Mucous Membrane Disorders

Definition

Aphthous stomatitis is a common, recurrent, idiopathic disorder of the mouth most often manifest by multiple small, “punched-out” ulcers ( Fig. 22.1 ).

Incidence

Recurrent aphthous stomatitis is a common disease, occurring in 20% to 60% of the general population. It is most common in young adults; the 60% prevalence was found in a survey of students attending professional schools.

History

A history of previous episodes is invariable. Recurrences are sometimes precipitated by trauma from biting or misguided toothbrushes. Some patients correlate outbreaks with emotional stress. Lesions are usually preceded by a 1-day prodrome of discomfort in the area of involvement. The ulcers are painful and sometimes interfere with eating.

Physical Examination

Lesions in aphthous stomatitis appear as 2- to 5-mm, round, punched-out ulcers with a yellowish necrotic surface and surrounding erythema. Lesions may be single but more often are multiple. The buccal and labial mucosae are the most common locations.

Differential Diagnosis

Recurrent aphthous stomatitis is most often confused with herpes simplex infection . Recurrent herpes simplex rarely occurs inside the mouth. When it does, it appears as grouped small vesicles or erosions on an erythematous base. A Tzanck preparation or culture proves the diagnosis of herpes infection.

The oral ulcerations in Behçeťs syndrome are indistinguishable from those of aphthous stomatitis. However, Behçeťs syndrome is distinguished by its extraoral manifestations. The classic triad consists of oral ulcerations, genital ulcerations, and ocular inflammation (iridocyclitis) ( Fig. 22.2 ). Erythema nodosum, thrombophlebitis, arthritis, and neurologic and intestinal involvement may also occur. Patients with inflammatory bowel disease, particularly ulcerative colitis , occasionally have oral ulcerations that resemble aphthous stomatitis.

Laboratory and Biopsy

Usually, a biopsy is not required. If a biopsy is performed, the findings will not be diagnostic and will show only ulceration and nonspecific inflammation, composed primarily of lymphocytes. The only other laboratory test to consider is a complete blood count, to screen for the questionable association of iron or folate deficiency anemia in some patients with aphthous stomatitis.

Therapy

The variety of therapies that have been recommended for this disease indicates that a highly successful treatment is lacking. If an underlying iron or folate deficiency is detected, it should be corrected. The ulcerations are usually treated topically. Tetracycline suspension (250 mg/5 mL) “swished and swallowed” four times daily helps in some patients. Patients in whom tetracycline therapy fails are treated with topical steroids in a gel (e.g., fluocinonide, Lidex gel) or a special adherent base (e.g., triamcinolone, Kenalog in Orabase) applied three times daily or with a spray preparation (e.g., beclomethasone, Vanceril) applied three to four times daily. Intralesional steroids (triamcinolone, Kenalog-10) are useful in patients with large aphthous ulcerations. Oral prednisone is effective in aphthous stomatitis but should be used for only a short course in patients with severe, incapacitating disease. Colchicine and pentoxifylline (Trental) have also been reported to be helpful in preventing recurrent disease, but the clinical trials were not controlled.

Pain relief can be obtained with topical anesthetics such as dyclonine hydrochloride (Dyclone liquid) or topical lidocaine (viscous Xylocaine) used 20 minutes before meals. These preparations numb the entire mouth, including the taste buds, for 1 to 2 hours and allow for pain-free, albeit taste-free, dining.

Course and Complications

For minor aphthous stomatitis, spontaneous healing occurs within 4 to 14 days. Large aphthous ulcers (major aphthous ulcers) take as long as 6 weeks to heal. Individual ulcers lasting much longer than that should be examined by biopsy to rule out malignancy. Recurrences are common and range in frequency from occasional to almost continuous. In most patients, the disease eventually remits, but the time course is highly variable – from 5 to 15 years or longer.

Pathogenesis

Factors implicated in the pathogenesis include emotional and physical stress, hormones, infection, and autoimmunity. An immune mechanism is the most favored cause. Circulating T lymphocytes cytotoxic against oral mucosa have been identified and appear to play a role.

Definition

Leukoplakia literally means “white plaque” ( Fig. 22.3 ). Some clinicians simply use that as the definition of the disease, defining leukoplakia as “a white patch or plaque that cannot be characterized clinically or pathologically as any other disease.” Others use the term leukokeratosis to describe a white patch that is histologically benign, and reserve the term leukoplakia for a white patch or plaque in which epithelial dysplasia is present pathologically. The authors prefer the second definition. Either way, the important point to remember is that, for white plaques on mucous membranes, a dysplastic change should be considered a possible cause.

The white color is due to macerated hyperkeratosis, which, in most cases, is caused by chronic irritation. Smoking is the most frequent origin, but physical irritation from dentures or ragged teeth may also be causative.

Incidence

Leukoplakia is an uncommon disorder affecting primarily middle-aged and elderly adults. The incidence depends, of course, on the definition. The disease is about one-tenth as common when dysplastic histologic changes are required criteria.

History

The onset is gradual and usually asymptomatic. Accordingly, leukoplakia is sometimes an incidental finding during a routine physical examination. Some patients seek medical attention because of irritation, which may be the original cause of the problem. Many patients are smokers or have used smokeless tobacco.

Physical Findings

Leukoplakia appears as a white patch or plaque on the mucous membrane. The surface may be flat or verrucous, and the color varies from pure white to gray. It can be located anywhere in the mouth, including the lips. The tongue is a common location, but leukoplakia can occur on the tonsils, pharynx, or larynx. Leukoplakia may also be found on genital mucosa.

All white lesions should be palpated for induration. Induration and ulceration are important physical findings that strongly suggest carcinoma ( Fig. 22.4 ). Sometimes, only part of a white plaque is indurated, and this area should be examined by biopsy to rule out cancer.

Differential Diagnosis

The differential diagnosis of white lesions in the mouth is given in Table 22.1 . The reticulated form of oral lichen planus is usually clinically distinctive. Mucous patches in secondary syphilis are accompanied by other manifestations of that disease, including skin rash and constitutional symptoms. White sponge nevus is a hereditary condition that begins in childhood and results in a white lesion that appears “spongy” ( Fig. 22.5 ). Leukokeratosis is a diagnosis of exclusion that clinically does not fit another known entity and histopathologically shows no dysplastic changes. The diagnosis then often rests with the biopsy.

Oral hairy leukoplakia affects the sides of the tongue with white papules and plaques that sometimes have a filiform (“hairy”) surface ( Fig. 22.6 ). This disorder occurs almost exclusively in patients with acquired immune deficiency syndrome (AIDS) and may be the first sign of human immunodeficiency virus (HIV) infection. It is asymptomatic, not premalignant, and is now known to be caused by infection with Epstein–Barr virus. Treatment with acyclovir and other antiviral agents can cause the condition to regress. With advances in treatment for HIV infection, this disease is rarely seen in the United States.