兔实验性膝骨性关节炎的组织病理学及发病机理

Histo-Pathological Basis of Osteoarthrities:Observation and Study of Etiological Mechanism on Rabbit's Experimental Model

目的 :探讨骨性关节炎发生的病理学基础。方法 :40只健康雄性家兔随机分为对照组和模型组。模型组用Hulth法复制出实验性膝骨性关节炎模型。对照组不作任何处理。 1月后处死家兔并切取家兔股骨内髁关节软骨作光镜及透射电镜观察 ,光镜所见依据Mankin’s评分标准评分 ,测定血清中红细胞超氧化物歧化酶 (SOD)活性并作统计学处理。结果 :模型组家兔膝关节滑膜均存在不同程度增生、肥厚、水肿 ,光镜及电镜下见模型组关节软骨呈明显退行性变 ,Mankin’s评分结果模型组得分显著高于对照组 (P <0 .0 5 ) ,模型组SOD活性显著低于对照组 (P <0 .0 5 )。结论 :滑膜组织的炎症、骨内压的增高以及自由基的改变是导致骨性关节炎发生的病理学基础 。

Objective: In order to study the histo pathological basis of OA.Methods:Forty rabbits were randomly divided into two groups:the compared group and the OA model group.The OA model group were duplicated by Hulth's technique.All the rabbits were fed under the same conditions.Excised the condylar cartilage of femur after one month for the observation by photo microscope and transmissive electron microscope.Each case was recorded according to Mankin's index.Detected the activity of the superoxide dismutase(SOD).Results:The knee joint's synovium of the OA model group were found adhesion,swelling and overgrowth.Obviously degenerative changes.were found in the OA model group by microscope.The OA model group's scores were significantly higher than the compared group according to Mankin's index(P<0.05).The activity of SOD in the OA model group were significantly decreased than the compared group(P<0.05).Conclusion:The inflammation of synovium,the intra articular pressure and the change of SOD activity were the histo pathological basis of OA occur.It was important to inhibit the histo pathological changes in OA prevention and treatment.