INTRODUCTION: Scoliosis is a three-dimensional spinal deformity that presents predominantly as a lateral curve in the coronal plane >10. In children and adolescents scoliosis is caused either by congenital vertebral anomalies or is acquired as a consequence of disease (syndromic, neuromuscular), but most often the etiology is idiopathic. Stokes hypothesized that spinal deformity progresses as a “vicious cycle” in which asymmetric stresses applied to the growing spine induce deformity of both osseous and non-osseous tissues, causing growth modulation in agreement with the Hueter-Volkmann Principle (i.e., tension applied to the physis stimulates growth, compression inhibits growth). Currently, it is unknown how asymmetric loading alters the growth of the intervertebral disc (IVD) relative to the vertebrae (VB). In this work we investigate the influence of asymmetric loading on a growing pig to create a reciprocal model of scoliosis. The goal of this study is to characterize a progressive thoracolumbar spinal deformity and transitions in osseous and non-osseous tissues. Our long-term goal is to map the structural, mechanical, and biological transitions with the progression of the spinal deformity to inform clinical interventions (cable tension, timing of correction surgery, and new tethering systems).

­­­­­­­METHODS: With IACUC approval, a 12-week-old Yorkshire pig was instrumented with a CoCr cable spanning T13 to L5; this offset tether created a lateral bending moment and an initial scoliosis that progressed as the pig matured (Fig 1). Anatomical changes to the IVD and VB as a function of time were measured with serial CT scans at -2, 0, 6, 12, and 19 weeks post-op and MRI at 6 and 19 weeks post-op. CT scans were used to quantify lateral wedging and axial rotation between the instrumented levels. Two MRI sequences were utilized, a T₁-weighted FLASH sequence to evaluate IVD volume and a T₂-weighted CPMG echo sequence to evaluate IVD T₂ relaxation time. The T₂ relaxation time, which is positively correlated with water and is decreased in IVD degeneration, was calculated for the nucleus pulposus.

RESULTS: 3D CT reconstructions demonstrate progression of spinal deformity and vertebral growth modulation due to the tether (Fig 2). A 17° Cobb angle, localized primarily through the lumbar IVDs, was produced immediately post-op (Fig 3). At 6 weeks, deformity progression was approximately equally distributed between the thoracolumbar (45%) and lumbar (41%) regions (Fig 3A) with VB wedging accounting for 60% of the total deformity (Fig 3B). From 12 to 19 weeks post-op, the spine deformity transitioned from nearly equal contributions of IVD and VB to only VB (Fig 3B). A 19 weeks post-op, the spine developed a 41° Cobb angle and 9° axial rotation. The T₂ times (290 ± 40 ms) were similar to an age-matched untreated pig (340 ± 10 ms) suggesting that the tether did not induce degeneration. 

DISCUSSION: The asymmetric loading produced by the tether provoked asymmetric spinal growth. Early-stage deformity was localized to the lumbar and thoracolumbar regions in both the IVD and VB. However, from 12 to 19 weeks the deformity transitioned to be primarily located in the VB.