Intervertebral disc health preservation after six months of spinal growth modulation.

Idiopathic scoliosis is a common disorder of the pediatric spine that results in a three-dimensional deformity. Asymmetric spinal growth and biomechanical imbalance have been postulated as causes of this progressive deformity1. Although various treatment methods have been proposed, only bracing and surgical fusion affect the natural history of idiopathic scoliosis compared with the deformity seen after observation alone2,3. However, even these two options have limitations. Bracing may prevent curve progression but generally affords little curve correction, despite optimal compliance3,4, while surgical treatments sacrifice spinal flexibility to obtain and maintain curve correction. Ideally, a third option that would permanently straighten the spinal deformity while preserving spinal mobility and long-term function would be available. Mechanical alteration of spinal growth by shortening the anterior vertebral column with an “internal brace” has been proposed as an attractive non-fusion treatment option for this multiplane deformity. Limiting anterior spinal overgrowth5,6 has been considered since Blount and Clarke7 and Haas8 reported their initial work on epiphysiodesis in long bones. Recent studies on growth modulation in the axial skeleton have focused on retarding growth at the convexity of the deformity9-13. Use of an anterolateral flexible vertebral tether has also been shown to modulate spinal growth in animal models14,15. However, further evaluation of intervertebral disc health and spinal mobility is needed to determine if these techniques will be successful in the adolescent population. The intervertebral disc is a flexible fibrocartilaginous structure that supports spinal loads while facilitating spinal movement. Disc degeneration has a multifactorial etiology, but decreased disc nutrition has been proposed as a common degenerative pathway, as the primary nutrition source for the avascular disc is diffusion from anular fibrosus and vertebral end-plate blood vessels16. Disc degeneration may develop prematurely secondary to compressive forces or it may occur as a result of natural aging leading to a breakdown of the large aggregating proteoglycans and loss of type-II collagen in the nucleus pulposus16,17. Decreased proteoglycans then reduce the capacity of the disc to attract and bind water, leading to a loss of hydration and decreased hydrostatic pressure18. Progressive disc degeneration leads to anular tears, rim lesions, decreased disc height, structural changes in the lamellar architecture of the anulus fibrosus, and formation of osteophytes. Traditionally, biochemical analyses and the Thompson grading scale19 have been used to characterize the state of disc degeneration. Pathomorphological and biochemical methods of grading intervertebral disc degeneration have been found to correlate well and are the gold standard for the analysis of cadaveric tissue. Differences in Thompson grades are reflected by changes in the concentration of disc constituents such as collagen and proteoglycans in both the anulus fibrosus and the nucleus pulposus. Clinically, magnetic resonance imaging (MRI) is the most sensitive and specific diagnostic tool for detection of disc degeneration. The purpose of this study was to assess the creation of three-dimensional spinal deformity during six months of growth modulation compared with what was found in sham-surgery controls, and to compare disc health between tethered and control animals through use of MRI, gross morphological, histological, and biochemical analyses. We hypothesized that the spinal tether would create significant spinal deformity while preserving intervertebral disc health.