Narrative review reveals cellular senescence drives chronic stromal inflammation in oral lichen planus, highlighting novel avenues for targeted therapeutics.
Key Points
To critically evaluate the direct and indirect evidence linking cellular senescence and its associated secretory phenotype to the chronic inflammatory circuit in oral lichen planus.
Conducted a focused narrative search across PubMed/MEDLINE, Scopus, and Web of Science through July 31, 2026.
Synthesized molecular, cellular, and multimodal data regarding senescence markers, stromal communication pathways, and in vitro experimental models.
Senescence-associated gene and protein signatures localize primarily to PDGFRα-positive mesenchymal cells, showing elevated CXCL12–CXCR4 and extracellular matrix–CD44 interactions with cytotoxic CD8-positive T cells.
Conditioned medium from senescent fibroblasts experimentally amplifies lymphoid-cell activation and epithelial keratinocyte damage.
Historical markers including p16, p21, p53, and oxidative DNA damage support senescence involvement but remain insufficient as standalone diagnostic proof.