Abstract
Increasing imaging data point to a link between deep endometriotic nodules (DENs) and uterine adenomyosis (AD). The study aimed to investigate this link at the histological level and detect potential features shared by the two diseases. We collected formalin-fixed paraffin-embedded tissue (endometrium and lesions) from women with DENs of the rectovaginal septum (n = 13), AD (n = 14), and control subjects (n = 14). Immunohistochemical analyses of CD41 and CD68 were conducted to explore the roles of platelets and macrophages, respectively. Picrosirius red staining was carried out to gather evidence of fibrosis. Vascular endothelial growth factor (VEGF) was assessed, and total numbers of CD31-positive vessels were calculated to investigate the mechanism governing angiogenesis. Double immunohistochemistry for CD31 and alpha smooth muscle actin (αSMA) was performed to discern stable vessels. Platelet aggregation was significantly decreased in both types of lesions compared to their corresponding eutopic endometrium and healthy controls. Macrophage numbers were higher in both lesions than in their corresponding endometrium and healthy subjects. Significantly higher rates of collagen accumulation were detected in DENs and AD lesions compared to their corresponding eutopic and healthy endometrium. VEGF expression was downregulated in the stromal compartment of AD lesions compared to the healthy endometrium. The total number of vessels per area was significantly higher in DENs and AD lesions than in the healthy endometrium. Rates of αSMA-surrounded vessels were decreased in DENs and AD lesions compared to their corresponding eutopic and healthy endometrium. We report common pathogenic mechanisms between DENs and AD, namely excessive macrophage accumulation, fibrosis, and irregular angiogenesis. Our results further support the notion of DENs and AD being linked at the histological level.
Highlights
Endometriosis is a benign disease histologically characterized by the presence of endometrium-like tissue outside the uterus, typically inside the pelvic peritoneum, the ovaries, or the rectovaginal septum [1]
Rates of vessels surrounded by αSMA-positive cells out of total vessels were significantly lower in Deep endometriotic nodules (DENs) and AD lesions than in their corresponding eutopic (** p = 0.001; *** p = 0.0002) and healthy (** p = 0.002; *** p = 0.0004) tissues (Figures 3 and 4d)
By comparing DENs and AD side by side, we identified specific pathogenic features shared by the two diseases, namely a drop in platelet numbers, excess macrophage accumulation, fibrosis, and irregular angiogenesis
Summary
Endometriosis is a benign disease histologically characterized by the presence of endometrium-like tissue outside the uterus, typically inside the pelvic peritoneum, the ovaries, or the rectovaginal septum [1]. It is the cause of chronic pelvic pain, abnormal menstrual bleeding, and infertility, diminishing quality of life in up to 10% of the female population worldwide [2,3]. To assess the role of these processes in DENs and AD, we examined aggregation patterns of the two cell populations as well as evidence of collagen accumulation. The present study aimed to identify patterns of modifications potentially common to both diseases at the histological level
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