AN INVESTIGATION OF JOINT DEGENERATION

我们计划研究促进进行性软骨破坏的因素， 骨关节病的动物模型，以了解病理生理学 这种情况。 这些模型的有效性已经建立 以前的实验。 对关节组织进行生物化学研究， 代谢和生物力学。 由于骨关节病的病理 包括关节软骨的破坏和 骨关节附近，我们必须使用体内制剂，因为 骨关节病主要影响成熟，老年人及其发展 涉及到各种组织、器官培养、 使用胎儿材料是不合适的 这项研究涉及 协同生物化学、生物力学、解剖学、病理学和 这些模型的临床分析，应该提供更好的理解， 希望有一天这个过程可以停止， 颠倒了 我们建议利用缺乏保护的重复 生理上合理量的脉冲负荷， 兔右膝骨关节病。 左膝被用作 控制 我们想建立关节炎的阈值水平 软骨是机械损伤，负荷的性质，这是最 有害的，和机械因素负责的进展， 关节退化 我们将首先预测最有害的力量 通过有限元分析和测试假设 实验性的 我们还将利用硬化，造成重塑的一个 局部区域的软骨下骨覆盖着植入的塞子， 研究骨硬化与骨密度的关系， 进行性软骨退化 有限元分析表明， 这种重塑的实现确实增加了深层的应力， 覆盖软骨。 我们计划在长期和短期的动物中研究这一点 来描述变化的进程 实验结果与 分析理解的扩展应有助于确定重要的 导致骨关节病关节退化的机械参数。

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.