Immunohistological analysis of experimental gingivitis in humans was carried out to provide a baseline for the study of immunoregulatory mechanisms in chronic inflammatory periodontal disease. Using a panel of monoclonal antibodies in an avidin biotin immunoperoxidase technique, T cell subsets were identified and the pattern of Class II major histocompatibility complex (MHC) antigens determined. Twenty third-year dental students took part in the study. Following the cessation of oral hygiene procedures, gingival biopsies were taken from each of five students at days 0, 4, 8 and 21 during the development of the inflammatory lesion. Each student had one biopsy which healed uneventfully. The T4:T8 ratio showed only slight variation over the time course of the lesion varying from 2.18:1 at day 0 to 2.48:1 at day 4. At all stages the T cells displayed both HLA-DR and HLA-DQ antigens, but less than 10% had detectable IL-2 receptors. The predominant macrophage population was acid phosphatase + ve, adenosine triphosphatase -ve, HLA-DR+ and HLA-DQ+ antigens suggesting an activated phagocytic population. During the development of the lesion, the number of intraepithelial Langerhans cells (T6+) increased but there appeared to be a discrepancy between HLA-DR and HLA-DQ expression on these cells. Similarly, the keratinocytes expressed HLA-DR but failed to express HLA-DQ at any stage. These results suggest that the developing gingival lesion is a well controlled lesion and follows a similar pattern to a controlled delayed type hypersensitivity (DTH) response
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