Nicotine down-regulates the proliferation of the cementoblasts (OCCM.30)

Abstract

Aim Smoking is a well known risk factor for periodontitis and it has definitely negative impacts on the results of periodontal therapies. Nicotine, which is the main active component of tobacco, affects cell functions including proliferation, adhesion and differentiation of the cells. The aim of this study was to explore the effects of nicotine on the proliferation of cementoblasts. Methods Immortalized mouse cementoblasts (OCCM-30) were treated with different concentrations (0.001, 0.01, 0.1, 1, 10, 100, 1000, 10,000, 100,000 nM, 1 mM, 10 mM) of nicotine and analyzed for proliferation using a real-time cell analyzer (xCelligence; RTCA-SP) for 130 hours and the cells were photographed after different concentrations of nicotine applications. Results Findings demonstrated that immediately after 10 mM nicotine application, OCCM cells were not alive. 10 mM concentration of nicotin was severely cytotoxic. Other concentrations of nicotine even when it was used picoM level, significantly inhibited proliferation of cementoblasts at 72 hrs (p<0.05). Inverted microscopy images exhibited rounded dead cells at highest concentration of nictoine parallel with the proliferation findings. Conclusions Results of this study displayed that nicotine suppressed proliferation potentials of OCCM.30 cells which is critical for new cementum formation. Further studies are warranted to understand whether nicotine affects the gene expressions profile of the cementoblasts.

Keywords

• cementoblasts
• nicotine
• smoking