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MECHANICALLY INDUCED DISRUPTION OF THE NUCLEUS PULPOSUS AND A COMPUTER BASED PREDICTIVE MODEL



Abstract

Aim: To investigate, quantify and model the influence of three biomechanical factors on the severity of mechanically induced nuclear disruption in healthy bovine, caudal, intervertebral discs.

Method: A preliminary study was conducted with a fully divided annular wall to investigate the cohesive nature of the isolated nucleus and its tendency to form clefts when loaded. A second more clinically relevant model using whole bovine discs was then conducted to investigate whether significant clefts could be induced in healthy discs by controlling flexion, hydration and rate of compressive loading.. A finite element model of the bovine caudal disc was constructed to predict the complex stress conditions that exist within the disc.

Results: We found that high degrees of flexion and hydration were significant risk factors in nuclear disruption (P < 0.005), while the rate of loading showed no significant effect (P = 0.37). The intact disc study also showed that flexion and hydration are significant risk factors (P < 0.002). In contrast with the preliminary study, the rate of loading was also shown to be mildly significant (P < 0.1). The finite element model predicted relatively high concentrations of stress and strain energy density within the nucleus. This is consistent with the experimental observations of cleft formation.

Conclusions: While it is well established that dehydration of the nucleus is a symptom of degeneration this study suggested that the healthy nucleus, when maximally hydrated, is more susceptible to nuclear disruption when loaded. This supports the hypothesis that the histologically abnormal and degenerate nuclear material removed at surgery, may well have attained this state as a result of biomechanical and biochemical changes occurring in the disc following rather than preceding a prolapse. This study further defined the rôle of trauma in disc injury and prolapse of the normal disc.

The abstracts were prepared by Professor Alan Thurston. Correspondence should be addressed to him at the New Zealand Orthopaedic Association, PO Box 7451, Wellington, New Zealand.

Acknowledgements: This research was supported by grants from the Wishbone Orthopaedic Trust and the Health Research Council of New Zealand.