As. Hilibrand et al., THE ROLE OF MELATONIN IN THE PATHOGENESIS OF ADOLESCENT IDIOPATHIC SCOLIOSIS, Spine (Philadelphia, Pa. 1976), 21(10), 1996, pp. 1140-1146
Study Design. A matched, case-control study comparing melatonin produc
tion in female patients with and without adolescent idiopathic scolios
is. Objectives. To determine whether melatonin production is decreased
in adolescent idiopathic scoliosis. Summary of Background Data. A cen
tral etiology for idiopathic scoliosis has never been established. Pre
vious authors have produced experimental scoliosis in chickens after p
inealectomy, preventable by administration of melatonin. They suggeste
d that a defect in melatonin synthesis might be involved in the pathog
enesis of human idiopathic scoliosis. Methods. Nine female adolescents
with no medical problems, normal neurologic examinations, radiographi
c idiopathic scoliosis of 15-40 degrees, and Risser Stage:-III were in
the patient group. Eighteen healthy adolescent girls With no medical
problems, a negative school screening, and no family history of scolio
sis were control subjects. Patients and control subjects were matched
for age, weight, Tanner stage, sleep duration, and light exposure by m
ultiple linear regression. Nighttime and daytime urine samples were an
alyzed for melatonin by high-performance liquid chromatography. Result
s. Although nighttime melatonin levels were significantly higher than
daytime levels in all volunteers (P < 0.00002), there were no signific
ant differences in nighttime (P > 0.63) or daytime (P > 0.78) melatoni
n levels between patients and control subjects, even after matching by
multiple linear regression analysis. A statistical analysis demonstra
ted that if a melatonin deficiency of 25% or more did exist in patient
s with scoliosis compared with control subjects, the likelihood that i
t would have been detected in this study was more than 98%. Conclusion
. Although melatonin deficiency may cause scoliosis in the chicken, th
is study suggests that it is not a mechanism in the pathogenesis of ad
olescent idiopathic scoliosis in humans.