Inflammatory osteoclastogenesis can be induced by GM-CSF and activated under TNF immunity

Biochemical and Biophysical Research Communications
Koji NomuraTetsuya Tomita

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.

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Citations

Aug 25, 2010·Best Practice & Research. Clinical Rheumatology·Axel J HueberAshley M Miller
Nov 26, 2014·Nature Reviews. Rheumatology·Iannis E Adamopoulos, Elizabeth D Mellins
Dec 15, 2017·Nihon Rinshō Men'eki Gakkai kaishi = Japanese journal of clinical immunology·Kazuhiro Yokota
Sep 28, 2017·Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Médicas E Biológicas·L LiX Yu
Jul 5, 2016·Inflammation and Regeneration·Aoi ShiomiTsuneyo Mimori

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