Secondary Vulvodynia Patients Show Reduced Bacterial Diversity in Vestibular Microbiome
Aalto, A. P.; Mishra, P.; Tuomisto, S.; Ceder, T.; Sundstrom, K.; Leppanen, R.; Ahinko, K.; Maenpaa, J.; Lehtimaki, T.; Karhunen, P.; Staff, S.
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IntroductionLocalized Provoked Vulvodynia (LPV) is a quite common form of sexual pain among young women. Primary LPV (e.g. pain from the first attempted intercourse) and secondary LPV (pain-free time period before the initiation of symptoms) have been suggested to develop via different pathomechanisms. As inflammation is one possible trigger in LPV, changes in vaginal and/or vulvar microbiome may be an initiator of the inflammatory process leading to peripheral neurosensitization and predisposing women to LPV. AimAim of this pilot study was to find out, whether there are differences in vestibular microbiome between LPV patients and controls. Materials and MethodsThirty women with LPV (8 with primary and 22 with secondary LPV) and 21 controls were prospectively recruited to the study from Kanta-Hame Central Hospital and Tampere University Hospital (TAUH). Paired vestibular samples were collected in clinical outpatient setting and analyzed with 16s rRNA sequencing. ResultsLPV patients had lower BMI, were younger and more often nulliparous than controls. Patients with secondary vulvodynia had reduced (p = 0.06) bacterial species diversity (alpha diversity) and more clustered (p= 0.05) vaginal microbiome community (beta diversity) compared to healthy controls. Differential abundance analysis identified 31 bacterial taxa that contributed to the difference in bacterial composition between secondary cases and controls (p < 0.05). Bacteria taxa that were increased among patients were Gardneralla vaginalis (p<0.0001), Peptoniphilus spp (p<0.0001), Prevotella amnii (p<0.0001) and Streptococcus spp (p=0.0001). Several bacterial species were more abundant among healthy controls reflecting reduced bacterial diversity among patients. ConclusionIn patients with secondary LPV changes in vulvar microbiome may contribute to pathogenesis of LPV and ultimately lead to targeted therapeutic options. These preliminary findings need to be confirmed in a larger study.
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