Send to

Choose Destination
J Oral Maxillofac Pathol. 2019 May-Aug;23(2):224-230. doi: 10.4103/jomfp.JOMFP_299_18.

Expression of p-16, Ki-67 and p-53 markers in dysplastic and malignant lesions of the oral cavity and oropharynx.

Author information

Department of Pathology, Gandhi Medical College, Bhopal, Madhya Pradesh, India.



Understanding the markers for predicting degree of dysplasia and progression to malignancy can help early identification and prompt treatment of patients with oral cancers. In this study, we aim to identify and characterize different tumor suppressor genes such as p-53 and p-16 and proliferation marker Ki-67 in defining stages of dysplasia of oral mucosa and grading of tumor.

Settings and Design:

Oral biopsy tissues (for neoplastic lesions) received for histopathological evaluation were included in the study. The sections were processed for H&E staining, and 112 cases were chosen for immunohistochemical study. The data were analyzed by Chi-square and z-tests using software SPSS.


We found significant correlation between degree of dysplasia and p-16 immunoexpression with 16.7% of cases showing positivity in oral intraepithelial neoplasia (OIN) I cases as compared to 25% in OIN II and 77.8% in OIN III. Ki-67 immunoexpression correlated significantly with both histological type and grade of tumor with increased expression and intensity seen in malignant cases (66.3%) as compared to benign (10%) and premalignant cases (37%) and higher Ki-67 immunoexpression in poorly differentiated tumors (75%) than well-differentiated tumors (12.2%). Regarding p-53 immunoexpression, positive staining was seen in only malignant cases and premalignant cases.


Ki-67 and p-16 can be useful as a marker of degree of dysplasia and transformation to malignancy. Ki-67 can also serve as a marker of degree of differentiation of tumors. Hence, they can serve as important ancillary markers to analyze the transition to carcinoma, dysplasia and progression of tumor.


Dysplasia; Ki-67; oral squamous oral carcinoma; p-16; p-53

Supplemental Content

Full text links

Icon for Medknow Publications and Media Pvt Ltd Icon for PubMed Central
Loading ...
Support Center