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Heterogeneity in microstructural deterioration following spinal cord injury. | LitMetric

Heterogeneity in microstructural deterioration following spinal cord injury.

Bone

Depts of Medicine and Endocrinology, Austin Health, The University of Melbourne, Melbourne, Australia; Dept of Endocrinology, Austin Health, The University of Melbourne, Melbourne, Australia.

Published: January 2021

AI Article Synopsis

  • The study examines how spinal cord injuries (tetraplegia and paraplegia) affect bone density and structure in specific bones (tibia, fibula, and radius) among 31 men compared to healthy controls.
  • Findings indicate significant reductions in volumetric bone mineral density (vBMD) in the tibia and fibula for both groups, with those with tetraplegia showing the most severe deficits.
  • The research suggests that weight-bearing bones (like the tibia) experience greater deterioration due to decreased strain after injury, while bone loss does not significantly differ in the radius despite mobility, indicating selective vulnerability based on bone location and loading conditions.

Article Abstract

Background: Modelling and remodelling adapt bone morphology to accommodate strains commonly encountered during loading. If strains exceed a threshold threatening fracture, modelling-based bone formation increases bone volume reducing these strains. If unloading reduces strains below a threshold that inhibits resorption, increased remodelling-based bone resorption reduces bone volume restoring strains, but at the price of compromised bone volume and microstructure. As weight-bearing regions are adapted to greater strains, we hypothesized that microstructural deterioration will be more severe than at regions commonly adapted to low strains following spinal cord injury.

Methods: We quantified distal tibial, fibula and radius volumetric bone mineral density (vBMD) using high-resolution peripheral quantitative computed tomography in 31 men, mean age 43.5 years (range 23.5-75.0), 12 with tetraplegia and 19 with paraplegia of 0.7 to 18.6 years duration, and 102 healthy age- and sex-matched controls. Differences in morphology relative to controls were expressed as standardized deviation (SD) scores (mean ± SD). Standardized between-region differences in vBMD were expressed as SDs (95% confidence intervals, CI).

Results: Relative to controls, men with tetraplegia had deficits in total vBMD of -1.72 ± 1.38 SD at the distal tibia (p < 0.001) and - 0.68 ± 0.69 SD at distal fibula (p = 0.041), but not at the distal radius, despite paralysis. Deficits in men with paraplegia were -2.14 ± 1.50 SD (p < 0.001) at the distal tibia and -0.83 ± 0.98 SD (p = 0.005) at the distal fibula while distal radial total vBMD was 0.23 ± 1.02 (p = 0.371), not significantly increased, despite upper limb mobility. Comparing regions, in men with tetraplegia, distal tibial total vBMD was 1.04 SD (95%CI 0.07, 2.01) lower than at the distal fibula (p = 0.037) and 1.51 SD (95%CI 0.45, 2.57) lower than at the distal radius (p = 0.007); the latter two sites did not differ from each other. Results were similar in men with paraplegia, but total vBMD at the distal fibula was 1.06 SD (95%CI 0.35, 1.77) lower than at the distal radius (p = 0.004).

Conclusion: Microarchitectural deterioration following spinal cord injury is heterogeneous, perhaps partly because strain thresholds regulating the cellular activity of mechano-transduction are region specific.

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Source
http://dx.doi.org/10.1016/j.bone.2020.115778DOI Listing

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