Abstract

BACKGROUND: One of the clinical course features of ovarian endometriosis is its recurrent nature, which leads to repeated operations and increased damage to the ovarian follicular apparatus.
 AIM: The aim of this study was to evaluate morphological and molecular features of recurrent endometrioid ovarian cysts in patients of reproductive age.
 MATERIALS AND METHODS: Morphological and immunohistochemical studies of the surgical material of 196 observations of endometrioid ovarian cysts were performed 23 observations of the first surgical intervention with further diagnosed relapse, 22 observations of repeated surgery and 151 observations of a relapse-free course of endometriosis. Monoclonal mouse antibodies to CD68, transforming growth factor -1, CD34, and -smooth muscle actin were used.
 RESULTS: CD68 (macrophage) expression was detected in lympho-macrophage infiltrates of the cytogenic stroma and endometrioid cyst capsule. Significantly greater values of the expression were obtained in recurrent endometrioid cysts in the surgical material of both the first (cytogenic stroma 31 [8; 53]%, capsule 23 [3; 42]%) and second operation (23 [12; 36] and 9 [5; 20]%, respectively) compared to the relapse-free course of the disease (8 [6; 9] and 2 [0; 4]%, respectively). The transforming growth factor -1 expression area in the endometrioid cyst capsule was significantly higher in the surgical material of both the first (22.8 [21.6; 24.8]%) and second operation (31.2 [30.5; 32.2]%) with recurrent endometriosis compared to cases with no relapse (12.7 [11.2; 13.9]%). But in the cytogenic stroma was it only detected in cases of repeated surgical endometrioid cyst treatment (18.7 [18.0; 19.7]%). The positive -smooth muscle actin expression area was higher in the surgical material of the second operation with recurrent endometriosis in both the cytogenic stroma (68.3 [66.3; 69.6]%) and endometrioma capsule (82.5 [80.5; 83.8]%). A large area of CD34 expression was also detected in the recurrent course of ovarian endometriosis in the surgical material of both the first (cytogenic stroma 34.8 [33.4; 35.8]%, capsule 52.6 [50.4; 55.0]%) and second operation (51.3 [49.0; 53.3] and 48.7 [46.7; 49.8]%, respectively).
 CONCLUSIONS: The recurrent course of ovarian endometriosis is characterized by more pronounced inflammation, angiogenesis, myofibroblast proliferation, and fibrogenesis, which indicates the importance of these pathological processes in the chronicity of the disease. Further study of the role of macrophages and the cascade of regenerative and reparative processes that they trigger is important for understanding the pathogenesis of endometriosis and searching for diagnostic markers of its recurrent course.

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