[External endometriosis: histogenesis, etiology and natural course].

A Audebert, A J Audebert
La Revue du praticien · 1990 · vol. 40(12) , pp. 1077–81 · PMID:2345849 · W2412339686
article OA: closed CC0 ⤵ 11 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This paper reviews theories on endometriosis histogenesis, including coelomic metaplasia and endometrial dissemination, alongside contributing factors like menstrual reflux and hormonal influences, to better understand its natural course and treatment.

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Abstract

Since the initial description of endometriosis, several histogenetic theories have been put forward. Endometriosis has been attributed either to coelomic metaplasia, or to embryonic remnants or to the dissemination by various routes and subsequent grafting of endometrial fragments; this would explain the different anatomical locations of the disease as found clinically. Several contributing factors are also involved, including menstrual reflux or, more hypothetically, disturbances of local hormonal conditions, familial and genetic factors and possibly immune disorders. The role played by these factors has been demonstrated by clinical, epidemiological or experimental studies. Owing to our knowledge of histogenesis and of the aetiological factors involved in the development of endometriosis, the risk factors of the disease and its natural history are now better understood, and a better approach to its treatment will perhaps be found in the near future.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometriosis Endometriosis Endometriosis Female Humans Time 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.

Cited by (11)

Source provenance

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