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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.

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,
including tuberculosis. The dental and oral health
The global pandemic of HIV infection and AIDS professions therefore have a key role in early diagnosis,
continues unabated. In much of the Western world a and in the management of these distressing infections.
degree of complacency has set in because being HIV- The highest standards of infection control must be
positive is no longer a death sentence: we have seen a maintained in all clinical situations and appropriate
remarkable transition to a chronic, and largely man- action taken should a clinician find him or herself HIV
ageable disease. This is due to the efficacy of modern positive.
highly active antiretroviral therapy (HAART). How- The single most useful entry point for all matters to
ever, the situation remains a global disaster and do with HIV diseases and the dental profession is the
awareness amongst professionals and the public must HIVdent website.1 This site itself has extensive current
remain high. Many of the earliest manifestations of the information on facts, policies and procedures, many
immune suppression associated with HIV infection links to other valuable internet sites, as well as to
occur in the mouth – particularly oral candidiasis, but current periodical literature.
ª 2010 Australian Dental Association 85

predominantly because of increasingly effective higher numbers.NW Johnson Current status of the global pandemic biggest challenge: in Zwaziland 25. there were some 33. and to 0. about HIV and ⁄ or AIDS in South and South-East Asia. Whilst the total HIV infection in adults aged 15–49 range from 0. the 2007 estimates of prevalence of Figure 2 is perhaps some good news. and India 0. 23. More than 97% of disease in our region: 3.4% in The latest data available from the global databases Lesotho. 18. and a nation with well- burden remains sub-Saharan Africa but our region. provides data showing there is now a gradual decline Such averages.1–35. we have a responsi- South and South-East Asia.8 million) December 2009 4 Fig 1. 2005. India is in bility to help stem the epidemic in these countries and fact the single country on earth with the highest number to assist in helping the afflicted. at the end of 2008. 59 000 in Oceania.3 In a nation with a population of over a continues to rise. disguise some astoundingly in the numbers of people living with HIV ⁄ AIDS high infection rates. of cases. and 2 million deaths.69% and 5. it therapy.6% in North and Latin America. 86 ª 2010 Australian Dental Association . social.1% in Zimbabwe and 16.4 million (31. with 2. World Health Organization Adults and children estimated to be living with HIV.38% among men serious situations. respectively.5 which describes in Eastern Europe. of those comparatively small number.4% in 2006. The major As a regional power. there is a considerable burden of new infections per day in 2008. in Botswana 25%. Again we need to look at the prevalence of HIV high proportion of these will die or remain chronically infections country by country: the Indonesian Province severely unwell.71%. 2008 (source UNAIDS 2009). Figure 1 shows the global distribution. 2008 Total: 33. ranks second.and middle-income countries. However.9% in the managed by the United Nations (UN) and the World Republic of South Africa. Again. Health Organization (WHO)2 reveal that.2% number of people in the world living with HIV ⁄ AIDS to 0. These are breathtaking numbers. Among injecting drug users (IDUs). in adults. through 0. prevalence of 2. sub-Saharan Africa is the (PLHA). the personal. including in our part of the world. India has an excellent National range from 5.5%. the billion (1 151 147 600) souls. There were more than 7400 As given in Fig 1. largely 2 400 000 infected individuals – both figures growing due to health promotion campaigns. these statistics disguise some serious situa- 40% are among young people aged 15–24. economic and of Papua was estimated by UNAIDS to have a political consequences for societies with high preva.4 this translates to some number of new infections per annum is falling. inevitably.7 million new The situation in the Asia-Pacific region infections that year alone. 0.6% in lence of HIV disease are clearly immense. 5. Given that a tions.3%. In India.4 million people living with HIV ⁄ AIDS in the world. developed professional standards. almost 48% are among women and about However.3% in South and South-East Asia and in Oceania. partly due to population growth.2% in sub-Saharan Africa. a 1200 are in children under 15 years of age and. High-risk groups. who have sex with men (MSM) and female sex workers Prevalence rates of HIV infection around the world (FSWs). Death rates are also by the second. these generalizations cover many is as high as 8. the considerable national programme therein.9% of the popula- tion is HIV positive. however.7% AIDS Control Organisation (NACO). Cambodia 0. Adults and children living with HIV.8 million people living with these are in low. show falling.

largely explained by Australia’s continuing the situation in Australia. tend Chemotherapy for HIV infection per se has advanced to be concentrated in clinics conducted by colleagues dramatically in both efficacy and coverage. officially estimated at 0. 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.2% (0.5% in Vietnam and in Malaysia. the prevalence in adults aged 15–49 is Figure 4 suggests that the rate of newly diagnosed estimated at 1. In Australia. With some dating from the mid 1990s (Fig 6). Papua New Guinea Torres Strait Islander citizens are over-represented. and ⁄ or patients with increasing efficacy. and those patients largely explained by the increasing availability. below). 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.1–0. population growth (Fig 5). This seems a small number. Most near neighbours in South-East Asia. few of us will downturn in AIDS diagnoses from that time (Fig 7).2% in Indonesia overall. and indeed it is death rate from AIDS-related illnesses.5%. majority of infected individuals in Australia are under ª 2010 Australian Dental Association 87 . 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. of HAART. including However.6 (PNG). The mouth in HIV ⁄ AIDS Global estimates 1900–2008 Number of people living with HIV Adult (15–49) HIV prevalence (%) 40 1.6 % 10 0. be caring for such an individual. the number of Australians estimated to be and 0. HIV infections may have plateaued. the downturn compared to the numbers given above.3%): some 18 000 During this time there has been a dramatic fall in the PLHA. However. with 54 000 PLHA. infected with hepatitis C is approximately 200 000. Global estimates 1990–2008 (source UNAIDS 2009). oral ⁄ dental problems associated with HIV disease. Prevalence (see below). have be unknown. and known to be HIV positive. Also. The vast with a special interest or skill in their management. this shows no significant change in the number of newly acquired infections.9 20 0. In PNG. as the HIV status of an individual will usually popular tourist destinations and trading partners. This follows the 11 000 practising dentists in the nation. universal precautions remain mandatory substantially higher rates than Australia.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 2.8% in Cambodia. the vast majority of sons where informative. 0. with international compari.2 Number (millions) 30 0. 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.

1% Guam 0.8 88 ª 2010 Australian Dental Association . World Health 2009 AIDS epidemic update Figure 27 Organization Fig 3. with various mixtures of protease inhibitors (PI). 1999–2008 (source60).NW Johnson Proportion of all HIV and AIDS cases in different Pacific island countries and territories.1% Fiji 1. those not receiving such care having Year fallen from around 15% of cases at the turn of the Fig 5. the paper by Guy et al.7 and in (NNRTIs). Newly diagnosed HIV infection in Australia.8% All others 0. Most are now on triple 1990–2007 (source61). 1984–2007 New Caledonia 1.0% Sources: The Secretariat of the Pacific Community and Papua New Guinea Department of Health. 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. Number of people living with HIV. 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. 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2003 2004 2005 2006 2007 treatment (Fig 8).8% Papua New Guniea 95. People living with HIV and AIDS (PLHA) in Australia. Newly diagnosed HIV infections in Australia. therapies.2% French Polynesia 1. 1990–2007 including diagnoses of newly acquired HIV 1200 infection. Proportion of HIV ⁄ AIDS in the Pacific (source UNAIDS 2009). millennium to 10% today.

IDU. 1999–2008 (source63). This is amplified below. the risk of transmission via saliva ⁄ oral fluids and the risk of becoming infected through Fig 7. and lacks Langerhans’ cells. Treatment uptake and modalities for HIV-infected people in amongst young women. this is now 10 the most common route. 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. Because most sexual 1999 2000 2001 2002 2003 2004 2005 2006 2007 2008 Year activity takes place between men and women.63 the mouth. In some Western countries. Whilst a 1500 proportion of these are also IDUs. 1990–2007 (source62). without effective condom use. and could have Number acquired their infection by either route. Diagnoses of HIV infection and AIDS in Australia Risk factors for transmission of HIV: MSM. There are risks in HIV diagnoses AIDS diagnoses Source: state and territory health authorities both directions. Free virus can be present in 500 ejaculate and anal mucosa is both thin and physically fragile. most infections are Fig 8. and it was always so in the high-incidence countries in Africa and in Eastern 0 Europe and South-East Asia. 2500 heterosexual.9 year1 These data indicate that the practice of safe sex is not universally followed in this high-risk community. an AIDS defining illness. (In Africa. It has been shown that a major route of transmission of human herpes virus 8 (HHV-8). most of the 1000 transmission would be from anal intercourse. Estimated deaths due to AIDS in Australia. mother-to-child. Percent 20 The next major route is heterosexual. in Aboriginal and Torres Strait Islander peoples are ª 2010 Australian Dental Association 89 . the UK for example. 1999–2008. 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. not NNRTI) of disease being spread throughout a population are 3+ (NRTI + NNRTI. 30 indicating a continuing challenge for education and social support networks. 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. the risks None Monotherapy Double therapy 3+ (NRTI +/– PI. New HIV infections and diagnoses of AIDS in Australia. The mouth in HIV ⁄ AIDS 1600 Estimated number of deaths due to AIDS. clinical settings 2000 Within Australia.) Whilst rates of HIV infection Australia. the major routes of transmission (Fig 9) remain those involved with MSM. 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. the causative agent of Kaposi’s sarcoma.

but there are no the birth canal. ways: free virus particles and virus within infected Transmission of HIV from an infected mother to her immune cells. Figure 11 shows HIV diagnoses in Australian born cases. offspring occurs predominantly during passage down tears. 2004–2008. pre-ejaculate. but unfortunately remains a major It is prudent to remind ourselves of the changes over problem in Africa where paediatric AIDS cases are time in viral loads in circulating blood and the distressingly common. and The natural history of HIV infection MSM is again the major route. and the appropriate antiviral drugs are given to the mother risk of infection is minimal. or breast milk. semen.NW Johnson HIV infection. It is possible to find HIV in the saliva. before labour. similar to those of non-Indigenous Australians. vaginal fluid. 2004–2008 (source63). Sharing of drug injection equipment has long been Within these body fluids. growing epidemic. Transmission in Indigenous and non-Indigenous Australians (source64). 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. indicating risk of a Infection with HIV occurs by the transfer of blood. and urine of infected individuals. It is almost entirely preventable if recorded cases of infection by these secretions.10 development of an immune response. 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. HIV is present in two different recognized as a very dangerous practice. 90 ª 2010 Australian Dental Association . Routes of transmission for new HIV infections in Australia. heterosexual transmis- sion is a larger proportion (Fig 10).

Antiret- false negative result.3% (0. of this workshop conclude that the evidence now ª 2010 Australian Dental Association 91 . e. to gathering of global expertise. Changes over time in blood levels of HIV and of antibodies to turn is much less infectious than hepatitis B (HBV). There are wide international varia- Clearly. HIV the recipient seroconverting following injury with a core protein antigen p24 – green. In Infectious viremia HIV DNA (PCR) the context of HIV.0% will develop clinical hepatitis and 23–37% days of exposure. The HIV-positive health care worker: current policies This has been an area of considerable controversy. in the USA (CDC data – op cit. HIV p24 Ag therefore. which took place from and Prevention (CDC) in the USA. the Centers for Disease Control Health and Disease in AIDS. this is an area of great interest to oral health tions.washington. and this is the important report to an occupational health clinic where advice on ‘‘window’’ when antibody-based HIV tests can give a post-exposure prophylaxis (PEP) will be given. the participants Australian Dental Association. 21–24 April 2009 in Beijing.15 No doubt the new national HIV RNA (RT-PCR) in plasma Dental Board of Australia will proscribe such also. It 1. roviral drugs given at this stage are very effective. from operator to patient. rises again in free extant across Australia and New Zealand.jpg) hepatitis and 37–62% serological evidence of HBV infection. For a ‘‘donor’’ who is HBsAg+ and HBeAg-.. only virus in plasma and is shedding these in secretions.11 and the Organiza.5% range). the beginning of an infectious viraemia within a few 1. and Transmission of HIV in clinical settings evolving policy. Within Australia. syringe contaminated from a patient who is HBsAg+ (Source http://depts. from an HCV positive ‘‘donor’’.) indicate that the risk of PCR) – red: HIV DNA in peripheral blood mononuclear cells (PBMC) – yellow.17 This states: prevent cross-infection. research to the global dental community’’. This is why we have universal precau. The mouth in HIV ⁄ AIDS tional dental boards.2–0.0% will develop clinical serv041b. Infection control procedures are designed to minimize Relative level above detection HIV antibody the risk of transmission of all micro-organisms. those considered the inconsistencies in the regulation of the from the National Health and Medical Research Coun. first aid is mandatory: wounds must be made to three weeks or so for antibodies to build up sufficiently bleed and washed with saline. there is website of the Australasian Society for HIV Medicine successive immune suppression with falls in peripheral (ASHM) is a good starting point for the range of polices blood CD4 lymphocyte counts. and AIDS.14 and all of the jurisdic.16 and cell-associated virus.0–31. HIV components following infection. It is. during which the subject has large numbers of In contrast. welcomed the tion for Safety and Asepsis Procedures (OSAP).0–6. draft out to consultation. or today preferably called standard precautions.8% (0–7% range) will seroconvert and from an HIV takes a little longer for viral load to rise within positive donor. immunoglobulin antibodies to HIV – blue. This rises to a peak some three weeks develop serological evidence of HBV infection. Virus RNA levels in plasma Extensive monitoring following needle stick injuries measured by reverse-transcriptase polymerase chain reaction (RT. After months or years (not shown). The if there is no or ineffective antiviral therapy. 0 10 20 30 40 50 60 70 80 HIV has a comparatively low risk of transmission: HIV Days post-infectious viremia is much less infectious than hepatitis C (HCV) which in Fig 11.12 The opportunity to assess the evidence relating to the latter is ‘‘dedicated to promoting infection control and transmission of HIV in the dental setting from oral safety policies and practices supported by science and health care professionals to patients. entering a new host. only 0. It takes theless. the risks are associated with infected Exposure in PBMC fluids – blood or saliva ⁄ oral fluids – or instruments contaminated with such. The recipients must to suppress the virus. It is not the intent of this review BEIJING DECLARATION 2009 to repeat details of these protocols. the ‘‘Beijing Declaration’’ was approved by a and HBeAg+ is that 22. Never- peripheral blood mononuclear cells (PBMC).13 Amongst those which Having analysed the scientific evidence that has morally and legally guide us are those from the become available over the last 20 years. increasing infectivity and illness. patient to patient and also to other clinical and laboratory staff. salient to remind ourselves of the viral loads – the ‘‘dose’’ – necessary for infection to be transmitted. ability of an HIV positive oral health care professional cil (NHMRC) are currently under review with a 2010 to continue practice. At the 2009 6th World Workshop on The Mouth professionals. Their advice Participants from over 30 countries noted and is current and comprehensive. They are available The participants of the 6th World Workshop on Oral from many sources.g. China. later. patient to operator.

RTI = respiratory tract infection. and Ragas Dental College. Given the low risk of transmission (as and Ranganathan. = tuberculosis. TB It remains to be seen how widely regulatory author.2. (2) The individual remains aware of his ⁄ her health status and acts appropriately Oral manifestations of HIV and AIDS (3) Standard Infection Control is observed (4) Scientific evidence related to HIV transmission will The common opportunistic infections: their diagnosis continue to be reviewed.22 Today it is more fruitful – Failure by such a Dental Practitioner to cease certainly more logical – to deal with lesions according performing exposure prone procedures may constitute to type of opportunistic infection. suppression and the stage at which various opportunis- plinary action before the Health Practitioners Tribunal. and considerable regional varia- the field of infectious diseases. this 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. or oral manifesta- must immediately cease to perform exposure prone tions. assuming the conduct of standard precau- with HIV do not pose a risk of transmission to patients in tions.2. with predictive value for treatment failure. The mode of transmission AN S IN PL TE S C LM LM PE M V N PE BA E C XO M EN O AL PU U ER YT ER C P C AP T TO O O C has never been established. provided that the following criteria are met: unless and until they are cognitively impaired. A ‘‘staircase’’ of progressive immune suppression and the are less likely to come to light. There remains only a 150 148 144 133 118 single established case of an HIV-positive dentist having 100 EX ER N L S S M B B I S P Y IS transmitted his infection to a patient – the infamous Acer RT H SI SI YT YT I PC TH O SU IT IT O PL ST TI O IA IN G L PA AR AR IO C M IA M ID IN ZO ET RO FE AS G N N TE SI D EN O O TA R case in Florida in late 1987. Chennai. appliances and instruments. wires. importantly. They can continue a career in clinical positive dentist conveys minimal risk to his ⁄ her patients practice. has changed. available. or decade into the epidemic. PCP = pneumocystis carinii pneumonia. from a large cohort of South Indian patients in the days before HAART was widely in monitoring the scientific literature. Many regard this as 200 192 192 190 190 187 unnecessarily restrictive and. and then by the unsatisfactory professional conduct leading to disci. the 5.) (Source: Courtesy of Professor Suniti Solomon and Drs Kumarasamy Workshop.2 ‘‘sentinels and signposts’’ of HIV infection. These manifestations have long been regarded as Dental Practitioners who meets the criteria of 5. CMV = cyto- ities around the world accept the view of the Beijing megalovirus.24 (OHL = oral hairy leukoplakia. and the availability of modern HAART. relative frequency of these lesions. Clearly. largely due to the impact of procedures. and seek expert advice.1 Hepatitis C antibody and PCR positive. from a specialist in HAART in the West. YRG Centre for AIDS Research and Epidemiol- identified above) when small volumes of blood are ogy. the oral states:18 medicine ⁄ oral pathology community around the world ‘‘Paragraph 5. or type of 5.2 A Dental Practitioner who discovers agreed upon a classification of oral manifestations of that he ⁄ she returns test results in any of the following HIV ⁄ AIDS and.) 92 ª 2010 Australian Dental Association . an HIV- the dental setting. The latter include teeth.21 categories: This was based on how common each lesion. and the risk of RY O R D M C these may be higher in resource-poor settings where they Fig 12. Exposure-prone procedures are those where the HIV INFECTION:INDIAN SCENARIO operator’s fingers are out of sight and likely to come into MEAN CD4 COUNTS close contact with sharp objects. This is (1) The individual is under ongoing care by a suitably the rationale for requiring ongoing care by a suitably qualified HIV Health Care Professional qualified HIV health care professional. Board immediately of their status may constitute Figure 12 shows the ‘‘staircase’’ of progressive immune unsatisfactory professional conduct leading to disci. OP = oropharyngeal. hence continued vigilance stage at which various opportunistic infections emerged. lesion. India. such concerns are 180 154 the basis of the Beijing Declaration.NW Johnson supports the view that Oral Health Care Professionals involved. indeed. major organ involved. tions have been described. a little over a positive. was seen in known AIDS patients at that time – 5. plinary action before the Health Practitioners Tribunal. have value in monitoring the efficacy of anti-HIV Failure by such a Dental Practitioner to notify the therapy. the Dental Board of Queensland currently In the early days of the HIV epidemic.3 HIV antibody positive.19 malice is suspected. As the years have passed.2. their diagnostic criteria.2 Hepatitis B e antigen or hepatitis B virus DNA the classification was published in 1993.20 Of EN PH M H TR H C TR U O R O SC AS C EX R AT O U U G M PT EC LL ER course there could be unknown cases. bone.23 and now have an obligation to notify the Board of their status. and management As but one example of an Australian jurisdictional guideline.

patients require close medical monitoring. glabrata and C. There Fig 14. These infections include cryptococcosis. with their many stresses following a diagnosis of HIV infection. Candida albicans is the most common species. topical amphotericin. Within this complexity. no less than any member of society.24 The dental ⁄ oral health professions have a duty of care to manage oral and dental conditions in HIV- positive patients. Figures 13 and 14 show cases of overt oral candidiasis Other so-called ‘‘deep mycoses’’ can infect oral in AIDS patients. sometimes neglect their oral hygiene. and to maintenance and repair of the dentition. liver toxicity and other side effects.28 Infection can practice protocols are widely available from many spread to the oesophagus. summarized below are derived mostly from the WHO. and who had a raised specific antibody titre to this fungus. as in conjunction with the patient’s HIV physician. Whilst in an emergency national and international sources and the approaches situation. base affecting hard and soft palate. This applies to ‘‘routine’’ aspects of preventive den- tistry. para- coccidiomycosis. interactions. penicilliosis and aspergilosis. quired through droplet infection – coughing. nystatin. may be in financial difficulties. Acute candidiasis with thrush deposits on an erythematous is good evidence that the outcomes of. Ketoconazole or itraco- for patients. The mouth in HIV ⁄ AIDS tic infections emerged in a study of a large cohort of patients in South India in the days before HAART was widely available. and may present with severe caries or unresolved periodontal problems. shouting by an already infected individual nearby.27 nazole have poor absorption from the gut and are not Effective treatment of opportunistic infections is also first-line treatment. endodontic treatments are not compromised. in any event. Management of the opportunistic oral infections described below may require referral to an oral common in severe immunosuppression and even in medicine specialist and. sneezing. clotrimazole or posaconazole can be effective. or in mild infections. Such florid infections are more tissues. This can be challenging because patients. There are increasing reports of dependent on effective antiretroviral treatment and oral azole resistance. and ª 2010 Australian Dental Association 93 . Acute pseudomembranous candidiasis in an AIDS patient. so patients should ideally be referred clinicians also need to be alert to the possible emergence for culture and antifungal sensitivity testing before of immune reconstitution inflammatory syndrome prescribing these drugs – and because of the risk of drug (IRIS) (see later). but Infections with Candida albicans and other fungi C. Mycobacterium tuberculosis is usually ac- Fig 13.30 Significant bacterial infections Mycobacterial infections: The WHO estimates that tuberculosis (TB) is the cause of death in 13% of AIDS patients. Xerostomia asso- ciated with anti-HIV drugs often compounds the problems. there are no funda- mental reasons why an HIV-positive patient should not receive the full range of high quality dental care. histoplasmosis. Heavy deposits of ‘‘thrush’’ cover the gingivae and tooth surfaces. dubliniensis are described. particularly in tropical and some developing countries where these organisms are more commonly picked up from the soil of other natural habitats. USA25 and Australian sources through the gateway of systemic treatment with fluconazole is usually required the ASHM.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. should be planned the era of HAART remain a major clinical problem. Best recently reviewed by Thompson et al.26 These include user-friendly information in established HIV infection. for example.

but severe oral with a literature review. of immunity to herpes simplex viruses. Granular inflammation of free and attached gingiva caused by nity. simplex virus infections: usually HSV1 – occasionally nary TB is more common. such a patient is a danger for transmission to others. Ganciclovir or famciclovir Occasionally other mycobacteria are involved. 94 ª 2010 Australian Dental Association . caused by herpes simplex virus.31 Our blistering can occur in HIV patients (Fig 17).32 drome. lesions caused by Mycobacterium avium intracellulare.33 and there may be widespread involvement of paranasal sinuses. are mostly members of the human herpes virus (HHV) family or are human papilloma viruses (HPV). having developed reasonable immunity from subclinical infec- tions earlier in life. There. a primary herpetic gingivostomatitis less frequently than fore. TB diagnosis must be of modern antiviral drugs are required. because a Management is systemic in the hands of a specialist child with an acute febrile illness is not usually taken to physician. the dentist. and be transmit- infection with the fungus Histoplasma capsulatum. presence of OC was 4. If lesions are widespread. With Oral health practitioners are familiar with herpes increasing degrees of immunodeficiency. This AIDS patient also had extensive pulmonary and lymphatic involve. We see sites. oral would be preferred today.34 Viral infections Viral infections are very common in the immunocom- promised. but also occasionally the mouth (Fig 16). Unsur- work amongst HIV patients in Kenya reveals oral prisingly these are very painful. lesions in the mouth can lead to diagnosis. is given by Miziara. high systemic doses high-incidence communities. active infections may re-emerge. Fig 17. ted via saliva. has susceptible recipient.0. Typical punched-out TB ulcers in the retromolar area. indicating that. In many countries where TB is decreased dramatically. In the era of HAART the prevalence of usually results in an acute pulmonary infection in the these lesions – at least in the Western world. and patients are usually candidiasis (OC) in 72% of patients. and a high proportion of healthy adults silently harbour these viruses. affecting many internal body HSV2 – in the form or recurrent herpes labialis. With progressively failing immu- Fig 15. Herpes simplex (HHV1 and HHV2) infections vated when he ⁄ she becomes immunosuppressed. this can be reached by sending blood for herpes simplex antibody titres – Fig 16. Those affecting the head and neck. a subject may have acquired TB long ago and has remained in a latent state which becomes reacti. If diagnosis is in doubt. Severe blistering of the tongue in an HIV-positive patient ment. so that early vir. treatment in in the body) in 57%: the crude odds ratio for TB in the collaboration with the patient’s physician is advisable. Their major reservoirs are salivary glands and oropharyngeal lymphoid tissues. Clearly. Almost all adults will have acquired a degree A review of 18 cases in AIDS patients from Brazil. and TB (anywhere quite febrile. or mouth. our general medical practitioner colleagues. HHVs cause a spectrum of disease in the head and neck.35 endemic. extra-pulmo. especially in For the management of oral lesions. Topical acyclo- sought when a patient presents with OC. often used for recurrent herpes labialis on pro- treatment can be initiated. will have no effect.NW Johnson are occasionally seen.

any spreading infection. Non-specific ulcers of the buccal mucosa caused by cyto- Herpes zoster. if facilities exist. orally and ⁄ or intravenously will be required for a child. or cido. obtundant gels (topical steroids should not be used). EBV is again harboured cause encephalitis. In the Western world. OHL has no aetiological or pathological associations with other forms of oral leukoplakia. the vast majority – probably in excess of 90% of adults in Australia – will be VZV seropositive. Further information is available gastro-intestinal tract.39 EBV also drives a range of malignancies of the lymphatic system. The ‘‘hairy’’ descriptor arises from the appearance of elongated filiform papillae and these are associated with white. EBV. Blisters caused by herpes zoster virus (shingles) which affected the mandibular branch of the right trigeminal nerve in this HIV The pain and swelling in the right mandible in this HIV- patient: lesions existed across the skin of his lower face.37 tis.40 These were very common in the pre- HAART era. and cause a terminal pneumoni. or shingles. Fig 18. (EBV). can cause relatively innocu. Described by dental colleagues in San Francisco in the early days of the HIV epidemic there. a minority of which have the potential to transform over time into squamous cell carcinomas. IM). but the first is the major cause of retinitis in HIV patients. foscarnet. For dentists. assumed ª 2010 Australian Dental Association 95 . Unless they resolve adolescence. A smear for light microscopy may reveal characteristic Tzank cells. CMV disease can spread elsewhere in the this anatomical area. However. and neck (Fig 18). for identification of the presence and type of HSV by polymerase chain reaction. Like any oral ulcer these can be very painful. acquired through chicken pox as fovir. and well known to the public and the profession alike. ganciclovir. a disease endemic in the malaria belt of Africa. Supportive treatment by way of analgesic mouth- washes. Cytomegalovirus (HHV5) infections Epstein-Barr virus (HHV4) infections Another member of the human herpes virus family. often plaque-like changes.36 The acute primary infection is glandular rapidly. Such a case is shown in Figs 24 and 25. Intensive treatment with modern antiviral drugs EBV is also the primary cause of Burkitt’s lymphoma. predominantly B-cell non-Hodgkin’s lymphomas.38 it is a lesion renowned as an early marker of HIV infection. may affect nerves of the head megalovirus. Perhaps the most ubiquitous HHV is Epstein-Barr virus cytomegalovirus (CMV). and can infection is often subclinical. maintenance of fluid balance should be provided. positive patient was. the signature EBV-associated lesion is so-called oral hairy leukoplakia (OHL) (Figs 20–23). Systemic antivirals are unlikely to be helpful in established infections such as that illustrated. perhaps not surprisingly. The mouth in HIV ⁄ AIDS rising titres if sequential samples are taken in acute phase or. and of a number of other lymphoproliferative diseases (see below). such as benzydamine hydrochloride (Difflam). as many as 95% of adults ous-looking ulcers of the lining mucosa of the mouth between 35 and 40 years of age have been infected with (Fig 19). Indeed before the era of HAART in the upper aerodigestive tract – IM is not called ‘‘the some 30% of patients in the West developed CMV kissing disease’’ for nothing – and it re-emerges in retinitis sometime between the time of AIDS diagnosis the immune-suppressed with disease manifestations in and death. further advice should be sought because CMV fever (infectious mononucleosis. though may be indicated under medical guidance to avoid risk of spread. Once again. such as valganciclovir. having had a primary infection in childhood or and require symptomatic treatment. Herpes zoster (HHV3) infections Fig 19. on the ‘‘Virology Down Under’’ website.

Fig 24. Swelling over the posterior part of the body of the right mandible. the diagnosis being lymphoma eroding mandibular bone and spilling into a soft tissue tumour. especially as the original radiograph probably sis in lytic infection but not latent infection. the oral tongue. the tongue to the ventral tongue and floor of mouth mucosa. There is increased thickness of the upper layers of the epithelium. Oral hairy leukoplakia extending from the lateral borders of infection. In fact. The process known as in situ hybridization localizes EB-virus Fig 20. Haematoxylin and eosin-stained section from an OHL lesion. Fig 25. Endodontic therapy treatment of lymphomata requires more complex 96 ª 2010 Australian Dental Association . attempted obturation of both roots and a metal crown. predominantly within the nuclei of these balloon cells. by his dentist to be the result of an odontogenic Acyclovir (acycloguanosine) inhibits viral DNA synthe- infection. the radiolucency was caused by an AIDS-associated lymphoma. Typical oral hairy leukoplakia affecting the lateral border of particles. An orthopantomogram of the patient in Fig 23 reveals periapical radiolucencies on tooth 46. so revealed a periapical radiolucency. had no effect.NW Johnson Fig 23. Fig 22. The differential diagnosis would include an odontogenic Fig 21. with ‘‘balloon’’ or clear cells and a conspicuous absence of inflammation in the connective tissue.

36 The virus resides primarily DNA-antiviral drugs described earlier for other HHV in the oropharynx. These present in infecting endothelial cells which are driven to a form of advanced AIDS and are likely to be multiple. 33) problem in sub-Saharan Africa. Transmission occurs more are all employed. penile and anal cancers. The mouth in HIV ⁄ AIDS cytokine or cytotoxic therapies in the hands of specialist oncologists. Lesions of KS demonstrated a close association of HHV8. Oral lesions gingiva. Such traditional forms of the disease tended to occur in the elderly and affect peripheral tissues. especially the head and neck. gingival tissues in this patient with AIDS. can grow to a very considerable size. cancer cytotoxic drugs and radiation therapy source of transmission. early Kaposi sarcoma presenting on the palatal centrally. Subsequent research step leading to diagnosis of HIV disease.g. A group known HAART in the West. Oral clinicians need to be aware of such appearances. HHV8. destruction of population carry latent infections. and may approach infection itself is the key to treatment. initially with minimal tumour forma. and saliva ⁄ oral fluids are the major infections. A massive Kaposi sarcoma engulfing all of the maxillary finger in an HIV-positive patient. a proportion of the of haemorrhage. A small. indeed the deeper gastro-intestinal tract can be affected. mucosa (Fig 27). There are no com. Its prevalence has declined sharply in the era of skin – others for mucous membranes. bone and periodontium and are a serious aesthetic and prehensive data from Australia but in the USA the functional problem. KS has been known for decades as a rare neoplasm with a predilection for Ashkenazi Jews and races of Medi- terranean descent.. Adequate management of HIV overall sero-prevalence is <5%. the skin of the limbs. At the beginning of the AIDS epidemic in California and New York in the 1980s. The family of 80% in groups of MSM. were common. We have Human papilloma virus infections recently reviewed the methods for laboratory diagno. it is have attracted much interest in recent years because practically unknown in India. as they can be the first Fig 26. can be the first presentation. Early Kaposi sarcoma lesions on back of hand and middle Fig 28. or KSHV. and some vulval. purple vascular lesions began to appear more Fig 27. Clearly neoplastic hyperproliferaiton. e. ª 2010 Australian Dental Association 97 .9 large family of over 100 known genotypes. They are KS has long been regarded as an AIDS-defining epitheliotropic. certain types having predilection for lesion. 31. secondary infection. vaginal. 18. All of tion. but it is still a major clinical as ‘‘high-risk’’ HPVs (especially HPV 16. commonly in MSM because of oral–genital contact and carriage of oral fluids to rectal mucosa. The human papilloma viruses (HPVs) comprise a very sis41 and the value of saliva as a diagnostic fluid. they have a clear role in the causation of certain Subtle discolourations of skin (Fig 26) or of oral epithelial malignancies – notable of the uterine cervix. growths of the kind shown in Fig 28 risk complications As with other herpes viruses. as can viscera. Kaposi sarcoma virus (HHV8) infections It is now well established that Kaposi’s sarcoma (KS) is caused by another of the human herpes viruses. Astonishingly.

This patient had widespread bruising elsewhere in his mouth.. membranes. Tags of mucosa at the commissure of the mouth in an HIV Fig 31.47 They can be unsightly.44 ‘‘Low-risk’’ HPVs. Sometimes these can be Fig 29. Surgical excision. and these are seen more commonly in HIV such as one would employ in a patient without any patients. positive patient. The same range of therapies those of the perianal mucosa (Fig 29). These are also HPV-induced.g. occurs in HIV- common viral wart. have long been known to be the cause of the minor.49 mucosal lesions. gluten sensitivity or other food allergies. HPV-related flat condylomas on the vermillion lip mucosa of an HIV-positive patient. will take decades to see if this impacts on the incidence of cervical cancer in the population as a whole. swimming pools.51 (Figs 33 and 34). routine screening for haematological abnormalities. frequently as flat condylomata. Diagnosis is based on clinical history. Minor aphthous ulcers. Typical ‘‘papil. picked up by children from positive persons. in an HIV- patient. this appears to act by inhibition In the era of HAART there has been a notable of TNF alpha – but because of its teratogenicity should increase in the prevalence of benign HPV-related oral only be used on a named-patient basis. 98 ª 2010 Australian Dental Association .46.NW Johnson these malignancies are more common in HIV-infected irritating to the patient. but sometime the major type. and Intra-mucosal haemorrhages ⁄ purpura HIV infection can cause a marked thrombocytopaenia. However. This can present to dental clinicians as intramucosal haemor- rhages. increased melanin deposits are common in longstanding HIV disease50. usually of the and 11. is employed – many simply giving symptomatic relief. similar to suggestion of HIV disease. These Recurrent oral ulceration of the aphthous stomatitis high risk HPVs are also associated with a subset of type upper aerodigestive tract cancers. especially HPV 6 Recurrent aphthous stomatitis (RAS).43. though it ablation such as is commonly used on the skin. lomatous’’ or pedunculated lesions also occur. e. The latter family also cause papillomas on mucous bowel disease. and conjunctival and intra-ocular bleeding. been used successfully. or transmitted from lesions on the typical appearances (Fig 31) and the same type of hands by direct contact. with typical appearance. explained as a side effect of drugs.42 Vaccination programmes are now underway or cryotherapy are employed. especially antimal- Fig 30. particularly in the acute or initial phase. laser excision persons. Topical steroids do have a place48 and thalidomide has times as simple tags of mucosa45 (Fig 30). Lesions on wet mucosal in Australia and in other countries with proven efficacy surfaces are not easily amenable to topical chemical for developing a protective immune response. Hyperpigmentation of the oral mucosa Patchy pigmentation of the oral mucosa is a common finding in dark-skinned races. particularly of the oropharynx. such as that seen in Fig 32. some.

This is now rare in the West. often containing considerable numbers of candida species. judicious (limited) use of disinfectant mouthwashes and. acute necrotizing ulcerative gingivitis (ANUG) is seen in Fig 34. Although this patient is dark-skinned. Complex classifications were proposed and their diagnostic criteria hotly debated. a great deal of attention was paid to periodontal mani- festations. Marked pigmentation of the dorsal tongue. they Fig 33. if Candida is identified. As in patients severely debilitated for other reasons. Bleeding within the tongue in a recently HIV-infected individual. the term ‘‘linear gingival erythema’’ having been used. with adrenal gland involve- ment. This particular patient had an extremely low platelet count. resembling that sometimes described as ‘‘linear gingival erythema’’ in an HIV patient. These appearances should trigger investigations of adrenal function. Unsurprisingly. It is amenable to improved oral hygiene. The mouth in HIV ⁄ AIDS arials. In advanced disease. Distinctive marginal gingivitis. Fig 35. the intensity and distribution of the oral pigmentation is more than normally seen as racial pigmentation.52 This has now been simplified. with slight keratosis. antifungal drugs (see above). it represents a manifestation of Addison’s disease. extension of ANUG to produce local exposure and necrosis of bone – termed necrotizing periodontitis – was seen (Fig 37). Such lesions may progress to sequestration of a significant piece of alveolar bone. are extremely painful. Local debridement as part of ª 2010 Australian Dental Association 99 . Fig 32. poor nutrition. but remains a major problem in Africa. In the early days of the HIV epidemic. particularly if they have psychological ⁄ motivational problems. and use tobacco or other drugs. A quite distinctive fiery red marginal gingivitis may be seen (Fig 35). Pigmented patches on the buccal mucosa. This is usually associated with deposits of dental plaque ⁄ oral biofilm at the gingival margin. immunocompromised patients (Fig 36). Periodontal diseases in HIV infection In the early days of the HIV epidemic in the West.

Note the exposed and necrotic bone lingual to teeth 43 and 44. may be needed. such as ANUG. and amoxicillin-clavulanate potassium. amox- icillin. Fig 38. and on the quality of periodontal care.55 In our London cohort of and disinfection. with an exaggerated response that can make the symptoms of the infection worsen. it depends on the quality of therapy for HIV disease itself.54 In the early days of the epidemic in New York. may extend to adjacent soft tissues.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. we found that measures of periodontal disease had some predictive value for HIV. Acute necrotizing ulcerative periodontitis in an HIV patient. should be combined with debridement of necrotic tissues. comprehensive periodontal care is effective if other opportunistic infections are under control and especially if antiretroviral therapy is in place. This is similar to the appearance of Noma or Cancrum oris. and old infection. concurrent. producing a necrotizing stomatitis (Fig 38). The lesion seen in Fig 38 a few days after local debridement severely immunosuppressed. Necrotic ulcer in the retromolar area 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. as listed above. which may have become occult. or antigens from dead organisms sequestered in necrotic tissue. such as metronidazole. 100 ª 2010 Australian Dental Association . Systemic antibiotics.56 However. Acute necrotizing ulcerative gingivitis in an HIV patient. As systemic antibiotics increase the patient’s risk of devel- oping candidiasis. a high quality longitudinal study did show greater disease progression in the more Fig 39. empirical administration of an antifungal agent should be considered. Broad spectrum antibiotics. Fig 37. Again.58 Cell- mediated immunity is raised. Fig 36.NW Johnson the 1990s there was not compelling evidence for greater progression of disease. tetracycline.57 Necrotizing stomatitis Occasionally an oral infection. Local debridement with disinfectants such as chlorhexidine or povidone iodine can result in rapid resolution (Fig 39). a recent study from the USA confirms increased severity in HIV patients and emphasizes the need for continuing periodontal care. whether directed against a new infection. In our Indian cohort of largely untreated subjects. clindamycin.

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