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 microg/ml to 500 microg/ml and their effect on different functions of GF was studied. The proliferation of GF was evaluated by the incorporation of 3H-thymidine. A dose-dependent inhibition was observed with nicotine concentrations > or =100 microg/ml. Similar results were observed when studying the total protein synthesis of GF by incorporation of 3H-proline into non-dialyzable material. RESULTS: When collagen production was evaluated by 3H-proline incorporation into collagenase-sensitive protein, a dose-dependent reduction was observed: the degree of inhibition varied from 25% with 50 microg/ml nicotine, to almost 60% with 500 microg/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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Giannopoulou et al. (2001) studied this question.
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