These authors Contribute to this paper equally.
Melatonin influences proliferation and differentiation of rat dental papilla cells in vitro and dentine formation in vivo by altering mitochondrial activity
Article first published online: 4 SEP 2012
© 2012 John Wiley & Sons A/S
Journal of Pineal Research
Volume 54, Issue 2, pages 170–178, March 2013
How to Cite
Liu, J., Zhou, H., Fan, W., Dong, W., Fu, S., He, H. and Huang, F. (2013), Melatonin influences proliferation and differentiation of rat dental papilla cells in vitro and dentine formation in vivo by altering mitochondrial activity. Journal of Pineal Research, 54: 170–178. doi: 10.1111/jpi.12002
Re-use of this article is permitted in accordance with the Terms and Conditions set out at http://wileyonlinelibrary.com/onlineopen#OnlineOpen_Terms
- Issue published online: 6 FEB 2013
- Article first published online: 4 SEP 2012
- Accepted manuscript online: 7 AUG 2012 09:32AM EST
- Manuscript Accepted: 27 JUL 2012
- Manuscript Received: 30 MAY 2012
- dental papilla cell;
Melatonin mediates a variety of biological processes ranging from the control of circadian rhythms to immune regulation. Melatonin also influences bone formation and osteointegration of dental implants. However, the effects of melatonin on dentine formation have not been examined. This study investigated the effects of melatonin on the proliferation and differentiation of rat dental papilla cells (rDPCs) in vitro and dentine formation in vivo. We found that melatonin (0, 10−12, 10−10,10−8 m) induced a dose-dependent reduction in rDPCs proliferation, increased alkaline phosphatase (ALP) activity, the expression of dentine sialoprotein (DSP), and mineralized matrix formation in vitro. In vivo melatonin (50 mg/kg, BW, i.p.) inhibited dentine formation. Melatonin (10−8 m) suppressed the activity of complex I and IV in the basal medium (OS−) and enhanced the activity of complex I and complex IV in osteogenic medium (OS+). These results demonstrate that melatonin suppresses the proliferation and promotes differentiation of rDPCs, the mechanisms of which may be related to activity of mitochondrial complex I and complex IV.