| Research Abstract |
We previously demonstrated the in vivo relationship between pulp apoptosis and pulp cell proliferation and differentiation during wound healing (J Dent Res, 2001; J Dent Res, 2003). We also demonstrated in vitro that pulp cells exposed to heat stress show apoptosis and thermotolerance, which was modified by LPS through the regulation of HSF1, HSP27, Akt, and NFkB/IkBa (J Cell Biochem, 2005, 2006). We also found that hypoxia induces cell cycle arrest and apoptosis through the regulation of p21, cyclin D2, Rb, and p53 (J Dent Res, 2006). In this research, to clarify the mechanism of pulp wound healing and establish dentin/pulp regeneration therapy, we applied gelatin hydrogels incorporating FGF-2, and found that controlled release of FGF-2 from gelatin hydrogels induced formation of dentin-like particles in dentin defect above exposed pulp (J Endod, 2007). Further, we established rat dental pulp cell line with odontoblastic properties, and found that calcification ability of this odontoblastic cells was inhibited by LPS (J Endod, 2007). Now, we are continuing research on effects of glycosaminoglycan on pulp cells, odonotblasts, and neurons, which are constituents of dental pulp tissues.
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