Endometriosis a review of its pathogenesis

Paul J.Q. van der Linden, P J van der Linden, van der Linden PJ
Frontiers in Bioscience · 1997 · vol. 2(5) , pp. e48–52 · doi:10.2741/a226 · PMID:9254645 · W2412391948
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This review discusses theories on endometriosis pathogenesis, focusing on endometrial cell implantation, peritoneal mesothelium induction, and the balance between retrograde menstruation and abdominal defense mechanisms.

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Abstract

Although peritoneal endometriosis was recognized in 1860, its pathogenesis still remains unclear. Several theories attempt to explain the pathogenesis of this condition. From these, the implantation theory maintains that peritoneal endometriosis is the result of implantation and subsequent growth of retrogradely shed viable endometrial cells. Based on a second theory, the peritoneal mesothelium transforms to an endometrium-like tissue under the influence of products of regurgitated endometrium (induction). Cell adhesion molecules could be functionally involved in the binding of the endometrial cells to the peritoneal lining. In peritoneal endometriosis, a delicate equilibrium seems to exist between attacking forces (retrograde menstruation) and the defense mechanisms. On one hand, the amount and the nature of the regurgitated menstrual debris seems important to the development of the disease. On the other hand, the active intra-abdominal milieu may be involved. This milieu probably converts the regurgitated endometrial tissue into single cells via loss of functional cell adhesion properties. Endometriosis may result form the impairment of the function of the peritoneal milieu in disposing of the regurgitated cells. Alternatively, the endometriosis may occur if the number of regurgitated cells is too large. An intact peritoneal lining may be an important additional line of defense in preventing the binding of the endometrial cells. Endometriosis is likely to develop if such defense mechanisms fail. Here, the scientific basis of the endometriosis theories is discussed.
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Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience. ENDOMETRIOSIS: A REVIEW OF ITS PATHOGENESIS 1 Deventer Ziekenhuis, Department of Obstetrics and Gynecology, P.O. Box 5001, 7400 GC Deventer, The Netherlands Abstract Although peritoneal endometriosis was recognized in 1860, its pathogenesis still remains unclear. Several theories attempt to explain the pathogenesis of this condition. From these, the implantation theory maintains that peritoneal endometriosis is the result of implantation and subsequent growth of retrogradely shed viable endometrial cells. Based on a second theory, the peritoneal mesothelium transforms to an endometrium-like tissue under the influence of products of regurgitated endometrium (induction). Cell adhesion molecules could be functionally involved in the binding of the endometrial cells to the peritoneal lining. In peritoneal endometriosis, a delicate equilibrium seems to exist between attacking forces (retrograde menstruation) and the defense mechanisms. On one hand, the amount and the nature of the regurgitated menstrual debris seems important to the development of the disease. On the other hand, the active intra-abdominal milieu may be involved. This milieu probably converts the regurgitated endometrial tissue into single cells via loss of functional cell adhesion properties. Endometriosis may result form the impairment of the function of the peritoneal milieu in disposing of the regurgitated cells. Alternatively, the endometriosis may occur if the number of regurgitated cells is too large. An intact peritoneal lining may be an important additional line of defense in preventing the binding of the endometrial cells. Endometriosis is likely to develop if such defense mechanisms fail. Here, the scientific basis of the endometriosis theories is discussed.

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Condition tags

endometriosis

MeSH descriptors

Cell Adhesion Endometriosis Endometrium Endometriosis Endometrium Female Humans Menstruation Disturbances Models, Theoretical

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.

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