Simulation of Progressive Deformities in Adolescent Idiopathic Scoliosis Using a Biomechanical Model Integrating Vertebral Growth Modulation

Abstract

While the etiology and pathogenesis of adolescent idiopathic scoliosis are still not well understood, it is generally recognized that it progresses within a biomechanical process involving asymmetrical loading of the spine and vertebral growth modulation. This study intends to develop a finite element model incorporating vertebral growth and growth modulation in order to represent the progression of scoliotic deformities. The biomechanical model was based on experimental and clinical observations, and was formulated with variables integrating a biomechanical stimulus of growth modulation along directions perpendicular (x) and parallel (y, z) to the growth plates, a sensitivity factor beta to that stimulus and time. It was integrated into a finite element model of the thoracic and lumbar spine, which was personalized to the geometry of a female subject without spinal deformity. An imbalance of 2 mm in the right direction at the 8th thoracic vertebra was imposed and two simulations were performed: one with only growth modulation perpendicular to growth plates (Sim1), and the other one with additional components in the transverse plane (Sim2). Semi-quantitative characterization of the scoliotic deformities at each growth cycle was made using regional scoliotic descriptors (thoracic Cobb angle and kyphosis) and local scoliotic descriptors (wedging angle and axial rotation of the thoracic apical vertebra). In all simulations, spinal profiles corresponded to clinically observable configurations. The Cobb angle increased non-linearly from 0.3 degree to 34 degrees (Sim1) and 20 degrees (Sim2) from the first to last growth cycle, adequately reproducing the amplifying thoracic scoliotic curve. The sagittal thoracic profile (kyphosis) remained quite constant. Similarly to clinical and experimental observations, vertebral wedging angle of the thoracic apex progressed from 2.6 degrees to 10.7 degrees (Sim1) and 7.8 degrees (Sim2) with curve progression. Concomitantly, vertebral rotation of the thoracic apex increased of 10 degrees (Sim1) and 6 degrees (Sim2) clockwise, adequately reproducing the evolution of axial rotation reported in several studies. Similar trends but of lesser magnitude (Sim2) suggests that growth modulation parallel to growth plates tend to counteract the growth modulation effects in longitudinal direction. Overall, the developed model adequately represents the self-sustaining progression of vertebral and spinal scoliotic deformities. This study demonstrates the feasibility of the modeling approach, and compared to other biomechanical studies of scoliosis it achieves a more complete representation of the scoliotic spine.

Expression of Runx2 and Type X Collagen in Vertebral Growth Plate of Patients with Adolescent Idiopathic Scoliosis

“…Following maturation, chondrocytes progress toward hypertrophy and secrete type X collagen, the matrix for the hypertrophic cartilage destined for endochondral ossification [52]. Runx2, a transcription factor that belongs to the Runx family [53], also regulates chondrocyte maturation and terminal differentiation during endochondral bone formation [6][7][8][9][10][11][12][13][14][15][16][17][18][19]54]. Many in vitro studies indicate that Runx2 is a positive regulator that can upregulate the expression of bone matrix genes, including type I collagen, type X collagen, osteopontin, bone sialoprotein (BSP), osteocalcin, and fibronectin [24,[55][56][57].…”

“…Some studies showed that the different growth rates between the right and the left side of the vertebrae generated the asymmetric growth and wedging of the vertebrae. This feature plays a main role in the progression of the curve [4][5][6][7][8]. Parent et al [9] investigated a large number of scoliotic specimens and found that the vertebral wedging was predominant in the front plane instead of the sagittal plane.…”

"Rehabilitation schools for scoliosis" thematic series: describing the methods and results

“…Whether or not the progression of an established scoliotic deformity is secondary to asymmetric loading, correction of the deformity using the principles of Hueter-Volkmann law is possible as long as there is sufficient residual growth. Other studies [20,21] have demonstrated the feasibility of the modeling approach achieving at the same time a complete representation of the scoliotic spine.…”

Mechanobiological bone growth: comparative analysis of two biomechanical modeling approaches

“…The sensitivity factor b l is determined from experimental data and is considered independent of the external environment. This modeling approach was integrated in beam-type finite element models by simulating the resulting strain increments as thermal loadings or equivalent forces to carry out bone geometrical changes [4,27,36,37].…”

“…According to experimental results, Stokes and Laible [27] hypothesized a linear relationship between compressive or tensile stresses and mechanobiological growth rate, in which growth plate stresses perpendicular to the growth plates are acting as mechanical stimuli to bone growth. This modeling approach was integrated in a beam finite element model of the thoracic and lumbar spine to simulate asymmetrical growth of the rib cage and/or vertebrae [27,28,36,37] and in a solid vertebral model to simulate the progression of scoliosis induced by the biomechanical growth modulation [26]. Carter et al proposed a theoretical relationship between bone growth, which incorporated the endochondral growth and ossification, and mechanical loading based on the physiological observations of the ossification of the hand in a 32-month-old child [2,5,6,[22][23][24][25].…”