Cited by 344Endometriosis Research and TreatmentUterine Myomas and TreatmentsGynecological conditions and treatments

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Pathogenesis of uterine adenomyosis, invagination or metaplasia?

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García-Solares, Javier, Donnez, Jacques, Donnez, Olivier, Dolmans, Marie-Madeleine·2018·Fertility and Sterility

DOI 10.1016/j.fertnstert.2017.12.030

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Abstract

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.

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Authors: García-Solares, J., Donnez, J., Donnez, O., & Dolmans, M.-M.
Affiliations: UCLouvain (BE)
Cliniques Universitaires Saint-Luc (BE)
Corresponding author: Dolmans, Marie-Madeleine
ORCID: Donnez, Jacques
Donnez, Olivier
Dolmans, Marie-Madeleine
Venue: Fertility and Sterility
Publisher: Elsevier BV
Published: 2018-03
Volume: 109
Issue: 3
Pages: 371-379
ISSN: 0015-0282 (ISSN-L)
DOI: 10.1016/j.fertnstert.2017.12.030
OpenAlex: W2794246050
Cited by: 339
References: 100
Citations by year: 2026: 39 · 2025: 46 · 2024: 33 · 2023: 48 · 2022: 57 · 2021: 53 · 2020: 41 · 2019: 17 · 2018: 4
FWCI: 4.55
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1548 d)
Locations: Fertility and Sterility (publishedVersion)
PubMed (publishedVersion)
Digital Access to Libraries (Université catholique de Louvain (UCL), l'Université de Namur (UNamur) and the Université Saint-Louis (USL-B)) (submittedVersion)
Topics: Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
Health Sciences › Medicine › Obstetrics and Gynecology › Uterine Myomas and Treatments
Health Sciences › Medicine › Obstetrics and Gynecology › Gynecological conditions and treatments
Keywords: adenomyosis, pathogenesis, metaplasia, Müllerian remnants, stem cell differentiation, epithelial-mesenchymal transition, collective cell migration, baboon model, myometrium, estrogen-dependent disease
MeSH terms: Animals, Cell Movement, Estradiol, Female, Humans, Metaplasia, Mullerian Ducts, Time Factors, Uterine Diseases, Uterus, Signal Transduction, Disease Progression, Pluripotent Stem Cells, Epigenesis, Genetic, Embryonic Stem Cells, Adult Stem Cells, Epithelial-Mesenchymal Transition, Adenomyosis

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Pathogenesis of uterine adenomyosis, invagination or metaplasia?

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