Pathogenesis of Bowel Endometriosis

In: Clinical Management of Bowel Endometriosis · 2020 · pp. 3–11 · doi:10.1007/978-3-030-50446-5_1 · W3083622689
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Deep pelvic endometriosis, particularly intestinal involvement, is characterized by fibrosis and the action of myofibroblasts, smooth muscle cells, TGF-β, and collagen deposition.

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The paper reviews the pathogenesis of deep pelvic (including bowel) endometriosis, describing its defining feature as endometriotic lesions extending more than 5 mm under the peritoneum and detailing common intestinal sites such as the rectovaginal septum, recto-sigmoid region, rectum, ileum, appendix, and cecum. It synthesizes several proposed mechanisms—retrograde menstruation, coelomic remnants metaplasia, and a stem cell model—while also noting a role for genetic susceptibility and emphasizing histologic and profibrotic processes (e.g., myofibroblast/smooth muscle involvement, TGF-β, epithelial-to-mesenchymal transition, transdifferentiation, and collagen deposition) in disease progression; a major caveat is that endometrial-like tissue is reported as a minor component of deep lesions, limiting how directly classic endometrial elements explain the lesion microenvironment. The paper does not explicitly discuss adenomyosis in a central experimental or population framework. This paper is centrally about endometriosis — specifically the pathogenesis and profibrotic mechanisms of deep pelvic and bowel endometriosis.

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Abstract

Deep pelvic endometriosis is a specific entity defined by endometriotic lesions extending more than 5 mm under the peritoneum, including the infiltrative forms involving vital structures, such as the bowel, ureters, bladder, and rectovaginal lesions. Intestinal endometriosis is the most common extra-pelvic site and involves more frequently the rectovaginal septum, the recto-sigmoid followed by the rectum, ileum, appendix, and cecum. Several theories have been proposed for the pathogenesis of deep pelvic endometriosis: the retrograde menstruation theory, the theory of coelomic remnants metaplasia and the stem cells theory. In addition, genetic factors seem to play a role on individual’s susceptibility to endometriosis. In the last years, advances in knowledge regarding the histological definition of endometriosis occurred, introducing the profibrotic nature of the disease inside its “new” definition. In general, the natural history of endometriosis toward fibrosis resembles that characteristic of other fibrotic disease, involving myofibroblast and smooth muscle cell action, as well as the production of high levels of Transforming Growth Factor (TGF)-β, epithelial-to-mesenchymal transition, fibroblast-to-myofibroblast transdifferentiation and finally collagen deposition. In line with these concepts, histologic analyses show that in deep lesions, endometrial-like tissue represents a minor component. Access this chapter Tax calculation will be finalised at checkout Purchases are for personal use only Similar content being viewed by others

References

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Author information Authors and Affiliations Corresponding author Editor information Editors and Affiliations Rights and permissions Copyright information © 2020 Springer Nature Switzerland AG About this chapter Cite this chapter Ottolina, J., Bartiromo, L., Schimberni, M., Viganò, P., Candiani, M. (2020). Pathogenesis of Bowel Endometriosis. In: Ferrero, S., Ceccaroni, M. (eds) Clinical Management of Bowel Endometriosis. Springer, Cham. https://doi.org/10.1007/978-3-030-50446-5_1 Download citation DOI: https://doi.org/10.1007/978-3-030-50446-5_1 Published: Publisher Name: Springer, Cham Print ISBN: 978-3-030-50445-8 Online ISBN: 978-3-030-50446-5 eBook Packages: MedicineMedicine (R0)

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