Pathogenesis of uterine adenomyosis: invagination or metaplasia?

被引:241
作者
Garcia-Solares, Javier [1 ]
Donnez, Jacques [2 ]
Donnez, Olivier [3 ]
Dolmans, Marie-Madeleine [1 ,4 ]
机构
[1] Catholic Univ Louvain, Inst Rech Expt, Pole Rech Gynecol, Brussels, Belgium
[2] Soc Rech Infertil, Brussels, Belgium
[3] Polyclin Urbain V, ELSAN Grp, Inst Sein & Chirurg Gynecol Avignon, Avignon, France
[4] Clin Univ St Luc, Dept Gynecol, Brussels, Belgium
关键词
Tissue injury and repair; stem cells; Mullerian remnants; epithelial-mesenchymal transition; collective cell migration; EPITHELIAL-MESENCHYMAL TRANSITION; MYOMETRIAL JUNCTIONAL ZONE; RECTOVAGINAL SEPTUM; MATRIX METALLOPROTEINASE-2; NORMAL ENDOMETRIUM; STEM-CELLS; GENERALIZED HYPERALGESIA; PERITONEAL ENDOMETRIOSIS; SYMPTOMATIC ADENOMYOSIS; PHTHALATE EXPOSURE;
D O I
10.1016/j.fertnstert.2017.12.030
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
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 Mullerian 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. (C) 2018 by American Society for Reproductive Medicine.
引用
收藏
页码:371 / 379
页数:9
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