Pathogenesis Of Oral Lichen Planus Research Articles

Immunohistochemical evaluation of Langerhans cells in oral lichen planus and oral lichenoid lesions

Objectivethe aim of this study was to evaluate the density of Langerhans cells in oral lichen planus (OLP) and oral lichenoid lesions (OLL). Design14 cases of OLP, 15 cases of OLL and 14 cases of oral inflammatory fibrous hyperplasia (OIFH), were selected for immunohistochemical analysis of CD1a, CD207 and S100 expression. The OIFH group was subdivided according to the presence (OIFHL n = 14) or absence (OIFHNL n = 14) of lichenoid inflammatory infiltrate. Positive cells were counted in intraepithelial and subepithelial areas. Results were analyzed by multivariate comparative analysis, correlation analysis, linear regression models and Student’s T-test. ResultsA significantly higher amount of CD207+ cells in OLL vs OLP was observed (p = 0.015). The prevailing reticular pattern observed was CD207high for OLP (p = 0.0329). A statistically significant difference in the expression of CD1a and CD207 was observed for intraepithelial vs subepithelial areas (p = 0.024 and p=0.015, for CD1a and CD207, respectively). Significant correlations were also observed between the expression of CD1a + and CD207+ cells in the pathogenesis of OLP and OLL. ConclusionHigh levels of CD207+cells in OLP compared with OLL may help explain the differences in the immunopathogenesis of both diseases. Additionally, CD1a + and CD207+ cells appear to be more essential to immunopathogenesis of OLL than to the pathogenesis of OLP.

Gene polymorphism in oral lichen planus

Oral lichen planus (OLP) is a common chronic inflammatory disease of the oral mucosa. The prevalence rate of OLP in adults is 0.5%-2%. The etiology and pathogenesis of OLP are still unclear. The pathogenesis of OLP may be related to the genetic polymorphism of some genes. Currently, the gene families, including tumor necrosis factor, interferon, interleukin, enzyme, and receptor, have been extensively studied. This work reviews related studies on gene polymorphism of OLP.

Serum Levels of IL-22in Patients with Oral Lichen Planus and Cutaneous Lichen Planus.

Statement of the Problem: Lichen planus disease is a chronic inflammatory disorder of mucosal and cutaneous tissues with yet unclear etiology and pathogenesis. Cytokines play an important role in the initiation, maintenance of inflammatory and intercellular crosstalk.Purpose: We assessed serum levels of IL-22 in patients with oral and cutaneous lichen planus and made comparison with healthy individuals.Materials and Method: In this case-control study, peripheral blood samples of 40 patients with lichen planus disease, included two groups of oral lichen planus (n=20) and cutaneous lichen planus (n=20) were compared with 32 healthy individuals in this case-control study. Serum samples were prepared from patients with lichen planus and IL-22 concentration was measured in each serum sample by using a commercial ELISA Kit. The obtained data were then analyzed using the Kruskal-Wallis (one-way ANOVA) test. Results: The IL-22 serum levels were significantly higher in patients with oral lichen planus compared to the healthy control group (p< 0.001). No statistically significant differences were observed in serum levels of IL-22 in cutaneous lichen planus patients compared to the controls (p= 0.183).Conclusion: Increased IL-22 serum levels in patients with oral lichen planus may play an important role in the pathogenesis of oral lichen planus. The administration of the recombinant or antagonist of IL-22 could be a new therapeutic opportunity in the treatment of oral lichen planus.

Genomic Analysis of Oral Lichen Planus and Related Oral Microbiome Pathogens.

Oral lichen planus (OLP) is a common chronic inflammatory disease affecting the oral mucosa. The pathogenesis of OLP is incompletely understood but is thought to be related to the immune system. As the oral cavity is a major reservoir and transmission gateway for bacteria, viruses, and fungi, the microbial composition of the oral cavity could play a role in the pathogenesis of OLP. However, limited by analytic technology and knowledge of the microbial community in the oral cavity, it is not yet clear which pathogens are associated with OLP. Next generation sequencing (NGS) is a powerful tool to identify pathogens for many infectious diseases. In this study, we compared the host cell gene expression profiles and the microbial profiles between OLP patients and matched healthy individuals. We identified the activation of the hepatocyte nuclear factor alpha (HNF4A) network in OLP patients and potential pathogens, including Corynebacterium matruchotii, Fusobacterium periodonticum, Streptococcus intermedius, Streptococcus oralis, and Prevotella denticola. Prevotella denticola is capable of activating the HNF4A gene network. Our findings shed light on the previously elusive association of OLP with various diseases like hepatitis, and indicate that OLP is a T-helper type 17 (Th17) mediated mucosal inflammatory process. The identified molecular pathways and microbes could be used to inform future investigations into OLP pathogenesis and to develop novel therapeutics for OLP treatment.

T cell-derived exosomes induced macrophage inflammatory protein-1α/β drive the trafficking of CD8+ T cells in oral lichen planus.

Oral lichen planus (OLP) is a T cell–mediated chronic inflammatory disease with uncertain aetiology. Exosomes are nanosized particles with biological capacities. Here, we aimed to study the effects of T cell–derived exosomes (T‐exos) on the pathogenesis of OLP and its mechanism. T‐exos were incubated with Jurkat cells for 48 hours, and 26 cytokines in the supernatant were measured by luminex assay. The expression of macrophage inflammatory protein (MIP)‐1α/β was detected using immunohistochemistry and ELISA; that of CCR1/3/5 on peripheral T cells was determined by flow cytometry. Transwell assay was performed to investigate the chemotactic effect of MIP‐1α/β, and cells in the lower chambers were examinated by flow cytometry. As a result, OLP T‐exos elevated the production of MIP‐1α/β, which were highly expressed in OLP tissues and plasma. CCR1/5 were markedly expressed on OLP peripheral T cells, and the majority of CCR1/5+ T cells were CD8+ T cells. Besides, MIP‐1α/β promoted the migration of OLP mononuclear cells, while inhibiting CCR1/5 significantly decreased the trafficking of mononuclear cells, especially that of CD8+ T cells. Conclusively, OLP T‐exos‐induced MIP‐1α/β may drive the trafficking of CD8+ T cells after binding with CCR1/5 in OLP, contributing to the development of OLP.

Correlation of VEGF and MMP-2 levels in oral lichen planus: An in vivo immunohistochemical study

BackgroundThis study aimed to investigate the relation between vascular endothelial growth factors (VEGF) and matrix metalloproteinase-2 (MMP-2) in different oral lichen planus (OLP) forms compared to control patients. MethodsBiopsies from 60 patients were selected and equally distributed as follows: reticular/popular OLP (R/PLP), atrophic/erosive OLP (A/ELP) patients, healthy subjects (Control). All biopsies were immune-histochemical stained and statistically analyzed for VEGF and MMP-2 expression. ResultsImmune-expression of VEGF was significant between OLP and control (P-value <0.001). OLP showed a higher epithelial expression of VEGF in A/ELP compared to R/PLP (15.19 ± 2.53). In connective tissue (CT), R/PLP showed a higher VEGF expression (11.57 ± 2.32) compared to A/ELP (9.87 ± 2.48); (p < 0.001), with no significant difference (P-value ≥ 0.05). A significant epithelial expression of MMP-2 was seen in A/ELP compared to R/PLP (21.32 ± 7.08). R/PLP showed a higher expression of MMP-2 (20.45 ± 6.28) in CT compared to A/ELP group (17.66 ± 6.94), with a non-significant difference (P-value = 1.000). In A/ELP, a positive correlation between VEGF and MMP-2 was detected in CT, r = 0.761, with a weak correlation was noticed in epithelium r = 0.163. A negative correlation was noted between VEGF and MMP-2 in R/PLP in CT, r = −0.368, with a moderate positive correlation in epithelium, r = 0.655. ConclusionMMP-2 and VEGF protein profiles support a role in the pathogenesis of OLP. Based the MMP-2 and VEGF findings in the A/ELP group, this pathway may have a role in the malignant transformation of these lesions. Both observations invite further study.

Role of serum immunoglobulins in patients of oral lichen planus and oral lichenoid reaction

The aim of the study is to find out the role of immunoglobulin IgA and IgM as indicators of humoral immune response in the etiopathogenesis and for the differentiation between oral lichen planus (OLP) and oral lichenoid reaction (OLR). The study comprises of 50 patients. From them 20 patients were of OLP, 20 patients of OLR and 10 patients as controls. After histopathological confirmation, approximately 5 ml of venous blood was collected by venepuncture from OLP patients, OLR patients and from control patients. The serum IgA and IgM were measured by immunoturbidimetry method using automated chemistry analyzer and data were analysed using t-test. The mean serum level of IgA and IgM was 2.14±1.19g/L and 0.88±0.47g/L respectively in reticular OLP, 2.21±0.98g/L and 0.78±0.49g/L respectively in erosive OLP, 1.64±0.60g/L and 0.99±0.34g/L respectively in OLR, 2.62±0.40g/L and 1.51±0.47g/L respectively in control patients. The results showed statistically significant IgM level for reticular and erosive OLP (p value=0.007 and 0.042 respectively). Patients with OLP shows systemic immunologic alterations suggest that humoral immune system may play a part in pathogenesis of OLP and also OLP and OLR lesions can be differentiate on the basis of serum level of IgM.

The association between Epstein-Barr virus and oral lichen planus: A systematic review and meta-analysis.

Oral lichen planus (OLP) is a relatively common inflammatory disease, with unclear etiology. A number of studies have linked Epstein-Barr virus (EBV) with OLP. The present systematic review and meta-analysis aimed to evaluate the available evidence regarding the potential association between EBV and OLP. Online databases (PubMed, Scopus, Web of Science, ProQuest, and Google Scholar) were searched from date of inception till May 2020. Studies were included if they met the following criteria: 1) observational studies that assessed the relationship between EBV and OLP, 2) the study comprised OLP patients and control subjects, 3) diagnosis of OLP was confirmed histopathologically, and 4) articles were in English. Studies without control groups, experimental studies, case reports, and reviews were excluded. The fixed-effects model was performed for meta-analyses using RevMan 5.3 software. A total of 10 studies comprising 386 OLP cases and 304 controls were included. Of these, only 8 studies were eligible for the meta-analysis. The results of the quality assessment showed that only 2 studies were of high quality, while the remaining studies were of moderate quality. The results of the pooled eight studies revealed a significant positive association between EBV and OLP (OR=4.41, 95% CI: [2.74, 7.11], P<.0001). The results of the present systematic review suggest that EBV infection is statistically associated with increased risk of OLP. However, these results are preliminary, and high-quality, large-scale studies are warranted to further explore the potential role of EBV in the pathogenesis of OLP.

Altered expression of CCN1 in oral lichen planus associated with keratinocyte activation and IL-1β, ICAM1, and CCL5 up-regulation.

Emerging evidence indicates that CCN1 is a novel inflammation-regulated mediator involved in the pathogenesis of some immune-mediated inflammatory diseases. The objective of this study was to investigate the preliminary roles of CCN1 and its related cytokines IL-1β, CCL5, and ICAM1 in oral lichen planus (OLP). CCN1 expression levels in biopsies from OLP patients against normal oral mucosa (NOM) using immunohistochemistry (42 OLP vs 9 NOM) and RT-qPCR (20 OLP vs 20 NOM) were compared, respectively. The correlation of CCN1 and IL-1β, CCL5, and ICAM1 expression was examined by RT-qPCR in tissue samples and an in vitro cell culture system using keratinocyte HaCaT cells incubated with lipopolysaccharides. Immunohistochemistry showed that CCN1 protein mainly expressed in the cytoplasm of epithelial keratinocytes of OLP. Consistently, RT-qPCR revealed that mRNA expression of CCN1 was increased in OLP compared with NOM (P<.05) and positively correlated with the high expression of IL-1β, ICAM1, and CCL5 (P<.001), respectively. Importantly, an in vitro study showed that keratinocyte proliferation significantly (P<.05) increased by CCN1 stimulation. Moreover, IL-1β, ICAM1, and CCL5 expression in keratinocytes stimulated by CCN1 was increased (P<.05), respectively. This preliminary study for the first time reported that altered expression of CCN1 was associated with high expression of IL-1β, ICAM1, and CCL5 in OLP. And we demonstrated CCN1 promoted keratinocyte activation, as well as IL-1β, ICAM1, and CCL5 production in keratinocytes. Our data indicated that the potential role of CCN1 and its related cytokines was involved in the pathogenesis of OLP.

Omega-3 polyunsaturated fatty acids: a promising approach for the management of oral lichen planus.

Oral lichen planus (OLP) is a T-cell-mediated inflammatory disease with a risk of malignant transformation. Although the etiology of OLP is still uncertain, growing evidence suggests that oral microbiota, antigen-specific, and non-specific mechanisms are involved in the pathogenesis of OLP. Antigen-specific mechanisms include antigen presentation, T-cell activation, nuclear factor-kappa B signaling pathway, and cytokine secretion, while non-specific mechanisms consist of matrix metalloproteinases (MMP)-9 upregulation, psychological pressure, oxidative damage, aberrant expression of microRNAs (miRNAs), and autophagy. Till now, there is no cure for OLP, and the main purpose of OLP therapy is symptomatic control. Seafood and its derivative omega-3 polyunsaturated fatty acids (n-3 PUFAs) can suppress antigen presentation, T-cell activation, and nuclear factor-kappa B signaling pathway, modulate the overexpressed inflammatory cytokines, inhibit the expression of MMP-9, as well as regulate the expression of miRNAs and autophagy. And they are possible agents for ameliorating psychological disorder and oxidative damage. Moreover, n-3 PUFAs supplementation has a beneficial effect on preventing tumorigenesis. n-3 PUFAs consumption may provide a non-toxic, inexpensive administration for OLP.

Increased Serum Level and High Tissue Immunoexpression of Interleukin 17 in Cutaneous Lichen Planus: A Novel Therapeutic Target for Recalcitrant Cases?

Background Interleukin-17 is supposed to play an important role in the pathogenesis of oral lichen planus (OLP). However, there is scarce data in the literature on its significance in the cutaneous variant of the disease. Objectives To determine the serum level and tissue immunoexpression of IL-17 in cutaneous lichen planus (CLP). Methods Fifty-two adult patients with CLP, without any significant autoimmune or inflammatory conditions, were included in the first part of the study. The control group consisted of 27 age- and sex-matched healthy volunteers. Serum concentration of IL-17 was quantified using enzyme-linked immunosorbent assay (ELISA) kit. In the second part of the study, the tissue expression of IL-17 was assessed in archival paraffin-embedded biopsy specimens from CLP (n = 14) against normal control tissues (n = 11) using immunohistochemical assays. The expression was evaluated using Zeiss Axio Imager A2 light microscope. Positively stained cells were counted in 10 fields of view for biopsy specimen at 200x magnification, and the mean value was calculated. Results The serum level of IL-17 was significantly elevated in patients with CLP, compared with healthy volunteers (0.218 ± 0.221 ng/ml versus 0.126 ± 0.058 ng/ml, respectively; p = 0.025). No correlation was found between the serum concentration of IL-17 and patient age, gender, disease duration, extent of skin involvement, the presence or intensity of pruritus, and coexistence of mucosal lesions. In tissue samples from CLP lesions, significantly higher numbers of cells expressing IL-17 were found when compared to a healthy skin (p < 0.001). Conclusion Elevated serum concentration of IL-17 and high expression in a lesional skin support the hypothesis that IL-17 is implicated in the immunopathogenesis of CLP. These findings may constitute a premise for the future use of anti-IL-17 monoclonal antibodies in the treatment of severe and recalcitrant forms of CLP.

The expression of Cathepsin L in oral lichen planus

BackgroundMalignant transformation of oral lichen planus (OLP) was reported particularly in erosive type, however, it remains inconclusive. Cathepsin L was shown to promote tumor growth and invasion in many cancers. Therefore, cathepsin L expression in erosive and non-erosive OLP compared with oral epithelial dysplasia and oral squamous cell carcinoma (OSCC) were investigated. MethodsThirty specimens of OLP (15 cases each of erosive and non-erosive OLP), 10 cases of oral epithelial dysplasia and 10 cases of OSCC were included. Ten healthy gingiva specimens were served as controls. All specimens were stained with cathepsin L antibody using immunohistochemistry technique. ResultsCathepsin L was expressed in all OLP and OSCC cases. In oral epithelial dysplasia and healthy gingiva, the expression was found at 90% and 50% respectively. The percentage of positive cells was the highest in erosive OLP (27.26 ± 12.09%), followed by non-erosive OLP (20.85 ± 7.43%), OSCC (20.15 ± 15.70%), oral epithelial dysplasia (9.24 ± 7.00%) and healthy gingiva (2.27 ± 5.65%). Most of non-erosive OLP cases showed mild staining intensity while erosive OLP and OSCC showed moderate staining intensity. Cathepsin L was mainly expressed at basement membrane zone and inflammatory cells of OLP. In OSCC, the expression was found in tumor islands and keratin pearls. In oral epithelial dysplasia and normal gingiva, cathepsin L expressions were low and presented in scattered pattern in both epithelium and connective tissue. ConclusionAccording to the patterns of expression in this study, cathepsin L could be implicated in pathogenesis and severity of OLP.

Microbial Community Analysis of Saliva and Biopsies in Patients With Oral Lichen Planus.

The specific etiology and pathogenesis of oral lichen planus (OLP) remain elusive, and microbial dysbiosis may play an important role in OLP. We evaluated the saliva and tissue bacterial community of patients with OLP and identified the colonization of bacteria in OLP tissues. The saliva (n = 60) and tissue (n = 24) samples from OLP patients and the healthy controls were characterized by 16S rDNA gene sequencing and the bacterial signals in OLP tissues were detected by fluorescence in situ hybridization (FISH) targeting the bacterial 16S rDNA gene. Results indicate that the OLP tissue microbiome was different from the microbiota of OLP saliva. Compared with the healthy controls, Capnocytophaga and Gemella were higher in OLP saliva, while Escherichia–Shigella and Megasphaera were higher in OLP tissues, whereas seven taxa, including Carnobacteriaceae, Flavobacteriaceae, and Megasphaera, were enriched in both saliva and tissues of OLP patients. Furthermore, FISH found that the average optical density (AOD) of bacteria in the lamina propria of OLP tissues was higher than that of the healthy controls, and the AOD of bacteria in OLP epithelium and lamina propria was positively correlated. These data provide a different perspective for future investigation on the OLP microbiome.

The effect of smoking on clinical presentation and expression of TLR-2 and CD34 in Oral lichen Planus patients: clinical and immunohistochemical study

BackgroundOral lichen planus is a chronic inflammatory disease which is considered as a potential precancerous condition. Numerous studies have confirmed that inflammation is a strong risk factor for cancer development. Smoking is associated with potentially malignant disorders of the oral and oropharyngeal mucosa. The adverse consequences of smoking in various pathologies are mediated by its effects on the immune-inflammatory system. Little is known about the influence of cigarette smoke content on the course of OLP and inflammatory response.MethodsTwenty oral lichen planus smoker patients, 20 oral lichen planus non-smoker patients and 20 control patients were included in this work. Pain and clinical scores were calculated for each patient. Image analysis to calculate area percent for TLR-2 and CD34 immuno-expression was performed. Data was tabulated and statistically analyzed.ResultsThe present study showed no statistically significant difference in clinical and pain scores between the smoker and non-smoker groups. However, there was a significant difference in area percent values for TLR-2 and CD34 immuno-expression between the smoker and the non-smoker groups.ConclusionSmoking enhanced TLR-2 and CD34 expression in OLP which are considered as inflammatory mediators and are contributing factors in the pathogenesis of oral lichen planus.

Assessment of miR-155 in Saliva of Oral Lichen Planus Patients as a Potential Biomarker of Malignant Transformation Before and After Topical Corticosteroid Therapy

Background: Immune dysregulation is undoubtedly implicated in the pathogenesis of oral lichen planus (OLP) and considering the importance of miR-155 in the regulation of the immune response the present study is conducted to assess salivary levels of miR-155 in patients with oral lichen planus lesions and compare these levels before and after corticosteroid therapy to explore its possible implication in the pathogenesis OLP. Methods: Thirty patients were enrolled in this study, 15 healthy individuals with normal mucosa as controls and 15 patients diagnosed with atrophic/erosive OLP lesions. Patients were treated with topical corticosteroid. Salivary levels of miR-155 were assessed before and after 4 weeks of topical steroids therapy. Clinical improvement was assessed via VAS score and Thongprasom scale. Results: A significant reduction of miR-155 levels four weeks post treatment was recorded with a value of 55.67%. There was a highly significant direct correlation between miR-155 levels and VAS score. Conclusion: The overexpression of miR-155 in OLP patients before treatment with its obvious reduction four weeks after therapy suggests it could be directly involved in OLP pathogenesis and shedding a light on the potential of miR-155 to act as an innovative therapeutic target for OLP.

A pilot study: a possible implication of Candida as an etiologically endogenous pathogen for oral lichen planus

BackgroundThe aim of this study was to investigate the prevalence and genotypic profiles of Candida albicans in patients with oral lichen planus (OLP).Materials and methodsPositive rates and genotypic profiles of Candida albicans strains from OLP patients and healthy controls were analyzed. Random amplified polymorphic DNA and internal transcribed spacer of ribosome DNA polymerase chain reactions were used to sequence the DNA of these strains, and then their genetic similarity was measured using BLAST, UIV Band, and Vector NTI Suite Sequence Analyses Software.ResultsThe prevalence of C. albicans strains detected from erosive-OLP, non-erosive OLP, and normal individuals was 18.87, 18.75, and 7.92%, respectively. Four different genotypes were revealed by the two methods. To be specific, type I was found only in the healthy subjects; type II a and II b were found in non-erosive OLP, and type III was identified in erosive OLP. Intragroup similarity coefficients, i.e. SAB were 100%, and inter-groups similarity coefficients, i.e. SAB were less than 30%.ConclusionsThe genotypic results of C. albicans in OLP revealed an endogenous rather than exogenous infection of C. albicans. In addition, a possible pathogenic role of C. albicans in OLP, with the etiologic sense contributing to a more proper recognition on the pathogenesis, development, and progression of OLP, as well as some strategies for its diagnosis and treatment were identified.

Serum and Salivary Level of Nitric Oxide (NOx) and CRP in Oral Lichen Planus (OLP) Patients.

Statement of the Problem: Oral lichen planus (OLP) is a chronic inflammatory oral mucosal disease with unclear etiology while a few cases of disease become malignant.Purpose: This study aimed to evaluate the level of nitric oxide (NOx) and C-reactive protein (CRP) as oxidative stress and inflammation status in sample of OLP patients.Materials and Method: In this case-control study, serum and salivary NOx and CRP levels were evaluated in twenty two OLP patients as the case group confirmed by clinical and histopathological diagnosis, and twenty two healthy control groups collected from Tooba Oral Pathology Laboratory in Sari in 2016. The data were analyzed by using independent-samples t-test, Mann-Whitney U-test and Chi-square by using SPSS version 21. The statistical significant level was considered at p< 0.05.Results: Salivary and serum NOx levels in case group showed statistically significantly higher than healthy control group (p= 0.035 and p= 0.001, respectively). CRP values were significantly higher both in serum (p= 0.001) and in saliva (p= 0.035). A significant correlation was found between CRP and NOx values in serum (r= 0.521, p= 0.0001) and saliva (r= 0.427, p= 0.045).Conclusion: Oxidative stress causes damage to organs in the human body. Correct understanding of oxidative stress and its association with free radicals and inflammatory markers related to oral disease are important for effective treatments. The results of the study advocate the effects of NOx and CRP levels in pathogenesis of OLP. Therefore, antioxidant drugs might probably be considered in the treatment of OLP.

Characterization of intratissue bacterial communities and isolation of Escherichia coli from oral lichen planus lesions

Oral lichen planus (OLP) is a chronic T cell-mediated inflammatory disease of unknown etiology. We previously proposed that the intracellular bacteria detected in OLP lesions are important triggering factors for T cell infiltration. This study aimed to identify OLP-associated bacterial species through the characterization of intratissue bacterial communities of OLP lesions. Seven pairs of bacterial communities collected from the mucosal surface and biopsied tissues of OLP lesions were analyzed by high-throughput sequencing of the 16S rRNA gene. The intratissue bacterial communities were characterized by decreased alpha diversity but increased beta diversity compared with those on the mucosal surface. While the relative abundance of most taxa was decreased within the tissues, that of Escherichia coli was significantly increased. Four E. coli strains were isolated from additional OLP biopsies and verified as K12 strains by whole-genome sequencing. The distribution of E. coli in sections of control (n = 12) and OLP (n = 22) tissues was examined by in situ hybridization. E. coli was detected in most OLP tissues, suggesting its potential role in the pathogenesis of OLP. The oral E. coli strains isolated from OLP tissues will be useful to investigate their role as triggering factors for T cell infiltration.

Evidence for a significant role of B-cells in the pathogenesis of oral lichen planus: Preliminary results of a cross-sectional study.

Evidence for a significant role of B-cells in the pathogenesis of oral lichen planus: Preliminary results of a cross-sectional study.

Role of interleukin-4 in pathogenesis of oral lichen planus: A systematic review.

Background Oral lichen planus (OLP) is a premalignant mucocutaneous disease that affects 1-2% of the adult population. Immunological factor may act as etiological factor. The cellular immune cells such as T cells are important in pathogenesis of OLP. Interleukin-4 (IL-4) is secreted by T-helper 2 (Th2). Several studies have been carried out on the role of IL-4 in OLP. The aim of this study was to review the level of IL-4 in OLP, effective factors in the production of IL-4 and its role in the development of OLP. Material and Methods A search in PubMed was performed on the literature published from 2000 until august 2019 using the following keywords: “oral lichen planus” or “OLP” and “interleukin-4” or “IL-4”. Results Originally, 37 articles were considered, of which 28 case-control articles were selected according to the inclusion/exclusion criteria. Conclusions This review study shows that IL-4 plays a key role in the development of OLP. According to the past studies, there are several factors contributing to the production of this cytokine. Identification of the routes of production of IL-4 and its role in OLP might be useful for development of new preventive and therapeutic methods in management of patients with OLP. Key words:Interleukin 4, oral lichen planus, pathogenesis.