Nievelstein R A, van der Werff J F, Verbeek F J, Valk J, Vermeij-Keers C
Department of Diagnostic Radiology, Free University Hospital, Amsterdam, The Netherlands.
Teratology. 1998 Feb;57(2):70-8. doi: 10.1002/(SICI)1096-9926(199802)57:2<70::AID-TERA5>3.0.CO;2-A.
In the literature, some controversy still exists about the normal and abnormal development of the human anorectum. Therefore, a three-dimensional and histological study was performed on human embryos. In early anorectal development (< or = 49 days postfertilization), the cloaca plays a crucial role, separated from the amniotic cavity by its cloacal membrane. In the cloaca, the yolk sac/primitive hindgut and allantois/primitive urogenital sinus enter. During the embryonic caudal folding process, incorporation of these structures occurs, including their surrounding extraembryonic mesoderm, which fuses to form the urorectal septum. Consequently, this septum does not grow in the direction of the cloacal membrane, and fusion of these structures is likewise never observed. The cloaca remains as such until the cloacal membrane ruptures by apoptotic cell death. The dorsal part of the cloaca then becomes part of the amniotic cavity, and is by no means involved in the development of the anorectum. The tip of the urorectal septum will become the perineal area. Soon after rupture of the cloacal membrane, during late anorectal development (> or = 49 days postfertilization), a secondary occlusion of the anorectal canal occurs, first due to adhesion, followed by formation of an epithelial "plug" at the level of the anal orifice. Recanalization, by apoptotic cell death, of this secondary occluded anal orifice occurs later during development. Based on these embryological observations, congenital anorectal malformations with an abnormal communication to the exterior are best explained as early embryonic defects. The abnormal communications, usually called fistulae, should be regarded as ectopic anal orifices. Anorectal malformations with the anus in normal position are best explained as late embryonic defects.
在文献中，关于人类肛门直肠的正常和异常发育仍存在一些争议。因此，对人类胚胎进行了三维和组织学研究。在肛门直肠发育早期（受精后≤49天），泄殖腔起着关键作用，其泄殖腔膜将其与羊膜腔分隔开。在泄殖腔内，卵黄囊/原始后肠和尿囊/原始泌尿生殖窦进入。在胚胎尾侧折叠过程中，这些结构包括其周围的胚外中胚层会合并，融合形成尿直肠隔。因此，这个隔不会朝着泄殖腔膜的方向生长，同样也从未观察到这些结构的融合。泄殖腔一直保持这样，直到泄殖腔膜通过凋亡性细胞死亡破裂。泄殖腔的背侧部分随后成为羊膜腔的一部分，绝不参与肛门直肠的发育。尿直肠隔的尖端将成为会阴区域。在泄殖腔膜破裂后不久，在肛门直肠发育后期（受精后≥49天），肛管会发生继发性闭塞，首先是由于粘连，随后在肛门开口处形成上皮“栓”。在发育后期，这个继发性闭塞的肛门开口会通过凋亡性细胞死亡进行再通。基于这些胚胎学观察结果，与外界有异常连通的先天性肛门直肠畸形最好解释为早期胚胎缺陷。通常称为瘘管的异常连通应被视为异位肛门开口。肛门位置正常的肛门直肠畸形最好解释为晚期胚胎缺陷。
