Idiopathic scoliosis is a common cause of spinal deformity in children and adolescents. Despite extensive studies, the etiology and pathogenesis remain unknown. Idiopathic scoliosis probably results from a multifactorial abnormality involving genetic, biochemical, and neuromuscular factors. Numerous experiments on various animal models and clinical studies have suggested possible anatomic or functional influences for the etiology, but many of them may be epiphenomena rather than etiologic causes. Recently, great emphasis has been placed on the role of the central nervous system. There is mounting evidence that a primary defect of central nervous system function - namely, a defect of posture, proprioception, or equilibrium control -is responsible for the development of scoliosis. More recently, results of studies indicate that calmodulin and/or melatonin are associated with the progression of idiopathic scoliosis. We have found that pinealectomy in chickens consistently produces scoliosis, which had similar anatomic characteristic of human idiopathic scoliosis. In addition, the intramuscular implantation of the pineal gland and interperitoneal injection of melatonin prevented the development of scoliosis. Furthermore, we demonstrated experimentally that induced scoliosis in pinealectomized rats occurs only in bipedal but not in quadrupedal rats.
From our series of experimental studies we have proposed that a defect of melatonin synthesis may contribute to the etiology of experimental scoliosis model in chickens and rats, and bipedal condition may also be an important factor for the development of scoliosis.
In a human study we found significantly decreased integrated concentration of melatonin over a 24-hour period and at night in adolescent idiopathic scolosis patients with progressive curves, while those with stable curves were similar to the control. We postulated that balanced muscle tone controlled by postural reflex is important to maintain normal posture with a straight spine in a bipedal condition. The disturbance of equilibrium and posture mechanism, secondary to a defect of melatonin synthesis, may promote development of rotational lordoscoliosis, especially in bipedal posture.
