Pathogenesis of endometriosis

Emre Seli, Seli E, Murat Berkkanoglu, Murat Berkkanoğlu, Aydın Arıcı, Arici A, Aydin Arici
Obstetrics and Gynecology Clinics of North America · 2003 · vol. 30(1) , pp. 41–61 · doi:10.1016/s0889-8545(02)00052-9 · PMID:12699257 · W4211184040
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This paper investigates the underlying biological mechanisms and processes that contribute to the development and progression of endometriosis in affected individuals.

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Abstract

Endometriosis is a common gynecologic disorder characterized by the presence of endometrial tissue outside the uterine cavity. Various theories have been put forth to explain the mechanisms for the development of this disease. Although no single theory can explain all cases of endometriosis, the retrograde menstruation theory has gained the widest acceptance. This theory proposes that viable endometrial tissue is refluxed through the fallopian tubes during menstruation and implants on peritoneal surface or pelvic organs. Retrograde menstruation occurs in 76% to 90% of women. The much lower prevalence of endometriosis suggests that additional factors determine susceptibility to endometriosis. Once in the peritoneal cavity, the survival and implantation of endometrial cells seem to be mediated by abnormal MMP and TIMP expression, altered immune milieu, aberrant local aromatase activity, and genetic and environmental factors.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Female Humans

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

europepmc
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openalex
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License: CC0 · commercial use OK