 152
c
dry mouth 89 bruxism 93
224 oral mucositis (table) 87 225
 bupivacaine casein phosphopeptide-amorphous choking 174 contraceptives (oral) see oral
adverse effects 113 calcium phosphate chronic obstructive pulmonary disease contraceptives
cl inical pha rmacology 112 clinical pharmacology 51 dental management issues 145 COPD see chronic obstructive
pregnancy & breastfeeding (ta ble) 210 pregnancy & breastfeed ing (table) 210 chronic pain see pain pu lmonary disease
therapeutic use therapeutic use clastic (definition) 218 coronal (definition) 218
dental procedures 117 dental caries 51 clavulanate (see a/so coronary artery bypass surgery
trigeminal neu ralgia 159 dry mouth 88 amoxycillin + clavu lanate) 22 dental management issues 142
burning mouth syndrome 91 cavity (dental) see caries clindamycin coronary artery stents
burns (chemical) cementum (definition) 218 clinical pharmacology 23 dental management issues 142
ocular 184 cephalexin pregnancy & breastfeed ing (table) 210 coronary heart disease
cli nical pharmacology 22 therape utic use dental management issues 142
c pregnancy & breastfeed ing (table) 210
therapeutic use
acute ulcerative gingivitis 59 emergency management 169
calculus (dental) (definition) 218 dentoalveolar su rgical infections 68 coronary ischaemic syndromes see
cancer therapy endocarditis prophylaxis 106 endocarditis prophylaxis 105 acute coronary syndromes
adverse effects cephalosporins odontogenic infections corticosteroids 34
dry mouth 87 clinical pharmacology 22 (spreading) 64,65,66 intradental 34
ora l mucositis 85 hypersensitivity (allergy) 18 periodontal abscess 60 systemic
dental management issues cephazolin salivary gland infections 70 clinical pharmacology 40
chemotherapy 162 cl inical pharmacology 22 surgical prophylaxis 108 therapeutic use
pregnancy & breastfeeding (table) 210 clodronate angioedema 181
head and neck cancer 161
Candida species therapeutic use adverse effects mucous membrane pemphigoid 82
see candidosis
candidiasis see candidosis odontogen ic infections (deep osteonecrosis of the jaws 152 pemphigus vu lgaris 82
candidosis spreading) 66 precautions topical
cetirizine dental procedures 153 adverse effects 38
angular cheilitis 85
therapeutic use clonazepam clinical pharmacology 35
oral 82
denture hygiene 83 urticaria (box) 181 therapeutic use contraindications 38
pred isposing fa ctors (table) 83 cheilitis (angular) 85 burning mouth syndrome 93 potency (table) 36
carbamazepine chemical eye injuries 184 clopidogrel preca utions 38
therapeutic use chemotherapy precautions prescribi ng considerations (box) 38
adverse effects dentoalveolar su rgery 139 principles of use 37
trigem inal nerve injury 159
cardiac arrest 169 oral mucositis 85 Clostridium difficile coxsackie vi ruses
cardiac implanted electronic devices dental management issues 162 antibiotic-associated diarrhoea 20 oral ulcers 79
dental management issues 142 chest pain (box) 170 codeine CPP-ACP see casein phosphopeptide-
'16
.... cardiopulmonary resuscitation chlorhexidine adverse effects 32 amorphou s ca lcium phosphate
c basic life support flow chart adverse effects clinical pharmacology 32 CPR see cardiopul monary resuscitation
Q)
Q (figure) 183 hairy tongue 75 third molar model (figure) 131 cracked teeth 191
'C cardiovascular conditions cli nical pharmacology 44 interactions 32 crepitus (definition) 218
c pregnancy & breastfeed ing (table) 210 precautions 32 cricothyroidotomy
Ctl
dental management issues 137
anticoagulant and anti platelet therapeutic use pregnancy & breastfeeding (table) 210 emergency management of an inha led

0
...
'16 drugs 138 dental caries
dentoalveolar su rgica l infections 68
51 therapeutic use
dental pain (post-treatment)
object (box)
crowns
176
see restorations (dental)
coronary heart disease 142
Ui heart fai lure 143 dent ure hygiene 83 adults 133 C-terminal telopeptide concentration
QJ
hypertension 140 dry mouth (table) 87 children 136 dental procedures in patients taking
c gingivitis 56
a; cardiovascular emergencies 168 combini ng ibuprofen with bisphosphonates 154
:Q acute coronary syndromes 169 acute ulcerative 58, 59 paracetamol+codeine (box) 134 interpretation (box) 155
~ halitosis 99 cold sores 79 CTX concentration see C-terminal
<.!J
angina 169
odontogenic infections (localised) complex regional pain syndromes telopeptide concentration
()
cardiac arrest 169
.;:::; (box) 63 dental management issues 163 cyclosporin
syncope 168
~
QJ caries 47-53 ora l mucocutaneous herpes 80 conscious seqation see sedation therapeutic use
Q. management 48 oral mucositis (table) 87 consent mucous membrane pemphigoid 82 ><
~ pathology 47 tooth avulsion 196 anxiolysis 122 pemph igus vulgaris 82 Q.)
QJ "0
.c chlorine dioxide procedures in patients taking cyproheptadine
f-
ri sk assessment 48 c
stages (schematic diagram) 62 pregnancy & breastfeeding 210 bisphosphonates 153 therapeutic use
therapeutic use sedation 122 urticaria (box) 181
226 ha litosis 99 227
 cytochrome P450 enzymes dental pain see pain diazepam (cont.) endocrine emergencies 178
(definition) 218 dental problems in medical interactions 41 hypoglycaemia 178
cytomegalovirus practice 191-201 preca utions 41 endodontics (definition) 218
oral ulcers 79 dental procedures pregnancy & breastfeeding (table) 211 enoxaparin
anti biotic prophylaxis 101- 9 therapeutic use precautions
D anxiolysis 121- 4 anxiolysis 124 dentoalveolar surgery 140
dabigatran complications after tooth sedation 124 epilepsy
preca utions extraction 198 dicloxacillin see di/flucloxac illin dental ma nagement issues 157
dentoalveolar surgery 140 local anaesthesia 111-19 dipyridamole emergency management 177
decay (tooth) see caries post-treatment pain 127- 36 preca utions equipment required for
defibrillator (automated external) precautions dentoalveolar surgery 140 emergencies 188
emergencies (desired equipment) 189 adrenal insufficiency or directed antimicrobial therapy erythema migrans 75
demeclocycline 25 suppression 151 (principles) 14 erythema multiforme 82
denosumab anticoagulant and antipl atelet diuretics (definition) 218 erythematous candidosis (oral) 82
adverse effects drugs 138 DKA see diabetic ketoacidosis erythromycin
osteonecrosis of the jaws 152 bisphosphonates 153 doxycyc Ii ne cli nical pharmacology 24
dental abscess see abscess (dental) vira l hepatitis 160 clinical pharmacology 25 etidronate
dental caries see cari es sedation 121- 6 pregnancy & breastfeeding (table) 211 adverse effects
dental cavity see ca ries surgical infections 67 therapeutic use osteonecrosis of the j aws 152
dental extractions see tooth extractions dental restorations see restorati ons tooth avul sion 196 precautions
dental implants (dental) doxylamine dental procedures 153
antibiotic prophylaxis for placement dentine (definition) 218 pregnancy & breastfeed ing (table) 211 eugenol (definition) 218
endocarditis 103 dentoalveolar procedures see denta l therapeutic use examination (principles) 2
in patients with viral hepatitis 160 procedures dental pai n (post -treatment) 133 extractions (tooth) see tooth extractions
surgica l site infection denture drug addiction see addiction (d ru g) eye emergencies see ocular
109
definition 219 defin ition 218 drug dependence see emergencies
precautions in patients taking hygiene 83 dependence (drug)
bisphosphonates 153 dependence (drug) 42 drug information 13- 45
denta l ma nagement issues 164 F
dental infections see odontogenic sources 10 facial nerve palsy 186
infections desloratadine drugs and sport 203-4
therapeutic use facial nerve weakness
dental management of patients with drugs required fo r emergencies 188 dental management issues 157
medical conditions 137- 66 urticaria (box) 181 dry mouth 87
dexchlorpheniramine famciclovir
adrenal disorders 151 oral preparations (table) 87 clinical pharmacology 26
i6
.... anticoagulant drugs 138 therapeutic use practical advice for patients (box) 89
c urticaria (box) pregnancy & breastfeedi ng (table) 211
Q) anti platelet drugs 138 181 dry socket see alveolar osteitis
di/flucloxacillin felypressin
Q asthma 144 dysaesthesia (oral)
adverse effe cts clinical pharmacology 113
'tl bone and calcium disorders 152 21 burning rnouth syndrome 91 pregnancy & breastfeedirg (table) 211
c chemotherapy 162 cli nical pharmacology 21 defin ition 218
('0
pregnancy & breastfeeding (table) 211 t herapeutic use
chronic musculoskeletal disorders 163 local anaesthetic complication 114 118
0
...
i6 chronic obstructive pulmonary therapeutic use
salivary glan d infections 70
dysarthria (definition) 218
local anaesthesia (table)
fexofenadine
disease 145 dysgeusia (definition) 218 therapeutic use
Ui coronary heart disease 142 diabet es mellitus dysphonia (definition) 218
Q) dental ma nagement issues 147 urticaria (box) 181
c diabetes 147
approach to gene ral dental fibromyalgia
epilepsy 157
Q)
treatment (box) 149
E dental management issues 163
~ head and neck cancer 161
hypoglycaemia emergencies see medical emergencies fillings (dental)
::J heart fai lu re 143 178 194
(.!J
diabetic ketoacidosis empirical antimicrobial therapy fracture
huma n immunodeficiency virus 161 194
(.)
dental management issues 148 (principles) 14 loss
~ hypertension 140
::J diagnosis (principles) 1
enamel (tooth) (definition) 218 flucloxacillin see di/fl ucloxaci llin
Q) obstructive sleep apnoea 146
Cl. diagnostic tests (principles) 2
endocarditis prophylaxis 101 fluconazole
~
psychological and psychiatric
diaphoresis (definition) endocrine conditions clinical pharm acology ><
(1)
Q) disorders 164 218
..c diarrhoea (a ntibiotic-associated) 20 dental management issues 147 common dru gs used in dentistry "C
stroke 156
f- diazepam ad renal disorders 151 (table) 17 c
thyroid disorders 150
adverse effects bone and calcium disorders 152 pregnancy & breastteeding (table) 211
trigeminal neuralgia 158 41
228 clinical pharmacology 42 diabetes 147 therapeutic use
viral hepat itis 159 thyroid di sorders 150 candidosis (oral) 84 229
 fluorapatite (definition) 218 halitosis 97-100 hypertension implants (and implantabl e d E~vices)
fluorhydroxyapatite (definition) 219 causes (box) 98 dental management issues 140 (cont.)
fluoride diagnosis 98 hyperthyroidism dental procedures in patien t~; with
adverse effects management 98 dental management issues 150 card iac devices 142
dental fluorosis 50 hand, foot and mouth disease hyperventilation syndrome incidence (definition) 219
clinica l pharmacology 50 oral ulcers 79 emergency management 171 infiltration anaesthesia 111
pregnancy & breastfeeding (table) 211 head cancer signs and symptoms (table) 171 information resources
therapeu tic use dental ma nagement issues 161 hypnotic drugs 40 (drug-related) 10
dental cari es 50 heart disease see cardiovascu lar drug dependence 42 informed consent see consent
dry mouth 88 co nditions hypochlorite solution inhaled objects
fluorosis (dental) 50 heart failure de nture hygi ene 83 emergency management 174
foreign body dental management issues 143 hypoglycaemia prevent ion 174
inhaled 174 hepatitis (viral) emerge ncy management 178 signs of airway obstruction (table) 175
lodged on the surface of the eye 185 dental ma nagement issues 159 symptoms (table) 179 intraligamentous injection
swallowed 174 heroin hypothyroidism (definition) 219
fractures adverse effects dental management issues 150 intraosseous injection (definition) 219
fi lling 194 dry mouth 87 ischaemic heart disease S6.e coronary
tooth 194 herpangina heart disease
oral ulcers 79 itraconazole
ibandronate
G herpes labialis 79 clinical pharmacology
adverse effects
herpes simplex virus common drugs used in dehtistry
geographic tongue 75 osteonecrosis of the jaws 152
erythema multiforme 82 (table) 17
gingiva (definition) 219 precautions
oral mucocuta neous ulcers 79 pregnancy & breastfeeding (\able) 211
gingival bleeding dental procedures 153
herpetic gingivostomatitis 79 therapeutic use
denta l problems see n in medical ibuprofen
herpetiform aphthous ulceration 78 cand idosis (oral) 84
practice (table) 201 adverse effects 28
history and history-taking
gingival hype rpl asia clinical pharmacology 27
(principles) 1
anti epileptic drug adverse effect 157 thi rd molar model (figure) 131 J
rel ating to bisphosphonates (box) 155 28
gingivitis 55 interactions joint prostheses
acute ulcerative 57 HIV see human immu nodeficiency vi rus 28 prevention of infection
precautions 106
HSV see herpes simplex vi rus 143
location (schematic diagram) 62 heart fa il ure
human immunodeficiency virus 142
gingivostomatitis (herpetic) 79 hypertension
K
glossary 217-21 dental management issues 161 risk factors for upper gastrointesti nal
glucose hydrocortisone 29
keratosis (definition) 219
bleeding or perforation (box) ketoacidosis (definition)
(6 therapeutic use adverse effects 38 160 219
+' vi ral hepati tis knocked-out tooth
c clinical pharmacology 35 pregnancy & breastfeeding (table) 211
194
Q)
emergencies (desired drug) 189
potency (table) 36
c hypoglycaemia (box) 179
con traind ications 38
therapeu tic use
"C glyceryl trinitrate dental pain (post-treatment) l
c therapeutic use precautions 38 adults 132, 133 Lactobacillus species
C"ll pregnancy & breastfeed ing (table) 211
acute coron ary syndrome (box) 170 children 136 dental caries 47
...
(6
0
angina (box) 170 principles of use
prescribing considerations (box)
37
38
combined with paracetamol (or laryngeal airways
emergencies (desired equiprn ent)
emergencies (desi red dru g) 189 paracetamol+ codeine) for 189
hydrogen peroxide latex a lle rgy
Ui glycopeptides 23 enhanced pain re li ef (box) 134 180
(j) pregnancy & breastfeed ing (table) 211 legislation
c Gram stain (definition) 219 imidazoles
therapeutic use prescriptions
Qj guanine analogues 26 miconazole 26 11
:Q
acute ulcerative gingivitis 58 immunoglobulin E (definition) 219 leukoplakia (oral} 72
::J hydroxyapatite (definition) 219 impacted tooth (definition) 219 hairy 76
CD H hyperbaric oxygen lichen planus (oral)
() haemostasis
implants (and implantable devices) 74
:;:::; therapeutic use life support flow chart (figur~) 183
antibiotic prophylaxis for dental impla nt
::J bleed ing tooth socket (table) 200 tooth extractions after head and neck lignocaine
(j) placement
0.. local measu res in surgery 139 radiotherapy 162 adverse effects ><
rn endocarditis 103 113
hairy leukoplakia (oral) 76 hypercalcaemia Q)
'-
(j) in patients with viral hepatitis 160 clinical pharmacology 112 "0
..c hairy tongue 75 dental manage ment issues 152
1- half-life of a drug (definition) 219 hyperplastic candidosis (oral) 83
surgica l site infection 109 dosing 117 c
dental implants in patients taking pregnancy & breastfeeding ~able) 211
hypersensitivity see all ergic reactions bisphosphonates 153
230 231
 lignocaine (cont.) malodou r (oral) see halitosis metronidazole (cont.) N
therapeutic use management of dental problems for pregnancy & breastfeeding (table) 211 narcotics see opioids
dental procedures 116 medical practitioners 191-201 therapeutic use neck cancer
topica l use 111 management (principles) 3 acute ulcerative gingivitis 58, 59 dental management issues 161
dry mouth (table) 87 marijuana dentoalveolar su rgical infectio ns 68 neck pain
oral mucocutaneous herpes 80 adverse effects odontogenic infections dental management issues 163
oral mucositis (table) 87 dry mouth 87 (spread ing) 65, 66 necrotising infections
recurrent aphthous ulcerat ive maxillofacia l trauma 197 miconazole acute ulcerative gingivitis 57
disease 79 medical conditions and dental cli nical pharmacology 26 needlestick injuries
lincomycin management issues 137- 66 pregnancy & breastfeedi ng (table) 211 de ntal management issues 160
cli nical pharmaco logy 23 medical emergencies 167-89 therapeutic use nerve injuries
pregnancy & breastfeeding (table) 211 acute coronary syndromes 169 angu lar cheilitis 85 loca l anaesthetic complication 114
therapeutic use all ergic reactions 179 candidosis (oral) 84 trigeminal nerve injury 159
endocarditis prophylaxis 105 anaphylaxis 182 mometasone neurological conditions
odontogenic infections (deep angioedema 181 adverse effects 38 dental management issues 156
spread ing) 66 urticaria 180 clinical pharmacology 35 epilepsy 157
salivary gland infections 70 angi na 169 potency (table) 36 stroke 156
surgica l prophylaxis 108 asthma 172 contrai nd ications 38 trigeminal neuralgia 158
lincosamides 23 basic life support flow chart precautions 38 neurological emergencies 176
local anaesthesia 111- 19 (figure) 183 pregnancy & breastfeeding (table) 211 seizu res 177
addition of vasoconstri ctors 112 cardiac arrest 169 principles of use 37 stroke 176
adverse effects 113 drugs required 187 prescribing considerations (box) 38 neuropathic pain 128
local complications 114 equipment requ ired 187 morphine neurotoxicity
systemic toxicity 115 hyperventilation syndrome 171 clinical pharmacology 31 loca l anaesthetic complication 114
temporary paralysis of the hypoglycaemia 178 mouth ulcers see ulcers (oral) nitroimidazoles 24
periocular muscles 186 in haled objects 174 mouth rinses see mouthwashes nitrous oxide
uni lateral bli ndness 186 ocular inju ri es 184 mouthwashes 43 pregnancy & breastfeed ing (table) 212
cli nical pharmaco logy 112 seizu res 177 alcohol use in 44 therapeutic use
dosing 117 stroke 176 antiseptic 44 sedation (inhalational) 124
techniques for administration 111 swallowed objects 174 benzydamine 45 nociceptive pain 127
therapeutic use syncope 168 flu orid e 50 nonsteroidal anti-inflammatory drugs
bleed ing tooth socket (table) 200 mepivaca ine mucosal disease (oral) 71-90 adverse effects 28
dental procedures 116 adverse effects 113 angu lar cheilitis 85 cli nical pharmacology 27
i haemostasis in su rgery 139 clinical pharmacology 112 ca nd idosis 82 interactions 28
..... pulpitis (irreversible) dosing 117 discolourations 71 28
c precautions
Q) initial management by medical pregnancy & breastfeed ing (table) 211 erythema multiforme 82 heart fail ure 143
c practitioners (table) 192 therapeutic use geograph ic tongue 75 hypertension 142
"C trigeminal neuralgia 159 dental procedures 117 hairy leukoplakia 76 risk factors for upper gastrointestinal
c
l1l local anaesthetics see local methaemoglobinaemia hairy tongue 75 bleeding or perforat ion (box) 29
i anaesthesia local anaesthetic adverse effect 113 herpes sim plex infection 79 160
...
0 local analgesia see local anaesthesia articaine 116 leu koplakia 72
viral hepatitis
t herapeuti c use
loratadine prilocaine 116 lichen planus 74 dental pain (post-treatment) 129
en
QJ therapeutic use methoxyflurane mucositis 85 dentoalveolar surgical infections 69
c urticaria (box) 181 precautions 125 mucous membrane pemphigoid 81 initial management of acute pain
Qi lost fi lling 194 methylprednisolone aceponate pemphigus vulgaris 81 by medical practitioners
:Q 77 192-3
::J Ludwig's angina 67 adverse effects 38 ulcers (table)
(!) luxation (definition) 219 clinical pharmacology 35 mucositis (oral) 85 NSAIDs see nonsteroidal
(.)
..::::; potency (table) 36 oral prepa rations (table) 87 anti-inflammatory drugs
contra ind ications 38 mucous membrane pemphigoid 81 nucleic acid tests (definition) 219
::J
QJ M ><
0. 24 precautions 38 musculoskeletal disorders nystatin
~
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pregnancy & breastfeeding (table) 211 dental management issues 163 clin ical pharmacology 26 a>
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principles of use 37 myocardial infarction pregnancy & breastfeedi ng (t able) 212 c:
1- prescribing considerations (box) 38 dental management issues 142 therapeutic use
chemotherapy 162 169
head and neck cancer 161 metronidazole emergency management angu lar cheil itis 85
232 cli nical pharmacology 24 cand idosis (oral) 84 233
squamous cell carcinoma (photo) 73
 0 osseointegration (definition) 220 paracetamol (cont.) phenoxymethylpenicillin (cont.)
obstruction of the airway see airway osteitis (a lveolar) see alveo lar osteit is therapeutic use pregnancy & breastfeeding (table) :212
obstruction osteoarthritis dental pain (post-treatment) t herapeutic use
obstructive sleep apnoea dental management issues 163 adu lts 133 acute ulcerative gingivitis 59
dental management issues 146 osteonecrosis of the j aws children 136 dentoalveolar su rgica l infections 68
occlusion (dental) (definition) 219 (bisphosphonate-related) 152 combined wit h ibuprofen for odontogenic infections (superficia l
ocular emergencies 184 osteopenia enhanced pain relief (box) 134 spread ing) 64,, 65
chemical injuries 184 dental management issues 152 dentoalveolar su rgical infections 69 periodontal abscess 60
foreign bodies lodged on the osteoporosis paraesthesia surgical prophylaxis :t08
su rface 185 dental management issues 152 dental problems seen in medical phobic disorders
penetrating injuri es 185 osteoradionecrosis 162 practice (table) 201 dental management issues :164
temporary para lysis 186 oximetry see pu lse oximetry local anaesthetic complication 114 plaque (dental)
unilateral blindness 186 oxycodone paralysis of the periocular caries 47
odontogenic (definition) 220 clinical pharmacology 31 muscles 186 periodontal disease 55
odontogenic infections 61- 9 oxygen parenteral (definition) 220 polyene antifungal drugs 26
denta l caries 47-53 therapeutic use parotitis 69 povidone-iodine
dentoalveolar surgical infections 67 acute coronary syndrome (box) 170 pemphigoid (mucous membrane) 81 clinical pharmacology 45
localised infections 61 anaphylaxis and anaphylactoid pemphigus vulgaris 81 pregnancy & breastfeed ing (table) ~12
locations (schematic diagram) 62 reactions (box) 182 penciclovir prasugrel
Ludwig's angina 67 asthma (box) 173 cl inical pha rmacology 27 precautions
periodonta l disease 55-60 emergencies (requ ired drug) 188 pregnancy & breastfeeding (table) 212 dentoalveolar surgery :1_39
spreading infectio ns 63 tooth extractions after head and therapeutic use prednisolone
surgica l prophylaxis 107 neck radiotherapy (hyperbaric oral mucocutaneous herpes 80 clinical pharmacology 40
operculum (definition) 220 oxygen) 162 penetrating eye injuries 185 pregnancy & breastfeeding (table) ~12
opioids penicillin G see benzylpenicillin prednisone see prednisol<me
adverse effects 32 p penicillin V see pregnancy
clin ica l pha rmacology 31 pacemakers phenoxymethylpenicillin dental procedures ~ 05
interactions 32 dental management issues 142 penicillins dru g use ~ 05
precautions 32 Paget 's disease of bone cli nical pha rmacology 21 risk categorisation (table) 210--13
t he rapeutic use dental management issues 152 hypersensitivity (allergy) 18 radiographs (intraoral) :;,05
dental pain (post-treatment) 129 pain periapical abscess 61 prescriptions and prescription-
oral contraceptives acute 128 location (schematic diagram) 62 writing 5--12
drug interactions with chronic 128 periapical inflammation see apica l prevalence (definition) :;,20
antimicrobials 20 dental management issues 163 periodontitis Prevotella species
oral leukop lakia see leukoplakia (oral) initial management by medical pericoronal abscess 61 ha litosis 97
oral lichen planus 74 practitioners 191 location (schematic diagram) 62 prilocaine
oral malodour see halitosis orofacia l 91- 6 pericoronal infection 61 adverse effects
oral mucocutaneous herpes post-treatment management 127-36 location (schematic diagram) 62 clinical pharmacology
simplex 79 pamidron ate pericoronitis (defin ition ) 220 dosing
oral mucosal disease see mucosal adverse effects periodontal abscess 59 pregnancy & breastfeeding (table)
disease (oral) osteonecrosis of the jaws 152 location (schematic diagram) 62 t herapeutic use
oral sedation see sedation precautions periodontal disease 55-60 dental procedures
oral ulcers see ulcers (oral) dental procedures 153 gingivitis 55 topical use
orofacial symptoms paracet amol acute ulcerative 57 principles
dental problems seen in medical adverse effects 30 locations (schematic diagram) 62 3 Ds 4
practice 199 clinical pharmacology 30 periodontal abscess 59 analgesic use 128
pain 91-6 third molar model (figure) 131 periodontitis 56 antimicrobial use 13
bruxism 93 interactions 30 periodontal ligament (definition) 220 corticosteroid (topical) use 37
burning mouth syndrome 91 overdose 31 periodontitis 56 diagnosis 1
temporomand ibula r disorders 95 precautions 30 location (schematic diagram) 62 management 3
trismus 93 pH (definition) 220 prescribing
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pregnancy & breastfeeding (table) 212 5
OSA see obstructive sleep apnoea phenoxymethylpenicillin procedures see dental procedutes "C
adverse effects 21 promethazine c
clinical pharmacology 21 therapeutic use
234 urticaria (box) 131 235
 prophylactic antibiotic therapy see Reye syndrome (definition) 220 salivary gland hypofunction see dry swallowed objects
antibiotic prophylaxis rheumatoid arthritis mouth emergency management 174
prosthetic joint infections dental management issues 163 salivary gland infections 69 prevention 174
prevention 106 rheumatological diseases scaling (dental) (definition) 221 syncope 168
pseudomembranous candidosis dental management issues 163 sedation 121-6
(oral) 82 risedronate assessment and preparation 122 T
psychiatric disorders adverse effects inhalational 124 T cells (definition) 221
dental management issues 164 osteonecrosis of the jaws 152 instructions for patients (box) 123 teicoplanin
psychological disorders precautions intravenous 125 clinical pharmacology 23
dental management issues 164 dental procedures 153 management of the patient 123 pregnancy & breastfeeding (table) 212
psychosomatic (definition) 220 rivaroxaban oral 124 therapeutic use
pulp (dental) (definition) 220 precautions sedative drugs 40 endocarditis prophylaxis 106
pulpitis dentoalveolar surgery 140 drug dependence 42 temazepam
definition 220 root canal system infection precautions adverse effects 41
initial management by medical initial management by medical viral hepatitis 160 clinical pharmacology 42
practitioners (table) 192 practitioners (table) 192 seizures interactions 41
pulpotomy (definition) 220 root canal treatment (definition) 220 dental management issues 157 precautions 41
pulse oximetry root planing (definition) 220 emergency management 177 pregnancy & breastfeeding (table) 212
anxiolysis and sedation 124 ropivacaine sharps injuries therapeutic use
emergencies (desired equipment) 189 adverse effects 113 dental management issues 160 anxiolysis 124
clinical pharmacology 112 sialadenitis 69 sedation 124
pregnancy & breastfeeding (table) 212 Sjogren syndrome 221
R dry mouth 87
temporise (definition)
therapeutic use temporomandibular disorders 95
radicular (definition) 220 snoring
radiographs (intraoral) and
dental procedures 117 tetracyclines 25
route of drug administration dental management issues 146 third molar model (figure) 131
pregnancy 205 sodium chloride see saline
radiotherapy (head and neck)
analgesics (general principles) 130 thrush (oral) 82
antimicrobials (general principles) 16 sodium hypochlorite thyroid disorders
adverse effects 83
roxithromycin denture hygiene dental management issues 150
dry mouth 87 somatisation (definition) 221
oral mucositis 85 cl inical pharmacology 24 tiludronate
pregnancy & breastfeeding (table) 212 spacer devices adverse effects
head and neck cancer 173
therapeutic use asthma (box) osteonecrosis of the jaws 152
dental management issues 162 emergencies (desired eq uipment) 189
de ntoalveolar surgical infections 68 precautions
recurrent aphthous ulcerative 203- 4
odontogenic infections (superlicial sport and drug use dental procedures 153
disease 78 squamous cell carcinoma of the
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regional block anaesthesia
regulations (legislation)
111 spreading)
periodontal abscess 60 tongue (photo) 73
tinidazole
clinical pharmacology 24
Q) rubber dam (definition) 221 Staphylococcus species pregnancy & breastfeeding (table) 212
c prescriptions 11 angular chei litis 85 therapeutic use
't:l relative analgesia see nitrous oxide
69
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resistance to antimicrobials 14 s salivary gland infections
stents (coronary artery)
acute ulcerative gingivitis 58
TMD (temporomandibular

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respiratory conditions
dental management issues
220

143
salbutamol
therapeutic use
asthma (box) 173
dental management issues
stomatitis
Streptococcus mutans
142
85
disorders)
tolerance (drug)
95
42
Ui asthma 144 emergencies (desired drug) 189 tooth avulsion 194
Q) dental caries 47 tooth decay see caries
c chronic obstructive pulmonary saline
Streptococcus species tooth extractions
03 disease 145 therapeutic use
angular cheilitis 85
obstructive sleep apnoea 146 alveolar osteitis antibiotic prophylaxis
:2 dental caries 47
:::J respiratory emergencies 171 initial management by medical endocarditis 103
<!J stroke surgical site infection 108
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asthma 172 practioners (table) 193 dental management issues 156
.p hyperventilation syndrome 171 dentoa lveolar surgical infections 68 complications 198
:::J emergency management 176 alveolar osteitis 69
Q) inhaled objects 174 odontogenic infections (local ised)
a. restorations (dental) (box) 63
surgery see dental procedures
bleeding 198 ><
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Q) definition 220 swelling post-tooth extraction 199 surgical site infections
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I- prevention 107 pain and swel li ng 198
loss 194 saliva (artificial) see artific ial saliva
treatment 67
retrognathia (definition) 220 237
236
 tooth extractions (cont.) ulcers (oral) (cont.)
precautions
anticoagulant and anti platelet
pemphigus vu lgaris
recurrent aphthous ulcerative
81 Request for comment
drugs 138
bisphosphonates 153
disease
viral ulcers
78
79 on guidelines
dry mouth 89 unilateral blindness 186
head and neck radiotherapy 162 urticaria 180
viral hepatitis 160
tooth fracture
tooth infections
194
see odontogenic
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valaciclovir
infections
clinical pharmacology 26
tramadol
pregnancy & breastfeeding (table) 212
cl inical pharmacology 31
vancomycin Help us to help you
tranexamic acid
clinical pharmacology 23
pregnancy & breastfeeding (table) 212 As the final user of this volume, you can give us valuable advice about
pregnancy & breastfeeding (table) 212
therapeutic use the content, layout and usability of this book. Your comments wi ll be
therapeutic use
dentoalveolar surgery in patients
taking warfarin (box) 141
endocarditis prophylaxis 106 most appreciated and will be considered during the preparation of the
varicella-zoster virus next edition.
transient ischaemic attack 176
oral ulcers 79
trauma
vasoconstrictors
maxillofacial 197
bleeding tooth socket (table) 200 Therapeutic Guidelines: Oral and Dental,
ocular 184
local anaesthesia 112
tooth avulsion 194
ulcers (oral) 77
unilateral blindness (adverse version 2, 2012
effect) 186
trench mouth 57
triamcinolone
Veillonella species Comments
halitosis 97
adverse effects 38
clinical pharmacology 35 veneers see restorations (dental)
Vincent's disease 57
potency (table) 36
vinegar
contraind ications 38
denture hygiene 83
precautions 38
viral hepatitis
pregnancy & breastfeeding (table) 212
dental management issues 159
principles of use 37
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(6 prescribing considerations (box) 38
triclosan w
Cl) clini cal pharmacology 45 warfarin
c Name
pregnancy & breastfeeding (table) 212 precautions
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c therapeutic use dentoalveolar surgery 139
C"CI halitosis 99 management (box) 141 Address
~ tricyclic antidepressants
adverse effects
withdrawal (drug) 42
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dry mouth 87 X
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Q) therapeutic use
c xerostomia see dry mouth
burning mouth syndrome 93 Detach this page and return to:
Qj trigeminal nerve injury 159
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::::l trigeminal neuralgia z Therapeutic Guidelines Limited
<.!J dental management issues 158 zinc lozenges
(.) trismus 93 halitosis 99 Ground Floor, 4 73 Victoria Street,
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erythema multiforme 82
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238 zygomatic complex (definition) 221
239