Siriraj Medical Journal (Aug 2016)
Are There Processes of Occlusion and Recanalization in the Esophageal Development?
Abstract
Background: Esophageal atresia (EA) or stenosis is well known among the congenital abnormalities of the esophagus which may result from the failure or incomplete recanalization after solid stage during the 8th week of human development or deviation of the tracheo-esophageal septum. The occlusion and recanalization theory of gut development cannot explain some types of esophageal atresia. Objective: To study the serial section of continuous stages of esophageal development of chick embryos from related human Carnegie stages 14-23, observe histologically whether there are occlusion and recanalization processes, at which stages and to calculate the mitotic and apoptotic indices of the epithelial lining of the esophageal lumen as well as measuring the lumen areas of each stage of esophageal development. Methods: The fertilized Leghorn hen eggs (Gallus domesticus) were incubated at different time intervals to gain five embryos for each developing stage 14-23. They were processed histologically into serial sections after the total bodies were photographed. The serial sections were observed at the esophageal area by one skipped five sections technique. The length and lumen area were measured, total epithelial cell count, mitotic and apoptotic cell counts were performed and the mitotic and apoptotic indices were calculated. Results: The lengths of the esophagus increased with advanced age from 126.80 ± 3.03 μm at stages 14 to 7, 234.80 ± 396.62 µm at stage 23. The lumen areas decreased from stages 14-16 and increased from stages 17-23. There was no evidence of occlusion at any stage. At the stages of increasing the lumen area there was also no evidence of vacuole formation. The mitotic indices decreased from stages 15-20 and were constant from stage 21-23, which showed no correlation with the lumen area. The apoptotic index was highest at stage 16 which also showed no correlation with the process of recanalization. Conclusion: By studying in the continuous stages of esophageal development, we could not demonstrate histologically the occuluded esophageal lumens, or vacuolation of the lumens at any stage. In the same way, the mitotic and apoptotic indices show no correlation with the lumen area. These results lead to the conclusion that processes of occlusion and recanalization never occur in the normal esophageal development.
