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目的 :探讨应用口服Ⅱ型胶原诱导免疫耐受对创伤性骨性关节炎的影响。材料和方法 :应用切断大鼠膝关节内侧副韧带和内侧半月板的方法制备大鼠膝关节骨性关节炎的动物模型 ,以关节软骨组织学和组织化学染色以及T淋巴细胞转化实验为观察指标 ,观察口服Ⅱ型胶原对其病程发展的影响 ,并以经典的大鼠胶原引发关节炎症的类风湿性关节炎模型为对照。结果 :在创伤性骨性关节炎时 ,大鼠的T淋巴细胞增殖程度受到口服Ⅱ型胶原的抑制 ,从一个侧面反映针对Ⅱ型胶原的自家免疫可能参与了病变的发生和发展过程。但是 ,从病理改变来看 ,口服Ⅱ型胶原却不能抑制OA的发展 ,因此 ,创伤性骨性关节炎虽然在病变发生和发展过程中可能有免疫因素的参与 ,但是 ,相比RA ,这种参与不是主要的 ,OA的发病过程仍然是由于机械因素导致关节软骨破坏 ,在此基础上逐步发展起来的。口服Ⅱ胶原不能减轻OA的发病程度 ,因此不能应用口服Ⅱ型胶原的方法来治疗OA。
Objective: To investigate the effect of oral administration of type Ⅱ collagen on immune tolerance induced traumatic osteoarthritis. MATERIAL AND METHODS: Animal models of knee osteoarthritis in rats were established by cutting off the medial collateral ligament and the medial meniscus in the knee joint of rats. The articular cartilage histological and histochemical staining and T lymphocyte transformation were used as the observation indexes , Observed oral type Ⅱ collagen on the course of its development, and the classic rat collagen-induced arthritis rheumatoid arthritis model as a control. Results: T cell proliferation in rats was inhibited by oral type Ⅱ collagen during traumatic osteoarthritis. From one side, the autoimmunity against type Ⅱ collagen might be involved in the pathogenesis and progression of the disease. However, from the pathological changes, oral administration of type Ⅱ collagen can not inhibit the development of OA, therefore, although traumatic osteoarthritis may have immune factors in the pathogenesis and development of disease involved, but compared to RA, this Participation is not the main, OA is still due to the pathogenesis of mechanical factors leading to the destruction of articular cartilage, and gradually developed on this basis. Oral Ⅱ collagen can not reduce the incidence of OA, it can not be applied oral method of type Ⅱ collagen to treat OA.