title: The pathogenesis of adolescent idiopathic scoliosis: review of the literature.
abstract: METHODS
  Review of the literature on the pathogenesis of adolescent idiopathic scoliosis (AIS).
  
  
  OBJECTIVE
  To discuss the different theories that have appeared on this subject.
  
  
  BACKGROUND
  The pathogenesis of AIS, a condition exclusive to humans, has been the subject of many studies. Over the years, practically every structure of the body has been mentioned in the pathogenesis of AIS; however, the cause of this spinal deformity remains little understood. The pathogenesis of this condition is termed multifactorial.
  
  
  METHODS
  PubMed and Google Scholar electronic databases were searched focused on parameters concerning the pathogenesis of adolescent idiopathic scoliosis. The search was limited to the English language.
  
  
  RESULTS
  No single causative factor for the development of idiopathic scoliosis has been identified, it is thus termed multifactorial. AIS is a complex genetic disorder. The fully erect posture, which is unique to humans, seems to be a prerequisite for the development of AIS.
  
  
  CONCLUSIONS
  Although any or all of the mentioned factors in this review may play a certain role in the initiation and progression of AIS at a certain stage, the presented material suggests that in the observed deformation, genetics, and the unique mechanics of the fully upright human spine play a decisive role.
authors.affiliation: Department of Orthopedics, University Medical Center Utrecht, Utrecht, The Netherlands.
authors.forename: Jan-Willem M
authors.initials: JW
authors.lastname: Kouwenhoven
authors.forename: René M
authors.initials: RM
authors.lastname: Castelein
mesh_terms: D000293:Adolescent; D000818:Animals; D005075:Biological Evolution; D001696:Biomechanical Phenomena / Q000502:physiology; D006801:Humans; D011187:Posture / Q000502:physiology; D012600:Scoliosis / Q000209:etiology* / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology; D013904:Thoracic Vertebrae / Q000473:pathology / Q000502:physiology