PATHOGENESIS OF ENDOMETRIOSIS

Engin Oral, E Oral, A Arici, Aydın Arıcı
Obstetrics and gynecology clinics of North America · 1997 · vol. 24(2) , pp. 219–233 · doi:10.1016/s0889-8545(05)70301-6 · PMID:9163764 · W2125165447
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⚙ AI-generated summary by claude@2026-06, 2026-06-06 ⓘ

This review discusses endometriosis pathogenesis, citing retrograde endometrial dissemination or in situ metaplasia, possibly influenced by genetics and hormones, and involving peritoneal immune cells and their secretions.

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Abstract

This article reviews the pathogenesis of endometriosis, which involves retrograde dissemination of endometrium and/or development in situ by metaplasia, and there is evidence suggesting that genetic and hormonal factors may play a role. There is also substantial evidence that immunologic factors, namely peritoneal macrophages, T cells, natural killer cells, and soluble products secreted by these cells, are involved in the pathogenesis of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Antibody Formation Ascitic Fluid Ascitic Fluid Endometriosis Endometriosis Endometriosis Female Humans Immunity, Cellular Integrins Integrins Menstruation Risk Factors

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.

References (100)

Cited by (50)

Source provenance

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License: CC0 · commercial use OK