BACKGROUND/AIM: Cigarette smoking is one of the most significant risk factors in the development and further advancement of inflammatory periodontal disease. However, no study has been performed to investigate the effect of smoking on the attachment of human periodontal ligament fibroblasts to either periodontally diseased or healthy roots. The present study was conducted to evaluate the attachment of fibroblasts derived from healthy human periodontal ligament (PDL) to periodontally diseased root surfaces of smokers. METHOD: The subjects included 14 smokers and seven nonsmokers with at least a single periodontally involved anterior tooth planned for extraction. In addition, seven impacted third molars, which had been removed from nonsmoking adolescents, were used as a healthy control. The smoking status of each patient was determined by classifying the volunteers into four groups according to their level of cigarette consumption at the initial examination (seven patients each). Nonsmoking subjects who had never smoked cigarettes and had healthy periodontium were called healthy control (G1). In subjects with periodontal diseases, nonsmoking subjects who had never regularly smoked cigarettes (< 2 cigarettes/week) were called positive control (G2), smokers consuming <or=19 cigarettes/day were placed in group G3, and smokers consuming >or=20 cigarettes/day were located in group G4. To exclude the effects of all local irritants except for the adsorbed tobacco products, all teeth were subjected to thorough scaling and root planing 1 week before extraction. After 1 week of meticulous home care and continued smoking experience, teeth were extracted and the periodontally involved test areas were prepared for PDL culturing. PDL cells were cultured on root segments for 24 h. Samples were prepared for SEM viewing, photographing and counting at x750 in a standard area. RESULTS: The results of this study indicated that smokers' data (G3, G4) revealed a significant reduction of attached PDL cells when compared to that of nonsmokers' healthy and positive controls (G1, G2). No significant difference in the mean number of attached cells was found between data derived from smokers' groups (G3 vs. G4). The attached cells in all groups varied in shape; they were flatter in the control groups, while they were round in smokers' groups, with no dose-dependent effect. CONCLUSION: The present results suggest that cigarette smoking compromises PDL cell adhesion to root planed surfaces, which might affect periodontal regeneration following therapy.
BACKGROUND/AIM: Cigarette smoking is one of the most significant risk factors in the development and further advancement of inflammatory periodontal disease. However, no study has been performed to investigate the effect of smoking on the attachment of human periodontal ligament fibroblasts to either periodontally diseased or healthy roots. The present study was conducted to evaluate the attachment of fibroblasts derived from healthy human periodontal ligament (PDL) to periodontally diseased root surfaces of smokers. METHOD: The subjects included 14 smokers and seven nonsmokers with at least a single periodontally involved anterior tooth planned for extraction. In addition, seven impacted third molars, which had been removed from nonsmoking adolescents, were used as a healthy control. The smoking status of each patient was determined by classifying the volunteers into four groups according to their level of cigarette consumption at the initial examination (seven patients each). Nonsmoking subjects who had never smoked cigarettes and had healthy periodontium were called healthy control (G1). In subjects with periodontal diseases, nonsmoking subjects who had never regularly smoked cigarettes (< 2 cigarettes/week) were called positive control (G2), smokers consuming <or=19 cigarettes/day were placed in group G3, and smokers consuming >or=20 cigarettes/day were located in group G4. To exclude the effects of all local irritants except for the adsorbed tobacco products, all teeth were subjected to thorough scaling and root planing 1 week before extraction. After 1 week of meticulous home care and continued smoking experience, teeth were extracted and the periodontally involved test areas were prepared for PDL culturing. PDL cells were cultured on root segments for 24 h. Samples were prepared for SEM viewing, photographing and counting at x750 in a standard area. RESULTS: The results of this study indicated that smokers' data (G3, G4) revealed a significant reduction of attached PDL cells when compared to that of nonsmokers' healthy and positive controls (G1, G2). No significant difference in the mean number of attached cells was found between data derived from smokers' groups (G3 vs. G4). The attached cells in all groups varied in shape; they were flatter in the control groups, while they were round in smokers' groups, with no dose-dependent effect. CONCLUSION: The present results suggest that cigarette smoking compromises PDL cell adhesion to root planed surfaces, which might affect periodontal regeneration following therapy.