Endometriosis-associated pain and adhesions — new pathogenetic aspects and therapeutic approach
This review explores the role of the immune system and fibrosis in endometriosis-associated pain and adhesions and evaluates the efficacy of a combined therapy for treating pain, infertility, and preventing adhesions.
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This paper discusses endometriosis-associated pelvic pain and adhesion formation by synthesizing evidence on how chronic inflammation and reactive fibrosis translate into clinical symptoms. It highlights mechanisms involving activated platelets and macrophages (including M1-to-M2 transitions) that drive TGF-β1/Smad3 signaling, epithelial–mesenchymal transition, α-SMA–positive myofibroblast activity, and extracellular matrix collagen deposition, linking these processes to pain mediators such as IL-1β, IL-6, TNF-α, VEGF, MCP-1, and neurotrophic pathways involving BDNF and NGF. The major limitation stated in the text is that pathogenetic mechanisms are still fragmentary and require further clarification, with fibrosis also complicating histologic interpretation and potentially causing mismatches between preoperative diagnosis and pathology. Relevance to endometriosis: the paper is directly centered on endometriosis-associated pain, fibrosis, and adhesions, including described roles of inflammatory mediators and immune-platelet-macrophage pathways in endometriosis.
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