Aetiology of idiopathic scoliosis: current concepts

The aetiology of the three-dimensional spinal deformity of idiopathic scoliosis (IS) is unknown. Progressive adolescent idiopathic scoliosis (AIS) that mainly affects girls is generally attributed to relative anterior spinal overgrowth from a mechanical mechanism (torsion) during the adolescent growth spurt. Established biological risk factors to AIS are growth velocity and potential residual spinal growth assessed by maturity indicators. Spine slenderness and ectomorphy in girls are thought to be risk factors for AIS. Claimed biomechanical susceptibilities are (1) a fixed lordotic area and hypokyphosis and (2) concave periapical rib overgrowth. MRI has revealed neuroanatomical abnormalities in ∼ 20% of younger children with IS. A neuromuscular cause for AIS is probable but not established. Possible susceptibilities to AIS in tissues relate to muscles, ligaments, discs, skeletal proportions and asymmetries, the latter also affecting soft tissues (e.g. dermatoglyphics). AIS is generally considered to be multi-factorial in origin. The many anomalies detected, particularly left–right asymmetries, have led to spatiotemporal aetiologic concepts involving chronomics and the genome altered by nurture without the necessity for a disease process. Genetic susceptibilities defined in twins are being evaluated in family studies; polymorphisms in the oestrogen receptor gene are associated with curve severity. A neurodevelopmental concept is outlined for the aetiology of progressive AIS. This concept involves lipid peroxidation and, if substantiated, has initial therapeutic potential by dietary anti-oxidants. Growth saltations have not been evaluated in IS.