Abstract
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 NFκB ligand (RANKL), as well as anti‐osteoclastogenic cytokines such as osteoprotegerin (OPG) and transforming growth factor beta (TGFβ). Although several studies have suggested that expansion of the 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 µMT(−/−) mice which are specifically deficient in mature B cells. Analysis of bone mineral density (BMD) by dual‐energy X‐ray absorptiometry (DXA) and micro‐computed 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. © 2006 Wiley‐Liss, Inc.