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Pathological mechanism of idiopathic scoliosis: experimental scoliosis in pinealectomized rats

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Abstract

The pathological mechanism of curve progression in idiopathic scoliosis is still obscure. In this study we investigated the pathological mechanism of idiopathic scoliosis in experimentally induced scoliosis in rats. A total 30 rats were divided into three groups: ten bipedal rats with a sham operation, which served as the control; ten quadrupedal rats with pinealectomy; and ten bipedal rats with pinealectomy. Scoliosis developed only in pinealectomized bipedal rats and not in pinealectomized quadrupedal rats. Cervicothoracic lordosis developed in bipedal rats with or without pinealectomy. These deformities of lordoscoliosis in pinealectomized bipedal rats were similar to human idiopathic scoliosis. Lordosis or lordotic tendency was sufficient to cause the spine to rotate to the side. Rotational instability of the spine with rotation of lordotic segment appears to produce a characteristic scoliotic deformity as a secondary phenomenon. Our findings suggest that lordosis may develop in bipedal rats, but pinealectomy is required for the development of lordoscoliosis. Balanced muscle tone controlled by the postural reflex is important to maintain normal posture with a straight spine in the bipedal condition. The disturbance of equilibrium and other postural mechanisms secondary to a deficiency of melatonin after pinealectomy may promote development of lordoscoliosis with vertebral rotation especially in the bipedal posture.

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Acknowledgements

This study was conducted at the Department of Orthopaedic Surgery, Nihon University School of Medicine, Tokyo, Japan. None of the authors received financial support for this study.

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Correspondence to Masafumi Machida.

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Machida, M., Saito, M., Dubousset, J. et al. Pathological mechanism of idiopathic scoliosis: experimental scoliosis in pinealectomized rats. Eur Spine J 14, 843–848 (2005). https://doi.org/10.1007/s00586-004-0806-1

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  • DOI: https://doi.org/10.1007/s00586-004-0806-1

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