Despite significant evidence regarding the increased risk of cartilage degeneration due to traumatic injuries to joints, there is still a lack of understanding of the mechanisms underlying osteoarthritis development following a joint injury. Injuries in knee cartilage are often characterized by lesions or tears. In addition to acute traumatic joint injuries, microscale damages, which may form because of wear, are thought to be a contributing factor in the development of osteoarthritis.

While the overall function of a joint may not be affected by the presence of microcracks, we hypothesized that strain magnification in the vicinity of microcracks might be significant. We tested this hypothesis by creating partial cuts in articular cartilages and measuring the strain within 20 µm from the edge of these cuts. Measurements were made in the superficial and middle zones of articular cartilage extract samples. We found that local strain in the vicinity of cuts is magnified by a factor of 1.2–1.6 compared to strains in intact regions for nominal compressions exceeding 5%. For nominal compressions of less than 5%, no strain magnification was detected in the vicinity of the cracks. We concluded that articular cartilage cracks magnify local strains by damaging the structural integrity and decreasing the fluid pressure in the matrix.

尽管有大量证据表明由于关节外伤导致软骨退变的风险增加，但是仍然缺乏对关节损伤后骨关节炎发展的机制的了解。膝关节软骨损伤通常以病变或眼泪为特征。除了急性外伤性关节损伤外，由于磨损可能造成的微观损伤也被认为是骨关节炎发展的一个重要因素。

虽然关节的整体功能可能不受微裂纹的存在的影响，但我们假设微裂纹附近的应变放大率可能很大。我们通过在关节软骨上局部切开并在距切开边缘20 µm的范围内测量应变来检验该假设。在关节软骨提取物样品的浅层和中层进行测量。我们发现，与名义压力超过5％的完整区域的应变相比，切口附近的局部应变放大了1.2-1.6倍。对于名义压缩小于5％的情况，在裂纹附近未检测到应变放大率。我们得出的结论是，关节软骨裂纹会通过破坏结构完整性并降低基质中的流体压力来放大局部应变。