期刊
JOURNAL OF CLINICAL PERIODONTOLOGY
卷 28, 期 8, 页码 769-775出版社
WILEY
DOI: 10.1034/j.1600-051X.2001.280808.x
关键词
nicotine; gingival fibroblasts; epithelial cells; proliferation; protein synthesis; collagen production
Background, aims: Several in vitro and in vivo studies have indicated that tobacco smoking may be an important risk factor for the development and severity of inflammatory periodontal disease. Method: In the present study, we developed an in vitro model to study the interactions between nicotine-treated epithelial cells (EC) and gingival fibroblasts (GF) derived from the same patient. EC were treated with nicotine concentrations varying from 1 mug/ml to 500 mug/ml and their effect on different functions of GF was studied. The proliferation of GF was evaluated by the incorporation of H-3-thymidine. A dose-dependent inhibition was observed with nicotine concentrations greater than or equal to 100 mug/ml. Similar results were observed when studying the total protein synthesis of GF by incorporation of H-3-proline into non-dialyzable material. Results: When collagen production was evaluated by H-3-proline incorporation into collagenase-sensitive protein, a dose-dependent reduction was observed: the degree of inhibition varied from 25% with 50 mug/ml nicotine, to almost 60% with 500 mug/ml. Interestingly, the production of non-collagenous proteins decreased by almost 50% only when EC were treated with the highest concentration of nicotine. Conclusions: The results suggest that epithelial cells, acting as mechanical barrier, can reduce but not completely eliminate the deleterious effect of nicotine on gingival fibroblasts.
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