Recurrent aphthous stomatitis

RAS, also known as canker sores, is a common and usually painful ulcerative condition of the mouth. Its prevalence in the United States may be as high as 20%. RAS is a recurring condition and may involve buccal, labial, tongue, and hard and soft palate mucosal surfaces. Ulcers are usually shallow; covered by gray, yellow, or white plaques; and accompanied by surrounding erythema.

RAS can be quite painful and may interfere with food intake and speech in some patients. Etiology of this condition is unknown; however, a strong genetic predisposition is observed.6 Precipitating factors include local trauma (e.g., dentures, orthodontic braces, toothbrush abrasion), salivary gland dysfunction, stress, local infections, nutritional deficiencies, GI disorders, systemic disorders, food allergy or hypersensitivity, hormonal fluctuations, and exposure to certain chemicals.7 RAS can occasionally be associated with such systemic conditions as HIV infection, Behcet’s syndrome, inflammatory bowel disease, and celiac disease.


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The three primary types of RAS are minor, major, and herpetiform, with the minor form being the most common. Minor aphthous ulcers are <10 mm in diameter and usually heal spontaneously in 10-14 days. Major aphthous ulcers (also called Sutton’s disease) are >1 cm in diameter, may take up to 30 days or more to heal, and may leave scars.8 Herpetiform ulcers are multiple, clustered, 1-3 mm lesions that may coalesce into plaques and usually heal in seven to 10 days.

Initial treatment goals include decreasing the number of ulcers, relieving pain, and, at times, reducing frequency.9 Most patients with minor aphthae require no treatment or only periodic topical therapy. Commonly used therapies include such topical corticosteroids as fluocinonide gel (Lidex) and triamcinolone acetonide with carboxymethylcellulose paste (Kenalog in Orabase). However, evidence in support of such treatments remains scarce.10

Chlorhexidine gluconate (Peridex) mouthwash decreases the severity of an episode but does not reduce the incidence of ulcers. Amlexanox 5% paste (Aphthasol) may promote healing and lessen pain. In severe or recurring cases, systemic therapy with such agents as thalidomide (Thalomid) may be necessary. Because of the risk of serious adverse effects and its off-label status, thalidomide generally is reserved for severe cases associated with HIV infection.11 A biopsy should be considered for solitary or multiple ulcers that last longer than three weeks. The need for additional analyses (e.g., serologic tests for rheumatologic disease), cultures, or other specific tests for infectious agents (i.e., herpes simplex virus, cytomegalovirus, or HIV) and evaluation for GI disease should be guided by the presence of features suggestive of these disorders.12

Leukoedema

Leukoedema, a very common condition of unknown origin that occurs in the oral mucosa, is characterized by diffuse, grayish-white wrinkles or streaks that cannot be removed but disappear upon stretching the cheek. This condition is commonly found bilaterally. Leukoedema occurs far more commonly in African-Americans than Caucasians, and it may be a variation of normal mucosa rather than a disease. Changes in mucosal pigmentation may make leukoedema easier to identify in African-Americans. Smoking may cause this condition to become more evident on examination. Leukoedema is considered a benign lesion and requires no treatment.13

Leukoplakia

The term leukoplakia applies to any white plaque or patch that does not fit the profile of any other disease, which makes it a diagnosis of exclusion. Other potential lesions must be ruled out before a diagnosis of leukoplakia can be justified. Sometimes, leukoplakia is considered a precancerous or premalignant lesion, and it usually affects people older than age 40 years, with a strong male predilection (2:1). There is also a close association between smoking and leukoplakia. Leukoplakia can be found on the lip vermillion, buccal mucosa, and gingiva and may have a translucent, fissured, wrinkled, soft, and flat appearance.13

The hyperkeratosis associated with leukoplakia is derived from the thickened keratin layer on the surface epithelium, which is visible microscopically. The keratin layer may consist of parakeratin, orthokeratin, or both, and this differentiation may help determine further classification of the leukoplakia in question. Leukoplakia may or may not show dysplastic changes on microscopic examination. If dysplastic changes exist, the severity is determined based on the layers of epithelium involved. Mild is limited to the basal and parabasal layers. Moderate involves the basal to the midportion of the spinous layer. Severe epithelial dysplasia incorporates changes from the basal layer to a point above the midline of the epithelium. When involving the entire epithelium, however, the term carcinoma in situ (CIS) is used. In contrast to SCC, CIS does not penetrate the basement membrane.13

It is impossible to determine which leukoplakic lesions have a serious histologic picture on clinical evaluation alone. Therefore, any leukoplakic lesion present for two weeks or more must be biopsied. The specimen should be taken from the area showing the most (or most severe) change. The treatment is dependent on the histologic features. If possible, a leukoplakia lesion with moderate dysplasia should be completely removed by surgical excision, electrocautery, laser ablation, or cryosurgery. Leukoplakia without dysplasia or with less severe dysplasia should be monitored and treated conservatively. If the lesion grows larger or shows increase in severity, additional biopsy should be performed. The patient should be encouraged to discontinue all irritants, including smoking and alcohol consumption.13

Squamous cell carcinoma

SCC comprises approximately 94% of all oral malignancies, and the cause is multifactorial. Multiple extrinsic and intrinsic factors have been identified, including tobacco, alcohol, syphilis, sunlight, radiation, immunosuppression, malnutrition, iron deficiency anemia, vitamin A deficiency, and presence of a precancerous lesion (e.g., leukoplakia). Oral SCC typically has one of the following presentations: Exophytic, endophytic, leukoplakic, erythroplakic, or erythroleukoplakic. The most common sites of occurrence for oral SCC are the posterior lateral and ventral surface of the tongue. Other possible locations include the soft palate, gingiva, buccal mucosa, labial mucosa, and hard palate.13

More than half of all intraoral cancers in the United States are located on the tongue, with two thirds of these lesions appearing as painless, firm masses or ulcerations of the posterior surface. Carcinomas of the oropharynx and soft palate tend to be more closely associated with increased size and metastasis. This is attributable to the patient being unaware of its existence thus delaying detection and diagnosis.13

Oral SCC is quantified by using the TNM classification system, which takes into consideration tumor size, presence of nodal involvement, and metastasis. Treatment for intraoral SCC is dependent on its clinical stage and can involve surgical excision, radiation therapy, or both. Chemotherapy agents are also used depending on clinical presentation and stage of the tumor. Patients with a small intraoral SCC should choose a single treatment modality, while those with larger or metastasized lesions should consider combination therapy.13