Vulvar Lichen Sclerosus from Pathophysiology to Therapeutic Approaches: Evidence and Prospects
Vulvar lichen sclerosus (VLS) is a chronic, distressing, inflammatory disease with an enormous impact on quality of life. Treatment goals are relieving symptoms, reversing signs and preventing anatomical changes. Despite the availability of numerous therapeutic options, treatment outcome may not be...
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MDPI AG
2021-08-01
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Online Access: | https://www.mdpi.com/2227-9059/9/8/950 |
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author | Monica Corazza Natale Schettini Pierantonia Zedde Alessandro Borghi |
author_facet | Monica Corazza Natale Schettini Pierantonia Zedde Alessandro Borghi |
author_sort | Monica Corazza |
collection | DOAJ |
description | Vulvar lichen sclerosus (VLS) is a chronic, distressing, inflammatory disease with an enormous impact on quality of life. Treatment goals are relieving symptoms, reversing signs and preventing anatomical changes. Despite the availability of numerous therapeutic options, treatment outcome may not be entirely satisfactory and a definitive cure does not exist. This may be due to the fact that the exact VLS etiopathogenesis remains unknown. The objectives of this paper were to review the most up-to-date knowledge on VLS etiopathogenesis and to consider the available therapies through the lens of a plausible pathogenetic model. An electronic search on both VLS etiopathogenesis and its treatment was performed using the National Library of Medicine PubMed database. Based on current knowledge, it is conceivable that various, heterogeneous environmental factors acting on a genetic background trigger an autoimmune, Th-1 response, which leads to a chronic inflammatory state. This, in turn, can determine both tissue and micro-vascular injury and activation of signaling pathways involved in fibroblast and collagen metabolism. This pathogenetic sequence may explain the effectiveness of anti-inflammatory treatments, mostly topical corticosteroids, in improving VLS clinical-pathological changes. Further deepening of the disease pathways will presumably allow key mediators to become new therapeutic targets and optimize the available treatments. |
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issn | 2227-9059 |
language | English |
last_indexed | 2024-03-10T08:59:17Z |
publishDate | 2021-08-01 |
publisher | MDPI AG |
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series | Biomedicines |
spelling | doaj.art-3a427dd6a5184454bad07bfff5066c942023-11-22T06:52:26ZengMDPI AGBiomedicines2227-90592021-08-019895010.3390/biomedicines9080950Vulvar Lichen Sclerosus from Pathophysiology to Therapeutic Approaches: Evidence and ProspectsMonica Corazza0Natale Schettini1Pierantonia Zedde2Alessandro Borghi3Section of Dermatology and Infectious Diseases, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, ItalySection of Dermatology and Infectious Diseases, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, ItalySection of Dermatology and Infectious Diseases, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, ItalySection of Dermatology and Infectious Diseases, Department of Medical Sciences, University of Ferrara, 44121 Ferrara, ItalyVulvar lichen sclerosus (VLS) is a chronic, distressing, inflammatory disease with an enormous impact on quality of life. Treatment goals are relieving symptoms, reversing signs and preventing anatomical changes. Despite the availability of numerous therapeutic options, treatment outcome may not be entirely satisfactory and a definitive cure does not exist. This may be due to the fact that the exact VLS etiopathogenesis remains unknown. The objectives of this paper were to review the most up-to-date knowledge on VLS etiopathogenesis and to consider the available therapies through the lens of a plausible pathogenetic model. An electronic search on both VLS etiopathogenesis and its treatment was performed using the National Library of Medicine PubMed database. Based on current knowledge, it is conceivable that various, heterogeneous environmental factors acting on a genetic background trigger an autoimmune, Th-1 response, which leads to a chronic inflammatory state. This, in turn, can determine both tissue and micro-vascular injury and activation of signaling pathways involved in fibroblast and collagen metabolism. This pathogenetic sequence may explain the effectiveness of anti-inflammatory treatments, mostly topical corticosteroids, in improving VLS clinical-pathological changes. Further deepening of the disease pathways will presumably allow key mediators to become new therapeutic targets and optimize the available treatments.https://www.mdpi.com/2227-9059/9/8/950vulvar lichen sclerosusetiopathogenesispathwayimmunityfibroblastscollagen metabolism |
spellingShingle | Monica Corazza Natale Schettini Pierantonia Zedde Alessandro Borghi Vulvar Lichen Sclerosus from Pathophysiology to Therapeutic Approaches: Evidence and Prospects Biomedicines vulvar lichen sclerosus etiopathogenesis pathway immunity fibroblasts collagen metabolism |
title | Vulvar Lichen Sclerosus from Pathophysiology to Therapeutic Approaches: Evidence and Prospects |
title_full | Vulvar Lichen Sclerosus from Pathophysiology to Therapeutic Approaches: Evidence and Prospects |
title_fullStr | Vulvar Lichen Sclerosus from Pathophysiology to Therapeutic Approaches: Evidence and Prospects |
title_full_unstemmed | Vulvar Lichen Sclerosus from Pathophysiology to Therapeutic Approaches: Evidence and Prospects |
title_short | Vulvar Lichen Sclerosus from Pathophysiology to Therapeutic Approaches: Evidence and Prospects |
title_sort | vulvar lichen sclerosus from pathophysiology to therapeutic approaches evidence and prospects |
topic | vulvar lichen sclerosus etiopathogenesis pathway immunity fibroblasts collagen metabolism |
url | https://www.mdpi.com/2227-9059/9/8/950 |
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