The exact pathogenesis of<unk>  is not fully understood. It is thought that<unk>  is the result of nutritional, endocrine, or genetic factors.The observation that curve development and progression correlate with the period of rapid adolescent growth appears to support a biomechanical contribution. However, multiple theories exist that attempt to explain the process by which the development takes place, and while each makes sense from a biomechanical standpoint. Malfunctioning melatonin and calmodulin signal pathway have been proposed for development of idiopathic<unk> . In addition, theories suggesting a relative anterior spinal overgrowth (RASO) or an uncoupled neuro-osseus growth as a cause of idiopathic<unk> . Skeletal immaturity is the major risk factor for the curve progression. It has been noted that girls with adolescent IS are taller and have a higher growth velocity during puberty in comparison to healthy individuals. A lower bone mineral density, leptin, cartilage oligomeric matrix protein and a high levels of growth hormone have seen to be influencing development of the disease. The effect of genetics on idiopathic<unk>  is well established. From the genetic standpoint,<unk>  is not easily explained by existing inheritance models. It has been recently seen the disease to be associated with loci on OS1, OS2, OS3, OS4, OS5, CHD7 and PAX1 gene.
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