Expressions of CD 138 and CD43 in Oral Leukoplakia

Introduction: Oral Leukoplakia is the second most common oral potentially malignant disorder encountered in day-to-day clinical practice, with an overall global prevalence of 4.11%. The rate of its malignant transformation varies worldwide. Aims & Objectives: The aim of the study was to assess CD 138 and CD43 immunoreactivity in oral epithelial dysplasia. Materials & Methods: Immunohistochemistry was performed on fifteen formalin-fixed oral epithelial dysplasia tissues for CD 43 (n=15) and CD 138 (n=15) which were obtained from archives at Oral cancer research and coordinating centre, Malaysia. Results: The expression of CD 43 in non-hematopoietic tissues was negative in all cases, but epithelium with dysplastic alterations had low or weak CD 138 expression between dysplastic tissue and non-dysplastic epithelium, there was a substantial difference in staining intensity. Conclusion: Oral carcinogenesis is a multistep process, and cancer driver genes have been shown to have vastly diverse effects in various tissues. CD 138 expression was shown to be lower in tissues undergoing dysplastic alterations, which could be a sign of oral epithelial dysplasia with a high risk of malignancy.

Altered ß-catenin expression in oral mucosal dysplasia: a comparative study

Objective The current study aimed to investigate the β-catenin expression in oral leukoplakia (OL) with different degrees of epithelial dysplasia and normal oral mucosa.Material and Methods Formalin-fixed, paraffin-embedded tissue samples of 39 OL (mild dysplasia n=19, moderate dysplasia n=13, and severe dysplasia n=7), and 10 normal oral mucosa (control group) were submitted to immunohistochemical reactions to anti-β-catenin primary antibody. A qualitative β-catenin analysis was performed based on the percentage of positive cells. The cellular location and the epithelial layer were also considered. The Chi-square test and the Fisher’s exact test were used to verify possible differences in the β-catenin expression among the OL groups. A p-value of <0.05 was considered statistically significant.Results Membranous expression of β-catenin in parabasal and basal layers was gradually lost in the higher degrees of epithelial dysplasia. In normal oral mucosa, β-catenin was detected only in the cytoplasmic membrane. However, a significant increase in cytoplasmic β-catenin could be observed between mild and moderate dysplasia (Fisher Exact test - p<0.001) and between mild and severe dysplasia (p<0.001).Conclusions The β-catenin cytoplasmic expression observed in this study may represent the initial stage of modifications in the E-cadherin-catenin complex, along with morphological cellular changes.

Overexpression of cyclin A in oral dysplasia: An international comparison and literature review.

Oral squamous cell carcinoma (OSCC) is one of the most debilitating cancers in the world and while its causes have been heavily researched, the outcome remains grim. Most of these cancers are identified in the late stage and as a result treatment options are limited. Therefore, researchers have focused their efforts on recognizing and identifying dysplastic tissue that has an increased chance of progressing to cancer. Research has begun to look at cell cycle dysfunctions and in particular, aberrant protein functions as a way of identifying the cellular mechanism at fault. The overexpression of a group of regulatory proteins called cyclins has been demonstrated in many types of dysplasia and carcinomas. Although researchers have identified several different types of cyclins as potential culprits, we chose to focus our study primarily on the overexpression of cyclin A. While most research on oral dysplasia and OSCC has been focused on cyclin D, studies have been done on cyclin A. While the etiology of oral dysplasia/SCC appears to be multifactorial, we chose to compare our results with those of similar studies performed across the globe. The social factors, such as the increased use of tobacco that may have contributed to our results, were compared with similar studies performed in Europe and Asia. While our results were remarkably similar and demonstrated a link between the overexpression of cyclin A in oral dysplasia, there exists some differences and thus may require a multicenter, longitudinal study.