Pathophysiological aspects of pain syndrome in endometriosis: A review
This review identifies and compares six sequential pathophysiological mechanisms contributing to the persistent pain syndrome in endometriosis, highlighting areas for further clinical investigation.
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This 2022 literature review synthesizes current knowledge on the pathophysiological mechanisms underlying pain syndrome in endometriosis, focusing on how inflammatory and nociceptive processes evolve beyond purely lesion burden, using published clinical and mechanistic studies. The authors summarize six interrelated mechanisms that sequentially activate and reinforce each other to produce persistent pain, emphasizing that pain intensity often does not correlate with the volume or morphological stage of affected tissue and may persist after lesion removal; they also note that gaps remain in the described mechanisms and that additional clinical studies are needed. Key components highlighted include cyclic bleeding from ectopic endometrial tissue with associated inflammation, elevated inflammatory mediators (e.g., PGE2, TNF-α, nerve growth factor, interleukins), oxidative stress products that can activate nociceptors, and mediator-induced irritation of nerve endings. This paper is centrally about endometriosis — it reviews mechanisms of chronic pelvic pain pathophysiology in endometriosis.
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