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Transcriptome Analysis Reveals Distinct Molecular Signatures Between Erosive and Non-Erosive Oral Lichen Planus
Kisung Sheen1,2, Chaerim Song1,3, Kanghyun Kwon1,4
1Translational-Transdisciplinary Research Center, Clinical Research Institute, Kyung Hee University Hospital at Gangdong, Kyung Hee University College of Medicine, Seoul, Republic of Korea.
Oral Diseases
|July 21, 2026
Summary
Erosive oral lichen planus (EOLP) exhibits distinct molecular signatures, including disrupted metabolic-inflammatory coordination and myeloid-dominant inflammation, differentiating it from non-erosive OLP (NEOLP). These findings suggest microbial triggers driving myeloid reprogramming in EOLP.
Area of Science:
- Oral pathology
- Molecular biology
- Immunology
Background:
- Oral lichen planus (OLP) is a chronic inflammatory condition with distinct clinical subtypes.
- The erosive subtype (EOLP) is often more severe and debilitating than the non-erosive subtype (NEOLP).
- Understanding the molecular differences between EOLP and NEOLP is crucial for targeted therapeutic strategies.
Purpose of the Study:
- To elucidate the molecular mechanisms underlying the distinction between EOLP and NEOLP.
- To identify key transcriptomic signatures that differentiate the two OLP subtypes.
Main Methods:
- Analysis of bulk RNA-sequencing data from 30 buccal mucosa samples (13 EOLP, 17 NEOLP).
- Utilized differential gene expression, Gene Set Enrichment Analysis (GSEA), transcription factor inference, and transcriptome deconvolution (xCell 2.0).
- Employed metabolic flux simulation and pathway correlation analysis (GSVA with DGCA).
Main Results:
- Identified three key molecular signatures distinguishing EOLP from NEOLP.
- Observed disrupted metabolic-inflammatory coordination and altered epithelial cell cycle/senescence programs in EOLP.
- Detected myeloid-skewed inflammation with elevated SPI1/PU.1, enhanced bacterial response pathways, and compromised epithelial barrier function in EOLP.
Conclusions:
- EOLP is characterized by dysregulated metabolic-inflammatory balance, epithelial alterations, and myeloid-driven inflammation.
- A model is proposed where microbial stimuli may induce myeloid-centered metabolic reprogramming, sustaining EOLP inflammation.
- Potential therapeutic targets include restoring metabolic-inflammatory equilibrium, modulating microbial factors, and repairing the epithelial barrier.
