Etiology: The release of the cinnamon ethereal oils and their constant contact with the oral mucosa, usually in the form of chewing gums, candies, toothpaste, dental floss, and mouthwashes may cause hypersensitivity reactions and oral lesions.
Clinical features: Clinically, erythema of the oral mucosa, white hyperkeratotic projections or plaques, and superficial erosions are the prominent features (▶ Fig. 1.21 and ▶ Fig. 1.22). A burning sensation and mild pain are common symptoms. The lateral border and the ventral surface of the tongue, the buccal mucosa, and the gingiva are more frequently affected. Exfoliative cheilitis and perioral dermatitis have also been described. The lesions may be localized or diffuse and mimic hairy leukoplakia, particularly, when they develop on the lateral aspect of the tongue, and lichen planus when they occur on the buccal mucosa. The diagnosis is mainly based on the history and clinical features.
Laboratory tests: Usually not required. In rare cases, biopsy and histopathologic examination may be needed.
Differential diagnosis: Candidiasis, lichen planus, hairy leukoplakia, leukoplakia chemical burn, chronic biting, leukoedema, amalgam contact reaction, plasma cell stomatitis, uremic stomatitis, and discoid lupus erythematosus.
Treatment: Discontinuation of any cinnamon product is the first step. This improves the signs and symptoms in approximately 2 weeks’ time. In severe and extended lesions with erosions, systemic corticosteroids in low dose (e.g., 10–20 mg/d prednisolone) for 5 to 7 days help the lesions to heal sooner.
Fig. 1.21 Cinnamon contact stomatitis of the lateral border of the tongue.
Fig. 1.22 Cinnamon contact stomatitis of the buccal mucosa.
1.10 Chemical Burn
Definition: Chemical burn of the oral mucosa is a relatively common lesion.
Etiology: It is caused by careless or inappropriate use of a large number of caustic chemical agents and local drugs in dental practice or by the patients. The most common causative agents include locally applied hydrogen peroxide, phenol, alcohol, iodine, silver nitrate, trichloroacetic acid, sodium perborate, eugenol, paraformaldehyde, household chemicals, etc.
Clinical features: Clinically, the affected oral mucosa is covered with pseudomembrane, usually white or whitish gray or black, due to epithelial necrosis (▶ Fig. 1.23, ▶ Fig. 1.24, and ▶ Fig. 1.25). The necrotic epithelium can easily be scraped off, leaving a red surface with or without bleeding, and occasionally erosions. The lesions are usual painful and heal within 4 to 6 days. The diagnosis is, exclusively, based on the history and clinical features.
Differential diagnosis: Thermal burn, mechanical trauma, chronic biting, candidiasis, cinnamon contact stomatitis, necrotizing ulcerative stomatitis and gingivitis, secondary herpetic oral lesions, lichen planus, and leukoplakia.
Treatment: It is symptomatic, as the lesions heal spontaneously within 4 to 6 days. Topically, oxygen-releasing mouthwashes are helpful. In severe cases, systemic corticosteroids in a low dose (10–15mg/d prednisolone for 3–6 days) improve the symptoms soon.
Fig. 1.23 Chemical burn of the buccal mucosa due to acetylsalicylic acid (aspirin).
Fig. 1.24 Trichloroacetic acid burn.
Fig. 1.25 Chemical burn caused by hydrogen peroxide.
1.11 Candidiasis
Definition: Candidiasis is the most frequent oral fungal infection. Over the last four decades, the disease has taken on major importance.
Etiology: Oral candidiasis is usually caused by Candida albicans, a fungus found in 20 to 50% of the normal oral flora of healthy people, and is rarely caused by other Candida strains (C. tropicalis, C. glabrata, C. krusei, C. parapsilosis, C. guilliermodii, etc.). The predisposing factors for oral candidiasis may be local (poor oral hygiene, xerostomia, chronic mucosal trauma, dentures, antibiotic mouthwashes, chronic use of inhalational or topical corticosteroids, and radiotherapy of the head and neck) and systemic (iron deficiency anemia, diabetes mellitus, primary immunodeficiency, HIV infection, hematological malignancies, neutropenia, aplastic anemia, systemic corticosteroids and immunosuppressive drugs, systemic antibiotics, hypoparathyroidism, and other endocrine diseases).
Clinical features: Oral candidiasis is classified into primary, including lesions exclusively in the mouth and the perioral skin, and secondary, including the oral lesions of mucocutaneous candidiasis. The primary oral candidiasis is classified into five clinical varieties: (1) pseudomembranous, (2) erythematous, (3) nodular or plaque-like, (4) papillary hyperplasia of palate, and (5) lesions contaminated with candida (angular cheilitis, median rhomboid glossitis, and denture stomatitis). The main forms of oral candidiasis that produce white lesions are: (1) pseudomembranous candidiasis, which is the most common form of the disease and may be acute or chronic (rare). Clinically, it is characterized by creamy white or whitish-yellow, slightly elevated spots or plaques which are easily detached, leaving a raw reddish or normal surface (▶ Fig. 1.26). The lesions may be localized or generalized, and more frequently appear on the buccal mucosa, tongue, palate, lips, and gingiva. Xerostomia, a burning sensation, unpleasant taste, and difficulty in swallowing are the most common symptoms. The diagnosis is usually based on the clinical features. (2) Nodular candidiasis, characterized by white, firm, and raised plaques that usually do not detach (▶ Fig. 1.27). The lesions may persist for a longer time and are usually located on the dorsum of the tongue and the commissures. (3) Mucocutaneous candidiasis, which is a heterogeneous and rare group of clinical syndromes, that are characterized by chronic lesions of the skin, nails, and mucosae, and are usually accompanied with immunological defects. Clinically, the oral lesions appear as white, multiple, plaques, which cannot be removed (▶ Fig. 1.28). Characteristically, the lesions are generalized, with a predilection for the tongue, buccal mucosa, commissures, and palate. Cutaneous and nail involvement are associated with the oral lesions.
Laboratory tests: Direct microscopic examination of smears and microbiological culture are suggested. In chronic forms biopsy and histopathologic examination with periodic acid-Schiff stain is indicated.
Differential diagnosis: Leukoplakia, hairy leukoplakia, cinnamon contact stomatitis, uremic stomatitis, lichen planus, lupus erythematosus, chronic biting, oral epitheliolysis, chemical and thermal burns, syphilitic mucous patches, and white sponge nevus.
Treatment: Systemic triazoles (fluconazole, itraconazole, and ketoconazole) are the drugs of choice. The dosage and duration of treatment depends on the form of candidiasis and the presence of predisposing factors. Meticulous oral hygiene and resolution of any local or systemic predisposing factor is also suggested. Topical treatment with nystatin or miconazole may also be used particularly for infants and children.