Kanami Itoh

TL;DR: It is suggested that IL-17 first acts on osteoblasts, which stimulates both COX-2-dependent PGE2 synthesis and ODF gene expression, which in turn induce differentiation of osteoclast progenitors into mature osteoclasts, and that IL -17 is a crucial cytokine for osteoclastic bone resorption in RA patients.

TL;DR: It is suggested that ODF/RANKL but not M-CSF mediates osteoblast-induced pit-forming activity of osteoclasts, and that bone-resorbing factors stimulate osteoclast activation through upregulation of ODF or RANKL by osteoblasts/stromal cells.

TL;DR: Findings suggest that OPG produced by osteoblasts/stromal cells is a physiologically important regulator in osteoclast differentiation and function and that RANKL expressed by osteobasts functions as a membrane-associated form.

TL;DR: Results suggest that osteoclast function is induced through a mechanism independent of p38 MAPK-mediated signaling, and LPS induced degradation of IkappaB and phosphorylation of ERK in osteoclasts as well as in osteOClast precursors.

TL;DR: The findings suggest that bone morphogenetic protein-mediated signals cross-communicate with RANKL-mediated ones in inducing osteoclast differentiation and survival and appear unrelated to nuclear factor-kappaB activation.