AGE-RELATED CHANGES IN DAMAGE ACCUMULATION IN CORTICAL AND SUBCHONDRAL BONE

软硬组织机械性能的有害变化 是关节炎和肌肉骨骼疾病的核心的核心 这些机械性能的变化是基质降解或损坏。 损伤定义为组织结构的永久性变化（例如裂纹） 这导致材料性能退化。超负荷，外伤，还有 重复的负荷导致关节软骨的退行性变化， 骨关节炎的潜在软骨下骨。据信 软骨下骨的硬化可能在软骨中起重要作用， 降解然而，增加骨形成的刺激不是 很好理解。基于先前对皮质骨的研究， 我们假设，损伤是重塑过程的刺激因素， 与骨关节炎相关的骨质变化代表了 修复反应改变损伤积累机制， 软骨下骨 在目前的研究中，我们建议测试是否损害 皮质骨和软骨下骨中的蓄积机制被改变， 年龄我们将分层次地解决这些问题， 在组织（mm尺度）和基质（微米尺度）结构上进行测试 程度.具体而言，我们建议实现以下目标： 1.确定组织水平的损伤累积机制是否存在 皮质骨随着年龄的增长而发生显着变化。 2.研制一种微机械测试系统， 量化皮质和皮质中基质水平损伤机制的改变， 软骨下骨 这项建议将提供机会，编制相关数据， 是研究疾病过程的基础， 微观层面的机械测试工具需要解决这些矩阵征 软骨下骨的变化。

Deleterious changes in the mechanical properties of soft and hard tissues are at the heart of arthritis and musculoskeletal disease. Central to these changes in mechanical properties is matrix degradation or damage. Damage is defined as a permanent change in tissue structure (e.g. crack) that results in material property degradation. Overload, trauma, and repetitive loading lead to degenerative changes in the joint cartilage and underlying subchondral bone in osteoarthritis. It is believed that sclerosis of the subchondral bone may play an important role in cartilage degradation. However, the stimulus for the increased bone formation is not well understood. Based on previous work in cortical bone which suggested that damage acts as a stimulus for the remodeling process, we postulate that the sclerotic changes associated with osteoarthritis represent a repair response to altered damage accumulation mechanisms in the subchondral bone. In the current study, we propose to test whether damage accumulation mechanisms in cortical and subchondral bone are altered with age. We will address these issues in a hierarchical manner by conducting tests at both the tissue (mm scale) and matrix (micron scale) structural levels. Specifically, we propose to accomplish the following: 1. To determine whether tissue-level damage accumulation mechanisms in cortical bone are significantly altered with age. 2. To develop a micro-mechanical testing system which is capable of quantifying alterations in matrix-level damage mechanisms in cortical and subchondral bone. This proposal will provide the opportunity to develop relevant data which is fundamental to studies of the disease process as well as to develop the micro-level mechanical testing tools needed to address these matrix levy changes in subchondral bone.