Abstract

Low peak bone mass and fast rate of postmenopausal bone loss, the two main determinants of postmenopausal osteoporosis are determined by complex interactions of genetic and environmental factors that regulate bone cell activity and bone turnover. Peak bone mass is mainly under genetic influence, whereas estrogen deficiency plays a major role in determining postmenopausal bone loss. Decisions for therapeutic intervention are made in individual patients. The level of intervention will depend not only on the severity of bone loss measured by DXA, but also on age, the existence or nonexistence of prevalent fractures, associated risk factors, and the benefit/risk ratio of the proposed therapeutic regimen. For intermediate values (neither high nor low) of BMD, the subsequent rate of bone loss is likely to be important in the assessment of risk. A high bone resorption assessed by specific biochemical markers is associated with increased risk of subsequent fracture, both at the spine and hip, with a predictive value similar to that obtained from bone mass assessment. There is evidence that an integrated strategy using major clinical risk factors (e.g., history of fractures, low body weight), measurement of BMD by DXA, and measurement of bone resorption by urinary or serum biochemical markers and potentially post translation modifications of type I collagen or other bone matrix proteins could be useful to detect high-risk patients.

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