Reduced bone density in women with fractures: contribution of low peak bone density and rapid bone loss.

Abstract

Osteoporosis is regarded as a disease of the elderly because fractures occur late in life. Although excessive bone loss during aging is likely to contribute to the deficit in bone density, patients with fractures do not consistently have more rapid bone loss, greater bone resorption or lower bone formation (measured using biochemical or histomorphometric markers of bone turnover). The pathogenesis of the low bone density and bone fragility that characterize osteoporosis may begin during the first two decades of life. There are differences in the hormonal regulation of regional growth and mineral accrual, differences in the age of onset, rate and duration of linear growth and mineral accrual of the axial and appendicular skeleton, of cortical and trabecular bone, and of proximal and distal limb segments. Illnesses, risk or protective factors, and disorders of hormonal deficiency or excess may affect longitudinal growth, mineral accrual, or both, depending on the timing of exposure. Quantitatively larger and qualitatively different effects on bone density may result when exposure occurs during growth rather than during adulthood. The magnitude of these deficits and their location are likely to establish the relevance of regional age-related and sex hormone dependent bone loss. Thus, any unifying hypothesis concerning the epidemiology and pathogenesis of osteoporosis must consider the relative contributions of low peak bone density and bone loss to the deficit in bone density in adulthood. A great deal of research is needed to examine the physiology of longitudinal growth and mineral accrual as the pathogenesis of osteoporosis is at least partly explained by events occurring during the first 20 years of life.