Articular cartilage adjacent to experimental defects is subject to atypical strains
Articular cartilage adjacent to experimental defects is subject to atypical strains
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DOI：
10.1097/01.blo.0000145990.58146.3d
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发表时间：
2005-01-01
影响因子：
4.2
通讯作者：
Chansky, HA
中科院分区：
文献类型：
--
作者：
Braman, JP;Bruckner, JD;Chansky, HA
我们测试了这样的假设：与实验性骨软骨缺陷相邻的关节软骨在负载下不会受到异常应变。在 10 只成年兔子的 15 个膝盖的股骨内侧髁上钻一个 2.5 毫米的钻孔。实验关节加载模拟股四头肌力，然后在负载下冷冻并通过冷冻替代固定保存。通过扫描电子和光学显微镜评估缺陷区域的变形，并与未钻孔和未负载的对照膝盖进行比较。为了模拟血凝块，在加载前将藻酸盐放入一些缺陷中。在承受负荷的膝盖中，钻孔边缘的关节软骨异常变平并折叠到缺损处。相对的胫骨软骨或半月板侵入股骨缺损，超出骨水泥线。藻酸盐不能阻止对向软骨的侵入。在这个标准钻孔模型中，当关节加载时，关节软骨缺陷被相对表面占据。任何在缺损处生长或通过手术植入的组织都会受到负载和位移的影响，因此使在类似钻孔模型中表征愈合或再生潜力的尝试变得复杂。缺损边缘处的软骨变形表明负荷集中或顺应性增加。这两种现象都会导致缺陷附近的软骨随后退化。
We tested the hypothesis that articular cartilage adjacent to experimental osteochondral defects is not subject to unusual strains under load. A 2.5-mm drill hole was made in the medial femoral condyle of 15 knees from 10 adult rabbits. Experimental joints were loaded with simulated quadriceps force, then frozen under load and preserved by freeze-substitution fixation. Deformation in the region of the defect was evaluated by scanning electron and light microscopy and compared with nondrilled and nonloaded control knees. To simulate blood clot, alginate was placed into some defects before loading. In loaded knees, articular cartilage at the edge of the drill hole was abnormally flattened and folded into the defect. Opposing tibial cartilage or meniscus intruded into the femoral defect beyond the cement line. Alginate did not prevent incursion of opposing cartilage. In this standard drill-hole model, the articular cartilage defect is occupied by the opposing surface when a joint is loaded. Any tissue growing or surgically implanted in the defect is subject to loading and displacement, therefore complicating attempts to characterize the healing or regenerative potential in similar drill-hole models. Deformation of cartilage at the defect edge suggests load concentration or increased compliance. Either phenomenon would contribute to subsequent degeneration of the cartilage adjacent to defects.