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Oral Cancer Prevention (PDQ®)

Health Professional Version

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.[12-15] 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.[10,22,24-26] 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. [PUBMED Abstract]
  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. [PUBMED Abstract]
  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. [PUBMED Abstract]
  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. [PUBMED Abstract]
  11. Firth NA: Marijuana use and oral cancer: a review. Oral Oncol 33 (6): 398-401, 1997. [PUBMED Abstract]
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  • Updated: April 24, 2015