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Orthopaedic Proceedings
Vol. 85-B, Issue SUPP_III | Pages 242 - 242
1 Mar 2003
Pollintine P Garbutt S Tobias J Dolan P Adams M
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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.


Orthopaedic Proceedings
Vol. 84-B, Issue SUPP_I | Pages - 95
1 Mar 2002
Pollintine P Garbutt S Tobias J McNally D Wakley G Dolan P Adams M
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Osteoporotic vertebral fractures are normally attributed to weakening of the vertebral body. However, the compressive strength of the spine also depends on the manner in which the intervertebral disc presses on the vertebral body, and on load-bearing by the neural arch. We present preliminary results from a large-scale investigation into the relative importance of these three influences on vertebral compressive strength.

Lumbar motion segments from elderly cadavers were subjected to 1.5 kN of compressive loading while the distribution of compressive stress was measured along the antero-posterior diameter of the intervertebral disc, using a miniature pressure-transducer. The overall compressive force on the disc, obtained by integrating the stress profile ( 1), was subtracted from the 1.5 kN applied load to give the force resisted by the neural arch. Stress profilometry was performed with each motion segment positioned to simulate the erect standing posture, and a forward stooping posture. Vertebral strength was measured by compressing the motion segments to failure in the forward stooping posture. In life, the spine is usually compressed most severely in this posture.

A univariate analysis of results from the first 9 motion segments (aged 72–92 yrs) showed that vertebral strength increased from 2.0 kN to 4.6 kN as the compressive force resisted by the neural arch in erect postures decreased from 1.1 kN to 0.4 kN (r2 = 0.42, p = 0.05). Updated results from this on-going study will be presented at the meeting.

Preliminary results suggest that habitual load-bearing by the neural arch in erect postures can lead to progressive weakening of the vertebral body, which is effectively “stress-shielded” by the neural arch. This weakening is exposed when the spine is loaded severely in a forward stooped posture, when it has a reduced compressive strength. This mechanism could explain some features of osteoporotic vertebral fractures in old people.