| pubmed-article:7067031 | pubmed:abstractText | In 1976, we decided to review the files of the scoliosis clinic at Ste-Justine Hospital in Montreal. We found 2,237 patients with scoliosis, 212 of them are classified as congenital. At this time, congenital scoliosis were the major unresolved problems. We decided to look at an experimental model, to study the physio-pathological mechanism of the induction of these malformations. We chose the mouse as the experimental animal, and "hypobaric hypoxia" as the teratogenic agent. With this model, we can produce, malformations at different levels of the spine, if we treat at different days of pregnancy. For example, if we treat the mothers in the 10th day of her pregnancy, we get 90% of malformed embryos, at the lumbar level. All the malformations reproduced in the mice, are similar to those found in humans. We have also demonstrated no difference in the morphology of these malformations from birth to maturity, in contradiction with Epstein, who said that the majority of cleft vertebrae will disappear with bone maturation. We have also demonstrated that these malformations are present in the cartilaginous stage of development of the vertebral column. Our findings are in contradiction with Nassim's who stated, that congenital vertebral malformations are produced by an abnormal ossification process on a normal cartilage primum. Finally, our findings are in agreements with those of Dr. Uhthoff, who showed that congenital vertebral malformations are present in cartilaginous stage of development in human embryos. | lld:pubmed |
