Ovariectomy-induced bone loss occurs independently of B cells

Estrogen withdrawal is associated with a significant expansion in B cell precursor and mature B cell populations. However, despite significant circumstantial evidence the role of B lineage cells in ovariectomy-induced bone loss in vivo is unclear. In vitro studies have demonstrated that mature B cells have the potential to both positively and negatively impact osteoclastogenesis by virtue of their capacity to secrete pro-osteoclastogenic cytokines including receptor activator of NF kappa B ligand (RANKL), as well as anti-osteoclastogenic cytokines such as osteoprotegerin (OPG) and transforming growth factor beta (TGF beta). Although several studies have suggested that expansion ofthe B lineage following ovariectomy may play a key role in the etiology of ovariectomy-induced bone loss, in vivo studies to directly test this notion have yet to be conducted. In this study, we performed ovariectomy on mu MT(-/-) mice which are specifically deficient in mature B cells. Analysis of bone mineral density (BMD) by dual-energy X-ray absorptiometry (DXA) and microcomputed tomography (CT) demonstrate that mature B cell-deficient mice undergo an identical loss of bone mass relative to wild-type (WT) control mice. Our data demonstrate that mature B cells are not central mediators of ovariectomy induced bone loss in vivo. J. Cell. Biochem. 100: 1370-1375, 2007. (c) 2006 Wiley-Liss, Inc.