Ovarian Endometriosis and Adenomyosis—Relevance, Pathophysiology of Ectopic Endometrium and Impact on Dysfunction of Eutopic Endometrium: A Narrative Review

Л.М. Михалева, Mekan R. Orazov, Evgeny D. Dolgov, S.A. Mikhalev, Z.V. Gioeva, A. V. Ilyichev, Н. Б. Тихонова, Lolita S. Bulatova
In: Biomedicines · 2026 · vol. 14(6) , pp. 1343 · doi:10.3390/biomedicines14061343 · W7164742572
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Abstract

A trend toward comorbid conditions is seen in around 50% of gynecological patients, with a significant contribution made by endometriosis as a common and incurable gynecological condition. Over the last decades, the global burdens of different forms of endometriosis have shown a progressive increase, while their diagnosis and management present persistent and significant challenges. Currently, endometriosis is divided into two primary types: genital (adenomyosis and external genital endometriosis, including ovarian endometriosis) and extragenital endometriosis. Regardless of the location of endometriosis, lesions or ectopic endometrium follow a consistent pathological process characterized by active proliferation, local inflammation, neoangiogenesis, and extracellular matrix remodeling. These pathogenetic patterns are associated not only with process progression, but also with the impact on the eutopic endometrium. External genital or extragenital endometriosis and adenomyosis (an internal genital endometriosis) are currently considered as a major cause of infertility and implantation failures due to the negative impact on the eutopic endometrium. However, it has been proven that the pathogenetic pathways for the development of eutopic endometrium dysfunction in these endometriosis phenotypes (despite the common pathophysiology of the ectopic endometrium) differ significantly. This narrative review is focused on highlighting the relevance and pathogenetic patterns of the two most frequently diagnosed forms of endometriosis—adenomyosis and ovarian endometrioid cysts—as key areas of research interest relating to their relevance, specific pathophysiology and impacts on the eutopic endometrium.

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