Neurath M F, Printz H, Stofft E
Department of Anatomy, University of Mainz, Germany.
Acta Orthop Scand. 1994 Feb;65(1):71-6. doi: 10.3109/17453679408993722.
To evaluate the cellular ultrastructure following injury, we examined the anterior cruciate ligaments in 55 patients with complete tears in different phases after the injury and compared them to a control group of 39 cadaver knees. Samples were analyzed by electron microscopy, immunofluorescence, and ultramorphometry. After an invasion of inflammatory cells into the stumps of the ruptured ligaments, a marked proliferation of fibroblasts was found at the end of Phase 1 (2-3 days after the ligament injury), that was even more pronounced at the beginning of Phase II (4-17 days). These cells were initially highly metabolically active and secreted Type III collagen precursors. In Phase III (4-45 days), fibroblast degeneration occurred with increasing frequency. Furthermore, some fibroblasts showed signs of cell death. Our findings suggest that the structural alterations of the intraligamentous fibroblasts diminish their function and, consecutively, disorganization of the developing repair tissue occurs. This mechanism might contribute to the poor healing potential of the ruptured anterior cruciate ligament.
为评估损伤后的细胞超微结构,我们检查了55例在损伤后不同阶段出现完全撕裂的前交叉韧带患者,并将其与39个尸体膝关节组成的对照组进行比较。通过电子显微镜、免疫荧光和超微形态测量法对样本进行分析。在炎性细胞侵入破裂韧带残端后,在第1阶段末期(韧带损伤后2 - 3天)发现成纤维细胞显著增殖,在第II阶段初期(4 - 17天)更为明显。这些细胞最初代谢活性很高,并分泌III型胶原前体。在第III阶段(4 - 45天),成纤维细胞变性的频率增加。此外,一些成纤维细胞显示出细胞死亡的迹象。我们的研究结果表明,韧带内成纤维细胞的结构改变削弱了它们的功能,进而导致正在形成的修复组织紊乱。这种机制可能导致破裂的前交叉韧带愈合潜力不佳。