Epithelial excrescence, protuberance, hypertrophy: the oral cicatrix

Preface: Oral Squamous Papilloma occurs preponderantly in females with a variable age of presentation. Specific clinical and physical attributes may be observed. Excision biopsy, histopathology and congruous immunohistochemical parameters may be appraised. Invasive squamous cell carcinoma with the progenitors such as cervical intraepithelial neoplasm (grade III) and carcinoma in situ may incorporate the nuclear (DNA) sequences of HPV 16 and 18 in numerous instances.4‒6 Human Papilloma Virus contamination activates the benign cellular expanse. Subsequent somatic mutations may assist the propagation of the virus. Pathogenic determinants of malignant conversion such as smoking, concomitant infections, dietary deficiencies, hormonal changes may expedite the cellular adaptations. The specific HPV-DNA may be amply evidenced in the neoplasm.2,3 The p53 protein assists the determination of the DNA repair or the activation of programmed cell death (apoptosis),7 a characteristic of the negatively coordinated cell growth. Initiation of p53 protein may competently inhibit cell growth and signify cell death (apoptosis). Protein E6 of the transforming HPV (16/18) may efficaciously combine with protein p53. The viral protein E6 engages the cellular protein E6 AP which is employed as a Ubiquitin ligase for the p53 comprising complex. Ubiquitination of the p53 emerges due to the protein retention, followed by marked degradation. In the absence of p53 protein, the cell is deprived of the ability to discern and restore the latent, devastated DNA. Thus the cell division may persist without cellular rejuvenation.1,7 Remodelled, invariable protein p53 may be ascertained by immune-histochemistry.1