Pathogenesis of Bowel Endometriosis

Jessica Ottolina, Ludovica Bartiromo, Matteo Schimberni, Paola Viganò, Massimo Candiani
In: Clinical Management of Bowel Endometriosis · 2020 · pp. 3–11 · doi:10.1007/978-3-030-50446-5_1 · W3083622689
book-chapter OA: closed CC0
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-07 ⓘ

Intestinal endometriosis, the most common extra-pelvic site, involves fibrosis driven by myofibroblasts, smooth muscle cells, TGF-β, and collagen deposition, with endometrial tissue being a minor component in deep lesions.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

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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Condition tags

endometriosisbowel_endometriosis

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