Cancers of the Oral Mucosa Clinical Presentation

Updated: Jun 29, 2017
  • Author: Chelsia Q Sim, DDS, MSc; Chief Editor: Dirk M Elston, MD  more...
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Presentation

History

Some oral squamous cell carcinomas (OSCCs) arise in apparently normal mucosa, but many are preceded by clinically obvious potentially malignant disorders, especially erythroplakia (red patch), leukoplakia (white patch), erythroleukoplakia (red and white patch), or verrucous leukoplakia. Many others are associated with such lesions (especially in Southeast Asia). The challenges in predicting which oral mucosal potentially malignant disorder will progress to neoplasia are discussed more fully elsewhere. [8]

Erythroplastic lesions are velvety red plaques, with a prevalence ranging from 0.01-0.21%, [9, 10] which, in at least 90% of cases, show severe dysplasia or frank malignancy. In contrast, most white lesions are not malignant or premalignant. Speckled or verrucous leukoplakias are more likely to be premalignant. The prevalence of leukoplakias as compared with erythroplakia is higher, and severe dysplasia or carcinomatous change is more common in erythroplakia. Homogeneous leukoplakias are only very occasionally premalignant, but speckled or verrucous leukoplakias are more likely to be premalignant. In a study of 257 patients with oral leukoplakia, Silverman et al followed these patients over a mean period of 7.2 years. Of these patients, 17.5% developed carcinoma. The time from initial diagnosis of either epithelial dysplasia or hyperkeratosis to carcinoma ranged from 6 months to 39 years. [11]

In most cases, a biopsy with histologic examination is required because dysplasia may precede malignant changes. The rate of malignant changes can be as high as 36% when moderate or severe dysplasia is present. Be aware that single ulcers, lumps, red patches, or white patches (particularly if they persist >3 wk) may be manifestations of malignancy.

OSCC may manifest as the following:

  • A red lesion (erythroplakia)

  • A granular ulcer with fissuring or raised exophytic margins

  • A white or mixed white and red lesion

  • An indurated lump/ulcer (ie, a firm infiltration beneath the mucosa)

  • A nonhealing extraction socket

  • A lesion fixed to deeper tissues or to overlying skin or mucosa

  • Cervical lymph node enlargement, especially if hardness is present in a lymph node or fixation. Enlarged nodes in a patient with oral carcinoma may be caused by infection, reactive hyperplasia secondary to the tumor, or metastatic disease. Occasionally, a lymph node is detected in the absence of any obvious primary tumor. Nodal enlargement is a feature particularly in oropharyngeal cancers.

These potentially malignant disorders and OSCC should be detected at an early stage; however, many OSCCs still are seen only when advanced. Diagnosis is often delayed by up to 6 months, even in developed countries, despite exhortations over the past 25 years to increase the index of suspicion. Early detection and treatment is the short-term goal because this results in considerably better survival rates. Early carcinomas may not be painful; however, later, they may cause pain and difficulty with speech and swallowing.

Dental practitioners and dental care professionals should remain vigilant for signs of potentially malignant disorders and oral cancer while performing routine oral examinations. [12]

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Physical Examination

A systematic and thorough examination of the mouth, fauces, and cervical lymph nodes should be performed by a clinician trained in the diagnosis of oral diseases, and a general physical examination is indicated. Dental practitioners and dental care professionals are trained in the examination of the mouth. Examine the teeth, periodontium, and entire mucosa in good lighting.

In those with oral squamous cell carcinoma (OSCC), advanced caries, periodontal disease, or periapical lesions may need early attention, especially if radiotherapy is to be used in the management of OSCC.

The most common sites of OSCC include the tongue, mainly the lateral and ventrolateral aspects, and the floor of the mouth; however, all areas should be scrutinized. A common site for OSCC is the posterior portion of the tongue, which may be missed on cursory inspection; hence, special care is needed to ensure close examination.

The clinical appearance of oral cancer is highly variable and includes ulcers, red or white areas, lumps, or fissures. Lesions always must be palpated after inspection to detect induration and fixation to deeper tissues.

Erythroplakia is a red and often velvety lesion, which, unlike leukoplakias, may not form a plaque but is level with or depressed below the surrounding mucosa. Of these lesions, 75-90% may show severe epithelial dysplasia, carcinoma in situ, or invasive changes. Erythroplakia can affect patients of either sex in their sixth and seventh decades and typically involves the floor of the mouth, the ventral surface of the tongue, or the soft palate. Red oral lesions usually are more dangerous than white oral lesions.

Oral mucosal white patches usually result from increased keratinization or candidosis. Leukoplakia is restricted to white patches for which a cause cannot be established; therefore, the term implies a diagnosis by exclusion (eg, lichen planus, candidiasis). The term leukoplakia is also used irrespective of the presence or absence of epithelial dysplasia. Leukoplakia is a clinical term for a persistent adherent white patch with no histologic connotation and no implied premalignant potential. Some OSCC can also appear as a white patch.

Late OSCC may manifest as an exophytic lesion or an area of ulceration with induration.

A typical malignant ulcer is hard with heaped-up and often everted or rolled edges and a granular floor, as shown in the image below.

Oral squamous cell carcinoma (OSCC) presenting as Oral squamous cell carcinoma (OSCC) presenting as a large, ulcerated lump on the left anterior lateral border of the tongue.

 The floor of the mouth is the second most common intraoral site for cancer and more commonly is associated with leukoplakia. Most cancer arises in the anterior floor of the mouth as an indurated mass that soon ulcerates, resulting in slurring of speech.

Carcinomas of the alveolus or gingiva can present as an exophytic mass or a persistent ulcer. The underlying alveolar bone is invaded in 50% of cases, even in the absence of radiographic changes, and adjacent teeth may be loose.

Carcinomas of the buccal mucosa are mostly seen at the commissure or in the retromolar area. Most are ulcerated lumps, and some arise in candidal leukoplakias.

Any single lesion that persists more than 3 weeks, especially if red, ulcerated, or a lump, especially with induration (ie, the RULE mnemonic) should be regarded with suspicion and a histopathological diagnosis established. [2]

Second primary tumors are additional primary carcinomas (synchronous tumors) present in as many as 10-15% of persons with oral carcinoma and are most commonly seen in the mouth in patients with gingival, floor of mouth, lingual, or buccal carcinoma. Second primary tumors may also be present elsewhere in the upper aerodigestive tract.

Lymph node examination is of paramount importance, and general examination and, possibly, endoscopy, may be indicated to detect metastases or second primary tumors. From 30-80% of patients with oral cancer have metastases in the cervical lymph nodes at presentation. Oral cancer predominantly metastasizes locally and to regional lymph nodes, primarily in the anterior neck. Later, dissemination to the lungs, liver, or bones may occur.

Any chronic oral lesion should be regarded with suspicion, especially when found in an older patient, when lesions appear (see History), with induration, with fixation to underlying tissues, with any recent changes in appearance, with associated lymphadenopathy, or with no obvious explanation for the lesion. Examine the entire mucosa because widespread dysplastic mucosa (field change) or a second neoplasm (see Staging) may be present. Carefully record the location of suspicious lesions, preferably on a standard topographic diagram.

Table 1. Practical Clinical Tool for Evaluating Oral Mucosal Lesions (Open Table in a new window)

Issue

 

No Serious Concern

Concern: Consider Referral to Specialist if Clinician or Patient Concerned, Especially if Multiple Issues Apply

Serious Concern: Referral to a Specialist

Historical Features

Size

No change

No reduction in size, even after eliminating trauma to lesion after 10-14 days

Increasing size, even after eliminating trauma to lesion after 10-14 days

 

Chronology

Lesion heals

No resolution over brief observation period

Rapid symptom onset

Solitary lesion or change in one area of lesion

Lesion persisting 3 weeks or longer

Persistent ulceration

Persistent swelling

Loosening of a tooth

Nonhealing tooth extraction socket

 

Neurological

None

Lack of pain

Pain

Dysphagia

Odynophagia

Otalgia

Numbness/paresthesia

Speech or voice change

 

Weight

Normal

No weight loss

Weight loss

History

Lifestyle Habits

None

Tobacco consumption mild/moderate

Betel quid or khat consumption mild/moderate

Marijuana consumption mild/moderate

UV light exposure mild/moderate (lip surface exposure)

Late-onset sexual debut

Few or moderate numbers of lifetime sexual partners

Tobacco consumption high

Betel quid or khat consumption high

Alcohol consumption high

Marijuana consumption mild/moderate

UV light exposure high

Early sexual debut

Numerous lifetime sexual partners

 

Medical History

Clear

Deficiencies of iron or vitamins A, C, or E

Fanconi anemia

High-risk human papillomavirus (HPV) infection

Immune defects, including HIV/AIDS or chronic candidosis

Medications: Immunosuppressants, antihypertensives

Periodontitis, poor hygiene

Plummer-Vinson syndrome

Scleroderma

Xeroderma pigmentosum

Deficiencies of iron or vitamins A, C, or E

Fanconi anemia

High-risk HPV infection

Immune defects, including HIV/AIDS or chronic candidosis

Medications: Immunosuppressants, antihypertensives

Periodontitis, poor hygiene

Plummer-Vinson syndrome

Scleroderma

Xeroderma pigmentosum

Examination and Imaging

Potentially Malignant Disorder

None

Leukoplakia

Lichen planus/lichenoid mucositis

Oral submucous fibrosis

Erythroplakia

Leukoplakia; speckled or verrucous

Lichen planus/lichenoid mucositis; unilateral

 

Lesion Features

Equivocal

White patch (leukoplakia)

Lichen/lichenoid

Oral submucous fibrosis

Red patch (erythroplakia)

Mixed red and white patch (erythroleukoplakia/speckled leukoplakia)

Granular surface

Rolled, elevated margins

Ulceration

Induration

 

Cervical Lymph Nodes

No enlargement

Possible enlargement

Enlarged, firm, fixed, nontender, asymmetric

 

Imaging

No abnormality

Any bone density change

Poorly defined, uncorticated, irregular radiolucency

Lamina dura loss

Teeth displaced and/or resorbed

Pathological fracture

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Causes

Tobacco and alcohol use are independent risk factors for mouth cancer and tongue cancer. Heavy tobacco smokers have a 20-fold greater risk; heavy alcohol drinkers a 5-fold greater risk; those who do both have a 50-fold greater risk. Betel-quid chewing and oral snuff are important risk factors in people from specific geographic areas (eg, betel chewing in Southeast Asia). Finally, a diet low in fresh vegetables and fruits has also been implicated in causing oral squamous cell carcinoma (OSCC), and human papillomaviruses (HPVs) have been implicated in oropharyngeal cancers. [13]

  • Cigarette smoking: Compared with persons who do not smoke, the risk of oral cancer in persons who smoke low/medium-tar cigarettes and high-tar cigarettes was 8.5- and 16.4-fold greater, respectively. (Note that cigarettes are classified as low/medium if the tar yield is less than 22 mg and high tar if the tar yield is greater than 22 mg). Note the image below.

    Early oral squamous cell carcinoma in the buccal m Early oral squamous cell carcinoma in the buccal mucosa arising from a chronic candidal leukoplakia in a person who smokes heavily. The lesion was a painless, chronic indurated lump.
  • Alcohol: Growing evidence is associating increased alcohol consumption with the risk of developing OSCC. [14] Alcoholic beverages may contain carcinogens or procarcinogens, including nitrosamine and urethane contaminants and ethanol. Ethanol is metabolized by alcohol dehydrogenase and, to some extent, by cytochrome P450 to acetaldehyde, which may be carcinogenic. The combined effects of tobacco use and alcohol consumption are found to be multiplicative. Compared with persons who do not drink and do not smoke, the risk of developing OSCC is increased 80-fold in persons with the highest levels of smoking and alcohol consumption.

  • Betel and similar habits [15] : The betel quid contains a variety of ingredients, including betel vine leaf, betel (areca) nut, catechu, and, often, slaked lime together with tobacco. Some persons chew the nut only, and others prefer paan, which includes tobacco and sometimes lime and catechu. In 1986, the International Agency for Research on Cancer deemed betel-quid chewing an important risk factor, and the areca (betel) nut habit with or without tobacco use can cause cytogenetic changes in oral epithelium. Various other chewing habits, usually combinations that contain tobacco, are used in different cultures (eg, Qat, Shammah, Toombak). Tobacco chewing in people from parts of Asia appears to predispose to OSCC, particularly when it is started early in life and is used frequently and for prolonged periods. [16, 17] Studies from India have confirmed the association between paan tobacco chewing and OSCC, particularly cancer of the buccal and labial mucosa.

  • Diet: Dietary habits may play a role in the development of oral cancer. A diet rich in fresh fruits and vegetables with limited consumption of meats is recommended for prevention of cancer. Health supplements (vitamins, minerals, and other bioactive compounds) have not been shown to confer the same level of effectiveness in replacing these nutrients. Hence, these health supplements should not be used as substitute for vegetables and fruits in meals. [18]

  • Oral health [19] : A case-control study (ie, every oral cancer case prior to surgery and every control at the time of interview had a structured oral examination) from China found that wearing dentures, per se, is not a risk factor, although the risk was increased in men who wore dentures made from metal. Poor dentition, as reflected by missing teeth, emerged as a strong risk factor independent of other established risk factors.

  • Mouthwash use: The effect of the alcohol in mouthwash appears to be similar to that of alcohol used for drinking, although the contribution of mouthwash use to oral cancer must be small in terms of attributable risk. This controversy continues. [20, 21]

  • Socioeconomic status: Behaviors that lead to social instability or social instability itself have been linked to an increased risk of oral cancer, but many other explanations may exist (eg, habits, oral health, diet, nutrition).

  • Infective agents: Candida albicans and viruses, such as herpes viruses and papillomaviruses, may be implicated in some cases. HPVs are particularly implicated in oropharyngeal cancers. [22] HPV-related tumors tend to be seen in younger patients, in the fauces, and have usually a better prognosis.

  • Others: Associations also are apparent between oral cancer and other various oral conditions (eg, oral submucous fibrosis, oral lichen planus, lupus erythematosus, dyskeratosis congenita, Fanconi anemia).

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