Oral cancer refers to malignancies that develop in the tissues of the mouth and throat, including the lips, tongue, cheeks, and gums. The development of this disease is not attributed to a single cause but a combination of factors that increase risk. These cancers arise from genetic mutations in cells, leading to their uncontrolled growth and the formation of tumors.
Tobacco and Alcohol Use
Tobacco use is an established risk factor for oral cancers, including all forms like cigarettes, cigars, pipes, and smokeless products. Chemicals in tobacco directly damage the DNA of cells lining the oral cavity, disrupting the normal cell cycle and leading to cancerous growth. For instance, pipe smoking is linked to cancer where the pipe stem rests on the lips.
Heavy alcohol consumption also elevates the risk. Alcohol acts as a solvent, increasing the permeability of the oral mucosa and allowing carcinogens from sources like tobacco to penetrate tissues more easily. This effect is compounded by epithelial atrophy, a thinning of the protective cell layer in the mouth caused by alcohol.
When used together, tobacco and alcohol have a synergistic effect, increasing the risk of oral cancer by about 30 times compared to non-users. In addition to increasing tissue permeability, alcohol can accelerate the metabolic conversion of substances in tobacco into more potent cancer-causing agents. This interaction creates a highly conducive environment for the cellular changes that initiate cancer.
Human Papillomavirus and Sun Exposure
Certain strains of the human papillomavirus (HPV) cause cancers affecting the oropharynx, which includes the back of the throat, base of the tongue, and tonsils. HPV-16 is the high-risk type most commonly associated with these cancers, accounting for a majority of cases. The virus integrates its DNA into host cells, disrupting tumor-suppressing genes and leading to uncontrolled cell division. This pathway is a leading cause of throat cancers, especially in younger, non-smoking individuals.
Exposure to ultraviolet (UV) radiation from the sun is a primary cause of cancer on the lips. The skin on the lips is thin and contains less protective melanin, making it vulnerable to UV rays, with the lower lip being the most common site. Most lip cancers are squamous cell carcinomas, originating in the flat cells on the outer surface of the skin.
Lip cancer risk is related to cumulative sun exposure over a lifetime. A precancerous condition known as actinic cheilitis, appearing as dry, scaly patches, can develop from chronic sun exposure and may progress to squamous cell carcinoma. Using lip balm with SPF 30 or higher and wearing a wide-brimmed hat can reduce this risk.
Underlying Health and Genetic Factors
An individual’s biological and health status can influence their susceptibility to oral cancer. The risk increases with age, with most diagnoses occurring in people over 40. Men are about twice as likely as women to develop these cancers, a difference linked to historically higher rates of tobacco and alcohol use. A personal or family history of cancer can also indicate a predisposition.
Certain rare genetic syndromes caused by inherited mutations also elevate the risk. Conditions like Fanconi anemia and Dyskeratosis congenita are associated with a high risk of these cancers, often at a younger age. These disorders can impair the body’s ability to repair DNA damage, making cells more vulnerable to cancer-causing mutations.
A compromised immune system heightens the risk. Individuals with conditions like HIV/AIDS or those taking immunosuppressant drugs after an organ transplant have a reduced ability to destroy abnormal cells. This weakened immune surveillance allows cells with cancerous changes to proliferate. A suppressed immune system can also increase susceptibility to infections like HPV, another risk factor for oral cancer.