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A Review of Drug-Induced Oral Reactions

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A Review of Drug-Induced Oral Reactions A Review of Drug-Induced Oral Reactions Abstract Every drug can produce untoward consequences, even when used according to standard or recommended methods of administration. Adverse drug reactions can involve every organ and system of the body and are frequently mistaken for signs of underlying disease. Similarly, the mouth and associated structures can be affected by many drugs or chemicals. Good oral health, including salivary function, is very important in maintaining whole body health. Regarding different parts of the oral system, these reactions can be catego- rized to oral mucosa and tongue, periodontal tissues, dental structures, salivary glands, cleft lip and palate, muscular and neurological disorders, taste disturbances, drug-induced oral infection, and facial edema. In this article, the drugs that may cause adverse effects in the mouth and related structures are reviewed. The knowledge about drug-induced oral adverse effects helps health professionals to better diagnose oral disease, administer drugs, improve patient compliance during drug therapy, and may influence a more ratio- nal use of drugs. Keywords: Oral reactions, drug reactions, adverse drug effects, side effects, oral mucosal reactions Citation: Abdollahi M, Radfar M. A Review of Drug-Induced Oral Reactions. J Contemp Dent Pract 2003 February;(4)1:010-031. © Seer Publishing 1 The Journal of Contemporary Dental Practice, Volume 3, No. 4, November 15, 2002 Etiology and Pathogenesis of Oral Adverse mimic erosive lichen planus known as lichenoid Drug Reactions1-3 drug reactions. Although the skin is more commonly involved in adverse reactions to drugs, the oral mucosa is Histopathology of Oral Adverse Drug also frequently affected. Virtually any drug has Reactions1,2 the potential to cause an untoward reaction, but Histologic features or findings of drug reac- some have a greater ability to do so than others. tions include nonspecific features as spongiosis, Pathogenesis of drug reactions may be related to apoptotic keratinocytes, lymphoid infiltrates, either immunologic or nonimmunologic mecha- eosinophils, and ulceration. Also, mononuclear or nisms. Most adverse reactions to drugs are medi- polymorphonuclear infiltrations in a subepithelial ated by the immune system and are drug aller- or perivascular distribution, basal cell destruction, gies. Three mechanisms have been proposed edema, and keratinocyte necrosis are seen. for drug allergies. Firstly, IgE-mediated reactions occur when the drug Diagnosis of Adverse Drug Reactions1,2 reacts with IgE antibod- The diagnosis of drug reactions requires a high ies bound to mast cells. index of suspicion and careful history taking. Secondly, drug allergies Recent use of a drug is important. Withdrawal of can involve a cytotoxic the suspected drug should result in improvement, reaction in which an and reinstitution of the drug should exacerbate antibody binds to a the patient’s condition. The clinical expression of drug that is already lesions in drug reactions is generally allergic in attached to a cell sur- nature that can help with the diagnosis. face. The third mecha- nism in a drug allergy Effects of Drugs on Oral Mucosa and involves circulation of Tongue1,2,4 the antigen for extend- Oral mucosal membranes may be the sole site of ed periods allowing involvement, or they may be a part of a more gen- sensitization of the patient’s immune system and eralized skin reaction to the offending drug. The production of a new antibody. Nonimmunologic main type of hypersensitivity reaction that affects drug reactions are not antibody dependent and oral mucosa is a delayed reaction mediated by may directly affect mast cells causing the release sensitized T-lymphocyte. Stomatitis medicamen- of chemical mediators. Also some nonimmuno- tosa, or fixed drug eruption, occurs with systemic logic drug-induced reactions result from a drug drug usage and stomatitis venenata appears overdose or toxicity. with contact hypersensitivity. Lesions associated with fixed drug eruption are erythematous in mild Clinical Features of Oral Adverse Drug 1,2 cases and appear ulcerated in severe cases. The Reactions reactions usually appear in 24 hours post-inges- Manifestations of drug reactions are dependent tion of the drug. Delayed reaction (up to two on the type of drug, drug dose, and individual weeks) has been noted after use of ampicillin.2 patient differences. These reactions can be Withdrawal of the causative drug results in reso- seen either rapidly or several days after drug lution of the lesions. Drugs with the potential to use. Acquired angioedema is an IgE-mediated cause fixed drug eruptions are shown in Table 1. drug allergy that is commonly observed as drug and food reactions. Other cutaneous manifesta- Contact stomatitis is a local reaction of the tions of drug reactions include urticaria, macu- mucosa after repeated contact with the causative lopapular rash, erythema, vesicles, ulcers, and agent. Reactions can be seen as erythematous target lesions. An unusual form of drug reaction to ulcerative lesions. The patient may complain is known as fixed drug reaction during which an of a burning sensation in the mouth together with erythematous lesion appears in the same location xerostomia. The reaction may develop from days with each antigenic challenge. Oral manifesta- to years post-exposure to the causative agent. tions of drug reactions may be erythematous, Compounds with potential to cause contact sto- vesicular, or ulcerative in nature. They may also matitis are shown in Table 2. 2 The Journal of Contemporary Dental Practice, Volume 3, No. 4, November 15, 2002 Aphthous Stomatitis5 drugs, however, 80% of cases occur in Stevens– Aphthous stomatitis (canker sores) is commonly Johnson Syndrome. Drugs with potential to cause observed and is mediated by the immune sys- erythema multiforme are shown in Table 5. tem. Lesions usually appear as painful, tiny, discrete, or grouped papules and vesicles. These Oral Ulceration1,13-16 lesions are small in diameter with round, shallow A number of chemicals used by dental surgeons ulcerations predominantly seen over the labial can cause “burns” of the oral and buccal mucosa. The reactions heal without mucosa, i.e., trichloroacetic scarring in 10-14 days, however, recurrence is acid used in the treatment of common. Drugs with potential to cause aphthous pericoronitis. Others that may stomatitis are shown in Table 3. cause local irritation or ulcer- ation of the mouth include Burning Mouth Syndrome those listed in Table 6. This syndrome may occur due to psychogenic factors, hormonal withdrawal, folate, iron, pyridox- Vesiculo–bullous Lesions1 ine deficiency, or hypersensitivity reactions to the The exact mechanism of this reaction is unclear, 1 materials utilized in dental prostheses. There is but it seems to be the consequence of a direct a case report of burning mouth syndrome after irritant effect. Patients using steroid inhalers for 6 taking clonazepam. Cases of “scalded mouth” more than 5 years are more prone to the devel- caused by captopril, lisinopril, and enalapril have opment of oral blistering. This type of reaction 7-9 been described. The mechanism of ACE-inhibi- has also been reported for naproxen and penicil- tor “scalded mouth” is uncertain, but it may be a lamine. subclinical manifestation of lichen planus. Lichenoid Eruptions1,2 Glossitis5 Unlike true lichen planus, drug-induced lichen- Glossitis is inflammation of the tongue that is oid eruptions disappear after drug withdrawal. characterized by swelling and intense pain that Lichenoid drug eruptions rarely affect the buc- may be referred to the ear area. Salivation, fever, cal mucosa. A characteristic white lace pattern and enlarged regional lymph nodes may develop may be present. It is thought that drugs causing during an infectious disease or after a burn, bile, lichenoid reactions only uncover the latent dis- or other injury. Drugs that have potential to cause ease of lichen planus, or amplify a previous dis- glossitis are shown in Table 4. order, rather than inducing the disease de novo. Such drugs are listed in Table 7. Erythema Multiforme (Stevens–Johnson Syndrome)1,5,10-12 Color Changes of Oral Mucosa and Teeth Erythema muultiforme, which when severe is Discoloration can occur after direct contact termed Stevens–Johnson Syndrome, is a muco- with or following systemic absorption of a drug. cutaneous disorder characterized by various Historically, exposure to metals like silver, bis- clinical types of lesions. Young male adults are muth, gold, lead, mercury, zinc, and copper were predominantly affected. The lips are swollen, the main causative agents of tissue discoloration. crusted, and bleeding. Widespread erythema can Color changes are typically seen along the gin- be seen within the mouth. The oral lesions disap- gival margins and are caused by the formation pear within 14 days of drug withdrawal. Only 4% of metallic sulphides as a result of reactions with of erythema multiforme reactions are caused by plaque products in gingival pockets. The exact 3 The Journal of Contemporary Dental Practice, Volume 3, No. 4, November 15, 2002 4 The Journal of Contemporary Dental Practice, Volume 3, No. 4, November 15, 2002 5 The Journal of Contemporary Dental Practice, Volume 3, No. 4, November 15, 2002 mechanism of tissue discoloration by many drugs Pigmented lesions of the tongue (dark macular is uncertain but generally resolves within weeks patches) are reported to occur in heroin addicts to months when the offending drug is
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