This dissertation, "Role of Pineal Gland and Melatonin in the Development of Scoliosis" by M C, Kenneth, Cheung, 張文智, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: ABSTRACT A central etiology for idiopathic scoliosis has never been established. This together with the absence of an appropriate animal model hampers research in this area. Recently, there has been great interest in the effect of pinealectomy in new born chickens, resulting in scoliosis that closely resembles adolescent idiopathic scoliosis. Published data suggested that pinealectomy, loss of melatonin secretion and a bipedal posture are important elements in the development of scoliosis in lower animal models. The findings in the lower animal models would make more sense if these could be reproduced in a model closely resembling humans. If pinealectomy produced scoliosis in a bipedal non-human primate model such as rhesus monkeys, the findings in chickens could be related to human beings, and it would serve as a good model for studying the mechanism of scoliosis development in the future. It has been shown that strong light can suppress the circadian release of melatonin from the pineal gland in chickens; however it is not known whether this alone can result in scoliosis. A non-invasive procedure being the priority for the primate model, the first study was undertaken to compare the effect of suppression of melatonin secretion by bright light in chickens with ithat of surgical pinealectomy. It was found that none of the chickens subjected to constant light developed scoliosis, placing doubt on the role of melatonin as the sole etiological factor and suggesting that the surgical operation itself is important. Therefore, constant light could not be used in primates to suppress melatonin production in order for them to develop scoliosis, but do argue against pursuing this method of altering melatonin production as a way to induce scoliosis. As part of the above work, a detailed anatomic study of the scoliotic chicken spines was carried out which formed our second study. Contrary to the literature, radiographs of the chicken spines with all soft tissues removed revealed that all the curves were thoracolumbar with structural changes including lordosis, rotation, and wedging, which was further confirmed by computed tomography imaging. However, the reason why scoliosis does not develop in all pinealectomized chickens is still unknown. Our third study investigated the binding properties of melatonin receptors in the thoracic spinal cord. Changes were detected in melatonin receptor binding after pinealectomy but regardless of the development of scoliosis. Thus, neither low serum melatonin level nor changes in spinal cord melatonin binding can be a sole etiologic factor in the pathogenesis of scoliosis in pinealectomized chickens. iiPinealectomy being the essential criterion for the production of scoliosis, our fourth study was undertaken to evaluate whether pinealectomy in rhesus monkeys will result in the development of scoliosis. Only some of the pinealectomised monkeys demonstrated a loss of melatonin secretion and none had developed scoliosis, suggesting that the possible etiologic factors producing idiopathic scoliosis in lower animals are different from primates, and cannot necessarily be extrapolated to human beings. Overall, these series of studies would suggest that melatonin suppression by pinealectomy is not a direct cause of scoliosis, and its relevance as an etiological factor in humans still needs to be proven. Further work on establishin