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dc.contributor.advisorWilson, David-
dc.contributor.advisorPierce, Angela-
dc.contributor.authorLogan, Richard M.-
dc.description.abstractOral hairy leukoplakia (OHL) is an oral lesion that, prior to the advent of AIDS in 1981, had not been reported in the literature. In 1984, Greenspan et al, described a white, non-removable lesion, which they called oral "hairy" leukoplakia (OHL), which was confined to the lateral borders of the tongue. OHL was associated in this initial report with both papillomavirus and a herpes-type virus. It was also observed that the presence of this lesion was associated with progression of HIV disease in many of the patients in the study. The importance of OHL as an indicator of immunosuppression and prognosis of HIV disease was soon realised. It is included by the Centers for Disease Control in the 1993 Revised Classification System for HIV Infection and Expanded Case Surveillance Case Definition for AIDS Among Adolescents and Adults. In the 13 years since the first description of OHL, many studies, primarily from the United States and Europe, have investigated the lesion with respect to aetiology and pathogenesis, histologic features and relevance to HIV disease progression. A close relationship has been observed between OHL and Epstein-Barr virus (EBV). There has not been any Australian studies which have described, in detail, the behaviour and characteristics of OHL in Australian HIV-infected patients. Anecdotal evidence indicated that OHL may not be as strong an indicator of HIV progression or of immunosuppression in South Australian patients as had been reported by international studies This research project was designed in two sections. The first part of the project comprised a retrospective analysis of OHL in 197 patients who had attended the Medically Compromised Patient Unit of the Adelaide Dental Hospital. The prevalence of OHL in these patients was examined with respect to factors such as length of time of HIV infection, CD4+ T-lymphocyte counts, AIDS-defining illness and concurrent medication. The second, prospective analysis, of OHL examined the lesion in 20 patients who had clinical evidence of the lesion. Exfoliative cytology smears from OHL lesions of these patients were examined using light microscopy and transmission electron microscopy. The results from this project found that the prevalence of OHL in South Australian patients was comparable to that found in international studies. The presence of OHL was not related to CD4+ T-lymphocyte count or AIDS-defining illness, nor did the length of time a patient had been infected with HIV relate to the presence of OHL. An association was observed between a reduced prevalence of OHL in patients taking the antiviral medications AZT and aciclovir. The prevalence of oral Candida infection in relation to the presence of OHL was not statistically significant. The prospective analysis of OHL found that the clinical appearance of OHL in the group of 20 patients was varied. It could present as a smooth, flat white lesion, to one that was corrugated and "shaggy". The size of the lesions was not related to medication or CD4+ T-lymphocyte count. OHL was observed to occur over a large range of CD4+ T-lymphocyte counts. Examination of exfoliative cytology specimens revealed Candida infection in 25% of cases. The light microscopic appearance of squamous epithelial cells did not reveal any marked changes in the morphology of the cells. Ultrastructural examination of squamous epithelial cells demonstrated the presence of herpes-type viruses (consistent with EBV) within the cell nuclei and extracellularly. Nuclear degeneration, as described in other studies, was also observed, as was the presence of fungal organisms. Generally, these results concur with those from other repofts in the literature relating to OHL. These results do support the notion that OHL is not an indicator of immunosuppression in South Australian patients, of course longitudinal studies are required to ascertain the relationship of OHL to HIV disease progression. Although supporting the possible role for EBV in the aetiology of OHL, these results do not provide unequivocal support for EBV as the sole aetiologic agent for the pathogenesis of OHL. The role of co-factors in the pathogenesis of this lesion requires further investigation.en
dc.titleA retrospective and prospective analysis of oral hairy leukoplakia in a South Australian HIV-infected populationen
dc.contributor.schoolDepartment of Dentistryen
dc.provenanceThis electronic version is made publicly available by the University of Adelaide in accordance with its open access policy for student theses. Copyright in this thesis remains with the author. This thesis may incorporate third party material which has been used by the author pursuant to Fair Dealing exceptions. If you are the owner of any included third party copyright material you wish to be removed from this electronic version, please complete the take down form located at:
dc.description.dissertationThesis (M.D.S.)--University of Adelaide, Dept. of Dentistry, 1998en
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