Kerin Alex J, Coleman Alexis, Wisnom Michael R, Adams Michael A
Department of Anatomy, University of Bristol, Southwell Street, Bristol BS2 8EJ, UK.
Clin Biomech (Bristol). 2003 Dec;18(10):960-8. doi: 10.1016/j.clinbiomech.2003.07.001.
Mechanical overloading of synovial joints can damage the articular cartilage surface and may lead to osteoarthritis. However, causal links between mechanical and biological events in cartilage are poorly understood.
To test the hypothesis that surface fissures in cartilage can propagate mechanically if the joint surface is subjected to vigorous cyclic loading.
Thirty-five cartilage-on-bone specimens, 15-mm square, were removed from mature bovine knee and shoulder joints. Specimens were loaded by means of a 9-mm-diameter flat indenter with a beveled edge, and their compressive strength determined. Failure occurred in the cartilage surface at an average stress of 36 MPa. Cartilage fissures were marked with Indian ink, photographed, and their length and width measured using image analysis software. Each damaged specimen was subjected to cyclic loading at 40% of its compressive strength, at 0.5 Hz, for up to 5 h. Fissure length and width were measured at regular intervals. After testing, fissure depth was measured from histological sections, and compared with measurements from damaged cartilage which was not cyclically loaded.
Cyclic loading caused cartilage fissures to increase in length (mean 353%, P<0.01) and width (360%, P<0.01) but not depth. Propagation was rapid at first, but approached equilibrium after several hundred cycles. Rehydration in saline had no effect on fissure length, but width returned to pre-cyclic loading values.
Cartilage fissures can propagate mechanically when a joint surface is subjected to cyclic compressive loading in vitro. The transient opening-up of fissures to form wide surface "wounds" during cyclic loading could be of biological significance if it occurred in living people.
In living joints, wide open fissures in the cartilage surface could promote degenerative changes in the tissue.
滑膜关节的机械性过载会损伤关节软骨表面，并可能导致骨关节炎。然而，软骨中机械事件与生物学事件之间的因果联系尚不清楚。
验证如下假设：如果关节表面受到剧烈的循环载荷，软骨表面的裂隙会发生机械性扩展。
从成年牛的膝关节和肩关节取下35个边长为15毫米的骨软骨标本。通过一个直径9毫米、边缘带斜角的平面压头对标本施加载荷，并测定其抗压强度。软骨表面在平均应力为36兆帕时发生破坏。用印度墨水标记软骨裂隙，拍照，并使用图像分析软件测量其长度和宽度。每个受损标本在其抗压强度的40%、频率为0.5赫兹的条件下进行循环加载，持续5小时。定期测量裂隙的长度和宽度。测试后，从组织学切片测量裂隙深度，并与未进行循环加载的受损软骨的测量结果进行比较。
循环加载导致软骨裂隙长度（平均增加353%，P<0.01）和宽度（增加360%，P<0.01）增加，但深度不变。起初扩展迅速，但在数百次循环后趋于平衡。在盐水中复水对裂隙长度没有影响，但宽度恢复到循环加载前的值。
在体外，当关节表面受到循环压缩载荷时，软骨裂隙会发生机械性扩展。如果这种情况发生在活人身上，循环加载过程中裂隙短暂张开形成宽的表面“伤口”可能具有生物学意义。
在活体关节中，软骨表面的宽裂隙可能会促进组织的退行性变化。
