While TNF-α is pivotal to the pathogenesis of inflammatory osteolysis, the means by which it
recruits osteoclasts and promotes bone destruction are unknown. We find that a pure …

It is well-established that receptor activator of NF-κB ligand (RANKL) is the inducer of
physiological osteoclast differentiation. However, the specific drivers and mechanisms …

Tumor necrosis factor-α (TNF) and the ligand for receptor activator of NF-κB (RANKL) are
abundant in sites of inflammatory bone erosion. Because these cytokines are potent …

Osteoblasts or bone marrow stromal cells are required as supporting cells for the in vitro
differentiation of osteoclasts from their progenitor cells. Soluble receptor activator of nuclear …

Tumor necrosis factor‐α (TNF‐α) is a cytokine produced by monocytes, macrophages, and T
cells and is induced by pathogens, endotoxins, or related substances. TNF‐α may play a key …

NF-κB is a pleiotropic transcription factor, which regulates osteoclast formation, function, and
survival. The finding that the deletion of both NF-κB p50 and p52 subunits resulted in …

TNF-induced receptor activator NF-κB ligand (RANKL) synthesis by bone marrow stromal
cells is a fundamental component of inflammatory osteolysis. We found that this process was …

Osteoclasts are multinucleated cells formed mainly on bone surfaces in response to
cytokines by fusion of bone marrow-derived myeloid lineage precursors that circulate in the …

Receptor activator of nuclear factor-κB ligand [RANK ligand (RANK-L)] stimulates mature
osteoclasts to resorb bone, a process associated with NF-κB activation. RANK-L also …

To address the controversy of whether TNFα can compensate for RANKL in
osteoclastogenesis in vivo, we used a TNFα‐induced animal model of inflammatory arthritis …