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的年龄相关变化的影响，骨组织组成的变化改变了超微结构和微观结构水平上的损伤积累过程。我们特别感兴趣的是年龄对循环加载阻力的影响，因为长期损伤积累与反复加载有关。本研究的目的是研究年轻和年老皮质骨的长、短疲劳裂纹扩展动力学。本文将检验两种假设：1)由于骨皮质在超微结构和显微结构水平上发生了与年龄相关的变化，骨皮质的疲劳裂纹起裂和抗短疲劳裂纹生长能力随年龄的增长而降低；2)随着年龄的增长，骨皮质的抗长疲劳裂纹扩展能力下降，这是由于骨皮质在超微结构和显微结构水平上发生了衰老相关的变化。为了解决这些假设，疲劳裂纹扩展试验将从年轻的和老骨头的标本进行。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。将评估两组骨之间的成分和形态差异，以及以微裂纹形式累积的损伤程度。具体的成分、形态和损伤积累参数对疲劳裂纹扩展阻力的影响将在每个年龄组和年龄组之间进行检查。声发射将用于识别疲劳裂纹扩展过程中微结构或超微结构损伤机制的差异。我们的方法是从检查皮质骨疲劳裂纹生长的动力学开始，相信结果也应该让我们深入了解小梁骨在组织水平上的行为。未来的目标是表征小梁骨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。识别受老化影响最大的疲劳损伤过程，以及最终确定导致疲劳损伤过程改变的超微结构和显微组织改变，可能在制定有效的治疗策略以降低断裂风险方面发挥重要作用。

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.