The many causes of<unk>  include neuromuscular problems and inherited diseases or conditions caused by the environment. An estimated 65% of<unk>  cases are idiopathic, about 15% are congenital, and about 10% are secondary to a neuromuscular disease. About 38% of variance in<unk>  risk is due to genetic factors, and 62% is due to the environment. The genetics are likely complex, however, given the inconsistent inheritance and discordance among monozygotic twins. The specific genes that contribute to development of<unk>  have not been conclusively identified. At least one gene, CHD7, has been associated with the idiopathic form of<unk> . Several candidate gene studies have found associations between idiopathic<unk>  and genes mediating bone formation, bone metabolism, and connective tissue structure. Several genome-wide studies have identified a number of loci as significantly linked to idiopathic<unk> . In 2006, idiopathic<unk>  was linked with three microsatellite polymorphisms in the MATN1 gene (encoding for matrilin 1, cartilage matrix protein). Fifty-three single nucleotide polymorphism markers in the DNA that are significantly associated with adolescent idiopathic<unk>  were identified through a genome-wide association study. Adolescent idiopathic<unk>  has no clear causal agent, and is generally believed to be multifactorial; leading to "progressive functional limitations" for individuals. Research suggests that Posterior Spinal Fusion (PSF) can be used to correct the more severe deformities caused by adolescent idiopathic<unk> . Such procedures can result in a return to physical activity in about 6 months, which is very promising, although minimal back pain is still to be expected in the most severe cases. The prevalence of<unk>  is 1% to 2% among adolescents, but the likelihood of progression among adolescents with a Cobb angle less than 20° is about 10% to 20%. Congenital<unk>  can be attributed to a malformation of the spine during weeks three to six in utero due to a failure of formation, a failure of segmentation, or a combination of stimuli. Incomplete and abnormal segmentation results in an abnormally shaped vertebra, at times fused to a normal vertebra or unilaterally fused vertebrae, leading to the abnormal lateral curvature of the spine. Resulting from other conditions Secondary<unk>  due to neuropathic and myopathic conditions can lead to a loss of muscular support for the spinal column so that the spinal column is pulled in abnormal directions. Some conditions which may cause secondary<unk>  include muscular dystrophy, spinal muscular atrophy, poliomyelitis, cerebral palsy, spinal cord trauma, and myotonia.<unk>  often presents itself, or worsens, during an adolescent's growth spurt and is more often diagnosed in females than males.<unk>  associated with known syndromes is often subclassified as "syndromic<unk> ".<unk>  can be associated with amniotic band syndrome, Arnold–Chiari malformation, Charcot–Marie–Tooth disease, cerebral palsy, congenital diaphragmatic hernia, connective tissue disorders, muscular dystrophy, familial dysautonomia, CHARGE syndrome, Ehlers–Danlos syndrome (hyperflexibility, "floppy baby" syndrome, and other variants of the condition), fragile X syndrome, Friedreich's ataxia, hemihypertrophy, Loeys–Dietz syndrome, Marfan syndrome, nail–patella syndrome, neurofibromatosis, osteogenesis imperfecta, Prader–Willi syndrome, proteus syndrome, spina bifida, spinal muscular atrophy, syringomyelia, and pectus carinatum. Another form of secondary<unk>  is degenerative<unk> , also known as de novo<unk> , which develops later in life secondary to degenerative (may or may not be associated with aging) changes. This is a type of deformity that starts and progresses because of the collapse of the vertebral column in an asymmetrical manner. As bones start to become weaker and the ligaments and discs located in the spine become worn as a result of age-related changes, the spine begins to curve.
Scoliosis
Poliosis
Kyphoscoliosis
Hip dysplasia
Multiple epiphyseal dysplasia
Tooth ankylosis
Back strain
Metaphyseal dysplasia