Theories of endometriosis

Vinatier D; D. Vinatier; Orazi G; G. Orazi; M Cosson; Cosson M; Michel Cosson; P. Dufour; Dufour P

doi:10.1016/s0301-2115(00)00405-x

Theories of endometriosis

Vinatier D, D. Vinatier, Orazi G, G. Orazi, M Cosson, Cosson M, Michel Cosson, P. Dufour, Dufour P

European journal of obstetrics, gynecology, and reproductive biology · 2001 · vol. 96(1) , pp. 21–34 · doi:10.1016/s0301-2115(00)00405-x · PMID:11311757 · W2048386911

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This paper reviews current theories regarding the pathogenesis of endometriosis, exploring potential cellular and molecular mechanisms underlying its development.

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Abstract

Endometriosis is characterised by the presence of abnormally located tissue resembling the endometrium with glands and stroma. Several hypotheses have attempted to explain the development of such tissue. The oldest theory, that of metaplasia, suggests that under diverse influences coelomic tissue could be transformed into endometrium. The most often cited theory, that of implantation, proposes that the physiological phenomenon of endometrial reflux in the fallopian tubes during menstruation may, in certain conditions, overcome local defense mechanisms, implant, and proliferate. The peritoneal fluid in unaffected women possesses the capacity to prevent endometriotic tissue from becoming established. The reasons for the occurrence of endometriosis and its consequences (pain, sterility, adhesions) are probably numerous and involve the endometrium, the immune system (macrophages, natural killer cells), the peritoneum, and fallopian tubes. The failure to clear the peritoneal cavity of fragments of endometrium could cause a state of local inflammation with hyperactivation of macrophages secreting a variety of different compounds. Some of these compounds may bring about metaplasia of the peritoneum or the development of Mullerian residues.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometrium Apoptosis Cell Division Endometriosis Endometriosis Endometriosis Endometrium Endometrium Estrogens Estrogens Female Heat-Shock Proteins Heat-Shock Proteins Humans Immune System Immune System Neovascularization, Pathologic Peritoneum Peritoneum

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References (100)

Cited by (50)

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