The objective of this study was to characterize the fatigue behavior and damage mechanism of trabecular bone in compression using both mechanical testing and modeling.

First, we studied the fatigue behavior of bovine trabecular bone using cubic specimens. The fatigue was characterized by decreased secant modulus, increased nonlinearity, and increased hysteresis. The number of cycles to failure was strongly correlated with the initial global maximum strain. Microscopic examination of the failure zones revealed two failure modes:​ a transverse brittle-like fracture and a buckling-like failure in the trabeculae. Modulus degradation with number of cycles showed that for low cycle fatigue, there was a continuous drop in modulus. In contrast, for high-cycle fatigue, there was an initial increase in modulus, followed by a rapid drop in modulus. This initial increase in modulus was an experimental artifact associated with crushing of the specimen ends.

To eliminate the end-crushing artifact associated with cubic specimens, we developed a technique to test waisted cylindrical specimens in fatigue. For the waisted cylindrical specimens, there was no initial increase in modulus for high-cycle fatigue and most fatigued specimens showed an oblique failure within the gage length. Moreover, the number of cycles to failure was strongly correlated with the normalized stress range Ao/E.

Next, a finite element model of trabecular bone was developed to study damage accumulation during cyclic loading. To study crack propagation, the trabecular bone was modeled as a 2-D hexagonal honeycomb-like structure. Initial microcracks were assumed to exist within the oblique trabeculae and to grow according to the Paris law until fracture occurred. Between loading cycles, fractured trabeculae were removed from the l'inile element mesh, and force and moment distributions were calculated for the next cycle. To study creep failure, a single cell model was applied to trabecular bone. The results from these models suggest that the primary failure mechanism for high-cycle fatigue of cubic trabecular bone specimens is crack propagation, while the primary failure mechanism for low-cycle fatigue of cubic trabecular bone specimens is creep deformation. For waisted trabecular bone specimens, creep dominates the damage mechanism. Other mechanisms, such as crack propagation, may play a role at very low stress level.