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Browsing by Subject "suppressed bone turnover"
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Item A computational assessment of the independent contribution of changes in canine trabecular bone volume fraction and microarchitecture to increased bone strength with suppression of bone turnover(2007-05) Eswaran, Senthil K; Allen, Matthew R.; Burr, David B.; Keaveny, Tony MThis study addressed the effects of changes in trabecular microarchitecture induced by suppressed bone turnover—including changes to the remodeling space—on the trabecular bone strength–volume fraction characteristics independent of changes in tissue material properties. Twenty female beagle dogs, aged 1–2 years, were treated daily with either oral saline (n=10 control) or high doses of oral risedronate (0.5 mg/kg/day, n=10 suppressed) for a period of 1 year, the latter designed (and confirmed) to substantially suppress bone turnover. High-resolution micro-CT-based finite element models (18-μm voxel size) of canine trabecular bone cores (n=2 per vertebral body) extracted from the T-10 vertebrae were analyzed in both compressive and torsional loading cases. The same tissue-level material properties were used in all models, thus providing measures of tissue-normalized strength due only to changes in the microarchitecture. Suppressed bone turnover resulted in more plate-like architecture with a thicker and more dense trabecular structure, but the relationship between the microarchitectural parameters and volume fraction was unaltered (p>0.05). Though the suppressed group had a greater tissue-normalized strength as compared to the control group (p<0.001) for both compressive and torsional loading, the relationship between tissue-normalized strength and volume fraction was not significantly altered for compression (p>0.13) or torsion (p>0.09). In this high-density, non-osteoporotic animal model, the increases in tissue-normalized strength seen with suppression of bone turnover were entirely commensurate with increases in bone volume fraction and thus, no evidence of microarchitecture-related or “stress-riser” effects which may disproportionately affect strength were found.Item Effects of suppression of bone turnover on cortical and trabecular load sharing in the canine vertebral body(2009-03) Eswaran, Senthil K; Bevill, Grant; Nagarathnam, Prem; Allen, Matthew R.; Burr, David B.; Keaveny, Tony MThe relative biomechanical effects of antiresorptive treatment on cortical thickness vs. trabecular bone microarchitecture in the spine are not well understood. To address this, T-10 vertebral bodies were analyzed from skeletally mature female beagle dogs that had been treated with oral saline (n=8 control) or a high dose of oral risedronate (0.5 mg/kg/day, n=9 RIS-suppressed) for 1 year. Two linearly elastic finite element models (36-μm voxel size) were generated for each vertebral body—a whole-vertebra model and a trabecular-compartment model—and subjected to uniform compressive loading. Tissue-level material properties were kept constant to isolate the effects of changes in microstructure alone. Suppression of bone turnover resulted in increased stiffness of the whole vertebra (20.9%, p=0.02) and the trabecular compartment (26.0%, p=0.01), while the computed stiffness of the cortical shell (difference between whole-vertebra and trabecular-compartment stiffnesses, 11.7%, p=0.15) was statistically unaltered. Regression analyses indicated subtle but significant changes in the relative structural roles of the cortical shell and the trabecular compartment. Despite higher average cortical shell thickness in RIS-suppressed vertebrae (23.1%, p=0.002), the maximum load taken by the shell for a given value of shell mass fraction was lower (p=0.005) for the RIS-suppressed group. Taken together, our results suggest that—in this canine model—the overall changes in the compressive stiffness of the vertebral body due to suppression of bone turnover were attributable more to the changes in the trabecular compartment than in the cortical shell. Such biomechanical studies provide an unique insight into higher-scale effects such as the biomechanical responses of the whole vertebra.