Abstract: The present invention demonstrates that human parathyroid hormone 1-34 [hPTH(1-34)] exerts anti-apoptotic effects on osteoblasts when administered in an intermittent fashion to mice in vivo. The present invention further demonstrates that bovine PTH(1-34) [bPTH(1-34)] prevents glucocorticoid-induced apoptosis of osteoblastic and osteocytic cells in vitro. Therefore, the present invention demonstrates that the previously established anabolic effects of PTH on the skeleton are mediated by its ability to postpone osteoblast apoptosis, as opposed to a stimulatory effect on osteoblastogenesis. The present invention provides methods of screening agents for anti-apoptotic effects on osteoblasts, wherein such agents stimulate and/or restore bone in osteopenic individuals, or prevent bone loss caused by agents such as glucocorticoids.

Abstract: The invention as disclosed provides a method to increase bone mass without compromising bone strength or quality, through the administration to a host of a compound that binds to the estrogen or androgen receptor without causing hormonal transcriptional activation.