Abstract
Endometriosis is a chronic and debilitating condition affecting ∼10% of women. Endometriosis is characterized by infertility and chronic pelvic pain, yet treatment options remain limited. In many respects this is related to an underlying lack of knowledge of the etiology and mechanisms contributing to endometriosis-induced pain. Whilst many studies focus on retrograde menstruation, and the formation and development of lesions in the pathogenesis of endometriosis, the mechanisms underlying the associated pain remain poorly described. Here we review the recent clinical and experimental evidence of the mechanisms contributing to chronic pain in endometriosis. This includes the roles of inflammation, neurogenic inflammation, neuroangiogenesis, peripheral sensitization and central sensitization. As endometriosis patients are also known to have co-morbidities such as irritable bowel syndrome and overactive bladder syndrome, we highlight how common nerve pathways innervating the colon, bladder and female reproductive tract can contribute to co-morbidity via cross-organ sensitization.
Highlights
Endometriosis is a chronic and debilitating condition characterized by chronic pelvic pain (CPP) and infertility
Endometriosis is commonly co-diagnosed with bladder and colon disorders that are characterized by sensory dysfunction, such as overactive bladder syndrome (OAB), and irritable bowel syndrome (IBS) (Surrey et al, 2018)
prostaglandin E2 (PGE2), tumor necrosis factorα (TNFα), nerve growth factor (NGF), Regulated on Activation Normal T cell Expressed and Secreted (RANTES, known as C-C chemokine ligand 5: CCL5), and interleukin (IL) IL8 and IL-1β are all elevated within the peritoneal fluid of endometriosis patients who reported CPP pain (Ryan et al, 1995; Barcz et al, 2000; Bedaiwy et al, 2002; Scholl et al, 2009)
Summary
Jessica Maddern1,2†, Luke Grundy1,2†, Joel Castro1,2* and Stuart M. Reviewed by: Wakako Fujita, Nagasaki University, Japan Fuminori Taniguchi, Tottori University, Japan. Specialty section: This article was submitted to Cellular Neurophysiology, a section of the journal
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