Ghadially J A, Ghadially F N
Virchows Arch B Cell Pathol. 1975 Jul 18;18(3):193-204. doi: 10.1007/BF02889247.
Full thickness defects (core defects) violating subchondral bone were created in the weight-bearing area of articular cartilage lining the rabbit medial femoral condyle. The repair reaction that follows has two components: (1) a sliding and flowing of cartilage over the edge of the defect and (2) a filling of the defect by repair tissue arising from the marrow spaces. Past studies have paid little or no attention to cartilage flow but this first scanning electron microscopic study of deep defects shows that it is an important phenomenon which materially affects the changes that occur and also the outcome of such injuries. Briefly, we have found that in most cases the cartilage flows downwards into the core defect. The repair tissue then grows along and over the "toed-in" catilage. In other cases the flowing cartilage rides over the repair tissue from the marrow spaces and as a result of load bearing and joint movement, becomes frayed and drawn out into long ribbons and rope-like structures.
在兔股骨内侧髁关节软骨的负重区制造穿透软骨下骨的全层缺损(核心缺损)。随后的修复反应有两个组成部分:(1)软骨在缺损边缘滑动和流动;(2)骨髓腔产生的修复组织填充缺损。过去的研究很少或根本没有关注软骨流动,但这项首次对深部缺损的扫描电子显微镜研究表明,它是一个重要现象,会实质性地影响损伤后发生的变化以及损伤的结果。简而言之,我们发现,在大多数情况下,软骨向下流入核心缺损。然后修复组织沿着“内翻”的软骨生长并覆盖其上。在其他情况下,流动的软骨从骨髓腔的修复组织上滑过,由于负重和关节运动,变得磨损并被拉伸成长条和绳状结构。