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Updated: Jul 3, 2026

Accessing the Cytotoxicity and Cell Response to Biomaterials
Published on: July 8, 2021
[Effects and molecular mechanism of nicotine on odontoblasts]
Li-An Wu1, Ling-Ying Wen, Fu-Sheng Yang
1Department of Pediatric Dentistry, College of Stomatology, The Fourth Military Medical University, Xi'an 710032, China.
Objective:
To observe the effects of nicotine on the proliferation of odontoblasts and explore the possible mechanism.
Methods:
Odontoblasts MDPC-23 were cultured, inoculated and divided into two groups randomly. With no stimuli added for the control group, the experimental group was stimulated by 100 microg/mL nicotine. After 8 hours, 10 micromol/L BrdU was added to label cells at S stage in cell cycle. 24 hours later, odontoblasts were fixed and immunofluorescence staining was performed with specific mouse BrdU antibody. After counterstaining with propidium iodide, BrdU positive cells were arbitrarily scored microscopically by an independent estimation conducted three times, and the corresponding total cell number in the same vision were counted in both groups. BrdU positive cell rates were calculated and compared statistically. At the same time, odontoblasts MDPC-23 were cultured and stimulated by 100 microg/mL nicotine, the dynamic Ca2+ concentration inside the cytoplasm were detected immediately by a confocal laser scanning microscope.
Results:
The ratio of S stage cells in the experimental group was 36.3% significantly lower than that (48.2%) in the control group. After the addition of 100 microg/mL nicotine, the Ca2+ concentration inside the cytoplasm rose rapidly, sustained at a high level for a short time and then relapsed gradually.
Conclusion:
Nicotine had inhibitory effects on the proliferation of odontoblasts MDPC-23, which might be related to the increased Ca2+ concentration in the cytoplasm.
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