[Endometriosis: physiopathology and investigation lines (part two)].

Ginecologia y obstetricia de Mexico · 2008 · vol. 76(9) , pp. 549–57 · PMID:18798462 · W2416035154
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AI-generated summary by claude@2026-06, 2026-06-08

This paper reviews endometriosis physiopathology, detailing Sampson's reflux theory and the roles of inflammation, angiogenesis, endocrine factors, genetic, and antioxidant components in its development and manifestations.

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Abstract

Sampson's menstrual reflux theory (1927) is widely accepted as an explanation of endometriosis physiopathology, it proposes five basic necessary processes to its development: adhesion, invasion, recruitment, angiogenesis and proliferation. Several factors and physiologic processes are necessary for the survival and growth of endometrial tissue. Clinical manifestations of these disease are: dysmenorrhoea, dyspareunia, and peritoneal adhesions, that with other findings reveal an inflammatory process that requires cytokines, macrophages, NK cells, lymphocytes and prostaglandins whose qualitative functions may be compromised or may contribute to the peripheral generation of estrogens. Angiogenesis benefits the development of these endometrial tissue foci and probably stimulates several vascular growth factors, and sexual steroids. Endocrine factors are capital for this entity, as is demonstrated by the presence of estrogen receptors in macrophages, fibroblasts and endometrium among others, as well as the clinical symptoms control trough the blockage of the hypothalamus-pituitary-ovary axis. Studies on the genetic and antioxidant factors have revealed key points that may be helpful in determining a proper diagnosis and treatment for endometriosis.

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Condition tags

endometriosisdysmenorrheadyspareunia

MeSH descriptors

Endometriosis Endometriosis Female Hormones Hormones Humans Macrophages Macrophages Neovascularization, Pathologic

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