Archives of oral biology · 2025
Patterns of circulating autoantibodies against desmoglein-1 and desmoglein-3 in the progression of oral lichen planus: A scoping review.
СтатьяScoping ReviewНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Ошибки и ограничения
История · было → стало
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Sarasati Andari, Wibawa Kadek Gede Putra, Surboyo Meircurius Dwi Condro, Panico Rene Luis, Santosh Arvind Babu Rajendra, Viany Adhistya, Agustina Dewi, Ernawati Diah Savitri
Аннотация
OBJECTIVE: The potential role of autoantibodies targeting desmosomal proteins, particularly desmoglein 1 (Dsg-1) and desmoglein 3 (Dsg-3), in modulating disease severity and epithelial integrity in oral lichen planus (OLP) remains a subject of growing interest. Distinct patterns of anti-Dsg-1 and anti-Dsg-3 autoantibodies across OLP subtypes may correlate with disease progression. This scoping review investigates the expression patterns of circulating anti-Dsg-1 and anti-Dsg-3 autoantibodies in reticular, erosive, and ulcerative forms of OLP to elucidate their potential roles in epithelial disruption and disease advancement.
DESIGN: Following PRISMA guidelines, a systematic search of four electronic databases was conducted. Eligible studies included case reports, case series, case-control and cross-sectional studies that reported serum levels of anti-Dsg-1 and anti-Dsg-3 autoantibodies in OLP patients.
RESULTS: Reticular-type OLP showed variable anti-Dsg-1 and anti-Dsg-3 autoantibody levels, with some patients testing positive while others were negative, indicating an inconsistent involvement of desmosomal autoimmunity in this milder form of the disease. In erosive-type OLP, the presence of both autoantibodies indicated deeper epithelial damage and an active autoimmune response. Interestingly, ulcerative-type OLP consistently tested negative for both antibodies despite extensive epithelial breakdown, implying a potential shift from desmosomal autoimmunity to chronic inflammation-driven tissue destruction that could compromise human health.
CONCLUSION: These findings suggest a potential continuum in which reticular OLP may progress to erosive OLP, with Dsg-3 autoantibodies as a possible early marker of worsening pathology. Ulcerative OLP appears to represent a late-stage, inflammation-driven phenotype with minimal autoantibody involvement. Given the limited and heterogeneous data, these observations are preliminary and should be interpreted cautiously.
DESIGN: Following PRISMA guidelines, a systematic search of four electronic databases was conducted. Eligible studies included case reports, case series, case-control and cross-sectional studies that reported serum levels of anti-Dsg-1 and anti-Dsg-3 autoantibodies in OLP patients.
RESULTS: Reticular-type OLP showed variable anti-Dsg-1 and anti-Dsg-3 autoantibody levels, with some patients testing positive while others were negative, indicating an inconsistent involvement of desmosomal autoimmunity in this milder form of the disease. In erosive-type OLP, the presence of both autoantibodies indicated deeper epithelial damage and an active autoimmune response. Interestingly, ulcerative-type OLP consistently tested negative for both antibodies despite extensive epithelial breakdown, implying a potential shift from desmosomal autoimmunity to chronic inflammation-driven tissue destruction that could compromise human health.
CONCLUSION: These findings suggest a potential continuum in which reticular OLP may progress to erosive OLP, with Dsg-3 autoantibodies as a possible early marker of worsening pathology. Ulcerative OLP appears to represent a late-stage, inflammation-driven phenotype with minimal autoantibody involvement. Given the limited and heterogeneous data, these observations are preliminary and should be interpreted cautiously.