The biomechanical role of the vertebral cortical shell remains poorly understood. Using highresolution finite element modeling of a cohort of elderly vertebrae, we found that the biomechanical role of the shell can be substantial and that the load sharing between the cortical and trabecular bone is complex. As a result, a more integrative measure of the trabecular and cortical bone should improve noninvasive assessment of fracture risk and treatments.Introduction: A fundamental but poorly understood issue in the assessment of both osteoporotic vertebral fracture risk and effects of treatment is the role of the trabecular bone and cortical shell in the load-carrying capacity of the vertebral body. Materials and Methods: High-resolution CT-based finite element models were developed for 13 elderly human vertebrae (age range: 54-87 years; 74.6 ± 9.4 years), and parameter studies-with and without endplates-were performed to determine the role of the shell versus trabecular bone and the effect of model assumptions. Results: Across vertebrae, whereas the average thickness of the cortical shell was only 0.38 ± 0.06 mm, the shell mass fraction (shell mass/total bone mass)-not including the endplates-ranged from 0.21 to 0.39. The maximum load fraction taken by the shell varied from 0.38 to 0.54 across vertebrae and occurred at the narrowest section. The maximum load fraction taken by the trabecular bone varied from 0.76 to 0.89 across vertebrae and occurred near the endplates. Neither the maximum shell load fraction nor the maximum trabecular load fraction depended on any of the densitometric or morphologic properties of the vertebra, indicating the complex nature of the load sharing mechanism. The variation of the shell load-carrying capacity across vertebrae was significantly altered by the removal of endplates, although these models captured the overall trend within a vertebra. Conclusions:The biomechanical role of the thin cortical shell in the vertebral body can be substantial, being about 45% at the midtransverse section but as low as 15% close to the endplates. As a result of the complexity of load sharing, sampling of only midsection trabecular bone as a strength surrogate misses important biomechanical information. A more integrative approach that combines the structural role of both cortical and trabecular bone should improve noninvasive assessment of vertebral bone strength in vivo.
The role of trabecular microarchitecture in whole-vertebral biomechanical behavior remains unclear, and its influence may be obscured by such factors as overall bone mass, bone geometry, and the presence of the cortical shell. To address this issue, 22 human T 9 vertebral bodies (11 female; 11 male; age range: 53-97 yr, 81.5 ± 9.6 yr) were scanned with mCT and analyzed for measures of trabecular microarchitecture, BMC, cross-sectional area, and cortical thickness. Sixteen of the vertebrae were biomechanically tested to measure compressive strength. To estimate vertebral compressive stiffness with and without the cortical shell for all 22 vertebrae, two high-resolution finite element models per specimen-one intact model and one with the shell removed-were created from the mCT scans and virtually compressed. Results indicated that BMC and the structural model index (SMI) were the individual parameters most highly associated with strength (R 2 = 0.57 each). Adding microarchitecture variables to BMC in a stepwise multiple regression model improved this association (R 2 = 0.85). However, the microarchitecture variables in that regression model (degree of anisotropy, bone volume fraction) differed from those when BMC was not included in the model (SMI, mean trabecular thickness), and the association was slightly weaker for the latter (R 2 = 0.76). The finite element results indicated that the physical presence of the cortical shell did not alter the relationships between microarchitecture and vertebral stiffness. We conclude that trabecular microarchitecture is associated with whole-vertebral biomechanical behavior and that the role of microarchitecture is mediated by BMC but not by the cortical shell.
Knowledge of the location of initial regions of failure within the vertebra -cortical shell, cortical endplates vs. trabecular bone, as well as anatomic location -may lead to improved understanding of the mechanisms of aging, disease and treatment. The overall objective of this study was to identify the location of the bone tissue at highest risk of initial failure within the vertebral body when subjected to compressive loading. Toward this end, micro-CT based 60-micron voxel-sized, linearly elastic, finite element models of a cohort of thirteen elderly (age range: 54-87 years, 75 ± 9 years) female whole vertebrae without posterior elements were virtually loaded in compression through a simulated disc. All bone tissue within each vertebra having either the maximum or minimum principal strain beyond its 90 th percentile was defined as the tissue at highest risk of initial failure within that particular vertebral body. Our results showed that such high-risk tissue first occurred in the trabecular bone and that the largest proportion of the high-risk tissue also occurred in the trabecular bone. The amount of high-risk tissue was significantly greater in and adjacent to the cortical endplates than in the mid-transverse region. The amount of high-risk tissue in the cortical endplates was comparable to or greater than that in the cortical shell regardless of the assumed Poisson's ratio of the simulated disc. Our results provide new insight into the micromechanics of failure of trabecular and cortical bone within the human vertebra, and taken together, suggest that during strenuous compressive loading of the vertebra, the tissue near and including the endplates is at the highest risk of initial failure.
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