Frost Harold M
Department of Orthopaedics, Southern Colorado Clinic, 3676 Parker Blvd, Pueblo, CO 81008-9000, USA.
Angle Orthod. 2004 Feb;74(1):3-15. doi: 10.1043/0003-3219(2004)074<0003:AUOBPA>2.0.CO;2.
By 1892, Julius Wolff and others realized that mechanical loads can affect bone architecture in living beings, but the mechanisms responsible for this effect were unknown, and it had no known clinical applications. In 2003 we know how this effect occurs and some of its applications. Our load-bearing bones (LBBs) include tibias, femurs, humeri, vertebrae, radii, mandibles, maxillae, wrists, hips, etc (so LBBs are not limited to weight-bearing ones). The strength of such bones and their trabeculae would represent their most important physiologic feature but in the special sense of relative to the size of the typical peak voluntary loads on them. The biologic "machinery" that determines whole-bone strength forms a tissue-level negative feedback system called the mechanostat. Two thresholds make a bone's strains determine its strength by switching on and off the biologic mechanisms that increase or decrease its strength. Equally, two thermostats can determine a room's temperature by switching on and off the room's heating and cooling systems. General features show that the largest voluntary loads on LBBs determine most of their strength after birth. These loads come from muscle forces so muscle strength strongly influences the strength of our LBBs. This process affects, in part, the healing of fractures, bone grafts, osteotomies, and arthrodeses; the bone's ability to endure load-bearing joint and dental endoprostheses; why healthy bones are stronger than the minimum needed to keep voluntary loads from breaking them suddenly or from fatigue; some general functions and disorders of bone modeling and basic multicellular unit-based bone remodeling; some limitations of in vitro data and of pharmaceutical actions; and the fact that many bone-active humoral and local agents have permissive roles in a bone's adaptations and healing, instead of forcing them to occur.
到1892年，尤利乌斯·沃尔夫等人意识到机械负荷会影响生物的骨骼结构，但造成这种影响的机制尚不清楚，也没有已知的临床应用。2003年，我们了解了这种影响是如何发生的以及它的一些应用。我们的承重骨（LBBs）包括胫骨、股骨、肱骨、椎骨、桡骨、下颌骨、上颌骨、手腕、髋部等（所以承重骨不限于承担体重的骨头）。这类骨头及其骨小梁的强度将代表其最重要的生理特征，但这里是相对于作用于它们的典型峰值随意负荷的大小而言的特殊意义上的重要特征。决定全骨强度的生物“机制”形成了一个组织水平的负反馈系统，称为机械稳态器。两个阈值使骨骼的应变通过开启和关闭增加或降低其强度的生物机制来决定其强度。同样，两个恒温器可以通过开启和关闭房间的加热和冷却系统来决定房间的温度。一般特征表明，出生后LBBs上最大的随意负荷决定了它们的大部分强度。这些负荷来自肌肉力量，因此肌肉力量强烈影响我们LBBs的强度。这个过程部分影响骨折、骨移植、截骨术和关节融合术的愈合；骨骼承受承重关节和牙科假体的能力；为什么健康的骨骼比防止随意负荷使其突然断裂或疲劳所需的最低强度更强；基于基本多细胞单位的骨建模和骨重塑的一些一般功能和紊乱；体外数据和药物作用的一些局限性；以及许多骨活性体液和局部因子在骨骼适应和愈合中起允许作用，而不是强制它们发生这一事实。
