Oral lichen planus (OLP) is a chronic inflammatory disorder of oral mucosa of unknown etiology with an unpredictable and prolonged course affecting 0.1%-4% of the general population, especially women aged over 40 years. 1 Mounting evidence points to a T-cell-mediated immune response against epithelial cells in the pathogenesis of the disease. 2 The key components of the Abstract Backgrounds: To explore the expression and functions of the tripartite motif-containing protein 21 (TRIM21) in oral lichen planus(OLP) lesions. Methods: Paraffin sections of buccal mucosa samples from 15 cases of reticular oral lichen planus (OLP) patients and 10 healthy controls were used for immunohistochemistry to determine expression and distribution of TRIM21. Buccal mucosae from 11 OLP patients and seven healthy controls were analyzed by qPCR to quantify its gene expression. Peripheral blood mononuclear cells and CD3+ cells from four pairs of age-and sex-matched OLP patients and healthy controls were isolated for immunocytochemistry and culture. Following lentivirus-mediated overexpression of TRIM21 gene in CD3+ cells, CCK-8 was applied to evaluate cell proliferation.Cytokines including IL-2, IL-4, IL-5, IL-6, IL-10, TNF-α, and IFN-γ in the supernatants were measured by the cytometric bead array and verified by ELISA. Results:A larger number of TRIM21-positive cells infiltrating the lamina propria were observed in OLP lesions by immunohistochemistry than those of healthy controls.Significantly higher transcription of TRIM21 was revealed by qPCR. TRIM21 overexpression in CD3+ cells significantly enhanced the proliferation and IL-6 secretion in CD3+ cells from 12 to 72 hours. Conclusion:Overexpressed TRIM21 in OLP may be a primary proinflammatory molecule rather than a secondary and inducible regulatory factor in immunopathogenesis of OLP. K E Y W O R D SIL-6, oral lichen planus, proliferation, T cells, TRIM21

Background: Recurrent aphthous stomatitis (RAS) is the most common oral mucosal disease, and ulcer-free periods are a major concern for patients. Thalidomide has been shown to be an effective systemic drug in the treatment of RAS, but the value of undertaking a trial to evaluate various maintenance doses was warranted. Methods:We performed this randomized controlled clinical trial with a two-stage design. Firstly, all the 125 cases of RAS received prednisone at a starting dose of 15 mg/d for one week as an initial therapeutic drug. Secondly, the 100 cases of RAS in the experimental group received thalidomide (50 mg/d vs. 25 mg/d) as a maintenance drug to observe its efficacy and safety. Results:During maintenance medication at the fourth and eighth weekend, the two doses (50 and 25 mg/d) of thalidomide were equivalent in reducing the incidence of ulcers, ulcer number, and ulcer pain, respectively (all p > 0.05). Notably, the ulcer-free period in the group using 25 mg/d thalidomide for eight weeks was longer (mean, >3 months) than those in the other groups (all p < 0.05). Importantly, the total adverse events in the group using 25 mg/d thalidomide were significantly less than those in the group using 50 mg/d (p < 0.001). Moreover, the effect of 50 mg/d thalidomide on the levels of various salivary cytokines was not superior to 25 mg/d medication (p > 0.05). Conclusion:This dose optimization study concluded that 25 mg/d thalidomide had a long-term effect on extending the recurrence interval of RAS with better safety.