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INTERVERTEBRAL DISC DEGENERATION INCREASES VERTEBRAL BODY VULNERABILITY TO OSTEOPOROTIC FRACTURE



Abstract

Introduction: Osteoporotic fractures affect certain bones more than others, suggesting that systemic bone loss is not the only underlying cause. We have shown that age-related intervertebral disc degeneration causes the anterior vertebral body (VB) to be stress-shielded in erect postures, and yet severely loaded when the spine is flexed (1). We hypothesise that this unequal loading causes exaggerated bone loss from the anterior vertebral body, making it vulnerable to fracture when the spine is heavily loaded in a forward stooping (flexed) posture.

Materials and Methods: Regional volumetric bone mineral density (BMD) was measured in 35 thoracolumbar motion segments (aged 64–92 yrs) using dual-energy x-ray absorptiometry. The distribution of compressive stress was measured along the mid-sagittal diameter of each intervertebral disc using a miniature pressure transducer. Stresses were integrated over area to give the compressive force acting on the anterior and posterior halves of the VB (1). Motion segment compressive strength was measured in moderate flexion.

Results: BMD of the anterior half of the VB was 26% (STD 13%) lower than that of the posterior half (p< 0.0001), was correlated with % load on the anterior VB in erect posture (r2=0.48, p< 0.0001), and was a better predictor of motion segment compressive strength (in flexion) than was BMD of the whole vertebral body (r2 = 0.79 compared to r2 = 0.59).

Conclusion: These results clearly support our hypothesis. It appears that intervertebral disc degeneration leads to exaggerated bone loss from the anterior VB, leaving it more vulnerable to fracture when the spine is flexed. Future work aims to confirm this important result on a larger number of specimens, and to compare the relative importance of disc degeneration and overall bone loss on vertebral compressive strength.

Pollintine P et al (2001). SBPR Annual Meeting, Bristol. Backcare Research Award 2002.

Correspondence should be addressed to the editorial secretary: Dr Charles Pither, c/o British Orthopaedic Society, Royal College of Surgeons, 35-43 Lincoln’s Inn Fields, London WC2A 3PN.