An immunohistochemical study of the distribution of p 16 protein in oral mucosa in smokers, non-smokers and in frictional keratosis

Abstract

Objective: Our study aimed to characterize alteration in the immunohistochemical p16 expression in normal oral mucosa and non-neoplastic hyperproliferative disorders (i.e. frictional keratosis and mucosa from smokers). Study design: 43 specimen of oral mucosa were examined using immunohistochemistry. Results: In normal mucosa, there was strong positive nuclear staining in a proportion of fibroblasts and endothelial cells in the lamina propria, with variable expression in nuclei of the epithelial layer. However, when the patient's tobacco smoking was examined, p16 nuclear staining in oral epithelium was seen in 4/20 (20%) of smokers and 0/23 (0%) of non-smokers. In every case of frictional keratosis (n=11), there was strong nuclear staining of some basal and supra-basal cells. In addition, there was strong nuclear staining of parakeratinizing squamous in a band above the spinous layer. In clinically normal oral epithelium of smokers and in frictional keratosis, basal and supra-basal cells expressed strong p16 nuclear staining which was absent in the control tissue examined. Conclusion: Our data suggest that p16 expression may be involved in the long-term loss of proliferation in cell senescence of oral mucosa.

Liquid-based cytology in oral cavity squamous cell cancer

“…The nuclear expression of Ki67, a cell proliferation marker, may provide useful information to evaluate the grading of oral epithelial dysplasia and the risk of evolution into OSCC [35][36][37]. The overexpression of the protein p16, a negative regulator of the cell cycle, in OPML may also be significant to recognize evolution of precancerous diseases in the oral cavity [36,38]. A recently described lymphatic endothelial biomarker, useful to predict the risk of transformation of oral leukoplakias, is podoplanin [39]: in a long-term follow-up study of 150 leukoplakias, immunohistochemical basal and suprabasal expression of podoplanin was the only independent factor for oral cancer development (P ¼ 0.002).…”

Histological and Immunohistochemical Investigation of Smoking-Induced Changes in Human Gingival Tissue: A Focus on p16 and CD34 Expression

“…Even in smokers' healthy-appearing mucosa, smoking has been shown to affect p16 immunoexpression. 10 Additionally, several writers claimed that the inflammatory and hyperplastic oral epithelium overexpressed the gene p16. An earlier investigation found that in non-neoplastic oral epithelium, smokers had considerably higher p16 immunoexpression than non-smokers.…”

“…9 CDKN2 gene produces the protein p16, which is a negative cell cycle regulator. 10 p16 expression has been suggested as a marker for oral mucosal dysplasia and malignant transformation. 11,12,13 In non-small cell lung carcinomas and squamous cell carcinomas of the head and neck, a relationship between pl6 and smoking has been reported.…”