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Spontaneous generation of functional osteoclasts from synovial fluid mononuclear cells as a model of inflammatory osteoclastogenesis
Author(s) -
Greisen Stinne R.,
Einarsson Halldór Bjarki,
Hvid Malene,
Hauge EllenMargrethe,
Deleuran Bent,
Kragstrup Tue Wenzel
Publication year - 2015
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12416
Subject(s) - rankl , cathepsin k , osteoclast , osteoimmunology , chemistry , immune system , macrophage colony stimulating factor , tartrate resistant acid phosphatase , immunology , monocyte , medicine , receptor , macrophage , in vitro , activator (genetics) , biochemistry
In osteoimmunology, osteoclastogenesis is understood in the context of the immune system. Today, the in vitro model for osteoclastogenesis necessitates the addition of recombinant human receptor activator of nuclear factor kappa‐B ligand ( RANKL ) and macrophage colony‐stimulating factor (M‐ CSF ). The peripheral joints of patients with rheumatoid arthritis ( RA ) and spondyloarthritis (SpA) are characterized by an immune‐mediated inflammation that can lead to bone destruction. Here, we evaluate spontaneous in vitro osteoclastogenesis in cultures of synovial fluid mononuclear cells ( SFMC s) activated only in vivo . SFMC s were isolated and cultured for 21 days at 0.5–1.0 × 10 6 cells/mL in culture medium. SFMC s and healthy control peripheral blood monocytes were cultured with RANKL and M‐ CSF as controls. Tartrate‐resistant acid phosphatase ( TRAP ) positive multinucleated cells were found in the SFMC cultures after 21 days. These cells expressed the osteoclast genes calcitonin receptor, cathepsin K, and integrin β3, formed lacunae on dentin plates and secreted matrix metalloproteinase 9 ( MMP 9) and TRAP . Adding RANKL and M‐ CSF potentiated this secretion. In conclusion, we show that SFMC s from inflamed peripheral joints can spontaneously develop into functionally active osteoclasts ex vivo . Our study provides a simple in vitro model for studying inflammatory osteoclastogenesis.