Australian Dental Journal

The official journal of the Australian Dental Association

Australian Dental Journal 2010; 55:(1 Suppl): 85–102

doi: 10.1111/j.1834-7819.2010.01203.x

The mouth in HIV⁄AIDS: markers of disease status and

management challenges for the dental profession
NW Johnson*
*Professor of Dental Research, Griffith Institute for Health and Medical Research; Foundation Dean, School of Dentistry and Oral Health, Griffith
University, 2005–2009.

ABSTRACT
There are over 30 million people in the world with HIV infection and, whilst the rate of new infections is slowing, this
number continues to grow. Although in Australia the overall prevalence of HIV infection in adults aged 15–49 is officially
estimated at only 0.2%, representing less than 20 000 people living with HIV and AIDS, our geographical area contains
populations with prevalences exceeding 10 times this. Oral health professionals must therefore practise safe, standard
infection control at all times and be aware of the oral manifestations of HIV disease. These are predominantly opportunistic
infections with fungi such as Candida albicans or with viruses of the herpes family, particularly herpes simplex, herpes
zoster and Epstein-Barr virus infections. Warts or papillomas may arise due to human papilloma viruses – even in
individuals on effective antiretroviral therapy. Rare types of fungal infection can occur, and severe bacterial infections,
notably tuberculosis, are an ever-present risk. Susceptibility to periodontal breakdown is somewhat enhanced by the effects
of HIV disease itself, and caries activity may increase because the patient neglects attention to diet and oral hygiene.
Restorative and periodontal care need, therefore, to be maintained at a high level. Oral opportunistic infections cause much
distress and the diagnosis and management of these is the responsibility of our profession.
Keywords: HIV, AIDS, blood-borne viruses, infected health care worker, oral manifestations, Candidiasis, herpes viruses, papilloma
viruses, tuberculosis, periodontal diseases.
Abbreviations and acronyms: ANUG = acute necrotizing ulcerative gingivitis; ASHM = Australian Society for HIV Medicine; CDC =
Centers for Disease Control and Prevention; CMV = cytomegalovirus; EBV = Epstein-Barr virus; FSW = female sex workers; HAART =
highly active antiretroviral therapy; HBV = hepatitis B; HCV = hepatitis C; HHV = human herpes virus; HPV = human papilloma virus;
HSV = herpes simplex virus; IDU = injecting drug users; IRIS = immune reconstitution inflammatory syndrome; KS = Kaposi sarcoma;
MAC = mycobacterium avium complex; MSM = men who have sex with men; NACO = National AIDS Control Organization; NHMRC =
National Health and Medical Research Council; NNRTI = non-nucleoside reverse transcriptase inhibitors; NRTIs = nucleoside reverse
transcriptase inhibitors; OC = oral candidiasis; OHL = oral hairy leukoplakia; OSAP = Organization for Safety and Asepsis Proceedures;
PEP = post-exposure prophylaxis; PI = protease inhibitors; PLHA = people living with AIDS ⁄ HIV; PMBC = peripheral blood mononuclear
cells; RAS = recurrent aphthous stomatitis; TB = tuberculosis; UN = United Nations; WHO = World Health Organization.

also viral and sometimes severe bacterial infections,

INTRODUCTION
The global pandemic of HIV infection and AIDS
continues unabated. In much of the Western world a
degree of complacency has set in because being HIV-
positive is no longer a death sentence: we have seen a
remarkable transition to a chronic, and largely man-
ageable disease. This is due to the efficacy of modern
highly active antiretroviral therapy (HAART). How-
ever, the situation remains a global disaster and
awareness amongst professionals and the public must
remain high. Many of the earliest manifestations of the
immune suppression associated with HIV infection
occur in the mouth – particularly oral candidiasis, but
ª 2010 Australian Dental Association
including tuberculosis. The dental and oral health
professions therefore have a key role in early diagnosis,
and in the management of these distressing infections.
The highest standards of infection control must be
maintained in all clinical situations and appropriate
action taken should a clinician find him or herself HIV
positive.
The single most useful entry point for all matters to
do with HIV diseases and the dental profession is the
HIVdent website.1 This site itself has extensive current
information on facts, policies and procedures, many
links to other valuable internet sites, as well as to
current periodical literature.
85
NW Johnson
Current status of the global pandemic
The latest data available from the global databases
managed by the United Nations (UN) and the World
Health Organization (WHO)2 reveal that, at the end of
2008, there were some 33.4 million people living with
HIV ⁄ AIDS in the world, with 2.7 million new
infections that year alone, and 2 million deaths. These
are breathtaking numbers. There were more than 7400
new infections per day in 2008. More than 97% of
these are in low- and middle-income countries, about
1200 are in children under 15 years of age and, of those
in adults, almost 48% are among women and about
40% are among young people aged 15–24. Given that a
high proportion of these will die or remain chronically
severely unwell, the personal, social, economic and
political consequences for societies with high preva-
lence of HIV disease are clearly immense.
Figure 1 shows the global distribution. The major
burden remains sub-Saharan Africa but our region,
South and South-East Asia, ranks second. India is in
fact the single country on earth with the highest number
of cases.
Figure 2 is perhaps some good news. Whilst the total
number of people in the world living with HIV ⁄ AIDS
continues to rise, partly due to population growth, the
number of new infections per annum is falling, largely
due to health promotion campaigns. Death rates are also
falling, predominantly because of increasingly effective
therapy. However, these generalizations cover many
serious situations, including in our part of the world.
Prevalence rates of HIV infection around the world
range from 5.2% in sub-Saharan Africa, through 0.7%
in Eastern Europe, 0.6% in North and Latin America,
to 0.3% in South and South-East Asia and in Oceania.
Such averages, however, disguise some astoundingly
high infection rates. Again, sub-Saharan Africa is the
World Health
Organization
Adults and children estimated to be living with HIV, 2008
Total: 33.4 million (31.1–35.8 million)
December 2009
Fig 1. Adults and children living with HIV, 2008 (source UNAIDS 2009).
86
biggest challenge: in Zwaziland 25.9% of the popula-
tion is HIV positive; in Botswana 25%; 23.4% in
Lesotho; 18.1% in Zimbabwe and 16.9% in the
Republic of South Africa.
The situation in the Asia-Pacific region
As given in Fig 1, there is a considerable burden of
disease in our region: 3.8 million people living with
HIV and ⁄ or AIDS in South and South-East Asia; a
comparatively small number, 59 000 in Oceania.
However, these statistics disguise some serious situa-
tions. Again we need to look at the prevalence of HIV
infections country by country: the Indonesian Province
of Papua was estimated by UNAIDS to have a
prevalence of 2.4% in 2006; Cambodia 0.6% in
2005; and India 0.3%.
As a regional power, and a nation with well-
developed professional standards, we have a responsi-
bility to help stem the epidemic in these countries and
to assist in helping the afflicted.
In India, the 2007 estimates of prevalence of
HIV infection in adults aged 15–49 range from 0.2%
to 0.5%.3 In a nation with a population of over a
billion (1 151 147 600) souls,4 this translates to some
2 400 000 infected individuals – both figures growing
by the second. High-risk groups, inevitably, show
higher numbers. Among injecting drug users (IDUs), it
is as high as 8.71%, 5.69% and 5.38% among men
who have sex with men (MSM) and female sex workers
(FSWs), respectively. India has an excellent National
AIDS Control Organisation (NACO),5 which describes
the considerable national programme therein, and
provides data showing there is now a gradual decline
in the numbers of people living with HIV ⁄ AIDS
(PLHA).
4
ª 2010 Australian Dental Association
 The mouth in HIV ⁄ AIDS

Global estimates 1900–2008

Number of people living with HIV Adult (15–49) HIV prevalence (%)

40 1.2
Number (millions)

30 0.9

20 0.6

%
10 0.3

0 0
1990 1993 1996 1999 2002 2005 2008 1990 1993 1996 1999 2002 2005 2008

Number of people newly infected with HIV Number of adult and child deaths due to AIDS
5 5
Number (millions)

Number (millions)
4 4

3 3

2 2

1 1

0 0
1990 1993 1996 1999 2002 2005 2008 1990 1993 1996 1999 2002 2005 2008

Estimate High and low estimates

Source: UNAIDS/WHO World Health

Figure 1 Organization
2009 AIDS epidemic update

Fig 2. Global estimates 1990–2008 (source UNAIDS 2009).

Most near neighbours in South-East Asia, including However, as the HIV status of an individual will usually
popular tourist destinations and trading partners, have be unknown, universal precautions remain mandatory
substantially higher rates than Australia. Prevalence (see below). It is also prudent to remember that HIV is
rates in adults aged 15–49 are currently estimated at the least infectious of the blood-borne viruses (see
0.8% in Cambodia; 0.5% in Vietnam and in Malaysia; below); the number of Australians estimated to be
and 0.2% in Indonesia overall. infected with hepatitis C is approximately 200 000, and
Figure 3 shows how the situation in the Pacific is 90–160 000 with hepatitis B – again Aboriginal and
dominated by our near neighbour, Papua New Guinea Torres Strait Islander citizens are over-represented.6
(PNG). In PNG, the prevalence in adults aged 15–49 is Figure 4 suggests that the rate of newly diagnosed
estimated at 1.5%, with 54 000 PLHA. HIV infections may have plateaued. However, this
shows no significant change in the number of newly
acquired infections. A more detailed look at data up to
The situation in Australia
2007 shows a steady rise in the number of infected
The remainder of this paper will mainly concentrate on individuals, largely explained by Australia’s continuing
the situation in Australia, with international compari- population growth (Fig 5). Also, the vast majority of
sons where informative. In Australia, the overall new cases in Australia are in people born outside
prevalence of HIV infection in adults aged 15–49 is Australia – especially those from sub-Saharan Africa.
officially estimated at 0.2% (0.1–0.3%): some 18 000 During this time there has been a dramatic fall in the
PLHA. This seems a small number, and indeed it is death rate from AIDS-related illnesses, the downturn
compared to the numbers given above. With some dating from the mid 1990s (Fig 6). This follows the
11 000 practising dentists in the nation, few of us will downturn in AIDS diagnoses from that time (Fig 7),
be caring for such an individual, and those patients largely explained by the increasing availability, and
known to be HIV positive, and ⁄ or patients with increasing efficacy, of HAART.
oral ⁄ dental problems associated with HIV disease, tend Chemotherapy for HIV infection per se has advanced
to be concentrated in clinics conducted by colleagues dramatically in both efficacy and coverage. The vast
with a special interest or skill in their management. majority of infected individuals in Australia are under
ª 2010 Australian Dental Association 87
NW Johnson

Proportion of all HIV and AIDS cases in different Pacific island

countries and territories, 1984–2007

New Caledonia 1.2%

French Polynesia 1.1%

Fiji 1.1%

Guam 0.8%

All others 0.8%

Papua New Guniea 95.0%

Sources: The Secretariat of the Pacific Community and Papua New Guinea Department of Health.
World Health
2009 AIDS epidemic update Figure 27 Organization

Fig 3. Proportion of HIV ⁄ AIDS in the Pacific (source UNAIDS 2009).

Newly diagnosed HIV infection in Australia, Number of people living with HIV, 1990–2007
including diagnoses of newly acquired HIV
1200 infection, by year Number of people living with HIV
High estimate
1000 Low estimate
40 000
800
Number

600
30 000
People living with HIV

400

200
20 000
0
1999 2000 2001 2002 2003 2004 2005 2006 2007 2008
Year
Other HIV diagnoses Newly acquired HIV 10 000
Source: state and territory health authorities

Fig 4. Newly diagnosed HIV infections in Australia, 1999–2008

(source60).
1990
1991
1992
1993
1994
1995
1996
1997
1998
1999
2000
2001
2002
2003
2004
2005
2006
2007

treatment (Fig 8), those not receiving such care having

Year
fallen from around 15% of cases at the turn of the
Fig 5. People living with HIV and AIDS (PLHA) in Australia,
millennium to 10% today. Most are now on triple 1990–2007 (source61).
therapies, with various mixtures of protease inhibitors
(PI), nucleoside reverse transcriptase inhibitors (NRTIs) Trends across and within Australia in all these
or non-nucleoside reverse transcriptase inhibitors measures can be seen on the NCHER website,7 and in
(NNRTIs). the paper by Guy et al.8
88 ª 2010 Australian Dental Association
 The mouth in HIV ⁄ AIDS

1600
Estimated number of deaths due to AIDS, 1990–2007

1400 Annual number of deaths due to AIDS

1200 High estimate
Low estimate
1000

800

600

400

200

1990 1992 1994 1996 1998 2000 2002 2004 2006

1991 1993 1995 1997 1999 2001 2003 2005 2007
Year

Fig 6. Estimated deaths due to AIDS in Australia, 1990–2007 (source62).

Diagnoses of HIV infection and AIDS in Australia Risk factors for transmission of HIV: MSM,
2500
heterosexual, IDU, mother-to-child, clinical settings
2000 Within Australia, the major routes of transmission
(Fig 9) remain those involved with MSM. Whilst a
1500 proportion of these are also IDUs, and could have
Number

acquired their infection by either route, most of the

1000
transmission would be from anal intercourse, without
effective condom use. Free virus can be present in
500
ejaculate and anal mucosa is both thin and physically
fragile, and lacks Langerhans’ cells. Of interest to us
0
1981 1983 1985 1987 1989 1991 1993 1995 1997 1999 2001 2003 2005 2007 as oral health clinicians are the risks associated with
Year oral fluids and oral–genital contact. There are risks in
HIV diagnoses AIDS diagnoses
Source: state and territory health authorities both directions; the risk of transmission via saliva ⁄
oral fluids and the risk of becoming infected through
Fig 7. New HIV infections and diagnoses of AIDS in Australia,
1999–2008.63 the mouth. This is amplified below. It has been
shown that a major route of transmission of human
herpes virus 8 (HHV-8), the causative agent of
Kaposi’s sarcoma, an AIDS defining illness, is the
use of saliva as a lubricant during anal intercourse –
Treatment uptake among people enrolled on the oropharynx being the major reservoir of this
40
the Australian HIV observational database by virus.9
year1
These data indicate that the practice of safe sex is not
universally followed in this high-risk community,
30
indicating a continuing challenge for education and
social support networks.
Percent

20
The next major route is heterosexual. In some
Western countries, the UK for example, this is now
10 the most common route, and it was always so in the
high-incidence countries in Africa and in Eastern
0 Europe and South-East Asia. Because most sexual
1999 2000 2001 2002 2003 2004 2005 2006 2007 2008
Year
activity takes place between men and women, the risks
None Monotherapy
Double therapy 3+ (NRTI +/– PI, not NNRTI) of disease being spread throughout a population are
3+ (NRTI + NNRTI, not PI) 3+ (PI + NNRTI +/– NRTI)
1 Dashed lines indicate the years of retrospective data collection
vastly increased once HIV infection becomes estab-
Source: Australian HIV observational database
lished in this majority. (In Africa, most infections are
Fig 8. Treatment uptake and modalities for HIV-infected people in amongst young women.) Whilst rates of HIV infection
Australia, 1999–2008 (source63). in Aboriginal and Torres Strait Islander peoples are
ª 2010 Australian Dental Association 89
NW Johnson

HIV infection, 2004–2008, by HIV exposure

category
Newly diagnosed HIV infection Newly acquired HIV infection

3% 3%
8% 1%

4% 10%
21%

4% 64%

82%
Men who have sex with men
Men who have sex with men and injecting drug use
Heterosexual contact
Injecting drug use
Other/undetermined
Source: state and territory health authorities
Fig 9. Routes of transmission for new HIV infections in Australia, 2004–2008 (source63).

similar to those of non-Indigenous Australians, and

MSM is again the major route, heterosexual transmis-
sion is a larger proportion (Fig 10), indicating risk of a
growing epidemic.
Sharing of drug injection equipment has long been
recognized as a very dangerous practice.
Transmission of HIV from an infected mother to her
offspring occurs predominantly during passage down
the birth canal. It is almost entirely preventable if
appropriate antiviral drugs are given to the mother
before labour, but unfortunately remains a major
problem in Africa where paediatric AIDS cases are
distressingly common.10
The natural history of HIV infection
Infection with HIV occurs by the transfer of blood,
semen, vaginal fluid, pre-ejaculate, or breast milk.
Within these body fluids, HIV is present in two different
ways: free virus particles and virus within infected
immune cells. It is possible to find HIV in the saliva,
tears, and urine of infected individuals, but there are no
recorded cases of infection by these secretions, and the
risk of infection is minimal.
It is prudent to remind ourselves of the changes over
time in viral loads in circulating blood and the
development of an immune response. Figure 11 shows

HIV diagnoses in Australian born cases, 2004–2008, by Aboriginal

and Torres Strait Islander status and HIV exposure category
Aboriginal and Torres Non-
Strait islander Indigenous

48%

1% 75%

6%
5%
23%
22% 12% 3% 5%
Male homosexual contact
Male homosexual contact and injecting drug use
Injecting drug use
Heterosexual contact
Other/undetermined

Fig 10. Transmission in Indigenous and non-Indigenous Australians (source64).

90 ª 2010 Australian Dental Association


HIV RNA (RT-PCR)
Relative level above detection
Infectious
viremia
Exposure
0 10 20
Days post-infectious viremia
Fig 11. Changes over time in blood levels of HIV and of antibodies to
HIV components following infection. Virus RNA levels in plasma
measured by reverse-transcriptase polymerase chain reaction (RT-
PCR) – red: HIV DNA in peripheral blood mononuclear cells
(PBMC) – yellow; immunoglobulin antibodies to HIV – blue; HIV
core protein antigen p24 – green.
(Source http://depts.washington.edu/labweb/Divisions/viro/HIV_
serv041b.jpg)
the beginning of an infectious viraemia within a few
days of exposure. This rises to a peak some three weeks
later, during which the subject has large numbers of
virus in plasma and is shedding these in secretions. It
takes a little longer for viral load to rise within
peripheral blood mononuclear cells (PBMC). It takes
three weeks or so for antibodies to build up sufficiently
to suppress the virus, and this is the important
‘‘window’’ when antibody-based HIV tests can give a
false negative result. After months or years (not shown),
if there is no or ineffective antiviral therapy, there is
successive immune suppression with falls in peripheral
blood CD4 lymphocyte counts, rises again in free
and cell-associated virus, increasing infectivity and
illness.
Transmission of HIV in clinical settings
Clearly, this is an area of great interest to oral health
professionals. This is why we have universal precau-
tions, or today preferably called standard precautions, to
prevent cross-infection. It is not the intent of this review
to repeat details of these protocols. They are available
from many sources, e.g., the Centers for Disease Control
and Prevention (CDC) in the USA,11 and the Organiza-
tion for Safety and Asepsis Procedures (OSAP).12 The
latter is ‘‘dedicated to promoting infection control and
safety policies and practices supported by science and
research to the global dental community’’. Their advice
is current and comprehensive. Within Australia, those
from the National Health and Medical Research Coun-
cil (NHMRC) are currently under review with a 2010
draft out to consultation.13 Amongst those which
morally and legally guide us are those from the
Australian Dental Association,14 and all of the jurisdic-
ª 2010 Australian Dental Association
The mouth in HIV ⁄ AIDS
tional dental boards.15 No doubt the new national
in plasma Dental Board of Australia will proscribe such also.
Infection control procedures are designed to minimize
HIV antibody the risk of transmission of all micro-organisms, from
operator to patient, patient to operator, patient to
patient and also to other clinical and laboratory staff. In
HIV DNA (PCR)
the context of HIV, the risks are associated with infected
in PBMC fluids – blood or saliva ⁄ oral fluids – or instruments
contaminated with such, entering a new host. It is,
HIV p24 Ag
therefore, salient to remind ourselves of the viral loads –
the ‘‘dose’’ – necessary for infection to be transmitted.
30 40 50 60 70 80
HIV has a comparatively low risk of transmission: HIV
is much less infectious than hepatitis C (HCV) which in
turn is much less infectious than hepatitis B (HBV).
Extensive monitoring following needle stick injuries
in the USA (CDC data – op cit.) indicate that the risk of
the recipient seroconverting following injury with a
syringe contaminated from a patient who is HBsAg+
and HBeAg+ is that 22.0–31.0% will develop clinical
hepatitis and 37–62% serological evidence of HBV
infection. For a ‘‘donor’’ who is HBsAg+ and HBeAg-,
1.0–6.0% will develop clinical hepatitis and 23–37%
develop serological evidence of HBV infection.
In contrast, from an HCV positive ‘‘donor’’, only
1.8% (0–7% range) will seroconvert and from an HIV
positive donor, only 0.3% (0.2–0.5% range). Never-
theless, first aid is mandatory: wounds must be made to
bleed and washed with saline. The recipients must
report to an occupational health clinic where advice on
post-exposure prophylaxis (PEP) will be given. Antiret-
roviral drugs given at this stage are very effective. The
website of the Australasian Society for HIV Medicine
(ASHM) is a good starting point for the range of polices
extant across Australia and New Zealand.16
The HIV-positive health care worker: current policies
This has been an area of considerable controversy, and
evolving policy. There are wide international varia-
tions. At the 2009 6th World Workshop on The Mouth
and AIDS, the ‘‘Beijing Declaration’’ was approved by a
gathering of global expertise.17 This states:
BEIJING DECLARATION 2009
The participants of the 6th World Workshop on Oral
Health and Disease in AIDS, which took place from
21–24 April 2009 in Beijing, China, welcomed the
opportunity to assess the evidence relating to the
transmission of HIV in the dental setting from oral
health care professionals to patients.
Participants from over 30 countries noted and
considered the inconsistencies in the regulation of the
ability of an HIV positive oral health care professional
to continue practice.
Having analysed the scientific evidence that has
become available over the last 20 years, the participants
of this workshop conclude that the evidence now
91
NW Johnson

supports the view that Oral Health Care Professionals
with HIV do not pose a risk of transmission to patients in
the dental setting. They can continue a career in clinical
practice, provided that the following criteria are met:
(1) The individual is under ongoing care by a suitably
qualified HIV Health Care Professional
(2) The individual remains aware of his ⁄ her health
status and acts appropriately
(3) Standard Infection Control is observed
(4) Scientific evidence related to HIV transmission will
continue to be reviewed.
As but one example of an Australian jurisdictional
guideline, the Dental Board of Queensland currently
states:18
‘‘Paragraph 5.2 A Dental Practitioner who discovers
that he ⁄ she returns test results in any of the following
categories:
5.2.1 Hepatitis C antibody and PCR positive;
5.2.2 Hepatitis B e antigen or hepatitis B virus DNA
positive; or
5.2.3 HIV antibody positive.
must immediately cease to perform exposure prone
procedures; and seek expert advice, from a specialist in
the field of infectious diseases.
Failure by such a Dental Practitioner to cease
performing exposure prone procedures may constitute
unsatisfactory professional conduct leading to disci-
plinary action before the Health Practitioners Tribunal.
Dental Practitioners who meets the criteria of 5.2
have an obligation to notify the Board of their status.
Failure by such a Dental Practitioner to notify the
Board immediately of their status may constitute
unsatisfactory professional conduct leading to disci-
plinary action before the Health Practitioners Tribunal.
Exposure-prone procedures are those where the
operator’s fingers are out of sight and likely to come into
close contact with sharp objects. The latter include teeth,
bone, wires, appliances and instruments. Clearly, this
involved, assuming the conduct of standard precau-
tions, and the availability of modern HAART, an HIV-
positive dentist conveys minimal risk to his ⁄ her patients
unless and until they are cognitively impaired. This is
the rationale for requiring ongoing care by a suitably
qualified HIV health care professional.
Oral manifestations of HIV and AIDS
The common opportunistic infections: their diagnosis
and management
In the early days of the HIV epidemic, the oral
medicine ⁄ oral pathology community around the world
agreed upon a classification of oral manifestations of
HIV ⁄ AIDS and, importantly, their diagnostic criteria.21
This was based on how common each lesion, or type of
lesion, was seen in known AIDS patients at that time –
the classification was published in 1993, a little over a
decade into the epidemic. As the years have passed, the
relative frequency of these lesions, or oral manifesta-
tions, has changed, largely due to the impact of
HAART in the West, and considerable regional varia-
tions have been described.22 Today it is more fruitful –
certainly more logical – to deal with lesions according
to type of opportunistic infection, and then by the
major organ involved.
These manifestations have long been regarded as
‘‘sentinels and signposts’’ of HIV infection,23 and now
have value in monitoring the efficacy of anti-HIV
therapy, with predictive value for treatment failure.
Figure 12 shows the ‘‘staircase’’ of progressive immune
suppression and the stage at which various opportunis-
HIV INFECTION:INDIAN SCENARIO
MEAN CD4 COUNTS
350

encompasses almost all procedures in clinical dentistry – 300

315
303

effectively barring the infected health care worker from 270

any clinical work – save the taking of radiographs and

MEAN CD4

250

impressions in an edentulous patient. Many regard this as 200 192 192 190 190 187
unnecessarily restrictive and, indeed, such concerns are 180

154
the basis of the Beijing Declaration. There remains only a 150 148 144
133
118
single established case of an HIV-positive dentist having 100
EX

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transmitted his infection to a patient – the infamous Acer

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PC

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ET

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case in Florida in late 1987. The mode of transmission

AN
S

IN

PL

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S

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LM

LM
PE

M
V
N
PE

BA
E

C
XO

EN
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has never been established;19 malice is suspected.20 Of

EN
PH

M
H

TR
H

C
TR
U

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O

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course there could be unknown cases, and the risk of

RY
O

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D

these may be higher in resource-poor settings where they
are less likely to come to light, hence continued vigilance
in monitoring the scientific literature.
It remains to be seen how widely regulatory author-
ities around the world accept the view of the Beijing
Workshop. Given the low risk of transmission (as
identified above) when small volumes of blood are
92
Fig 12. A ‘‘staircase’’ of progressive immune suppression and the
stage at which various opportunistic infections emerged; from a large
cohort of South Indian patients in the days before HAART was widely
available.24 (OHL = oral hairy leukoplakia; OP = oropharyngeal; TB
= tuberculosis; RTI = respiratory tract infection; CMV = cyto-
megalovirus; PCP = pneumocystis carinii pneumonia.)
(Source: Courtesy of Professor Suniti Solomon and Drs Kumarasamy
and Ranganathan, YRG Centre for AIDS Research and Epidemiol-
ogy, and Ragas Dental College, Chennai, India.)
ª 2010 Australian Dental Association

tic infections emerged in a study of a large cohort of
patients in South India in the days before HAART was
widely available.24
The dental ⁄ oral health professions have a duty of
care to manage oral and dental conditions in HIV-
positive patients, no less than any member of society.
This applies to ‘‘routine’’ aspects of preventive den-
tistry, and to maintenance and repair of the dentition.
This can be challenging because patients, with their
many stresses following a diagnosis of HIV infection,
sometimes neglect their oral hygiene, may be in
financial difficulties, and may present with severe caries
or unresolved periodontal problems. Xerostomia asso-
ciated with anti-HIV drugs often compounds the
problems. Within this complexity, there are no funda-
mental reasons why an HIV-positive patient should not
receive the full range of high quality dental care. There
is good evidence that the outcomes of, for example,
endodontic treatments are not compromised.
Management of the opportunistic oral infections
described below may require referral to an oral
medicine specialist and, in any event, should be planned
in conjunction with the patient’s HIV physician. Best
practice protocols are widely available from many
national and international sources and the approaches
summarized below are derived mostly from the WHO,
USA25 and Australian sources through the gateway of
the ASHM.26 These include user-friendly information
for patients.27
Effective treatment of opportunistic infections is also
dependent on effective antiretroviral treatment and oral
clinicians also need to be alert to the possible emergence
of immune reconstitution inflammatory syndrome
(IRIS) (see later).
Infections with Candida albicans and other fungi
Figures 13 and 14 show cases of overt oral candidiasis
in AIDS patients. Such florid infections are more
Fig 13. Acute pseudomembranous candidiasis in an AIDS patient.
Heavy deposits of ‘‘thrush’’ cover the gingivae and tooth surfaces.
ª 2010 Australian Dental Association
The mouth in HIV ⁄ AIDS
Fig 14. Acute candidiasis with thrush deposits on an erythematous
base affecting hard and soft palate.
common in severe immunosuppression and even in
the era of HAART remain a major clinical problem, as
recently reviewed by Thompson et al.28 Infection can
spread to the oesophagus. Whilst in an emergency
situation, or in mild infections, topical amphotericin,
nystatin, clotrimazole or posaconazole can be effective,
systemic treatment with fluconazole is usually required
in established HIV infection. Ketoconazole or itraco-
nazole have poor absorption from the gut and are not
first-line treatment. There are increasing reports of
azole resistance, so patients should ideally be referred
for culture and antifungal sensitivity testing before
prescribing these drugs – and because of the risk of drug
interactions, liver toxicity and other side effects,
patients require close medical monitoring.
Candida albicans is the most common species, but
C. glabrata and C. dubliniensis are described.
Other so-called ‘‘deep mycoses’’ can infect oral
tissues, particularly in tropical and some developing
countries where these organisms are more commonly
picked up from the soil of other natural habitats. These
infections include cryptococcosis, histoplasmosis, para-
coccidiomycosis, penicilliosis and aspergilosis.29 Fig-
ure 15 shows an HIV-positive African patient who
presented with a granulomatous gingival enlargement
which proved to harbour histoplasma spores on biopsy,
and who had a raised specific antibody titre to this
fungus.30
Significant bacterial infections
Mycobacterial infections: The WHO estimates that
tuberculosis (TB) is the cause of death in 13% of AIDS
patients. Mycobacterium tuberculosis is usually ac-
quired through droplet infection – coughing, sneezing,
shouting by an already infected individual nearby, and
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Fig 15. Granular inflammation of free and attached gingiva caused by
infection with the fungus Histoplasma capsulatum.
usually results in an acute pulmonary infection in the
susceptible recipient. In many countries where TB is
endemic, a subject may have acquired TB long ago and
has remained in a latent state which becomes reacti-
vated when he ⁄ she becomes immunosuppressed. With
increasing degrees of immunodeficiency, extra-pulmo-
nary TB is more common, affecting many internal body
sites, but also occasionally the mouth (Fig 16). There-
fore, lesions in the mouth can lead to diagnosis.
Management is systemic in the hands of a specialist
physician.
A review of 18 cases in AIDS patients from Brazil,
with a literature review, is given by Miziara.31 Our
work amongst HIV patients in Kenya reveals oral
candidiasis (OC) in 72% of patients, and TB (anywhere
in the body) in 57%: the crude odds ratio for TB in the
presence of OC was 4.0, indicating that, especially in
high-incidence communities, TB diagnosis must be
sought when a patient presents with OC, so that early
treatment can be initiated.32
Occasionally other mycobacteria are involved, oral
lesions caused by Mycobacterium avium intracellulare,
Fig 16. Typical punched-out TB ulcers in the retromolar area. This
AIDS patient also had extensive pulmonary and lymphatic involve-
ment. Clearly, such a patient is a danger for transmission to others.
94
are occasionally seen,33 and there may be widespread
involvement of paranasal sinuses.34
Viral infections
Viral infections are very common in the immunocom-
promised. Those affecting the head and neck, or mouth,
are mostly members of the human herpes virus (HHV)
family or are human papilloma viruses (HPV).
HHVs cause a spectrum of disease in the head and
neck. Their major reservoirs are salivary glands and
oropharyngeal lymphoid tissues, and a high proportion
of healthy adults silently harbour these viruses, having
developed reasonable immunity from subclinical infec-
tions earlier in life. With progressively failing immu-
nity, active infections may re-emerge, and be transmit-
ted via saliva. In the era of HAART the prevalence of
these lesions – at least in the Western world, has
decreased dramatically.35
Herpes simplex (HHV1 and HHV2) infections
Oral health practitioners are familiar with herpes
simplex virus infections: usually HSV1 – occasionally
HSV2 – in the form or recurrent herpes labialis. We see
a primary herpetic gingivostomatitis less frequently than
our general medical practitioner colleagues, because a
child with an acute febrile illness is not usually taken to
the dentist. Almost all adults will have acquired a degree
of immunity to herpes simplex viruses, but severe oral
blistering can occur in HIV patients (Fig 17). Unsur-
prisingly these are very painful, and patients are usually
quite febrile. If lesions are widespread, treatment in
collaboration with the patient’s physician is advisable.
For the management of oral lesions, high systemic doses
of modern antiviral drugs are required. Topical acyclo-
vir, often used for recurrent herpes labialis on pro-
drome, will have no effect. Ganciclovir or famciclovir
would be preferred today.
If diagnosis is in doubt, this can be reached by
sending blood for herpes simplex antibody titres –
Fig 17. Severe blistering of the tongue in an HIV-positive patient
caused by herpes simplex virus.
ª 2010 Australian Dental Association

rising titres if sequential samples are taken in acute
phase or, if facilities exist, for identification of the
presence and type of HSV by polymerase chain
reaction. A smear for light microscopy may reveal
characteristic Tzank cells.
Supportive treatment by way of analgesic mouth-
washes, such as benzydamine hydrochloride (Difflam),
obtundant gels (topical steroids should not be used),
maintenance of fluid balance should be provided.
Systemic antivirals are unlikely to be helpful in
established infections such as that illustrated, though
may be indicated under medical guidance to avoid risk
of spread.
Herpes zoster (HHV3) infections
Herpes zoster, or shingles, may affect nerves of the head
and neck (Fig 18). Once again, the vast majority –
probably in excess of 90% of adults in Australia – will
be VZV seropositive, acquired through chicken pox as
a child.
Cytomegalovirus (HHV5) infections
Another member of the human herpes virus family,
cytomegalovirus (CMV), can cause relatively innocu-
ous-looking ulcers of the lining mucosa of the mouth
(Fig 19). Like any oral ulcer these can be very painful,
and require symptomatic treatment. Unless they resolve
rapidly, further advice should be sought because CMV
is the major cause of retinitis in HIV patients, and can
cause encephalitis. Indeed before the era of HAART
some 30% of patients in the West developed CMV
retinitis sometime between the time of AIDS diagnosis
and death. CMV disease can spread elsewhere in the
gastro-intestinal tract, and cause a terminal pneumoni-
tis. Intensive treatment with modern antiviral drugs
such as valganciclovir, ganciclovir, foscarnet, or cido-
Fig 18. Blisters caused by herpes zoster virus (shingles) which affected
the mandibular branch of the right trigeminal nerve in this HIV
patient: lesions existed across the skin of his lower face.
ª 2010 Australian Dental Association
The mouth in HIV ⁄ AIDS
Fig 19. Non-specific ulcers of the buccal mucosa caused by cyto-
megalovirus.
fovir, orally and ⁄ or intravenously will be required for
any spreading infection.
Epstein-Barr virus (HHV4) infections
Perhaps the most ubiquitous HHV is Epstein-Barr virus
(EBV). In the Western world, as many as 95% of adults
between 35 and 40 years of age have been infected with
EBV, having had a primary infection in childhood or
adolescence.36 The acute primary infection is glandular
fever (infectious mononucleosis, IM), but the first
infection is often subclinical. EBV is again harboured
in the upper aerodigestive tract – IM is not called ‘‘the
kissing disease’’ for nothing – and it re-emerges in
the immune-suppressed with disease manifestations in
this anatomical area. Further information is available
on the ‘‘Virology Down Under’’ website.37
EBV is also the primary cause of Burkitt’s lymphoma,
a disease endemic in the malaria belt of Africa, and of a
number of other lymphoproliferative diseases (see
below). For dentists, the signature EBV-associated
lesion is so-called oral hairy leukoplakia (OHL)
(Figs 20–23). Described by dental colleagues in San
Francisco in the early days of the HIV epidemic there,38
it is a lesion renowned as an early marker of HIV
infection, and well known to the public and the
profession alike. The ‘‘hairy’’ descriptor arises from
the appearance of elongated filiform papillae and these
are associated with white, often plaque-like changes.
However, OHL has no aetiological or pathological
associations with other forms of oral leukoplakia, a
minority of which have the potential to transform over
time into squamous cell carcinomas.39
EBV also drives a range of malignancies of the
lymphatic system, predominantly B-cell non-Hodgkin’s
lymphomas.40 These were very common in the pre-
HAART era. Such a case is shown in Figs 24 and 25.
The pain and swelling in the right mandible in this HIV-
positive patient was, perhaps not surprisingly, assumed
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Fig 20. Typical oral hairy leukoplakia affecting the lateral border of
the oral tongue.
Fig 21. Oral hairy leukoplakia extending from the lateral borders of
the tongue to the ventral tongue and floor of mouth mucosa.
Fig 22. Haematoxylin and eosin-stained section from an OHL lesion.
There is increased thickness of the upper layers of the epithelium, with
‘‘balloon’’ or clear cells and a conspicuous absence of inflammation in
the connective tissue.
by his dentist to be the result of an odontogenic
infection, especially as the original radiograph probably
revealed a periapical radiolucency. Endodontic therapy
96
Fig 23. The process known as in situ hybridization localizes EB-virus
particles, predominantly within the nuclei of these balloon cells.
Fig 24. Swelling over the posterior part of the body of the right
mandible. The differential diagnosis would include an odontogenic
infection.
Fig 25. An orthopantomogram of the patient in Fig 23 reveals
periapical radiolucencies on tooth 46, attempted obturation of both
roots and a metal crown. In fact, the radiolucency was caused by an
AIDS-associated lymphoma.
had no effect, the diagnosis being lymphoma eroding
mandibular bone and spilling into a soft tissue tumour.
Acyclovir (acycloguanosine) inhibits viral DNA synthe-
sis in lytic infection but not latent infection, so
treatment of lymphomata requires more complex
ª 2010 Australian Dental Association

cytokine or cytotoxic therapies in the hands of specialist
oncologists.
Kaposi sarcoma virus (HHV8) infections
It is now well established that Kaposi’s sarcoma (KS) is
caused by another of the human herpes viruses, HHV8.
KS has been known for decades as a rare neoplasm with
a predilection for Ashkenazi Jews and races of Medi-
terranean descent. Such traditional forms of the disease
tended to occur in the elderly and affect peripheral
tissues, e.g., the skin of the limbs. At the beginning of
the AIDS epidemic in California and New York in the
1980s, purple vascular lesions began to appear more
centrally, especially the head and neck. Oral lesions
were common; indeed the deeper gastro-intestinal tract
can be affected, as can viscera. Subsequent research
demonstrated a close association of HHV8, or KSHV,
infecting endothelial cells which are driven to a form of
neoplastic hyperproliferaiton.
As with other herpes viruses, a proportion of the
population carry latent infections. There are no com-
prehensive data from Australia but in the USA the
overall sero-prevalence is <5%, and may approach
80% in groups of MSM.36 The virus resides primarily
in the oropharynx, and saliva ⁄ oral fluids are the major
source of transmission. Transmission occurs more
commonly in MSM because of oral–genital contact
and carriage of oral fluids to rectal mucosa. We have
recently reviewed the methods for laboratory diagno-
sis41 and the value of saliva as a diagnostic fluid.9
KS has long been regarded as an AIDS-defining
lesion. Its prevalence has declined sharply in the era of
HAART in the West, but it is still a major clinical
problem in sub-Saharan Africa. Astonishingly, it is
practically unknown in India.
Subtle discolourations of skin (Fig 26) or of oral
mucosa (Fig 27), initially with minimal tumour forma-
tion, can be the first presentation. Oral clinicians need
to be aware of such appearances, as they can be the first
Fig 26. Early Kaposi sarcoma lesions on back of hand and middle
finger in an HIV-positive patient.
ª 2010 Australian Dental Association
The mouth in HIV ⁄ AIDS
Fig 27. A small, early Kaposi sarcoma presenting on the palatal
gingiva.
step leading to diagnosis of HIV disease. Lesions of KS
can grow to a very considerable size. These present in
advanced AIDS and are likely to be multiple. Clearly
growths of the kind shown in Fig 28 risk complications
of haemorrhage, secondary infection, destruction of
bone and periodontium and are a serious aesthetic and
functional problem. Adequate management of HIV
infection itself is the key to treatment. The family of
DNA-antiviral drugs described earlier for other HHV
infections, cancer cytotoxic drugs and radiation therapy
are all employed.
Human papilloma virus infections
The human papilloma viruses (HPVs) comprise a very
large family of over 100 known genotypes. They are
epitheliotropic, certain types having predilection for
skin – others for mucous membranes. A group known
as ‘‘high-risk’’ HPVs (especially HPV 16, 18, 31, 33)
have attracted much interest in recent years because
they have a clear role in the causation of certain
epithelial malignancies – notable of the uterine cervix,
and some vulval, vaginal, penile and anal cancers. All of
Fig 28. A massive Kaposi sarcoma engulfing all of the maxillary
gingival tissues in this patient with AIDS.
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these malignancies are more common in HIV-infected
persons.42 Vaccination programmes are now underway
in Australia and in other countries with proven efficacy
for developing a protective immune response, though it
will take decades to see if this impacts on the incidence
of cervical cancer in the population as a whole. These
high risk HPVs are also associated with a subset of
upper aerodigestive tract cancers, particularly of the
oropharynx.43,44 ‘‘Low-risk’’ HPVs, especially HPV 6
and 11, have long been known to be the cause of the
common viral wart, e.g., picked up by children from
swimming pools, or transmitted from lesions on the
hands by direct contact.
The latter family also cause papillomas on mucous
membranes, and these are seen more commonly in HIV
patients, frequently as flat condylomata, similar to
those of the perianal mucosa (Fig 29). Typical ‘‘papil-
lomatous’’ or pedunculated lesions also occur, some-
times as simple tags of mucosa45 (Fig 30).
In the era of HAART there has been a notable
increase in the prevalence of benign HPV-related oral
mucosal lesions.46,47 They can be unsightly, and
Fig 29. HPV-related flat condylomas on the vermillion lip mucosa of
an HIV-positive patient.
Fig 30. Tags of mucosa at the commissure of the mouth in an HIV
patient. These are also HPV-induced.
98
irritating to the patient. Surgical excision, laser excision
or cryotherapy are employed. Lesions on wet mucosal
surfaces are not easily amenable to topical chemical
ablation such as is commonly used on the skin.
Recurrent oral ulceration of the aphthous stomatitis
type
Recurrent aphthous stomatitis (RAS), usually of the
minor, but sometime the major type, occurs in HIV-
positive persons. Diagnosis is based on clinical history,
typical appearances (Fig 31) and the same type of
routine screening for haematological abnormalities,
bowel disease, gluten sensitivity or other food allergies,
such as one would employ in a patient without any
suggestion of HIV disease. The same range of therapies
is employed – many simply giving symptomatic relief.
Topical steroids do have a place48 and thalidomide has
been used successfully; this appears to act by inhibition
of TNF alpha – but because of its teratogenicity should
only be used on a named-patient basis.49
Intra-mucosal haemorrhages ⁄ purpura
HIV infection can cause a marked thrombocytopaenia,
particularly in the acute or initial phase. This can
present to dental clinicians as intramucosal haemor-
rhages, such as that seen in Fig 32. This patient had
widespread bruising elsewhere in his mouth, and
conjunctival and intra-ocular bleeding.
Hyperpigmentation of the oral mucosa
Patchy pigmentation of the oral mucosa is a common
finding in dark-skinned races. However, increased
melanin deposits are common in longstanding HIV
disease50,51 (Figs 33 and 34). Sometimes these can be
explained as a side effect of drugs, especially antimal-
Fig 31. Minor aphthous ulcers, with typical appearance, in an HIV-
positive patient.
ª 2010 Australian Dental Association
 The mouth in HIV ⁄ AIDS

arials. In advanced disease, with adrenal gland involve-

ment, it represents a manifestation of Addison’s disease.
These appearances should trigger investigations of
adrenal function.

Periodontal diseases in HIV infection

In the early days of the HIV epidemic in the West, a
great deal of attention was paid to periodontal mani-
festations. Complex classifications were proposed and
their diagnostic criteria hotly debated.52 This has now
been simplified.
A quite distinctive fiery red marginal gingivitis may be
seen (Fig 35), the term ‘‘linear gingival erythema’’
having been used. This is usually associated with
deposits of dental plaque ⁄ oral biofilm at the gingival
margin, often containing considerable numbers of
candida species. It is amenable to improved oral hygiene,
judicious (limited) use of disinfectant mouthwashes and,
if Candida is identified, antifungal drugs (see above).
As in patients severely debilitated for other reasons,
acute necrotizing ulcerative gingivitis (ANUG) is seen in

Fig 34. Marked pigmentation of the dorsal tongue. Although this

patient is dark-skinned, the intensity and distribution of the oral
pigmentation is more than normally seen as racial pigmentation.

Fig 32. Bleeding within the tongue in a recently HIV-infected

individual. This particular patient had an extremely low platelet count.

Fig 35. Distinctive marginal gingivitis, resembling that sometimes

described as ‘‘linear gingival erythema’’ in an HIV patient.

immunocompromised patients (Fig 36), particularly if

Fig 33. Pigmented patches on the buccal mucosa, with slight keratosis.
ª 2010 Australian Dental Association
they have psychological ⁄ motivational problems, poor
nutrition, and use tobacco or other drugs. In the early
days of the HIV epidemic, extension of ANUG to
produce local exposure and necrosis of bone – termed
necrotizing periodontitis – was seen (Fig 37). This is
now rare in the West, but remains a major problem in
Africa. Such lesions may progress to sequestration of a
significant piece of alveolar bone. Unsurprisingly, they
are extremely painful. Local debridement as part of
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the 1990s there was not compelling evidence for greater

progression of disease.56 However, a recent study from
the USA confirms increased severity in HIV patients and
emphasizes the need for continuing periodontal care.57

Necrotizing stomatitis
Occasionally an oral infection, such as ANUG, may
extend to adjacent soft tissues, producing a necrotizing
stomatitis (Fig 38). This is similar to the appearance of
Noma or Cancrum oris. Local debridement with
disinfectants such as chlorhexidine or povidone iodine
can result in rapid resolution (Fig 39). Broad spectrum
antibiotics, as listed above, may be needed.

Fig 36. Acute necrotizing ulcerative gingivitis in an HIV patient.
Immune reconstitution inflammatory syndrome (IRIS)
This is a now well recognized situation in which a
recovering immune system responds to a previously
acquired opportunistic infection, which may have
become occult, with an exaggerated response that can
make the symptoms of the infection worsen.58 Cell-
mediated immunity is raised, whether directed against a
new infection, and old infection, or antigens from dead
organisms sequestered in necrotic tissue.

Fig 37. Acute necrotizing ulcerative periodontitis in an HIV patient.

Note the exposed and necrotic bone lingual to teeth 43 and 44.

comprehensive periodontal care is effective if other

opportunistic infections are under control and especially
if antiretroviral therapy is in place. Systemic antibiotics, Fig 38. Necrotic ulcer in the retromolar area in an HIV patient.
such as metronidazole, tetracycline, clindamycin, amox-
icillin, and amoxicillin-clavulanate potassium, should
be combined with debridement of necrotic tissues. As
systemic antibiotics increase the patient’s risk of devel-
oping candidiasis, concurrent, empirical administration
of an antifungal agent should be considered.53
There is some controversy as to whether or not the
severity and extent of the common forms of destructive
periodontitis are increased in those with HIV ⁄ AIDS.
Again, it depends on the quality of therapy for HIV
disease itself, and on the quality of periodontal care. In
our Indian cohort of largely untreated subjects, we
found that measures of periodontal disease had some
predictive value for HIV.54 In the early days of the
epidemic in New York, a high quality longitudinal
study did show greater disease progression in the more Fig 39. The lesion seen in Fig 38 a few days after local debridement
severely immunosuppressed.55 In our London cohort of and disinfection.
100 ª 2010 Australian Dental Association

AIDS patients are more at risk for IRIS if they are
starting HAART for the first time, or if they have
recently been treated for an opportunistic infection. It is
generally advised that when patients have low initial
CD4 T cell count and opportunistic infection at the time
of their HIV diagnosis, they receive treatment to control
the opportunistic infections before HAART is initiated.
Overall, the infections most commonly associated
with IRIS include cytomegalovirus, herpes zoster,
Mycobacterium avium complex (MAC), Pneumocystis
pneumonia, and Mycobacterium tuberculosis. There
are no detailed incidence data for oral infections,
though KS, candidiasis and oral warts have all been
described.59
The response to IRIS has to be use of the appropriate
antibiotic or antiviral drugs for the causative agent, and
concomitant corticosteroids to suppress inflammation
until the infection has been managed are often required.
Continuing challenges for the dental profession
Although the number of cases of HIV disease in
Australia is fairly small, the epidemic remains a threat,
especially because certain groups continue to practise
risky behaviours, and because there is continuous
‘‘leakage’’ into the heterosexual community. Dental
practitioners have opportunities for early diagnosis, and
infection control for the types of invasive procedures we
engage in on a daily basis remains essential. We have a
duty of care to all patients, and we may choose to work
in regions with a high prevalence of HIV disease
requiring skills in diagnosis and management of oral
manifestations; the latter may be without ready access
to specialist advice. Oral clinicians must therefore
maintain knowledge of both the global and local
epidemics, of the oral manifestations of HIV ⁄ AIDS,
and be able to provide treatment for oral conditions.
ACKNOWLEDGEMENTS
I thank colleagues past and present from many
continents who have contributed to my experience of
the oral manifestations of HIV disease and who have
contributed to my library of images.
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Address for correspondence:
Professor Newell W Johnson
Building GO5, Room 3.22a
Gold Coast Campus
Griffith University QLD 4222
Email: n.johnson@griffith.edu.au
ª 2010 Australian Dental Association