DAMAGE TO ORAL SOFT TISSUES
Color changes to the oral mucosa Mucosal pigmentation Many agents affect the coloration of the oral mucosa. Discoloration of the oral mucosa may have intrinsic or extrinsic causes (Sreeja et al., 2015; Rosebush, Briody, & Cordell 2019). Extrinsic discoloration is usually caused by habits (e.g., tobacco, betel nut use) or by consuming colored foods or beverages (e.g., red wine, coffee, tea). Some medications (e.g., chlorhexidine, iron salts, minocycline, bismuth subsalicylate, lansoprazole) may discolor the oral mucosa. Extrinsic staining is rarely serious. Intrinsic mucosal hyperpigmentation has many potential causes, ranging from non-serious conditions such as amalgam tattoo to serious conditions such as neoplasms (e.g., malignant melanoma, Kaposi sarcoma; Sreeja et al., 2015). Other causes of intrinsic hyperpigmentation include nevus, melanotic macule, Peutz-Jeghers syndrome, racial pigmentation, decorative or cultural tattoo practices, pregnancy, and Addison’s disease. Evaluation of a patient presenting with a pigmented lesion should include a full medical and dental history, extraoral and Black hairy tongue Black hairy tongue (lingua villosa nigra) consists of elongated filiform papillae of the tongue that become stained because of growth of chromogenic microorganisms (Gurvits & Tan, 2014; Hamad & Warren, 2018). Administration of oral antibiotics, poor dental hygiene, and excessive smoking have been associated with black hairy tongue. Specific medications that have been reported to cause this condition include antibiotics (e.g., penicillin, aureomycin, erythromycin, doxycycline, neomycin and linezolid), antipsychotics (e.g., olanzapine, chlorpromazine), and chemotherapeutics (e.g., erlotinib; Gurvits & Tan, 2014; Hamad & Warren, 2018). In most cases, empirical approaches adequately resolve black hairy tongue: brushing or scraping the tongue, improving oral hygiene, and eliminating potential associated factors (e.g.,
intraoral examinations, and in some cases biopsy and laboratory investigations. The exact mechanism of intrinsic tissue discoloration varies by drug and is uncertain in many cases. Generally, discoloration resolves within weeks to months after removal of the drug, but sometimes the discoloration is permanent. The discoloration caused by antimalarial drugs such as chloroquine and mepacrine (quinolones) is ascribed to deposition of melanin or iron in mucosal tissues (Jallouli et al., 2013). The hyperpigmentation caused by tetracycline and minocycline has been attributed to the interaction of the drug with bone during its formation. Use of oral contraceptives may also cause pigmentation of the oral mucosa. It is postulated that estrogens produce high levels of cortisol-binding globulin, which decreases the level of plasma free cortisol. This decrease results in hypersecretion of adrenocorticotropic hormone and melanocyte-stimulating hormone, which in turn causes increased oral pigmentation (Sreeja et al., 2015). tobacco, strong mouthwashes, antibiotics; Gurvits & Tan, 2014; Hamad & Warren, 2018). Older case reports describe successful treatment of black hairy tongue with triamcinolone acetonide (Weinstein & Rosencrans, 1962). Educating patients regarding proper oral hygiene and encouraging routine tongue brushing are the best preventive and therapeutic measures. Treatment usually does not require pharmacological intervention; however, if fungal overgrowth is present and the condition is symptomatic, the clinician may prescribe a topical antifungal agent. Additionally, the clinician should counsel the patient that this is a benign process and prognosis is favorable. With black hairy tongue, the patient may see improvement with lifestyle modification, or spontaneous resolution (Gurvits & Tan, 2014; Hamad & Warren, 2018).
DRUG-RELATED GINGIVAL ENLARGEMENT
Enlargement of the gingiva is a well-recognized side effect of drug therapy, especially with medications such as anticonvulsants (e.g., phenytoin, phenobarbital, ethosuximide), oral contraceptives, immunosuppressants (e.g., cyclosporine), and calcium channel blockers (e.g., nifedipine, amlodipine; Kalmar, 2016; Raizada, Varghese, Bhat, & Gupta, 2016; Sarda & Rathod, 2015; Seymour & Rudralingham, 2008). Table 2 lists the drugs with potential to cause gingival enlargement. Table 2: Drugs with Potential to Cause Gingival
dihydropyridine class of medications) and cyclosporine have also been associated with this reaction. In the calcium channel blocker family, nifedipine, diltiazem, verapamil, and amlodipine are among the most commonly reported causative agents (Charles, Ramesh, Babu, & Premalatha, 2012). However, drug- related gingival enlargement is not observed in all patients. The prevalence ranges between 25% and 50%, with no clear relationship between the dose of the drug and the severity of the overgrowth (Kalmar, 2016). Drug-induced gingival enlargement was previously termed gingival hypertrophy or gingival hyperplasia because of an increased number of fibroblasts in gingival connective tissue on histological analysis (Mohan, Rastogi, Bhushan, & Verma, 2013; Teoh, Moses, & McCullough, 2019). However, the terms hypertrophy and hyperplasia inaccurately reflect the histological composition of enlarged gingiva. It is not the increased proliferation of gingival fibroblasts, but the accumulation of extracellular matrix, particularly collagenous components, within the gingival connective tissue that is responsible for gingival enlargement. Although it is known that the pathogenic process of drug-related gingival enlargement is characterized by chronic inflammation and accumulation of extracellular matrix within the gingival connective tissue, the exact mechanism is still being investigated (Trackman & Kantarci, 2015). Clinically, gingival enlargement typically occurs 1 to 3 months after initiation of drug therapy and starts as a beadlike enlargement of the interdental papilla (Mohan et al., 2013). Over time, this painless enlargement extends to the facial and lingual gingival margins. Although the enlargement is usually generalized throughout the mouth, enlargement in the anterior regions is frequently more severe.
Enlargement • Amlodipine • Candesartan • Captopril • Clopidogrel • Eprosartan • Losartan • Midodrine
• Nicarpidine • Nifedipine • Nitrendipine
• Phenytoin • Valsartan • Verapamil
Note. Adapted from “Cardiovascular Drugs-Induced Oral Toxicities: A Murky Area to be Revisited and Illuminated,” by P. Balakumar, M. Kavitha, and S. Nanditha, 2015, Pharmacological Research, 102 , pp. 81-89; and “Drugs, Medications and Periodontal Disease,” by P. A. Heasman and F. J. Hughes, 2014, British Dental Journal, 217 (8), pp. 411-419. Diffuse, non-neoplastic enlargement of the gingival tissues was initially recognized in patients using phenytoin (Chen et al., 2015). Calcium channel blockers (members of the
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