Objective: To better understand the potential disease triggers of neurogenic inflammation in provoked localized vulvodynia (PLV), our objective was to determine whether the types of infiltrating lymphocytes were different in vestibular biopsies from women with primary PLV, secondary PLV, and unaffected controls.
Methods: Secondary retrospective analysis of archived vestibular biopsies from a series of adult premenopausal women with primary PLV (n = 10), secondary PLV (n = 10), and unaffected controls (n = 4) was performed. All study patients had severe entry dyspareunia for more than 1 year. Subjects were excluded if pregnant, or they had a known infection, or history of generalized vulvodynia. Biopsies were performed during the midfollicular phase. Lymphocyte subtypes were highlighted in histologic sections using antibodies against CD3, CD4, and CD8 and scored as the mean number of T-cell subtypes per high-power field. Flow cytometry was also used to test fresh biopsies from a de novo prospective series of primary PLV (n = 4) and unaffected controls (n = 2).
Results: Unaffected control biopsies showed more CD8-positive than CD4-positive T cells, similar to previous reports of the gynecologic tract. In contrast, biopsies from women with primary PLV showed significantly more CD4-positive T cells than those from women with secondary PLV and unaffected controls (p = .003). This observation was further supported by flow cytometry.
Conclusions: CD4-positive T cells are more numerous in vestibular biopsies from premenopausal women with primary PLV. This may be important because subtypes of CD4-positive T cells are specifically recruited by infectious, allergic, or autoimmune triggers. Future studies distinguishing these subtypes may lead to new insights into this common disease.
CD4-positive T-cell recruitment in primary-provoked localized vulvodynia may yield insights into potential disease triggers such as infection, allergy, or autoimmunity.
Departments of 1Obstetrics and Gynecology and 2Pathology, Oregon Health & Science University, Portland, OR
Reprint requests to: Terry K. Morgan, MD, PhD, Department of Pathology and Obstetrics and Gynecology, Oregon Health & Science University, 3181 SW Sam Jackson, Mail Code L471, Portland, OR 97239. E-mail: email@example.com
This study was funded in part by the National Vulvodynia Association, the Oregon Medical Research Foundation, and the Office of Research on Women’s Health at the National Institute of Child Health and Human Development, Oregon BIRCWH HD043488-08.
The authors have declared they have no conflicts of interest.
Presented at the United States and Canadian Academy of Pathology, San Antonio, TX, 2011.