Pathogenesis of bowel endometriosis

The pathogenesis of bowel endometriosis is multifactorial. There is a predilection for disease of the rectum/sigmoid colon because refluxed endometrium is more likely to settle in the pouch of Douglas and its movement is delimited by the sigmoid colon, in addition to the close proximity of the rectum/sigmoid to posterior extrinsic uterine adenomyosis and to ovarian endometriomas. Once situated, deep bowel endometriosis has features of invasion, angiogenesis, and fibrosis (repeated tissue injury and repair), with emerging research on oxidative stress and the microbiome. Furthermore, deep bowel endometriosis is associated with neurogenesis and/or the recruitment of local nerve fibers and is capable of invading existing nerves, which in turn may also promote fibrosis. Recently, somatic cancer driver mutations (e.g., in KRAS) were identified in deep bowel endometriosis, which may play a role in the genetic/epigenetic theory of endometriosis. In the future, it is possible that bowel endometriosis could be classified based on molecular features. (c) 2021 Elsevier Ltd. All rights reserved.

Automated summary

The pathogenesis of bowel endometriosis is multifactorial and involves factors such as reflux of endometrium, uterine attachment rupture and fibrosis, oxidative stress, microbiome, neurogenesis, nerve fiber recruitment, and genetic mutations. Bowel endometriosis may be classified based on molecular features in the future.