Abstract
Cutaneous lichen planus (CLP) is a chronic immune-mediated inflammatory dermatosis in which oxidative stress and mitochondrial dysfunction are increasingly implicated, yet integrated biomarker evidence remains limited. Methods: In this cross-sectional pilot study, 30 histopathologically confirmed CLP patients and 30 age- and sex-matched healthy controls were enrolled. Relative mtDNA copy number and telomere length were measured using quantitative real-time PCR, while serum TOS was estimated by a colorimetric assay. CLP patients had a markedly reduced mtDNA content in comparison to controls (246.95±69.95 versus 289.40±73.60; p=0.026). The relative telomere length was significantly greater in the CLP group (16279.92±2363.58 vs 14677.06±2528.51; p=0.021). TOS levels were elevated in CLP patients (32.11±14.67 vs 16.59±7.06 µmol H₂O₂ equivalents/L; p<0.0001), indicating a substantially more oxidative stress. CLP is linked to mitochondrial DNA depletion, modified telomere dynamics, and significant oxidative stress. These results support the hypothesis that mitochondrial malfunction and oxidative imbalance are pivotal in CLP development. Therapeutic approaches aimed at oxidative stress and mitochondrial well-being may provide potential advantages. Further long-term studies are needed to better understand the cause-and-effect correlations and therapeutic consequences.
Keywords: Lichen planus; Mitochondria; DNA content; Oxidative stress
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