Polarization of macrophage cellular center during endometrioid cyst evolution

Author:

Ukrainets R. V.1ORCID,Korneva Y. S.1ORCID

Affiliation:

1. Smolensk State Medical University; Smolensk Regional Institute of Pathology

Abstract

Introduction. Macrophages are the center of homeostasis regulation in endometrioid heterotopia tissue. Being one of the most important elements in understanding the pathogenesis of endometriosis, macrophages control the changes in the cooperation of cellular elements.Aim. The aim of the study was to assess the location, nature, and strength of correlation relationships between the macrophages/ siderophages and other cell populations in the endometrioid cysts wall at various stages of their formation.Material and Methods. The study comprised 57 patients with a histologically verified diagnosis of endometrioid ovarian cyst. All the studied endometrioid cysts were divided into “young”, “mature”, and “old” based on the morphological features. The macrophages/siderophages, lymphocytes, neutrophils, and eosinophils were counted in 10 visual fields in the cyst wall after staining with hematoxylin and eosin at ×400 magnification at the different layers of cyst wall.Results. The dynamics of changes in the location, direction, and strength of correlations showed that the functional destruction of macrophage cell center occurred during maturation and aging of the ovarian endometrioid cyst. This process was caused by an insufficient vascularization of endometrioid heterotopia, increasing pressure inside the cyst, and the gradual compaction of underlying fibrous layer, which lead to the atrophy of endometrioid lining and inability of macrophage cell center to maintain homeostasis. These changes caused a complete depletion of macrophage cell center due to macrophage polarization and subsequent formation of siderophages.Conclusion. In the absence of endometrium-associated macrophage pool renewal, endometrioid heterotopia eventually subside due to the destruction of macrophage cell center that controls its homeostasis.

Publisher

Cardiology Research Institute

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