Division of Rheumatology, University of Washington, Seattle, WA, USA.
Rheumatology (Oxford). 2018 Mar 1;57(3):414-418. doi: 10.1093/rheumatology/kex274.
Most students of articular mechanics consider impact loads to be compressive forces that are borne by an intraosseous, trabecular scaffold. The possible role of marrow fat, which comprises about 75% of the structure, is generally ignored, and the potential contribution of type 1 collagen, the prototypic tensile protein, is not considered. Here, I question the evidence underlying these omissions and reject the conclusion of exclusive trabecular compression. Instead, I suggest that impact loading pressurizes the fat in subchondral compartments, and those pressures stretch the elastic trabecular walls, which are thereby subjected to tensile loading. The load-driven pressure pulses then diminish as they pass from each compartment to its adjoining neighbours. The resulting pressure gradient distributes the burden throughout the subchondrium, stores energy for ensuing recovery and subjects individual trabeculae only to the net pressure differences between adjacent compartments.
大多数关节力学的学生认为，冲击载荷是由骨内的小梁支架承受的压缩力。通常忽略了骨髓脂肪（约占结构的 75%）的可能作用，也没有考虑到 1 型胶原蛋白（典型的拉伸蛋白）的潜在贡献。在这里，我对这些遗漏的证据提出质疑，并拒绝了仅发生小梁压缩的结论。相反，我认为冲击加载会对软骨下隔室中的脂肪施加压力，并且这些压力会拉伸弹性小梁壁，从而使小梁壁受到拉伸载荷。随着压力脉冲从一个隔室传递到相邻的隔室，其压力会逐渐减小。由此产生的压力梯度将负担分布在整个软骨下区域，为随后的恢复储存能量，并使各个小梁仅承受相邻隔室之间的净压力差。
