Sex Steroids

The effect of sex steroids on skeletal homeostasis is well established, although, the mechanisms mediating those effects are unclear. Estrogen plays a pivotal role in regulating bone metabolism not only in women but also in men (Khosla et al., 2002). Sex steroids (estrogen and androgens) decrease the genesis of osteoblasts and osteoclasts; however, they stimulate apoptosis in osteoclasts and prolong the life span of osteoblasts (Manola-gas, 2000). Sex steroids inhibit bone resorption via effects on the RANKL/RANK/OPG system, as well as by altering cell-mediated release of various cytokines (inter-leukins, MCSF, TNF-a, TGFft BMP-6), insulin-like growth factor-I (IGF-I), prostaglandins, and NO (Khosla et al., 2002). Overwhelming data, including the Women's Health Initiative study, suggest that HRT reverses bone loss associated during the postmenopausal period (Riggs et al., 2002; Rossouw et al., 2002). Cross-sectional and interventional studies have demonstrated cardioprotective actions of estrogen. However, recent prospective randomized intervention trials have failed to show such beneficial actions (Rossouw et al., 2002). The dose of estrogen, timing of initiating hormone replacement, and presence of prior atherosclerotic vascular disease may have contributed to the apparently contradictory results. Interestingly, coronary artery plaque calcium content and burden have been shown to be associated with estrogen levels in pre- and postmenopau-sal women (Christian et al., 2002). Estrogen is known to modulate OPG, MGP, RANKL/RANK, and NO, and may mediate some of its actions on arterial calcification.

In contrast to estrogen, well-designed and adequately powered interventional trials examining the effects of testosterone replacement on bone metabolism in elderly men are lacking. Therefore, the effects of androgen supplementation on BMD are largely unknown. Testosterone has been shown to retard atherosclerosis in rodent models; however, prospective or cross-sectional studies have failed to reveal any consistent association of testosterone levels and coronary artery disease (Alexandersen et al., 1999). Similarly, there is no convincing evidence supporting an association of DHEA(S) with atherosclerosis. These studies suggest that estrogen, but not testosterone or DHEA(S), plays a key role in osteoporosis and atherosclerosis.

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