Eun-Ju Chang

TL;DR: It is suggested that intracellular S1P produced in response to RANKL forms a negative feedback loop in BMM single cultures and plays an important role in osteoclastogenesis regulation and in communication between osteoclasts and osteoblasts or T cells.

TL;DR: It is suggested that IL-17 can function as a signal to induce extensive bone turnover by regulating hMSC recruitment, proliferation, motility, and differentiation by supporting osteoclastogenesis both in vivo and in vitro.

TL;DR: Alpha-LA greatly suppressed in vivo bone loss induced by RANKL or TNF-alpha in a calvarial remodeling model, providing evidence that ROS plays an important role in osteoclast differentiation through NF-kappaB regulation and the antioxidant alpha-lipoic acid has a therapeutic potential for bone erosive diseases.

TL;DR: It is shown that inhibition of p38 activity with SB203580 reduced osteoclastogenesis from primary precursor cells, with concomitant suppression in the induction of both c-Fos and nuclear factor of activated T cells (NFAT) c1 by receptor activator of nuclear factor kappaB ligand (RANKL), the key osteOClast differentiation factor.

TL;DR: Results clearly show that hyaluronan inhibits osteoclast differentiation through TLR4 by interfering with M-CSF signaling, and point that the interaction between ECM components and innate immune receptors can play an important role in the regulation of bone metabolism.