Oral Lichen Planus Cell Research Articles

Function of unconventional T cells in oral lichen planus revealed by single-cell RNA sequencing.

We intended to map the single-cell profile of OLP, explore the molecular characteristics of unconventional T cells in OLP tissues. Buccal mucosa samples from OLP patients and healthy individuals were used to prepare single-cell suspension. Single-cell RNA sequencing was used to analyze the proportion of all the cells, and the molecular characteristics of unconventional T cells. Immunohistochemical staining was used to detect the expression of unconventional T cells marker genes. The cell clusters from buccal mucosa were categorized into immune cells, fibroblasts, endothelial cells, and epithelial cells. Unconventional T cells with phenotype of CD247+TRDC+NCAM1+ were identified. Immunohistochemical staining revealed higher expression of unconventional T cell marker genes in OLP tissue, predominantly in the lamina propria. In OLP, unconventional T cells are in a unique stress response state, exhibited enhanced NF-κB signaling and apoptosis inhibition, enhanced heat shock protein genes expression, weakened cytotoxic function. A large number of ligand-receptor pairs were found between unconventional T cells and other cells, particularly with fibroblasts and endothelial cells. This study mapped the single-cell profile of OLP, delineated the molecular characteristics of unconventional T cells in OLP, and uncovered that these unconventional T cells are in a stress response state.

Mast cells in oral lichen planus and oral lichenoid lesions related to dental amalgam contact.

The aim of this study was to analyze the expression of mast cell markers toluidine blue, c-kit, and tryptase and presence of mononuclear inflammatory cells in oral lichen planus (OLP) and oral lichenoid lesions related to dental amalgam. Nineteen specimens of OLP, OLLC, and healthy oral mucosa were selected. Mononuclear inflammatory cells were analyzed. Histochemical and immunohistochemical analyses were performed using toluidine blue, anti-c-kit and anti-tryptase reagents, and the results were quantified in areas A and B of connective tissue. Mast cells of all OLP and OLLC samples were positive for toluidine blue, c-kit, and tryptase. The density of toluidine blue+, c-kit+ and tryptase+ mast cells was higher in tissue with OLP and OLLC compared with healthy controls (p < 0.05). No difference was noted in mast cells density between OLP and OLLC (p > 0.05). The density of tryptase+ mast cells was higher in the subepithelial region (area A) than the region below it (Area B) in OLLC (p = 0.047). The mononuclear inflammatory cell density was higher in OLLC compared to OLP, but without statistical significance (p > 0.05). A positive statistical correlation was found between mononuclear immune cells and density of c-kit+ and tryptase+ mast cells in OLP (r = 0.943 and r = 0.886, respectively). Our data demonstrate that the etiopathogenesis process of OLP and OLLC modulates the expansion and degranulation of mast cells; mast cells density, however, was similar between OLP and OLLC. The distribution of mast cells appears to vary along the lamina propria.

TRIM21 Promotes Inflammation by Ubiquitylating NF-κB in T Cells of Oral Lichen Planus.

Oral lichen planus (OLP) is a mucocutaneous inflammatory disease affecting 1% general population. Tripartite motif-containing protein 21 (TRIM21) shows a significant role in OLP. This study aimed to explore the function and mechanism of TRIM21 in T cells of OLP. Differential gene expression profile in OLP vs. healthy controls (HCs) was constructed by RNA sequencing. Protein expression level and infiltration sites of TRIM21 in OLP were detected by immunoblot, immunohistochemistry and immunofluorescence. Expression of proinflammatory cytokines and chemokines including IL-6, TNF-α, ICAM1, CXCL1, CXCL8, CXCL9, and CXCL11 in CD3+ TRIM21hi T cells were measured by quantitative real-time polymerase chain reaction analysis. Downstream pathways and substrates of TRIM21 were explored by immunoblot and immunoprecipitation. Whether TRIM21 ubiquitination its substrate and ubiquitination form were tested by ubiquitination assay in vitro. Compared with HCs, TRIM21 exhibited a higher level in OLP, which expressed mainly in CD3+ T lymphocytes in OLP tissues. Overexpressed TRIM21 enhanced the expression of IL-6, TNF-α, CXCL1, CXCL8, CXCL9, and CXCL11 in CD3+ T cell line through ubiquitinating nuclear factor-κB (NF-κB) via a lysine 63 (K63) linkage, which eventually activating NF-κB signaling pathway. In OLP, TRIM21 promoted inflammation through ubiquitylating NF-κB and activating NF-κB signaling pathway.

Characterization of Mucosal-Associated Invariant T Cells in Oral Lichen Planus.

Oral lichen planus (OLP) is an inflammatory condition of unknown cause that has been associated with concurrent candidal infection. Mucosal-associated invariant T (MAIT) cells express the T cell receptor TCRVα7.2 and are activated by riboflavin intermediates produced by microbes. The interaction between MAIT cells, Candida, and OLP is unknown. This study aimed to determine mucosal-associated T cell presence in OLP and whether the abundance of these cells changed due to the presence of either Candida or symptoms, using multiplex immunohistochemistry (mIHC). Ninety formalin fixed-paraffin-embedded (FFPE) tissue samples were assessed using mIHC for the cellular markers CD3, interleukin 18 receptor one (IL18R1), TCRVα7.2, CD161, CD8, and major histocompatibility complex class I-related (MR-1) protein. The samples were stratified into five groups on the basis of clinical (presence/absence of symptoms) and microbiological (presence/absence of Candida) criteria. Results demonstrated the presence of MAIT cell phenotypes in OLP inflammatory infiltrate within the connective tissue. Significant differences existed between different OLP groups with the percentage of log(CD3+ CD161+) and log(CD3+ TCRVα7.2+) positive cells (p < 0.001 and p = 0.005 respectively). Significant differences also existed with the relative abundance of triple-stained log(CD3+ CD161+ IL18R1+) cells (p = 0.004). A reduction in log(CD3+ CD161+ IL18R1+) cells was observed in lesional tissue of patients with symptomatic OLP with and without Candida when compared to controls. When present in OLP, MAIT cells were identified within the connective tissue. This study demonstrates that mIHC can be used to identify MAIT cell phenotypes in OLP. Reduced percentage of log(CD3+ CD161+ IL18R1+) cells seen in symptomatic OLP with and without Candida suggests a role for these cells in OLP pathogenesis.

Senescence in oral lichen planus as assessed by the immunohistochemical evaluation of senescence marker protein-30 (Regucalcin).

Oral lichen planus is a T-cell-mediated chronic inflammatory disease affecting approximately 1% to 2% of the population, the etiology of which is currently unknown. The objectives of this study were to observe if senescence occurs in oral lichen planus, through the assessment of the immunohistochemical expression of a novel marker for senescence called Senescence marker protein-30 or regucalcin, and compare the expression to that in oral lichenoid reaction and non-specific inflammation. The study material consisted of 30 cases of oral lichen planus, 15 cases of oral lichenoid reaction and 15 cases of non-specific inflammation. The number of positive cells in ten randomly selected high power fields were counted in the epithelium and the connective tissue separately and the mean was determined. Mann-Whitney U test was used to statistically analyze if there was any significant difference in the expression of Senescence marker protein-30 between oral lichen planus, oral lichenoid reaction and non-specific inflammation. Even though a greater expression was seen in the oral lichen planus cases than oral lichenoid reaction, the difference in both the epithelium and connective tissue was not statistically significant. This study shows that in addition to the already known mechanisms like apoptosis and increased cell proliferation rates, the activated T-lymphocytes may also trigger a senescent change in the cells of oral lichen planus. As with the other mechanisms, this is also seen only in a small proportion of the cases.

Autophagy-related 9 homolog B regulates T-cell-mediated immune responses in oral lichen planus

ObjectivesThis study aimed to explore the impacts of autophagy-related 9 homolog B (ATG9B)-mediated autophagy on T-cell immune responses in oral lichen planus. DesignATG9B expression was detected in lesions and local T cells by immunohistochemical analysis and immunofluorescence assay. The effects of ATG9B-mediated autophagy on T-cell immune responses were explored after ATG9B-overexpression or ATG9B-knockdown lentivirus transfection. A coculture system of activated T cells and lipopolysaccharide-induced keratinocytes was used to simulate the main cell crosstalk in oral lichen planus. ResultsThe expression of ATG9B upregulated in lesions and local T cells of oral lichen planus, especially in non-erosive oral lichen planus, suggesting that ATG9B may be a diagnostic factor for oral lichen planus. Notably, ATG9B-knockdown T cells of oral lichen planus demonstrated autophagy suppression, enhanced proliferation, and attenuated apoptosis, whereas overexpression of ATG9B showed opposite effects on T cells. In the coculture system of T cells and keratinocytes, ATG9B-knockdown T cells of oral lichen planus, but not ATG9B-overexpression T cells, promoted the proliferation and apoptosis of their cocultured keratinocytes. Additionally, exogenous insulin-like growth factor 1 (IGF1) significantly reversed the apoptosis rates of keratinocytes cocultured with T cells expressing abnormal ATG9B. Furthermore, ATG9B-overexpression T cells showed decreased secretion of interferon-γ and tumor necrosis factor-α in the coculture system. ConclusionsThis study revealed the regulatory roles of ATG9B-mediated T-cell autophagy on T-cell immune responses and crosstalk between T cells and keratinocytes in of oral lichen planus.

A potential reciprocal emergence of regulatory T cells in oral lichen planus and pemphigus vulgaris: A meta-analysis

Oral lichen planus (OLP) and pemphigus vulgaris (PV) are 2 common inflammatory mucocutaneous diseases of immune-based etiology. Evidence indicates regulatory T (Treg) cells maybe play a role in the pathogenesis of OLP and PV, which are caused by aberrant immune responses. In this report, 7 eligible case–control studies containing 517 OLP patients and 261 healthy controls (HC) were identified. The level of Tregs was significantly higher in OLP patients than HC (mean difference: 1.79; 95%CI: 0.99, 2.60). On the other hand, 7 eligible case–control studies containing 169 PV patients and 121 HC were identified. Conversely, the level of Tregs was significantly lower in PV patients than HC (mean difference: −2.49; 95%CI: −3.90, −1.08). Collectively, this analysis for the first time reported reciprocal emergence of Tregs in OLP and PV using meta-analysis, and provided an interesting insight into a previously undescribed the linkage of the 2 mucocutaneous diseases.

Infiltration of Mature KLRG1 Expressing Cytotoxic T Cells in Oral Lichen Planus.

Oral lichen planus (OLP) is a chronic inflammatory disease affecting oral mucosa. Its pathogenesis includes T cell infiltration. T cells may be naïve or in response to antigen stimulation, progress through differentiation stages. The differentiated states of T cells in OLP mucosa have not previously been reported. Available OLP microarray gene expression data from Gene Expression Omnibus were analyzed for markers of T cell cytotoxicity. Immunohistochemical studies of T cell subset markers CD4 and CD8 and the T cell differentiation marker killer cell lectin-like receptor G1 (KLRG1) were performed on paraffin embedded formalin fixed oral mucosa biopsy samples from 10 patients with OLP. Gene expression analysis of OLP oral mucosa samples disclosed increased transcript expression of KLRG1, CD8A, and granzyme K (GZMK). By immunohistochemistry, prominent CD4 + and CD8 + T cell infiltration was seen in all patient samples. KLRG1 + T cells were abundant, constituting a mean of 51% (range 40-65%) of the number of CD8 + T cells. KLRG1 + T cells localized at the epithelium and lamina propria junction, infiltrating both basal and intraepithelial regions and adjacent to both basal and intraepithelial keratinocytes. OLP oral mucosa T cell infiltration includes KLRG1 + highly differentiated cytotoxic T cells, suggesting continued antigen exposure driving T cells to a highly differentiated phenotype. The known phenotype of these cells, together with microarray detected increases in cytotoxic molecules, suggests that highly differentiated cytotoxic T cells contribute to oral mucosa injury in OLP.

MAIT cells and their implication in human oral diseases.

Mucosal-associated invariant T (MAIT) cells are unique innate-like T cells that are abundant in humans, accounting for 1-10% of circulating T cells and about 2% of total T cells in human oral cavity. MAIT cells can mount a strong immune response quickly without exogenous antigens and undergo a phenotypic transformation in the development of diseases. They produce cytokines involved in the Th1 and Th17 immune response and cytotoxic proteins, promote the dysfunction of autoreactive B cell and inhibit the function of NK cells. MAIT cells have been widely explored in autoimmune diseases, inflammatory diseases and tumors, and these mechanisms may also be involved in the pathogenesis of some oral diseases, while MAIT cells have not been systematically discussed in oral diseases. We searched PubMed/MEDLINE, EMBASE and Microsoft Bing databases to review and analyze relevant literatures on the impact of MAIT cells in the pathogenesis of human oral diseases. Collected evidence elucidated the characteristics of MAIT cells and emphasized the potential roles of MAIT cells in oral lichen planus (OLP), chronic graft-versus-host disease (cGVHD), oral squamous cell carcinoma (OSCC), apical periodontitis (AP) and primary Sjogren's syndrome (pSS).

Langerhans Cells, T Cells, and B Cells in Oral Lichen Planus and Oral Leukoplakia.

Although oral lichen planus (OLP) and oral leukoplakia (LPL) have different pathogenetic profiles, both may involve chronic inflammation. The aim of this observational study was to evaluate the inflammatory cell profiles of OLP and LPL. The inflammatory cell infiltrates in patients with OLP and LPL were analyzed for the presence of Langerhans cells (LCs; CD1a), T cells (CD3), and B cells (CD20), as well as for the proliferation marker Ki-67. Biopsied specimens from patients with OLP (N = 14) and LPL without dysplasia (N = 13) were immunohistochemically stained with antibodies directed against CD1a, CD3, CD20, and Ki-67, followed by quantitative analyses. A significant increase in the number of CD3+ cells and CD20+ cells was found in the submucosa of OLP, as compared to LPL (p < 0.01). Likewise, the number of CD3+ cells was significantly higher in the epithelium of OLP than of LPL (p < 0.05). No differences were found in the expression of Ki-67 and the number of CD1a+ cells between the two groups. Although an immune response is elicited in both conditions, there are differences at the cellular level between OLP and LPL. A more robust immune activation involving T cells and B cells is seen in OLP. The role of B cells in OLP needs to be further elucidated. Although the number of B cells in LPL is low, their role in the inflammatory response cannot be ruled out.

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.

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.

Characterization and function of circulating mucosal-associated invariant T cells and γδT cells in oral lichen planus.

Oral lichen planus (OLP) is a T-cell-mediated chronic inflammatory disease with uncertain aetiology. Mucosal-associated invariant T (MAIT) cells and γδT cells are unconventional, innate-like T cells with immunoregulatory capacity. This study aimed to investigate the potential effects of MAIT and γδT cells on the pathogenesis of OLP. Circulating MAIT cells and γδT cells were identified using flow cytometry. Surface proteins including CD4, CD8, CD69, CD103, CD49d, programmed death-1 (PD-1) and its ligand PD-L1 were assessed. Cytokines containing interleukin (IL)-4, IL-17, interferon (IFN)-γ, granzyme B and tumour necrosis factor (TNF)-α released by MAIT and γδT cells were measured following PMA and ionomycin stimulation. Circulating MAIT and γδT cells were deficient in OLP. The percentage of CD4+ , CD69+ , CD103+ and PD-1+ MAIT cells was increased in OLP, while that of CD8+ and CD49d+ MAIT cells was decreased. The percentage of CD103+ , PD-1+ and PD-L1+ γδT cells was upregulated in OLP. Both the MAIT and γδT cells in OLP produced less IL-4 than controls. The granzyme B-producing MAIT cells were increased, while γδT cells secreting granzyme B and TNF-α were reduced in OLP. IL-17 and IFN-γ in OLP MAIT and γδT cells were not significantly different from that in controls. The frequency of OLP MAIT cells and the MAIT/γδT rate were positively associated with the disease severity. The deficient MAIT and γδT cells expressing functional proteins and releasing cytokines may play an immunoregulatory role in the pathogenesis of OLP.

Systemic and local changes of regulatory T cells in oral lichen planus.

Systemic and local changes of regulatory T cells in oral lichen planus.

The role of CD68+ and CD163+ macrophages in immunopathogenesis of oral lichen planus and oral lichenoid lesions

Macrophages are phagocytic cells with essential participation in immunological events of the oral cavity. However, the role of these cells in oral lichen planus (OLP) and oral lichenoid lesions (OLL) remains unclear. The present study aimed to evaluate the density of macrophages in OLP and OLL, and to compare it with that of oral inflammatory fibrous hyperplasia (OIFH) (control group). 14 cases of OLP, 14 cases of OLL and 14 cases of OIFH were selected for immunohistochemical analysis of CD68+ (M1) and CD163+ (M2) macrophage expression. CD68+ and CD163+ macrophages densities were measured in the intraepithelial and subepithelial areas. The statistical tests used were multivariate analysis of variance, as well as a correlation and linear regression. OLP has more CD68+ macrophages when comparing with OLL (p = 0.001) and OIFH (p = 0.045). There is a very strong relationship between the macrophages types (p < 0.0001) in OLP and OLL. The linear regression showed that to OLL development (p < 0.0001/R2′ = 0.9584), the presence of different types of macrophages are more essential than to OLP (p < 0.0001/R2′ = 0.8983). However, in the OLP these dependencies are also largely. CD68+ macrophages may be associated with immunopathogenesis of OLP, indicating a pro-inflammatory activity and regulatory role in the type of T-cell response. Besides, CD68+ macrophages can cooperate in the diagnosis of OLP. These results are essential to future studies that seek a therapeutic target for OLP and OLL.

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.

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.

Presence of B Cells and Plasma Cells in Oral Lichen Planus.

Statement of the Problem: Oral lichen planus (OLP) is a chronic inflammatory disease with unknown etiopathogenesis. It was believed that T cells played the major role in developing the lesions. It has been recently suggested that B lymphocyte cells (B cells) and plasma cells may play a role in OLP pathogenesis.Purpose: OLP is considered as a T-cell mediated disease. It was believed that the presence of B cells and plasma cells in the sub-epithelial inflammatory infiltrate, rules out the diagnosis of OLP. This study aims to investigate the presence of B cells and plasma cells in the inflammatory infiltrate of OLP. In addition, the association between the presence of B cells and plasma cells with histopathologic features of the lesion was assessed.Materials and Method: To assess the presence of B cells and plasma cells, 61 cases with the diagnosis of OLP were collected. The cases with definite clinical and histopathological diagnosis of lichen planus based on WHO criteria were included. For each case, demographic information and histological characteristics were recorded. Specimens underwent immunohistochemical (IHC) staining for CD20 and CD138 and the percentage of the positive cells were counted and scored.Results: CD20 positive cells existed in all OLP cases with the mean expression of 22.5%± 15.17% and small number of CD138 positive cells were seen in 62.3% of our cases with the mean expression of 4.74%±9.23%. No association was found between histopathological features and CD138 expression, however, CD20 expression level was higher in the cases with parakeratinized surface (p= 0.004).Conclusion: B cells existed in the inflammatory infiltrate of OLP in all cases. Small number of plasma cells could be occasionally found in OLP. Therefore, presence of B cells and plasma cells in the inflammatory infiltrate cannot rule out the diagnosis of OLP.

ALDH1 immunoexpression in epithelial and stromal cells of oral lichen planus and lesions with lichenoid inflammatory infiltrate.

Oral Lichen Planus is a potential malignant disorder and shares clinical and histopathological features with other similar lesions. ALDH1 is a specific biomarker for stem cells identification, however its role in stromal cells of immune inflammatory infiltrate has not been explored. The aim of this study was to investigate the ALDH1 immunoexpression in epithelial and stromal cells of Oral Lichen Planus and other lesions with lichenoid inflammatory infiltrate. 64 samples of Oral Lichen Planus, Oral Lichenoid Lesions, Oral Leukoplakia and Unspecific Chronic Inflammation were included. ALDH1 was evaluated in both epithelium and stromal cells. ALDH1+ cells ≥ 5% were considered positive in epithelium. Stromal cells were evaluated semi quantitatively. Fields were ranked in scores, according to criteria: 1 (0 to 10%); 2 (11 to 50%) and 3 (>50%). The mean value of the sum of the fields was the final score. Statistical differences among groups were investigated, considering p < 0.05. ALDH1 expression in epithelium was low in all groups without difference among them. ALDH1+ cells in the lamina propria were higher for Lichen Planus [2.0], followed by Leukoplakia [1.3], Lichenoid lesions [1.2] and control [1.1] (p<0.05). ALDH1 immunoexpression in epithelium of lichenoid potential malignant disorders did not show a contributory tool, however ALDH1 in stromal cells of lichen planus might be involved in the complex process of immune regulation associated with the pathogenesis of this disease.

Frequency of micronuclei in tobacco habitués and Non-Habitués with oral lichen planus

Background: Tobacco in any form is genotoxic to the oral epithelium and manifests as tobacco-associated mucosal lesions, some of which are OPMDs with a propensity for progression into OSCC (2-17%). The aberrations in the count and morphology of micronuclei in exfoliative cytological preparations have been demonstrated in all forms of oral tobacco usage and OLP independently. The more extensive these aberrations, the greater the possibility of undergoing malignant change. This study focused on assessing the extent of micronuclear damage in tobacco-habitues with OLP, thus placing them in a higher risk group as compared to non- habitues with OLP. Aim and Objectives: To evaluate the frequency of micronucleated exfoliative cells in oral lichen planus and to evaluate the effect of tobacco on the frequency of micronuclei in these patients. Material and Methods: Patients were divided into 3 groups: OLP with habit, OLP without habit and healthy controls. Exfoliated cells were obtained from the lesion, smeared on slides, stained by Papanicolaou's method and 1000 cells per slide evaluated for micronuclei according to the Tolbert et al criteria. Statistical Analysis: A statistically significant result was obtained using ANOVA and Bonferroni tests. Result: The genetic damage and increased potential for malignant transformation in OLP is compounded in tobacco habitues evidenced by the increase in the number of micronuclei. Conclusion: The Micronucleus Index was observed to be three-fold greater in tobacco habitues with OLP as compared to non-habitues with OLP.