High Risk Individuals
Who are at High Risk?
Two groups of risk factors - those that are well-established as causes of oral cancer and a second group of possibly relevant contributory factors. Age is included as an established risk factor because exposure to the risks listed increases with age but age on its own is not a risk factor. Also, oral cancer is not always a disease of old age. Clinicians treating oral cancer are concerned that its incidence appears to be increasing in younger age groups. Established risk factors
  • Smoking tobacco – cigarettes, cigars, pipes, bidis.
  • Chewing tobacco – betel quid/paan/gutkha/pan masala.
  • High alcohol consumption (synergistic with tobacco).
  • The presence of potentially malignant oral lesions and conditions.
  • Prior history of oral cavity or other aero-digestive tract cancer.
  • Age, in conjunction with other risks listed (more likely to strike after age 40).
  • Prolonged exposure to the sun increases the risk of lip cancer.
  • Oral cancers can occur in people who do not smoke and have no other known risk factors.
  • Studies suggest that a diet high in fruits and vegetables may prevent the development of potentially cancerous lesions.
Other possible risk factors
  • Dietary deficiencies, particularly of vitamins A, C and E and iron, trace elements such as selenium and zinc.
  • Viral infections, e.g. certain types of human papilloma viruses (HPVs).
  • Candida infection.
  • Excessive exposure to sunlight or radiation (for lip cancer).
  • Immune deficiency disease or immune suppression.
  • Familial or genetic predisposition.
  • Air pollution and environmental exposure to the burning of fossil fuels.
  • Chronic sepsis in the mouth.
Tobacco use, however, remains the most widely believed risk factor for oral cancer.
  • Tobacco use, however, remains the most widely believed risk factor for oral cancer. Oral cancer most often occurs in those who use tobacco in any form.
  • Although other lifestyle and environmental factors also have been identified as risk factors for oral cancer, tobacco use remains the single most important and preventable cause of this disease.
  • Although oral cancer undoubtedly has a multifaceted aetiology, tobacco use and alcohol consumption are widely considered to be its major risk factors.
  • It has been conclusively established that tobacco use, especially cigarette smoking, is causally related to at least eight major cancer sites and increases the mortality rate for several others.
  • Cigarette smoking is a major cause of cancers of the oral cavity. Individuals who smoke pipes or cigars experience a risk for oral cancer similar to that of the cigarette smoker.
  • Scientific evidence shows that use of snuff can cause cancer in humans, particularly cancers of the cheek and gum. The evidence for causality is strongest for cancer of the oral cavity, wherein cancer may occur several times more frequently in snuff dippers as compared to non- tobacco users.
  • Smoking, combined with alcohol use greatly increases risk.
  • Heavy drinkers usually are also heavy users of tobacco products.
  • Consumption of alcohol together with a poor diet may be an enhancing factor for oral cancer.
  • Alcohol intake and often- episodic nature of usage is often under reported. This makes it difficult for a patient to estimate ‘average’ use.

According to various studies, all three forms of alcohol (beer, hard liquor and wine) have been associated with oral cancer, though hard liquor and beer have a higher associated risk. The studies have also found that the level of consumption was also a deciding risk factor. For example, one study found increased risk only if 56 or more glasses of wine per week were consumed. Another study noted a significant increase only if the average daily consumption of alcohol exceeded 120 grams. That evidence contradicts about the role of alcohol in oral cancer and may relate to the difficulty in measuring intake or to alcohol's effect on other variables (or both). But it is reasonable to assume that any form of alcohol taken in excess may promote oral cancer.

Though there is insufficient evidence to establish that mouthwashes can cause oral cancer, this might be a cause if used frequently, because they have high alcohol content as high as 26 percent.
Dietary factors have been identified as having a possible association with oral cancer. But, accumulated scientific evidence shows that use of tobacco and alcohol increases oral cancer risk and far outweighs any evidence linking a deficient diet to increased risk.

Low beta-carotene intake has been associated with an increased risk of lung, laryngeal, gastric, ovarian, breast, cervical and oral cancers.

Various studies have shown that a low intake of fruits and vegetables, which are the primary sources of beta- carotene, is also related to a generalized increased cancer risk and mortality. At the same time, an increased consumption of fruits and/or vegetables has been associated with a decreased risk of oral or oropharyngeal cancer when compared with low intake levels.

Low intake of vitamin C has been associated with an increased risk of cancers of the stomach, oesophagus, oral cavity and larynx. Patients who consume high levels of vitamin C and fibre have half the risk of oral cancer as those with the lowest level of intake.

According to one study, patients with low serum levels of vitamin E had more than double the general risk of gastrointestinal cancers. In another study, which evaluated more than 2,000 cases, the use of vitamin E supplements showed a diminished risk for oral and pharyngeal cancer.

It has been found in dietary studies across multiple cultures that high fruit consumption has a protective effect and high alcohol consumption has a carcinogenic effect.

Actinic Radiation

Sunlight, through actinic radiation, is a factor that helps produce cancer along the vermilion border of the lip. One finds these ‘sunlight’ induced cancers are much more common in fair- skinned individuals exposed to the outdoor life than in individuals with darker pigmentation. That is because, darker pigmentation, it appears, protects against actinic radiation damage. (The wavelengths of the light thought to be responsible for the actinic damage are in the 2900-3200nm range).

Dental Factors

There is little evidence to suggest that poor oral hygiene, improperly fitting dental prostheses, defective dental restorations or misaligned or sharp teeth promotes oral cancer.

Viruses and their Interactions with Oncogenes

Alterations of cellular oncogenes, which lead to altered expression of their products, have been implicated in human cancers. Cellular oncogenes, also known as proto- oncogenes, get their transforming properties or become activated by gene amplification, point mutations and gene rearrangements.

Oncogenes can encode growth factors and growth factor receptors. They act on internal signalling molecules and regulate DNA transcription factors. Other genes encode proteins that inhibit the cell cycle or promote programmed cell death (apoptosis).

Tumour suppressor genes may become inactivated or mutated with consequential loss of control over cell division. The retinoblast and gene products are examples. It must be considered that many molecular events governing control of cell cycles are influenced by viruses.

The viruses most commonly implicated in oral cancer transformation have been the human papillomavirus (HPV), herpes group viruses and the adenoviruses. Of these, HPV and herpes have been the most thoroughly studied. They are now considered to be the most likely "synergistic viruses" involved in human oral cancer. The herpes viruses most often linked to oral cancer are the Epstein- Barr virus (EBV) and cytomegalovirus (CMV).


Oral cancer does not appear to be a common consequence of systemic immunosuppression. This is even though, among HIV- positive immunocompromised individuals, HIV- associated oral malignancies have been reported. The most common are Kaposi's sarcoma (KS) and non- Hodgkin's lymphomas. You can take steps to reduce your risk of developing oral cancer by avoiding behaviors that researchers have identified as being strongly associated with the development of oral cancer.

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