The role of melatonin in the pathogenesis of adolescent idiopathic scoliosis.

Abstract

A matched, case-control study comparing melatonin production in female patients with and without adolescent idiopathic scoliosis. To determine whether melatonin production is decreased in adolescent idiopathic scoliosis. A central etiology for idiopathic scoliosis has never been established. Previous authors have produced experimental scoliosis in chickens after pinealectomy, preventable by administration of melatonin. They suggested that a defect in melatonin synthesis might be involved in the pathogenesis of human idiopathic scoliosis. Nine female adolescents with no medical problems, normal neurologic examinations, radiographic idiopathic scoliosis of 15-40 degrees, and Risser Stage I-III were in the patient group. Eighteen healthy adolescent girls with no medical problems, a negative school screening, and no family history of scoliosis were control subjects. Patients and control subjects were matched for age, weight, Tanner stage, sleep duration, and light exposure by multiple linear regression. Nighttime and daytime urine samples were analyzed for melatonin by high-performance liquid chromatography. Although nighttime melatonin levels were significantly higher than daytime levels in all volunteers (P < 0.00002), there were no significant differences in nighttime (P > 0.63) or daytime (P > 0.78) melatonin levels between patients and control subjects, even after matching by multiple linear regression analysis. A statistical analysis demonstrated that if a melatonin deficiency of 25% or more did exist in patients with scoliosis compared with control subjects, the likelihood that it would have been detected in this study was more than 98%. Although melatonin deficiency may cause scoliosis in the chicken, this study suggests that it is not a mechanism in the pathogenesis of adolescent idiopathic scoliosis in humans.