Abstract
The aim of this study was to assess and compare quantitatively the presence of S100+ Langerhans cells (LC) by immunochemistry techniques in HIV+ and HIV- gingivitis and periodontitis subjects. Additionally, it aimed to evaluate the correlation among densities of these cells with CD4+ and CD8+ T cells, and viral load levels in HIV+ subjects, all using Highly Active Antiretroviral Therapy (HAART). The samples were allocated into four groups: 1) 15 subjects with moderate chronic periodontitis (MCP), HIV+; 2) 15 subjects with MCP, HIV-; 3) 10 subjects with gingivitis (G), HIV+; and 4) 10 subjects with G, HIV-. The S100+ cells were assessed in the pocket epithelium, gingival epithelium, and lamina propria. A statistically significant increase of total S100+ cells in HIV+ periodontitis subjects was observed in relation to HIV- periodontitis subjects. No increase of S100+ cells with increased inflammation was observed. No statistically significant correlation among S100+ cells and blood levels of CD4, CD8, and viral load was observed. In conclusion, the use of HAART can aid in achieving viral loads, and it is suggested that it may prevent the destruction of the LC.
Highlights
Langerhans cells (LC) are the first cells of the immune system capable of uptaking, processing, and presenting foreign antigens to T-lymphocytes.[1]
A larger number of cells was observed with increased inflammation,[4,5] a low quantitative difference was observed between gingivitis and periodontitis.[6]
As a result of this infection, in HIV+ patients with periodontitis, LC were decreased as compared with HIV− subjects[9]; the former showed a significant decrease in major histocompatibility complex class II (MHC-II) expression.[10]
Summary
Langerhans cells (LC) are the first cells of the immune system capable of uptaking, processing, and presenting foreign antigens to T-lymphocytes.[1]. HIV infection is a modifier factor for periodontal disease, responsible for the depletion of CD4+ T lymphocytes, macrophages and LC.[7,8] As a result of this infection, in HIV+ patients with periodontitis, LC were decreased as compared with HIV− subjects[9]; the former showed a significant decrease in major histocompatibility complex class II (MHC-II) expression.[10]. Recent reports have not indicated a major severity of periodontal disease in HIV+ patients under treatment with antiretroviral agents.[11,12] The antiretroviral treatment has resulted in a significant reduction in mortality and morbidity. Strong evidence has shown that the introduction of HAART for the medical management of HIV+ subjects has resulted in a marked decrease in the severity of periodontal diseases in this population.[8] the impact of this therapy on LC needs to be determined
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