Oral lichen planus (OLP) is a chronic inflammatory disease affecting the oral mucosa, with mechanisms of pathogenesis that remain only partially understood. It has a global prevalence of about 1.01% within the general population. Significantly, OLP is recognized for its potential to undergo malignant transformation at a rate of about 1.4%. The condition can be classified into erosive and non-erosive types, with erosive OLP carrying a higher risk of malignancy. Key histopathological features of OLP include T lymphocyte infiltration, basement membrane disruption, and basal keratinocyte degeneration.

The role of various cellular components in the immune-inflammatory response of OLP has been an area of intense research. Among these, oral keratinocytes have been noted for their antigen-presenting capabilities and their ability to upregulate the expression of cytokines, chemokines, and adhesion molecules. Keratins, the primary intermediate proteins in keratinocytes, play significant roles in cell structure, signaling, intracellular transport, cell cycle, and cell death processes. Changes in keratin expression have been linked to oral inflammation and epithelial barrier dysfunction.

A particular focus has been placed on keratin 17 (KRT17) owing to its potential role in the pathogenesis of OLP. KRT17 belongs to the family of type I epithelial keratins, which contribute to the structural integrity of the epidermis. It is usually found in basal cells of complex epithelia. KRT17 has been implicated in the pathogenesis of various immune diseases, including psoriasis, where it serves as an overexpressed autoantigen promoting disease development via T-cell-mediated mechanisms. However, research into KRT17's expression and clinical correlations in OLP is still in nascent stages.

Recently, Han et al. published article "CIncreased expression of keratin 17 in oral lichen planus and its correlation with disease severity" in the Journal of Dental Sciences. This study aimed to explore KRT17 expression in OLP and its correlation with the severity of the disease, potentially providing new targets for OLP prevention and treatment.

Materials and Methods

The study collected oral tissue samples from 5 OLP patients and 5 healthy controls. Tissues were processed using dispase and TRIzol for RNA extraction and sequencing. RNA libraries were constructed and sequenced using the NovaSeq 6000 platform. Differential gene expression was analyzed with DESeq2, and gene ontology and pathway analyses were conducted. Immunohistochemistry was used to assess KRT17 expression, and severity was evaluated with the REU scoring system. Statistical analyses included t-tests, Fisher's exact tests, and correlation analyses.

Results

KRT17 mRNA Expression

Principal component analysis of RNA-seq data demonstrated the reproducibility of results. A total of 15,493 genes were detected, with 1,492 significantly upregulated and 622 downregulated in OLP. KRT17 mRNA expression was markedly elevated in OLP tissues.

Fig. 1 RNA sequencing of HC and OLP epithelium.

GO and Pathway Analysis

GO analysis revealed that KRT17-associated biological processes were primarily involved in hair follicle development, cornification, and keratinization. Cellular components included the cell periphery, cytosol, and cytoplasm, while molecular functions were related to structural molecule activity. KEGG pathway analysis identified potential pathways involving KRT17, including staphylococcus aureus infection. GSEA showed that high KRT17 expression was associated with positive regulation of cell growth, translation, epithelial morphogenesis, intermediate filament organization, keratinization, and hair follicle development.

Fig. 2 Predicted functions and pathways associated with KRT17 expression in OLP.

Immunohistochemical Validation

IHC staining confirmed that KRT17 expression was significantly higher in OLP tissues compared to HC tissues. In OLP tissues, KRT17-positive cells were widespread throughout the epithelial layer, whereas HC tissues showed minimal KRT17 positivity. The median percentage of the KRT17-positive area was 19.30% in OLP and 0.01% in HC.

Fig. 3 KRT17 expression and distribution in HC and OLP tissues.

Correlation with OLP Severity

Analysis revealed that erosive OLP patients had a higher percentage of KRT17-positive area (27.25%) compared to non-erosive OLP patients (15.02%,). REU scores, which quantify disease severity, were positively correlated with the percentage of KRT17-positive area, suggesting that higher KRT17 expression is associated with greater disease severity.

Fig. 4 Correlation of severity of OLP and percentage of KRT17 positive area value.

Conclusion

The study demonstrated that KRT17 mRNA expression is elevated in OLP tissues compared to healthy controls, and this expression is positively correlated with the severity of OLP. These findings suggest that KRT17 may play a crucial role in OLP pathogenesis and could serve as a potential target for clinical prevention and treatment of the disease. However, further research is required to validate these findings and explore the underlying mechanisms involving KRT17 in OLP.

• Cytokeratin 17 Polyclonal Antibody
• Cytokeratin 17 Monoclonal Antibody
• Cytokeratin 17 ELISA Kit
• Cytokeratin 17 Protein