Role of abnormal Langerhans cells in oral epithelial dysplasia and oral squamous cell carcinoma: A pilot study

Abstract

Background:

The oral epithelial dysplasia (OED) and oral squamous cell carcinoma (OSCC), although initiated by tobacco carcinogens, their progression is due to inability of Langerhans cells (LCs) to detect these abnormal cells and promote lymphocytes to destroy these cells. We assessed and quantified the tumor associated LCs and inflammation in OED and OSCC to understand their role.

Materials and Methods:

Fifty-five microscopic sections were assessed (27 OED and 28 OSCC). The LCs were detected using S-100 immunohistochemical marker. The number of tumor associated LCs were counted. The presence of abnormal appearing large cells and its relation to histopathologic grade and inflammation was assessed.

Results:

Significant increase in the LC count was observed in OSCC when compared to dysplasia. Large, abnormal appearing cells were observed in dysplasia and carcinomas however, these were more pronounced in moderate dysplasia and poorly-differentiated carcinomas. The presence of these abnormal appearing cells was associated with decrease in lymphocytic infiltrate.

Conclusion:

The present study indicates more LC are recruited into the carcinoma. These accumulated nonfunctional LC in the tumor tissue are indicative of aggressive tumor with potential malignant transformation.