实验性兔膝骨关节炎滑液引起正常关节软骨的形态学改变

The morphological changes of normal cartilage induced by osteoarthritic synovial fluid of experimental rabbit knee

目的探讨内源性骨关节炎(osteoarthritis,O A)生物学致病因子对正常关节软骨的初始破坏作用。方法兔14只随机分为实验组和对照组。实验组切断一侧膝关节前交叉韧带,第12周晚期OA形成。抽取OA滑液随机注入自身一侧肘关节内(SF组),对侧肘关节注入等量生理盐水(N S组)。每周一次。对照组肘关节不注射任何液体。肘关节注射20周后SF组、NS组和对照组行大体、光镜和电镜观察。结果SF组、NS组和对照组肘关节关节软骨在大体上无明显区别。光镜下NS组和对照组关节软骨表面光滑,各层软骨细胞排列正常;SF组软骨细胞数量减少,移行层和放射层见到大量软骨细胞巢聚,出现双潮线,并且软骨钙化层增厚,非钙化层明显变薄。透射电镜下N S组和对照组软骨细胞形态大多正常,SF组软骨细胞发生退变和凋亡。扫描电镜下NS组和对照组软骨表面结构完整,SF组软骨表面出现表浅溃疡,胶原中断且排列紊乱。结论OA内源性生物学致病因子对正常关节软骨存在损害作用,但明显弱于力学因素。

Objective To investigate the incipient katogene of endogenous osteoarthritic biological causative agents on normal cartilage. Methods Fourteen white rabbits were divided into experimental group and control group randomly. The experimental rabbits received unilateral anterior cruciate ligament transection (ACLT), and advanced osteoarthritis was induced in the 12th week. Osteoarthritic synovial fluid of ACLT knee was extracted and then injected into one of the rabbit′s own elbow (SF group) and equale volume normal saline was injected into the contralateral elbow (NS group) once a week. No fluid was injected into the elbows of the control group. The cartilage of elbows of SF, NS and control groups were observed under gross observation, light and electron microscope. Results Elbow cartilage change without significant difference were observed in SF, NS and control groups under gross observation. Under light microscope the cartilage surface was smooth and normally aligned chondrocytes were observed in NS and control groups, but the decrease in the number of chondrocytes, chondrocyte nests in the transitional and radial zones and the double tide mark were observed in SF group with the thickened calcified layer and the significantly thinned noncalcified layer. The morphous of chondrocytes of NS and control groups were generally normal under transmission electron microscope, and cataplasis and apoptosis of chondrocytes of SF group were found. The surface structure of cartilage of NS and control groups were intact under scanning electron microscope, but superficial ulcer of cartilage and broken and derangment of collagen were observed in the SF group. Conclusion The incipient katogene of endogenous osteoarthritic biological causative agent on normal cartilage dose exist, but its effect on normal cartilage is weaker than that of mechanical agent.