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Bone mineral and stiffness loss at the distal femur and proximal tibia in acute spinal cord injury

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Abstract

Summary

Computed tomography and finite element modeling were used to assess bone mineral and stiffness loss at the knee following acute spinal cord injury (SCI). Marked bone mineral loss was observed from a combination of trabecular and endocortical resorption. Reductions in stiffness were 2-fold greater than reductions in integral bone mineral.

Introduction

SCI is associated with a rapid loss of bone mineral and an increased rate of fragility fracture. The large majority of these fractures occur around regions of the knee. Our purpose was to quantify changes to bone mineral, geometry, strength indices, and stiffness at the distal femur and proximal tibia in acute SCI.

Methods

Quantitative computed tomography (QCT) and patient-specific finite element analysis were 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 epiphyseal, metaphyseal, and diaphyseal regions of the distal femur and proximal tibia. Changes in bone volumes, cross-sectional areas, strength indices and stiffness were also determined.

Results

Bone mineral loss was similar in magnitude at the distal femur and proximal tibia. Reductions were most pronounced at epiphyseal regions, ranging from 3.0 % to 3.6 % per month for integral BMC (p < 0.001) and from 2.8 % to 3.4 % per month (p < 0.001) for integral vBMC. Trabecular BMC decreased by 3.1–4.4 %/month (p < 0.001) and trabecular vBMD by 2.7–4.7 %/month (p < 0.001). A 3.8–5.4 %/month reduction was observed for cortical BMC (p < 0.001); the reduction in cortical vBMD was noticeably lower (0.6–0.8 %/month; p ≤ 0.01). The cortical bone loss occurred primarily through endosteal resorption, and reductions in strength indices and stiffness were some 2-fold greater than reductions in integral bone mineral.

Conclusions

These findings highlight the need for therapeutic interventions targeting both trabecular and endocortical bone mineral preservation in acute SCI.

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Acknowledgments

The authors thank Danielle Barkema, M.S., Meghan Lipowski, and Narina Simonian for their help with subject recruitment and data collection. This project was funded in part by an investigator-initiated research grant from Merck & Co, Inc. to TJS and KLT.

Conflicts of interest

None.

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Authors and Affiliations

  1. Department of Kinesiology and Nutrition, University of Illinois at Chicago, 1919 W. Taylor Street, 650 AHSB, M/C 517, Chicago, IL, 60621, USA

    W. B. Edwards & K. L. Troy

  2. Department of Physical Medicine and Rehabilitation Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA

    T. J. Schnitzer

  3. Department of Bioengineering, University of Illinois at Chicago, Chicago, IL, 60612, USA

    K. L. Troy

Authors
  1. W. B. Edwards
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  2. T. J. Schnitzer
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  3. K. L. Troy
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Correspondence to W. B. Edwards.

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Edwards, W.B., Schnitzer, T.J. & Troy, K.L. Bone mineral and stiffness loss at the distal femur and proximal tibia in acute spinal cord injury. Osteoporos Int 25, 1005–1015 (2014). https://doi.org/10.1007/s00198-013-2557-5

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