Approximately 10% of the 250,000 hip fractures that occur each year in the United States and over 50% of the 500,000 age related spine fractures are thought to be spontaneous fractures associated with cyclic loading during the activities of daily living. Trabecular fatigue fractures are observed clinically as compressive stress fractures in the proximal femur, vertebrae, calcaneus and tibia. This study is aimed at predicting the compressive fatigue behavior of trabecular bone. We plan first to characterize the fatigue behavior of trabecular bone in compression by both mechanical testing and microscopy of fatigued specimens. Two hypothetical mechanisms for fatigue will be modelled: slow crack growth and creep. We hypothesize that slow crack growth will be the dominant mechanism of high cycle, low stress fatigue damage while creep will be the dominant mechanism of low cycle, high stress fatigue damage. The models we develop for these two mechanisms of fatigue should be capable of estimating the remaining fatigue life of trabecular bone of a given density and crack distribution at a given stress and temperature. Finally, the results of the models will be compared with the trabecular bone fatigue data to identify which mechanisms are responsible for fatigue. We expect these findings to improve our understanding of the relative importance of densitometric, morphological and loading factors in the etiology of spontaneous fractures of the hip and spine. Eventually, this improved understanding may lead to more successful approaches to the prevention of such age-related fractures in the elderly population most at risk.
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