Oral Cavity and Oropharyngeal Cancer Prevention–for health professionals (PDQ®)

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Overview

Note: Separate PDQ summaries on Oral Cavity and Oropharyngeal 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 a have high alcohol intake are at elevated risk of both cancers; they are at particularly high risk if they use both tobacco and alcohol. People who chew betel quid (whether mixed with tobacco or not) are also at high risk of cancer of the oral cavity and oropharynx.[1-3] People who have a personal history of cancer in the head and neck region also are at elevated risk of a future primary cancer of the oral cavity or oropharynx.[4] Human papillomavirus (HPV) 16 is a sufficient, but not necessary, cause of oropharyngeal cancer.[5]

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 increases the risk of cancers of the oral cavity and oropharynx.[6-8] .

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.[9-12]

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 greater than a simple multiplicative effect of the two individual risks.[10,13]

Magnitude of Effect: About two to three times greater than the simple multiplicative effect, with risks for persons who both smoke and drink heavily approximately 35-fold that of persons who both never smoke and never drink.[10,13]

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

Betel-quid chewing

Based on solid evidence, chewing betel quid alone or with added tobacco (gutka) increases the risk of both oral cavity and oropharyngeal cancers.[3,14] Of the three primary components of betel quid (betel leaf, areca nut, and lime), the areca nut is the only one considered to be carcinogenic when chewed.

Magnitude of Effect: Relative risks for oral cavity cancer are high and typically stronger for gutka than for betel quid alone. Both products appear to confer a modest yet statistically significant increase in risk for oropharyngeal cancer.[3]

  • Study Design: Ecologic, 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.[15]

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.[5] 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.[16,17]

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.[16]

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.[18] However, no data are available to assess whether vaccination at any age will lead to reduced risk of oropharyngeal cancer at current typical ages of diagnosis.

  • Study Design: No studies available.
  • Internal Validity: Not applicable (N/A).
  • Consistency: N/A.
  • External Validity: N/A.
References
  1. Huber MA, Tantiwongkosi B: Oral and oropharyngeal cancer. Med Clin North Am 98 (6): 1299-321, 2014. [PUBMED Abstract]
  2. 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]
  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. Atienza JA, Dasanu CA: Incidence of second primary malignancies in patients with treated head and neck cancer: a comprehensive review of literature. Curr Med Res Opin 28 (12): 1899-909, 2012. [PUBMED Abstract]
  5. 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]
  6. 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. Also available online. Last accessed February 4, 2016.
  7. 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 October 16, 2015.
  8. 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]
  9. 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]
  10. 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]
  11. 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]
  12. 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]
  13. 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]
  14. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans: Betel-quid and areca-nut chewing and some areca-nut derived nitrosamines. IARC Monogr Eval Carcinog Risks Hum 85: 1-334, 2004. [PUBMED Abstract]
  15. 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]
  16. 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]
  17. 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]
  18. 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]

Description of the Evidence

Background

Incidence and mortality

From 2008 to 2012, the estimated age-adjusted incidence of cancer of the oral cavity and pharynx in the United States was 11.0 cases per 100,000 persons per year. The estimated mortality rate for the same years was 2.5 per 100,000 persons per year. U.S. incidence and mortality rates are both about 2.6 times higher in men than in women.[1] It is estimated that there will be 48,330 new cases of oral cavity and pharynx cancer diagnosed in the United States in 2016 and 9,570 deaths due to this disease.[2] Cancer of the oral cavity will account for about 45% and cancer of the oropharynx will account for about 20% of the estimated incidence.[1] In 2012, the estimated age-standardized (World Standard Population) worldwide incidence rate of oral cavity and pharyngeal cancer was about 7.0 per 100,000 persons per year; the estimated mortality rate was 3.9 per 100,000 persons per year.[3] Cancer of the oral cavity accounts for about one-half of the incidence and mortality estimates, and cancer of the oropharynx accounts for about one-third of the incidence and mortality estimates. Rates of oral cavity cancer vary greatly across the world, primarily because of differences in alcohol use, tobacco use, and betel-quid chewing and the products chewed. In 2012, for example, the rate of oral cavity cancer in French Guiana was 0 per 100,000 persons; in Papua New Guinea, the rate was 25 per 100,000 persons. Rates of oropharyngeal cancer vary as well but less so; in 2012, rates varied from 0 per 100,000 persons in a number of countries to about 9 per 100,000 persons in Bangladesh.[3]

Oral cavity cancer includes cancer of the tongue, gums, floor of the mouth, and other parts of the mouth. In the United States, oropharyngeal cancer is the most common pharyngeal cancer.[1] Squamous cell carcinoma, which arises from the oral mucosal lining, accounts for more than 90% of the tumors in the oral cavity and oropharynx. Leukoplakia, erythroplakia, and erythroplasia are considered preneoplastic lesions, but most will not progress to carcinoma.[4]

The most important factor affecting long-term outcome after treatment is the stage of disease at diagnosis; however, overall outcome is stage and site dependent. Although localized cancers of the oral cavity and pharynx have an excellent anticipated 5-year survival rate of about 83%, the 5-year survival rate for patients with regional lymph node spread is only about 62%; the 5-year survival rate for patients with metastases is about 38%.[2] Separate stage-specific survival rates for oral cavity and oropharyngeal cancer are not available.

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

Tobacco use

Tobacco use is implicated in most cases of oral cavity and oropharyngeal cancer.[5] All forms of tobacco use (cigarettes, pipes, cigars, snuff, chewing tobacco, gutka [betel quid with tobacco added], and other smoked and smokeless products) increase the risk of these cancers.[6] Epidemiologic studies consistently demonstrate that cigarette smokers have a higher incidence of mortality from oral cavity and oropharyngeal cancers compared with lifetime nonsmokers, and there is general consensus that the relationship is causal. Among current smokers who smoke only cigarettes, the relative risk of cancer of the oral cavity or oropharynx was observed in a large cohort study to be approximately tenfold greater in men and fivefold greater in women compared with lifetime nonsmokers.[6] However, other epidemiologic studies have observed smaller and larger increases in risk, with some variation by anatomic location. Gutka chewing is prevalent in many countries in south and south-east Asia, including China and India, and is an important risk factor for both oral cavity and oropharyngeal cancer.[5]

Alcohol use

Alcohol use is a major independent risk factor for the development of oral cavity and oropharyngeal cancer.[7] Most epidemiologic studies demonstrate an increase in risk with increasing drinks per day, with a more than fivefold increase in risk for individuals who consume five or more drinks a day relative to nonconsumers.[8] Associations are observed in studies that control for confounding by smoking, as well as in studies of nonsmokers.[7] There is a suggestion that consumption of beer and hard liquor confers a greater risk than does wine consumption.[9]

Tobacco and alcohol use

Oral cavity and oropharyngeal cancer risk is highest in people who consume large amounts of both alcohol and tobacco.[8] When both risk factors are present, the risk of oral cavity and oropharyngeal cancer is typically about two to three times greater than a simple multiplicative effect.[9] In a case-control study, individuals who consumed two or more packs of cigarettes and more than four alcoholic drinks per day had slightly over a 35-fold increased risk for developing oral cavity or oropharyngeal cancer, relative to individuals who neither smoked nor drank.[9]

Betel-quid chewing

Betel quid is composed of betel leaf, areca nut, and lime; gutka is betel quid with added tobacco. Both betel-quid and gutka chewing increase the risk of cancer of the oral cavity and oropharynx.[5,10] The carcinogenic component of chewed betel quid arises from the areca nut.[5]

Relative risks are typically stronger for gutka than for betel quid alone.[10] A meta-analysis of oral cavity cancer studies conducted on the Indian subcontinent calculated a statistically significant eightfold increase in risk for gutka chewing and a statistically significant twofold increase in risk for betel-quid chewing. A statistically significant tenfold increase in oral cavity cancer risk for betel-quid chewing was demonstrated by studies conducted in China or Taiwan. A meta-analysis of oropharyngeal cancer studies conducted on the Indian subcontinent calculated a statistically significant fourfold increase in risk for gutka chewing and a statistically significant twofold increase in risk for betel-quid chewing.[10] Studies of head and neck cancer (without specification of subsite) suggest that increases in risk are positively correlated with chewing frequency and duration.[5]

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

Tobacco cessation

The cessation of cigarette smoking is associated with about a 50% reduction in risk of developing oral cavity and oropharyngeal cancer within 5 to 9 years [11] and a return to a cancer risk comparable to that of never-smokers within 20 years.[11]

Dentists can participate in the full scope of pharmacological and behavioral interventions for smoking cessation.[12] A study has shown that only 25% of tobacco users report receiving advice to quit tobacco use from their dentists,[13] a proportion less than tobacco users who received such advice from their physicians.

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

Cessation of alcohol consumption

Because alcohol is associated with oral cavity and oropharyngeal cancer in a dose-dependent fashion,[9,14-16] it is believed that cessation or avoidance of alcohol use would result in reduced incidence. However, the evidence for reduced oral cavity and oropharyngeal cancer among people who have stopped consuming alcohol is inadequate.[11] Most studies suggest that the risk of oral cavity cancer decreases as time from cessation increases; one meta-analysis of eight studies observed a statistically significant 35% reduction (95% confidence interval [CI], 0.26–0.78), relative to current drinkers, for those who ceased consumption 20 years or more ago. Data for oropharyngeal cancer alone are not available, but studies that examine oropharyngeal cancer in conjunction with at least one other pharyngeal cancer typically have demonstrated a smaller risk reduction than for oral cavity cancer.[11]

Factors With Adequate Evidence of an Increased Risk of Oropharyngeal Cancer

Human papillomavirus (HPV) infection

HPV 16 infection is a sufficient, but not necessary, cause of oropharyngeal cancer.[17] It is, however, present in more than 85% of HPV-associated oropharyngeal cancers.[8] A meta-analysis of five case-control studies of HPV 16 positivity in either serum or tissue calculated an odds ratio of 4.3 (95% CI, 2.1–8.9) for oropharyngeal cancer.[18] In a case-control study, the observed strong association of HPV 16 serologic status and oropharyngeal cancer did not vary at different levels of tobacco or alcohol use.[19]

Other high-risk HPV subtypes, including HPV 18, have been found in a small percentage of oropharyngeal cancers.[19,20] Given its association with cervical cancer, HPV 18 is believed to increase oropharyngeal cancer risk as well.[20]

Interventions With Inadequate Evidence of a Reduced Risk of Oropharyngeal Cancer

Vaccination against HPV 16 and 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.[21] Given the relatively recent adoption of vaccination 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.

References
  1. Howlader N, Noone AM, Krapcho M, et al., eds.: SEER Cancer Statistics Review, 1975-2012. Bethesda, Md: National Cancer Institute, 2015. Also available online. Last accessed February 8, 2016.
  2. American Cancer Society: Cancer Facts and Figures 2016. Atlanta, Ga: American Cancer Society, 2016. Available online. Last accessed January 14, 2016.
  3. Ferlay J, Soerjomataram I, Ervik M, et al.: GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide. Lyon, France: International Agency for Research on Cancer, 2013. IARC CancerBase No. 11. Available online. Last accessed February 2, 2016.
  4. Slootweg PJ, Eveson JW: Tumours of the oral cavity and oropharynx. In: Barnes L, Evenson J, Reichart P, et al., eds.: Pathology and Genetics of Head and Neck Tumours. Lyon, France: IARC Press, 2005. World Health Organization Classification of Tumours, 9, pp 163-208. Also available online. Last accessed October 16, 2015.
  5. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans: Betel-quid and areca-nut chewing and some areca-nut derived nitrosamines. IARC Monogr Eval Carcinog Risks Hum 85: 1-334, 2004. [PUBMED Abstract]
  6. Cancer. In: 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, pp 35-360. Also available online. Last accessed October 16, 2015.
  7. Goldstein BY, Chang SC, Hashibe M, et al.: Alcohol consumption and cancers of the oral cavity and pharynx from 1988 to 2009: an update. Eur J Cancer Prev 19 (6): 431-65, 2010. [PUBMED Abstract]
  8. Huber MA, Tantiwongkosi B: Oral and oropharyngeal cancer. Med Clin North Am 98 (6): 1299-321, 2014. [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. 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]
  11. 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]
  12. Mecklenburg RE, Christen AG, et al.: How to Help Your Patients Stop Using Tobacco: a National Cancer Institute Manual for the Oral Health Team. Bethesda, Md: National Institutes of Health, National Cancer Institute, 1993.
  13. Martin LM, Bouquot JE, Wingo PA, et al.: Cancer prevention in the dental practice: oral cancer screening and tobacco cessation advice. J Public Health Dent 56 (6): 336-40, 1996 Fall. [PUBMED Abstract]
  14. Macfarlane GJ, Zheng T, Marshall JR, et al.: Alcohol, tobacco, diet and the risk of oral cancer: a pooled analysis of three case-control studies. Eur J Cancer B Oral Oncol 31B (3): 181-7, 1995. [PUBMED Abstract]
  15. La Vecchia C, Tavani A, Franceschi S, et al.: Epidemiology and prevention of oral cancer. Oral Oncol 33 (5): 302-12, 1997. [PUBMED Abstract]
  16. Bagnardi V, Blangiardo M, La Vecchia C, et al.: Alcohol consumption and the risk of cancer: a meta-analysis. Alcohol Res Health 25 (4): 263-70, 2001. [PUBMED Abstract]
  17. 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]
  18. Hobbs CG, Sterne JA, Bailey M, et al.: Human papillomavirus and head and neck cancer: a systematic review and meta-analysis. Clin Otolaryngol 31 (4): 259-66, 2006. [PUBMED Abstract]
  19. 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]
  20. 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]
  21. 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]

Changes to This Summary (02/04/2016)

The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.

Description of the Evidence

Updated statistics with estimated new cases and deaths for 2016 (cited American Cancer Society as reference 2).

This summary is written and maintained by the PDQ Screening and Prevention Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ® - NCI's Comprehensive Cancer Database pages.

About This PDQ Summary

Purpose of This Summary

This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about oral cavity and oropharyngeal cancer prevention. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.

Reviewers and Updates

This summary is reviewed regularly and updated as necessary by the PDQ Screening and Prevention Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).

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Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.

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Levels of Evidence

Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Screening and Prevention Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.

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National Cancer Institute: PDQ® Oral Cavity and Oropharyngeal Cancer Prevention. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://www.cancer.gov/types/head-and-neck/hp/oral-prevention-pdq. Accessed <MM/DD/YYYY>.

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  • Updated: February 4, 2016

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