The quantitative and qualitative differences of the proliferative activity and the p53 protein expression in sporadic KCOT may be associated with intrinsic growth potential that could play a role in its development and explain locally aggressive biological behaviour. AgNOR count and p53 protein detection in odontogenic lesions can be of great consequence to predict the biological behaviour and prognosis.

The OSCC-OSMF was found to be a clinicopathologically distinct entity with a better grade of tumor differentiation, less incidence of nodal metastases, and early detection (early clinical TNM stage) compared to OSCC. All these factors probably contribute to a better prognosis and increased 3-year disease-free survival in OSCC-OSMF patients.

The result suggests that CD105 (endoglin) is strongly expressed in microvessels of KCOT compared with that in Dentigerous cyst and Normal oral mucosa. Thus, it suggests that angiogenesis may be associated with locally aggressive biological behavior of KCOT. These findings further stress on the hypothesis that the stroma of KCOT could be regarded not just as a structural support of the cyst wall, but as playing a part in the neoplastic behavior of cyst.

The aim was to evaluate and compare the presence of myofibroblasts in oral squamous cell carcinoma (OSCC), verrucous carcinoma (VC), high-risk epithelial dysplasia (HRED), low-risk epithelial dysplasia (LRED), and normal oral mucosa (NOM). The study consisted of 37 OSCC, 15 VC, 15 HRED, 15 LRED and 15 NOM. a-smooth muscle actin (a-SMA) antibody was used to identify myofibroblasts. The a-SMA expression was not observed in NOM and LRED. The a-SMA was expressed in 97.29% of OSCC, 86.66% of VC, 46.66 % of HRED. The a-SMA expression was significantly higher in OSCC than VC (p = 0.023) and HRED (p \ 0.000). The a-SMA expression was significantly higher in VC than HRED (p = 0.043). Myofibroblastic expression, as highlighted by a-SMA, is undetectable in NOM and LRED but increases as the disease progresses from potentially malignant disorders, as HRED to VC to invasive OSCC. Thus, proliferation of myofibroblasts may be used as a stromal marker of oral premalignancy and malignancy.

Chewing tobacco/betel quid is a strong risk factor in the development of PMD and oral cancer. Also age, gender, SES, education, and occupation influence the development of PMD and oral cancer.