Archives of Gynecology and Obstetrics

, Volume 289, Issue 1, pp 13–21

Mechanism of pain generation for endometriosis-associated pelvic pain

Authors

    • Department of Obstetrics and GynecologyNara Medical University
  • Yuki Yamada
    • Department of Obstetrics and GynecologyNara Medical University
  • Sachiko Morioka
    • Department of Obstetrics and GynecologyNara Medical University
  • Emiko Niiro
    • Department of Obstetrics and GynecologyNara Medical University
  • Aiko Shigemitsu
    • Department of Obstetrics and GynecologyNara Medical University
  • Fuminori Ito
    • Department of Obstetrics and GynecologyNara Medical University
Review

DOI: 10.1007/s00404-013-3049-8

Cite this article as:
Kobayashi, H., Yamada, Y., Morioka, S. et al. Arch Gynecol Obstet (2014) 289: 13. doi:10.1007/s00404-013-3049-8

Abstract

Purpose

Endometriosis-associated pelvic pain appears due to persistent nociceptive stimulation, but the precise mechanisms remain poorly understood.

Methods

A search was conducted to screen and select articles from PubMed.

Main results

Neurotrophins (NTs), a family of neuronal growth factors, are overexpressed in endometriosis and encompass NGF, BDNF and NT-3 and NT-4/5. NT receptors, TrkA and p75NTR, and NT receptor-interacting proteins, MAGE and NDN, were also expressed. NTs and their receptors play a role in the development and maintenance of neural tissues in non-neuronal cell types such as endometriosis. Nerve fibers contain unmyelinated sensory C, myelinated sensory Adelta and adrenergic nerve fibers that innervate abnormal cell growths. An increased release of proinflammatory cytokines from endometriotic lesions is responsible for the excessive sensory innervation and development of chronic pelvic pain.

Conclusions

The preponderance of the inflammatory milieu and subsequent hyperinnervation might be involved in the pathophysiology of pain generation in women with endometriosis.

Keywords

EndometriosisPainNeurotrophinInflammationNeuron

Copyright information

© Springer-Verlag Berlin Heidelberg 2013