Contact stomatitis describes an inflammatory reaction of the oral mucosa by contact with irritants or allergens (see the images below). Contact stomatitis is classified by its clinical features, pattern of distribution, or etiologic factors. Contact stomatitis frequently goes undetected because of the scarcity of clinical signs that are often less pronounced than subjective symptoms.[1, 2, 3]
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Irritant contact stomatitis of the tongue.
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Close-up view of irritant contact stomatitis of the tongue.
Ingredients of dentifrices, mouthwashes, and dental cleaners (rare) are possible causes of irritant or allergic contact stomatitis.[6, 7, 8, 9]
Flavoring agents (eg, cinnamon compounds, eugenol, menthol) have been implicated.[10]
Colophony in dental floss and denture adhesives have also been reported causes of irritant or allergic contact stomatitis.[5, 11, 12]
Antimicrobials reportedly to have caused irritant or allergic contact stomatitis include chlorhexidine and quaternary ammonium compounds.
Ingredients of candies and chewing gums that may cause irritant or allergic contact stomatitis include flavoring agents (rare) (cinnamon compounds, menthol) and propolis, a strong sensitizer often used in the oral cavity because of its antiseptic properties.
Cosmetic ingredients (fragrance and preservatives) are a common cause of contact cheilitis.[13]
Ingredients in dental restorations may be responsible.[14, 15] Amalgam fillings contain mercury compounds (45-60%) and often gold, palladium, and platinum.[16, 17, 18, 19, 20, 21, 22] Metallic and ammoniated mercury are common sensitizers. Dental cement used for sealing pulp canals may contain eugenol, balsam of Peru, and colophony. Acrylic fillings rarely cause problems in dental patients because polymerization of the resin occurs without contact between the sensitizing acrylic monomers and the oral mucosa, and the final polymerized acrylate is relatively free of allergens.[23]
Ingredients of dental prosthesis are reported to cause irritant or allergic contact stomatitis.[24] Metal prostheses may release nickel, especially when they are poorly made or corroded (see the image below).
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Allergic contact stomatitis on the gingiva in a patient with a positive patch test result to nickel, palladium, and mercury.
Nickel is also present in dental braces, bridges, and crowns (see the image below). Contact gastritis due to nickel has also been reported.[25]
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Allergic contact reaction due to nickel in a dental brace.
Stomatitis from acrylates is rare. Acrylate sensitization is a common occupational problem in dentists and dental technicians. It has been reported in 2-3% of dental patients.[26, 27, 28]
Topical drugs, such as antibiotics, anesthetics, antiseptics, and steroids, may cause sensitization.[29]
Rubber (eg, gloves, dams, orthodontic elastics, bite blocks) may cause sensitization.[30] Latex allergy is not rare (see the images below).
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Contact urticaria of the tongue in a patient with latex allergy.
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Close-up view of contact urticaria of the tongue in a patient with latex allergy.
Foods[31] rarely cause contact stomatitis. Children with atopic dermatitis and a food allergy may develop contact urticaria with lip swelling and stomatitis after contact with foods, especially fruits (eg, fruits of the Rosaceae family [eg, apple, peach, pear] in patients with birch pollinosis). Food allergy can worsen granulomatous cheilitis. Gallates in margarine and other oily foods can cause stomatitis and cheilitis.[32]
Ingredients in cosmetics, lipsticks, lip balms, and the sunscreens in these products (eg, propolis, ricinoleic acid, colophony derivatives) may cause contact stomatitis (see the images below).
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Acute allergic stomatitis involving the oral mucosa and the lip due to benzocaine.
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Allergic contact dermatitis involving the lips and the perioral area due to propolis.
Tobacco consumption can be responsible for nicotine stomatitis, black hairy tongue, periodontal disease, and contact stomatitis.[33, 34]
The exact incidence of contact stomatitis is unknown; however, numerous well-documented series of patients with this disorder are described in the literature. Irritant reactions appear to be more common than allergic reactions.
International
In Europe, an estimated 0.01% of the population has oral symptoms related to dental materials.[35] Patch testing identifies a contact allergy in no more than 10% of these patients. Allergic reactions are usually intraoral (68%), and responsible materials are more commonly latex, metals, resins, and hygiene products. Patients with oral mucosal diseases are significantly more likely to have demonstrable hypersensitivity to food additives, especially benzoic acid, and perfumes and flavorings, especially cinnamaldehyde, compared with controls.[36]
Sex
No sexual predilection is known for contact stomatitis, except for the burning mouth syndrome that almost exclusively affects women.
Age
Contact stomatitis may occur in persons of any age, but it is much more common in elderly individuals. A study evaluating oral lesions among elderly people revealed denture-induced stomatitis in 17.2% of patients aged 65-99 years.[37] Allergic contact stomatitis to nickel seems to be more frequent in young females with a clinical history of allergies; it is not associated with how long the patients are exposed to fixed orthodontic appliances.
The prognosis for contact stomatitis is excellent if the causative agent is detected and removed. Contact stomatitis usually resolves without sequelae.
Acute contact stomatitis is easily correlated to the causative agent; however, contact stomatitis most frequently presents as a chronic condition. Tracing the relationship between contact stomatitis and causative factors is difficult. The presence of lip and perioral eczema aids in making the diagnosis. Symptoms of contact stomatitis include the following[4, 38] :
Possible clinical presentations of contact stomatitis include erythematous lesions, erosions/ulcerations, leukoplakialike lesions, oral lichenoid reactions, contact urticaria, burning mouth syndrome, geographical tongue, intense itching of the tongue, and orofacial granulomatosis.[39] The disease may improve after removal of responsible sensitizers.[40]
Erythematous lesions of contact stomatitis
These lesions are often associated with swelling. They may be localized or diffuse. Common causes include ingredients of mouthwashes and toothpastes, dental materials, and chewing gum flavorings. A burning sensation is a common complaint.
Erosions/ulcerations of contact stomatitis
Erosions/ulcerations are usually painful; they represent the evolution of vesicles and blisters rarely seen in the mouth. Erosions appear as outlined, whitish, rough, macerated areas. Ulcerations are usually covered by a yellow-white exudate and may present with an erythematous halo. Chemical burns are not frequent because the oral mucosa is resistant to heat and acid or alkaline compounds. Possible causes include accidental ingestion of caustic agents, prolonged contact with aspirin or vitamin C tablets, or contact with irritants used for dental care. Allergic contact stomatitis from metal salts or acrylates rarely causes mouth ulcerations.
Leukoplakialike lesions of contact stomatitis
Contact sensitization from nickel and other metals occasionally produces whitish hyperkeratotic lesions that clinically resemble leukoplakia. Leukoplakialike lesions are asymptomatic and are commonly localized in the medial part of the cheek (see the image below).
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Leukoplakialike lesion in a patient who is allergic to mercury.
Oral lichenoid reactions of contact stomatitis
Lesions that resemble reticular or erosive lichen planus may occur at the site of mucosal contact with amalgam restorations (see the image below).[41, 42]
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Lichen planus–like lesion adjacent to a dental restoration.
These lesions are typically localized. Patients often have a positive patch test result to mercury.[43, 44]
Removal of restorations in patients with positive patch test results to mercury usually produces complete regression of the lichenoid lesions, especially when they are in close contact with amalgam fillings. Dental restoration removal occasionally improves the lesions even in patients with negative patch test results, if no cutaneus lichen planus is present.
Sensitization to gold, palladium chloride, and copper sulfate has also been associated with oral lichenoid reactions. A 2015 study suggests that palladium-sensitized patients should always undergo an oral examination, with particular attention to the presence of/exposure to dental crowns.[45]
Contact urticaria
Swelling of the lips, the tongue, the buccal mucosa, and the gingiva develops suddenly with intense itching. Severe cases may be associated with upper airway obstruction. Contact urticaria from latex occurs in patients undergoing dental treatment due to contact with gloves and dental dams. Latex sensitization is more common in patients with atopy and in children who have had multiple operations (eg, patients with spina bifida). Patients with latex sensitization may experience a severe type I immunoglobulin E–mediated allergy after ingestion of some fruits and vegetables, especially chestnuts, banana, avocado, and kiwi fruit (latex-fruit syndrome), due to cross-reactivity between latex allergens and plant-derived food allergens. Contact urticaria is rarely due to allergy to foods (see the image below).
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Contact urticaria of the lip due to food allergy.
Burning mouth syndrome
Burning mouth syndrome[46, 47] is characterized by a burning sensation and dryness of the oral mucosa in the absence of objective signs. Symptoms typically improve during meals. Although contact allergy (especially to mercury) has often been implicated, the disorder can have a psychogenic basis, with anxiety, if present, usually considered an exacerbating factor rather than a cause.
Orofacial granulomatosis
Orofacial granulomatosis can be worsened by contact allergy to mercury, gold, or foods. The disease may improve after removal of responsible sensitizers.
Serologic testing may be helpful. In vitro tests, such as a radioallergosorbent test (RAST), for specific immunoglobulin E are available for food and latex allergy. These tests can confirm sensitivity and establish the degree of allergy.
Patch testing (see the image below) is useful to distinguish irritant reactions from allergic reactions.[48, 49, 50, 51] Patch testing before placement of a prosthesis is not indicated. Reading at 10 days is recommended because reactions to gold, palladium, and mercury salts may be delayed. A patch test series for contact stomatitis should include the following[52, 53] :
Nickel sulfate 5% pet
Beryllium chloride 1% pet
Gold sodium thiosulfate 2% pet
Metallic mercury 1% pet (see image below)
Ammoniated mercury 1% pet (mercury ammonium chloride)
Palladium chloride 1% pet
Copper sulfate 2% pet
Amalgam without mercury 20% pet (contains silver 13.9%, copper 2.36%, tin 3.54%, and zinc 0.2%)
Amalgam with mercury 5% pet (contains mercury 2.5%, silver 1.73%, copper 0.3%, tin 0.44%, and zinc 0.03%)
Methacrylates: 2-Hydroxyethylmethacrylate 2% pet
2,2-bis (2-Hydroxy-3-methacryloxy-propoxyl)-phenylpropane (BIS-GMA) 2% pet
Balsam of Peru 25% pet
Menthol 1% pet
Eugenol 1% pet
Cinnamic aldehyde 1% pet
Propolis 10% pet
Fragrance mix 8% pet
Colophony 20% pet
Benzalkonium chloride 0.1% pet
Benzocaine 5% pet
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Positive patch test result to mercury.
For direct testing of the oral mucosa, the suspected allergen is placed on the lip mucosa as is, or it is incorporated in Orabase. Reading is performed at 24 hours.
Skin prick tests are routinely used for diagnosing a latex allergy. They are also useful in cases of suspected food allergy (see the image below).
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Positive prick test result to latex.
Use test with rubber latex gloves is often positive in patients with a latex allergy.
Histologic study excludes neoplasia in long-standing lesions. A 3- to 4-mm punch biopsy is usually sufficient. Histopathologic examination in contact stomatitis can show changes similar to those in allergic contact dermatitis, with epithelial spongiosis and perivascular lymphohistiocytic infiltration. In addition, lichenoid changes of lymphocytic effacement of the dermoepithelial junction with, at times, vacuolar changes and necrotic epithelial cells, may be seen.
Histopathology findings cannot help distinguish between oral lichenoid reactions associated with amalgam and oral lichen planus.
Advise patients with contact stomatitis to avoid spicy foods. Instruct contact stomatitis patients to avoid soft drinks, candies, and chewing gums in case of allergy to flavoring agents. Recommend that contact stomatitis patients avoid the causative food in cases of contact urticaria.
Replacement of dental restorations and prostheses may be very expensive and stressful for patients and should not be recommended when their causative role in contact stomatitis is doubtful.[54] Removal of fillings or restorations does not always produce a complete resolution of symptoms, even in patients with positive patch test results to mercury or other dental compounds. Replacement is advisable when the mucosal lesions are adjacent to dental restorations, especially in cases of localized lichenoid reactions.[55] Titanium may be a satisfactory alternative for patients who are allergic to palladium and other transition metals.
Sensitization to nickel is common in the general population. Establish relevance before removal of dental metal. Avoid prostheses containing transition metals in patients with history of nickel dermatitis.
Sensitization to palladium chloride is associated with nickel allergy due to cross-sensitization.
Establish relevance before removal of dental restorations in patients with sensitization to mercury derivatives.
Gold allergy is often not relevant, and dental gold removal may not prove curative.
Sensitization to acrylates is usually relevant. Patch testing with acrylates may cause active sensitization. Active sensitization to metals or acrylates as a consequence of dental procedures is rare.
Topical steroids are the first-line therapy for contact stomatitis. Available vehicles include topical gels, creams, pastes, ointments, sprays, and rinses. General guidelines for administration and usage can be found in standard pharmacology references.
Clinical Context:
Triamcinolone topical is for inflammatory dermatoses responsive to steroids; it decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. Use 0.1% gel.
Clinical Context:
Fluocinonide is a high-potency topical corticosteroid that inhibits cell proliferation. It is immunosuppressive and anti-inflammatory. Use 0.05% gel.
Clinical Context:
Clobetasol is a class I superpotent topical steroid; it suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Use 0.05% gel.
Clinical Context:
Prednisone is an immunosuppressant for the treatment of autoimmune disorders; it may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Prednisone stabilizes lysosomal membranes and suppresses lymphocyte and antibody production. It is useful in severe cases.
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
Antonella Tosti, MD, Professor of Dermatology, Department of Dermatology and Cutaneous Surgery, University of Miami, Leonard M Miller School of Medicine
Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: PharmaDerm<br/>Received income in an amount equal to or greater than $250 from: Valeant; Pharmaderm.
Coauthor(s)
Bianca Maria Piraccini, MD, PhD, Director of Outpatient Consultation for Hair and Nail Disorders, Researcher, Department of Dermatology, University of Bologna, Italy
Disclosure: Nothing to disclose.
Massimiliano Pazzaglia, MD, PhD, Fellow, Department of Dermatology, University of Bologna, Italy
Disclosure: Nothing to disclose.
Specialty Editors
Michael J Wells, MD, FAAD, Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology
Disclosure: Nothing to disclose.
Drore Eisen, MD, DDS, Consulting Staff, Dermatology of Southwest Ohio
Disclosure: Nothing to disclose.
Chief Editor
Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Craig A Elmets, MD, Professor and Chair, Department of Dermatology, Director, Chemoprevention Program Director, Comprehensive Cancer Center, UAB Skin Diseases Research Center, University of Alabama at Birmingham School of Medicine
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: University of Alabama at Birmingham; University of Alabama Health Services Foundation<br/>Serve(d) as a speaker or a member of a speakers bureau for: Ferndale Laboratories<br/>Received research grant from: NIH, Veterans Administration, California Grape Assn<br/>Received consulting fee from Astellas for review panel membership; Received salary from Massachusetts Medical Society for employment; Received salary from UpToDate for employment. for: Astellas.
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