Androgens are required to achieve peak bone mass in adolescence and are responsible for the higher BMD in men compared to women. Hypogonadism is associated with a decrease in bone mass and is one cause of osteoporosis in men. With aging, progressive loss of BMD is associated with increased fracture rates. Interestingly, the BMD in older men is more significantly correlated with serum free estradiol than with serum free testosterone levels (44,45). The few case reports of estrogen-receptor mutations and aromatase deficiency in males were all associated with severe osteoporosis (46-48). Thus, the current hypothesis is that estrogens are required for maintaining peak BMD in men. The concentration of serum E2, or the level of estrogen activity in the target tissues, that is required to maintain BMD is not known. Although it is apparent that some estrogenic action is required for normal BMD, it is probable that testosterone also directly effects bone mass through androgen receptors.
Hypogonadal men have lower BMD. Androgen replacement by injections or oral or transdermal preparations increases BMD in younger hypogonadal men (17,38,49). The androgen-induced increase in BMD is accompanied by initial elevations of bone formation markers and decreases in bone resorption markers (16,17,38,50). In older men, androgen administration increased BMD in some studies (18), but other studies showed no effect (51). In general, the lower the BMD and the lower the serum testosterone level before treatment, the greater the improvement in BMD after testosterone replacement (17,51). Although significant changes in BMD have occurred in hypogonadal men after long-term administration of androgen replacement, randomized controlled studies to examine whether androgens prevent fractures have not been performed.
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