Embryology of the Abdominal Wall and Associated Malformations—A Review

Abstract

In humans, the incidence of congenital defects of the intraembryonic celom and its associated structures has increased over recent decades. Surgical treatment of abdominal and diaphragmatic malformations resulting in congenital hernia requires deep knowledge of ventral body closure and the separation of the primary body cavities during embryogenesis. The correct development of both structures requires the coordinated and fine-tuned synergy of different anlagen, including a set of molecules governing those processes. They have mainly been investigated in a range of vertebrate species (e.g., mouse, birds, and fish), but studies of embryogenesis in humans are rather rare because samples are seldom available. Therefore, we have to deal with a large body of conflicting data concerning the formation of the abdominal wall and the etiology of diaphragmatic defects. This review summarizes the current state of knowledge and focuses on the histological and molecular events leading to the establishment of the abdominal and thoracic cavities in several vertebrate species. In chronological order, we start with the onset of gastrulation, continue with the establishment of the three-dimensional body shape, and end with the partition of body cavities. We also discuss well-known human etiologies.

Y-27632 Impairs Angiogenesis on Extra-Embryonic Vasculature in Post-Gastrulation Chick Embryos

“…Although similar in that both conditions involve herniation of abdominal contents through the ventral body wall, they differ in that omphalocele occurs through the base of the umbilical cord and has a peritoneal covering, whereas gastroschisis occurs usually to the right of the umbilical cord and herniated organs have no peritoneal covering. Both conditions are relatively infrequent, and their exact causes are still unknown [ 3 , 4 ].…”

“…Incomplete development and migration of the lateral plate mesoderm to form the body wall and incomplete differentiation and migration of somitic myotomes to form precursors of the body wall musculature may also contribute. Gene mutations and environmental factors have also been implicated in omphalocele formation [ 3 , 5 , 6 , 7 ].…”

“…The etiology of gastroschisis is reported to be the result of a disruption to blood flow to the developing body wall, leading to deficient development of the affected tissues and subsequently to an intestinal herniation through the defect [ 3 , 8 ]. It has been hypothesized that the abnormal involution of the right umbilical vein in particular leads to impaired growth and viability of the surrounding mesenchyme, which then results in a defect of skin formation in the periumbilical area and subsequent rupture of the intestines through the defect [ 1 , 7 , 9 , 10 ].…”