Oral manifestations of human papillomavirus infections

Abstract

Papillomaviruses are one of the oldest viruses known, dating back 330 million years. During this long evolution, human papillomaviruses (HPV) have developed into hijackers of human cellular and immune systems in which they replicate and remain silent. Systematic studies on oral HPV infections and their outcomes are still scarce. Oral HPV infections have been linked to sexual behaviour, but recent evidence supports their horizontal, mouth‐to‐mouth, transmission. Most HPV infections in infants are acquired vertically from the mother during the intrauterine period, during delivery, or later via saliva. The best‐known benign clinical manifestations of HPV infection are oral papilloma/condyloma and focal epithelial hyperplasia. Evidence is emerging which suggests that some oral HPV infections might persist. Persistent HPV infection is mandatory for HPV‐associated malignant transformation. However, progression of HPV‐induced lesions to malignancy requires additional cofactors. In the early 1980s, we provided the first evidence that a subset of oral cancers and other head and neck cancers might be causally linked to HPV infection. This review summarizes current knowledge on the virus itself, its transmission modes, as well as the full spectrum of oral HPV infections – from asymptomatic infections to benign, potentially malignant oral lesions, and squamous cell carcinoma.

Sexually transmitted infections in oral cavity lesions: Human papillomavirus,Chlamydia trachomatis, and Herpes simplex virus

“…In the present study, the prevalence of HPV in oral cavity lesions was 34%. Similar frequency of HPV detection was reported by Syrjänen et al [21] in a Finland population showing an oral prevalence of 15-30% among couples during the 6-year follow-up.…”

“…On the other hand, HPV DNA in asymptomatic infections in which HPV DNA is detectable without any clinical lesion is still a matter of debate. Kreimer et al [28] reported that asymptomatic oral HPV-16 infection and any HPV type were found in 1.3% and 4.5%, respectively, of the nearly 4.000 subjects included in the review [21]. In a previous local study, HPV in oral mucosa without lesion or injury was not detected [29], maybe because the number of healthy volunteers who were studied was small.…”

Predicted prevalence of oral human papillomavirus (HPV) by periodontitis status and HPV vaccination status

“…Ortiz et al's study concluded that an association between oral HPV and periodontitis was, however, specific to severe cases. Additionally, Syrjanen cautions that the evidence of an HPV‐periodontitis relationship is merely suggestive, and although biologically plausible, is currently inconclusive . In a study of 500 HPV+ participants of the NHANES 2009–2012 study cohort, Wiener et al showed that for persons aged 30–69 years, the adjusted odds ratio was just 1.04 (95% CI = 0.63–1.73) for the association of periodontitis with oral HPV infection.…”

Human papillomavirus (HPV) 16 infection is not detected in rectal carcinoma

“…A strong causal relationship has been demonstrated between HPV and some types of cancers such as cervix uteri, penis, vulva, vagina, anus and oropharynx [4,6]. Controversial results have been obtained regarding the role of HPVs in esophagus [6][7][8], oral cavity [6,9], breast [10][11][12] and lung cancers [13,14]. In cervical lesions the HPV DNA is frequently found integrated into the host genome particularly in high grade cervical intraepithelial neoplasia and invasive cancer cases [15,16].…”