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Endometriosis: harmful survival of an ectopic tissue
Janos Garai1,Valeria Molnar1,Tamas Varga1,Miklos Koppan1,Attila Torok1,Jozsef Bodis1
1
Department of Pathophysiology, Faculty of Medicine, University of Pecs, Hungary. janos.garai@aok.pte.hu
DOI: 10.2741/1821 Volume 11 Issue 1, pp.595-619
Published: 01 January 2006
Abstract

Endometriosis results from implantation of endometrial tissue outside the uterine cavity. Endometriosis might remain asymptomatic and discovered accidentally. However, it may cause symptoms, which include chronic pelvic pain, bleeding, infertility, and increases susceptibility to development of adenocarcinoma. The most prevailing hypothesis is that endometriosis results from implantation of endometrial tissue that gains access to peritoneal cavity by retrograde flow during menstruation. The factors contributing to the establishment and persistence of the endometriotic lesions (plaques) most probably include abnormalities of the genital tract, genetic predisposition, hormonal imbalance, altered immune surveillance, inflammatory response and abnormal regulation of the endometrial cells. The mediators that contribute to survival and progression of endometriosis are likely involved in the development of the symptoms of this process. Genomic studies have started to delineate the wide array of mediators involved and the complex genetic background required in the development of endometriosis. This review summarizes our current knowledge regarding the pathogenesis of endometriosis, including progress made with transgenic animals, and a clinical perspective on the diagnosis and management of this common process.

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Janos Garai, Valeria Molnar, Tamas Varga, Miklos Koppan, Attila Torok, Jozsef Bodis. Endometriosis: harmful survival of an ectopic tissue. Frontiers in Bioscience-Landmark. 2006. 11(1); 595-619.