2012 Volume 55 Issue 5 Pages 304-312
Purpose: Heat stress during restorative procedures can trigger damage to pulpodentin complex. It is universally known that dental pulp has tissue restoration ability. Odontoblast or odontoblast-like cells in dental pulp produce tertiary dentin in response to various irritations of pulpodentin as a defense reaction. However, the precise mechanism remains unclear. It is important to clarify this mechanism to save dental pulp and maintain healthy teeth. In the present study, we examined the effects of heat stress on dental pulp derived cells and the responses of the cells after heat stress. Materials and Methods: Viability and cell morphology of odontoblast-like cell line KN-3 were examined after exposure to heat stress at 43℃ for 45 minutes. The expression of several proteins (HSP25, HSP70, HSP90, Cyclin D1, Cyclin E, p21, p27, DSP and DMP-1) after heat stress was assessed by western blot analysis. Results: The viability of heat-stressed cells temporarily decreased and cells with nuclear fragmentation were observed at 12 hours after heat stress. The recovery of cell proliferation ability was observed at 1, 2 and 3 days after. Increase of the expression of HSP25, HSP70 and HSP90 was detected after heat stress. As for the expression of several proteins involving cell cycle, Cyclin D1 and Cyclin E increased at 6 and 24 hours after heat stress. However, expression of p21 and p27 peaked at 6 hours and decreased at 24 hours. The expression of odontoblast differentiation markers DSP and DMP-1 increased at 6 and 24 hours. Conclusion: After heat stress, the production of HSPs and transient cell-cycle arrest maintained the viability of KN-3 cells, and cell proliferation and differentiation into odontoblast-like cells were induced after heat stress.
