| [ Summary ] |
Osteoporosis is the most common bone disease. It is recognized that postmenopausal women lose bone due to a decrease in ovarian estrogen. Ovariectomized (OVX) animals have been used to understand the mechanism of bone loss due to estrogen deficiency. We have reported that loss of estrogen stimulates B-lymphopoiesis in OVX mice, resulting in an accumulation of B cells in mouse bone marrow. It was assumed that the increased B-lymphopoiesis caused by estrogen deficiency was involved in stimulated bone resorption. In OVX mice, the expression of receptor activator of nuclear factor KB ligand (RANKL) mRNA was elevated in trabecular bone and bone marrow compared with sham mice. When B cells were co-cultured with mouse osteoblasts, most of the B cells adhered to cell surface of osteoblasts, and the expression of RANKL in osteoblasts was markedly elevated by the contact with the B cells. On the other hand, previous studies suggested that bone-resorbing cytokines such as IL-1 and tumor necrosis factor alpha may be involved in bone loss in OVX mice. These studies are useful to consider the mechanism of action of estrogen in bone. |