Pathophysiology of pain in patients with peritoneal endometriosis

Simone Ferrero, Valerio Gaetano Vellone, Fabio Barra
Annals of translational medicine · 2019 · vol. 7(S1) , pp. S8 · doi:10.21037/atm.2019.01.36 · PMID:31032289 · PMC6462618 · W2909234313
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

This paper investigates the underlying biological mechanisms contributing to pain experienced by women with peritoneal endometriosis.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

This paper reviews the mechanisms underlying pain in patients with peritoneal endometriosis (PE), contrasting it with deep infiltrating disease (DIE) and discussing how lesion location and severity do not consistently track with symptom intensity. It synthesizes histological and immunohistochemical findings showing inflammatory mediators in peritoneal fluid, nerve sensitization, and direct nerve irritation/invasion by endometriotic lesions, alongside evidence that DIE and certain nerve-associated molecules (e.g., NGF and its receptors, neurotrophin pathways) are more abundant in painful cases. A major caveat highlighted throughout is the poor correlation between pain severity and overall endometriosis extent, implying multifactorial causes beyond lesion burden and limiting straightforward inference. This paper is centrally about endometriosis — it specifically focuses on the pathophysiology of pain in peritoneal endometriosis, including roles of nerve fiber density, neurotrophins, and neurogenesis.

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Abstract

Endometriosis is a chronic disease characterized by the presence of hormone-responsive endometriotic glands and stroma outside the uterus that affect at least 4% of reproductive age women (1). It may be asymptomatic, but it frequently causes pain symptoms that negative influence social activities, working efficiencies and sexual life (2,3).
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Acknowledgements

None. Footnote Conflicts of Interest: The authors have no conflicts of interest to declare.

References

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