MicroRNA-21, TP53, and TP63 expression in oral lichen planus: insights into molecular immunopathogenesis

Oral lichen planus is a chronic immune-mediated inflammatory disorder of the oral mucosa that is classified as an oral potentially malignant disorder, carrying a recognized risk of transformation into oral squamous cell carcinoma. This classification denotes a documented risk of malignant progression rather than an established premalignant biological state in every lesion. Although immune dysregulation plays a central role in its pathogenesis, the molecular mechanisms linking chronic inflammation to tumor-associated pathways remain incompletely understood. MicroRNAs (miRNAs), particularly miR-21, have emerged as key regulators of immune responses and oncogenic signaling, yet their contribution to OLP immunopathogenesis requires further clarification. Punch biopsy specimens were obtained from 85 individuals, including 52 patients with clinically and histopathologically confirmed OLP and 33 healthy controls. The expression levels of miR-21 and of two candidate genes selected through bioinformatic target screening and biological plausibility, TP53 and TP63 , were quantified using real-time polymerase chain reaction. Relative expression levels were calculated using the ΔCt method. Comparative and correlation analyses were performed to explore concurrent expression patterns; these analyses were exploratory and were not designed to establish regulatory relationships. Compared with healthy controls, OLP tissues exhibited significantly higher miR-21 transcript levels (U = 341.000, Z = − 4.133, p < 0.001; n = 50 vs. 30). TP53 transcript levels were also significantly higher (U = 470.000, Z = − 3.499, p < 0.001; n = 52 vs. 32), whereas TP63 did not differ significantly between groups (U = 774.000, Z = − 0.534, p = 0.593; n = 52 vs. 31). Within the OLP group, correlation analysis revealed a negligible, non-significant positive association between miR-21 and TP53 (rho = 0.048, n = 50, p = 0.740) and a weak, non-significant negative association between miR-21 and TP63 (rho = − 0.204, n = 50, p = 0.154). Given the limited magnitude of these coefficients, the observed associations do not establish a direct regulatory relationship. miR-21 and TP53 transcript levels differed between OLP and healthy control tissues, whereas TP63 transcript levels did not differ significantly. The observed associations were weak and exploratory. These findings are potentially relevant to molecular pathways associated with epithelial stress, inflammation, and carcinogenesis, but they do not constitute evidence of malignant progression. Confirmation in studies using age-matched controls, validated normalization strategies, protein-level analyses, functional experiments, and longitudinal clinical follow-up is required.