Frost H M
Clin Orthop Relat Res. 1985 Nov(200):198-225.
The disease osteoporosis is a manifestation of osteopenia and mechanical incompetence. The osteopenia (reduced bone tissue volume) can follow insufficient bone accumulation during growth, secondary to abnormalities in cortical bone modeling and/or remodeling of spongiosa. Or it can follow pathologic bone losses due to altered activation of bone remodeling units and to the special bone-balance-determining delta B X BMU function. Combinations of the above can occur. Mechanical incompetence (fracture and/or bone pain during normal mechanical usage) is due partly to the osteopenia, which reduces bone strength to 90% to occasionally 40% of normal. However, even 40% of normal strength should leave bones with approximately five times the strength needed to withstand maximum normal mechanical loads. Further weakening of osteoporotic bone to 10% of normal or less is due to accumulations of mechanical microdamage, which increase when less bone still carries normal loads. Microdamage also accumulates because malfunctions of the remodeling mechanism that normally repairs it occur consistently in most osteoporoses. Thus microdamage physiology emerges as a major feature of the pathophysiology of the osteoporoses. Future research must find what controls it in life and how to reduce it for medical needs.
骨质疏松症是骨质减少和力学功能不全的一种表现。骨质减少(骨组织体积减少)可因生长期间骨累积不足所致,继发于皮质骨塑形和/或松质骨重塑异常。或者,它可因骨重塑单位激活改变以及特殊的骨平衡决定因素ΔB×BMU功能导致的病理性骨质流失所致。上述情况可能会合并出现。力学功能不全(正常力学使用过程中发生骨折和/或骨痛)部分归因于骨质减少,骨质减少会使骨强度降至正常的90%,偶尔降至40%。然而,即使是正常强度的40%,骨骼的强度也应是承受最大正常力学负荷所需强度的约五倍。骨质疏松性骨进一步减弱至正常的10%或更低,是由于机械性微损伤的累积,当较少的骨仍承受正常负荷时,微损伤会增加。微损伤也会累积,因为在大多数骨质疏松症中,正常修复微损伤的重塑机制持续出现故障。因此,微损伤生理学成为骨质疏松症病理生理学的一个主要特征。未来的研究必须找出生活中控制微损伤的因素以及如何根据医疗需求减少微损伤。