Huynh Anne-Marie, Aubin Carl-Eric, Rajwani Talib, Bagnall Keith M, Villemure Isabelle
Mechanical/Biomedical Engineering Department, Ecole Polytechnique, Montreal, Quebec, Canada.
Eur Spine J. 2007 Apr;16(4):523-9. doi: 10.1007/s00586-006-0235-4. Epub 2006 Oct 10.
Over the last century the neurocentral junction (NCJ) has been identified as a potential cause of adolescent idiopathic scoliosis (AIS). Disparate growth at this site has been thought to lead to pedicle asymmetry, which then causes vertebral rotation and ultimately, the development of scoliotic curves. The objectives of this study are (1) to incorporate pedicle growth and growth modulation into an existing finite element model of the thoracic and lumbar spine already integrating vertebral body growth and growth modulation; (2) to use the model to investigate whether pedicle asymmetry, either alone or combined with other deformations, could be involved in scoliosis pathomechanisms. The model was personalized to the geometry of a nonpathological subject and used as the reference spinal configuration. Asymmetry of pedicle geometry (i.e. initial length) and asymmetry of the pedicle growth rate alone or in combination with other AIS potential pathogenesis (anterior, lateral, or rotational displacement of apical vertebra) were simulated over a period of 24 months. The Cobb angle and local scoliotic descriptors (wedging angle, axial rotation) were assessed at each monthly growth cycle. Simulations with asymmetrical pedicle geometry did not produce significant scoliosis, vertebral rotation, or wedging. Simulations with asymmetry of pedicle growth rate did not cause scoliosis independently and did not amplify the scoliotic deformity caused by other deformations tested in the previous model. The results of this model do not support the hypothesis that asymmetrical NCJ growth is a cause of AIS. This concurs with recent animal experiments in which NCJ growth was unilaterally restricted and no scoliosis, vertebral wedging, or rotation was noted.
在过去的一个世纪里，神经中央连接部（NCJ）已被确定为青少年特发性脊柱侧凸（AIS）的一个潜在病因。人们认为该部位的不均衡生长会导致椎弓根不对称，进而引起椎体旋转，最终导致脊柱侧凸曲线的发展。本研究的目的是：（1）将椎弓根生长和生长调节纳入已整合椎体生长和生长调节的现有胸腰椎有限元模型中；（2）使用该模型研究椎弓根不对称单独或与其他畸形相结合是否可能参与脊柱侧凸的发病机制。该模型根据一名非病理性受试者的几何形状进行个性化定制，并用作参考脊柱构型。在24个月的时间里，模拟了椎弓根几何形状的不对称（即初始长度）以及单独的椎弓根生长速率不对称或与其他AIS潜在发病机制（顶椎的前、侧方或旋转位移）相结合的情况。在每个月的生长周期评估Cobb角和局部脊柱侧凸描述符（楔角、轴向旋转）。椎弓根几何形状不对称的模拟未产生明显的脊柱侧凸、椎体旋转或楔变。椎弓根生长速率不对称的模拟单独不会导致脊柱侧凸，也不会放大先前模型中测试的其他畸形所引起的脊柱侧凸畸形。该模型的结果不支持不对称的NCJ生长是AIS病因这一假设。这与最近的动物实验结果一致，在这些实验中，NCJ生长被单侧限制，未观察到脊柱侧凸、椎体楔变或旋转。
