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