Spontaneous generation of functional osteoclasts from synovial fluid mononuclear cells as a model of inflammatory osteoclastogenesis. Issue 9 (30th June 2015)

• Record Type: Journal Article
• Authors: Greisen, Stinne R.; Einarsson, Halldór Bjarki; Hvid, Malene; Hauge, Ellen‐Margrethe; Deleuran, Bent; Kragstrup, Tue Wenzel
• Is Part Of: Apmis. Volume 123:Issue 9(2015:Sep.)
• Page Start: 779
• Page End: 786
• Publication Date: 2015-06-30
• Subjects: Pathology -- Periodicals; Microbiology -- Periodicals; Immunology -- Periodicals; 572
• DOI: 10.1111/apm.12416
• Languages: English
• ISSNs: 0903-4641

Abstract

<abstract abstract-type="main" id="apm12416-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <p>In osteoimmunology, osteoclastogenesis is understood in the context of the immune system. Today, the <italic>in vitro</italic> 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 <italic>in vitro</italic> osteoclastogenesis in cultures of synovial fluid mononuclear cells (SFMCs) activated only <italic>in vivo</italic>. SFMCs were isolated and cultured for 21 days at 0.5–1.0 × 10<sup>6</sup> cells/mL in culture medium. SFMCs 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 (MMP9) and TRAP. Adding RANKL and M‐CSF potentiated this secretion. In conclusion, we show that SFMCs from inflamed peripheral joints can spontaneously develop into functionally active osteoclasts <italic>ex vivo</italic>. Our study provides a simple <italic>in vitro</italic> model for studying inflammatory osteoclastogenesis.</p> </abstract>