High bone density masks architectural deficiencies in an individual with spinal cord injury.

Context Spinal cord injury (SCI) causes a decline of bone mineral density (BMD) in the paralyzed extremities via the gradual degradation and resorption of trabecular elements. Clinical tools that report BMD may not offer insight into trabecular architecture flaws that could affect bone's ability to withstand loading. We present a case of a woman with a 30-year history of SCI and abnormally high distal femur BMD. Findings Peripheral quantitative-computed tomography-based BMD for this subject was ∼20% higher than previously published non-SCI values. Computed tomography (CT) revealed evidence of sclerotic bone deposition in the trabecular envelope, most likely due to glucocorticoid-induced osteonecrosis. Volumetric topologic analysis of trabecular architecture indicated that the majority of the bone mineral was organized into thick, plate-like structures rather than a multi-branched trabecular network. Visual analysis of the CT stack confirmed that the sclerotic bone regions were continuous with the cortex at only a handful of points. Conclusions Conventional clinical BMD analysis could have led to erroneous assumptions about this subject's bone quality. CT-based analysis revealed that this subject's high BMD masked underlying architectural flaws. For patients who received prolonged glucocorticoid therapy, excessively high BMD should be viewed with caution. The ability of this subject's bone to resist fracture is, in our view, extremely suspect. A better understanding of the mechanical competency of this very dense, but architecturally flawed bone would be desirable before this subject engaged in activities that load the limbs.