What causes cancer of the mouth and throat?

All cancers are diseases in the cancer cells. Oncogenes are activated as a result of mutation of the DNA. The exact cause is often unknown. Risk factors that predispose a person to oral cancer have been identified in epidemiological studies. India being member of International Cancer Genome Consortium is leading efforts to map oral cancer's complete genome. In many Asian cultures chewing betel, paan and Areca is known to be a strong risk factor for developing oral cancer. In India where such practices are common, oral cancer represents up to 40% of all cancers, compared to just 4% in the UK.

Some oral cancers begin as leukoplakia a white patch (lesion), red patches, (erythroplakia) or non healing sores that have existed for more than 14 days. In the US oral cancer accounts for about 8 percent of all malignant growths. Men are affected twice as often as women, particularly men older than 40/60. In Indian subcontinent Oral submucous fibrosis is very common. This condition is characterized by limited opening of mouth and burning sensation on eating of spicy food. This is a progressive lesion in which the opening of the mouth becomes progressively limited, and later on even normal eating becomes difficult. It occurs almost exclusively in India and Indian communities living abroad.

Tobacco
Smoking and other tobacco use are associated with about 75 percent of oral cancer cases, caused by irritation of the mucous membranes of the mouth from smoke and heat of cigarettes, cigars, and pipes. Tobacco contains over 60 known carcinogens, and the combustion of it, and by products from this process, is the primary mode of involvement. Use of chewing tobacco or snuff causes irritation from direct contact with the mucous membranes.

Alcohol
Alcohol use is another high-risk activity associated with oral cancer. There is known to be a strong synergistic effect on oral cancer risk when a person is both a heavy smoker and drinker. Their risk is greatly increased compared to a heavy smoker, or a heavy drinker alone. Recent studies in Australia, Brazil and Germany point to alcohol-containing mouthwashes as also being etiologic agents in the oral cancer risk family. Constant exposure to these alcohol containing rinses, even in the absence of smoking and drinking, lead to significant increases in the development of oral cancer. A 2008 study suggests that acetaldehyde (a break-down product of alcohol) is implicated in oral cancer.

Human papillomavirus
Infection with human papillomavirus (HPV), particularly type 16 (there are over 120 types), is a known risk factor and independent causative factor for oral cancer. (Gilsion et al. Johns Hopkins) A fast growing segment of those diagnosed does not present with the historic stereotypical demographics. Historically that has been people over 50, blacks over whites 2 to 1, males over females 3 to 1, and 75% of the time people who have used tobacco products or are heavy users of alcohol. This new and rapidly growing sub population between 20 and 50 years old is predominantly non smoking, white, and males slightly outnumber females. Recent research from Johns Hopkins indicates that HPV is the primary risk factor in this new population of oral cancer victims. HPV16 (along with HPV18) is the same virus responsible for the vast majority of all cervical cancers and is the most common sexually transmitted infection in the US. Oral cancer in this group tends to favor the tonsil and tonsillar pillars, base of the tongue, and the oropharnyx. Recent data suggest that individuals that come to the disease from this particular etiology have some slight survival advantage.

Alcohol and tobacco use are the most common risk factors for head and neck cancer in the United States. Alcohol and tobacco are likely synergistic in causing cancer of the head and neck. Smokeless tobacco is an etiologic agent for oral and pharyngeal cancers. Cigar smoking is an important risk factor for oral cancers as well. Other potential environmental carcinogens include occupational exposures such as nickel refining, exposure to textile fibers, and woodworking. In one large, controlled study, marijuana use was shown to be associated with oral squamous cell carcinoma. In another study, marijuana use was even shown to be a potential protective factor against the development of head and neck squamous cell carcinoma. However, cigarette smokers have a lifetime increased risk for head and neck cancers that is 5- to 25-fold increased over the general population. The ex-smoker's risk for squamous cell cancer of the head and neck begins to approach the risk in the general population twenty years after smoking cessation. The high prevalence of tobacco and alcohol use worldwide and the high association of these cancers with these substances makes them ideal targets for enhanced cancer prevention.