Age-related bone fractures are a devastating public health problem in the United States and other nations. Approximately 700,000 vertebral fractures and 250,000 hip fractures occur annually in the United States at a cost of over $10 billion. While the majority of osteoporotic fractures are caused by falls, it has been estimated that almost 10% of these hip fractures and over 50% of these age-related vertebral body fractures are spontaneous fractures that occur without initial trauma but are associated with cyclic (fatigue) loading during the activities of daily living. These spontaneous fractures occur most frequently in trabecular bone sites, such as the proximal femur and the vertebral body. The limited published data on the fatigue behavior of trabecular bone suggest that both creep and slow crack growth contribute to fatigue failure. Therefore, the objective of this study was to thoroughly characterize the creep behavior of trabecular bone and to determine the phase (collagen or hydroxyapatite) responsible for creep, in the belief that this knowledge would lead to a greater understanding of the etiology of spontaneous age-related fractures of the hip and spine.

Creep tests were conducted on specimens of trabecular bone at a range of applied normalized stresses and temperatures using a custom-designed creep apparatus. Additional creep tests were conducted on specimens of demineralized cortical bone at a range of applied normalized stresses and temperatures to determine whether collagen was the phase responsible for the creep behavior of bone. The creep behaviors of trabecular and demineralized cortical bone were similar to the published creep behaviors of cortical bone and other engineering materials. Power-law relationships were developed between both steady-state creep rate and time-to-failure as functions of the applied normalized stress. The creep activation energies of trabecular, cortical, and demineralized cortical bone were within a narrow range, as were their creep exponents, together providing strong evidence that collagen is the phase responsible for the creep behavior of bone.

Clinically, the data indicate that the strength of trabecular bone can be reduced substantially if relatively large loads are applied for several hours. Therefore, it is likely that creep plays a role in the etiology of spontaneous fractures. The monotonic and creep properties of demineralized bone (i.e. bone collagen) and hydroxyapatite, the two primary constituents of bone, are sufficient to predict the creep behavior of trabecular bone when its cellular-solid architecture is taken into account. The mathematical model used to make these predictions may be helpful in developing strategies to prevent spontaneous fractures from occurring, by illustrating how bone constituents interact and influence whole-bone behavior during extended periods of loading.