Jean Ouellet1, Thierry Odent. 1. McGill Scoliosis and Spinal Research Chair, Deputy Chief Shriners Hospital, Montreal, Canada. jean.ouellet@Muhc.mcgill.com
Abstract
PURPOSE: The purpose of this study was to provide the readers with a reliable source of animal models currently being utilized to perform state-of-the-art scoliotic research. MATERIALS AND METHODS: A comprehensive search was undertaken to review all publications on animal models for the study of scoliosis within the database from 1946 to January 2011. RESULTS: The animal models have been grouped under specific headings reflecting the underlying pathophysiology behind the development of the spinal deformities produced in the animals: genetics, neuroendocrine, neuromuscular, external constraints, internal constraints with or without tissue injury, vertebral growth modulation and iatrogenic congenital malformations, in an attempt to organize and classify these multiple scoliotic animal models. As it stands, there are no animal models that mimic the human spinal anatomy with all its constraints and weaknesses, which puts it at risk of developing scoliosis. What we do have are a multitude of models, which produce spinal deformities that come close to the idiopathic scoliosis deformity. CONCLUSION: All these different animal models compel us to believe that the clinical phenotype of what we call idiopathic scoliosis may well be caused by a variety of different underlying pathologies.
PURPOSE: The purpose of this study was to provide the readers with a reliable source of animal models currently being utilized to perform state-of-the-art scoliotic research. MATERIALS AND METHODS: A comprehensive search was undertaken to review all publications on animal models for the study of scoliosis within the database from 1946 to January 2011. RESULTS: The animal models have been grouped under specific headings reflecting the underlying pathophysiology behind the development of the spinal deformities produced in the animals: genetics, neuroendocrine, neuromuscular, external constraints, internal constraints with or without tissue injury, vertebral growth modulation and iatrogenic congenital malformations, in an attempt to organize and classify these multiple scoliotic animal models. As it stands, there are no animal models that mimic the human spinal anatomy with all its constraints and weaknesses, which puts it at risk of developing scoliosis. What we do have are a multitude of models, which produce spinal deformities that come close to the idiopathic scoliosis deformity. CONCLUSION: All these different animal models compel us to believe that the clinical phenotype of what we call idiopathic scoliosis may well be caused by a variety of different underlying pathologies.
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