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Oral Cancer Prevention (PDQ)

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Overview
Description of the Evidence
Changes to This Summary (04/24/2015)
Questions or Comments About This Summary
About This PDQ Summary
Get More Information From NCI

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] [2] [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] [6] [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.

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] [9] [10] [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.

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]

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.

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.

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.

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.

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.
  2. Huber MA, Tantiwongkosi B: Oral and oropharyngeal cancer. Med Clin North Am 98 (6): 1299-321, 2014.
  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.
  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.
  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.
  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.
  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.
  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.
  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.
  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.
  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.
  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.
  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.
  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.

Description of the Evidence

Background

Incidence and mortality

From 2004 to 2008, the estimated incidence of oral cancer in the United States was 10.6 cases per 100,000 persons per year. The most recent estimated mortality rate (from 2007 to 2011) was 2.5 per 100,000 persons per year. U.S. incidence and mortality rates are about 2.5 and 2.8 times higher, respectively, in men than in women. [1] It is estimated that there will be 45,780 new cases of oral cancer diagnosed in the United States in 2015 and 8,650 deaths due to this disease. [2] The estimated age-standardized (World Standard Population) worldwide incidence and mortality rates of oropharyngeal cancer in 2008 were 5.9 and 3.3 per 100,000 persons per year, respectively. [3] Primarily because of differences in tobacco and alcohol use, rates vary widely across the world. [4] South central Asia and Melanesia have particularly high rates of oral cancer attributable to betel quid chewing.

Oral cancer can be divided into three clinicopathological categories: carcinoma of the lip vermillion, carcinoma of the oral cavity proper, and carcinoma of the oropharynx.

Squamous cell carcinoma, which arises from the oral mucosal lining, accounts for more than 90% of the tumors in the oral cavity and oropharynx. Other types of primary tumors arising in this area include lymphoma, sarcoma, melanoma, and minor salivary gland tumors. In the Western world, the most common locations of tumor development are the tongue and floor of the mouth; however, in parts of the world where tobacco or betel quid chewing is prominent, cancers of the retromolar trigone and buccal mucosa are common. Oral squamous cell carcinomas are sometimes preceded by oral preneoplastic lesions, which are often present as visible alterations of the mucosal surface and include leukoplakia and erythroplakia. [5]

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 early-stage tumors (without lymph node involvement) have an excellent anticipated 5-year survival rate (about 82%), the 5-year survival rates for patients with regional lymph node spread or metastases are only about 56% and 34%, respectively. [6] Some or all of the differences in prognosis among disease stages may result from lead-time bias rather than a benefit of early detection and treatment. (Refer to the PDQ summary on Cancer Screening Overview for more information.)

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

Tobacco use

Tobacco use is responsible for more than 90% of tumors of the oral cavity among men and 60% among women, [7] and is responsible for 90% of oral cancer deaths in men. [8] All forms of tobacco—cigarettes, pipes, cigars, and smokeless tobacco—have been implicated in the development of oral cancers. [9] While tobacco use confers the highest risk of cancer of the floor of the mouth, [10] it is associated with an increased risk of oral cancer for all sites.

Tobacco use is known to cause “field cancerization” resulting in a propensity for development of second primary tumors in patients with oral cancer. Case reports have also implicated marijuana smoking as a cause of oral cancer, particularly in younger patients. [11]

Alcohol use

Alcohol use is a second independent major risk factor for the development of oral cancer. [12] [13] [14] [15] There is a suggestion that consumption of beer and hard liquor confers a greater risk than does wine consumption. [12] 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. [12] 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. [16]

Tobacco and alcohol use

The combined use of alcohol and tobacco increases the risk of oral cancer far more than either factor independently. [17]

Interventions With Adequate Evidence of a Decreased Risk of Oral Cancer 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 [18] and a return to a normal level of risk of developing oral cancer within 10 years. [12] 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. [19] A study has shown that only 25% of tobacco users report receiving advice to quit tobacco use from their dentists, [20] 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, [21] 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, [10] [12] [22] [23] 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.

Dietary changes and dietary supplements

Several studies have shown an inverse association between fruit intake and the development of oral cancer, particularly in those who use tobacco. [10] [22] [24] [25] [26] Fiber, in the form of vegetable intake, has similarly been shown to be associated with a decreased risk of oral cancer. It is estimated that intake of fruits and vegetables may lower the risk of development of oral cancer by 30% to 50%. [24] [27] However, the evidence for reduced oral cancer among people who have made changes in their diet is inadequate.

Dietary supplementation with 50 mg of alpha-tocopherol acetate (vitamin E) per day and 20 mg beta carotene per day has been tested in a large, randomized, placebo-controlled, 2 2 factorial trial of 29,133 male smokers aged 50 to 69 years. [28] After a median follow-up of 6.1 years, there were 65 incidences of oropharyngeal cancers, with no statistically significant differences between the placebo and the active agents, whether alone or in combination. Moreover, in the same trial, beta carotene was associated with increased lung cancer incidence and mortality.

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. [29] Other high-risk HPV subtypes, including HPV 18, have been found in a small percentage of oropharyngeal cancers. [30] [31]

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. [30]

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. [32] 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, 1975-2011. Bethesda, Md: National Cancer Institute, 2014. Also available online. Last accessed February 6, 2015.
  2. American Cancer Society: Cancer Facts and Figures 2015. Atlanta, Ga: American Cancer Society, 2015. Available online. Last accessed April 1, 2015.
  3. Ferlay J, Shin HR, Bray F, et al.: GLOBOCAN 2008: Cancer Incidence and Mortality Worldwide in 2008. Lyon, France: IARC CancerBase No. 10. Available online. Last accessed April 24, 2015.
  4. Parkin DM, Bray F, Ferlay J, et al.: Global cancer statistics, 2002. CA Cancer J Clin 55 (2): 74-108, 2005 Mar-Apr.
  5. Noonan VL, Kabani S: Diagnosis and management of suspicious lesions of the oral cavity. Otolaryngol Clin North Am 38 (1): 21-35, vii, 2005.
  6. Howlader N, Noone AM, Krapcho M, et al., eds.: SEER Cancer Statistics Review, 1975-2008. Bethesda, Md: National Cancer Institute, 2011. Also available online. Last accessed February 6, 2015.
  7. Reducing the Health Consequences of Smoking: 25 Years of Progress - a Report of the Surgeon General. Rockville, Md : U.S. Dept. of Health and Human Services Public Health Service, Centers for Disease Control, Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 1989.
  8. Cinciripini PM, McClure JB: Smoking cessation: recent developments in behavioral and pharmacologic interventions. Oncology (Huntingt) 12 (2): 249-56, 259; discussion 260, 265, 2, 1998.
  9. Spitz MR, Newell GR: Descriptive epidemiology of squamous cell carcinoma of the upper aerodigestive tract. Cancer Bull 39(2): 79-81, 1987.
  10. 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.
  11. Firth NA: Marijuana use and oral cancer: a review. Oral Oncol 33 (6): 398-401, 1997.
  12. 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.
  13. 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.
  14. 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.
  15. 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.
  16. 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.
  17. 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.
  18. Samet JM: The health benefits of smoking cessation. Med Clin North Am 76 (2): 399-414, 1992.
  19. 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.
  20. 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.
  21. Nelson NJ: "Big Smoke" has big risks: daily cigar use causes cancer, heart disease. J Natl Cancer Inst 90 (8): 562-4, 1998.
  22. La Vecchia C, Tavani A, Franceschi S, et al.: Epidemiology and prevention of oral cancer. Oral Oncol 33 (5): 302-12, 1997.
  23. 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.
  24. Winn DM, Ziegler RG, Pickle LW, et al.: Diet in the etiology of oral and pharyngeal cancer among women from the southern United States. Cancer Res 44 (3): 1216-22, 1984.
  25. Winn DM: Diet and nutrition in the etiology of oral cancer. Am J Clin Nutr 61 (2): 437S-445S, 1995.
  26. Horn-Ross PL, Morrow M, Ljung BM: Diet and the risk of salivary gland cancer. Am J Epidemiol 146 (2): 171-6, 1997.
  27. Morse DE, Pendrys DG, Katz RV, et al.: Food group intake and the risk of oral epithelial dysplasia in a United States population. Cancer Causes Control 11 (8): 713-20, 2000.
  28. Wright ME, Virtamo J, Hartman AM, et al.: Effects of alpha-tocopherol and beta-carotene supplementation on upper aerodigestive tract cancers in a large, randomized controlled trial. Cancer 109 (5): 891-8, 2007.
  29. 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.
  30. 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.
  31. 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.
  32. 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.

Changes to This Summary (04/24/2015)

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 comprehensively reviewed and extensively revised.

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 Web site’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 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:

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 Web site's Contact Form. 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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PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”

The preferred citation for this PDQ summary is:

National Cancer Institute: PDQ Oral 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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Date last modified: 2015-04-24

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