Abstract
The etiopathogenesis of endometriosis is a multifactorial process resulting in a heterogeneous disease. Considering that endometriosis etiology and pathogenesis are still far from being fully elucidated, the current review aims to offer a comprehensive summary of the available evidence. We performed a narrative review synthesizing the findings of the English literature retrieved from computerized databases from inception to June 2019, using the Medical Subject Headings (MeSH) unique ID term “Endometriosis” (ID:D004715) with “Etiology” (ID:Q000209), “Immunology” (ID:Q000276), “Genetics” (ID:D005823) and “Epigenesis, Genetic” (ID:D044127). Endometriosis may origin from Müllerian or non-Müllerian stem cells including those from the endometrial basal layer, Müllerian remnants, bone marrow, or the peritoneum. The innate ability of endometrial stem cells to regenerate cyclically seems to play a key role, as well as the dysregulated hormonal pathways. The presence of such cells in the peritoneal cavity and what leads to the development of endometriosis is a complex process with a large number of interconnected factors, potentially both inherited and acquired. Genetic predisposition is complex and related to the combined action of several genes with limited influence. The epigenetic mechanisms control many of the processes involved in the immunologic, immunohistochemical, histological, and biological aberrations that characterize the eutopic and ectopic endometrium in affected patients. However, what triggers such alterations is not clear and may be both genetically and epigenetically inherited, or it may be acquired by the particular combination of several elements such as the persistent peritoneal menstrual reflux as well as exogenous factors. The heterogeneity of endometriosis and the different contexts in which it develops suggest that a single etiopathogenetic model is not sufficient to explain its complex pathobiology.
Highlights
The etiopathogenesis of endometriosis is a multifactorial process resulting in a heterogeneous disease [1]
The epigenetic mechanisms underlying endometriosis support the processes that promote the acquisition and maintenance of immunologic, immunohistochemical, histological, and biological aberrations that characterize both the eutopic and ectopic endometrium in patients affected by endometriosis
The etiopathogenesis of endometriosis is a multifactorial process that leads to the development of an extremely heterogeneous disease characterized by the variable acquisition and loss of cellular functions
Summary
The etiopathogenesis of endometriosis is a multifactorial process resulting in a heterogeneous disease [1]. The innate ability of endometrial stem cells to regenerate cyclically under the influence of estrogen followed by estrogen/progesterone stimulation and hormonal withdrawal seems to play a key role The presence of such cells in the peritoneal cavity and what leads to the development of endometriosis is a complex process with a large number of interconnected factors potentially both inherited and acquired [2]. The growing body of evidence confirms the multifactorial nature of endometriosis that is the result of the combined contribution of anatomical, hormonal, immunological, reactive, estrogenic, genetic, epigenetic, and environmental factors in affected women [7] These multiple interconnected factors may explain the complex and heterogeneous presentations of the disease with different locations, appearances, developments, and hormone responsiveness. Understanding the multiple pathogenetic pathways underlining the development of endometriosis is of paramount importance, as they may have implications in the prevention, diagnosis, treatment, and prognosis of the disease [6]
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