Abstract

BackgroundCervical spine fixation or immobilization has become a routine treatment for spinal fracture, dislocation, subluxation injuries, or spondylosis. The effects of immobilization of intervertebral discs of the cervical spine is unclear. The goal of this study was to evaluate the effects of long-segment in-situ immobilization of intervertebral discs of the caudal vertebra, thereby simulating human cervical spine immobilization.MethodsThirty-five fully grown, male Sprague-Dawley rats were used. Rats were randomly assigned to one of five groups: Group A, which served as controls, and Groups B, C, D, and E, in which the caudal vertebrae were in-situ immobilized using a custom-made external device that fixed four caudal vertebrae (Co7-Co10). After 2 weeks, 4 weeks, 6 weeks, and 8 weeks of in-situ immobilization, the caudal vertebrae were harvested, and the disc height, the T2 signal intensity of the discs, disc morphology, the gene expression of discs, and the structure and the elastic modulus of discs was measured.ResultsThe intervertebral disc height progressively decreased, starting at the 6th week. At week 6 and week 8, disc degeneration was classified as grade III, according to the modified Pfirrmann grading system criteria. Long-segment immobilization altered the gene expression of discs. The nucleus pulposus showed a typical cell cluster phenomenon over time. The annulus fibrosus inner layer began to appear disordered with fissure formation. The elastic modulus of collagen fibrils within the nucleus pulposus was significantly decreased in rats in group E compared to rats in group A (p < 0.05). On the contrary, the elastic modulus within the annulus was significantly increased in rats in group E compared to rats in group A (p < 0.05).ConclusionLong-segment in-situ immobilization caused target disc degeneration, and positively correlated with fixation time. The degeneration was not only associated with changes at the macroscale and microscale, but also indicated changes in collagen fibrils at the nanoscale. Long-segment immobilization of the spine (cervical spine) does not seem to be an innocuous strategy for the treatment of spine-related diseases and may be a predisposing factor in the development of the symptomatic spine.

Highlights

  • Cervical spine fixation or immobilization has become a routine treatment for spinal fracture, dislocation, subluxation injuries, or spondylosis

  • In this study, long-segment in-situ immobilization caused target disc degeneration, and positively correlated with fixation time. These findings showed that, over time, in-situ immobilization induced a progressive decrease in the intervertebral disc space height and T2 signal intensity of IVD

  • The effects on aggrecanase, collagenase, stromelysin of annulus fibrosus (AF) were not significant. These changes suggested that immobilization loading initiated a degenerative cascade, this trend was significantly observed in the nucleus pulposus (NP) compared to AF

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Summary

Introduction

Cervical spine fixation or immobilization has become a routine treatment for spinal fracture, dislocation, subluxation injuries, or spondylosis. The effects of immobilization of intervertebral discs of the cervical spine is unclear. The goal of this study was to evaluate the effects of long-segment in-situ immobilization of intervertebral discs of the caudal vertebra, thereby simulating human cervical spine immobilization. Immobilization using fixation of two caudal vertebrae, including one disc, downregulated the expression of anabolic genes [13]. Several studies have shown the effect induced by short-segment immobilization (usually fixation is less than/or equal to three caudal vertebrae, including two discs). Because of the anatomical features of the cervical vertebrae (C4–7 intervertebral discs is an easier segment to degenerate or protrude), cervical spine immobilization or fixation (a brace or Halo-Vest fixator) is more inclined to overall fixation (similar to long tube fixation). The effect of long-segment in-situ immobilization and the underlying mechanism involved in the onset of complications remains unknown

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