ABSTRACT
The etiology of the amniotic band syndrome is unknown, and has been subject of debate since the time of Hippocrates. The most accepted theories fail to cover all the abnomalities found in affected children. During organogenesis the epithelial-mesenchymal transition process (EMTP) participates in adequate formation of different organs from three embryo layers. Altered activation of EMTP occurs when the epithelial homeostasis is disturbed, the resulting myofibroblasts are able to secrete extracellular matrix proteins and deposit them on the tissues contributing to a fibrotic phenotype. If injury occurs during organogenesis, wound healing could be exaggerated and fibrotic response could be triggered. The molecule that regulates both of these processes (EMTP and fibrosis) is the transforming growth factor ß (TGFß); indeed null animals for TGFß isoforms show similar defects than those seen in the amniotic band syndrome. Based on documented evidence this review intends to explain how the epithelial mesenchymal transition process may contribute to the pathogenesis of amniotic band syndrome.
