Biomechanical analysis and modeling of different vertebral growth patterns in adolescent idiopathic scoliosis and healthy subjects

Abstract

BackgroundThe etiology of AIS remains unclear, thus various hypotheses concerning its pathomechanism have been proposed. To date, biomechanical modeling has not been used to thoroughly study the influence of the abnormal growth profile (i.e., the growth rate of the vertebral body during the growth period) on the pathomechanism of curve progression in AIS. This study investigated the hypothesis that AIS progression is associated with the abnormal growth profiles of the anterior column of the spine.MethodsA finite element model of the spinal column including growth dynamics was utilized. The initial geometric models were constructed from the bi-planar radiographs of a normal subject. Based on this model, five other geometric models were generated to emulate different coronal and sagittal curves. The detailed modeling integrated vertebral body growth plates and growth modulation spinal biomechanics. Ten years of spinal growth was simulated using AIS and normal growth profiles. Sequential measures of spinal alignments were compared.Results(1) Given the initial lateral deformity, the AIS growth profile induced a significant Cobb angle increase, which was roughly between three to five times larger compared to measures utilizing a normal growth profile. (2) Lateral deformities were absent in the models containing no initial coronal curvature. (3) The presence of a smaller kyphosis did not produce an increase lateral deformity on its own. (4) Significant reduction of the kyphosis was found in simulation results of AIS but not when using the growth profile of normal subjects.ConclusionResults from this analysis suggest that accelerated growth profiles may encourage supplementary scoliotic progression and, thus, may pose as a progressive risk factor.

Distraction magnitude and frequency affects the outcome in juvenile idiopathic patients with growth rods: finite element study using a representative scoliotic spine model

“…In our preliminary study, we ran these models both with (pure compression) and without (compression aligned with gravitational force) follower load to find the differences in results. We found insignificant variability in the result and, hence, we chose to use follower load to keep our methods consistent with the methodology of a previously published author [26]. Boundary conditions included restraining the inferior surface of S1 vertebra in all degrees of freedom [26].…”

“…We found insignificant variability in the result and, hence, we chose to use follower load to keep our methods consistent with the methodology of a previously published author [26]. Boundary conditions included restraining the inferior surface of S1 vertebra in all degrees of freedom [26]. The model also incorporated the increase in stiffness of spine as a function of time to take into consideration the effects of autofusion [16].…”

Lesiones del anillo apofisario vertebral: A proposito de un caso

“…1,5 Con respecto al desarrollo vertebral, a diferencia de otros vertebrados, el ser humano solo tiene centros primarios de osificación (uno central y dos en los arcos neurales) que crecen hasta dejar delimitado un anillo apofisario cartilaginoso separado del resto del cuerpo por una fisis, estructuras que se fusionan aproximadamente a los 14-15 años (Figura 3). 6 Se ha podido provocar la fractura del núcleo de osificación (epifisiólisis) en ensayos biomecánicos, aplicando sobre el cuerpo vertebral una fuerza que provoque cizallamiento, siempre que el raquis esté en flexión. 7 En una revisión de 12 casos mortales de lesión espinal en niños, los hallazgos necrópsicos mostraron una fractura del núcleo de osificación epifisario.…”

Whither the etiopathogenesis (and scoliogeny) of adolescent idiopathic scoliosis? Incorporating presentations on scoliogeny at the 2012 IRSSD and SRS meetings

“…The attainment of a grand unifying theory for adolescent idiopathic scoliogeny seems unlikely at present. Finite element analysis of spinal models of AIS pathogenesis (‘scoliosis in a box’) has provided for the testing of specific questions, recently in connection with how accelerated growth profiles may increase scoliosis progression and pose a progressive risk factor [130]. Building a unifying computer model for AIS pathogenesis might be considered using supercomputers with ever increasing memory (‘brain and scoliosis in a box’).…”