Neuroinflammation in Endometriosis : From Peripheral Lesions to Central Pain Sensitization

Hala Djihane Bahous
2026 · doi:10.5281/zenodo.22812630 · W7213498101
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This review examines how peripheral endometriosis lesions drive central sensitization via spinal microglial and astrocytic activation, linking neuroinflammation to chronic pelvic pain and affective comorbidities while identifying novel non-hormonal therapeutic targets.

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This review examines the role of neuroinflammation in endometriosis, highlighting how peripheral lesions drive central pain sensitization through spinal and supraspinal mechanisms. The authors describe how persistent inflammation leads to microglial M1 polarization and astrocytic activation in the dorsal horn, which amplifies hyperexcitability and contributes to affective comorbidities like anxiety and depression. They note that current surgical and hormonal treatments often fail because they do not address these underlying neurological alterations, despite targeting peripheral disease. Novel non-hormonal targets such as Glra3 modulation and microglial inhibition are proposed to restore neural homeostasis and alleviate chronic pelvic pain. This paper is centrally about endometriosis — specifically focusing on the pathophysiological link between peripheral lesions and central nervous system pain sensitization.

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Abstract

Endometriosis is a complex, chronic systemic condition characterized by the presence of endometrial-like tissue outside the uterine cavity, leading to chronic pelvic pain, dysmenorrhea, and infertility. Current diagnostic and therapeutic strategies remain limited due to the marked heterogeneity of endometriotic lesions—spanning superficial peritoneal implants, deep infiltrating endometriosis (DIE), and ovarian endometriomas—and their distinct cellular dynamics, such as altered aromatase activity and progesterone resistance. Crucially, surgical excision and hormonal suppression often fail to provide complete pain relief, as they target peripheral lesions rather than the underlying neurological alterations. Emerging evidence highlights that persistent peripheral inflammation and nerve fiber sprouting establish a state of central sensitization driven by spinal neuroglial adaptation. In the spinal dorsal horn, microglial M1 polarization—mediated via the CX_3CR1 / P2X_4R / NF-\kappa B pathway—and astrocytic activation (marked by elevated GFAP) amplify neuroinflammation and central hyperexcitability. Furthermore, chronic nociceptive signaling induces structural remodeling within supraspinal sensory and limbic networks, driving affective comorbidities such as anxiety and depression. Novel non-hormonal targets, including Glycine Receptor Subunit Alpha 3 (Glra3) modulation and targeted microglial inhibition, offer promising avenues to restore neural homeostasis and alleviate chronic pelvic pain.
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Neuroinflammation in Endometriosis : From Peripheral Lesions to Central Pain Sensitization Authors/Creators - 1. University of science and technology Mohammed Boudiaf Description Endometriosis is a complex, chronic systemic condition characterized by the presence of endometrial-like tissue outside the uterine cavity, leading to chronic pelvic pain, dysmenorrhea, and infertility. Current diagnostic and therapeutic strategies remain limited due to the marked heterogeneity of endometriotic lesions—spanning superficial peritoneal implants, deep infiltrating endometriosis (DIE), and ovarian endometriomas—and their distinct cellular dynamics, such as altered aromatase activity and progesterone resistance. Crucially, surgical excision and hormonal suppression often fail to provide complete pain relief, as they target peripheral lesions rather than the underlying neurological alterations. Emerging evidence highlights that persistent peripheral inflammation and nerve fiber sprouting establish a state of central sensitization driven by spinal neuroglial adaptation. In the spinal dorsal horn, microglial M1 polarization—mediated via the CX_3CR1 / P2X_4R / NF-\kappa B pathway—and astrocytic activation (marked by elevated GFAP) amplify neuroinflammation and central hyperexcitability. Furthermore, chronic nociceptive signaling induces structural remodeling within supraspinal sensory and limbic networks, driving affective comorbidities such as anxiety and depression. Novel non-hormonal targets, including Glycine Receptor Subunit Alpha 3 (Glra3) modulation and targeted microglial inhibition, offer promising avenues to restore neural homeostasis and alleviate chronic pelvic pain. Files Files (25.4 kB) | Name | Size | Download all | |---|---|---| | md5:2ba9cf949d9854af439a2052a7b47bfd | 25.4 kB | Download |

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