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DOI

10.1016/j.jds.2015.03.007

First Page

431

Last Page

436

Abstract

Abstract Background/purpose Cigarette smoking is an important risk factor in the pathogenesis of periodontal disease. Little is known about the effects of nicotine, the major component of cigarette smoke, on cementoblasts. The aim of this study was to investigate the cytopathologic effects of nicotine on murine immortalized cementoblast cell line (OCCM.30). Materials and methods Cell viability was judged by using the tetrazolium bromide reduction assay. Cell differentiation was examined by alkaline phosphatase assay. The production of prostaglandin E2 (PGE2) and nitric oxide (NO) were evaluated using an enzyme-linked immunosorbent assay and Griess reaction, respectively. Inducible nitric oxide synthase (iNOS) was evaluated by western blot. Results Nicotine demonstrated cytotoxicity to cementoblasts in a dose-dependent manner (P < 0.05). Nicotine was found to inhibit alkaline phosphatase activity in a time-dependent manner (P < 0.05). In addition, nicotine increased the secretion of PGE2 in a dose-dependent manner (P < 0.05). Nicotine was found to induce NO generation and iNOS expression in a dose-dependent manner (P < 0.05). Conclusion Our results suggest that nicotine could inhibit cementoblast growth and differentiation. In addition, nicotine could also induce the inflammatory effects by the augmentation of PGE2 secretion and iNOS/NO expression.

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