ENDOMETRIOSIS: A REVIEW OF ITS PATHOGENESIS

Deventer Ziekenhuis
1997 · W2556392052
Review OA: closed CC0 Metadata only
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This review discusses theories of endometriosis pathogenesis, including retrograde implantation, peritoneal mesothelial cell transformation, and the balance between retrograde menstruation and the body's defense mechanisms.

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Abstract

Although peritoneal endometriosis was recognizedin 1860, its pathogenesis still remains unclear. Severaltheories attempt to explain the pathogenesis of this condition.From these, the implantation theory maintains that peritonealendometriosis is the result of implantation and subsequentgrowth of retrogradely shed viable endometrial cells. Basedon a second theory, the peritoneal mesothelium transforms toan endometrium-like tissue under the influence of products ofregurgitated endometrium (induction). Cell adhesionmolecules could be functionally involved in the binding of theendometrial cells to the peritoneal lining. In peritonealendometriosis, a delicate equilibrium seems to exist betweenattacking forces (retrograde menstruation) and the defensemechanisms. On one hand, the amount and the nature of theregurgitated menstrual debris seems important to thedevelopment of the disease. On the other hand, the activeintra-abdominal milieu may be involved. This milieu probablyconverts the regurgitated endometrial tissue into single cellsvia loss of functional cell adhesion properties. Endometriosismay result form the impairment of the function of theperitoneal milieu in disposing of the regurgitated cells.Alternatively, the endometriosis may occur if the number ofregurgitated cells is too large. An intact peritoneal lining maybe an important additional line of defense in preventing thebinding of the endometrial cells. Endometriosis is likely todevelop if such defense mechanisms fail. . Here, the scientificbasis of the endometriosis theories is discussed.

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Condition tags

endometriosis

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (38)

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