Seeman E
Department of Medicine, Austin Hospital, University of Melbourne.
Osteoporos Int. 1994;4 Suppl 1:15-25. doi: 10.1007/BF01623430.
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.
骨质疏松症被视为一种老年疾病，因为骨折发生在生命后期。虽然衰老过程中过度的骨质流失可能导致骨密度降低，但骨折患者的骨质流失并不总是更快，骨吸收也不总是更多，或者骨形成更低（使用骨转换的生化或组织形态计量学标志物测量）。骨质疏松症所特有的低骨密度和骨脆性的发病机制可能始于生命的前二十年。区域生长和矿物质积累的激素调节存在差异，轴向和附属骨骼、皮质骨和小梁骨以及近端和远端肢体节段的线性生长和矿物质积累的发病年龄、速率和持续时间也存在差异。疾病、风险或保护因素以及激素缺乏或过多的紊乱可能会影响纵向生长、矿物质积累，或两者都有影响，这取决于暴露的时间。当暴露发生在生长期间而非成年期时，可能会对骨密度产生数量上更大、质量上不同的影响。这些缺陷的程度及其位置可能决定了与年龄相关的区域性和性激素依赖性骨质流失的相关性。因此，任何关于骨质疏松症流行病学和发病机制的统一假设都必须考虑低峰值骨密度和骨质流失对成年期骨密度降低的相对贡献。由于骨质疏松症的发病机制至少部分是由生命最初20年发生的事件所解释的，因此需要大量研究来研究纵向生长和矿物质积累的生理学。
