ArticleJournal of inflammation research2022
Characterization of Early Inflammatory Events Leading to Provoked Vulvodynia Development in Rats.
Article in Journal of inflammation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07257029 (A Multi-center, Randomized, Double-blind, Placebo-controlled Trial of Topical Ketotifen Fumarate 0.25% Cream for Females With Secondary Vestibulodynia), which is not on this map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Multi-center, Randomized, Double-blind, Placebo-controlled Trial of Topical Ketotifen Fumarate 0.25% Cream for Females With Secondary Vestibulodynia
Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Exploring Localized Provoked Vulvodynia: Insights from Animal Model Research.International journal of molecular sciences · 2024Pooled it
- Molecular mechanisms and therapeutic perspectives in vulvodynia: From current evidence to future investigations.Cell reports. Medicine · 2026Review
- Chronic stress increases the susceptibility to chronic vulvar pain following acute vulvar inflammation in a preclinical model of vulvodynia.Molecular brain · 2026Article
- Mitochondrial dysfunction in the spinal cord contributes to peripheral hypersensitivity in a nitroglycerin-induced migraine model.Journal of translational medicine · 2026Article
- Article
- The Involvement of Glutamate-mGluR5 Signaling in the Development of Vulvar Hypersensitivity.International journal of molecular sciences · 2025Article
- HBO treatment enhances motor function and modulates pain development after sciatic nerve injury via protection the mitochondrial function.Journal of translational medicine · 2023Article
- Inflammation, lipids, and pain in vulvar disease.Pharmacology & therapeutics · 2023Review
- Immune mechanisms in vulvodynia: key roles for mast cells and fibroblasts.Frontiers in cellular and infection microbiology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Provoked vulvodynia (PV) is the main cause of vulvar pain and dyspareunia. The etiology of PV has not yet been elucidated. However, PV is associated with a history of recurrent inflammation, and its often accompanied by increases in the numbers of mast cells (MCs) and sensory hyperinnervation in the vulva. Therefore, this study aimed to examine the role of MCs and the early inflammatory events in the development of chronic vulvar pain in a rat model of PV. Methods: Mechanical and thermal vulvar sensitivity was measured for 5 months following zymosan vulvar challenges. Vulvar changes in glutamate and nerve growth factor (NGF) were analyzed using ELISA. Immunofluorescence (IF) staining of the vulvar section after 20, 81, and 160 days of the zymosan challenge were performed to test MCs accumulation, hyperinnervation, and expression of pain channels (transient receptor potential vanilloid/ankyrin-1-TRPV1 & TRPA1) in vulvar neurons. Changes in the development of vulvar pain were evaluated following the administration of the MCs stabilizer ketotifen fumarate (KF) during zymosan vulvar challenges. Results: Zymosan-challenged rats developed significant mechanical and thermal vulvar sensitivity that persisted for over 160 days after the zymosan challenge. During inflammation, increased local concentrations of NGF and glutamate and a robust increase in MCs degranulation were observed in zymosan-challenged rats. In addition, zymosan-challenged rats displayed sensory hyperinnervation and an increase in the expression of TRPV1 and TRPA1. Treatment with KF attenuated the upregulated level of NGF during inflammation, modulated the neuronal modifications, reduced MCs accumulation, and enhanced mechanical hypersensitivity after repeated inflammation challenges. Conclusion: The present findings suggest that vulvar hypersensitivity is mediated by MCs accumulation, nerve growth, and neuromodulation of TRPV1 and TRPA1. Hence, KF treatment during the critical period of inflammation contributes to preventing chronic vulvar pain development.
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