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Oral Cavity and Oropharyngeal Cancer Prevention (PDQ®)

Health Professional Version

.

Published online: August 17, 2015.

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.

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).

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 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. Betel-nut chewing, a habit practiced by about 700 million people worldwide, is an important risk factor for oral cancer (whether mixed with tobacco or not) .[1] The relative risk for oral cancer increases with frequency of chewing and is typically in excess of tenfold at the highest exposure categories.[1-4] 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.[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 causes 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 typically about two to three times greater than it is for either risk factor individually.[13]

  • 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.[14]

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.[15,16]

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.[15]

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.[17]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. Huber MA, Tantiwongkosi B: Oral and oropharyngeal cancer. Med Clin North Am 98 (6): 1299-321, 2014. [PubMed: 25443678]
  2. 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. [PMC free article: PMC4781453] [PubMed: 15635762]
  3. 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: 23666841]
  4. 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: 24302487]
  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. [PMC free article: PMC3709056] [PubMed: 23775966]
  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 October 9, 2015.
  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 July 22, 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. [PMC free article: PMC4781254] [PubMed: 18335640]
  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. [PMC free article: PMC3304584] [PubMed: 21744095]
  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: 3365707]
  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: 15380168]
  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: 9862628]
  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: 23910467]
  14. 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. [PMC free article: PMC2817090] [PubMed: 19805488]
  15. 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: 17494927]
  16. 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. [PMC free article: PMC4012803] [PubMed: 24751181]
  17. 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. [PMC free article: PMC3714284] [PubMed: 23873171]

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 45,780 new cases of oral cavity and pharynx cancer diagnosed in the United States in 2015 and 8,650 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] The estimated age-standardized (World Standard Population) worldwide incidence and mortality rates of oral cavity and pharyngeal cancer in 2012 were about 7.0 and 3.9 per 100,000 persons per year, respectively.[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 tobacco and alcohol use, including betel-quid chewing. 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 (about 83%), the 5-year survival rates for patients with regional lymph node spread or metastases are only about 62% and 38%, respectively. 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, and other smoked and smokeless products) and betel-nut chewing 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 the general consensus is 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.

Alcohol use

Alcohol use is a second independent major risk factor for the development of oral cancer.[7-10] There is a suggestion that consumption of beer and hard liquor confers a greater risk than does wine consumption.[7] The risk of oral cancer increases with the number of cigarettes smoked per day and the number of alcoholic drinks consumed per day in a dose-dependent fashion.[7] Alcohol use has been shown to be an independent risk factor for development of premalignant oral lesions (leukoplakia or erythroplakia), which can progress to cancer.[11]

Tobacco and alcohol use

The combined use of alcohol and tobacco increases the risk of oral cancer far more than either factor independently.[12]

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

Tobacco cessation

The cessation of cigarette smoking is associated with a 50% reduction in risk of developing oral cancer within 3 to 5 years [13] and a return to a normal level of risk of developing oral cancer within 10 years.[7] Dentists and other health professionals can play an integral role in providing smoking cessation advice and encouragement.

Dentists can also participate in the full scope of pharmacological and behavioral interventions for smoking cessation.[14] A study has shown that only 25% of tobacco users report receiving advice to quit tobacco use from their dentists,[15] a proportion less than tobacco users who received such advice from their physicians. There was a dramatic increase in the use of cigars of about 250% between 1993 and 1998,[16] and heavy cigar use is particularly associated with oral cancer development.

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

Cessation of alcohol consumption

Because alcohol is associated with oral cancer in a dose-dependent fashion,[7,17- 19] it is believed that cessation or avoidance of alcohol use would result in a lower incidence of oral cancer. However, the evidence for reduced oral cancer among people who have stopped consuming alcohol is inadequate.

Factors With Adequate Evidence of an Increased Risk of Oropharyngeal Cancer

HPV infection

HPV 16 infection is a sufficient, but not necessary, cause of oropharyngeal cancer.[20] Other high-risk HPV subtypes, including HPV 18, have been found in a small percentage of oropharyngeal cancers.[21,22]

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.[21]

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.[23] 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.

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 July 16, 2015.
  2. American Cancer Society: Cancer Facts and Figures 2015. Atlanta, Ga: American Cancer Society, 2015. Available online. Last accessed July 1, 2015.
  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 July 22, 2015.
  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 July 17, 2015.
  5. Huber MA, Tantiwongkosi B: Oral and oropharyngeal cancer. Med Clin North Am 98 (6): 1299-321, 2014. [PubMed: 25443678]
  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 July 17, 2015.
  7. 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: 3365707]
  8. 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: 15380168]
  9. 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: 9862628]
  10. Talamini R, Franceschi S, Barra S, et al.: The role of alcohol in oral and pharyngeal cancer in non-smokers, and of tobacco in non-drinkers. Int J Cancer 46 (3): 391-3, 1990. [PubMed: 2394506]
  11. Hashibe M, Sankaranarayanan R, Thomas G, et al.: Alcohol drinking, body mass index and the risk of oral leukoplakia in an Indian population. Int J Cancer 88 (1): 129-34, 2000. [PubMed: 10962450]
  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: 23910467]
  13. Samet JM: The health benefits of smoking cessation. Med Clin North Am 76 (2): 399-414, 1992. [PubMed: 1548968]
  14. 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.
  15. 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: 9089529]
  16. Nelson NJ: "Big Smoke" has big risks: daily cigar use causes cancer, heart disease. J Natl Cancer Inst 90 (8): 562-4, 1998. [PubMed: 9554434]
  17. 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: 7549758]
  18. La Vecchia C, Tavani A, Franceschi S, et al.: Epidemiology and prevention of oral cancer. Oral Oncol 33 (5): 302-12, 1997. [PubMed: 9415327]
  19. 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. [PMC free article: PMC6705703] [PubMed: 11910703]
  20. 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. [PMC free article: PMC3709056] [PubMed: 23775966]
  21. 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: 17494927]
  22. 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. [PMC free article: PMC4012803] [PubMed: 24751181]
  23. 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. [PMC free article: PMC3714284] [PubMed: 23873171]

Changes to This Summary (08/17/2015)

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.

This summary was renamed from Oral Cancer Prevention.

Overview

Added text to state that betel-nut chewing, a habit practiced by about 700 million people worldwide, is an important risk factor for oral cancer; the relative risk for oral cancer increases with frequency of chewing and is typically in excess of tenfold at the highest exposure categories (cited IARC Working Group on the Evaluation of Carcinogenic Risks to Humans as reference 2).

Description of the Evidence

Revised text to state that from 2008 to 2012, the estimated age-adjusted incidence of cancer of the oral cavity and pharynx in the United State was 11.0 cases per 100,000 persons per year. Also added text to state that cancer of the oral cavity will account for about 45% and cancer of the oropharynx will account for about 20% of the 2015 estimated incidence; 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; however, rates of oral cavity cancer vary greatly across the world (cited Howlader et al. as reference 1 and Ferlay et al. as reference 3).

Added text to state that oral cavity cancer includes cancer of the tongue, gums, floor of the mouth, and other parts of the mouth, and in the United States, oropharyngeal cancer is the most common of the pharyngeal cancers; leukoplakia, erythroplakia, and erythroplasia are considered preneoplastic lesions, but most will not progress to carcinoma (cited Slootweg et al. as reference 4)

Added text to state that separate stage-specific survival rates for oral cavity and oropharyngeal cancer are not available.

Revised text to state that tobacco use is implicated in most cases of oral cavity and oropharyngeal cancer. Also added text to state that all forms of tobacco use increase the risk of these cancers; among current smokers who smoke only cigarettes, the relative risk of cancer of the oral cavity and oropharynx was observed in a large cohort study to be approximately tenfold greater in men and fivefold greater in women compared with lifetime nonsmokers; other epidemiologic studies have observed smaller and larger increases in risk with some variation by anatomic location (cited Huber et al. as reference 5 and the U.S. Department of Health and Human Services as reference 6).

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.

Questions or Comments About This Summary

If you have questions or comments about this summary, please send them to Cancer.gov through the website's E-mail Us. We can respond only to email messages written in English.

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).

Board members review recently published articles each month to determine whether an article should:

  • be discussed at a meeting,
  • be cited with text, or
  • replace or update an existing article that is already cited.

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.

Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.

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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The preferred citation for this PDQ summary is:

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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