osteoclastogenesis

osteoclastogenesis

The development of osteoclasts from blood cells, specifically from monocytes/macrophages.
References in periodicals archive ?
Several proinflammatory cytokines such as interleukin (IL)-1, tumor necrosis factor alpha (TNF-[alpha]), IL-6, IL-11, IL-15, and IL-17 are elevated in IBD and have been identified as stimulators of osteoclastogenesis (5).
On the one hand, IL-17A increases the expression of receptor activator of nuclear factor kappa beta ligand, which has a central role in the stimulation of osteoclastogenesis, and on the other, it inhibits the expression of osteoprotegerin, which reduces the production of osteoclasts.
Tumeric (Curcuma longa) inhibits inflammatory factor (NF) and NF-KB regulated gene products and induce death receptors leading to suppressed proliferation, induced chemosensitization and suppressed osteoclastogenesis.
Role of C-reactive protein in osteoclastogenesis in rheumatoid arthritis.
interleukin-1 (IL-1), and interleukin-6 (IL-6), tumor necrosis factor-alpha (TNFa)) associated with chronic HBV infection can increase receptor activator of nuclear factor kappa-B ligand (RANKL) to stimulate osteoclastogenesis and bone resorption.
Myricetin suppresses LPS-induced MMP expression in human gingival fibroblasts and inhibits osteoclastogenesis by downregulating NFATc1 in RANKL-induced RAW 264.
SC-514 is a new selective, reversible, and competitive with adenosine triphosphate (ATP) of IKK[sz] inhibitor and can attenuate RANKL-induced osteoclastogenesis and NF-?
IL-23 induces receptor activator of NF-kappaB ligand expression on CD4+ T cells and promotes osteoclastogenesis in an autoimmune arthritis model.
To maintain this balance, osteoblasts produce factors including RANKL and M-CSF, which directly mediate osteoclastogenesis and osteoclast activity.
6) El aumento en los niveles circulantes de citoquinas como la interleucina (IL) 1, la IL-6, la IL-7, el factor de necrosis tumoral (TNF)-a y el TNF-B pueden producir supresion del reclutamiento de osteoblastos y estimular la osteoclastogenesis, con el consiguiente desequilibrio en el recambio oseo.