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Figure 6 | Scoliosis

Figure 6

From: Adolescent idiopathic scoliosis (AIS), environment, exposome and epigenetics: a molecular perspective of postnatal normal spinal growth and the etiopathogenesis of AIS with consideration of a network approach and possible implications for medical therapy

Figure 6

Postnatal development of AIS in the spine over time to puberty initiated by genetic factors (pink) and environmental factors (internal pink for AIS, ? external orange) leading to AIS deformity (red). Etiopathogenetic hypotheses acting at cell, tissue, structure and organ levels are linked to putative epigenetic mechanisms affecting vertebral growth plates. For example, in the asynchronous spinal neuro-osseous growth concept [208–211] subclinical tether of a relatively short spinal cord causes a lordoscoliotic maladaption of the spine leading to relative anterior spinal overgrowth (RASO) and the AIS deformity. These adaptive changes in the anterior spinal column are viewed as occurring at cell, tissue and organ levels, and resulting from mechanically-induced effects in vertebral growth plates from epigenetic interactions and/or epigenetic modification in vertebral growth-plates (Adapted from Jamniczky [140]).

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Scoliosis and Spinal Disorders

ISSN: 2397-1789

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