Introduction: Various hypotheses concerning the pathomechanism of adolescent idiopathic scoliosis have been proposed, such as the abnormal growth of the anterior spine. Accelerated growth patterns in scoliotic over healthy patients encouraged speculation that such increase is involved in the pathomechanism of scoliotic spines.
Objectives : Explores this hypothesis using a finite element model (FEM) of the spine with integrated growth dynamics.
Materials and Methods: A baseline spine FEM was constructed from patient geometry. Coronal and sagittal profiles were then altered to emulate 5 new spinal configurations of interest (no, mild and moderate scoliosis; hypo and regular kyphosis). FEMs material properties abide with published values while growth dynamics respect the Hueter-Volkmann principle. Ten years of growth (8–18) was simulated for each model using documented growth patterns of scoliotic and healthy patients. Coronal (Cobb angle) and sagittal (kyphosis, lordosis) were quantified at 2 year intervals during growth.
Results: Following ten years of simulated growth and comparison of resulting spinal profiles, a significant increase in the mean coronal plane deformity progression was observed under scoliotic growth (44°) when compared to healthy growth (11°). Similarly, a mean hypokyphosis increase in the sagittal plane (13°) occurred when governed by scoliotic growth rates while healthy rates resulted in no significant alteration.
Conclusion: This preliminary analysis supports the hypothesis that increased anterior vertebral body growth of scoliotic spines may play a role in its pathomechanism by encouraging additional deformity under the Hueter-Volkmann principle.
Significance: Accelerated growth profiles clinically observed in scoliotic patients may then pose as a progressive risk factor.
Acknowledgements: Funded by NSERC Canada.