Biomechanical simulations of the spine deformation process in adolescent idiopathic scoliosis from different pathogenesis hypotheses.

It is generally recognized that progressive adolescent idiopathic scoliosis (AIS) evolves within a self-sustaining biomechanical process involving asymmetrical growth modulation of vertebrae due to altered spinal load distribution. A biomechanical finite element model of normal thoracic and lumbar spine integrating vertebral growth was used to simulate the progression of spinal deformities over 24 months. Five pathogenesis hypotheses of AIS were represented, using an initial geometrical eccentricity (gravity line imbalance of 3 mm or 2 degrees rotation) at the thoracic apex to trigger the self-sustaining deformation process. For each simulation, regional (thoracic Cobb angle, kyphosis) and local scoliotic descriptors (axial rotation and wedging of the thoracic apical vertebra) were evaluated at each growth cycle. The simulated AIS pathogeneses resulted in the development of different scoliotic deformities. Imbalance of 3 mm in the frontal plane, combined or not with the sagittal plane, resulted in the closest representation of typical scoliotic deformities, with the thoracic Cobb angle progressing up to 39 degrees (26 degrees when a sagittal offset was added). The apical vertebral rotation increased by 7 degrees towards the convexity of the curve, while the apical wedging increased to 8.5 degrees (7.3 degrees with the sagittal eccentricity) and this deformity evolved towards the vertebral frontal plane. A sole eccentricity in the sagittal plane generated a non-significant frontal plane deformity. Simulations involving an initial rotational shift (2 degrees ) in the transverse plane globally produced relatively small and non-typical scoliotic deformations. Overall, the thoracic segment predominantly was sensitive to imbalances in the frontal plane, although unidirectional geometrical eccentricities in different planes produced three-dimensional deformities at the regional and vertebral levels, and their deformities did not cumulate when combined. These results support the hypothesis of a prime lesion involving the precarious balance in the frontal plane, which could concomitantly be associated with a hypokyphotic component. They also suggest that coupling mechanisms are involved in the deformation process.