Oral and periodontal manifestation related during human papilloma virus infections: Update on early prognostic factors

Abstract

Human Papilloma Virus (HPV) is considered one of the most common sexually transmitted infections and has been shown to play an important role in the pathogenesis of squamous cell carcinomas (SCC) of the cervix and head and neck. Manifestations of HPV infections can be manifold, ranging from asymptomatic infections to benign or potentially malignant lesions to intraepithelial neoplasms and invasive carcinomas. The heterogeneity of clinical manifestations from HPV infection depends on the interactions between the viral agent and the host, a direct consequence of the ability on the part of HPV is to remain silent and to evade and convey the action of the host immune system. The oral mucosa represents one of the tissues for which HPV has a distinct tropism and is frequently affected by infection. While much information is available on the role that HPV infection plays in the development of SCC in the oral cavity, there is less information on asymptomatic infections and benign HPV-induced oral lesions. Therefore, the purpose of this review is to analyze, in light of current knowledge, the early clinical and bio-humoral prognostic features related to the risk of HPV malignant transformation, focusing on subclinical conditions, benign lesions, and the correlation between oral infection and infection in other districts. The data show that the main risk associated with HPV infection is related to malignant transformation of lesions. Although HPV-driven OPSCC is associated with a better prognosis than non-HPV-driven OPSCC, primary prevention and early detection of the infection and affected genotype are essential to reduce the risk of malignant neoplastic complications and improve the prognosis.

Keywords: Human papilloma virus; Oral cell; Oral mucosa; Periodontitis; Prognostic markers.

Fig. 1

The structure of human papillomavirus (HPV) and its function. HPV genome is composed of 8k base pairs and divided into early and late gene. The early genome encodes E1, E2, E4, E5, E6, and E7 and the late genome encodes L1 and L2. Oncoprotein E6 and E7 degrade tumor suppressor p53 and pRb, respectively. L1 and L2 build the structure of HPV capsid protein. LCR, long control region.

Fig. 2

The way of transmission of HPV for oral lesions. Oral HPV infection may occur vertically, from mother to child and horizontally between sexual partners.

Fig. 3

Three types of prevention. The use of vaccines represents primary prevention, which represents intervention in healthy oral mucosa. Secondary prevention may be conducted during latent but persistent HPV infection and or in the presence of precancerous lesions. At the end, in the advanced cases, that is to say the oncological cases, in which the oral lesions have been transformed in cancer the only chance of intervention is represented by tertiary prevention and treatment.