The spatial distribution of fatigue microdamage accumulation in cortical bone and factors influencing fracture risk

by Travis L. Turnbull Human cortical bone, like many engineering materials, exhibits damage and fracture, due to cyclic loading and overloading, such as that experienced by the loadbearing long bones. Unlike engineering materials, bone possesses a unique ability to repair damage and reduce fracture risk. However, in cases such as athletes and military recruits, the rate and extent of damage formation can exceed the rate of repair, resulting in increased fracture risk until the damage is diagnosed and rest prescribed. In the elderly, and especially those afflicted with metabolic bone diseases such as osteoporosis, the rate of bone resorption exceeds the rate of formation of new bone, resulting in reduced cortical thickness, increased intracortical porosity and, thus, increased fracture risk. The overall objective of this project was to nondestructively investigate the spatial distribution of fatigue microdamage accumulation in cortical bone and factors that, upon interaction with microdamage, influence fracture susceptibility. Contrast-enhanced micro-CT detected increased microdamage in whole rat femora loaded in cyclic three-