Tongue cancer risk factors

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]

Overview

The most potent risk factor in the development of oral cancer is alcohol intake, tobacco use and human papillomavirus transmitted through sexual contact. The other risk factors include history of betel quid intake, male gender, age over 55 year, ultraviolet light, Fanconi anemia, dyskeratosis congenita, lichen planus, graft-versus-host disease (GVHD), immune system suppression, mouthwash and irritation from dentures.

Risk Factors

The major risk factors in the development of tongue cancer includes the following:

• Tobacco smoking
  • Cancer of the tongue is correlated the closest with the use of tobacco products.
  • Approximately 90% of patients with oral cavity cancers use tobacco products and that the relative risk of oral cavity cancers increases with the amount smoked and the duration of the smoking.
  • In persons who smoke the incidence of oral cavity cancers is approximately six times that of those who do not smoke.
  • Tobacco exposure causes progressive sequential histological changes to the oral mucosa. Prolonged period of exposure eventually leads to neoplastic transformation, in particular changes in the expression of p53 mutations. If the tobacco exposure is discontinued, these changes may be reversible.
  • There is compelling evidence supporting the benefit for head and neck cancer patients to cease smoking after treatment for their cancer. Approximately 40% of patients who continued to smoke after definitive treatment for an oral cavity malignancy developed recurrence or developed a second head and neck malignancy. In patients who stopped smoking after treatment, approximately 6% went on to develop a recurrence.
  • There has been recent increase in the incidence of oral cavity cancer in young adults in the recent years. The explosive use of smokeless tobacco, or snuff, in certain regions of the United States has lead to increased numbers of mandibular alveolus, buccal mucosa, and tongue cancers.
• Alcohol ingestion
  • The correlation between alcohol consumption, particularly hard liquor, and oral cavity cancer is significant, especially in patients taking more than four consumptions per day.
  • Approximately 75% of patients who develop oral cavity cancers consume alcohol, and the cancer occurs six times more often in persons who drink than in those who do not drink. The role of alcohol consumption in the development of tongue cancer appears to be independent of smoking.
  • The use of alcohol has a synergistic effect on the risk of carcinogenesis rather than cumulative effect. The risk for a person who drinks alcohol and smokes tobacco is fifteen times that of an individual with neither of these habits.
• Human papillomavirus
  • The human papillomavirus, is an etiologic agent for carcinogenesis in the tongue cancer. Human papillomavirus (HPV) has been detected in various amounts in persons with leukoplakia, oral dysplasia, and malignancy. In the subset of patients without other risk factors, HPV should be considered as an etiologic factor. Human papillomavirus (HPV), especially HPV type 16.
• Plummer-Vinson syndrome
  • Plummer-Vinson syndrome (Fe deficiency anemia; achlorhydria; and mucosal atrophy of the mouth, pharynx, and esophagus) has been associated with an increased risk of cancer of the tongue. Studies have suggested that vitamins A and C, along with the carotenoids, may be protective against epithelial cancers. Iron and riboflavin deficiencies are known to produce dysplastic changes to the oral mucosa.

Precancerous lesions

Oral leukoplakia

• Leukoplaki is A white plaque it often occurs in individuals under the age of 40[12].
• Leukoplakia is seen six times more among smokers than among non-smokers[1].
• Leukoplakia can be divided into two subtypes including homogeneous and non-homogeneous types[1].
• Homogenous lesions are characterized by uniformly flat, thin, uniformly white in colour and shows shallow cracks of the surface keratin[1,13].
• Nonhomogenous lesions have been defined as a white and red lesion (known as erythroleukoplakia) that may be either irregularly flat (speckled) or nodular (Figure 1).
• Verrucous leukoplakia is yet another type of non-homogenous leukoplakia[ 14].
• Histopathologically, two distinct appearances may be seen as dysplastic or non-dysplastic leukoplakia.

Risk factors of malignant transformation

• Female gender
• Long duration of leukoplakia
• Leukoplakia in non-smokers
• Location on the tongue and/or floor of the mouth
• Size > 200 mm2
• Non-homogenous type
• Presence of epithelial dysplasia

The diseases should be considered in the differential diagnosis including aspirin burn, chemical injury, oral pseudomembranous and hyperplastic candidiasis,

frictional lesions, oral hairy leukoplakia, leukoedema, linea alba, lupus erythematosus, morsicatio buccarum, papilloma and allied lesions, mucous patches in secondary syphilis, tobacco-induced lesions, smoker’s palate (nicotinic stomatitis), stuff-induced lesion, white sponge nevus, oral lichen planus (OLP), and lichenoid reaction[1,13].

Oral leukoplakia should be confirmed by mucosal biopsy.

Surgical excision should be recommended in the presence of moderate and severe epithelial dysplasia.

Recurrence of leukoplakia was reported as approximately 50% after withdrawing the topical retinoic acid[21].

Oral erythroplakia

• Erythroplakia is a red patch that cannot be characterized clinically or pathologically as any other definable disease.
• It mainly occurs in the middle aged and the elderly.
• Most commonly affected areas were reported as the soft palate, the floor of the mouth, and the buccal mucosa[14,22].
• Chewing tobacco and alcohol use are the possible etiologic factors for the development erythroplakia.[23]
• Typical lesion of oral erythroplakia is less than 1.5 cm in diameter, but it also be less than 1 cm and larger than 4 cm[22].
• Histopathologically, moderate or severe dysplasia was usually seen in lesion with erythroplakia.
• Malignant transformation rates is very high (vary from 14% to 50%), so it needs to be treated expeditiously.[14,22].
• Early effective treatment is mandatory.[22]
• Surgery is the recommended therapy.[1]

Oral lichen planus

• The disease is a chronic, autoimmune, inflammatory disease which may affect skin, oral mucosa, genital mucosa, scalp, and nails[26].
• It mainly occurs among female gender and the age of onset is usually between third and sixth decade[25,27] [28].
• OLP may be seen as six types including papular, reticular, plaque-like, atrophic, erosive, and bullous type[25].

• lesions present symmetrically and bilaterally, and usually asymptomatic. Atrophic pattern presents as a red lesion. Erosive pattern is usually seen as irregular erosion or ulceration covered with a fibrinous plaque or pseudomembrane. atrophic and erosive pattern are generally associated with a burning sensation and pain that exacerbated by trauma and hot, spicy or acidic foods.

• Multifocal plaque type lesions may be seen.
• This subtype is more common among tobacco smokers.
• The papular pattern, which is rarely seen, is characterized by small, white, raised papules with fine white striation at the periphery of the lesion.
• Bullous pattern is the least common type of OLP that characterized by bullae formation range from a few millimeters to several centimeters in diameter[26].

• histologic features include liquefactive degeneration of the basal cells, colloid bodies (known as Civatte bodies), homogenous infiltrate of lymphocytes in a dense, band-like pattern along the epithelium-connective tissue interface in the superficial dermis, cytologically normal maturation of the epithelium, sawtooth rete ridges, and hyperkeratosis. In erosive lichen planus, ulceration may be seen in the surface epithelium[31].

• Malignant transformation ratio has been reported in 0% to 10% of patients, according to the sample’s characteristics and study design, after mean follow-up of 1.5 to 10 years[25].

• Increased malignant transformation risk occurs greater in erosive and atrophic forms and in cases of lesions of lateral border of the tongue[27].

• Other factors
  • A number of other factors have been associated with an increased incidence of tongue cancer such as the use of the product of the areca catechu tree, the betel nuts or quid as well as the use of slaked lime. This mixture is highly irritating to the oral mucosa, and as well as carcinogenic.
  • The mutations in tumor suppressor genes has been reported in patients with cancers of the oral cavity. The most abundant carcinogens in tobacco constitute nitrosamines. Nitrosamines can damage DNA, leading to point mutations. These point mutations lead to deregulation of tumor suppressor genes (TP53), which is located on chromosome 17. The other oncogenes associated with oral squamous cell cancers of tongue include c-myc and erb -b1.

Other less potent risk factors includes the following:

• Lifestyle
  • Betel quid
• Genetics
  • Fanconi anemia
  • Dyskeratosis congenital
  • Family history of squamous cell carcinoma
• General
  • Male gender
  • Ultraviolet light
  • Age over 55 year
  • Graft-versus-host disease(GVHD)
  • Immune system suppression
  • Lichen planus
• Unproven risk factors
  • Mouthwash
  • Irritation from dentures