Clinical Practice

Oral Cancer: Just the Facts

Contact Author
Denise M. Laronde, RDH, MSc; T. Greg Hislop, MDCM; Ms. Laronde
J. Mark Elwood, MD, MBA, FRCPSC; Miriam P. Rosin, BSc, PhD Email: dlaronde@
bccancer.bc.ca

ABSTRACT

Oral cancer screening should be an integral part of a clinician’s routine. This article
reviews facts about oral cancer that are relevant to screening. The relevance of some
issues in a particular dental practice will vary with the patient composition of the
practice.

For citation purposes, the electronic version is the definitive version of this article: www.cda-adc.ca/jcda/vol-74/issue-3/269.html

O
ral cancer, although prevalent world- a reduction in smoking.2 Like most cancers,
wide, is very common in some countries the incidence of oral cancers rises with age
such as India, Pakistan and Taiwan, (Fig. 1). Patients over 60 years of age are at
and in some areas of France.1 Although less the greatest risk; however, the incidence of
frequent in Canada, oral cancer was diag- oral cancer has increased in patients under
nosed in 3,200 people and responsible for 40 years of age, perhaps because of chan-
1,100 deaths in 2007.2 To put this into per- ging risk factors. About 6% of oral cancers
spective, currently in Canada, more cases occur among persons under 40 years of age.
of oral cancer are diagnosed in a year than Although the overall ratio of males to females
cervical or ovarian cancer, and more deaths with oral cancer in Canada is 2:1, the ratio is
occur from oral cancer than from melanoma almost 1:1 in patients under 40. The overall
or cervical cancer. 2 With growing immigra- incidence in Canada is about 12 per 100,000
tion from high-risk areas such as India, the per year in men and 5 per 100,000 in women.
number of cases of oral cancer will increase. Rates are somewhat higher in eastern than in
Since nasopharyngeal cancers are routinely western Canada.
included in oral cancer statistics, we estimate
that dental professionals could potentially de- What Can Be Done About This?
tect about 2,700 (84%) of these 3,200 cases. Early diagnosis of oral cancer through
The distribution of the sites of oral and re- screening and early detection is critical.
lated cancers that can be detected by dental Survival is much better when the lesion is
screening is shown in Table 1. For conven- diagnosed at an early stage. For example, the
ience, we refer to this group of 2,700 cancers 5-year survival rate for tongue cancer in the
as “oral cancers” in this paper. United States is 71% for stage 1 disease and
Oral cancer is often diagnosed at an ad- 37% for late-stage disease. 3 More than 40% of
vanced stage, and the overall survival rate 5 oral cancers are diagnosed at a late stage. 3
years after diagnosis is about 62% for all sites
combined 2 and 65% for the sites shown in Who Should Be Screened?
Table 1. Survival has improved a little over The first step in screening for oral cancer
the last several decades, perhaps because of involves reviewing the patient’s medical

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Table 1 Distribution and survival rates for oral cancers

amenable to dental screening and early detection 80
by subsite: Canada, 2007
Male
5-year 60 Female
Number of survival
Subsite of new cases % rate

Incidence
cancer (n = 2,690) distribution (mean 65) 40

Lip 341 13 94
20

Tongue 740 27 53
0
Gum and 509 19 60 20 30 40 50 60 70 80 90

other mouth Age

Floor of mouth 281 10 53 Figure 1: Annual incidence rate for new oral cancers by age and sex
(number per 100,000 population). From U.S. SEER data.4
Salivary 348 13 74
gland Patients from South Asian countries may also chew
betel quid or paan, a common habit in their culture.
Tonsil 379 14 50 Betel quid is a carcinogenic complex mixture of plant
components that frequently contains tobacco. Since im-
Oropharynx 93 3 50 migrants from these countries tend to retain the level of
oral cancer risk characteristic of their country of origin
Estimates based on data from the United States3 and Canada.2 for some time, they should be questioned about their con-
sumption of betel quid.

history to assess various risk factors, including a past Alcohol

history of disease, specific risk-related habits, medica- Alcohol consumption is also a strong risk factor for
tions and reasons for hospitalizations. A number of fac- oral cancer and premalignant lesions. The risk increases
tors are associated with an increased risk of oral cancer with increased consumption and duration of use of al-
(Table 2).1,5–8 cohol. Typically, one 8-ounce glass of beer, one 4-ounce
There is no single cause of oral cancer. It results from glass of wine and 1 ounce of spirits have equal amounts of
a variety of factors that operate over time and is de- alcohol.10 In many studies,10,11 heavy drinking is defined
pendent on each person’s unique response to these fac- as consumption of more than 14 to 21 drinks per week.
tors. However, patients without obvious risk factors can Again, the risk of oral cancer decreases when alcohol
develop oral cancer and premalignant lesions. The 2 most is no longer consumed, but it takes many years for a
important modifiable risk factors for oral cancer are to- drinker’s risk to reduce to that of someone who has never
been a drinker.1
bacco and alcohol consumption. Up to 75% of oral cancers
Tobacco and alcohol consumption work together syn-
may be attributed to exposure to tobacco or alcohol.6,9
ergistically, increasing the risk of oral cancer to more
Tobacco than 30 times that of those who do not smoke or drink.1,5,6
Tobacco smoke contains dozens of known carcino- Heavy drinkers and smokers are also more likely to be
gens. The risk of oral cancer and premalignant lesions diagnosed with late-stage disease. Ceasing to use tobacco
increases with the amount of tobacco consumed and the and alcohol greatly reduces the risk of developing oral
duration of tobacco use. This increased risk holds for all cancer and premalignant lesions.
types and uses of tobacco, whether it is smoked as a ciga- Human Papilloma Virus
rette, cigar, pipe or bidi (a small, hand-rolled cigarette Having human papilloma virus (HPV) is a strong risk
commonly used in Asia), or used smokeless as a chew, factor for oral cancers, especially when the lingual and
plug or snuff. Stopping smoking reduces the risk of oral palatine tonsils, the soft palate and the base of the tongue
cancer and premalignant lesions, although it may take 10 are involved. Of the more than 120 types of HPV, only a
to 20 years for a former smoker’s risk to reduce to that of few are high-risk factors for oral cancer, primarily HPV-
a nonsmoker.1 16 and HPV-18. Over 90% of HPV-positive oral cancers

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Table 2 Risk factors for oral cancers

Very strong risk factors (> 10-fold increased risk) Common Fallacies about Oral Cancer
Increased age1
Oral cancer happens only to smokers and alcohol
Using tobacco and alcohol, especially combined use
(risks for heavy smokers and drinkers are increased
drinkers.
more than 30-fold)1,5,6 About 25% of oral cancers occur in people with no
Using smokeless tobacco, including snuff and chewing history of tobacco or alcohol use.
tobacco 6
Chewing betel quid, areca nut and paan1,6 Oral cancer occurs only in the elderly.
Being immunologically compromised (e.g., after Although the risk of oral cancer increases with age,
bone-marrow transplantation)6–8
it can occur at any age and seems to be increasing in
Strong risk factors (4- to 10-fold increased risk)
patients less than 40 years of age.
Smoking cigarettes5,6
Drinking alcohol5,6 The risk of oral cancer does not decrease once a

Having a human papilloma virus infection, especially patient quits smoking.

type 161,5 The risk of oral cancer is reduced for former smokers
Moderate risk factors (≤ 4-fold increased risk) and approaches that of a nonsmoker after many years.
Being male1
It is not my job to question patients about their
Smoking pipes and cigars1,5,6
tobacco and alcohol use.
Smoking marijuana1
Being exposed to environmental tobacco smoke 6 A comprehensive health history should include
Having low fruit and vegetable intake1,5,6 questions about patients’ tobacco and alcohol use,
including the duration of use and amount consumed.

are HPV-16 positive.1 Since risk factors for HPV infection Talking to your patients about tobacco and alcohol
include having a large number of sexual partners and first cessation may play an important role in the prevention
intercourse at a younger age, changing sexual practices of disease.
in our society may increase the effect of HPV infection
on the development of oral cancers and premalignant I can quickly screen for oral cancer as I complete
lesions, especially in younger adults.12 The combination other parts of my treatment.
of smoking and HPV infection and of alcohol and HPV
infection may have an additive effect.13 Screening for oral cancer is a 3-part process: the
review of the health history, the extraoral examination
Diet and Vitamins
A diet rich in fruits and vegetables, particularly fruit, and the intraoral examination. Cursory looks are not
reduces the risk of oral cancer and premalignant le- sufficient because areas such as the posterior lingual
sions. 5,14 Several studies1,5 have shown that higher levels vestibule, the soft palate, tonsils, the floor of the
of vitamin C or carotene consumption reduce the risk of
oral cancer. The potentially increased risk associated with mouth, and the posterior lateral and ventral tongue
meat consumption is less clear.1 Results of intervention can easily be missed.
studies involving dietary change or dietary supplements
have shown no clear evidence of benefit.1
Other Issues premalignant lesions. One study 8 reported an 11-fold
Studies of the role of marijuana in oral cancer are increased risk of oral cancer for bone-marrow trans-
scarce. Marijuana smoke contains many of the same car- plant patients. This risk increases with time, after
cinogens found in tobacco smoke15 and has 4 times the transplantation.
tar burden.16 Eating spicy or hot foods, using mouthwash, or having
Studies 6–8 have reported that immunosuppressed poor oral hygiene, missing or broken teeth, or dentures
patients (due to medications, bone-marrow transplants do not seem to cause oral cancer. Reports1,5 of higher
or disease) have an increased risk of oral cancer and risks associated with infrequent tooth-brushing and

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with missing teeth may be due to other factors such as editors. Clinical oncology. 3rd ed. Orlando: Churchill Livingstone, an imprint
of Elsevier; 2004. p. 1499–500.
smoking. Reported increased risks in some occupational 7. Bhatia S, Louie AD, Bhatia R, O’Donnell MR, Fung H, Kashyap A, and
groups, such as rubber workers and cooks, may also be others. Solid cancers after bone marrow transplantation. J Clin Oncol 2001;
19(2):464–71.
due to such factors.1,5,6 8. Curtis RE, Rowlings PA, Deeg HJ, Shriner DA, Socíe G, Travis LB, and
others. Solid cancers after bone marrow transplantation. N Engl J Med 1997;
336(13):897–904.
What Risk Information Should Be Recorded and
9. La Vecchia C, Tavani A, Franceschi S, Levi F, Corrao G, Negri E. Epidemiology
Updated in the Patient’s Chart? and prevention of oral cancer. Oral Oncology 1997; 33(5):302–12.
Questions about tobacco and alcohol consumption 10. Franceschi S, Levi F, Dal Maso L, Talamini R, Conti E, Negri E, and other.
Cessation of alcohol drinking and risk of cancer of the oral cavity and pha-
are a vital part of the screening process and should be re- rynx. Int J Cancer 2000; 85(6):787–9.
corded in the patient’s chart. Frequency (current and past 11. Hashibe M, Brennan P, Benhamou S, Castellsague X, Chen C, Curado M,
and others. Alcohol drinking in never users of tobacco, cigarette smoking in
use), and amount and duration of use should be recorded never drinkers, and the risk of head and neck cancer: pooled analysis in the
and updated regularly. This information may indicate the International Head and Neck Cancer Epidemiology Consortium. J Natl Cancer
Inst 2007; 99(10):777–89.
need to counsel patients about tobacco and alcohol cessa- 12. D’Souza G, Kreimer AR, Viscidi R, Pawlita M, Fakrhy C, Koch WM, and
tion. Finally, screening should be done regularly because others. Case-control study of human papillomavirus and oropharyngeal
oral cancer can occur in patients without any apparent cancer. New Engl J Med 2007; 356(19):1944–56.
13. Smith EM, Ritchie JM, Summersgill KF, Hoffman HT, Wang DH, Haugen
risk factors. a TH, and other. Human papillomavirus in oral exfoliated cells and risk of head
and neck cancer. J Natl Cancer Inst 2004; 96(6):449–55.
14. World Cancer Research Fund International and American Institute for
THE AUTHORS Cancer Research. Mouth, pharynx, and larynx. In: Food, nutrition, physical
activity and the prevention of cancer: a global perspective. Washington (DC):
AICR; 2007. p. 245–9.
Acknowledgments: Ms. Laronde is supported by a Michael Smith
15. Hashibe M, Ford DE, Zhang ZF. Marijuana smoking and head and neck
Foundation for Health Research/BC Cancer Foundation Senior Trainee
cancer. J Clin Pharmacol 2002; 42(11 Suppl):103S–7S.
Award.
16. Lingen M, Sturgis EM, Kies MS. Squamous cell carcinoma of the head
Ms. Laronde is a dental hygienist and PhD candidate, applied science, and neck in nonsmokers: clinical and biologic characteristics and implications
Simon Fraser University and BC Oral Cancer Prevention Program, BC for management. Curr Opin Oncol 2001; 13(3):176–82.
Cancer Agency/Cancer Research Centre, Vancouver, British Columbia.
Dr. Hislop is an epidemiologist and clinical professor, medicine, Univer-
sity of British Columbia and senior scientist in the cancer control research
department, BC Cancer Agency/Cancer Research Centre, Vancouver,
British Columbia.
Dr. Elwood is an epidemiologist and clinical professor, medicine, Univer-
sity of British Columbia and vice-president, Family and Community
Oncology, BC Cancer Agency/Cancer Research Centre, Vancouver, British
Columbia.
Dr. Rosin is a translational scientist and professor, applied science,
Simon Fraser University, medicine, University of British Columbia and
director, BC Oral Cancer Prevention Program, BC Cancer Agency/Cancer
Research Centre, Vancouver, British Columbia.
Correspondence to: Ms. Denise M. Laronde, BC Oral Cancer Prevention
Program, BC Cancer Agency/Cancer Control Research Centre, 675 West
10th Ave., Vancouver, BC V5Z 1L3.
The authors have no declared financial interests.
This article has been peer reviewed.

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