Genital Lichen Sclerosus—The Role of the Vulvar Microbiome

<i>Background and Objectives:</i> Lichen sclerosus (LSc) is a chronic inflammatory and sclerosing condition that primarily affects the genital region. In women, vulvar lichen sclerosus presents with a wide range of clinical features, including pruritus, erythema, burning, pain, dysuria, architectural distortion, scarring, and the formation of ivory-white atrophic plaques. While the precise etiology of LSc remains unclear, increasing evidence indicates that prolonged exposure to urine and occlusion may play a central role in its pathogenesis. Additionally, the role of the genital microbiome has garnered increasing attention, with dysbiosis-an imbalance in microbial communities-emerging as a potential contributing factor. Prior investigations have reported an increased abundance of <i>Gardnerella</i> in women with LSc, but findings regarding <i>Streptococcus</i> and <i>Lactobacillus</i> have been inconsistent. This study aimed to investigate the relationship between the vulvar microbiome and LSc. <i>Materials and Methods:</i> Forty-seven women with LSc and seven healthy controls were recruited from the Division of Dermatology, Ryhov Hospital, Jönköping. Vulvar swabs were obtained from affected skin areas. The 16S rRNA regions were amplified and sequenced using the Illumina MiSeq system. Differential abundance analyses were conducted using four regression methods, and genera were considered significant only if identified by at least two methods. <i>Results:</i> Compared to controls, LSc patients showed reduced abundance of <i>Lactobacillus</i>, <i>Finegoldia</i>, <i>Lawsonella</i>, <i>Stapylococcus</i>, <i>Cutibacterium</i>, and an unidentified genus belonging to the <i>Actinomycetaceae</i> family. In contrast, <i>Porphyromonas</i> and <i>Ezekiella</i>, were significantly increased. Beta diversity analysis revealed significant differences in microbiome composition between groups (<i>p</i> = 0.022). <i>Conclusions:</i> The vulvar microbiome of women with LSc differs significantly from that of healthy controls. These findings support a possible role of microbial dysbiosis in LSc pathogenesis, highlighting the need for further research into microbiome-targeted interventions.