Vertebral strength, as estimated by finite element analysis of computed tomography (CT) scans, has not yet been compared against areal bone mineral density (BMD) by dual energy x-ray absorptiometry (DXA) for prospectively assessing the risk of new clinical vertebral fractures. To do so, we conducted a case-cohort analysis of 306 men aged 65 yrs and older, which included 63 men who developed new clinically-identified vertebral fractures and 243 men who did not, all observed over an average of 6.5 years. Non-linear finite element analysis was performed on the baseline CT scans, blinded to fracture status, to estimate L1 vertebral compressive strength and a load-to-strength ratio. Volumetric BMD by quantitative CT and areal BMD by DXA were also evaluated. We found that, for the risk of new clinical vertebral fracture, the age-adjusted hazard ratio per standard deviation change for areal BMD (3.2; 95% CI: 2.0–5.2) was significantly lower (p<0.005) than for strength (7.2; 3.6–14.1), numerically lower than for volumetric BMD (5.7; 3.1–10.3), and similar for the load-to-strength ratio (3.0; 2.1–4.3). After also adjusting for race, BMI, clinical center, and areal BMD, all these hazard ratios remained highly statistically significant, particularly those for strength (8.5; 3.6–20.1) and volumetric BMD (9.4; 4.1–21.6). The area-under-the-curve for areal BMD (AUC=0.76) was significantly lower than for strength (AUC=0.83, p=0.02), volumetric BMD (AUC=0.82, p=0.05), and the load-to-strength ratio (AUC=0.82, p=0.05). We conclude that, compared to areal BMD by DXA, vertebral compressive strength and volumetric BMD consistently improved vertebral fracture risk assessment in this cohort of elderly men.

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.

Vertebral strength, a key etiologic factor of osteoporotic fracture, may be affected by the relative amount of vertically oriented trabeculae. To better understand this issue, we performed experimental compression testing, high-resolution micro–computed tomography (µCT), and micro–finite-element analysis on 16 elderly human thoracic ninth (T9) whole vertebral bodies (ages 77.5 ± 10.1 years). Individual trabeculae segmentation of the µCT images was used to classify the trabeculae by their orientation. We found that the bone volume fraction (BV/TV) of just the vertical trabeculae accounted for substantially more of the observed variation in measured vertebral strength than did the bone volume fraction of all trabeculae (r2 = 0.83 versus 0.59, p < .005). The bone volume fraction of the oblique or horizontal trabeculae was not associated with vertebral strength. Finite-element analysis indicated that removal of the cortical shell did not appreciably alter these trends; it also revealed that the major load paths occur through parallel columns of vertically oriented bone. Taken together, these findings suggest that variation in vertebral strength across individuals is due primarily to variations in the bone volume fraction of vertical trabeculae. The vertical tissue fraction, a new bone quality parameter that we introduced to reflect these findings, was both a significant predictor of vertebral strength alone (r2 = 0.81) and after accounting for variations in total bone volume fraction in multiple regression (total R2 = 0.93). We conclude that the vertical tissue fraction is a potentially powerful microarchitectural determinant of vertebral strength. © 2011 American Society for Bone and Mineral Research.

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The mechanisms of age-related vertebral fragility remain unclear, but may be related to the degree of “structural redundancy” of the vertebra, that is, its ability to safely redistribute stress internally after local trabecular failure from an isolated mechanical overload. To better understand this issue, we performed biomechanical testing and nonlinear micro-CT-based finite element analysis on 12 elderly human thoracic ninth vertebral bodies (ages 76.9 ± 10.8 years). After experimentally overloading the vertebrae to measure strength, we used the nonlinear finite element analysis to estimate the amount of failed tissue and understand failure mechanisms. We found that the amount of failed tissue per unit bone mass decreased with decreasing bone volume fraction (r2 = 0.66, p < 0.01). Thus, for the weak vertebrae with low bone volume fraction, overall failure of the vertebra occurred after failure of just a tiny proportion of the bone tissue (< 5%). This small proportion of failed tissue had two sources: the existence of fewer vertically oriented load paths to which load could be redistributed from failed trabeculae; and the vulnerability of the trabeculae in these few load paths to undergo bending-type failure mechanisms, which further weaken the bone. Taken together, these characteristics suggest that diminished structural redundancy may be an important aspect of age-related vertebral fragility: vertebrae with low bone volume fraction are highly susceptible to collapse since so few trabeculae are available for load redistribution if the external loads cause any trabeculae to fail.