Oral Papillomatosis: Its Relation with Human Papilloma Virus Infection and Local Immunity-An Update

Abstract

Oral papilloma lesions may appear as a result of HPV infection, or not, and only special molecular methods could differentiate them. Low-risk and high-risk HPV types could induce oral HPV papillomatosis with different natural evolution, clearance and persistence mechanisms. The pathogenic mechanisms are based on the crosstalk between the oral epithelial and immune cells and this very efficient virus. HPV acts as a direct inducer in the process of transforming a benign lesion into a malignant one, the cancerization process being also debated in this paper. According to the degree of malignity, three types of papillomatous lesions can be described in the oral cavity: benign lesions, potential malign disorders and malignant lesions. The precise molecular diagnostic is important to identify the presence of various virus types and also the virus products responsible for its oncogenicity. An accurate diagnostic of oral papilloma can be established through a good knowledge of etiological and epidemiological factors, clinical examination and laboratory tests. This review intends to update the pathogenic mechanisms driving the macroscopic and histological features of oral papillomatosis having HPV infection as the main etiological factor, focusing on its interreference in the local immunity. In the absence of an accurate molecular diagnostic and knowledge of local immunological conditions, the therapeutic strategy could be difficult to decide.

Keywords: HPV immunity; HPV oncogenicity; HPV-related oral lesions; oral HPV infection; oral papilloma.

Figure 1

Schematic illustration of a high-risk HPV morphology.

Figure 2

The roles of high-risk HPV main gene products. E1-L2—HPV genes; Kc-Keratinocyte; HSPGs—heparan sulfate proteoglycans.

Figure 3

The central role of infected Kcs in suppressing the immune response. (see details in the text below).

Figure 4

HPV-negative oral papilloma (a,b) and HPV-positive papilloma (c,d). (a) Macroscopically, tumor lesion located at the jugal mucosa, round shape, size 0.75 mm, pinkish-whitish color, poorly vascularized, non-bleeding; (b) Histological aspect of jugal mucosa; acanthosis, parakeratosis and koilocytes presence in the epithelium, (trichrome stain × 200); (c) Macroscopically, tumor lesion located at the occlusal line of the jugal mucosa, round-oval shape, size 0.95 mm, red color, richly vascularized, bleeding at the slightest trauma; (d) Hiper- and parakeratosis, acanthosis and koilocytes presence in the epithelium; in the basal epithelial layer mitotic figures are present. Proinflammatory cells infiltrate the mucosa (trichrome stain × 400).