Effects of nicotine on differentiation, prostaglandin E2, and nitric oxide production in cementoblasts

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.

Keywords

• alkaline phosphatase
• cementoblasts
• nitric oxide
• nicotine
• prostaglandin E2