 |
Oral inflammation and ulcers, known as stomatitis, may be mild and localized or severe, widespread, and painful. Symptoms are caused by inflammation of the oral mucosa. Stomatitis may involve swelling and redness of the oral mucosa or discrete, painful ulcers (single or multiple). Less commonly, whitish lesions are produced, and, rarely, the mouth appears normal (burning mouth syndrome) despite significant symptoms. Symptoms hinder eating, sometimes leading to dehydration and malnutrition. Secondary infection occasionally occurs. Some conditions are recurrent.
Stomatitis may be caused by infection, systemic disease, a physical or chemical irritant, or an allergic reaction; many cases are idiopathic (see Approach to the Patient With Nasal, Oral, and Pharyngeal Symptoms: Recurrent Aphthous Stomatitis). Because the normal flow of saliva protects the mucosa against many insults, xerostomia (see Approach to the Patient With Nasal, Oral, and Pharyngeal Symptoms: Xerostomia) predisposes the mouth to stomatitis of any cause.
Infections:
Viral causes are most common, but bacteria and fungi are sometimes involved. Oral infections can be clinically significant in immunocompromised patients.
Primary herpes simplex infection produces multiple vesicular lesions on the intraoral mucosa on both keratinized and nonkeratinized surfaces and always includes the gingiva. These lesions rapidly ulcerate. Clinical manifestation occurs most often in children. Subsequent reactivations (secondary herpes simplex, “cold sore”), however, usually appear on the lip at the vermilion border and, rarely, on the hard palate.
Primary varicella zoster infection (chickenpox) often produces vesicles on the oral mucosa. Reactivation (shingles) produces similar lesions in the distribution of a nerve root; if the trigeminal nerve is involved, unilateral oral ulcers may result.
Many other viruses are involved. Coxsackievirus can produce hand-foot-and-mouth disease in young children, with both cutaneous and intraoral lesions, or herpangina, with isolated oral ulcers. Other infections include Epstein-Barr virus, influenza, cytomegalovirus, and HIV.
Acute necrotizing ulcerative gingivitis (see Common Dental Disorders: Acute Necrotizing Ulcerative Gingivitis (ANUG)) is a nonspecific, mainly fusospirochetal bacterial infection producing inflammation and punched-out ulcers on the dental papillae and marginal gingivae. A severe variant, termed noma (gangrenous stomatitis), can produce full-thickness tissue destruction (sometimes involving the lips or cheek), typically in a debilitated patient. It begins as a gingival, buccal, or palatal (midline lethal granuloma) ulcer that becomes necrotic and spreads rapidly. Tissue sloughing may occur.
Sexually transmitted diseases can produce stomatitis. Gonorrhea very rarely produces burning ulcers and erythema of the gingiva and tongue as well as the more common pharyngitis. Primary syphilis chancres may appear in the mouth, and about 20% of patients with secondary syphilis develop painless, shallow oral mucosal ulcers (mucous patch), typically with a yellow or gray base and slight surrounding erythema. Tertiary syphilis may produce oral gummas or a generalized glossitis and mucosal atrophy. The site of a gumma is the only time that squamous cell carcinoma will develop on the dorsum of the tongue.
Rare bacterial causes include Mycobacterium
tuberculosis
, inoculated by sputum from the lungs. Cervicofacial bacterial actinomycosis (lumpy jaw) may resemble a fungal infection and may contain pathognomonic yellow (sulfur) granules in purulent exudate.
Candida albicans and related species, which are normal oral flora, can overgrow in people who have taken antibiotics or corticosteroids or who are debilitated, such as patients with AIDS. Overgrowth may produce a pseudomembrane with a cheesy substance on friable mucosa. The chronic erythematous and erosive forms are more common but are also more difficult to recognize. Oral and perioral lesions occur infrequently in blastomycosis, histoplasmosis, coccidioidomycosis, cryptococcosis (mainly in debilitated patients), and mucormycosis (particularly in people with diabetes).
Systemic
diseases:
Behçet's syndrome, Stevens-Johnson syndrome, and inflammatory bowel disease can produce bullous or ulcerative oral mucosal lesions. Pemphigoid and pemphigus vulgaris cause oral vesicles and ulcers. Sprue (gluten-sensitive enteropathy) may produce oral ulcers. Hemorrhagic oral lesions may occur in erythema multiforme, scurvy, leukemia, thrombocytopenic purpura, and platelet disorders. Unprovoked bleeding, xerostomia, and an ammonia-like odor accompany uremia. The mucocutaneous lymph node syndrome (Kawasaki disease) affects children, causing erythema of the lips and oral mucosa. Stomatitis may result from hypovitaminosis (particularly B vitamins or vitamin C), iron-deficiency anemia with dysphagia (as in Plummer-Vinson syndrome), or agranulocytosis. Pellagra produces a smooth, fiery red tongue; painful mouth; and mucosal ulcers.
Cyclic neutropenia is a rare condition probably caused by a defect in neutrophil maturation, resulting in regular, cyclic bouts of neutropenia (< 500/μL) with fever, malaise, lymphadenopathy, and oral ulcers. It usually presents in childhood.
Irritants
and allergies:
Physical irritation is frequently involved. Cheek biting, mouth breathing, jagged teeth, orthodontic appliances, ill-fitting dentures, and nursing bottles with nipples that are hard or too long may cause stomatitis. Other contributors are excessive use of alcohol, tobacco, hot foods, and spices.
Drugs and chemicals may be sensitizing (typically resulting in a type IV hypersensitivity reaction) or directly irritating (ie, triggering inflammatory mediator release without involvement of memory T cells or IgE). Common substances include ingredients in toothpaste, mouthwash, candy, gum (especially if made from chicle), dyes, lipstick, and, rarely, dental materials. Stomatitis also may result from occupational exposure to dyes, heavy metals, acid fumes, or metal or mineral dust. Many drugs are implicated in stomatitis. The most common are cytotoxic cancer chemotherapy drugs, and gold salts. Nicorandil (K channel blocker), iodides, barbiturates, and NSAIDs are rare causes. Some foods, especially highly acidic ones, may produce oral ulcers.
Evaluation
History:
Occasionally, causes are obvious in the history (eg, cytotoxic chemotherapy). Relation of symptoms to food, drugs, and other substances is sought. Recurrent GI symptoms suggest inflammatory bowel disease or sprue. Ocular symptoms suggest Behçet's syndrome. Nonspecific symptoms suggesting chronic illness (weight loss, malaise, fever) and risk factors for HIV infection are important.
Physical examination:
Cutaneous bullae suggest Stevens-Johnson syndrome, pemphigus vulgaris, or pemphigoid. Cutaneous vesicles suggest chickenpox or herpes zoster. Other cutaneous lesions may implicate erythema multiforme, hand-foot-and-mouth disease, or secondary syphilis.
Location of oral lesions may help; interdental ulcers occur with herpes simplex or acute necrotizing ulcerative gingivitis. Lesions on keratinized surfaces suggest herpes simplex, recurrent aphthous stomatitis, or physical injury. Unilateral lesions suggest herpes zoster.
Testing:
Clues suggesting specific diseases are pursued, as discussed elsewhere in The Manual. Patients with acute stomatitis and no symptoms, signs, or risk factors for systemic illness probably require no testing. If stomatitis is recurrent, viral and bacterial cultures, CBC, serum iron, ferritin, vitamin B12, folate, zinc, and endomysial antibody (for sprue) are obtained. Biopsy at the periphery of normal and abnormal tissue can be done for persistent lesions that do not have an obvious etiology. Systematically eliminating foods from the diet can be useful, as can changing brands of toothpaste or mouthwash.
Treatment
Underlying disorders are treated. Meticulous oral hygiene (using a soft toothbrush) may help prevent secondary infection. A soft diet that does not include acidic or salty foods is followed.
Numerous topical treatments, alone or in combination, are used to ease symptoms. These treatments include anesthetics, protective coatings, corticosteroids, antibiotics, antihistamines, and physical measures such as cautery.
For topical anesthesia, 5 mL of 2% viscous lidocaine is diluted in 10 mL water and used as a rinse and then expectorated q 3 h. A carboxymethylcellulose paste with or without 1% triamcinolone qid reduces irritation of painful local lesions. Other topical drugs include sucralfate and aluminum-magnesium liquid antacids; 30 mL of these drugs may be used alone but are often mixed with 2% viscous lidocaine 5 mL and diphenhydramine (an antihistamine with mild local anesthetic properties) and, often, kaolin, 12.5 mg to rinse and expectorate. Some physicians add tetracycline or nystatin suspension. If an infectious etiology is unlikely, fluocinonide gel may be applied to each ulcer. Amlexanox 5% paste can be applied qid (1⁄4 on tip of finger, wiped across ulcer).
Chemical or physical cautery can ease pain. Silver nitrate sticks are not as effective as low-power (2- to 3-watt), defocused, pulsed-mode CO2 laser treatments, after which pain relief is immediate and lesions tend not to recur locally.
Recurrent
Aphthous Stomatitis
Recurrent
aphthous stomatitis is a common condition in which round or ovoid
painful ulcers recur on the oral mucosa. Etiology is unclear. Diagnosis
is clinical. Treatment is symptomatic and usually includes topical
corticosteroids.
Recurrent aphthous stomatitis (RAS) affects 20 to 30% of adults and a greater percentage of children at some time in their lives. Etiology is unclear, but RAS tends to run in families. The damage is predominately cell-mediated. Cytokines, such as IL-2, IL-10, and, particularly, tumor necrosis factor-α, play a role.
Predisposing factors include oral trauma, stress, and foods, particularly chocolate, coffee, peanuts, eggs, cereals, almonds, strawberries, cheese, and tomatoes, although allergy does not appear to be involved. Factors that may, for unknown reasons, be protective include oral contraceptives, pregnancy, and tobacco, including smokeless tobacco and nicotine -containing tablets.
Symptoms and Signs
Symptoms and signs usually begin in childhood (80% of patients are < 30 yr) and decrease in frequency and severity with aging. Symptoms may involve as few as one ulcer 2 to 4 times/yr or almost continuous disease, with new ulcers forming as old ones heal. Pain or burning for 1 to 2 days precedes ulcers, but there are no antecedent vesicles or bullae. Severe pain, disproportional to the size of the lesion, can last from 4 to 7 days.
Ulcers are well-demarcated, shallow, ovoid, or round and have a necrotic center with a yellow-gray pseudomembrane, a red halo, and slightly raised red margins.
Minor aphthae (Mikulicz's) account for 85% of cases. They occur on the floor of the mouth, lateral and ventral tongue, buccal mucosa, and pharynx; are < 8 mm (typically 2 to 3 mm); and heal in 10 days without scarring.
Major aphthae (Sutton's disease, periadenitis mucosa necrotica recurrens) constitute 10% of cases. Appearing after puberty, the prodrome is more intense and the ulcers deeper, larger (> 1 cm), and longer lasting (weeks to months) than minor aphthae. They appear in the lips, soft palate, and throat. Fever, dysphagia, malaise, and scarring may occur.
Herpetiform ulcers (morphologically resembling but unrelated to herpesvirus) account for 5% of cases. They begin as multiple (up to 100) 1- to 3-mm crops of small, painful clusters of ulcers on an erythematous base. They coalesce to form larger ulcers that last 2 wk. They tend to occur in women and at a later age of onset than do other forms of RAS.
Diagnosis
Evaluation proceeds as described above under stomatitis. Diagnosis is based on appearance and on exclusion, because there are no definitive histologic features or laboratory tests.
Primary oral herpes simplex may mimic RAS but usually occurs in younger children, always involves the gingiva and may affect any keratinized mucosa (hard palate, attached gingiva, dorsum of tongue), and is associated with systemic symptoms. Viral culture can be performed to identify herpes simplex. Recurrent herpetic lesions are usually unilateral.
Similar recurrent episodes can occur with Behçet's syndrome, inflammatory bowel disease, sprue, HIV infection, and nutritional deficiencies; these conditions generally have systemic symptoms and signs. Isolated recurrent oral ulcers can occur with herpes infection, HIV, and, rarely, nutritional deficiency. Viral testing and serum hematologic tests can identify these conditions.
Drug reactions may mimic RAS but are usually temporally related to ingestion. However, reactions to foods or dental products may be difficult to identify; sequential elimination may be necessary.
Treatment
General treatments for stomatitis (see Approach to the Patient With Nasal, Oral, and Pharyngeal Symptoms: Treatment) may help patients with RAS. Chlorhexidine gluconate mouthwashes and topical corticosteroids, the mainstays of therapy, should be used during the prodrome, if possible. The corticosteroid can be dexamethasone 0.5 mg/5 mL tid used as a rinse and then expectorated or clobetasol ointment 0.05% or fluocinonide ointment 0.05% in carbymethylcellulose mucosal protective paste (1:1) applied tid. Patients using these corticosteroids should be monitored for candidiasis. If topical corticosteroids are ineffective, prednisone (eg, 40 mg po once/day) may be needed for ≤ 5 days. Continuous or particularly severe RAS is best treated by a specialist in oral medicine. Treatment may require prolonged systemic corticosteroids, azathioprine or other immunosuppressants, pentoxifylline , or thalidomide . Intralesional injections can be done with betamethasone , dexamethasone , or triamcinolone . Supplemental B1, B2, B6, B12, folic acid, or iron lessens RAS in some patients.
Last full review/revision November 2005
Content last modified November 2005
| |
