UC Berkeley

Knowledge of the biomechanical behavior of the human vertebra is fundamental to improving clinical assessment of vertebral fracture risk and diagnosis of osteoporosis. In this context, the focus of this dissertation is to enhance the current understanding of the biomechanical mechanisms of vertebral strength and the etiology of vertebral fractures.

Combining the latest advances in micro-computed tomography, high-resolution finite element modeling, and biomechanical testing, we found that variation in vertebral strength across individuals was primarily due to the variation in the bone volume fraction of vertical trabeculae. This is because the major load paths were parallel columns of vertically-oriented bone. A new microarchitecture parameter, the vertical tissue fraction, was developed to reflect these findings. Whereas the role of traditional microarchitecture parameters in vertebral strength was mediated by bone mass and density, the role of this new parameter was independent of bone mass and density. From a biomechanics perspective, the vertical tissue fraction thus represents a mechanistic aspect of trabecular microarchitecture with the most potential for microarchitecture analysis of bone strength.

The work presented in this dissertation has also provided substantial insight into the etiology of vertebral fractures. We found that due to the variation in failure mechanisms between porous and dense vertebrae, the amount of tissue yielding that occurred during a mechanical overload of the vertebra was up to 5 times lower in porous vertebrae than in dense vertebrae. This illustrates a new aspect of vertebral fragility: as bone density decreases with aging and disease, not only is the vertebra becoming weaker, but it is also becoming much less structurally robust. Unique evidence was also obtained to help explain why the endplates are frequently involved in osteoporotic vertebral fractures. A detailed comparison of the biomechanical behavior of the endplates, cortical shell, and trabecular bone revealed that the endplates are at the highest risk of failure due to the development of high tensile strains, and that the development of such high tensile strains is directly associated with the material behavior of the intervertebral disc.

In closure, this dissertation answers fundamental questions regarding the role of trabecular microarchitecture in explaining the variation in vertebral strength across individuals, and provides new insight into the etiology of age-related vertebral fractures. This work also outlines areas of research to further advance our understanding of vertebral fracture etiology and describes a systematic approach for identifying architectural determinants of bone strength that could be used at other anatomic sites.