ArticleJournal of dentistry (Shiraz, Iran)2026
CD1a Expression in Oral Dysplastic Lesions: An Immunohistochemical Analysis.
Article in Journal of dentistry (Shiraz, Iran), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Leukoplakia is among the most prevalent oral potentially malignant disorders, and its association with oral epithelial dysplasia (OED) markedly increases the risk of malignant transformation. Although histopathological grading systems have evolved, accurately predicting which lesions will undergo malignant progression remains a significant challenge. CD1a, a marker expressed by Langerhans cells, may reflect local immune responses and serve as a potential indicator of dysplastic progression. Purpose: Given the inconsistencies in previous findings, the present study aimed to assess CD1a-positive cells in OED associated with leukoplakia and investigate their potential role in the pathogenesis of these lesions. Materials and Method: In this retrospective cross-sectional study, 60 formalin-fixed paraffin- embedded tissue samples were analyzed, comprising 53 OED cases and 7 control samples. Immunohistochemical staining was performed using a monoclonal anti-CD1a antibody. CD1a-positive cells were counted in five high-power fields (40×) in hotspot regions. The severity of dysplasia was categorized according to both 2022 WHO classification and binary grading system; inflammation severity was also scored. Statistical analyses were conducted using the Shapiro-Wilk test, Spearman's correlation, the Mann-Whitney U test, and the Kruskal-Wallis test in SPSS version 28. Results: CD1a expression was elevated in dysplastic tissues compared to controls; however, this difference was not statistically significant ( Conclusion: CD1a may contribute to the process of dysplastic transformation and serve as an indicator of local immune activation. Its increased expression in higher-grade dysplasia was associated with more pronounced inflammatory cell infiltration and a more immune-active microenvironment.
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