Etiopathology of Endometriosis

J. Bontis, J N Bontis, Dimitrios Vavilis, D T Vavilis
Annals of the New York Academy of Sciences · 1997 · vol. 816(1) , pp. 305–309 · doi:10.1111/j.1749-6632.1997.tb52155.x · PMID:9238281 · W2018568129
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This paper reviews proposed theories for endometriosis, including celomic metaplasia, transplantation, induction, and immune system dysfunction, noting that additional factors may influence disease expression.

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Abstract

Although endometriosis is one of the most frequent problems in gynecology, its pathogenesis remains controversial and poorly understood. Many theories relating to the etiopathology of this disorder have been proposed. The celomic metaplasia hypothesis states that peritoneal mesothelium undergoes metaplasia, forming typical endometrial-like glands and stroma. The transplantation theory suggests implantation and subsequent growth of retrogradely shed, viable endometrial cells. The induction theory states that unknown substances released from shed endometrium induce undifferentiated mesenchyma to form endometriotic tissue. Regardless of which theory is correct, additional factors may be responsible for the expression of the disease. The possibility that the development and progression of endometriosis is associated with abnormal immune function and an inadequate response of the peritoneal defense system is currently the most recent hypothesis for the etiopathology of this disease.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Endometriosis Adolescent Adult 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 (21)

Cited by (14)

Source provenance

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