Prevalence of human papillomavirus in oral epithelial dysplasia: Systematic review and meta‐analysis

Abstract

The purpose of this systematic review and meta‐analysis was to estimate the overall and type‐specific prevalence of human papillomavirus (HPV) DNA in oral epithelial dysplasia and assess p16INK4a overexpression in relation to HPV‐status. A systematic literature search identified 31 eligible studies (832 cases) evaluating the presence of HPV DNA in oral epithelial dysplasia cases by PCR. Of these, six studies evaluated p16INK4a overexpression in relation to HPV‐status. The overall pooled prevalence of HPV DNA in oral epithelial dysplasia was 27.2% (95% CI: 17.6‐38.1). We observed substantial interstudy heterogeneity, which could not be explained by differences in continent, tissue type, or severity of epithelial dysplasia. HPV16 was the predominant genotype detected. Moreover, 62.2% of HPV positive and 17.8% of HPV negative oral epithelial dysplasia samples stained intensively positive for p16INK4a. This meta‐analysis found that 27% of oral epithelial dysplasia harbor HPV DNA. Whether this represents a transient infection or has a carcinogenic role is unknown.

Oral epithelial dysplasia: Recognition, grading and clinical significance

“…was type 16 (de laCour et al, 2020). These prevalence figures seem high when compared to rarity of HPV-dysplasia confirmed by in situtechniques and are probably an overestimate.…”

The clinical utility of contemporary oral epithelial dysplasia grading systems

“…40,41 There was a low prevalence of HPVOED in this cohort (2.3%) compared with the 27.2% published in a recent meta-analysis on prevalence of HPV in OED. 42 The high prevalence values in the studies included in the meta-analysis could be due to the use of polymerase chain reaction (PCR)-based techniques as the method to detect HPV DNA. PCR-based methods though sensitive, lack specificity and may give a positive result even if the virus was not transcriptionally active (carrier/bystander).…”

High-Risk Human Papillomavirus and Epstein–Barr Virus Coinfection: A Potential Role in Head and Neck Carcinogenesis

“…These molecular changes are commonly detected in dysplastic epithelial cells [ 136 , 137 ], which are also more susceptible to EBV infection [ 116 ]. Interestingly, the pooled prevalence of HPV infection was 27.2% in oral epithelial dysplasia [ 138 ], whereas other authors found a 50% positivity in oral cavity and oropharyngeal dysplasia [ 139 ]. Guidry and Scott (2018) reported a significant reduction in EBV DNA replication in both HPV-positive and E7-immortalized human keratinocytes when compared with the EBV DNA replication observed in primary keratinocytes cultured in organotypic rafts [ 140 ], suggesting the contribution of HPV to the establishment of EBV latency.…”