Bone mass in early adult life, or peak bone mass, is primarily under genetic control, although recent data suggest that alterations in nutrition and life style during growth may modify the genetic potential. Cross-sectional data indicated that upon completion of growth, there was a period of skeletal consolidation that resulted primarily from increased width of cortical bones. Data on cancellous bone are conflicting. Cross-sectional data suggest that cancellous bone mass reaches a maximum at about age 18 years. Bone mass in the spine appears stable until the beginning of menopause, unless there are other disturbances of ovarian function. On the basis of cross-sectional data, significant bone loss in the femoral neck in premenopausal women appears to occur prior to changes in ovarian function. This decline in hip density is also independent of body size, nutritional influences, or other variables thought to influence bone mass. Longitudinal data are not available to confirm the reduction in femoral neck bone mass. Preliminary data indicate that modest disruptions of ovarian function, insufficient to result in frank amenorrhea, might impact negatively on bone mass. A detailed longitudinal study of menstrual and other factors controlling bone mass in premenopausal women is needed. If bone mass can be modified, ensuring a maximal skeletal mass becomes a viable possibility for prevention of osteoporosis.