Langerin-expressing and CD83-expressing cells in oral lichen planus lesions

OBJECTIVE: Dendritic Langerhans cells (LCs) have been attributed a role in the pathogenesis of lichen planus as autoantigen-presenting cells initiating expansion of autoreactive T cells. Langerin and CD83, which are cell molecules expressed on LCs, are associated with antigen presentation. The present study examined expression of Langerin and CD83 molecules on LCs in patients with oral lichen planus (OLP). MATERIAL AND METHODS: Biopsies were obtained from seven patients with OLP. Oral mucosa from seven healthy subjects served as controls. Monoclonal antibodies (mAbs) were used in standard immunohistochemical procedures to visualize CD1a-, Langerin-, and CD83-molecule-expressing cells. RESULTS: CD1a+ and Langerin+ cells were found in significantly higher frequencies in OLP epithelium compared with healthy oral epithelium (p<0.01 and p<0.05, respectively); however, the frequency of CD83+ cells did not differ (p>0.05). The connective tissue in OLP lesions showed significantly higher frequencies of CD1a+, Langerin+, and CD83+ cells compared with healthy connective tissue (p<0.01, p<0.01, and p<0.05). CD1a+ and Langerin+ cells in OLP and healthy epithelium had a dendritic morphology. CONCLUSIONS: The study shows increased numbers of CD1a- and Langerin-expressing LCs in OLP compared with healthy controls. In the connective tissue, CD83+ cells with dendritic morphology were localized to regions of lymphocyte clusters. The presence of CD83+ dendritic cells in areas of lymphocyte clusters in the connective tissue of OLP lesions indicates the possibility of ongoing autoantigen presentation.     

Perforin and granzyme B involvement in oral lesions of lichen planus and chronic GVHD

J Oral Pathol Med (2010) 39 : 741–746 Background: Oral lesions of lichen planus and chronic graft‐vs.‐host disease (cGVHD) have similar clinical and histological features, but distinct etiology. Apoptosis induced by cytotoxic T lymphocyte has been proposed as a mechanism of keratinocytes death. Cytotoxicity can be mediated by granules containing granzyme B and perforin. Since common features can reflect similarities in immunological mechanisms, we studied the role of those molecules in both diseases. Methods: We analyzed 29 cases of oral lichen planus and 27 of oral cGVHD. The sections were studied on H&E, perforin and granzyme B staining. Results: The total means (epithelium plus connective tissue number) of the granzyme B‐ and perforin‐positive cells were significantly higher in cGVHD than in oral lichen planus lesions (P < 0.05). Also, it was found that the higher the number of perforin+ cells, the higher the number of granzyme‐B+ cells in the epithelium and in the connective tissue for both groups (P < 0.05). In oral lichen planus, the number of single apoptotic bodies had a positive correlation with connective tissue granzyme immunostaining and a negative correlation with perforin (P < 0.01). On the contrary, in oral cGVHD, the number of apoptotic body clusters presented a positive correlation with connective tissue perforin (P < 0.01). Conclusions: Our findings indicate that apoptosis in oral lichen planus seems to be correlated with granzyme B release, while in oral cGVHD, perforin seems to be more important. Although these diseases present clinical and histological similarities, subtle differences seem to exist in their pathogenetic mechanisms.     

Immunophenotypic characterization and distribution of dendritic cells in odontogenic cystic lesions

Oral Diseases (2012) 19 , 85–91 Objective: To analyze the expression and distribution patterns of mature dendritic cells (mDCs) and immature DCs (imDCs) in radicular cysts (RCs), dentigerous cysts (DtCs), and keratocystic odontogenic tumors (KCOTs). Materials and methods: Forty‐nine odontogenic cystic lesions (OCLs) (RCs, n = 20; DtCs, n = 15; KCOTs, n = 14) were assessed using the following markers: S100, CD1a and CD207 for imDCs; and CD83 for mDCs. Results: Almost all cases were S100, CD1a, and CD207 positive, whereas 63% were CD83 positive. RCs presented greater number of immunostained cells, followed by DtCs, and KCOTs. The number of S100+ cells was greater than both CD1a+ and CD207+ cells (P < 0.001), which showed approximately similar amounts, followed by lower number of CD83+ cells (P < 0.001) in each OCL type. Different from S100+ cells, both CD1a+ and CD207+ cells on the epithelium (P < 0.05) and CD83+ cells on the capsule (P < 0.05) were preferentially observed. In RCs, significant correlation was found between the thickness epithelium with S100+ and CD1a+ cells, and between the degree of inflammation with CD83+ cells. Conclusions: Dendritic cell populations in OCLs can be phenotypically heterogeneous, and it could represent distinct lineages and/or functional stages. It is suggested that besides DC‐mediated immune cell interactions, DC‐mediated tissue differentiation and maintenance in OCLs should also be considered.     

Immunohistochemical localization of CD1a and S100 in gingival tissues of healthy and chronic periodontitis subjects

Oral Diseases (2012) 18, 778-785 Objective: The aim of this study was to evaluate the presence and distribution of CD1a and S100 protein markers in states of gingival health and chronic periodontitis in human subjects. Materials and Methods: Gingival tissue samples were derived from 10 healthy and 10 chronic periodontitis-affected human subjects. The presence and distribution of CD1a and S100 protein was assessed using immunohistochemistry, and the cell types involved in their expression was determined. Results: The presence and distribution of CD1a was confined only to the gingival epithelium, whereas S100 was seen in the epithelium and connective tissue. However, increased expression of both CD1a and S100 protein was seen in periodontitis-affected gingival tissues compared with healthy gingiva. Immunohistochemistry demonstrated that CD1a- and S100-positive cells in the epithelium are Langerhans cells (LCs) and S100 positive cells in the connective tissue are dendritic cells (DCs). Conclusion: Our findings suggest the transition of CD1a-positive LCs to S100-positive DCs from epithelium to connective tissue in response to an antigenic challenge. Demonstration of increased number of S100-positive DCs in the gingival connective tissue in chronic periodontitis possibly suggests their involvement in bone resorption in addition to their antigen presentation property.     

Effect of smoking on Langerhans and dendritic cells in patients with chronic gingivitis

Background: Previous literature showed contrasting results regarding dendritic cell (DC) counts in patients with periodontal diseases. Although smoking decreases the number of DCs in the lungs, the effect of smoking on the quantitative distribution of Langerhans cells (LCs) and DCs in patients with chronic gingivitis has not been investigated to our knowledge. Methods: Gingival samples were obtained from 30 patients (15 smokers and 15 non‐smokers). Immunohistochemical staining was performed to identify CD1a+ immature LCs and CD83+ mature DCs. The inflammatory infiltrate was evaluated and counted. Densities of cells were calculated within the oral epithelium (OE), sulcular epithelium (SE), and lamina propria (LP) for CD1a+ cells and within the LP for CD83+ cells. Results were compared between groups. This study evaluates whether the high number of cigarettes and smoking years affects densities of cells. Correlations among densities of LCs and DCs with densities of inflammatory infiltrate, number of cigarettes, and smoking years were performed. Results: Densities of inflammatory infiltrate and CD1a+ cells from the SE and LP were significantly lower for smokers than for non‐smokers (P <0.05). This result could not be identified for CD1a+ cells from the OE and for CD83+ cells from the LP. The number of cigarettes and smoking years did not affect densities of cells. No statistically significant correlations could be drawn among densities of LCs and DCs and inflammatory infiltrate, number of cigarettes, and smoking years. Conclusion: Smoking proved to affect the quantitative distribution of LCs and DCs in patients with chronic gingivitis.     

Oral mucosal expression of HIV-1 receptors, co-receptors, and alpha-defensins: tableau of resistance or susceptibility to HIV infection?

The basic premise of whether transmission of HIV-1 through the oral mucosa actually occurs, and through what route, is a topic of intense interest. Our work has focused on HIV-1 receptors/co-receptors and alpha-defensin-1 in situ in human gingiva. Regardless of HIV-1 infection, the role that C-type lectin receptors might play in periodontal pathogenesis is of great interest. We have shown that the gingival lamina propria, when inflamed, becomes increasingly infiltrated with DC-SIGN+MR+ dermal dendritic cells (DDCs), while the inflamed epithelium shows a decrease in Langerin+ Langerhans cells (LCs). Moreover, DDCs and LCs contribute to the mature CD83+ DC pool in situ, and form immune conjugates with CD4+ T-cells in the lamina propria (Jotwani and Cutler, 2003). This raises the intriguing possibility that oral mucosal DCs may be involved in HIV-1 transfer to T-cells in situ. However, this possibility is tendered by the challenges faced by the virus in gaining access to oral mucosal immune cells, including their ability to survive the salivary defenses, cross the mucosal barrier, resist inactivation by alpha-defensins, and overcome the paucity of co-receptor CCR5 in (healthy) oral mucosa (i.e., required for productive infection [Jotwani et al., 2004]). To date, there is little evidence of direct infection by HIV-1 of oral mucosal DCs/T cells and other cells in situ. Abbreviations used in this paper: CP, chronic periodontitis; CCR5, chemokine receptor 5; CXCR4, C-X-C receptor 4; DCs, dendritic cells; DC-SIGN, DC-specific ICAM-3 grabbing non-integrin; DDC, dermal dendritic cells; LCs, Langerhans cells; LP, lamina propria; MR, mannose receptor.     

Immunohistochemical study of oral lichen planus associated with hepatitis C virus infection,oral lichenoid contact sensitivity reaction and idiopathic oral lichen planus

OBJECTIVES: Oral lichen planus (OLP) is a common mucocutaneous disorder and might be associated to a possible pathogenic relationship with hepatitis C virus (HCV) infection or hypersensitivity to dental alloy. We examined the clinical and immunohistochemical features of OLP associated with HCV infection (OLP-HCV), oral lichenoid contact sensitivity reaction (OLCSR), and idiopathic oral lichen planus (iOLP). The immunohistochemical expressions of CD4, CD8, B cells, Class II major histocompatibility complex antigen (HLA-DR), S-100, HSP60, Proliferating cell nuclear antigen (PCNA) and Ki-67 were compared to study the pathogenic differences of the three OLP groups. MATERIALS AND METHODS: Three groups of OLP patients, (I) OLP-HCV patients (n = 17), (2) OLCSR patients (n = 10) and (3) iOLP patients (n = 14) were retrieved from clinical records and tissues examined immunohistochemically by the avidin-biotin-complex technique. RESULTS: The patients with OLP-HCV showed widespread lesions. The proportion of CD8+ cells was found to be significantly higher in the lamina propria of the OLP-HCV patients and a significantly lower proportion of CD8+ cells of the OLCSR patients was noticed in the epithelium or the connective tissue papillae than in the iOLP patients. There were no significant differences in either the number of CD4+ cells or B cells between the three OLP groups. No significant differences in the number of HLA-DR+ cells were found between the three OLP groups and some OLP-HCV patients showed a significant increase of S-100+ cells in the epithelium compared with iOLP patients. There were no significant differences in either the number of PCNA+ or Ki-67+ cells between the groups. The patients showed similar weak expressions of HSP60 in the three OLP groups. CONCLUSION: The different distributions of the CD8+ cells that could have functionally different roles might be related to the distinct pathogenic mechanisms in the three OLP groups.     

Overexpression and varied clinical significance of Th9 versus Th17 cells in distinct subtypes of oral lichen planus

ObjectiveOral lichen planus (OLP) presents with large numbers of T lymphocytes accumulating beneath the epithelium of the oral mucosa; however, its aetiology remains obscure. A potential role for an emerging novel T cell subset, Th9, in OLP has recently been suggested but remains to be clarified. The current aim was to investigate the expression and potential clinical significance of Th9 cells in distinct subtypes of OLP.Materials and methodsPeripheral blood samples were collected from 41 OLP patients and 18 healthy controls (HCs). Flow cytometric analysis was used to detect the CD4+ T helper subset Th9 (IL-9⁺IL-17⁻CD4⁺ Th cells) and Th17 (IL-9⁻IL-17⁺CD4⁺ Th cells) expression levels.ResultsFlow cytometry results showed significantly elevated levels of Th9 cells in reticular and erosive OLP compared to HCs. Th9 expression in erosive OLP was less than in reticular OLP, indicating that Th9 but not Th17 cells may play a predominant role in reticular disease. However, in erosive OLP patients, we found much higher levels of Th17 cells compared to reticular OLP patients and HCs, indicating that Th17 dominates in erosive OLP. Statistical analysis showed positive correlations of Th9 cells and Th17 cells in patients with reticular or erosive OLP but none in HCs.ConclusionsTh9 and Th17 cells may take the predominant roles in reticular and erosive OLP respectively, and their numbers were positively correlated in reticular and erosive OLP patients. Elevated circulating Th9 cells may help maintain immune balance in OLP immunopathogenesis, which requires further investigation.     

Increased submucosal factor XII la-positive dendrocytes in oral lichen planus

Factor XIIIa +“dendrocytes”, normal residents of the submucosa and dermis. are a morphologically and phenotypically distinctive subset of the monocyte-macrophage system. Because these cells arc believed to participate in the regulation of immune responses, we postulated that they may play a role in the pathogenesis of lichen planus, a condition of immune dysregulation. Tissue sections of oral lichen planus were evaluated immunohistochemically for evidence of differences in dendrocyte populations in lesional and non-lesional areas from the same patient. In addition to factor XIIIa, sections were stained for antigens (CD68, S-100 protein, CD36) that may be expressed by other cells that occasionally exhibit dendritic profiles. CDI8 (found on leukocytes and dendrocytes) and its ligand ICAM-I (intercellular adhesion molecule) were also identified in sections to determine if these antigens are operative in lichen planus. Results showed that XIIIa + dendrocytes were significantly increased in number (and size) in lichen planus. The mean number of dendrocytes in connective tissue subjacent to basement membrane (0.064 mm²) was 27 in lichen planus as compared to 10 in adjacent unaffected tissue. Similar increases were also evident in connective tissue deep to this zone (mean of 20 dendrocytes vs. mean of 8). CD68+ macrophages were also abundant in the lichen planus infiltrate, and S-100 + connective tissue cells were frequently seen. CD36 + dendritic cells were seen in relatively small numbers in the same sites where dendrocytes were found. ICAM-I + connective tissue dendritic cells of undetermined lineage were also evident in the diseased areas. Endothelial cells in and around the infiltrate were strongly reactive to anti-ICAM-1. Basal and parabasal keratinocytes overlying the lymphoid infiltrates were also strongly ICAM-1 +. It appears that XIIIa + dendrocytes have a role in the immunologic mechanisms of lichen planus, and that these cells may be acting in concert with other immunocompetent cells, such as macrophages and S-100 + epithelial dendritic cells, to activate T lymphocytes. ICAM-I expression by dendrocytes. endothelial cells, and keratinocytes may facilitate leukocyte migration to, and retention in. the disease focus.     

Intra-epithelial CD8+ T cells and basement membrane disruption in oral lichen planus.

BACKGROUND: We investigated basement membrane (BM) disruption and the distribution of mast cells (MCs) and T cell subsets, in oral lichen planus (OLP) and normal buccal mucosa (NBM) using immunohistochemistry. In OLP, there were increased numbers of tryptase+ MCs in areas of BM disruption (P < 0.05). METHOD: We identified clusters of intraepithelial CD8+ T cells in OLP, specifically in regions of BM disruption. The number of intraepithelial CD8+ T cells in regions of BM disruption was significantly greater than in regions of BM continuity (P < 0.05). RESULTS: There were comparable numbers of lamina propria CD8+ T cells in regions of BM disruption and BM continuity. The number of CD4+ T cells in the epithelium and lamina propria of OLP lesions did not vary between regions of BM disruption and BM continuity. CONCLUSION: These data suggest a role for MCs in epithelial BM disruption in OLP. CD8+ T cells may migrate through BM breaks to enter the OLP epithelium.     

Oral lichen planus and chronic junctional stomatitis: differences in lymphocyte subpopulations

Objective. Oral lichen planus (OLP) is an oral counterpart or oral manifestation of the common skin disease lichen planus. Chronic junctional stomatitis (CJS) is a relatively unknown condition characterized by a stromal lymphocyte infiltrate, which is also a diagnostic feature of OLP. The differential diagnosis of OLP and CJS is unclear and they have been suggested to represent variants of the same disease. Material and methods. To investigate possible differences in lymphocyte (sub)populations between these two conditions, we immunostained 10 OLP and 10 CJS specimens for CD1-a, and the lymphocyte markers, CD3, CD4, CD5, CD8, and CD20. We scored the staining results by a four-step grading system and used the Fisher exact test to analyze them statistically. Results. The proportional amount of (CD20 positive) B lymphocytes was higher in CJS than in OLP and the predominance of CD4 positive T lymphocytes over CD8 positive T lymphocytes was stronger in OLP than in CJS. The differences were statistically significant. Conclusion. The results reflect differences in the lymphatic infiltrate between OLP and CJS. Their significance needs further investigation.     

A novel application of the buccal micronucleus cytome assay in oral lichen planus: a pilot study

Background

The most important complication of oral lichen planus is malignancy transformation.

Objective

The aim of this study was to assess cellular and nuclear morphology in a group of patients with oral lichen planus measured by means of buccal micronucleus cytome assay.

Study design

This study included thirty patients with a clinicopathological diagnosis of oral lichen planus (all with atrophic–erosive clinical forms of OLP) and thirty healthy control subjects. Both samples were similar in age and gender. The buccal micronucleus cytome assay protocol consisted of: cell collection from both cheeks with a cytobrush; cell centrifuge; slide preparation, fixation and staining followed by fluorescent microscope analysis. 2 × 10⁶ exfoliated cells were screened for nuclear abnormalities: micronuclei, nuclear buds, binucleation, basal and differentiated cells, condensed chromatin, karyorrhectic cells, pyknosis and karyolytic cells.

Results

Patients with oral lichen planus showed significantly higher frequencies of micronuclei (p < 0.001), nuclear buds (p < 0.001), binucleated cells (p < 0.021) than the control group.

Conclusions

This method is an easy way for clinicians to assess DNA damage, proliferative potential of basal cells and cell death in buccal cells in cases of oral lichen planus.     

Detection of fascin and CCR-7 positive mature dendritic cells in oral lichen planus

Background: Dendritic cells (DC) play a crucial role in the pathogenesis of oral lichen planus (OLP) with respect to antigens presented to T cells. We performed immunohistochemical analysis to elucidate the process of activation of DC in OLP. Methods: Thirty biopsy specimens were obtained from the patients with OLP. The expressions of CD1a, Langerin, S‐100, fascin, chemokine receptor‐7 (CCR‐7), D2‐40, cyclooxygenase‐2 (COX‐2), and microsomal prostaglandin E synthase‐1 (mPGES‐1) in DC from OLP and disease free control were investigated using specific antibodies. The distribution and number (1 mm²) of DC were assessed in the intra‐epithelium and the submucosa specimens. Correlation between the number of DC and epithelium thickness was also determined. Result: Immature DC (Langerin⁺, CD1a⁺, and S‐100⁺) were identified in the epithelia from OLP patients and control, though the numbers of Langerin⁺ and CD1a⁺ positive cells were decreased in the OLP samples as compared to the control. Mature DC (fascin⁺) were identified in the submucosa specimens, not found in the epithelium from OLP or control. Double immunostaining revealed DC positive for fascin and CCR‐7 in the submucosa, which had migrated into D2‐40⁺ lymph vessels. Furthermore, keratinocytes expressed both Prostaglandin E₂ (PGE₂) converting enzymes, COX‐2, and mPGES‐1, indicating PGE₂ synthesis in the epithelial layer of the OLP specimens. Conclusion: Our results indicate that DC change from immature to mature in the epithelium and are then drawn out to the submucosa. We demonstrate that mature DC localized in the submucosa, it consequently migrates into lymph vessels. This maturation process of DC is an important immunopathological feature of OLP.     

Multiple dendritic cell (DC) subpopulations in human gingiva and association of mature DCs with CD4+ T-cells in situ

Gingival epithelium is a site of active trafficking of Langerhans cells (LCs), while the lamina propria in chronic periodontitis (CP) contains CD83+ mature dendritic cells (mDCs) and CD4+ T-cells. The immune cells that contribute to the mDCs, and whether mDCs engage with T-cells in situ, are unclear. Using several immunohistochemical approaches, combined with fluorescence-, light-, and scanning laser confocal-microscopy, we show that, in addition to LCs, the gingiva contains dermal DCs (DDCs) in the lamina propria; moreover, DDCs increase in number during CP. Furthermore, DDCs, LCs, and B-cells co-express CD83 in CP and contribute to the mDC pool. Double-staining for CD83 and CD4 revealed that mDCs associate with clusters of CD4+ T-cells in the lamina propria. Analysis of these data suggests that multiple DC subsets mature in the gingiva and that mature DCs engage in antigen presentation with T-cells in chronic periodontitis.     

MicroRNA‐137 promoter methylation in oral lichen planus and oral squamous cell carcinoma

Oral lichen planus (OLP) is a common oral mucosal disease, which is generally considered a potentially malignant lesion. To identify efficiently prognostic biomarker, we investigated the microRNA‐137 (miR‐137) promoter methylation in OLP and compared with the samples from healthy volunteers and patients with oral squamous cell carcinoma (OSCC). A total of 20 OLP and 12 patients with OSCC as well as 10 healthy subjects were subjected to miR‐137 promoter methylation analysis using methylation‐specific PCR (MSP). To address the malignancy prediction potential from miR‐137 promoter methylation status, methylation of the p16 gene, a well‐known tumor suppressor, was investigated in the same samples. The p16 methylation and miR‐137 promoter methylation were found to be 25% and 35% in patients with OLP, 50% and 58.3% in patients with OSCC, and 0% and 0% in healthy subjects, respectively. The differences between miR‐137 and p16 methylation levels were statistically significant between healthy controls and patients. Methylation levels of the two promoters were also influenced by age, gender, and lesion duration. Interestingly, aberrant promoter methylation of the p16 and miR‐137 genes was only found in the epithelium but not in the connective tissue from patients with OLP. This raises the possibility to use miR‐137 methylation as a biomarker for malignant prediction in patients with OLP.     

Do Langerhans cells behave similarly in elderly and younger patients with chronic periodontitis?

OBJECTIVE: The purpose of this study was to compare the number, the distribution and the expression of markers of maturation of Langerhans cells (LC) in elderly and younger patients with chronic periodontitis in order to evidence the effect of aging on LC in inflammatory gingival tissue. METHODS: Gingival tissue specimens presenting chronic periodontitis from 8 elderly patients aged >75 (group E) and from 8 younger patients aged 50-60 (considered as controls, group C) were used for immunohistochemistry with monoclonal antibodies against CD45RB (leucocytes), CD1a (LC), markers of LC maturation (DC-LAMP, CD83) and number of immunolabelled cell subsets was evaluated using image analysis. RESULTS: The difference in the number of CD45RB+ leucocytes in the upper connective tissue between groups was not significant. In group E, the number of CD1a+ LC was significantly decreased (P<0.002) in the epithelium and significantly increased (P<0.0004) in the upper connective tissue. Furthermore, in group E, intraepithelial CD1a+ LC are more often observed in the upper epithelium and their dendritic processes were shorter and less numerous. Concerning the expression of markers of maturation, the numbers of intraepithelial DC-LAMP+ cells and CD83+ cells were significantly increased (P<0.0007 and P<0.02, respectively) in group E. CONCLUSION: During chronic periodontitis in elderly patients, the decrease in the number of intraepithelial LC and the alteration of dendritic processes could be balanced by a cellular distribution often observed in the upper epithelium associated with changes in cell maturation in response to bacterial elements.     

Increase of gingival matured dendritic cells number in elderly patients with chronic periodontitis

Objective

The purpose of this study was to evaluate the inflammatory cell subset proportions in the upper gingival connective tissue, including mature dendritic cells (DC) in elderly and younger patients with generalized chronic periodontitis in order to further understand the effect of aging on gingival inflammatory phenomenon.

Methods

Gingival tissue specimens presenting chronic periodontitis from 8 elderly patients aged >75 (test group, group T) and from 8 younger patients aged 50-60 (considered as controls, group C) were analysed by immunohistochemistry using monoclonal antibodies against CD45RB, CD4, CD8, CD19, CD68, DC-SIGN, DC-LAMP molecules. The number of each immunolabelled cells subset was counted using image analysis.

Results

The difference in the number of CD45RB + leucocytes in the upper gingival connective tissue between groups was not significant permitting to use it as reference. As compared to group C, the lymphocyte subsets/CD45RB + leucocytes ratios tended to decrease in group T but the decrease was significant only for CD4 + T lymphocytes/CD45RB + cells ratio (p < 0.03). On the opposite, the ratios of antigen-presenting cells DC-SIGN + cells/CD45RB + cells and DC-LAMP + cells/CD45RB + cells were significantly increased (p < 0.03 and <0.0001, respectively) in group T. Moreover, in group T the DC-LAMP + cells/DC-SIGN + cells ratio was significantly increased (p < 0.05) showing an increased number of matured dendritic cells.

Conclusion

During chronic periodontitis in elderly patients, our results show a decrease in the ratio of gingival CD4 + lymphocyte subset associated with an increase in the ratios of antigen-presenting cells subsets and more particularly maturated DC-LAMP + dendritic cells.     

No detection of TSH or TSHR in oral lichen planus lesions in patients with or without hypothyroidism

Abstract

Objective: An association between hypothyroidism (HT) and oral lichen planus (OLP) has been reported. However, the mechanisms that could explain this association remain unresolved. This study aimed to evaluate the expression of thyroid-stimulating hormone (TSH) and thyroid-stimulating hormone receptor (TSHR) in healthy oral mucosa and in OLP lesions of individuals with and without HT.

Material and methods: Immunohistochemical expression of TSH and TSHR was studied in oral mucosal biopsies obtained from 14 OLP patients with HT, 14 OLP patients without HT and 10 healthy controls without oral mucosal lesions. Gene expression of TSHR was investigated by using three different PCR techniques in oral mucosal samples from 7 OLP patients with HT, 3 OLP patients without HT, 9 healthy controls and in cultured human oral epithelial cells. Gene expression of TSH was examined by employing 2 PCR techniques in oral mucosal samples from 2 OLP patients with HT, 2 OLP patients without HT and 4 healthy controls.

Results: TSH and TSHR stainings were negative in the studied oral mucosal specimens. Gene quantification assays demonstrated negative gene expression of TSH and TSHR in clinical and in vitro samples.

Conclusions: These results suggest that TSH and TSHR may not be commonly involved in the pathogenetic mechanism that could explain the association between OLP and hypothyroidism.     

Composition of hemidesmosomes in basal keratinocytes of normal buccal mucosa and oral lichen planus

Oral lichen planus (OLP) is a chronic inflammatory disease displaying ultrastructural disturbances in epithelial hemidesmosomes. The expression of several key hemidesmosomal components in OLP as well as in normal buccal mucosa is, however, unknown. The aim of the study was therefore to examine intracellular and extracellular components involved in hemidesmosomal attachment, in OLP (n = 20) and in normal buccal mucosa (n = 10), by immunofluorescence. In normal buccal mucosa, laminin-α3γ2, integrin-α6β4, CD151, collagen α-1(XVII) chain, and dystonin showed linear expression along the basal membrane, indicating the presence of type I hemidesmosomes. Plectin stained most epithelial cell membranes and remained unphosphorylated at S4642. In OLP, most hemidesmosomal molecules examined showed disturbed expression consisting of discontinuous increases, apicolateral location, and/or intracellular accumulation. Plectin showed S4642-phosphorylation at the basement membrane, and deposits of laminin-α3 and laminin-γ2 were found within the connective tissue. The disturbed expression of hemidesmosomal proteins in OLP indicates deficient attachment of the basal cell layer, which can contribute to detachment and cell death of basal keratinocytes seen in the disease.