Langerhans cells and their role in oral mucosal diseases.

Dendritic cells are arguably the most potent antigen-presenting cells and may be the only cells capable of initiating the adaptive immune response. The epithelial residents of dendritic cells are Langerhans cells, which serve as the "sentinels" of the mucosa, altering the immune system not only to pathogen entry but also of tolerance to self antigen and commensal microbes. Oral mucosal Langerhans cells are capable of engaging and internalizing a wide variety of pathogens and have been found responsive to nickel in patients with nickel allergies, oral Candida species, oral lichen planus, lichenoid drug eruptions, graft versus host diseases, periodontal diseases median rhomboid glossitis, human immunodeficiency virus infection, hairy leukoplakia of the tongue, and oral squamous cell carcinoma. Review focuses on the role of antigen-presenting cells in particular Langerhans cells to better understand the mechanisms underlying immune responses. In this review, comprehensive detail about mucosal diseases has been compiled using the PubMed database and through textbooks.

A comparative analysis of langerhans cell in oral epithelial dysplasia and oral squamous cell carcinoma using antibody CD-1a.

BACKGROUND: The integrity of the immune system is necessary to control tumor progression and a compromised state contributes to tumor escape. AIMS: The study intends to evaluate the presence and distribution pattern of Langerhans cells (LC) in Oral epithelial dysplasia (OED) and oral squamous cell carcinoma (OSCC) oral epithelial dysplasia and oral squamous cell carcinoma and elucidate their role. The study analyses LC in histological zones of the epithelium and connective tissue, which has seldom been attempted previously. MATERIALS AND METHODS: Forty-five microscopic sections (i.e. 5 normal, 15 OED and 25 OSCC) were examined for expression of LC marker CD1a using immunohistochemistry. LCs were counted in zones of epithelium and connective tissue. STATISTICAL ANALYSIS USED: Results were analyzed using SPSS Version 16.0 and subjected to one-way ANOVA comparison and Student's t-test and Wilcoxon Z test. RESULTS: Significant decline in LC count was observed with progressing grade of OED and OSCC. The basal and suprabasal zones in OED and superficial zone in OSCC exhibited the highest density of LCs. The low LC count in severe dysplasia was attributed to paucity in the basal zone. There was a significant paucity of LCs in the sub-epithelial zone of all the grades of OSCC, with high influx of LCs within the tumor stroma. Also, poorly differentiated OSCC exhibited a significant decrease in the LC count within the overlying epithelium as well as the tumor stroma. CONCLUSION: The present study suggests that there is a recruitment of LCs in the neoplastic process. Changes observed in LC distribution within the zones of dysplastic epithelium and tumor stroma can be interpreted as their pathophysiologic function.

Reliability of toluidine blue vital staining in detection of potentially malignant oral lesions--time to reconsider.

Being simple and inexpensive toluidine blue has been in use for more than two decades for the detection of potentially malignant oral lesions (PMOL's) and malignant lesions. Although there has been concensus that staining often assists in the identification of these lesions, results have been diverse. In most studies false negative were not recorded as biopsies of lesions that did not retain toluidine blue were not performed. Thus the present study attempted to evaluate the efficacy of toluidine blue vital dye for detection of PMOL's. The study included 47 biopsies (TBP:35 and TBN:12), of which 23 cases were confirmed as dysplastic (TBP=17 and TBN=6), 7 as hyperkeratosis (TBP=4 and TBN=3), 8 as epithelial hyperplasia (TBP=6 and TBN=3) and 5 as other benign lesions (TBP=4 and TBN=1). The validity test revealed a senstivity of 73.9% and specificity of 30%. The positive predictive value was 54.8% and negative predictive value of 50%. The study intends to highlight the false negative result (26.1%) which was mainly attributed to mild dysplasia and the false positive (32.6%) which included hyperkeratosis, hyperplasia, lichen planus and traumatic ulcer. The study concludes that toluidine blue staining should not blindly direct the clinician's opinion, and strongly discourages the use of toludine blue as a screening test and the results should be interpreted with caution.

Oxidative stress and antioxidant defense in oral lichen planus and oral lichenoid reaction.

BACKGROUND: Oral Lichen Planus (OLP) is an inflammatory disease of unknown etiology while Oral Lichenoid Reaction (OLR) is a condition mimicking OLP. As these conditions are exposed to oxidative stress, they could release reactive oxygen species (ROS) which are implicated in the pathogenesis of a plethora of inflammatory conditions to lethal diseases. We evaluated and compared the levels of a series of oxidative stress markers in patients with OLP and OLR with that of normal controls and tried to identify the role of these oxidative stress markers in these conditions. METHODS: Protein thiol oxidation, malondialdehyde (MDA) and total antioxidant activity were estimated in both the groups (OLP and OLR) and compared with that of normal subjects. RESULTS: There were significantly lower levels of serum protein thiols in OLP (p < 0.005) while in patients with OLR the difference was not statistically significant (p < 0.489) when compared with controls. Serum MDA levels were significantly higher in OLP (p < 0.001) and OLR (p < 0.001) than in controls. However, there was no significant difference in serum MDA levels between OLP and OLR patients (p > 0.05), but with a significant difference in serum thiol levels between the two (p < 0.047). Total antioxidant levels were lower in OLP (p < 0.016) and OLR (p < 0.017) when compared to normal subjects, while between the study group total antioxidant levels were not significantly different (p < 0.632). CONCLUSIONS: The findings from the present study demonstrate involvement of ROS in the pathogenesis of OLP and OLR, though both these disease conditions have a different clinical course.