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 Stomatitis: A Merck Manual of Patient Symptoms podcast
Oral inflammation and ulcers, known as stomatitis, may be mild and localized or severe and widespread. They are invariably painful. Stomatitis may involve swelling and redness of the oral mucosa or discrete, painful ulcers (single or multiple). Less commonly, whitish lesions form, 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.
Etiology
Stomatitis may be caused by local infection, systemic disease, a physical or chemical irritant, or an allergic reaction (see Table 2: Symptoms of Dental and Oral Disorders: Some Causes of Stomatitis ); many cases are idiopathic. Because the normal flow of saliva protects the mucosa against many insults, xerostomia predisposes the mouth to stomatitis of any cause.
The most common specific causes overall include
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Table 2
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| Some Causes of Stomatitis |
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Category
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Examples
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Bacterial infections
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Actinomycosis*
Acute necrotizing ulcerative gingivitis
Gonorrhea
Syphilis, primary or secondary
TB*
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Fungal infections
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Blastomycosis*
Candidal infections (most common)
Coccidioidomycosis*
Cryptococcosis*
Mucormycosis* (more common in diabetics)
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Viral infections
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Herpes simplex infection, primary (mostly in young children)
Herpes simplex infection, secondary (cold sore on lip or palate)
Varicella zoster, primary (chickenpox)
Varicella zoster reactivation (shingles)
Others (eg, infection by coxsackievirus, cytomegalovirus, Epstein-Barr virus, or HIV; condyloma acuminata; influenza; rubeola)
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Systemic disorders
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Behçet's syndrome
Celiac sprue
Cyclic neutropenia
Erythema multiforme
Inflammatory bowel disease
Iron deficiency
Kawasaki disease
Leukemia
Pemphigoid, pemphigus vulgaris
Platelet disorders
Stevens-Johnson syndrome
Thrombotic thrombocytopenic purpura
Vitamin B deficiency (pellagra)
Vitamin C deficiency (scurvy)
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Drugs
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Antibiotics*
Anticonvulsants*
Barbiturates*
Chemotherapy drugs
Gold
Iodides*
NSAIDs*
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Physical irritation
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Dentures that fit poorly
Jagged teeth
Mouth biting
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Irritants and allergies
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Acidic foods
Occupational exposure to dyes, heavy metals, acid fumes, metal or mineral dust
Tobacco (nicotinic stomatitis, particularly pipe smoker's palate [hyperkeratotic palate with red dots at the openings of minor salivary glands])
Type IV hypersensitivity reaction (eg, to ingredients in toothpaste, mouthwash, candy, gum, dyes, lipstick, or dental restorations)
Aspirin applied topically
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Other
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Burning mouth syndrome
Lichen planus
Recurrent aphthous stomatitis (most commonly, minor aphthae)
Head and neck radiation
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*Rare.
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Evaluation
History:
History of present illness should ascertain the duration of symptoms and whether the patient ever had them previously. Presence and severity of pain should be noted. The relation of symptoms to food, drugs, and other substances (particularly occupational exposure to chemicals, metals, fumes, or dust) is sought.
Review of systems seeks symptoms of possible causes, including chronic diarrhea and weakness (inflammatory bowel disease, celiac sprue); genital lesions (Behçet's syndrome, syphilis); eye irritation (Behçet's syndrome); and weight loss, malaise, and fever (nonspecific chronic illness).
Past medical history should ascertain known conditions that cause oral lesions, including herpes simplex, Behçet's syndrome, inflammatory bowel disease, and risk factors for oral lesions, including immunocompromised state (eg, cancer, diabetes, organ transplant, use of immunosuppressants, HIV infection). Whether chemotherapy or radiation therapy has ever been used to manage cancer needs to be determined. Drug history should note all recent drugs used. History of tobacco use should be noted. Social history should include sexual contact, particularly oral sex, unprotected sex, and sex with multiple partners.
Physical examination:
Vital signs are reviewed for fever. The patient's general appearance is noted for lethargy, discomfort, or other signs of significant systemic illness.
The mouth is inspected for the location and nature of any lesions.
The skin and other mucosal surfaces (including the genitals) are inspected for any lesions, rash, petechiae, or desquamation. Any bullous lesions are rubbed for Nikolsky's sign (peeling of epithelium with lateral pressure).
Red flags:
The following findings are of particular concern:
Interpretation of findings:
Occasionally, causes are obvious in the history (eg, cytotoxic chemotherapy; significant occupational exposure to chemicals, fumes, or dust). Recurrent episodes of oral lesions occur with RAS, herpes simplex, and Behçet's syndrome. History of diabetes, HIV infection or other immunocompromise, or recent antibiotic use should increase suspicion of Candida infection. Recent drug use (particularly sulfa drugs, other antibiotics, and antiepileptics) should increase suspicion of Stevens-Johnson syndrome (SJS).
Some causes typically have extraoral, noncutaneous findings, some of which suggest a cause. Recurrent GI symptoms suggest inflammatory bowel disease or celiac sprue. Ocular symptoms can occur with Behçet's syndrome and SJS. Genital lesions may occur with Behçet's syndrome and primary syphilis.
Some causes usually also have extraoral, cutaneous findings.
Cutaneous bullae suggest SJS, pemphigus vulgaris, or bullous pemphigoid. Prodrome of malaise, fever, conjunctivitis, and generalized macular target lesions suggests SJS. Pemphigus vulgaris starts with oral lesions, then progresses to flaccid cutaneous bullae. Bullous pemphigoid has tense bullae on normal-appearing skin. Nikolsky's sign is usually positive in SJS and pemphigus vulgaris.
Cutaneous vesicles are typical with chickenpox or herpes zoster. Unilateral lesions in a band after a dermatome suggest herpes zoster. Diffuse, scattered vesicular and pustular lesions in different stages suggest chickenpox.
Kawasaki disease usually has a macular rash, desquamation of hands and feet, and conjunctivitis; it occurs in children, usually those < 5 yr. Oral findings include erythema of the lips and oral mucosa.
Other cutaneous lesions may implicate erythema multiforme, hand-foot-and-mouth disease (from coxsackievirus), or secondary syphilis.
Some causes have isolated oral findings, including RAS, most viral infections, acute necrotizing ulcerative gingivitis, primary syphilis, gonorrhea, and Candida.
Location of oral lesions may help identify the cause. Interdental ulcers occur with primary herpes simplex or acute necrotizing ulcerative gingivitis. Lesions on keratinized surfaces suggest herpes simplex, RAS, or physical injury. Physical injury typically has an irregular appearance and occurs near projections of teeth, dental appliances, or where biting can injure the mucosa. An aspirin burn next to a tooth and pizza burn on the palate are common.
Primary herpes simplex infection causes 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) usually appear starting in puberty on the lip at the vermilion border and, rarely, on the hard palate.
Acute necrotizing ulcerative gingivitis causes severe inflammation and punched-out ulcers on the dental papillae and marginal gingivae. A severe variant called noma (gangrenous stomatitis) can cause 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.
Isolated oral gonorrhea very rarely causes burning ulcers and erythema of the gingiva and tongue, as well as the more common pharyngitis. Primary syphilis chancres may appear in the mouth. Tertiary syphilis may cause oral gummas or a generalized glossitis and mucosal atrophy. The site of a gumma is the only time that squamous cell carcinoma develops on the dorsum of the tongue. A common sign of HIV becoming AIDS is hairy leukoplakia (vertical white lines on the lateral border of the tongue).
C. albicans and related species, which are normal oral flora, can overgrow in people who have taken antibiotics or corticosteroids or who are immunocompromised, such as patients with AIDS. C. albicans can cause whitish, cheesy plaques that leave erosions when wiped off. Sometimes only flat, erythematous areas appear (erosive form of Candida).
Testing:
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 done. 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, chewing gum, or mouthwash.
Treatment
Specific disorders are treated, and any causative substances or drugs are avoided.
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.
Topical measures:
Numerous topical treatments, alone or in combination, are used to ease symptoms. These treatments include
For topical anesthesia of discomfort that may interfere with eating and drinking, the following may be effective:
A 2-min rinse is done with 15 mL (1 tbsp) 2% viscous lidocaine q 3 h prn; patient expectorates when done (no rinsing with water and no swallowing unless the pharynx is involved). A soothing coating may be prepared with sucralfate (1-g pill dissolved in 15 mL water) plus 30 mL of aluminum-magnesium liquid antacid; the patient should rinse with or without swallowing. Many institutions and pharmacies have their own variation of this formulation (magic mouthwash), which sometimes also contains an antihistamine.
If the physician is certain the inflammation is not caused by an infectious organism, the patient can
Chemical or physical cautery can ease pain of localized lesions. 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.
Key Points
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 life.
Etiology
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
Allergy does not seem 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. A prodrome of pain or burning for 1 to 2 days precedes ulcers, but there are no antecedent vesicles or bullae. Severe pain, disproportionate 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 disease) 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 are 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 previously under stomatitis (see Symptoms of Dental and Oral Disorders: 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 done 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 Symptoms of Dental and Oral Disorders: 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 carboxymethylcellulose 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 use of systemic corticosteroids, azathioprine or other immunosuppressants, pentoxifylline, or thalidomide. Intralesional injections can be done with betamethasone, dexamethasone, or triamcinolone. Supplemental B1, B2, B6, B12, folate, or iron lessens RAS in some patients.
Last full review/revision March 2009 by Robert B. Cohen, DMD
Content last modified March 2009
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