OBJECTIVE: Oral lichen planus (OLP) is a chronic inflammatory disease characterized by a dense T-cell infiltration and the degeneration of basal keratinocytes. The potential functions of mucosal associated invariant T (MAIT) cells in OLP have been analyzed in our previous study. Keratinocytes under proinflammatory conditions have been demonstrated to activate T cells. This study was aimed to investigate how keratinocytes stimulate MAIT cells in OLP, and to explore the role of activated MAIT cells on keratinocytes.
RESULTS: Increased MAIT cells and higher activation marker CD69 were detected in OLP lesions by flow cytometry. The enhanced expression of MHC class I-like molecule (MR1) required for MAIT cell activation in the epithelial layer of OLP lesions was determined by immunohistochemistry. Keratinocytes treated by 5-A-RU prodrug and lipopolysaccharide, respectively, exhibited higher expression of MR1 and secretion of IL-18. In direct coculture systems consisting of keratinocytes and peripheral blood mononuclear cells, both 5-A-RU prodrug-pretreated keratinocytes and lipopolysaccharide-pretreated keratinocytes activated MAIT cells to secrete granzyme B, contributing to elevated keratinocyte apoptosis.
CONCLUSIONS: Keratinocytes were capable to activate MAIT cells via MR1 and cytokines in OLP, and granzyme B produced by activated MAIT cells intensified keratinocyte apoptosis, engaging in the pathogenesis of OLP.

BACKGROUND: Oral lichen planus (OLP) is a common T cell-mediated oral mucosal immune inflammatory disease. Intraepithelial lymphocytes (IELs) are a unique subset of T cells that play an important role in regulating immune response. This study aims to investigate the phenotype and the differentiation mechanism of IELs in OLP.
METHODS: The expression of CD4, CD8α, CD8β, T-helper-inducing POZ/Krueppel-like factor (ThPOK), and RUNX family transcription factor 3 (Runx3) in the epithelium and peripheral blood mononuclear cells (PBMCs) of OLP was determined by immunofluorescence and immunohistochemistry. Then, the correlations among them were analyzed. Naïve CD4+ T cells were sorted from blood of OLP patients and stimulated with retinoic acid (RA) and transforming growth factor-β1 (TGF-β1). Then the expression of CD4, CD8α, CD8β, ThPOK, and Runx3 was investigated by immunocytochemistry.
RESULTS: CD8α expression and CD8αα+ cells were upregulated in the epithelium of OLP, whereas they were downregulated in PBMCs of OLP. CD8β was not expressed in the epithelium of OLP. CD4, CD8α, and Runx3 expression and CD4+CD8α+ cells were increased, whereas ThPOK expression was decreased in the epithelium of OLP. CD8α expression was positively correlated with Runx3 expression, whereas ThPOK expression was negatively correlated with Runx3 expression. After RA and TGF-β1 stimulation, CD8α and Runx3 expression was upregulated, and ThPOK expression was downregulated in naïve CD4+ T cells.
CONCLUSIONS: CD4+CD8αα+ IELs may be the dominant phenotype of IELs in OLP, and the differentiation of CD4+CD8αα+ IELs in OLP is negatively regulated by ThPOK and positively regulated by Runx3.

UNASSIGNED: Oral lichen planus (OLP) is a relatively common chronic T cell-mediated disease characterized by pain and inflammation. Clobetasol propionate (CLO) is the first-line drug in the treatment of OLP. The meta-analysis aimed to evaluate the efficacy and safety of CLO for treating patients with OLP.
UNASSIGNED: PubMed, Embase and Web of Science were systematically searched from the database inception date up to August 2023. There were no restrictions on language or date of publication. The outcomes of our interest were as follows: improvement of clinical signs and/or symptoms, total lesion size, relapse and adverse events.
UNASSIGNED: A total of 17 RCTs evaluating the effects of CLO were included in this study. The results revealed no significant difference in the clinical score (WMD = 0.14, 95% CI: -0.39, 0.66; p = 0.609) and pain score (WMD = 0.17, 95% CI: -0.44, 0.79; p = 0.582) between CLO and other treatments. However, clinical resolution (RR = 1.61, 95% CI: 1.17, 2.22; p = 0.003) and symptoms improvement (RR = 1.80, 95% CI: 1.17, 2.77; p = 0.008) were significantly different between CLO and other treatments. Moreover, there was a significant reduction in the total lesion size with CLO treatment (WMD = -0.58, 95% CI: -1.03, -0.13; p = 0.011). In addition, CLO showed no statistical incidence of adverse events (RR = 1.46, 95% CI: 0.86, 2.50; p = 0.161) and relapse (RR = 1.56, 95% CI: 0.66, 3.71; p = 0.314) than other therapies.
UNASSIGNED: This systematic review and meta-analysis of 17 randomized clinical trials supported the long-term application of CLO as an effective regimen in OLP patients.

BACKGROUND: Emerging evidence emphasized the role of oral microbiome in oral lichen planus (OLP). To date, no dominant pathogenic bacteria have been identified consistently. It is noteworthy that a decreased abundance of Streptococcus, a member of lactic acid bacteria (LAB) in OLP patients has been commonly reported, indicating its possible effect on OLP. This study aims to investigate the composition of LAB genera in OLP patients by high-throughput sequencing, and to explore the possible relationship between them.
METHODS: We collected saliva samples from patients with OLP (n = 21) and healthy controls (n = 22) and performed 16 S rRNA gene high-throughput sequencing. In addition, the abundance of LAB genera was comprehensively analyzed and compared between OLP and HC group. To verify the expression of Lactococcus lactis, real time PCR was conducted in buccal mucosa swab from another 14 patients with OLP and 10 HC. Furthermore, the correlation was conducted between clinical severity of OLP and LAB.
RESULTS: OLP and HC groups showed similar community richness and diversity. The members of LAB, Lactococcus and Lactococcus lactis significantly decreased in saliva of OLP cases and negatively associated with OLP severity. In addition, Lactococcus and Lactococcus lactis showed negative relationship with Fusobacterium and Aggregatibacter, which were considered as potential pathogens of OLP. Similarly, compared with healthy controls, the amount of Lactococcus lactis in mucosa lesion of OLP patients was significantly decreased.
CONCLUSIONS: A lower amount of Lactococcus at genus level, Lactococcus lactis at species level was observed in OLP cases and associated with disease severity. Further studies to verify the relationship between LAB and OLP, as well as to explore the precise mechanism is needed.

BACKGROUND: This study aimed to evaluate the incidence of implant failure in patients with oral lichen planus (OLP) and investigate the potential association between OLP and peri-implant diseases.
METHODS: Embase, Web of Science, PubMed, and Scopus databases were searched for studies with no time restrictions. Meta-analysis was performed calculating pooled proportion of peri-implantitis (PI), peri-implant mucositis (PIM), and bleeding on probing (BOP) prevalence using fixed-effects model. Odds ratio and corresponding 95% CI were calculated to assess the potential risk of PI, PIM, and BOP in dental implant patients with OLP compared to healthy controls.
RESULTS: Implant failure rate was 4.38% at the patient level and 4.37% at the implant level. Six patients (3.92%) from five studies were diagnosed with oral cancer after receiving implant. The prevalence of PI, PIM, and BOP at the implant level were 14.00%, 20.00%, and 40.00%, respectively. There was no significant difference in the occurrence of PI and PIM between OLP patients and healthy controls.
CONCLUSIONS: Stabilized OLP is not considered a significant risk factor for peri-implant diseases. It is advised against placing implants or prostheses during the acute phase of the disease. Histopathological investigation to differentiate OLP from oral lichenoid dysplasia is crucial.

Oral lichen planus (OLP) is a common chronic inflammatory disease of the oral mucosa, the mechanism of its inflammatory progression has not yet been fully elucidated. PA28γ plays a significant role in a variety of immune-related diseases. However, the exact role of PA28γ in the pathogenesis of OLP remains unclear. Here, we demonstrated that PA28γ is overexpressed in epithelial cells and inflammatory cells of OLP tissues but has no significant relationship with OLP subtypes. Functionally, keratinocytes with high PA28γ expression could induce dendritic cell (DC) maturation and promote the T-cell differentiation into Th1 cells in response to the immune response. In addition, we found that a high level of PA28γ expression is associated with high numbers of infiltrating mature DCs and activated T-cells in OLP tissues. Mechanistically, keratinocytes with high PA28γ expression could promote the secretion of C-C motif chemokine (CCL)5, blocking CCL5 or/and its receptor CD44 could inhibit the induction of T-cell differentiation by keratinocytes with high PA28γ expression. In conclusion, we reveal that keratinocytes with high expression of PA28γ in OLP can induce DC maturation and promote T-cell differentiation through the CCL5-CD44 pathway, providing previously unidentified mechanistic insights into the mechanism of inflammatory progression in OLP.

OBJECTIVE: Our previous studies have found that the composition ratio of Prevotella melaninogenica (Pm) on buccal mucosa surface of oral lichen planus (OLP) patients increased significantly compared with control. Furthermore, Pm could invade the epithelium of OLP patients. This study aimed to further explore the impact of Pm on oral keratinocytes.
METHODS: The Pm-human oral keratinocyte (HOK) co-culture model was established to detect monolayer permeability, zona occludens-1 (ZO-1) expression, and intracellular survival of Pm. We performed RNA-seq followed by identification of differentially expressed genes (DEGs) and Gene Ontology (GO) analysis, with a particular focus on myosin light chain kinase (MLCK). An MLCK inhibitor ML-7 was utilized in Pm-HOK co-culture model to assess its effects on monolayer permeability and ZO-1 expression.
RESULTS: HOK monolayer permeability was increased, and ZO-1 expression was decreased after co-culture (p < 0.05). Pm could survive in HOK cells. RNA-seq revealed MLCK was an upregulated common DEG. The expression of MLCK in the Pm-HOK co-culture model was upregulated. Inhibition of MLCK rescued the increased epithelial permeability, and ZO-1 expression was upregulated (p < 0.05).
CONCLUSIONS: MLCK may be involved in disrupting epithelial barrier function by Pm.

BACKGROUND: Oral lichen planus (OLP) is one of the most common oral mucosal diseases, exhibiting a higher prevalence in women than men, but its pathogenesis is still unclear. Current research suggests that microbial dysbiosis may play an important role in the pathogenesis of OLP. Our previous research has found that the increase of Prevotella melaninogenica and decrease of Streptococcus salivarius have been identified as a potential pathogenic factor in OLP. Consequently, the objective of this study is to examine whether S. salivarius can counteract the detrimental effects of P. melaninogenica on the integrity of the epithelial barrier function.
METHODS: Epithelial barrier disruption was induced by P. melaninogenica in human keratinocytes (HaCaT cells). HaCaT cells were pretreated with S. salivarius(MOI = 20) or cell-free supernatant for 3 h, followed by treatment with P. melaninogenica (MOI = 5) for 3 h. The epithelial barrier integrity of HaCaT cells was detected by FD4 permeability. The mRNA level of tight junction protein was detected by quantitative real-time polymerase chain reaction (PCR). Immunofluorescence and Western Blot were used to detect the protein expression of zonula occludin-1 (ZO-1). The serial dilution-spotting assay was applied to monitor the viability of P. melaninogenica at the end of 8 and 24 h incubation.
RESULTS: Challenge by P. melaninogenica decreased the levels of tight junction proteins, including occludin, ZO-1, and claudin in HaCaT cells. S. salivarius or its cell-free supernatant inhibited the down-regulation of ZO-1 mRNA and protein expression levels induced by P. melaninogenica and thus improved the epithelial barrier function. The inhibitory effect of the cell-free supernatant of S. salivarius on the growth of P. melaninogenica is associated with metabolic acid production rather than with bacteriocins and hydrogen peroxide.
CONCLUSIONS: These results suggest that live S. salivarius or its cell-free supernatant significantly ameliorated the disruption of epithelial tight junctions induced by P. melaninogenica, likely through the inhibition of P. melaninogenica growth mediated by metabolic acid production.

Compelling evidence indicates that dyslipidemia is positively associated with oral lichen planus (OLP). The types and magnitude of lipid metabolism disturbance in peripheral blood of OLP patients have been investigated in different studies. Yet, consensus on how these different lipid components varied in levels for the development of OLP lesions has not been reached so far. Herein, a total of 8 eligible studies were recognized, which enrolled 533 cases of OLP and 499 healthy controls. The analysis showed that the average total triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) levels were considerably higher, and high-density lipoprotein cholesterol (HDL-C) levels were significantly lower in OLP patients compared to healthy controls. Collectively, the lipid profile panel maybe serve as the potential predictive indicator for screening OLP.

Verrucous xanthoma is a rare benign muco-cutaneous lesion, whereas oral lichen planus is a chronic inflammatory disease relatively common in the clinical setting. Verrucous xanthoma and oral lichen planus can reportedly coexist according to foreign literature. Owing to the low incidence of verrucous xanthoma and the rarity of co-occurrence of these two diseases, the mechanism underlying the co-occurrence of the two diseases remains inconclusive. In this work, a case of oral verrucous xanthoma complicated with oral lichen planus was reported. Related literature was reviewed to discuss the clinical classification, pathological classification, and possible pathogenesis of the two diseases.
疣状黄瘤是一种罕见的良性黏膜皮肤病变，而口腔扁平苔藓则是口腔门诊中较为常见的一种慢性炎症性疾病。国外已有文献报道，疣状黄瘤与口腔扁平苔藓可以存在伴发现象。由于疣状黄瘤的低发病率，两病共存的情况较为罕见，目前，对于两种疾病伴发的内在机制尚无定论。本文报道了1例口腔疣状黄瘤合并口腔扁平苔藓的临床病例，并回顾相关文献，探讨两种疾病伴发的临床分类、病理分型及可能的发病机制。.