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Q61.1 Given the various conditions associated with erosive gingivitis, which conditions are best treated with (1) topical corticosteroids alone, (2) topical calcineurin inhibitors, (3) systemic corticosteroids or (4) other immunosuppressive therapies? (Pg. 666)
Q61.2 What are some factors which influence the choice of topical medication vehicle when treating oral diseases? (Pg. 666x2)
Q61.3 What are several of the principles clinicians can use to maximize the benefits of topical therapy for oral conditions? (Pg. 666)
Q61.4 What is the rationale behind using custom dental ‘trays’ with topical medications? (Pg. 667)
Q61.5 What are common oral complications of topical intraoral, inhaled or systemic corticosteroids? (Pg. 667)
Q61.6 What are potential complications of intraoral topical lidocaine? (Pg. 668)
Q61.7 What are commonly used topical and systemic options for managing oral candidiasis? (Pg. 668x2, 669)
Q61.8 What are several treatment options for recurrent aphthous ulcers? (Pg. 670x2)
Q61.9 What is the only FDA-approved drug for the treatment of recurrent aphthous stomatitis in HIV-positive individuals? (Pg. 670)
Q61.10 What are several systemic medications used to manage xerostomia? (Pg. 674x2)
Q61.11 What are some of the oral medications used for burning mouth syndrome (glossodynia)? (Pg. 675)
Acute necrotizing ulcerative gingivostomatitis
Burning mouth syndrome
Bullous pemphigoid
Human immunodeficiency virus
Herpes simplex virus
Lupus erythematosus
Lichen planus
Mucous membrane pemphigoid
Nil per os
Over the counter
Pemphigus vulgaris
Recurrent aphthous stomatitis
This chapter introduces the use of topical and systemic medications for the treatment of common oral conditions. The chapter is designed to meet the needs of dermatologists, dentists, and other healthcare providers, who care for patients with a variety of oral disorders. We highlight treatment pearls and potential pitfalls of therapy. Although many of the agents discussed are commercially available and US Food and Drug administration (FDA) approved, the dosing and regimens provided may vary based on the available literature, and thus may be considered to be ‘off-label.’ This chapter focuses on the treatment of erosive gingivostomatitis (desquamative gingivitis), herpetic gingivostomatitis, oral candidiasis, hairy tongue, recurrent aphthous stomatitis (RAS, canker sore), acute necrotizing ulcerative gingivostomatitis (ANUG), mucositis (stomatitis), xerostomia, and burning mouth syndrome (BMS, glossodynia).
There are a limited number of morphologic patterns that manifest orally. As a result, the differential diagnosis for these reaction patterns is often broad. For example, the differential diagnosis of white oral lesions includes infectious (viral warts), inflammatory (lichen planus [LP], lichenoid drug reactions, discoid lupus erythematosus [LE]), mechanical (morsicatio buccarum et labiorum), and neoplastic (dysplasia) etiologies. Thus, the first step in managing mucosal diseases is to obtain a definitive diagnosis. It is imperative to determine, by a complete history and physical examination, the full extent of disease involvement by a thorough assessment of all mucosal (conjunctiva, nose, ear, oral cavity, esophagus, larynx, vagina, vulva, anus) and cutaneous (skin, scalp, nails) sites. Diagnostic studies, including biopsy for routine histopathology and/or immunofluorescence microscopy, microbiologic cultures, and directed laboratory studies, may be necessary.
If the condition is limited to the oral cavity, topical therapy may be appropriate. However, systemic therapy is usually indicated when multiple mucosal sites or a combination of mucosal and cutaneous sites are affected. In the context of systemic therapy, the importance of adjunctive intraoral therapy and optimizing oral hygiene should not be overlooked. Topical corticosteroids (TCS) may enhance the effectiveness of systemic CS in patients with recalcitrant disease. Adjunctive intraoral nonsteroidal topical regimens may also permit a reduction in systemic medication.
Gingivitis is defined as nondestructive inflammation of the gums because of poor oral hygiene or a mixed bacterial infection. Dental plaque is a sticky, yellow or colorless film composed of decomposing food debris, sloughed keratinocytes, and accumulated bacteria. Dental plaque contributes to gingival inflammation and can be removed by tooth brushing and/or flossing. Dental plaque may calcify and form dental calculus , which is only removable upon mechanical debridement by a dentist/dental hygienist. Periodontitis is a destructive inflammatory reaction of the gingiva, periodontal ligament and alveolar bone. As inflammation progresses, the integrity and strength of the underlying alveolar bone is compromised, resulting in gingival retraction, bone resorption, and tooth mobility.
Erosive gingivostomatitis (desquamative gingivitis) presents with erythema, edema, tenderness, and superficial erosions on the gingiva and other mucosal sites. Vesicles may rupture owing to the fragile/thin nature of the epithelium and the mechanical trauma inherent to the oral cavity. Patients may complain of painful, bleeding or tender gums, or difficulty eating, swallowing and/or speaking. The mucosal surfaces are eroded and friable. These findings and associated pain may limit the patient’s ability to practice good oral hygiene or maintain adequate oral intake.
The differential diagnosis of both focal and diffuse erosive gingivostomatitis includes erosive LP, mucous membrane pemphigoid (MMP), pemphigus vulgaris (PV), LE, bullous pemphigoid (BP), erythema multiforme (EM), graft versus host disease (GVHD), drug reactions, infections and paraneoplastic disorders. In most of the aforementioned diagnoses, there is a predominance of findings at the marginal gingiva/dental papilla. Diagnostic biopsies for routine histopathology and immunofluorescence microscopy are required to distinguish between these clinically similar conditions, and directed serologic studies may provide additional diagnostic information.
A complete mucocutaneous examination (skin, scalp, nails, mucous membranes) should be performed, may provide helpful diagnostic clues and should direct treatment approach, based on extent of involvement. Symmetric white reticulated striae, with or without erythema and erosions, suggest a diagnosis of oral LP. Asymmetric white plaques on the buccal mucosa, labial mucosa, hard palate and vermilion lip suggest the diagnosis of discoid or systemic LE; findings, such as a malar rash with a history of photosensitivity and musculoskeletal complaints, may further support this diagnosis. In all patients with gingival involvement, dental consultation should be obtained to optimize oral hygiene, evaluate for dental and bone integrity, and facilitate local intraoral therapy (i.e., custom acrylic dental trays, see later).
Q61.1 Factors to consider when selecting a therapeutic regimen for patients who present with erosive gingivostomatitis include extent of oral mucosal involvement, impact on oral nutrition/food and fluid intake, involvement of additional mucosal sites, extent of skin involvement, patient comorbidities and access to medication (cost, availability). Once the diagnosis is established, the first line of therapy for limited oral erosive diseases, such as LP or MMP, is TCS. Topical calcineurin inhibitors (see Chapter 48 for explanation of FDA Boxed Warning for this drug group), tacrolimus and pimecrolimus, have been increasingly used as adjunct therapy and may be occasionally used as monotherapy. Systemic therapy (CS, azathioprine, rituximab, etc.) may be indicated in severe cases of LP, MMP, GVHD and PV.
Q61.2 Ointments and gel formulations are most effective for limited oral mucosal disease. Cream formulations have an unpleasant taste and are less likely to adhere to wet mucosa. For ulcers on the posterior pharynx or the soft and hard palate, or if the patient is unable to apply topical medications, elixirs and suspensions may be more effective.
Q61.3 To maximize the effectiveness of all topical agents in the oral cavity, the patient should be instructed to avoid eating, drinking or talking excessively (because of increased saliva production, resulting in dilution and reduced contact time of medication) for 30 to 60 minutes after each medication use. Patients should be instructed to dry the oral mucosa, apply the topical medication using a fingertip or cotton applicator, and rub the topical medication gently into the affected areas for 30 seconds.
Q61.2 The palatability (taste, texture) of medications should be considered. The authors prefer gel and ointment formulations because of their ease of use and smooth texture. Adhesive bases, such as Orabase, tend to have a gritty texture, have lower patient acceptance, and have not been shown to be more effective than other TCS preparations. In the context of more widespread or anatomically challenging (posterior oropharynx) disease, or for patients who are not able to apply topical medication (because of limitations in vision, maneuverability or hyperactive gag reflex), liquid formulations (elixir, suspension) may be helpful. Flavorings may be added to improve the taste of oral liquid medications. These flavorings should be free of sugar, gluten, and dyes; these are widely available at commercial pharmacies.
Q61.4 Custom acrylic dental ‘trays’ can be fashioned to facilitate the delivery of topical medications to the gingivae ( Fig. 61.1 ). Soft acrylic trays are readily made by dentists and are traditionally used to deliver bleaching agents. The dentist must be made aware that the purpose of trays is to facilitate longer duration of topical medication contact with the gingival mucosa, thereby acting as an occlusive agent (analogous to plastic wrap occlusion for topical medications). Therefore trays should be trimmed to extend over the affected gingiva. This is counterintuitive to dentists, who usually use acidic agents in bleaching teeth, and thus routinely trim the trays at the gingival margin. Medicated dental trays are typically applied for 10 to 20 minutes per use 2 to 4 times daily. The frequency of medication use should be titrated based on patient symptoms and severity of disease.
The importance of meticulous oral hygiene should be impressed upon every patient, as dental plaque is proinflammatory and worsens erosive gingivostomatitis. Adequate dental hygiene includes brushing of the teeth twice daily using a regular or sonic soft bristle toothbrush with toothpaste devoid of sodium lauryl sulfate, mint, or cinnamon flavorings, as well as tartar-control and whitening age. The immunocompetent patient should floss at least daily, using unflavored dental floss. The use of antibacterial oral rinses may also reduce bacterial plaque. Professional dental cleanings are recommended every 3 to 4 months.
Q61.5 Pitfalls that may be encountered in patients using topical, inhaled, or systemic CS include secondary oral candidiasis and reactivation of herpes simplex virus (HSV) stomatitis. Both of these conditions may present with pain, increased mucosal erosions, and perceived decreased effectiveness of current therapy. Thorough re-examination, microbiologic smears and cultures should be performed to identify any underlying cause. Candida albicans is the most common fungus in the oral cavity and can be isolated from asymptomatic adults (see ‘Oral candidiasis’ section). Patients who experience herpetic gingivostomatitis may benefit from long-term suppressive antiviral therapy, when immunomodulating medications (CS, topical calcineurin inhibitors) must be used (see Herpetic gingivostomatitis section).
Most mouth rinses are antibacterial products that can be used as adjuncts to various management programs discussed in this chapter. Some, such as Listerine, are over the counter (OTC), whereas others, such as chlorhexidine gluconate, are available by prescription.
OTC : Listerine
Disp : 250 mL, 500 mL, 1 L, 1.5 L, or 1.7 L
Sig : Rinse with 10 to 20 mL (2–4 tsp, 1/3–2/3 oz) for 30 seconds. Then expectorate. Use twice daily (BID) after toothbrushing.
NB : Product contains 26.7% alcohol.
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Rx : Chlorhexidine gluconate oral rinse, 0.12% (Oro Clense, Peridex, PerioGard, PerioRx)
Disp : 480 mL
Sig : Rinse with 15 mL (3 tsp, 0.5 oz) for 30 seconds. Then expectorate. Use BID after toothbrushing.
NB : Product contains 11.6% alcohol, saccharin and mint flavoring. PerioGard Oral Rinse can cause staining of teeth, dental restorations, and dorsum of the tongue. Increased calculus formation and altered taste perception may occur.
Rx : Triamcinolone acetonide 0.1% gel; fluocinonide 0.05% gel; clobetasol 0.05% gel
Disp : 30 to 60 g
Sig : Apply a thin film to affected areas, nil per os (NPO) 30 to 60 minutes or apply to inner surface of dentures or dental trays and leave in place for 10 to 20 minutes. Use four times per day (QID) as needed.
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Rx : Dexamethasone elixir 0.5 mg/5 mL (Decadron)
Disp : 400 mL
Sig : Swish and gargle 5 mL for 5 to 10 minutes, then expectorate. Use QID (after meals and at bedtime). NPO for 30 minutes.
NB : Avoid swallowing, to limit systemic adverse effects (AE), such as hypertension, diabetes mellitus, esophageal candidiasis, and osteoporosis.
Rx: Azathioprine rinse 5 mg/mL compounded in a methylcellulose vehicle with a flavoring agent
Disp: 600 mL
NB: Used for PV, MMP, chronic GVHD.
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Rx: Cyclosporine solution 100 mg/mL (Sandimmune)
Disp: 450 mL
Sig: Swish 5 mL (500 mg) for 5 to 10 minutes, then expectorate. Use TID. NPO for 30 minutes.
NB: Minimal systemic absorption has been shown. Use may be limited by high cost. Results typically noted after 4 to 8 weeks of treatment.
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Rx : Pimecrolimus 1% cream (Elidel)
Disp : 30, 60, or 100 g
Sig : Apply to affected areas BID. NPO for 30 minutes.
NB : Can be used as currently formulated or pimecrolimus 1% cream mixed 1:1 with a hydrophilic adhesive gel base. Burning or stinging often occurs.
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Rx: Sirolimus solution 1 mg/mL (Rapamune)
Disp: 60 mL
Sig: Apply 1 mL to erosions BID. NPO for 30 minutes.
NB: Burning or stinging is common but tends to decrease over time. Systemic absorption may occur.
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Rx : Tacrolimus 0.03% or 0.1% ointment (Protopic)
Disp : 30, 60, or 100 g
Sig : Apply a thin film to affected areas or apply to inner surface of dentures or dental ‘trays’ and leave in place for 30 minutes. Use QID as needed. NPO for 30 minutes.
NB : Burning or stinging often occurs. Systemic absorption may occur.
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Rx : Tacrolimus suspension 0.5 mg/mL (Prograf)
Disp : 5-mg capsules
Sig : Dissolve six individual 5-mg capsules with equal amounts of Ora-Plus and Simple Syrup, National Formulary, to make a final volume of 60 mL. Swish 5 mL for 5 to 10 minutes, then expectorate. Use BID. NPO for 30 minutes.
NB : Suspension is stable for up to 8 weeks at room temperature in glass or plastic amber prescription bottle. Simple syrup contains sugar and may predispose to dental caries and secondary oral candidiasis.
Rx : Lidocaine hydrochloride 2% viscous (Xylocaine)
Disp : 100 mL
Sig : Swish 5 to 15 mL for 5 minutes, then expectorate. Use before meals and every 3 hours as needed for pain.
NB : Maximum dose of 15 mL (0.225 mL/kg, 4.5 mg/kg) and 8 doses per day. Q61.6 Toxicity may occur if swallowed. Risk of aspiration caused by suppression of gag reflex in acutely ill or debilitated patients. Risk of aspiration is reduced by applying medication locally with fingertip or cotton applicator.
Rx : Triamcinolone acetonide injectable, 3 to 10 mg/mL (Kenalog)
Direction : Inject suspension into individual lesions using a 30-gauge needle. Injection may be repeated every 2 to 4 weeks.
NB: Best used for solitary (or relatively few) lesions recalcitrant to other therapy. Systemic absorption may occur. Ahmed AR and associates recommend a maximum dose of 40 mg triamcinolone acetonide per injection session. In an unusually severe case, a total dose of up to 60 to 80 mg per session is acceptable, ideally with at least 3 to 4 months interval between sessions.
It is common for oral disease to be the initial and/or most recalcitrant manifestation of immunobullous disorders. Systemic medications are therefore often necessary to achieve adequate disease control. For a complete discussion of systemic immunosuppressive therapies (azathioprine, cyclophosphamide, cyclosporine, intravenous immunoglobulin [IVIg], methotrexate, mycophenolate mofetil, prednisone, rituximab, tacrolimus, tumor necrosis factor [TNF]-α antagonists) and anti-inflammatory agents (dapsone, tetracycline/nicotinamide) used in the treatment of immunobullous and other inflammatory disorders that cause erosive gingivostomatitis, please refer to the appropriate individual chapters and relevant review articles.
Pain control is an important adjunct in the management of patients with erosive gingivostomatitis; depending on the severity of the patient’s discomfort, prescription analgesics and pain management consultation should be judiciously considered. Acute and chronic prophylactic treatment of concomitant HSV infection or secondary candidiasis should be undertaken. Referral for nutritional evaluation and maintenance is recommended.
Most cases of primary herpetic gingivostomatitis occur in early childhood and are often misdiagnosed as an unspecified viral illness. A recurrent episode may be the first indication that the patient was previously exposed to HSV. Recurrences may vary significantly in severity and extent of involvement. Although HSV1 may predominate in the oral cavity, HSV2 can also be found. Infection with HSV1 and HSV2 cannot be distinguished clinically. Oral recurrences occur less frequently with HSV1 than with HSV2.
The treatment goal is to minimize symptoms and accelerate resolution of herpetic lesions. Topical antiviral agents are of limited utility and will not be discussed. Oral therapy for HSV is covered in available reviews and in Chapter 11 of this book. The earlier in the course (within 24–48 hours of prodrome onset) that antiviral agents are initiated, the more effective they are. Daily suppressive antiviral therapy is indicated in patients who experience more than six episodes of oral/labial HSV infection per year.
OTC systemic analgesics (acetaminophen, ibuprofen) adequately manage the associated pain and malaise of HSV infection.
Rx : Lidocaine 2% viscous (Xylocaine)
C. albicans is an oral commensal fungus present in as many as 30% to 50% of healthy adult mouths. Predisposing factors to developing oral candidiasis include xerostomia, use of removable oral prosthesis (e.g., partial denture, full denture, mouthguard, nightguard, retainer, etc.), tobacco use, poor oral hygiene, and immunosuppression. A diagnosis of oral candidiasis cannot be made from cultures alone, but rather requires clinical and cytologic evidence of an infection or clinical overgrowth. Oral candidiasis can present as pseudomembranous candidiasis, erythematous candidiasis, angular cheilitis, median rhomboid glossitis and hyperplastic candidiasis. Demonstration of pseudohyphae and blastospores using a potassium hydroxide (KOH) preparation or a periodic acid-Schiff (PAS) stain is highly suggestive of infection. However, a negative KOH preparation does not exclude active infection. Culture results should be used in conjunction with the clinical presentation to determine whether C. albicans is clinically active. Early treatment of oral candidiasis will relieve the discomfort and prevent systemic spread of localized disease (noted in immunocompromised transplant patients or patients with severe human immunodeficiency virus [HIV] infection). C. albicans is the most commonly isolated pathogen in individuals infected with HIV. C. albicans accounts for almost 50% of all episodes of candidemia, followed by Candida tropicalis (20%) and Candida glabrata (10%). Cultures are necessary to speciate and to determine antifungal resistance.
Oral antifungal formulations (clotrimazole troches, nystatin pastilles) contain sucrose (presenting an increased risk of developing caries with prolonged use), worsen glucose intolerance and ironically promote the overgrowth of Candida. Q61.7 Oral appliances may harbor pathogenic organisms, and pseudohyphae have been found throughout the microscopic pores of these appliances. Soaking appliances in a dilute bleach solution (1 tsp of bleach per cup of water), for 20 minutes twice daily, reduces the fungal burden and limits recurrent infections. In addition, for further prophylactic effects antifungal powders (nystatin) may be applied to the inner aspect of these appliances before placing them in the mouth. Patients should be counseled to remove their oral appliances at night to help prevent denture stomatitis. No difference between the use of disinfective/antiseptic methods and antifungal therapy was demonstrated for the management of denture stomatitis. Innate resistance of C. glabrata to azole antimycotic therapy must be considered when treatment fails.
Q61.7
Rx: Gentian violet solution, 0.5% to 2%
Disp: 60 mL
Sig: Apply 1.5 mL to affected mucosa BID.
NB: Purple staining of skin and clothing limits this old standby antiseptic agent with both anticandidal and antistaphylococcal properties.
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Rx : Clotrimazole troches 10 mg (Mycelex)
Disp : 70 tablets (bottles contain either 70 or 140 tablets)
Sig : Slowly dissolve 1 tablet in mouth 5 times daily for 7 to 14 days.
NB : Difficult to dissolve in patients with xerostomia. Periodic assessment of hepatic function is advisable, particularly in patients with pre-existing liver disease. Clotrimazole troches 3 times daily can be used for prophylaxis in leukemic patients receiving chemotherapy.
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Rx : Nystatin lozenges (pastilles), 200,000 units
Disp : 60 tablets
Sig : Slowly dissolve 1 to 2 tablet in the mouth 4 times daily. NPO for 30 minutes. Continue use for 48 hours after symptoms resolve or for 7 to 14 days.
NB : Tablets are more effective than oral suspension and have a pleasant taste. Risk of nausea and vomiting. Difficult to dissolve in patients with xerostomia.
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Rx : Nystatin oral suspension, 100,000 units/mL (Mycostatin)
Disp : 240 mL (12-day supply)
Sig : Gargle 4 to 6 mL QID (after meals and at bedtime), hold in mouth for 5 to 10 minutes. Then swallow. NPO for 30 minutes. Continue use for 48 hours after symptoms resolve.
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Rx: Fluconazole 40 mg/mL powder for oral suspension
Disp: 35 mL
Sig: 200 mg (5 mL) by mouth the first day (loading dose) and then 100 mg (2.5 mL) every (Q)day for 2 weeks.
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Rx: Miconazole mucoadhesive buccal 50-mg tablet (Oravig)
Disp: 14 tablets
Sig: Apply the rounded side of 1 tablet to a depression in the upper gum, in the morning after brushing teeth. Apply pressure for 30 seconds. Reapply if the tablet does not adhere or if it is swallowed within 6 hours of placement. Continue for 7 to 14 days.
NB: Can be used in patients with oral ulcerations or dry mouth. Miconazole may alter the pharmacokinetics of drugs metabolized through cytochrome P-450 (CYP)2C9 (warfarin) and CYP3A4 (oral hypoglycemics, phenytoin, ergot alkaloids).
Q61.7 Systemic antifungals, such as itraconazole, are associated with increased potential for adverse drug–drug interactions owing to their strong inhibition of CYP3A4 hepatic metabolic pathways. They are typically reserved for use in immunocompromised patients.
Rx : Fluconazole tablets 100 mg (Diflucan)
Disp : 15 tablets
Sig : Take 2 tablets stat (loading dose) and 1 tablet daily thereafter for 2 weeks.
NB : Well absorbed at any gastric pH. Rare hepatic toxicity, albeit unlikely with short courses of therapy. Be aware of many drug interactions (see Chapters 10 , Chapters 66 ). Resistance may require higher doses. For patients with recurrent infection who require chronic suppressive therapy, administer 100 mg 3x/week. Avoid during pregnancy.
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Rx : Itraconazole oral solution 10 mg/mL or 100 mg capsules (Sporanox)
Disp : 200 to 280 mL or 10 to 14 capsules
Sig : 10 to 20 mL or 1 to 2 capsules orally (PO) daily with food. Continue for 1 week past resolution of symptoms.
NB : Take with food for improved absorption for the capsule; the oral solution is better absorbed on an empty stomach. Avoid concomitant antacids and H 2 antagonists, as they lead to decreased absorption. Avoid during pregnancy. Patients with fluconazole-refractory candidiasis may respond to itraconazole.
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Rx : Posaconazole suspension 40 mg/mL (Noxafil)
Disp : 105 mL
Sig : Loading dose of 100 mg (2.5 mL) BID for 1 day then 100 mg (2.5 mL) qday (QD) for an additional 13 days. May require 400 mg BID for 3 days followed by 400 mg QD or BID for 25 to 28 days for refractory disease. Avoid during pregnancy.
NB : Shake well before using to ensure proper even mixing. Must be taken with a full meal or with liquid nutritional supplement. Reserved for fluconazole-resistant strains or refractory disease.
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Rx: Voriconazole suspension 40 mg/mL and 200-mg tablet (Vfend)
Disp: 100 mL or 50 tablets
Sig: 200 mg (5 mL) PO Q12h for at least 14 days.
NB: Treatment should be continued for at least 7 days following resolution of symptoms. Indicated for treatment of esophageal candidiasis with or without oropharyngeal candidiasis. Tablets should be taken 1 hour before or after meals. Reserved for fluconazole-refractory disease. Contraindicated in pregnancy.
Hairy tongue (black hairy tongue, lingua villosa nigra) is a common, unsightly, reactive condition on the dorsal surface of the tongue. Keratin accumulates on elongated hypertrophic filiform papillae, with subsequent deposition of exogenous pigment from food/beverages, tobacco, medication (bismuth, chlorhexidine, doxycycline, erlotinib) and/or chromogenic bacteria or yeast. Most patients are asymptomatic; altered taste, gagging sensation, and malodor may occur. Risk factors include poor oral hygiene, tobacco use, ingestion of pigmented foods and drinks (coffee, tea, and licorice), use of hydrogen peroxide mouth rinses, use of broad-spectrum antibiotics, chemotherapy and radiation therapy. Contributing factors should be discontinued. Mechanical debridement using a toothbrush with or without a baking soda slurry or tongue scraper helps control this condition. There is no FDA-approved treatment for hairy tongue. The use of antifungals or other agents including urea 40% solution, salicylic acid 15% in glycerol, gentian violet, thymol, and trichloroacetic acid 30% to 50% have been reported.
Rx : Tretinoin 0.1% gel (Retin-A)
Disp : 20, 45 g
Sig : Apply to dorsal surface of tongue for 5 minutes. Then rinse with warm water. Brush treated area with a firm toothbrush, tongue cleaner, or tongue scraper.
RAS is the most common cause of oral ulceration. In contrast to the shaggy ulcers, frequently seen in vesiculobullous disease, RAS presents with well-circumscribed oval to round ulcers with an erythematous halo. They may be solitary or multiple and range in size from 1 to 2 mm up to 1 to 2 cm. Minor aphthae, ranging in size from 0.5 to 1 cm, account for 90% of all oral aphthae. Major aphthae are more than 1 cm in diameter and usually solitary, whereas herpetiform (grouped) aphthae present as crops of 1 to 2 mm ulcers that must be differentiated from HSV infection. Aphthous ulcers, regardless of size, characteristically occur on nonkeratinized mucosa (see later). A biopsy is indicated to evaluate for malignancy or infection in select persistent ulcers. The pathogenesis of RAS is unknown. Impaired cellular immunity and cytokine gene polymorphisms have been implicated.
Complex aphthosis describes patients with continuous oral ulceration or patients who have multiple mucosal sites (oral and genital) affected by aphthae. Complex aphthosis may be idiopathic or occur in the context of systemic illness (Behçet disease, HIV infection, Trisomy 8-positive myelodysplastic syndrome).
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