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• W2158486578 abstract "In inflammatory arthritis such as RA, osteoclastic activity is severely enhanced. GM-CSF was reportedly elevated in synovial fluid, but is a strong inhibitor of osteoclastogenesis; here lies a contradiction. Our objective was to examine what type of osteoclasts generate and resorb bone with resistance to GM-CSF in an inflammatory joint. Monocyte-derived cells generated in GM-CSF were morphologically and immunophenotypically different from both the conventional DC and macrophage. They could differentiate into osteoclasts in the presence of RANKL + M-CSF, acquiring a stronger osteoclastic activity under TNF treatment. Furthermore, their differentiation was not inhibited by GM-CSF, while monocyte-derived osteoclast differentiation was completely inhibited. The resorption was suppressed by GM-CSF, and the existence of another osteoclastic pathway has been suggested. Our findings indicate another type of osteoclast exists in inflammatory arthritis." @default.
• W2158486578 created "2016-06-24" @default.
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• W2158486578 creator A5068842257 @default.
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• W2158486578 date "2008-03-01" @default.
• W2158486578 modified "2023-09-26" @default.
• W2158486578 title "Inflammatory osteoclastogenesis can be induced by GM-CSF and activated under TNF immunity" @default.
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• W2158486578 doi "https://doi.org/10.1016/j.bbrc.2008.01.023" @default.
• W2158486578 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18201554" @default.
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