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Research

INTERNAL DISC DISRUPTION: THE ROLE OF STRESS GRADIENTS

British Orthopaedic Research Society (BORS)



Abstract

Background

In the annulus fibrosus of degenerated intervertebral discs, disruption to inter-lamellar cross-ties appears to lead to delamination, and the development of anulus fissures. We hypothesise that such internal disruption is likely to be driven by high gradients of compressive stress (i.e. large differences in stress from the nucleus to the mid anulus).

Methods

Eighty-nine thoracolumbar motion segements, from T7/8 to L4/5, were dissected from 38 cadavers aged 42-96 yrs. Each was subjected to 1 kN compressive loading, while intradiscal compressive stresses were measured by pulling a pressure transducer along the disc's mid-sagittal diameter. Measurements were repeated in flexed and extended postures. Stress gradients were measured, in the anterior and posterior anulus of each disc, as the average rate of increase in stress (MPa/mm) between the nucleus and the region of maximum compressive stress in the anulus. Average nucleus pressure (IDP) was also recorded.

Results

Stress gradients increased with grade of disc degeneration, especially in the posterior anulus (p<0.04 or better). Age had little additional influence, despite an inverse correlation with IDP (p<0.04). Stress gradients increased in the anterior anulus in flexion, and were greatest of all in the posterior anulus in extension, sometimes exceeding 0.5 MPa/mm. In the most severely degenerated discs, stress gradients remained high, even though peak anulus stresses and IDP were reduced as a result of load-bearing being transferred to the neural arch.

Discussion

Stress gradients are highest in the region of the disc (the middle posterior anulus) that is most disrupted by the degenerative process. Unlike the overall peak stresses, or IDP, stress gradients remain high in severely degenerated discs, and are not reduced when load-bearing is transferred to the neural arch. These results suggest that stress gradients play a major role in the internal disruption of degenerated human discs.

Acknowledgements

M Stefanakis would like to thank the Greek Institute of Scholarships (I.K.Y) for financial support.