Pathophysiological aspects of chronic pelvic pain and systemic inflammation in patients with endometriosis

This paper is a narrative review examining how chronic pelvic pain in endometriosis is linked to systemic and local inflammation, focusing on neuroimmune pathways. It synthesizes evidence that estrogen-driven dysregulation of macrophages and peripheral nerve changes promote chemokine release, macrophage recruitment/polarization in endometriotic lesions, and neurotrophin signaling that supports neurogenesis and peripheral sensitization, which can contribute to central hyperexcitability and neuropathic-like pain. A key finding emphasized across cited studies is the correlation between elevated peritoneal factors (e.g., TNFα, TGF-β1, macrophages) and central hyperexcitability/low pain thresholds, alongside altered densities of nerve fiber types in and around lesions. The authors explicitly frame this as an overview of proposed mechanisms and note that the pain–lesion relationship is complex and not fully understood, limiting causal certainty, and it does not present original new patient data. This paper is centrally about endometriosis — it reviews estrogen-, macrophage-, and cytokine-mediated neuroimmune mechanisms underlying chronic pelvic pain and systemic inflammation in endometriosis.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works