UC Berkeley

The overall objective of this work is to provide a fundamental understanding of changes in bone structure–function relationship and failure mechanism with the presence of a certain degree of degradation in bone micro–architecture. Since it is of scientific interest to illustrate the mechanism by which aging, disease, and environmental factors, such as ionizing radiation, affect bone morphology and consequently alter the bone mechanical behaviors. More importantly, such insights would also potentially enhance the assessment of bone fracture risk in a clinical setting.

Combing a small animal model, where the mouse vertebral body morphological changes were introduced by the whole–body ionizing radiation, with high–resolution micro–computed tomography (micro–CT) based finite element (FE) analysis, we demonstrated how ionizing radiation altered the mouse vertebral body micro–architecture, structure-function relationship, as well as the failure mechanism. Our key results showed a reduction in trabecular mass fraction (by 12.8% on average, p = 0.0014) and a reduction in trabecular load fraction as the trabecular mass fraction was controlled (by an 8% decrease in the linear correlation slope, p = 0.0264). Related to this, nonlinear FE results showed that there were a reduction in the mouse vertebral stiffness (by 7.4%, p = 0.0054), a reduction in the vertebral strength (by 8.8%, p = 0.0002), and an significant offset for the linear correlation between them (p = 0.011) due to changes in the volume of failure tissue (p = 0.036). Our results suggested that, following ionizing radiation, the loss of trabecular load sharing could be more substantial than the loss of mass sharing since the trabecular structure–function relationship was altered. Moreover, the loss of vertebral strength could be more significant than the loss of vertebral stiffness, as the failure mechanism was altered. Such insights may apply to changes in vertebral micro–architecture induced by aging and diseases.

Using eight human vertebral body specimens with high–resolution micro–CT based nonlinear FE analysis, we established the damage law for the human vertebrae. The key results were that the human vertebral body damaged tissue accumulated exponentially as the axial compressive load applied (max p = 0.04, min R2 = 0.98), and the damaged tissue growth rate was nonlinearly correlated with the whole–bone strength (p < 0.001). With the aid of two simplified analytical models, our results implied that a weak human vertebra accumulated fracture tissue at a higher rate than a strong one due to a low number of vertical load paths.

In closure, this work presents the fundamental mechanisms by which changes in vertebrae morphology translate into alterations in the vertebrae structure–function relationship and failure mechanism, then ultimately into alterations in vertebrae strength and fracture risk.