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Home  > HPV > Oral lesions caused by HPV

Oral lesions caused by HPV

Commonly mistaken as oral warts by patients are the circumvallate papillae which are arranged in an inverted V at the back of the tongue. These papillae are evenly distributed on the back of the tongue in an organized fashion and are part of the normal anatomy. Oral warts do, however, occur. 

In addition, a study has linked human papillomavirus (HPV) to an increased risk, in both men and women, of a kind of oral cancer more often seen in men.  Those infected with HPV were 32 times more likely to develop this type of oral cancer than those who did not have HPV. These findings show HPV to be far more dangerous than the increased risk of developing this oropharyngeal cancer associated with the two other known major risk factors, namely, smoking (3 times greater alone, without HPV), and drinking (2.5 times greater alone, without HPV).

Malays J Pathol 1998 Jun;20(1):1-10:

Biology and pathological associations of the human papillomaviruses: a review.

Cheah PL, Looi LM Department of Pathology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.

"Human papillomaviruses (HPVs) essentially induce skin and mucosal epithelial lesions. Various skin warts are well known to be HPV-associated (HPVs 1, 2, 3, 7 and 10). Besides HPVs 3 and 10, HPVs 5, 8, 17 and 20 have been recovered from Epidermodysplasia verruciformis lesions. Anogenital condyloma acuminatum, strongly linked with HPVs 6 and 11 are probably sexually transmitted.

The same HPVs, demonstrable in recurrent juvenile laryngeal papillomas, are probably transmitted by passage through an infected birth canal. HPVs described in uterine cervical lesions are generally categorized into those associated with high (16, 18), intermediate (31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68) and low (6, 11, 26, 40, 42, 43, 44, 53, 54, 55, 62, 66) risk of cervical squamous carcinoma. Other lesions reported to be HPV-associated are: papillomas, dysplasia and carcinomas in the nasal cavity (HPV 6, 11, 57); squamous papilloma, condyloma acuminatum, and verruca vulgaris of the oral cavity (HPV 6, 11), oral focal epithelial hyperplasia (HPV 13, 32); warty lip lesions (HPV 2): and conjunctival papillomas (HPV 6, 11)."

N Engl J Med 2007 May 10; 356 (19):1944-1956: 

Case-Control Study of Human Papillomavirus and Oropharyngeal Cancer.

"Objective and Background: Substantial molecular evidence suggests a role for human papillomavirus (HPV) in the pathogenesis of oropharyngeal squamous-cell carcinoma, but epidemiologic data have been inconsistent.  

Methods: We performed a hospital-based, case–control study of 100 patients with newly diagnosed oropharyngeal cancer and 200 control patients without cancer to evaluate associations between HPV infection and oropharyngeal cancer. Multivariate logistic-regression models were used for case–control comparisons.  

Results: A high lifetime number of vaginal-sex partners (26 or more) was associated with oropharyngeal cancer (odds ratio, 3.1), as was a high lifetime number of oral-sex partners (6 or more). The degree of association increased with the number of vaginal-sex and oral-sex partners. Oropharyngeal cancer was significantly associated with oral HPV type 16 (HPV-16) infection, oral infection with any of 37 types of HPV, and seropositivity for the HPV-16 L1 capsid protein. HPV-16 DNA was detected in 72% of 100 paraffin-embedded tumor specimens, and 64% of patients with cancer were seropositive for the HPV-16 oncoprotein E6, E7, or both. HPV-16 L1 seropositivity was highly associated with oropharyngeal cancer among subjects with a history of heavy tobacco and alcohol use and among those without such a history. The association was similarly increased among subjects with oral HPV-16 infection, regardless of their tobacco and alcohol use. By contrast, tobacco and alcohol use increased the association with oropharyngeal cancer primarily among subjects without exposure to HPV-16.  

Conclusion:  Oral HPV infection is strongly associated with oropharyngeal cancer among subjects with or without the established risk factors of tobacco and alcohol use."

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Dr. Joe Glickman, Jr., M.D.

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