AN INVESTIGATION OF JOINT DEGENERATION

我们计划研究促进进行性软骨破坏的因素。 骨关节病动物模型的建立及其病理生理意义 在这种情况下。这些模型的有效性已经被证实。 根据之前的实验。对关节组织进行生化研究， 在新陈代谢和生物力学方面。自骨关节病的病理学以来 涉及关节软骨的破坏和关节的重塑 骨与关节相邻时，必须使用体内制剂，因为 骨关节病主要影响成熟、老年个体及其发育 涉及各种组织、器官培养之间的相互关系 使用胎儿材料是不合适的。这项研究，涉及 协同生化、生物力学、解剖学、病理学和 对这些模型的临床分析，应该提供更好的理解 骨关节病，希望有一天这个过程可以停止和 颠倒了。我们建议使用保护不力的-防止重复 冲动地加载生理上合理的量来创造 兔右膝骨关节病。左膝被用作 控制力。我们想要确定关节的门槛水平 软骨是机械性损伤的，其性质是负荷最大 有害的，和机械因素导致的进展 关节恶化。我们将首先预测最有害的力量 通过有限元分析进行分析并验证假设 试验性的。我们还将利用由一个 软骨下骨覆盖在种植塞上的局部区域 绵羊膝关节骨僵硬与骨质疏松症关系的研究 进行性软骨退化。有限元分析表明， 这样的重塑确实增加了深层的应力。 覆盖着软骨。我们计划在长期和短期动物身上研究这一点。 勾勒出变化的进程。实验结果与 分析理解的扩展应该有助于确定重要的 导致骨关节病关节恶化的力学参数。

We plan to study the factors promoting progressive cartilage destruction in animal models of osteoarthrosis in order to understand the pathophysiology of this condition. The effectiveness of these models has been established by previous experimentation. The joint tissues are studied biochemically, metabolically, and biomechanically. Since the pathology of osteoarthrosis involves destruction of the articular cartilage and the remodeling of the bone adjacent to the joints, we must use in vivo preparations because osteoarthrosis mainly affects mature, older individuals and its development involves an inter-relationship between a variety of tissues, organ cultures utilizing fetal materials are inappropriate. This study, involving collaborative biochemical, biomechanical, anatomical, pathological, and clinical analyses of these models, should provide a better understanding of osteoarthrosis with the hope that the process can some day be halted and reversed. We propose utilizing poorly-protected-against repetitive impulsive loading of a physiologically reasonable amount to create osteoarthrosis in the right knees of rabbits. The left knee is used as a control. We want to establish the threshold levels at which articular cartilage is mechanically injured, the nature of the load which is most deleterious, and the mechanical factors responsible for progression of the joint deterioration. We will first predict the most deleterious force analytically by finite element analysis and test that hypothesis experimentally. We will also utilize stiffening, caused by remodeling of a local area of subchondral bone overlying an implanted plug just under the knee joint of a sheep to study the relationship of bone stiffening and progressive cartilage deterioration. Finite element analysis reveals that such remodeling achieved does increase the stress in the deep layers of the overlying cartilage. We plan to study this in long- and short-term animals to delineate the progression of changes. Experimental results coupled with an expansion of analytical understanding should help define the important mechanical parameters causing joint deterioration in osteoarthrosis.