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Local and systemic TCR V gene expression in advanced periodontal disease
Author(s) -
Berglundh T.,
Liljenberg B.,
Tarkowski A.,
Lindhe J.
Publication year - 1998
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.1998.tb02418.x
Subject(s) - periodontitis , t cell receptor , pathology , immunohistochemistry , biopsy , gingivitis , biology , medicine , lesion , molar , immunology , t cell , dentistry , immune system
. The aim of the present investigation was to study the expression of specific α/β T cell receptor (TCR) gene products in relation to some microbiological and immunological features of advanced destructive periodontitis, 21 individuals with advanced periodontal disease (diseased group) and 16 age‐ and sex‐matched healthy subjects (healthy group) were recruited. Following a clinical examination of the diseased group, the 3 deepest interproximal sites in the upper and lower premolar‐ or molar segments (i.e., 12 sites in each individual) were selected for further analysis. Samples from the subgingival microbiota were obtained from the pocket of the selected sites and were prepared for a microbiological examination. The gingival tissue at one of the selected sites was also biopsied. Each excised soft tissue specimen was divided into 2 equal portions. One portion of the biopsy was prepared for histometric and morphometric analyses. The 2nd portion was snap frozen and prepared for immunohistochemical analysis, A sample of peripheral blood was obtained from each individual of the diseased and the healthy group and prepared for immunohistochemical analysis. The selected sites of the diseased group harbored varying numbers of microorganisms which have been associated with periodontal disease. The excised gingival tissue contained inflammatory lesions with substantial numbers of lymphocytes and plasma cells including T‐ and B‐cells and a TCR Vα/β gene repertoire dominated by Vβ 17. The TCR profile of the lesion, however, differed markedly from that of the circulating blood of the diseased subjects. While only minor differences were observed between the blood samples of the diseased and the healthy subjects regarding the TCR genes, CD5, HLA‐DR and CD5+CD19 positive cells occurred in higher proportions in the blood samples of the subjects susceptible to periodontal disease than in healthy controls. It may be suggested that (i) TCR Vα/Vβ expression in peripheral blood samples of subjects with periodontal disease does not differ from that of healthy individuals, and (ii) the periodontal lesion expresses a unique TCR repertoire in which the Vβ 17 gene dominates.