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Oral Cancer Prevention (PDQ®)

Health Professional Version

Overview

Note: Separate PDQ summaries on Oral Cancer Screening; Lip and Oral Cavity Cancer Treatment; and Cigarette Smoking: Health Risks and How to Quit are also available.

Who Is at Risk?

Oral cavity cancer and oropharyngeal cancer are two distinct diseases, although they have some risk factors in common. People who use tobacco in any of the commonly available forms (cigarettes, cigars, pipes, and smokeless tobacco) or have high alcohol intake are at elevated risk of both cancers; and they are at particularly high risk if they use both tobacco and alcohol. People who chew betel quid (whether mixed with tobacco or not)—a common practice in south central Asia and Melanesia—are also at high risk of cancer of the oral cavity and oropharynx.[1-3] People who have a personal history of oral cancer are also at elevated risk. Human papillomavirus (HPV) 16 is a sufficient, but not necessary, cause of oropharyngeal cancer.[4]

Factors With Adequate Evidence of an Increased Risk of Oral Cavity and Oropharyngeal Cancer

Tobacco use

Based on solid evidence from numerous observational studies, tobacco use causes cancers of the oral cavity and oropharynx.[5-7] .

Magnitude of Effect: Large. Risk for current smokers is about tenfold that of never-smokers, and is dose related. Most cancers of the oral cavity are attributable to the use of tobacco products.

  • Study Design: Numerous observational case-control and cohort studies.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Alcohol use

Based on solid evidence, alcohol use is a risk factor for the development of oral cavity and oropharyngeal cancer. Its effects are independent of those of tobacco use.[8-11]

Magnitude of Effect: Lower than the risk associated with tobacco use, but the risk is approximately doubled for people who drink three to four alcoholic beverages per day compared with nondrinkers, and is dose related.

  • Study Design: Case-control and cohort studies.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Tobacco and alcohol use

Oral cavity and oropharyngeal cancer risk is highest in people who consume large amounts of both alcohol and tobacco. When both risk factors are present, the risk of oral cavity and oropharyngeal cancer is typically about two to three times greater than it is for either risk factor individually.[12]

  • Study Design: Case-control and cohort studies.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Interventions With Adequate Evidence of a Decreased Risk of Oral Cavity and Oropharyngeal Cancer

Tobacco cessation

Based on solid evidence, cessation of exposure to tobacco (e.g., cigarettes, pipes, cigars, and smokeless tobacco) leads to a decrease in the risk of cancer of the oral cavity and oropharynx.

Magnitude of Effect: Decreased risk, moderate to large magnitude.

  • Study Design: Case-control and cohort studies.
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Interventions With Inadequate Evidence of a Reduced Risk of Oral Cavity and Oropharyngeal Cancer

Cessation of alcohol consumption

Based on fair evidence, cessation of alcohol consumption leads to a decrease in oral cavity cancer, but not until approximately 10 years after cessation. For cancer of the oropharynx, reduction in risk does not occur until approximately 20 years after cessation.[13]

Magnitude of Effect: Decreased risk, small to moderate magnitude.

  • Study Design: Case-control studies.
  • Internal Validity: Fair.
  • Consistency: Fair.
  • External Validity: Fair.

Factors With Adequate Evidence of an Increased Risk of Oropharyngeal Cancer

Human papillomavirus (HPV) infection

Based on solid evidence, HPV 16 infection causes oropharyngeal cancer.[4] HPV 16 is a sufficient but not necessary cause. Other high-risk HPV subtypes, including HPV 18, have been found in a small percentage of oropharyngeal cancers.[14,15]

Tobacco and alcohol use does not appear to be associated with increased risk among people with evidence of HPV 16 L1 seropositivity or oral HPV 16 infection.[14]

Magnitude of Effect: Large. Oral infection with HPV 16 confers about a 15-fold increase in risk relative to individuals without oral HPV 16 infection.

  • Study Design: Case-control and cohort studies, including one conducted using data collected prospectively (nested case-control study).
  • Internal Validity: Good.
  • Consistency: Good.
  • External Validity: Good.

Interventions With Inadequate Evidence of a Reduced Risk of Oropharyngeal Cancer

Vaccination against HPV 16 and the other high-risk subtypes

Vaccination against HPV 16 and 18 has been shown to prevent more than 90% of oral HPV 16/18 infections within 4 years of vaccination.[16] Given the relatively recent onset of vaccination adoption and the age at which individuals are vaccinated, there is not yet evidence that vaccination at a young age will lead to a substantially reduced risk of HPV-associated oropharyngeal cancer later in life. In addition, no data are available to examine whether incidence or mortality would be reduced if vaccination occurred at an age closer to that at which oropharyngeal cancers tend to present.

  • Study Design: No studies available.
  • Internal Validity: Not applicable (N/A).
  • Consistency: N/A.
  • External Validity: N/A.

References

  1. Song H, Wan Y, Xu YY: Betel Quid Chewing Without Tobacco: A Meta-analysis of Carcinogenic and Precarcinogenic Effects. Asia Pac J Public Health 27 (2): NP47-57, 2015. [PUBMED Abstract]
  2. Huber MA, Tantiwongkosi B: Oral and oropharyngeal cancer. Med Clin North Am 98 (6): 1299-321, 2014. [PUBMED Abstract]
  3. Guha N, Warnakulasuriya S, Vlaanderen J, et al.: Betel quid chewing and the risk of oral and oropharyngeal cancers: a meta-analysis with implications for cancer control. Int J Cancer 135 (6): 1433-43, 2014. [PUBMED Abstract]
  4. Kreimer AR, Johansson M, Waterboer T, et al.: Evaluation of human papillomavirus antibodies and risk of subsequent head and neck cancer. J Clin Oncol 31 (21): 2708-15, 2013. [PUBMED Abstract]
  5. U.S. Department of Health and Human Services: The Health Consequences of Smoking: A Report of the Surgeon General. Atlanta, Ga: U.S. Department of Health and Human Services, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Available online. Last accessed April 24, 2015.
  6. National Cancer Institute: Cigars: Health Effects and Trends. Bethesda, MD: U.S. Department of Health and Human Services, National Institutes of Health, National Cancer Institute, [1998]. Smoking and Tobacco Control Monograph 9. Available online. Last accessed February 9, 2015.
  7. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans: Smokeless tobacco and some tobacco-specific N-nitrosamines. IARC Monogr Eval Carcinog Risks Hum 89: 1-592, 2007. [PUBMED Abstract]
  8. Lubin JH, Muscat J, Gaudet MM, et al.: An examination of male and female odds ratios by BMI, cigarette smoking, and alcohol consumption for cancers of the oral cavity, pharynx, and larynx in pooled data from 15 case-control studies. Cancer Causes Control 22 (9): 1217-31, 2011. [PUBMED Abstract]
  9. Blot WJ, McLaughlin JK, Winn DM, et al.: Smoking and drinking in relation to oral and pharyngeal cancer. Cancer Res 48 (11): 3282-7, 1988. [PUBMED Abstract]
  10. Altieri A, Bosetti C, Gallus S, et al.: Wine, beer and spirits and risk of oral and pharyngeal cancer: a case-control study from Italy and Switzerland. Oral Oncol 40 (9): 904-9, 2004. [PUBMED Abstract]
  11. Talamini R, La Vecchia C, Levi F, et al.: Cancer of the oral cavity and pharynx in nonsmokers who drink alcohol and in nondrinkers who smoke tobacco. J Natl Cancer Inst 90 (24): 1901-3, 1998. [PUBMED Abstract]
  12. Hashibe M, Sturgis EM: Epidemiology of oral-cavity and oropharyngeal carcinomas: controlling a tobacco epidemic while a human papillomavirus epidemic emerges. Otolaryngol Clin North Am 46 (4): 507-20, 2013. [PUBMED Abstract]
  13. Marron M, Boffetta P, Zhang ZF, et al.: Cessation of alcohol drinking, tobacco smoking and the reversal of head and neck cancer risk. Int J Epidemiol 39 (1): 182-96, 2010. [PUBMED Abstract]
  14. D'Souza G, Kreimer AR, Viscidi R, et al.: Case-control study of human papillomavirus and oropharyngeal cancer. N Engl J Med 356 (19): 1944-56, 2007. [PUBMED Abstract]
  15. Steinau M, Saraiya M, Goodman MT, et al.: Human papillomavirus prevalence in oropharyngeal cancer before vaccine introduction, United States. Emerg Infect Dis 20 (5): 822-8, 2014. [PUBMED Abstract]
  16. Herrero R, Quint W, Hildesheim A, et al.: Reduced prevalence of oral human papillomavirus (HPV) 4 years after bivalent HPV vaccination in a randomized clinical trial in Costa Rica. PLoS One 8 (7): e68329, 2013. [PUBMED Abstract]
  • Updated: April 24, 2015