Effects of nicotine on cell growth, migration, and production of inflammatory cytokines and reactive oxygen species by cementoblasts

Background/purposeCigarette smoking is an important risk factor in the pathogenesis of periodontal disease. However, little is known about the effect of nicotine, the major component of cigarette smoke, on cementoblasts. The aim of this study was to investigate the pathological effects of nicotine on the murine immortalized cementoblast cell line (OCCM.30).Materials and methodsCell viability was judged by using the Alamar Blue reduction assay. Cell migration was evaluated by transwell and wound-healing assays. The protein concentrations of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) were measured by using enzyme linked immunosorbent assay (ELISA). The semiquantitative 2′,7′-dichlorfluorescein-diacetate (DCFH-DA) fluorescence technique was used to detect the intracellular level of reactive oxygen species (ROS).ResultsConcentrations of nicotine > 1.5mM demonstrated cytotoxicity to cementoblasts (P < 0.05). Nicotine attenuated cell migration in a dose-dependent manner (P < 0.05). In addition, nicotine augmented the production of IL-6 and TNF-α in a dose-dependent manner (P < 0.05). The concentration of 1mM nicotine enhanced the generation of intracellular ROS in a time-dependent manner (P < 0.05).ConclusionTaken together, these results suggest that nicotine could inhibit the growth and migration of cementoblasts. In addition, nicotine could also induce the generation of inflammatory cytokines and ROS by cementoblasts.