Toshihiro Miyazaki

TL;DR: These findings indicate that the maturity and turnover rate of bone are determined by the level of functional Runx2 and Run x2 is responsible for bone loss in estrogen deficiency, but that Runx 2 is not essential for maintenance of the expression of major bone matrix protein genes in postnatal bone development and maintenance.

TL;DR: Results indicate that Runx2 is required for the proliferation of osteoblast progenitors and induces proliferation, at least partly, by regulating F gfr2 and Fgfr3 expression.

TL;DR: It is demonstrated that Ocn is required for bone quality and strength by adjusting the alignment of BAp crystallites parallel to collagen fibrils; but it does not function as a hormone.

TL;DR: It is suggested that the osteocyte network negatively regulate bone mass by inhibiting osteoblast function and activating osteoclastogenesis, and these functions are augmented in the unloaded condition at least partly through the upregulation of Rankl expression in osteoblasts and that of Sost in osteocytes.

TL;DR: Findings indicate that Runx2 inhibits the terminal differentiation of odontoblasts, and that Run x2 induces transdifferentiation of odonoblasts into osteoblasts forming a bone structure.