Background     Spinal cord injury (SCI) causes rapid bone loss due to a reduction in bone formation at the basic cellular unit (BMU) level and increased rate of bone remodelling at the surface level, changes that result in microstructural deterioration and increased fracture risk.   There is lack of information concerning the effects of paralysis on bone microstructure. We hypothesised that SCI individuals have i) a severe trabecular bone microstructural deterioration ii) higher cortical porosity in comparison to controls.

Methods        We studied 31men with chronic complete SCI (age 43.5±14.2 yrs, duration of paralysis of 1.7-22 yrs), and 90 age and sex-matched healthy ambulatory controls, recruited at Austin Health, University of Melbourne.  Images of the non-dominant distal tibia were obtained using high-resolution quantitative computed tomography (HR-pQCT, Scanco, 82 micron isotropic voxel size). Manufacturer’s and StrAx algorithm (StraxCorp, Melbourne, Australia) were used to quantify trabecular and cortical compartments indices.

Results          Compared with controls, SCI cases had 2.2(95% CI 1.8 to 2.6), 1.7SD (1.31 to 2.13), 2.3SD (1.95 to 2.78) and 1.74 SD (1.32 to 2.15) higher porosity in the total cortex, compact cortex, inner and outer transitional zones and 1.7SD (-2.15 to -1.3) lower matrix mineralisation density. Total and cortical vBMD were reduced by 2.22 SD and 2.25 SD, respectively, all (p<0.01). Trabecular bone volume fraction was 1.8 SD (-2.21 to -1.38) lower in cases due to1.74 SD (-2.17 to -1.34) lower number of trabeculae and 2.3SD (1.81 to 2.78) higher separation. Trabecular bone surface and connectivity density were decreased by 0.9(0.5 to 1.3) and 1.4 SD (1.1 to 2.2), respectively (all p<0.01). 

Conclusion    We infer that spinal paralysis produces profound and rapid loss of cortical and trabecular bone suggesting antiresorptive therapy should be commenced at the time of presentation.