Ankara Spine Center, Iran caddesi 45/2, Kavaklidere, Ankara, Turkey.
Eur Spine J. 2012 Jun;21(6):1033-42. doi: 10.1007/s00586-012-2245-8. Epub 2012 Mar 9.
The purpose of this review is to elucidate the metabolic processes involved in the pathogenesis of adolescent idiopathic scoliosis (AIS) in light of research by the present authors as well as current literature.
Pathogenetic mechanisms involved in AIS were modeled as (a) a form of neuromuscular scoliosis (in conjunction with an adverse mechanical environment such as bipedality), in which hormonal and other chemical factors act as regulators of skeletal muscle tone and function; (b) as a consequence of an abnormality in growth of the spinal column (in conjunction with an adverse mechanical environment such as bipedality), in which hormones and other chemical factors act as regulators of growth; and (c) as a mechanical failure of one side of the vertebral column due to a defect in trabecular formation or mineralization (in conjunction with an adverse mechanical environment such as bipedality); in which hormonal and other chemical factors act as regulators of bone formation, mineralization and/or resorption.
Current evidence supporting these models individually or in combination is discussed.
本综述旨在根据作者的研究以及当前文献阐明青少年特发性脊柱侧凸(AIS)发病机制中涉及的代谢过程。
将 AIS 涉及的发病机制建模为:(a)一种神经肌肉性脊柱侧凸形式(与双足等不良机械环境相结合),其中激素和其他化学因素作为骨骼肌张力和功能的调节剂;(b)脊柱生长异常(与双足等不良机械环境相结合),其中激素和其他化学因素作为生长调节剂;(c)由于小梁形成或矿化缺陷导致脊柱单侧发生机械故障(与双足等不良机械环境相结合);其中激素和其他化学因素作为骨形成、矿化和/或吸收的调节剂。
讨论了支持这些模型单独或联合应用的当前证据。