The effect of sex steroids on the skeleton in premenopausal women.

Abstract

Whereas peak bone mass is genetically determined, the skeletal growth, maturation, and maintenance required to reach this peak may be influenced by physical activity, ovarian function, and nutrition. Estrogen deficiency at menopause leads to increased skeletal remodeling and loss of bone mass, which can result in osteoporotic fractures. Entering menopause with low bone mass is a risk factor itself, because bone mass predicts future risk of fracture. The administration of exogenous steroids can reverse the setting of the "mechanostat" to lower levels after ovarian dysfunction, although it is unclear whether oral contraceptives can modify bone mass in the ovulatory premenopausal woman. Our recent data suggest that the use of steroidal hormones to treat menstrual irregularity (presumably relative to ovarian dysfunction), as opposed to fertility control, is more likely to positively affect bone mass. It is even less clear whether hyperestrogenic states (e.g., pregnancy) affect the skeleton. Recent evidence from bone mass changes that occur in women with ovulatory cycles and inadequate luteal phase function suggests that progestins may also influence skeletal metabolism.