Nicotine suppresses proliferation and mineralized tissue‐associated gene expressions of cementoblasts

Background Previous studies reported that nicotine, which is the prominent constituent of tobacco, has negative effects on periodontium cells. However, the precise role of nicotine in cementoblast functions remains unclear. In the present study, we investigated the effects of nicotine on the functions of cementoblasts (OCCM‐30) in terms of proliferation, migration, and mineralized tissue‐associated gene expression. Methods Immortalized murine cementoblasts were exposed to various concentrations (0, 10−6, 10−5, 10−4, 10−3, 10−2, 10−1, 1, 2.5, 5, and 10 mM) of nicotine, and cementoblast proliferation was then evaluated using a real‐time cell analyzer for 142 hours. Using an in vitro wound healing assay, cell migration was evaluated 2, 4, 6, and 24 hours after exposure to different concentrations of nicotine (1, 2.5, 5, and 10 mM). The mRNA expressions of bone sialoprotein (BSP), collagen type I (COL‐I), osteocalcin (OCN), runt‐related transcription factor 2 (Runx2), and alkaline phosphatase (ALP) were assessed in the nicotine‐treated (0, 10−3, 10−2, 10−1, 1, 2.5, 5, and 10 mM) OCCM‐30 cells by reverse transcription quantitative polymerase chain reaction at 8 and 24 hours exposure. Results At concentrations of 1 to 10 mM, nicotine significantly reduced cementoblast proliferation (P