SHORT AND LONG FATIGUE CRACK GROWTH IN BONE

该建议的总体假设是，骨骼脆性随年龄的增加受到骨组织组成中与年龄相关的变化的影响，这改变了超微结构和微观结构水平上的损伤累积过程。 我们特别感兴趣的是与年龄有关的抗循环荷载的影响，因为长期的损伤积累与重复加载。 本建议的目的是研究年轻和老年皮质骨中短和长疲劳裂纹扩展的动力学。 将检验两个假设：1）由于皮质骨在超微结构和显微结构水平上的年龄相关变化，皮质骨的疲劳裂纹萌生和短疲劳裂纹扩展阻力随年龄而降低; 2）由于皮质骨在超微结构和显微结构水平上的年龄相关变化，皮质骨的长疲劳裂纹扩展阻力随年龄而降低。 为了解决这些假设，将对来自年轻骨和老年骨的样本进行疲劳裂纹扩展试验。 将使用断裂力学方法确定每个年龄组的疲劳裂纹扩展动力学。 将评价两组骨之间的成分和形态差异，以及微裂纹形式的损伤累积程度。 将针对每个年龄组和年龄组之间检查特定成分、形态和损伤累积参数对疲劳裂纹扩展阻力的影响。 声发射将用于识别疲劳裂纹扩展过程中微观或超微结构损伤机制的差异。 我们的方法是开始通过检查疲劳裂纹生长的动力学在皮质骨的信念，结果也应该给我们洞察的行为，骨小梁在组织水平。 未来的目标是表征骨小梁中疲劳裂纹扩展的动力学。 这项研究的长期目标是降低老年人骨折的风险。 确定疲劳损伤过程中，最改变的老化，并最终，负责改变疲劳损伤过程的超微结构和微观结构组织的变化，可能会在开发有效的治疗策略，降低骨折风险发挥至关重要的作用。

The global hypothesis of this proposal is that the increase in skeletal fragility with age is affected by age-related changes in bone tissue composition which alters the damage accumulation process at the ultrastructural and microstructural levels. We are particularly interested in age-related effects on resistance to cyclic loading, because long-term damage accumulation is associated with repeated loading. The purpose of this proposal is to investigate the kinetics of short and long fatigue crack growth in younger and older cortical bone. Two hypotheses will be tested: 1) the fatigue crack initiation and short fatigue crack growth resistance of cortical bone is decreased with age due to age-related changes in cortical bone at the ultrastructural and microstructural levels; and 2) the long fatigue crack growth resistance of cortical bone is decreased with age due to age-related changes in cortical bone at the ultrastructural and microstructural levels. To address these hypotheses, fatigue crack propagation tests will be conducted on specimens from younger and older bone. The kinetics of fatigue crack growth will be determined for each age group using a fracture mechanics approach. Compositional and morphological differences between the two bone groups will be evaluated, as will the extent of damage accumulation in the form of microcracks. The effect of specific compostional, morphological, and damage accumulation parameters on fatigue crack growth resistance will be examined for each age group and between age groups. Acoustic emission will be used to identify differences in microstructural or ultrastructural damage mechanisms during fatigue crack growth. Our approach is to begin by examining the kinetics of fatigue crack growth in cortical bone with the belief that the results should also give us insight into the behavior of trabecular bone at the tissue level. A future objective is to characterize the kinetics of fatigue crack growth in trabecular bone. The long term goal of this research is to reduce the risk of fracture in the elderly. Identifying the fatigue damage processes that are most altered by aging, and, eventually, the ultrastructural and microstructural tissue alterations responsible for the altered fatigue damage processes, could potentially play a vital role in developing effective treatment strategies for reducing fracture risk.