BONE MASS AND THE MECHANOSTAT - A PROPOSAL
BONE MASS AND THE MECHANOSTAT - A PROPOSAL
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DOI：
10.1002/ar.1092190104
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发表时间：
1987-09-01
影响因子：
--
通讯作者：
FROST, HM
中科院分区：
文献类型：
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作者：
FROST, HM
观察到的骨量与健康动物典型机械使用的拟合表明，某些机制监测该使用并控制直接确定骨量的三个纵向生长、骨建模和基于BMU的重塑活动。这种机制可以被命名为机械稳定器。累积的证据表明，它包括骨骼本身，加上将其机械使用转化为适当信号的机制，以及检测这些信号然后指导上述三种生物活动的其他机制。体内研究表明，在1500-3000微应变范围内或以上的骨应变导致骨建模增加皮质骨量，而低于100-300微应变范围的应变释放基于BMU的重塑，然后去除现有的皮质-骨内膜和骨小梁。该布置提供了双重系统，其中骨建模将使骨量适应于总过载，而基于BMU的重塑将使骨量适应于总欠载，并且上述应变范围将是这些响应的近似“设定点”。这些机械使用效应的解剖学分布是众所周知的。如果循环因子或疾病改变了这些响应的有效设定点，则其骨量效应应复制机械使用效应的解剖分布。这似乎是许多代理商和疾病的情况下，并讨论了几个例子，包括绝经后骨质疏松症，氟化物的影响，在眼眶骨丢失，和骨生成arrhythmia。机械恒温器的建议是一个开创性的想法，适合不同的证据，但它需要批判和实验研究。
The observed fit of bone mass to a healthy animal''s typical mechanical usage indicates some mechanism or mechanisms monitor that usage and control the three longitudinal growth, bone modeling, and BMU-based remodeling activities that directly determine bone mass. That mechanisms could be named a mechanostat. Accumulated evidence suggests it includes the bone itself, plus mechanisms that transform its mechanical usage into appropriate signals, plus other mechanisms that detect those signals and then direct the above three biologic activities. In vivo studies have shown that bone strains in or above the 1500-3000 microstrain range cause bone modelling to increase cortical bone mass, while strains below the 100-300 microstrain range release BMU-based remodeling which then removes existing cortical-endosteal and trabecular bone. That arrangement provides a dual system in which bone modeling would adapt bone mass to gross overloading, while BMU-based remodeling would adapt bone mass to gross underloading, and the above strain ranges would be the approximate "setpoints" of those responses. The anatomical distribution of those mechanical usage effects are well known. If circulating agents or disease changes the effective setpoints of those responses their bone mass effects should copy the anatomical distribution of the mechanical usage effects. That seems to be the case for many agents and diseases, and several examples are discussed, including postmenopausal osteoporosis, fluoride effects, bone loss in orbit, and osteogenesis imperfecta. The mechanostat proposal is a seminal idea which fits diverse evidence but it requires critique and experimental study.