SHORT AND LONG FATIGUE CRACK GROWTH IN BONE

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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.