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• Eutopic (inside the uterus) and ectopic (outside the uterus) endometria are distinctly different, both morphologically and functionally, which is difficult to reconcile with the notion that endomelriotic implants represent autotransplants of normal endometrial tissue."
Alternatively, circulating stem cells originating from the bone marrow might differentiate into endomelriotic tissue in various locations.01' This may explain how ectopic endometrium can occur in locations outside of the pelvis, such as the lung and central nervous system.
CXCL12, also knowm as stromal cell-derived factor I (SDFI), is a che- mokine involved in regulating cell migration.0* Increased expression of CXCL12 in endomelriotic implants attracts stem cells preferentially to endometriotic lesions, preventing their normal migration to the endometrium.0*-07 CXCR4, a chcmokine receptor, and its ligand CXCL12 not only are important in stem cell recruitment but can also induce angiogenesis and tissue growth.0" CXCR7, another receptor for CXCL12, is increased in inflammation and tumor growth.0' Recently, CXCR7 was found to have increased expression in endomelriotic lesions, where it enhances BMDSC recruitment to lesions and perpetuates their growth.07 Lastly, estrogens enhance recruitment of BMDSCs, through increasing CXCL12; as endometriotic lesions have an increased local estrogenic environment, this provides yet another mechanism by which lesions can further ensure their growth and survival.08
Interventions that reduce ovarian estradiol production are the most reliable ways to cause atrophy of endomelriotic lesions and the most effective treatment for pain.
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