Abstract
Osteoporosis heightens vertebral fragility owing to the biomechanical effects of diminished bone structure and composition. These biomechanical effects are only partially explained by loss in bone mass, so additional factors that are independent of bone mass are also thought to play an important role in vertebral fragility. Recent advances in imaging equipment, imaging-processing methods, and computational capacity allow researchers to quantify trabecular architecture in the vertebra at the level of the individual trabecular elements and to derive biomechanics-based measures of architecture that are independent of bone mass and density. These advances have shed light on the role of architecture in vertebral fragility. In addition to the adverse biomechanical consequences associated with trabecular thinning and loss of connectivity, a reduction in the number of vertical trabecular plates appears to be particularly harmful to vertebral strength. In the clinic, detailed architecture analysis is primarily applied to peripheral sites such as the distal radius and tibia. Analysis of trabecular architecture at these peripheral sites has shown mixed results for discriminating between patients with and without a vertebral fracture independent of bone mass, but has the potential to provide unique insight into the effects of therapeutic treatments. Overall, it does appear that trabecular architecture has an independent role on vertebral strength. Additional research is required to determine how and where architecture should be measured in vivo and whether assessment of trabecular architecture in a clinical setting improves prospective fracture risk assessment for the vertebra.
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