Studies have started appreciating the fact that the prevalence of osteoporosis in older men is substantial. Estrogen deficiency states such as delayed puberty, amenorrhea of any cause, and, perhaps, the use of progestational agents for contraception, can lead to suboptimal acquisition of peak bone mass. In the male, androgens are thought to be critical to the establishment of peak bone mass. Delayed puberty in otherwise normal boys is associated with reduced bone density for as long as 10 years thereafter compared with boys who entered puberty on time. In sex steroid-sufficient, growing boys and girls, a 7% to 10% difference in the achievement of peak bone mass is believed to be a key protective factor in the male. Thus, not only do men not normally experience an abrupt cessation of androgen production in their middle years, but they also achieve a greater reservoir of bone owing to the attainment of greater peak bone mass in youth. Results from the short-term interventional observations also opened the way to studies on the use of estrogenic compounds in men. Short-term low doses of estradiol have been successfully employed to increase growth velocity in prepubertal boys. Major concerns of either androgen and estrogen treatment in men relate to their possible collateral negative implications in other estrogen targets, such as the gonads, the prostate, and the cardiovascular system. Thus, it is likely that the therapeutic skeletal effects of androgens in men are owing, at least in part, to their conversion to estrogens.
|Original language||English (US)|
|Title of host publication||Principles of Bone Biology, Two-Volume Set|
|Number of pages||18|
|State||Published - Dec 1 2008|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)