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.
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