Update of recent studies of adenomyosis-associated dysmenorrhea

In: Gynecology and Minimally Invasive Therapy · 2016 · vol. 5(4) , pp. 137–140 · doi:10.1016/j.gmit.2016.06.002 · W2490076638
article OA: diamond CC0 ⤵ 11 in-corpus citations
AI-generated summary by claude@2026-06, 2026-06-07

This review examines the pathophysiology of adenomyosis-associated dysmenorrhea, highlighting the roles of oxytocin, inflammatory factors, prostaglandin F2α, and pelvic splanchnic nerve pathways.

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Abstract

Adenomyosis is characterized by invasion of endometrial glands and stromal cells into the myometrium. It is a common gynecological disorder that usually occurs in women during their reproductive years. The primary clinical manifestations of adenomyosis are menorrhagia and progressive dysmenorrhea. The pathogenesis of adenomyosis-associated dysmenorrhea is complicated. However, it is predicted that oxytocin, inflammatory factors, and prostaglandin F2α are responsible for adenomyosis-associated dysmenorrhea via the induction of uterine smooth muscle contractions. Additionally, the pain conductivity of the pelvic viscera (internal organs) involves both the sympathetic (T10–L1) and parasympathetic (S2–4) nervous systems located in the abdominal region. This article provides a review of the pathophysiology of dysmenorrhea in adenomyosis and the nociceptive afferent pathway of the pelvic splanchnic nerves.

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adenomyosisdysmenorrhea

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