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      Diagnosis of Oral Hairy Leukoplakia: The Importance of EBV In Situ Hybridization

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          Abstract

          Oral hairy leukoplakia (OHL) is caused by the Epstein-Barr virus (EBV), which has been related to HIV infection. In situ hybridization (ISH) is the gold-standard diagnosis of OHL, but some authors believe in the possibility of performing the diagnosis based on clinical basis. The aim of this study is diagnose incipient lesions of OHL by EBV ISH of HIV-infected patients and the possible correlations with clinical characteristics of the patients. Ninety-four patients were examined and those presenting with clinical lesions compatible to OHL were submitted to biopsy prior to EBV ISH. Twenty-eight patients had lesions clinically compatible to the diagnosis of OHL, but only 20 lesions were confirmed by EBV ISH. The patients with OHL had a mean age of 41.9 years and were HIV-infected for 11.2 years, on average, including CD4 count of 504.7 cells/mm 3 and log 10 viral load = 1.1. Among the quantitative variables, there was a statistically significant correlation with age only ( P = 0.030). In conclusion, the presence of OHL in patients with HIV/AIDS results in changes in the epidemiological characteristics of the disease, and this fact allied with subtle clinical-morphological features makes clinical diagnosis very difficult. Therefore, EBV ISH is important for a definitive diagnosis of OHL.

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          Oral manifestations of an HIV positive cohort in the era of highly active anti-retroviral therapy (HAART) in South London.

          Human Immunodeficiency Virus (HIV) infection is associated with oral manifestations of diagnostic and prognostic importance. With the advent of Highly Active Anti-retroviral Therapy (HAART) there is anecdotal evidence to suggest that the prevalence of oral lesions has declined. The number of prevalence studies, carried out in the era of HAART is, however, meagre. Our aim was to study the prevalence of the oral manifestations of HIV in a population, predominantly on HAART, attending a Genito-Urinary Medicine Centre in South London. This cross sectional study included 203 adult volunteers, comprising 76% males and 24% females. One third of the subjects were from the predominantly African or Afro- Caribbean ethnic minority groups resident in London. The relationship between the prevalence of oral lesions and demographic variables, therapeutic regimes, viral load and CD4 counts were evaluated. One hundred (49%) of the patients had no detectable oral lesions. Oral lesions detected most frequently included oral hairy leukoplakia (9.9%), HIV associated periodontal diseases (9.9%) and oral candidiasis (4.9%). Three subjects had multiple papillomatous growths. Most cases (n = 17/20) of oral hairy leukoplakia were in individuals with a detectable (> 400 copies/ml) plasma RNA viral load. The majority (n = 8/10) of our patients with oral candidiasis had a plasma RNA viral load > 10,000 copies/ml and half (n = 5/10) had a CD4 count < 200 cells/mm3. Logistic regression analysis suggested that the presence of an oral lesion was not associated with any demographic features except for periodontal diseases which were associated with tobacco smoking (P = 0.023). The prevalence of so called 'strongly associated' oral lesions of HIV is low in this South London HIV-infected population on HAART, and the relative frequency is different from that cited in the literature from the pre-HAART era. The oral lesions detected were found mostly in people with low CD4 counts and high HIV-1 RNA viral loads, suggesting they were very immunocompromised, not on, or declining therapy, or that their therapy was failing.
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            Oral hairy leukoplakia and oral candidiasis as predictors of HIV viral load.

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              Risk indicators for oral candidiasis and oral hairy leukoplakia in HIV-infected adults.

              Oral candidiasis (OC) and oral hairy leukoplakia (OHL) are the most common oral mucosal diseases associated with HIV infection. Independent risk indicators associated with these sentinel opportunistic diseases have not been established in mixed race and gender adult populations in the southeast USA. The purposes of this study were 1) to estimate prevalence of OC and OHL among an HIV-1 positive adult population, and 2) to develop explanatory multivariable models for each disease outcome. This cross-sectional study evaluated 631 adult dentate HIV-1 seropositive persons examined for HIV-associated oral mucosal diseases between 1995 and 2000 at University of North Carolina Hospitals in Chapel Hill, North Carolina using data collected from medical record review, interview questionnaire and clinical examination. We analyzed the data using t-tests, anova, and unconditional logistic regression. Prevalent OC was associated with low CD4+ cell count [<200 cells/microl, adj. OR = 12.7 (95%CI: 4.9-32.9)], antiretroviral combination therapy [OR = 0.6 (0.3-0.9)], and current smoking [OR = 2.5 (1.3-4.8)]. Prevalent OHL was associated with low CD4+ cell count [<200 cells/microl, OR = 7.2 (2.7-18.9)], antifungal medication use [OR = 1.8 (1.1-2.9)], current recreational drug use [OR = 2.5 (1.3-4.9)], and male gender [OR = 2.5 (1.3-4.8)]. While CD4+ cell count, and antiretroviral medication were important risk indicators for OC, and OHL, cigarette smoking appears to be an important risk indicator for OC in HIV-1-infected populations. Copyright Blackwell Munksgaard, 2005.
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                Author and article information

                Journal
                Int J Dent
                Int J Dent
                IJD
                International Journal of Dentistry
                Hindawi
                1687-8728
                1687-8736
                2017
                17 July 2017
                : 2017
                : 3457479
                Affiliations
                1Special Care Dentistry Center, Division of Oral and Maxillofacial Pathology, Department of Stomatology, School of Dentistry, University of Sao Paulo, Sao Paulo, SP, Brazil
                2Division of General Pathology, Department of Stomatology, School of Dentistry, University of Sao Paulo, Sao Paulo, SP, Brazil
                3Laboratory of Virology, Institute of Tropical Medicine of Sao Paulo, University of Sao Paulo, Sao Paulo, SP, Brazil
                Author notes
                *Karem L. Ortega: klortega@ 123456usp.br

                Academic Editor: Tommaso Lombardi

                Author information
                http://orcid.org/0000-0001-5945-8401
                http://orcid.org/0000-0001-7787-4062
                http://orcid.org/0000-0002-1842-9521
                http://orcid.org/0000-0002-9573-2858
                Article
                10.1155/2017/3457479
                5536144
                d9d257ea-4cef-43a9-93fe-210ee804b2a0
                Copyright © 2017 Luana L. Martins et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 19 December 2016
                : 29 May 2017
                : 19 June 2017
                Categories
                Research Article

                Dentistry
                Dentistry

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