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TNFα blockade mediates bone protection in antigen-induced arthritis by reducing osteoclast precursor supply

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Uster Stephanie, Coelho Fernanda Matos, Aeberli Daniel, Stein Jens V., Hofstetter Wilhelm, Engelhardt Britta, Seitz Michael,
Project Osteoklastogenese und chronisch entzündliche rheumatische Erkrankungen
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Original article (peer-reviewed)

Journal Bone
Volume (Issue) 107
Page(s) 56 - 65
Title of proceedings Bone
DOI 10.1016/j.bone.2017.10.020

Abstract

Bone protective effects of TNFα inhibition in rheumatoid arthritis are thought to be mediated by inhibiting synovial osteoclast differentiation and activity. However, it has not been addressed, if TNFα inhibitors alter the pool of peripheral osteoclast precursor cells (OPCs). Here, we blocked TNFα function in C57BL/6 mice with antigen induced arthritis (AIA) using the soluble TNFα receptor etanercept. Synovial bone lesions and osteoclasts were markedly reduced upon Etanercept in the early chronic phase of AIA. Unexpectedly this was not associated with a reduced recruitment of circulating OPCs to the arthritic joint nor to reduced synovial inflammation. In contrast we found that OPC numbers in bone marrow and blood were significantly reduced. Overall our study suggests that arrest of osteoclast mediated bone lesions upon inhibition of TNFα is, at least initially, based on reduced OPC availability in the periphery, and not on OPC recruitment or local anti-inflammatory effects in the arthritic joint
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