Abstract

Bone damage occurs as a result of repetitive loading in-vivo [1] and has been implicated as a contributing factor governing bone fragility in diseases such as osteoporosis and in repetitive loading injuries such as stress fractures. In response to damage or microcracks in-vivo, healthy bone will self-repair by removing the damaged bone and replacing it with newly formed bone [2]. However, when the rate of damage accumulation is greater than the rate of repair in healthy bone, a fracture may result.

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