Oral lichen planus (OLP) is a chronic immune-mediated mucosal disease with a prolonged, recurrent course. Although conventional models explain basal keratinocyte injury through T-cell-mediated cytotoxicity, they do not fully account for site-restricted chronicity or recurrence after clinical improvement. Single-cell, immune repertoire, and spatial studies have identified tissue-associated CD8+ T-cell states, fibroblast subsets, and organized lymphoid structures within the affected mucosa. OLP-specific studies link tissue-resident memory T (TRM)-like CD8+ cells near the epithelial basement membrane to erosive disease and recurrent erosions. Tertiary lymphoid structures (TLSs) are frequently observed in OLP. CCL19+ fibroblast-associated TLS organization has been linked to atrophic erosive disease and greater clinical activity, and TLS-related humoral activation has been associated with erosive and recurrent phenotypes. SFRP2+WNT5A+ fibroblasts may further amplify T-cell–epithelial inflammation. In contrast, a recent multiomics study of cutaneous and mucosal lichen planus found no prominent canonical TRM signature and identified CXCL13+ cytotoxic CD8+ T-cells associated with an inferred classical type 2 dendritic cell subset A– interleukin-15 interaction and spatially linked to epithelial responses. This review compares these findings through two nonexclusive hypotheses: cellular persistence, in which pathogenic lymphocytes remain within the affected mucosa, and niche persistence, in which local stromal, myeloid, and lymphoid components retain the capacity to reactivate or regenerate cytotoxic T-cell states. Because current evidence is predominantly cross-sectional, persistent clonotypes, direct TRM–TLS interactions, and causal roles in recurrence remain undetermined. Longitudinal same-site sampling with clonotype tracking and spatial profiling is required to identify which tissue features remain after clinical improvement and which features predict recurrence.

Introduction
From Epithelial Cytotoxicity to LocalImmune Persistence
Tissue-resident Memory T-cells andPersistent CD8+ T-cell States
Tertiary Lymphoid Structures asOrganizers of Local Immunity
Stromal and Dendritic-cell NetworksConnect Persistent Immunity to EpithelialInjury
An Integrated Model of Local ImmunePersistence
Clinical Implications and Future Directions
Conclusion
Funding
Conflicts of Interest
References

• Cheul Kim(Department of Oral Medicine and Diagnosis, Research Institute of Oral Science, College of Dentistry, Kangwon National University, Gangneung 25457, Republic of Korea)
• Kyu Hwan Kwack(Department of Oral Microbiology, College of Dentistry, Kyung Hee University, Seoul 02447, Republic of Korea) Corresponding author