Screening for Oral Cancer

Edward T. Lahey III

There are estimated to be at least 23,000 new cases of oral cancer diagnosed each year in the United States, with oral cancer causing more than 5,000 deaths yearly. The anatomical borders within which oral cancer occurs are the lips, oral tongue (that portion in front of circumvallate papillae), buccal and alveolar mucosae, floor of mouth, and hard palate. Oral cancer is distinct from oropharyngeal cancer (cancer of the soft palate, tongue base, tonsils, and pharyngeal walls) with regard to risk factors and natural history though in both anatomic areas, squamous cell carcinoma represents more than 90% of diagnosed malignancies. This chapter focuses predominantly on oral cancer but includes some consideration of oropharyngeal malignancy since it may present in the oral cavity.

Despite the ready accessibility of the oral cavity to inspection by physicians, dentists, and patients, 50% of oral cancers have already metastasized at the time of initial diagnosis due to early lesions usually being painless and often going undetected during routine care visits. There is a precipitous decline in prognosis once oral cancer has progressed beyond early, localized disease, so the primary care physician can play an important role in early detection. Counseling patients on prevention is another responsibility, given that 90% of oral cancer cases are linked to alterable risk factors.

EPIDEMIOLOGY AND RISK FACTORS (1, 2, 3, 4, 5, 6, 7, 8, 9, 10 and 11)

More than 97% of oral cancers occur among patients older than 35 years of age, with a peak incidence in the sixth decade for women and fifth decade for men. Demographically, black men have the highest risk of developing oral cancer. Risk factors include increased age, smoking and alcohol abuse, history of previous cancer of the upper aerodigestive tract, and chronic immunocompromise. While the precise etiology of oral cancer remains unknown, many of these risk factors probably act as cocarcinogens, effecting malignant change in concert with some primary factor not yet elucidated. Increased chromosomal fragility has been found in nonsmokers who develop oral cancers.

Tobacco and alcohol abuse warrant special attention in that they are synergistic cocarcinogens. It is theorized that the solvent effect of alcohol allows better penetration of tobacco smoke carcinogens into the oral mucosa. Patients with a history of combined tobacco and alcohol abuse often present with multiple dysplastic and malignant lesions due to “field cancerization.” Nonsmoking oral cancer patients are more likely to present at the extremes of age with lesions of the lateral borders of the tongue and rarely develop cancer of the floor of the mouth.

Mucosal atrophy increases the risk of oral cancers. Chronic iron deficiency leading to Plummer-Vinson syndrome alters mucosal tissues, which might account for the increased incidence of oral carcinoma associated with the condition. The atrophic glossitis of tertiary syphilis might account for the increased incidence of tongue cancer associated with the condition.

Use of betel quid, a stimulant composed of a betel leaf combined with areca nut and/or tobacco and placed between the lip/cheeks and gingiva, is common among natives of southeastern Asia and is another well-established risk factor for oral cancer.

Purported, but not fully established, risk factors include chronic mucosal irritation, use of smokeless tobacco, and human papillomavirus (HPV) infection. Chronic irritation of the oral mucosa by ill-fitting dentures, poorly restored teeth, or particularly spicy diets has often been mentioned as contributing to the development of oral carcinoma; however, no epidemiologic data support this view. Similarly, while smokeless tobacco use can be detrimental to oral and systemic health, its role as an independent risk factor for oral cancer development remains controversial. Human papillomavirus is an important risk factor for oropharyngeal cancer (see later discussion) but is less well established as a risk factor for oral cancer, identified in 0% to 10% of oral cancer tumors.

Epidemiology and Risk Factors for Oropharyngeal Cancer

Overall incidence is increasing due to the rise in sexually transmitted oral human papillomavirus (HPV) infection. HPV-positive disease (especially involving the HPV-16 strain) now accounts for as much as 42% to 87% of cases. These squamous cell cancers constitute at least two distinct clinicopathologic entities related to their risk factors. Those associated with smoking and alcohol excess demonstrate a worse prognosis and greater refractoriness to treatment than HPV-positive disease. Epidemiologic evidence finds little interaction between HPV-positive and HPV-negative disease, suggesting separate disease mechanisms, although smoking worsens the prognosis for both.

Risk Factors for Lip Cancer

Cancer of the lip has a risk-factor profile more similar to skin cancer having a particularly high incidence among fair-skinned people whose occupation or residence subjects them to prolonged sun exposure. Pipe smoking also increases risk for cancer of the lip.