Abstract
Endometriosis is a chronic, estrogen-dependent inflammatory disorder characterized
by ectopic endometrium-like tissue, leading to debilitating pain and reduced quality
of life. Pain is the hallmark of endometriosis, with individuals experiencing dysmenorrhea,
dysuria, dyschezia, dyspareunia, and chronic pelvic pain. However, pain does not always
correlate with the severity or location of the lesions, which suggests additional
factors are involved in the generation of endometriosis-associated pain. The underlying
mechanisms are multifactorial, involving peripheral and central sensitization, inflammation,
aberrant innervation, immune dysregulation, and hormonally influenced processes. Additionally,
many individuals with endometriosis experience comorbid pain syndromes, including
pelvic floor dysfunction (PFD), irritable bowel syndrome, interstitial cystitis, abdomino-pelvic
myalgia, and vulvar vestibulodynia. These conditions share overlapping pathophysiological
mechanisms, such as cross-sensitization of pelvic organs and maladaptive neuroplastic
changes, further amplifying pain perception. Despite advances in understanding these
mechanisms, current treatment strategies remain inadequate, with hormonal suppression
and surgical intervention providing variable relief. A comprehensive, multimodal approach
targeting neuroinflammatory pathways, PFD, and central sensitization may be essential
for improving pain management. Further research is needed to refine therapeutic strategies
and develop targeted interventions for this challenging condition.
Keywords
endometriosis - pelvic pain - cross sensitization - comorbid pain syndromes - endometriosis-associated
pain
