New Insights in Pathogenesis of Endometriosis

Pietro G Signorile, Rosa Viceconte, Alfonso Baldi
Frontiers in medicine · 2022 · vol. 9 , pp. 879015 · doi:10.3389/fmed.2022.879015 · PMID:35572957 · PMC9095948 · W4224997926
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review revises proposed pathogenetic mechanisms for endometriosis, emphasizing recent evidence linking fetal development alterations to the disease's later onset.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 ⓘ

This paper reviews proposed mechanisms for the pathogenesis of endometriosis, focusing particularly on embryologic theories, and reports that a PubMed systematic search (1957–2021) identified over 3,000 articles with about 200 selected for detailed reading. It summarizes leading hypotheses including retrograde menstruation, coelomic metaplasia, hematogenous/lymphatic spread, and stem cell recruitment, and discusses limitations of retrograde menstruation for deep lesions and extra-peritoneal sites, as well as challenges for cell spread and lack of definitive evidence across models. A key emphasis is that developmental alterations during a critical fetal window may prompt later disease, with embryogenetic persistence of residual Wolffian or Müllerian duct cells suggested to develop into endometriotic lesions in response to estrogen. The paper is limited by its narrative/review design rather than presenting new experimental results, and it notes that the underlying pathogenetic mechanism remains undefined. This paper is centrally about endometriosis — it specifically revises and compares theories of endometriosis pathogenesis with emphasis on an embryologic mechanism.

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Abstract

Endometriosis is a gynecological disease characterized by the growth of endometrial glands and stroma outside the uterine cavity. The incidence of the disease is very high, there are currently no reliable early diagnostic tests, the therapies are only symptomatic and, consequently, the social impact of endometriosis is very important, also considering the related fertility problems. Despite this, the pathogenesis of endometriosis is still not fully defined. Retrograde menstruation and coelomic metaplasia are currently the most recognized pathogenetic hypotheses. Recent experimental evidences generated by our research group and by others have indicated an alteration of the fine-tuning of the female genital system developmental program during a critical window of time in the fetal life as the pathogenetic event prompting to the development of endometriosis later in life. Goal of this article is to present a revision of the recent literature about the different pathogenetic mechanisms proposed for endometriosis with particular emphasis on the embryologic theory. The possible clinical and pathological implications of these findings will be discussed.

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Condition tags

endometriosis

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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