Abstract
OBJECTIVE:
The purpose of this review is to elucidate the metabolic processes involved in the pathogenesis of adolescent idiopathic scoliosis (AIS) in light of research by the present authors as well as current literature.
METHODS:
Pathogenetic mechanisms involved in AIS were modeled as (a) a form of neuromuscular scoliosis (in conjunction with an adverse mechanical environment such as bipedality), in which hormonal and other chemical factors act as regulators of skeletal muscle tone and function; (b) as a consequence of an abnormality in growth of the spinal column (in conjunction with an adverse mechanical environment such as bipedality), in which hormones and other chemical factors act as regulators of growth; and (c) as a mechanical failure of one side of the vertebral column due to a defect in trabecular formation or mineralization (in conjunction with an adverse mechanical environment such as bipedality); in which hormonal and other chemical factors act as regulators of bone formation, mineralization and/or resorption.
RESULTS AND CONCLUSION:
Current evidence supporting these models individually or in combination is discussed.
Source: PubMed
Dr. Morningstar’s take: This is a highlight of the current etiological models of scoliosis development in which hormonal and other non-spinal factors are of central importance. Scoliosis is much more than an orthopedic spine problem.
