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Pathogenesis of uterine adenomyosis: invagination or metaplasia?

https://doi.org/10.1016/j.fertnstert.2017.12.030Get rights and content
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Adenomyosis is a commonly diagnosed estrogen-dependent gynecological disorder that causes pelvic pain, abnormal uterine bleeding, and infertility. Despite its prevalence and severity of symptoms, its pathogenesis and etiology have not yet been elucidated. The aim of this manuscript is to review the different hypotheses on the origin of adenomyotic lesions and the mechanisms involved in the evolution and progression of the disease. Two main theories have been proposed to explain the origin of adenomyosis. The most common suggests involvement of tissue injury and the repair mechanism and claims that adenomyosis results from invagination of the endometrial basalis into the myometrium. An alternative theory maintains that adenomyotic lesions result from metaplasia of displaced embryonic pluripotent Müllerian remnants or differentiation of adult stem cells. Previous investigations performed in human adenomyotic lesions and corroborated by studies in mice supported the involvement of the epithelial-mesenchymal transition process in the early stages of progression and spread of adenomyosis. However, studies conducted in a recently developed baboon model indicate that collective cell migration may be implicated in the later events of invasion. This suggests that the invasiveness of this complex uterine disorder is not driven by a single mechanism of migration but by a time-dependent combination of two processes.

Key Words

Tissue injury and repair
stem cells
Müllerian remnants
epithelial-mesenchymal transition
collective cell migration

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J.G.-S. has nothing to disclose. J.D. has been a member of the Scientific Advisory Board of PregLem S.A. since 2007. He receives grants and fees for lectures and coverage of travel expenses to investigator meetings of PEARL studies from the Gedeon Richter Group. O.D. receives grants and fees for lectures and coverage of travel expenses to investigator meetings of PEARL studies from the Gedeon Richter Group. M.-M.D. has no conflict of interest in relation to the paper, but her salary is partially (50%) paid by the Fonds National de la Recherche Scientifique de Belgique-FNRS for grant no. 5/4/150/5.