HPV-16 accounts for most of the cervical cancers and 95% of the HPV positive oropharyngeal cancers. Although virtually all cervical cancers are HPV induced, oropharyngeal carcinoma (OPC) has two distinct etiologies: tobacco and alcohol consumption or HPV infection. HPV positive patients with OPC tend to be male,younger (median age of 54), have less exposure to tobacco and alcohol, and improved overall outcomes compared with their HPV negative counterparts. The incidence of HPV positive OPC is on the rise and has now surpassed the cervix as the most common site of HPV-related cancer.
Male predominance may be largely due to higher prevalence of oral HPV-16 infections in men than in women (5:1 in the US). Also, transmissibility or oral HPV may be greater for men performing oral sex on women possibly because of higher vaginal / cervical HPV copy numbers.
The principal risk factor for both cervical cancer and HPV positive OPC is sexual behavior. Women acquire HPV usually via sexual intercourse. Men acquire oral HPV as a result of oral sexual partners. In both cervical cancer and OPC, cigarette smoking increases the risk three-fold.
An increasing number of studies and reviews are focusing on the cause of the rapidly rising incidence of oropharyngeal carcinoma in this country, especially in men. The identification of HPV-16 in most of these tumors has broadened the extent of studies in this population. Several observations have been made that are clinically relevant.
The incidence of oral HPV infection in men is several times that of women.
The percentage of HPV-related oral tumors (non-alcohol or tobacco related) is quickly rising even as tobacco usage decreases.
There is a relatively good prognosis associated with HPV-related tumors of the oropharynx.
There are studies that point to a significant number of men in this country who harbor HPV-16 in their oral cavity and oropharynx who represent the population at risk for oropharyngeal cancer and who would benefit from oral HPV screening, a simple procedure.
Also found in these studies was the relatively rapid disappearance of oral HPV when newly acquired. Oral HPV infection is often undetectable after 12 months of infection; however, HPV-16, when acquired orally, tends to be more persistent which may explain its presence and causal relationships to oropharyngeal cancer.
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