Abstract
Nievelstein and Vermeij-Keers call attention to their work on the normal and abnormal development of the cloaca in relation to anorectal malformations [1,2]. In these studies they confirmed for the greater part new ideas that had emerged from my earlier investigation in normal pig embryos and pig embryos with hereditary congenital anorectal malformations [3,4], and had been related to the human condition [5]. There were also some differences of opinion. Those related to normal development, reiterated in their letter, have been discussed in a preceding monograph about the normal development of the human perineum [6] and were not repeated in the present article [7], which was primarily focused on malformations. In that monograph I have demonstrated that: (1) the cloaca becomes divided into urogenital and anal compartments by the disproportionate growth of the urogenital part over the anal part, and the classical descending urorectal (Letter: urogenital) septum does not exist; (2) the dorsal (anal) part of the cloaca forms the deep part of the permanent anal canal, which is also proven by the zone of typically cloacal pseudostratified columnar epithelium with anal glands at the linea dentata of the definitive anorectum; and (3) a “secondary occlusion” of the anorectal canal is a deceptive phenomenon caused by a high epithelium in a narrow segment of the canal that obscures a (persisting) central lumen.
With secondary occlusion an illusion, defective recanalization cannot be considered as the mechanism responsible for causing a malformed or occluded anus at the normal position (apart from the unlikely process that persistence of a purely epithelial “plug” would lead to the essentially stromal permanent “imperforate anal membrane,” stenosis and buckle handle). The present study points at narrow, occasionally microscopic, canals between the dilated anorectum and the surface, i.e., ectopic anorectal canals, which may disappear later with blind-ending anorectum as a result. The observations disqualify the categorization proposed by the authors.
Their magnetic resonance imaging study, which is impressive from a clinical point of view, was not referred in the present article [7] because it did not provide additional data to the much more detailed histological information of the present investigation.