Lewis Jack L, Deloria Laurel B, Oyen-Tiesma Michelle, Thompson Roby C, Ericson Marna, Oegema Theodore R
Department of Orthopaedic Surgery, University of Minnesota, Minneapolis, MN 55455, USA.
J Orthop Res. 2003 Sep;21(5):881-7. doi: 10.1016/S0736-0266(03)00039-1.
The damage from rapid high energy impacts to cartilage may contribute to the development of osteoarthritis (OA). Understanding how and when cells are damaged during and after the impact may provide insight into how these lesions progress. Mature bovine articular cartilage on the intact patella was impacted with a flat impacter to 53 MPa in 250 ms. Cell viability was determined by culturing the cartilage with nitroblue tetrazolium for 18 h or for 4 days in medium containing 5% serum before labeling (5-day sample) and compared to adjacent, non-impacted tissue as viable cells per area. There was a decrease in viable cell density only in specimens with macroscopic cracks and the loss was localized primarily near matrix cracks, which were in the upper 25% of the tissue. This was confirmed using confocal microscopy with a fluorescent live/dead assay, using 5'-chloromethylfluorescein diacetate and propidium iodide. Cell viability in the impacted regions distant from visible cracks was no different than the non-impacted control. At 5 days, viable cell density decreased in the surface layer in both the control and impacted tissue, but there was no additional impact-related change. In summary, cell death after the impaction of cartilage on bone occurred around impact induced cracks, but not in impacted areas without cracks. If true in vivo, early stabilization of the damaged area may prevent late sequelae that lead to OA.
快速高能冲击对软骨造成的损伤可能会促使骨关节炎（OA）的发展。了解细胞在冲击过程中及之后如何以及何时受到损伤，可能有助于深入了解这些损伤是如何进展的。完整髌骨上的成熟牛关节软骨用扁平冲击器在250毫秒内冲击至53兆帕。通过在含有5%血清的培养基中用硝基蓝四氮唑培养软骨18小时或4天（5天样本），然后进行标记，来确定细胞活力，并将其与相邻的未受冲击组织作为每单位面积的活细胞进行比较。仅在有宏观裂纹的标本中活细胞密度降低，且损失主要局限于基质裂纹附近，这些裂纹位于组织的上25%。使用5'-氯甲基荧光素二乙酸酯和碘化丙啶进行荧光活/死检测的共聚焦显微镜证实了这一点。远离可见裂纹的受冲击区域的细胞活力与未受冲击的对照无差异。在第5天，对照组织和受冲击组织的表层活细胞密度均降低，但没有与冲击相关的额外变化。总之，软骨撞击骨后细胞死亡发生在冲击诱导的裂纹周围，但在没有裂纹的受冲击区域则不会发生。如果在体内情况属实，受损区域的早期稳定可能会预防导致OA的晚期后遗症。
