Beyond the uterus: is the fascial system a missing piece in primary dysmenorrhea?

To the editor, Primary dysmenorrhea is one of the most common gynecological disorders affecting women of reproductive age. Its pathophysiology has traditionally been attributed to excessive prostaglandin production, uterine hypercontractility, and transient uterine ischemia. Although these mechanisms explain the initiation of menstrual pain, they do not fully account for its broad clinical presentation. Many women experience pain extending beyond the uterus, including the lower abdomen, groin, lower back, and proximal thighs, suggesting that additional pain-modulating mechanisms may contribute to symptom generation. One anatomical structure that has received remarkably little attention in this context is the fascial system. Far from being merely a passive connective tissue envelope, fascia has been proposed as one of the body's largest sensory organs, containing abundant free nerve endings, proprioceptors, and nociceptors that actively participate in pain perception and modulation. Moreover, experimental and histological studies have demonstrated that certain fascial tissues exhibit a higher density of sensory innervation than the adjacent muscles, further supporting the concept that fascia functions as an active sensory tissue rather than simply a mechanical covering1. Interestingly, contemporary fascial concepts have expanded beyond musculoskeletal disorders. In the fascial manipulation model, dysmenorrhea is recognized alongside gastritis, irritable bowel syndrome, and constipation as a visceral disorder in which fascial dysfunction may contribute to symptom generation2. Despite these evolving concepts, the potential role of the fascial system in primary dysmenorrhea has received remarkably little scientific attention. Several indirect observations further support this hypothesis. Abdominal wall myofascial trigger points have been proposed as a potential contributor to menstrual pain3. Likewise, a recent literature review demonstrated an association between primary dysmenorrhea and pelvic floor dysfunction, including increased pelvic floor muscle tone and a higher prevalence of pelvic floor myofascial trigger points4. Although these findings primarily concern muscles, the close anatomical and functional continuity between muscle and fascia raises the possibility that the surrounding fascial network may also contribute to menstrual pain. A possible neurophysiological explanation is that menstrual pain is not confined to the uterus. Nociceptive signals arising from the uterus converge with somatic afferents within the spinal cord through viscerosomatic convergence, providing a plausible explanation for the characteristic distribution of pain beyond the uterus5,6. Persistent visceral nociceptive input may subsequently influence muscle tone and alter the mechanical loading of surrounding fascial tissues. Such alterations in fascial biomechanics may function as secondary pain amplifiers, contributing to the propagation and persistence of menstrual pain rather than its initiation.

A possible neurophysiological explanation is that menstrual pain is not confined to the uterus. Nociceptive signals arising from the uterus converge with somatic afferents within the spinal cord through viscerosomatic convergence, providing a plausible explanation for the characteristic distribution of pain beyond the uterus5,6. Persistent visceral nociceptive input may subsequently influence muscle tone and alter the mechanical loading of surrounding fascial tissues. Such alterations in fascial biomechanics may function as secondary pain amplifiers, contributing to the propagation and persistence of menstrual pain rather than its initiation.