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<p>Vulvar lichen sclerosus (VLS) is a chronic, inflammatory, and progressive skin disease mainly involved in the anogenital area. Platelet-rich fibrin (PRF) is a fibrin adhesive-concentrated platelet-rich plasma (PRP) used for tissue repair and angiogenesis. In this study, we explored the effects of PRF on VLS patients, further to utilize the established VLS animal model, to confirm the therapeutic effect of PRF and regulation on the TGF-β/SMAD3 pathway. Among the 46 VLS patients included in the analysis, injectable RPF (i-PRF) treatment improved the symptoms of VLS. The immunohistochemical analysis showed that i-PRF decreased the local blurring of the dermal-epidermal boundary and increased the number of basal keratinocytes. I-PRF increased positive PGD9.5, CD34, and Melan A cell numbers, and decreases positive IL-17 and INF-γ cell numbers in VLS tissues. In the VLS rat model, i-PRF reduced inflammatory factors IL-17 and INF-γ via inhibition of NF-κB and increased CD31 and VEGF expression in external genital tissue. The i-PRF decreases fibronectin and collagen-I by inhibiting TGF-β/SMAD3 in VLS, which is the main factor that triggers inflammation and fibrosis of the external genital skin.</p>

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Platelet-rich fibrin attenuates inflammation and fibrosis in vulvar lichen sclerosus via the TGF-β/SMAD3 pathway

  • 期刊论文

  • 发表日期：

    2025年2月7日

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  • Shu-Hong Sun,
  • Hong-He Fan,
  • Xiao-Wei Wang,
  • Bo-Dong Bing,
  • Yuan-Jing Hu

摘要

Vulvar lichen sclerosus (VLS) is a chronic, inflammatory, and progressive skin disease mainly involved in the anogenital area. Platelet-rich fibrin (PRF) is a fibrin adhesive-concentrated platelet-rich plasma (PRP) used for tissue repair and angiogenesis. In this study, we explored the effects of PRF on VLS patients, further to utilize the established VLS animal model, to confirm the therapeutic effect of PRF and regulation on the TGF-β/SMAD3 pathway. Among the 46 VLS patients included in the analysis, injectable RPF (i-PRF) treatment improved the symptoms of VLS. The immunohistochemical analysis showed that i-PRF decreased the local blurring of the dermal-epidermal boundary and increased the number of basal keratinocytes. I-PRF increased positive PGD9.5, CD34, and Melan A cell numbers, and decreases positive IL-17 and INF-γ cell numbers in VLS tissues. In the VLS rat model, i-PRF reduced inflammatory factors IL-17 and INF-γ via inhibition of NF-κB and increased CD31 and VEGF expression in external genital tissue. The i-PRF decreases fibronectin and collagen-I by inhibiting TGF-β/SMAD3 in VLS, which is the main factor that triggers inflammation and fibrosis of the external genital skin.