, Volume 24, Issue 9, pp 2461-2469

Bone mineral loss at the proximal femur in acute spinal cord injury

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Abstract

Summary

This study used quantitative computed tomography to assess changes in bone mineral at the proximal femur after acute spinal cord injury (SCI). Individuals with acute SCI experienced a marked loss of bone mineral from a combination of trabecular and endocortical resorption. Targeted therapeutic interventions are thus warranted in this population.

Introduction

SCI is associated with a rapid loss of bone mineral and an increased rate of fragility fracture. Some 10 to 20 % of these fractures occur at the proximal femur. The purpose of this study was to quantify changes to bone mineral, geometry, and measures of strength at the proximal femur in acute SCI.

Methods

Quantitative computed tomography analysis was performed on 13 subjects with acute SCI at serial time points separated by a mean of 3.5 months (range, 2.6–4.8 months). Changes in bone mineral content (BMC) and volumetric bone mineral density (vBMD) were quantified for integral, trabecular, and cortical bone at the femoral neck, trochanteric, and total proximal femur regions. Changes in bone volumes, cross-sectional areas, and surrogate measures of compressive and bending strength were also determined.

Results

During the acute period of SCI, subjects experienced a 2.7–3.3 %/month reduction in integral BMC (p < 0.001) and a 2.5–3.1 %/month reduction in integral vBMD (p < 0.001). Trabecular BMC decreased by 3.1–4.7 %/month (p < 0.001) and trabecular vBMD by 2.8–4.4 %/month (p < 0.001). A 3.9–4.0 %/month reduction was observed for cortical BMC (p < 0.001), while the reduction in cortical vBMD was noticeably lower (0.8–1.0 %/month; p ≤ 0.01). Changes in bone volume and cross-sectional area suggested that cortical bone loss occurred primarily through endosteal resorption. Declines in bone mineral were associated with a 4.9–5.9 %/month reduction in surrogate measures of strength.

Conclusions

These data highlight the need for therapeutic interventions in this population that target both trabecular and endocortical bone mineral preservation.