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In Situ Lymphocyte Subpopulations from Active versus Stable Periodontal Sites
Author(s) -
Reinhardt Richard A.,
Bolton Ronald W.,
McDonald Thomas L.,
DuBois Linda M.,
Kaidahl Wayne B.
Publication year - 1988
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.1988.59.10.656
Subject(s) - lymphocyte , clinical attachment loss , biopsy , t lymphocyte , monoclonal antibody , pathology , medicine , periodontal disease , antibody , immune system , immunology , dentistry
T he purpose of this study was to evaluate lymphocyte subset densities and distributions within gingival biopsies from active sites (>2 mm clinical attachment loss within three months of biopsy) versus clinically similar but stable or healthy sites. Small interproximal gingival biopsies representing at least one of each of the above categories were obtained from each of 20 periodontal maintenance patients. Serial cryostat sections displaying a cross section of the gingiva were labeled with monoclonal antibodies for (1) pan T cells, (2) T cytotoxic/suppressor cells, (3) T helper/inducer cells and (4) pan B cells and were developed using an avidin‐biotin‐peroxidase system. Lymphocyte populations were enumerated in repeatable fields from the sulcular, middle and oral one‐third of each section. Relative proportions of the same lymphocyte subsets were analyzed in peripheral blood samples from the same patients using direct immunofluorescence. Pan B cells were significantly more prevalent in infiltrates from active sites than in stable ( P < 0.05) or healthy ( P < 0.01) sites. The T/B cell ratio was also significantly lower in active than stable biopsies ( P < 0.05), and in active biopsies versus blood ( P < 0.05). The T helper/T suppressor cell ratio did not vary significantly between blood and any gingival tissue disease group or location, but a trend toward lower relative numbers of T helper cells in the sulcular infiltrates of active sites was noted. These results support the premise that active periodontal sites display elevated B cell populations and abnormal immune regulation possibly involving the T helper cell subset.