| First Author | Uster S | Year | 2018 |
| Journal | Bone | Volume | 107 |
| Pages | 56-65 | PubMed ID | 29081378 |
| Mgi Jnum | J:256982 | Mgi Id | MGI:6113114 |
| Doi | 10.1016/j.bone.2017.10.020 | Citation | Uster S, et al. (2018) TNFalpha blockade mediates bone protection in antigen-induced arthritis by reducing osteoclast precursor supply. Bone 107:56-65 |
| abstractText | Bone protective effects of TNFalpha inhibition in rheumatoid arthritis are thought to be mediated by inhibiting synovial osteoclast differentiation and activity. However, it has not been addressed, if TNFalpha inhibitors alter the pool of peripheral osteoclast precursor cells (OPCs). Here, we blocked TNFalpha function in C57BL/6 mice with antigen induced arthritis (AIA) using the soluble TNFalpha 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 TNFalpha 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. |
