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Increased vanilloid receptor VR1 innervation in vulvodynia
Author(s) -
Tympanidis Penelope,
Casula Maria Anna,
Yiangou Yiangos,
Terenghi Giorgio,
Dowd Pauline,
Anand Praveen
Publication year - 2004
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1016/s1090-3801(03)00085-5
Subject(s) - vulvodynia , trpv1 , nociceptor , nociception , medicine , capsaicin , jacalin , endocrinology , receptor , chemistry , immunology , transient receptor potential channel , surgery , pelvic pain , lectin
Vulvodynia is characterised by painful burning sensation, allodynia and hyperalgesia in the region of the vulval vestibulus. While in many patients the cause of vulvodynia remains uncertain, we and others have previously shown increased intraepithelial and papillary innervation in vulvodynia. The vanilloid receptor VR1 (TRPV1) is expressed by nociceptors, and is triggered by capsaicin, noxious heat, protons, and chemicals produced during inflammation. In the present study we show increased papillary VR1 fibres by immunostaining and image analysis in vulvodynia tissues compared to controls ( P <0.002). VR1 expression was found to be significantly increased when the percentage area immunostained was expressed as a ratio of VR1 to PGP 9.5, a pan‐neuronal marker ( P =0.01). VR1‐positive fine epidermal fibres also appeared to be increased in vulvodynia tissues, by inspection. Fibres immunoreactive to the voltage‐gated sodium channel SNS1/PN3 (Nav1.8), also expressed by nociceptors, were relatively scarce in both vulvodynia and control tissues. We hypothesize that increased expression of VR1 by nociceptors could mediate some of the symptoms in vulvodynia, for which systemic or topical specific VR1 antagonists may provide novel treatment.