Oral Cancer

Causes

Most cases of oral carcinomas can be attributed to certain life-style risk factors and are thus preventable. The most important are the use of tobacco and drinking alcohol to excess. For some populations, regular areca nut and betel quid use is relevant (Figures 1-3).

Amongst younger patients, known risk factors are absent, producing a challenge for research into their aetiology (Llewleyn et al., 2001). Human papillomavirius (HPV) infection is emerging as a likely cause of oral cancer and particularly of the oro-pharynx in this age group.

Diet plays an important role; regular consumption of fresh fruits and vegetables provides protection against cancer and precancer.

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Figure 1. Doctors and dentists should enquire about their patient’s smoking habits

Tobacco

Tobacco use – smoked or in smokeless forms – is far and away the most important risk factor for oral cancer. Over 75% of mouth and pharyngeal cancers are directly attributed to smoking (and alcohol) use. Within Europe, smoking cigarettes (Figure 1) is the most commonly encountered risk factor, but rolled-up (non-filter) cigarettes have higher risks. Smokeless tobacco products also could cause mouth and pancreatic cancer (Warnakulasuriya, 2004).

DownloadLeafletThe risk of oral cancer increases with the amount of tobacco consumed per day, and the number of years of consumption. All tobacco products are carcinogenic (IARC, 2012), and there is no evidence to suggest that replacing smoking with another tobacco product Is harmless.

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Figure 2. Excessive consumption of alcohol is the second most important risk factor

Alcohol

Excessive consumption of alcohol (>21 units/week for men; >14 units/week for women) is the second most important risk factor (Figure 2). Alcohol acts synergistically with tobacco so that the combined damage is more than multiplied.

DownloadLeafletThough ethanol per se has not been shown to carcinogenic, acetaldehyde – a metabolite of alcohol – is carcinogenic to man. Alcohol can be broken down to acetaldehyde in the mouth by bacteria in oral biofilms.

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Figure 3. Areca fruit; unripe Areca fruit as used in Taiwan; Areca nut (endosperm of the Areca fruit); packaged commercial products of Areca nut.

Areca Nut

Areca nut with tobacco consumed as betel quid has traditionally been known to cause a high disease burden of oral cancer in South and Southeast Asia and Asia, Pacific islands and among Asian migrants living in Europe.

Areca nut alone (without tobacco) can be carcinogenic and appears to be responsible for the high incidence of oral cancer in some countries e.g. Papua New Guinea (in Melanesia), Guam (in Micronesia), and Taiwan, where it is often consumed without tobacco. The International Agency on Research for Cancer (IARC) has recently classified areca nut (Figure 3) as a Class I carcinogen. Areca nut is the major cause of the distressing condition Oral Submucous Fibrosis, which has a high rate of malignant transformation (up to 7% over 10 to 15 years) to oral cancer.

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 Figure 4. A healthy diet protects

Diet

Diet is probably the next most powerful factor in cancer control: a healthy diet is protective (Figure 4). The antioxidant vitamins A, C and E scavenge potentially mutagenic free radicals from damaged cells. They are best delivered naturally in red, yellow and green fresh fruits and vegetables, and we should encourage people to eat about five helpings of such foods a day.

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Figure 5. Human Papillomavirus

Human papillomavirus

Of great current interest is the possibility of a role for human papillomavirus (HPV; Figure 5). The so-called high oncogenic HPVs types 16 and 18 are known to be important in causing cancers of the uterine cervix, and are increasingly being found in the oral cavity (particularly in cancers of the tonsils and oropharynx). Screening for their presence may become a useful component of the early detection of patients and disorders at risk of malignant transformation.

DownloadLeafletAnti-HPV vaccines are now available and when given in early teens they protect against epithelial cancers.

Other Factors

  • The presence of oral potentially malignant disorders (OPMDs) such as white plaques (leukoplakia), red plaques (erythroplakia), white and red plaques (erythroleukoplakia), oral lichen planus and submucous fibrosis certainly indicate that a patient is at an increased risk of developing an oral cancer.

    It is estimated that someone with leukoplakia may have an increased risk one hundred times greater than a person with a healthy normal mucosa. For erythroplakia, the risk is much higher. This will usually justify removal of risky white/red patches or other treatment; excision reduces the risk of transformation but does not completely eliminate that risk. These OPMDs result from the same life-style risk factors discussed above, elimination of which is therefore even more important in such patients.

  • Infections of oral mucosa may also be important. It has long been known that oral keratosis harbouring yeasts or hyphae of the fungus Candida albicans carry an increased risk of progressing to malignancy and where present appropriate anti-fungal therapy (local and/or systemic) should be prescribed.

  • There is no strong evidence to suggest that oral cancer is familial, although few hereditary syndromes are known.

  • People with poor dental health such as sharp, broken teeth, dental sepsis or trauma from ill-fitting dentures are at slightly increased risk. The evidence available though is weak. Oral sepsis (commensal bacteria) in mouths of alcoholics might contribute to the metabolism of alcohol to acetaldehyde, a known carcinogen.

  • Immunosuppression regimes, for example following renal or other organ transplantation, increase the risk of ultra-violet-induced cancers of skin and lip. There appears to be no increased risk of intra-oral squamous cell carcinoma in those with HIV disease, and there is as yet no evidence that the characteristic, so-called, oral hairy leukoplakia in HIV/AIDS patients has malignant potential. However other neoplasms such as Kaposi’s Sarcoma and Non-Hodgkin’s lymphomas are certainly increased in HIV seropositve or AIDS patients.

This is the end of the What causes oral cancer module, please select the next module to continue through the guide.

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