Bone densitometry in premenopausal women: synthesis and review.

Bone loss prior to menopause is being increasingly identified in women. Clearly, low bone mineral density (BMD) is a significant risk factor for fracture in the estrogen-deficient female postmenopause. The significance of low bone density prior to menopause needs to be addressed. Low bone density in the premenopausal female may reflect attainment of a lower peak bone mass. It may also be secondary to progressive bone loss following achievement of peak bone density. The etiology of low bone density in the premenopausal female needs to be clarified with meticulous exclusion of secondary causes of bone loss. Menstrual status is an important determinant of peak bone mass as well as the development of bone loss in women prior to the onset of menopause. Subclinical decreases in circulating gonadal steroids may be associated with a lower peak bone mass as well as progressive bone loss in otherwise reproductively normal women. Elevations of follicle-stimulating hormone (FSH) of greater than 20 miu/L are associated with evidence of increased bone turnover marker activity and correlate with progressive bone loss in perimenopausal women. This transitional period requires further study with respect to the magnitude of bone loss experienced and the potential benefits of antiresorptive therapy. Detailed assessment of menstrual status is necessary in the evaluation of low bone density in premenopausal women. The majority of the cross-sectional and longitudinal studies completed evaluating BMD in the premenopausal years suggest that minimal bone loss does occur prior to menopause after attainment of peak bone mass. The magnitude of premenopausal bone loss, however, is controversial and may be site-dependent. More rapid rates of bone loss are seen in the transitional period beginning 2-3 yr prior to the onset of menopause. Prospective data are needed to understand further the relationship between BMD and fracture in the premenopausal period. Women with steroid-induced bone loss as well as other secondary causes of osteoporosis respond to antiresorptive therapy with documented improvements in BMD. Biomarkers can identify perimenopausal women with increased bone turnover. Lifestyle modification can improve BMD in the pre- and the perimenopausal period. Antiresorptive therapy has not been evaluated in pre- or perimenopausal women with low BMD in the absence of secondary causes of osteoporosis. As new treatment options are evaluated and become available, biomarker assessment may be of value in identifying women at risk of fracture.