ABSTRACT
BACKGROUND: Despite considerable advances in the past few decades, there is no generally accepted "top theory or theories" of the etiology of adolescent idiopathic scoliosis (AIS). This article aims to provide an overview of the current main hypothetical "concepts" on the etiopathogenesis of AIS. METHODS: An extensive literature review on hypothetical concepts on the etiology and etiopathogenesis of AIS. RESULTS: Concepts of etiopathogenesis in AIS were summarized and highlighted under 6 subgroups: genetics factors, abnormalities in nervous system, abnormal skeletal growth, hormones and metabolic dysfunction, biomechanical factors, and environmental and life style factors. An integrative model on the etiopathogenesis of AIS is proposed. CONCLUSIONS: The current knowledge is still fragmented and many fundamental questions have remained to be answered. In moving forward in the perusal of further advancement of our understanding of the etiopathogenetic mechanisms and future evidence-based prevention and management of AIS, multidisciplinary and multicenter innovative research collaboration is imminently important and necessary. CLINICAL RELEVANCE: With a relatively comprehensive review on the current understanding on the etiology and etiopathogenesis of AIS, the article would help to stimulate further innovative thoughts, research, and especially collaborative research in this area of great interest.
Subject(s)
Models, Theoretical , Scoliosis/etiology , Adolescent , Animals , Cooperative Behavior , Evidence-Based Medicine , Humans , Research Design , Scoliosis/physiopathology , Stress, PsychologicalABSTRACT
Altered paraspinal muscle activity was suggested by Lowe et al (2002) to explain a relationship between Cobb angle changes and platelet calmodulin level changes in adolescent idiopathic scoliosis (AIS). We formulate an alternative platelet-skeletal hypothesis which involves: (1) a small scoliosis curve; (2) axial loads transmitted directly from the intervertebral discs to vertebral body growth plates (endplate physes) as axial inward bulges that create mechanical micro-insults; (3) the latter cause dilatation of juxta-physeal vessels and, in deforming vertebrae, vascular damage with exposure of subendothelial collagen and other agonist proteins; (4) subject to predisposition, platelet activation with calmodulin changes occurs within dilated vessels of deforming vertebral bodies; (5) the activated platelets in juxta-physeal vessels release growth factors that, after extravasation, abet the hormone-driven growth of the already mechanically-compromised vertebral endplate physes to promote the relative anterior spinal overgrowth and curve progression of AIS. The hypothesis links several fields in each of which research within ethical restraints is suggested to refute it.
