Pathogenesis Of Oral Lichen Planus Research Articles

Molecular detection of human papillomavirus DNA in dysplastic and non-dysplastic oral lichen planus patients

Introduction: Oral Lichen Planus (OLP) is a chronic inflammatory disease of cell-mediated dysregulation characterized by relapses and remissions. The aetiology of OLP has been extensively studied for decades. The pathogenesis is unclear with a debatable malignant transformation. The pathogenesis and malignant transformation of OLP may be affected by viruses such as Hepatitis C Virus (HCV), Human Papillomavirus (HPV), Herpes Simplex Virus (HSV), and stress. HPV has been proved to be an etiological agent in oropharyngeal cancers and non-tobacco-associated leukoplakia. The role of human papillomavirus in the pathogenesis of OLP and its malignant transformation has to be studied extensively. Aim: This study aims to detect the presence of HPV DNA in the biopsy samples of dysplastic and non-dysplastic OLP and thus determine the role the virus played in the malignant transformation of OLP. Materials and Methods: Biopsy samples comprising 250 OLP tissues were collected. The DNA was extracted from the fixed tissue by using the Cetyltrimethylammonium bromide (CTAB) method. Polymerase Chain Reaction (PCR) was performed using primers to amplify the HPV E6 gene. Results: Hundred and three out of 250 (41.2%) OLP cases were positive for HPV DNA.

DNA Fragmentation and mRNA Expression of Bcl-2, Bcl-xL, p53, p21 and HSP70 Genes in Nondysplastic and Dysplastic Oral Lichen Planus.

Background:Oral lichen planus (OLP) is a chronic inflammatory disease. Apoptosis of the basal keratinocytes is a causative factor for OLP pathogenesis but the detailed mechanism of apoptosis among nondysplastic and dysplastic OLP lesions is yet unraveled.Aims:This study aims to evaluate the involvement of cellular DNA fragmentation and alteration in the expression of Bcl-2 and B-cell lymphoma extra-large (Bcl-xL), p53, p21 and heat shock protein 70 (HSP70) in nondysplastic and dysplastic OLP lesions.Materials and Methods:Untreated, fifteen OLP patients each with nondysplastic and dysplastic lesions were enrolled for this study. Their DNA fragmentation was analyzed by the agarose gel electrophoresis method. The mRNA expression of Bcl-2, Bcl-xL, p53, p21 and HSP70 were measured using semi-quantitative reverse transcription-polymerase chain reaction.Results:Elevated DNA fragmentations were found in dysplastic lesions compared to nondysplastic type. Significantly higher expression of Bcl-2, Bcl-xL, p53 and p21 were found in both types of OLP lesion compared to the control. Expression of Bcl-2 and Bcl-xL were significantly elevated in nondysplastic lesions, whereas significantly overexpression of p53 and p21 were found in dysplastic lesions. Anti-stress protein HSP70 was overtly expressed in dysplastic lesions compared to other groups.Conclusion:Reduced expression of Bcl-2 and Bcl-xL, with elevated DNA fragmentation, may be associated with increased apoptosis in dysplastic lesions which aid in the resolution of the chronic inflammatory process. Higher expression of p53 and p21 in dysplastic lesions reflect its malignant potentiality. Overexpression of HSP70 in dysplastic lesions is a useful marker for higher cellular stress.

MiR-155-5p modulates inflammatory phenotype of activated oral lichen-planus-associated-fibroblasts by targeting SOCS1.

Oral lichen planus (OLP) is a chronic inflammatory oral mucosal disease. Cytokines are closely associated with OLP development. In addition to immune cells, fibroblasts have been reported to induce regional inflammation. MicroRNA(miR)-155-5p is reportedly increased significantly in OLP and is known to regulate inflammation. This study aimed to investigate the role of miR-155-5p in fibroblasts of OLP lesions. Normal mucosal fibroblasts (NFs) and OLP associated-fibroblasts (OLP AFs) were isolated from the oral mucosa of 15 healthy controls and 30 OLP patients. We detected the expression of miR-155-5p and fibroblast activation protein alpha (FAP-α) using quantitative RT-PCR and analyzed their correlation. Interleukin (IL)-6 and IL-8 levels were determined using ELISA. Expression of suppressor of cytokine signaling (SOCS) 1 was analyzed by western blotting. A dual-luciferase reporter assay was performed to investigate the interaction between miR-155-5p and SOCS1. MiR-155-5p and FAP-α were significantly increased and positively correlated in OLP AFs. Overexpression of miR-155-5p in OLP AFs augmented IL-6 and IL-8 release and decreased SOCS1 expression, whereas knockdown of miR-155-5p in OLP AFs decreased IL-6 and IL-8 release. The expression of SOCS1 was downregulated in OLP AFs, and SOCS1 silencing augmented IL-6 and IL-8 production in OLP AFs. Furthermore, miR-155-5p inhibited SOCS1 expression by directly targeting its 3'-UTR in OLP AFs. MiR-155-5p regulates the secretion of IL-6 and IL-8 by downregulating the expression of SOCS1 in activated OLP AFs. Our results provide novel insights into the pathogenesis of OLP and identify a potential new target for OLP therapy.

FAP-α+ immunofibroblasts in oral lichen planus promote CD4+ T-cell infiltration via CCL5 secretion.

Oral lichen planus (OLP) is a T cell-mediated, chronic inflammatory disease. CD4+ T-cell infiltration plays a crucial role in the pathogenesis of OLP. Fibroblasts are activated under pathological conditions and perform various functions. This study was designed to explore the immune activation and biological functions of OLP fibroblasts on CD4+ T cells. We detected the expression of fibroblast activation protein-alpha (FAP-α) in the oral tissues of patients with OLP and healthy controls using immunohistochemistry. Furthermore, expression of FAP-α and C-C motif chemokine ligand 5 (CCL5) in fibroblasts isolated from oral tissues of patients with OLP and healthy controls was assayed by quantitative PCR, Western blotting and enzyme-linked immunosorbent assay. Moreover, we assessed the effects of fibroblasts on CD4+ T-cell proliferation, apoptosis and migration using flow cytometry and Transwell assays. We found that FAP-α expression in the oral tissues of patients with OLP was significantly higher than that in healthy controls. FAP-α and CCL5 expression levels were significantly upregulated in OLP fibroblasts. Moreover, OLP fibroblasts promoted CD4+ T-cell proliferation and migration and inhibited CD4+ T cell apoptosis. In summary, our findings indicate that OLP fibroblasts are immunologically activated and induce CD4+ T-cell infiltration in OLP.

Potential role of INTERLEUKIN-17 in the pathogenesis of oral lichen planus: a systematic review with META-analysis.

Oral lichen planus (OLP) is a chronic inflammatory mucocutaneous disease of unknown aetiology, which may evolve into squamous cell carcinoma. Recent advances on OLP pathogenesis suggest the presence of Th17 cells and the up-regulation of interleukin-17 (IL-17) expression are crucial events. Our aim was to test the hypothesis in the literature about an important role of IL-17 in OLP by systematically investigating the overexpression of IL-17 in the lesional tissue and blood from OLP patients and healthy controls. A total of 22 studies comprising 658 OLP patients and 362 control subjects fulfilled inclusion criteria were subjected to meta-analysis. The assessment of IL-17 in the lesional tissue by quantitative real-time polymerase chain reaction (PCR) revealed a significant elevation in the OLP group (RR:1.35 95%CI: 0.20-2.50, I2 = 92%). There was a statistical overexpression of IL-17 in the serum of OLP group detected by ELISA (RR:2.47 95%CI: 1.17-3.77, I2 = 97%) and flow cytometry (RR:3.04 95%CI: 0.69-5.39, I2 = 97%). In the erosive OLP group, the tissue IL-17 assessed by PCR was higher than in reticular OLP patients (RR:0.78 95%CI: 0.21-1.36, I2 = 0%). Peripheral assessment of IL-17 by ELISA (RR:1.43 95%CI: 0.01-2.85, I2 = 94%) and flow cytometry (RR:1.55 95%CI: 0.29-2.81, I2 = 89%) revealed significant elevation in erosive OLP group. The dominating overexpression of IL-17 and Th17 cells in the local inflammatory infíltrate and serum of OLP patients confirms its role, probably in the interaction between T cells and keratinocytes. Notably, the upregulation of IL-17 is more intense in erosive than in reticular OLP suggesting a positive correlation between IL-17 levels and disease severity. Further research is warranted to investigate the potential role of anti-IL-17 drugs to manage this chronic condition.

Role of human papillomavirus in the pathogenesis of oral lichen planus

Oral Lichen Planus (OLP) is a chronic inflammatory disease with a cell-mediated immunopathologic response. Although OLP has been studied extensively for decades, its exactaetiologyremains unclear. Autoimmunity, viruses like Hepatitis C Virus (HCV), Human Papillomavirus (HPV), and stress have all beenhypothesized in recent articles. HPVs are epitheliotropic viruses with an affinity for keratinocytes and are principally found in the anogenital tract, urethra, skin, larynx, tracheobronchial and oral mucosa. This article aimed to review the frequency of HPV prevalence in OLP. A computer database search was performed through the use of PubMed from 1987 to 2021. The summary showed that the association of HPV and OLP varied significantly by geographic population. The correlation of HPV and erosive-atrophic oral lichen planus was comparable and well above that of HPV and non-EA-OLP. Among HPV genotypes, HPV 16 showed an extremely strong association with OLP, and HPV 18 showed a relatively strong one.

Cell-Free DNA Promotes Inflammation in Patients With Oral Lichen Planus via the STING Pathway.

BackgroundDamaged and dead cells release cell-free DNA (cfDNA) that activates cyclic GMP–AMP (cGAMP) synthase (cGAS), which leads to the activation of stimulator of interferon genes (STING) via the second messenger cGAMP. STING promotes the production of inflammatory cytokines and type I interferons to induce an inflammatory response. Oral lichen planus (OLP), a chronic autoimmune disease involving oral mucosa characterized by the apoptosis of keratinocytes mediated by T-lymphocytes, is related to the activation of multiple inflammatory signaling pathways. Currently, the relationship between cfDNA and OLP has not been confirmed. We hypothesized that cfDNA may be a potential therapeutic target for OLP.MethodscfDNA was extracted from the saliva and plasma of OLP patients; its concentration was measured using the Quanti-iT-PicoGree kit and its relationship with OLP inflammation was assessed. cfDNA of OLP patients (cfDNA-OLP) was transfected into THP-1 macrophages and the expression of inflammatory factors was investigated by performing quantitative real time PCR (qRT-PCR), western blotting, and enzyme-linked immunosorbent assay (ELISA). STING expression was analyzed in the tissues of OLP patients and healthy controls using immunohistochemical staining and western blotting. siRNA was used to knockdown STING expression in THP-1 macrophages, and the inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) secreted by cells following cfDNA-OLP transfection were detected using ELISA. Finally, the effect of the cationic polymer PAMAM-G3 was evaluated on the treatment of inflammation induced by cfDNA-OLP.ResultsThe concentration of cfDNA in the saliva and plasma of OLP patients was considerably higher than that of healthy controls, and it positively correlated with the levels of inflammatory cytokines and clinical characteristics. cfDNA-OLP induced an inflammatory response in THP-1 macrophages. STING expression was significantly higher in OLP tissues than in the gingival tissues of healthy controls. STING knockdown suppressed cfDNA-OLP-induced inflammation in THP-1 macrophages. PAMAM-G3 inhibited the inflammatory response caused by cfDNA-OLP.ConclusionThe cfDNA level is increased in OLP patients, and the STING pathway activated by cfDNA-OLP might play a critical role in OLP pathogenesis. Treatment with PAMAM-G3 reduced the inflammation induced by cfDNA-OLP, and therefore, may be a potential treatment strategy for OLP.

Probiotics as Potential Biological Immunomodulators in the Management of Oral Lichen Planus: What's New?

Oral lichen planus (OLP) is a T cell-mediated chronic inflammatory disorder with multifactorial aetiology and malignant transformation potential. Despite the treatments so far identified, new tailored and safe specific measures are needed. Recently, human microbiota imbalance has been linked to several immune-mediated diseases, opening new therapeutic perspectives for probiotics; besides their ability to directly interact with the host microbiota, they also display a strain-specific immune-modulatory effect. Thus, this non-systematic review aims to elucidate the molecular pathways underlying probiotic activity, mainly those of Lactobacilli and Bifidobacteria and their metabolites in OLP pathogenesis and malignant transformation, focusing on the most recent in vitro and in vivo research evidence. Findings related to their activity in other immune-mediated diseases are here included, suggesting a probiotic translational use in OLP. Probiotics show immune-modulatory and microbiota-balancing activities; they protect the host from pathogens, hamper an excessive effector T cell response, reduce nuclear factor-kappa B (NF-kB) signalling and basal keratinocytes abnormal apoptosis, shifting the mucosal response towards the production of anti-inflammatory cytokines, thus preventing uncontrolled damage. Therefore, probiotics could be a highly encouraging prevention and immunotherapeutic approach for a safer and more sustainable OLP management.

Protein disulfide isomerase family A member 3 expression is upregulated in tissue-derived extracellular vesicles in oral lichen planus and oral lichenoid lesions

ObjectivesThe aim of this study was to identify the tissue-derived extracellular vesicles immunogen involved in the pathogenesis of oral lichen planus (OLP) and its variation oral lichenoid lesions (OLL). DesignSix pooled tissue-derived extracellular vesicles from participants with OLP/OLL and three from healthy controls were isolated and enriched. The extracellular vesicles were characterized with transmission electronic microscopy, nanoparticle tracking analysis and western blotting. Proteins from extracellular vesicles were identified with proteomics analysis and differentially expressed proteins (DEPs) were further identified with a 2-fold (p < 0.05) increase or a 0.5-fold decrease. ResultsA total of 1805 peptides and 141 proteins were identified. Ten DEPs were further identified, with five upregulated proteins of fibrinogen alpha chain, lamin isoform A, 40S ribosomal protein, protein disulfide isomerase family A member 3 (PDIA3) and elongation factor 1-alpha 1, and five downregulated proteins of plakophilin-1, katanin p80 repeat-containing subunit B1, collagen alpha-3 chain, mitochondrial 2-oxoglutarate/malate carrier protein and guanine nucleotide-binding protein subunit gamma-12. PDIA3 was found to be immune-associated and to be involved in the antigen processing and presentation pathway. The upregulation of PDIA3 was confirmed in a verification cohort composed of three pairs of OLP/OLL-extracellular vesicles and healthy controls-extracellular vesicles with western blotting. ConclusionsProtein disulfide isomerase family A member 3 in extracellular vesicles may play a significant role in the local immune responses and the pathogenesis of oral lichen planus and oral lichenoid lesions.

Structural Analysis of Salivary Bacterial and Fungal Microbiome in Oral Lichen Planus Patients

To explore the differences of oral mycobiome and bacteriome between the healthy controls (H) and oral lichen planus (OLP) patients, and the co-occurrence patterns of the salivary mycobiome and bacteriome and the association with host immunity. Saliva samples were collected from clinical OLP patients (n=35) and healthy volunteers (n=18). Microbiome DNA was extracted for bacterial 16S rRNA genes sequencing and fungal internal transcribed spacer 2 (ITS2) sequencing. Bioinformatics analysis was performed on the data.The levels of IL-17 and IL-23, two pro-inflammatory cytokines, in the saliva were examined, and their correlation with the bacteria was analyzed. There was no significant difference in the overall community structure of the mycobiome and the bacteriome between OLP patients and healthy controls. The abundance of Prevotellaand Solobacterium in the saliva bacteriome was significantly increased in the OLP group (P<0.05), and the relative abundance of Candidaand Aspergillusin the saliva mycobiome was also significantly increased (P<0.05). The co-occurrence pattern of the salivary mycobiome and bacteriome showed that the aforementioned difference was not related. However, the correlation between Aspergillusand bacteria was altered in the H group and the OLP group, and co-occurrence was reduced in the latter group. The level of IL-17 in the saliva was significantly increased in the OLP group. IL-17 and clinical scores were significantly correlated with the abundance of Porphyromonas. The increased abundance of Prevotella, Solobacterium, Candida, and Aspergillus was associated with the pathogenesis of OLP, and the changes of the microbiome co-occurrence relationship and host immunity may be involved in the pathogenesis of OLP.

Identification of Potential Key Biomarkers and Immune Infiltration in Oral Lichen Planus.

Background Oral lichen planus (OLP) is a chronic autoimmune oral mucosal disease that seriously affects the life quality of the patients. But till now, the exact etiology and pathogenesis of OLP remain unclear. Our study is aimed at finding the key molecules and pathways involved in the pathogenesis mechanisms of OLP, providing more effective therapeutic strategies for OLP. Methods Data from GSE52130 were downloaded from GEO datasets for analysis. Then, we carried out enrichment analysis of the differentially expressed genes (DEGs) using Gene Ontology (GO) and KEGG pathway analyses. Next, the CIBERSORT algorithm was used to assess immune cell infiltration in OLP patients. Furthermore, we also constructed a protein-protein interaction network using STRING and Cytoscape and simultaneously sought potential transcription factors plug-in including MCODE CytoHubba and iRegulon. In addition, ROC analysis was employed to assess the diagnostic performance of these hub genes. Lastly, we identified 6 promising novel drugs to treat OLP through Connectivity Map. Results We illustrated that 255 DEGs were mainly enriched in the focal adhesion pathway and metabolism pathways. Besides, Cibersort analysis showed that M1 macrophages, T follicular helper cells, and T regulatory cells are more infiltrated in OLP samples. In addition, ROC analysis demonstrated that these hub genes owned higher diagnostic value in OLP, in which SPRR1B had the highest diagnostic value. And we also predicted that SOX7 was the most relevant transcription factor of those hub genes. Lastly, through the CMap database, we identified 6 small molecules as possible treatment drugs of OLP. Conclusion Our research identified that SPRR1B could be used as potential biomarkers for the early diagnosis of OLP. In addition, as a chronic autoimmune oral mucosal disease, OLP has different infiltration types of immune cells. Furthermore, 6 small molecules were proposed as promising novel treatment drugs for OLP patients. Therefore, our research may provide new impetus for the development of effective OLP biological treatment options.

Immune mechanisms in oral lichen planus.

Oral lichen planus (OLP) is a T cell-mediated inflammatory disease of the oral mucosa that has been extensively researched over many years but as yet the mechanisms of pathogenesis are still not fully understood. Whilst the specific aetiological factors driving OLP remain ambiguous, evidence points to the development of a chronic, dysregulated immune response to OLP-mediating antigens presented by innate immune cells and oral keratinocytes leading to increased cytokine, chemokine and adhesion molecule expression. These molecules recruit T cells and mast cells to the diseased site and orchestrate a complex interplay between cells that culminates in keratinocyte cell death, mucosal basement membrane destruction and long-term chronicity of the disease. The main lymphocytes involved are thought to be CD8+ cytotoxic and CD4+ Th1 polarised T cells although recent evidence indicates the involvement of other Th subsets such as Th9, Th17 and Tregs, suggesting that a more complex immune cell relationship exists during the disease process. This review provides an overview of the immune mechanisms at play in OLP pathogenesis with particular emphasis on the role of the different Th subsets and how these recent discoveries may guide research towards identifying potential therapeutic targets.

Immunohistochemical Evaluation of Transforming Growth Factor-β Expression in Oral Lichen Planus

Background: In oral lichen planus (OLP), which is a persistent inflammatory condition of the autoimmune system, cytotoxic T lymphocytes are triggered against epithelial cells. OLP resists treatment more than its cutaneous counterpart and potentially transforms into malignancy as oral squamous cell carcinoma (OSCC). Transforming growth factor β (TGF-β) is produced by various cells, such as leukocytes and epithelial cells, whereby epithelial-mesenchymal-epithelialn (EMT) forms the phenotype of invasive cancerous cells and promotes tumors. Objectives: We investigated the role of TGF-β in the pathogenesis and biological behavior of dysplastic and non-dysplastic OLP. Methods: Thirty samples of erosive/atrophic OLP (15 dysplastic and 15 non-dysplastic) and 10 samples of normal mucosa of the oral cavity were immunohistochemically examined for the expression of TGF-β. Statistical analysis was performed using the Kruskal-Wallis and chi-squared tests. Results: TGF-β expressed to varying degrees in the epithelium of the studied groups. The groups significantly differed in terms of the expression of TGF-β. In pairwise comparisons, the dysplastic OLP group showed significantly higher immunoreactivity than the normal and non-dysplastic groups, although there was no significant difference between the normal and non-dysplastic OLP groups. The expression of TGF-β in the sub-epithelial lymphocytes of the dysplastic and non-dysplastic OLP groups showed a statistically significant difference. Conclusions: According to the results, TGF-β, as a marker of the inflammatory process in chronic inflammatory conditions, was expressed in epithelial cells and sub-epithelial lymphocytes of all OLPs. This suggests a possible role of this marker in the pathogenesis of OLP. In addition, the increased expression of TGF-β, a marker also involved in carcinogenesis, in the epithelial keratinocytes indicates the role it might play in the development of carcinoma in OLP.

Metal Allergy Mediates the Development of Oral Lichen Planus via TSLP-TSLPR Signaling.

Metal allergy is a T-cell-mediated delayed type of hypersensitive reaction. The pathogenetic mechanisms underlying the allergy are unclear, although the condition has been reported to be related to oral lichen planus (OLP), despite an absence of immunological studies to support this relationship. In this study, histopathological samples of OLP patients were examined to compare the metal allergy-positive and -negative groups, with a focus on the network of epidermal keratinocytes and T cells induced by thymic stromal lymphopoietin (TSLP) and its receptor, TSLPR. Infiltration of T cells into the epithelium was revealed to be higher in the OLP lesions of metal allergy-positive patients than in those of metal allergy-negative patients. Moreover, TSLP-TSLPR signaling and TNF-α production were higher in the epithelial tissue samples of the metal allergy-positive patients than in the metal allergy-negative patients. Metal allergy is associated with both increased expressions of TSLP in keratinocytes and increased TNF-α levels in the epithelium. We propose that this would promote the accumulation of T cells at the lesion site, contributing to the formation of the disease. These results suggest that metal allergy may be an aggravating factor in the pathogenesis of OLP.

New Progress of T Cells in Oral Lichen Planus

Oral lichen planus (OLP) is a relatively common chronic oral mucosal disease mediated by T cells, and its pathogenesis may include antigen-specific and non-specific. The etiology is unknown and the course of the disease is chronic and prolonged. The treatment has become a rather difficult clinical problem. There is no cure for OLP at present. Histologically, it is characterized by band-like infiltration of subepithelial T lymphocytes, rupture of the basement membrane, and liquefaction and degeneration of basal cells. Its etiology is not yet fully understood, its course is chronic, and its treatment has become a difficult clinical problem. Because of the malignant phenomenon of long-term erosion lesions, WHO lists it as a precancerous state. The main pathological changes of OLP are liquefaction and degeneration of basal cells and infiltration of subepithelial lymphocytes. The pathogenesis of OLP is not yet fully understood. OLP is an inflammatory disease mediated by T cells, which is related to autoimmune function. Various pathogenic factors lead to changes in the antigenicity of epithelial keratinocytes. The altered antigens are taken up by Langerhans cells and presented to T cells, these cells release and activate various cytokines to destroy the epithelium, and these cytokines activate T cells to initiate a series of immune responses, leading to the formation of OLP lesions. Studies have found that the pathogenesis of OLP is a process of immune damage mediated by T cells, which is related to the body's autoimmune function.

Mechanisms of reactive oxygen species in oral lichen planus: A literature review

Oral lichen planus is a chronic non-infectious mucosal inflammatory disease caused by an imbalance between reactive oxygen species homeostasis and antioxidant defense systems. Notably, excessive oxidative stress products result in related autoimmune reactions. Further, it activates signaling pathways related to the development of oral lichen planus, as evidenced by the detection of damage to deoxyribonucleic acid, protein, and lipid. Thus, the mechanisms of reactive oxygen species-mediated oxidative stress in the pathogenesis of oral lichen planus are numerous and complex. In this review, we first introduce oxidative stress and oxidative products. Then, we summarize the role and possible mechanisms of reactive oxygen species-mediated oxidative stress in the pathogenesis of oral lichen planus and present a clinical correlation between oxidative stress and oral lichen planus. Finally, we discuss the current challenges and future perspectives.

Salivary Antioxidants Levels in Patients with Oral Lichen Planus.

Oral lichen planus (OLP) is one of the most common diseases of the oral mucosa, which exact pathogenesis remains unknown. Free radicals and reactive oxygen species could play an important role in the pathogenesis of oral lichen planus. This study aimed to compare the salivary levels of uric acid, superoxide dismutase, glutathione peroxidase, and albumin in the patients with oral lichen planus and healthy subjects. Thirty patients with oral lichen planus and 30 healthy subjects, who were matched for age and sex, were enrolled in this case-control study. The salivary concentration of uric acid, superoxide dismutase, glutathione peroxidase, and albumin were examined in these individuals using the spectrophotometry and coulometric technique. The data were analyzed through Mann-Whitney test and T test by SPSS software (ver. 19). Salivary uric acid and albumin levels in patients with oral lichen planus and healthy controls were not statistically different (p > 0.05); however, the concentrations of salivary superoxide dismutase in OLP patients (660.4 ± 266.4 U/g protein) and healthy controls (935.73 ± 561.9 U/g protein) were significantly different (p < 0/05). Also, salivary glutathione peroxidase levels in healthy controls (1049.98 ± 964.56 mU/mL) were remarkably higher than OLP patients (244.12 ± 170.78 mU/mL) (p < 0/001). The salivary superoxide dismutase concentration, as an indicator of antioxidant system, in OLP patients was significantly higher than healthy subjects. The glutathione peroxidase levels in these patients were remarkably lower than healthy controls. It is suggestive that these markers could be effective in pathogenesis of OLP.

Curcuma Longa in the Treatment of Symptomatic oral lichen planus: A non-randomized controlled trial.

Oxidative stress has been suggested as pathogenesis of oral lichen planus (OLP), implicating the vital role of antioxidants in its treatment. Curcumin, naturally found in turmeric has potent antioxidant and inflammatory properties and can be useful in reducing spread and subsiding burning and pain sensation in patients with OLP. The present study was done to evaluate the role of curcumin in the treatment of symptomatic OLP compared with the control group. A total of 40 patients with symptomatic OLP were divided into 2 groups of 20 subjects each. Group A was treated with curcumin oral gel and a multivitamin capsule containing zinc, whereas Group B was given multivitamin containing zinc only. Patients were followed-up twice, that is, after 1 month and 3 months. A modified REU (reticulation/keratosis, erythema and ulceration) score for spread and Visual analogue scale for pain/burning sensation was used and the difference of score was calculated by t test. During F1 period, 0.61 (Group A) and 0.19 (Group B) points improvement and in F2 period, the REU score further increased significantly to 1.36 (Group A) and 0.43 (Group B), respectively. The mean score reduction in Visual analogue scale during F1 period was 1.71 and 0.71, which further increased significantly to 2.88 and 1.24 during F2 period in Groups A and B, respectively. Curcumin, an active ingredient of turmeric is commercially available in gel form to treat different oral lesions and significantly effective in reducing spread and providing symptomatic relief in OLP without any adverse effects.

Origin of langerin (CD207)-expressing antigen presenting cells in the normal oral mucosa and in oral lichen planus lesions.

The number of langerin-expressing antigen-presenting cells is higher in oral lichen planus than in normal oral mucosa. However, langerin may be expressed by several functionally different lineages of antigen presenting cells (APCs), and this has important implications for our understanding of the pathogenesis of oral lichen planus. The aim of this study was to determine the origin of the langerin-expressing APCs. To this end, we examined oral mucosal biopsies from healthy persons and patients with oral lichen planus using multicolor immunofluorescence. In normal oral mucosa, a substantial fraction of Langerhans cells expressed Ki-67, indicating that steady-state oral mucosal Langerhans cells are at least partially maintained by self-renewal. In oral lichen planus, the numbers of Langerhans cells were higher but proliferation was not altered, indicating that the higher cell numbers appeared to depend on recruited dendritic cell (DC)-precursors. Moreover, we found a markedly higher number of langerin+ APCs within the lamina propria of oral lichen planus lesions. Such cells did not display monocyte- or macrophage markers, but rather showed a phenotype compatible with tissue-elicited IRF4+ cDC2. Detailed understanding of how the oral mucosal APC network is regulated and the functional capacities of the different ontogenies may identify novel treatment targets for oral lichen planus.

Literature review of cancer stem cells in oral lichen planus: a premalignant lesion.

As there is no review study about cancer stem cells (CSCs) involved in the pathogenesis of oral lichen planus (OLP), for the first time we review the role of these cells in OLP and this hypothesis may be a clue for the evaluation of the premalignancy of OLP. Cellular mediated immune responses are the main etiopathogenesis in OLP and it is a potentially premalignant lesion. One of the factors proposed in the pathogenesis of OLP and the comparable trend of this autoimmune disease to squamous cell carcinoma (SCC) are CSCs. CSCs have been detected in several solid tumors including head and neck cancers, and have special characteristics including metastasis and resistance to chemotherapy. Related keywords were searched and risk of bias assessment was done for each study. Among all of the studies reviewed in this article, all markers had increased expression in OLP compared to controls that are consistent with SCC. Only CD44 was in contradiction to other papers, in which different expression of CD44 strains was measured in different samples such as saliva and tissue. Based on the results of this review and more studies in the future by investigating the levels of these markers in OLP, it may be possible to determine the prognosis and course of the disease for each patient individually.