Oral cancer is an age-related disease and 98% of patients are over the age of 40. While the overall incidence in the population is only about 1 in 20  000, this rises to 1 in 1100 in males of 75 and over. There is a sharp and virtually linear rise in mouth cancer with age, as with carcinoma in many other sites.

Cancer of the mouth is considerably more common in men than women in most countries, and carcinoma of the lip is at least eight times as common in men as in women in Britain. Intraoral cancer used to be several times more frequent in men than women, but the male to female ratio is overall about 3:2 and, in south-east England, recent figures show little difference in incidence between the genders. The change is the result of the progressive decline in oral cancer in men, but a low, static rate in women.

The incidence of oral cancer rises steeply with age and, with an ageing population, oral cancer will become more common.

The earliest recorded tobacco-related death was in 1621 when a Thomas Herriot, who introduced clay pipe smoking to England, died (appropriately) of lip cancer. It was not thought at the time that pipe smoking had anything to do with Herriot’s death.

The effects of tobacco on the mouth depend on the way it is used and this varies in different countries. In Westernised countries, cigarette smoking predominates and pipe smoking has declined. In some countries, notably in India, the southern states of the USA and Sweden, tobacco chewing or snuffdipping (unsmoked tobacco held in the mouth for prolonged periods) is a habit. Methods of processing tobacco before use also vary widely, so that its products released into the mouth differ considerably in their effect.

Alcohol consumption has steadily risen in Britain, particularly in the past half-century when oral cancer was declining. However, as noted above, the incidence may now be rising. In some countries, such as Denmark, there is good epidemiological evidence to link alcohol intake with oral carcinoma and, in the Bas Rhin area of France, alcohol is held to be responsible for the highest oral and pharyngeal cancer incidence in Europe. The low incidence of mouth cancer among Mormons and Seventh Day Adventists, who neither drink nor smoke, supports this idea.

It is generally considered that the combination of smoking and drinking is the most important aetiological factor for mouth cancer and, as noted above, many oral cancer patients smoke and drink heavily. The relative risks for alcohol and tobacco consumption are shown in Figure 17.1.

Alcoholic drinks are not usually allowed to reside in the mouth for long periods and there is no specific alcohol-related oral lesion. The mechanism by which alcoholic drinks might cause carcinomas is unclear and may not be their ethanol content. Drinks with the highest content of congeners, such as raw home-brewed spirits, appear to have the closest association with carcinoma. By contrast, evidence from the USA suggests that beer-drinking is associated with a greater risk. It is also possible that alcohol might predispose to carcinoma through its action on the liver and some studies have found a correlation between mouth cancer and cirrhosis. As with smoking, the total consumption is probably a critical factor.

Concern over the possible carcinogenic effects of alcohol has led to a proposal that it should be banned from mouthwashes, some of which contain more than 25% alcohol. There is as yet no conclusive link between mouthwash use and oral carcinoma.

The oncogenic potential of viruses is well recognised and some evidence has been produced to suggest that the human papillomavirus (particularly HPV 16) genomes can be found to be incorporated into mouth cancer cells. The importance of this finding remains unclear, especially as HPV is equally frequently found in normal mucosa. Screening exfoliated mucosal cells for the presence of HPV DNA has not proved to be useful as a screening test. If HPV played a significant role in oral carcinogenesis, it would be expected that the immunosuppressed, who suffer enhanced HPV infection, would be at greater risk of oral carcinoma. However, though uterine cervical and anal cancer in patients with AIDS is HPV-associated, oral carcinoma is uncommon and usually associated with other risk factors such as heavy tobacco or alcohol use. There is also no evidence of any greater susceptibility to intraoral cancer among patients who are deeply immunosuppressed therapeutically, though many are HPV carriers. Such patients have high rates of lip cancer, but only if exposed to strong sunshine.

There is better evidence that HPV plays a role in tonsil and oropharyngeal carcinoma. At these sites, up to 10% of carcinomas can be shown to contain HPV DNA integrated into the genome, but its precise contribution remains unclear and the focus of considerable research interest.

Syphilitic leukoplakia held pride of place as an infectious precancerous disease, in that the suggested rate of malignant change was between 30 and 100%. However, tertiary syphilis has become so rare that investigation of possible mechanisms has now become impossible and, even in developing countries, syphilitic leukoplakia is no longer a significant risk factor (Ch. 16).

Chronic candidosis can lead to formation of hyperkeratotic plaques or speckled leukoplakias with epithelial dysplasia. There have been isolated reports of malignant change in such lesions but, overall, this accounts for a very small proportion of cases (Ch. 16)

There is a high incidence of mouth as well as oesophageal cancer in Paterson–Kelly syndrome, in which iron deficiency is a feature. However, this disease is no longer a significant risk factor.

Epidemiologically, a low vitamin A intake has been associated with oral carcinoma, but deficiency of beta-carotene has now been dismissed as contributing to cancer. In India, malnutrition is widespread and may contribute, together with betel quid chewing, to the high incidence. However, there appears to be no comparably high frequency of mouth cancer in other areas, such as many parts of Africa, where malnutrition is at least as severe.

Oral sepsis has traditionally been regarded as contributing to mouth cancer. The latter is most common in low socioeconomic groups, which tend to have the most neglected mouths. Oral cancer also progressively declined in frequency in Britain, where a slow but steady improvement in oral health is well documented.

Despite such considerations, the aetiological role of oral sepsis in mouth cancer remains unproven.

Exposure to the ultraviolet component of sunlight is a risk factor, with the result that lip cancer is predominantly a disease of outdoor workers, particularly farmers and fishermen. As with other skin cancers, fair-skinned persons are at most risk. There may be multiple lesions in the most severely affected.

The relationship between exposure to sunlight and lip cancer has been clearly shown in hot countries such as Australia and the USA with large immigrant, fair-skinned populations of European origin. In the USA, for example, the risk of lip cancer approximately doubles for every 250 miles nearer the equator to the site of residence.

Dysplastic lesions caused by sunlight may precede the carcinoma and sun-damaged lip may be identified clinically by its loss of elasticity and atrophic epithelium. Changes due to sunlight are preventable and dentists should encourage the need to wear a high-factor sun-block when exposed to strong sunlight.

There are a few genetic disorders, notably dyskeratosis congenita (Ch. 16), of which oral cancer is a frequent feature, but such disorders are rare. Mice with a high susceptibility to oral cancer have also been bred. However, the genetics of oral cancer are highly complex and causative genes have not been identified in humans.

Several premalignant lesions are recognised (Ch. 16). In general, the risk of malignant transformation in the more common white lesions is very low, but the risk from speckled leukoplakia and erythroplasia is high. However, it is not known what proportion of carcinomas arise in clinically recognisable premalignant lesion.

Key features of cancer of the mouth are summarised in Box 17.2.