Nicotinic Stomatitis
Definition: Nicotinic stomatitis or smoker’s palate is a relatively common tobacco-related type of hyperkeratosis that occurs exclusively on the hard palate, and is classically associated with heavy pipe, cigar, or cigarette smoking.
Etiology: Mainly the elevated temperature and lesser the tobacco chemicals are the etiologic factors.
Clinical features: Clinically, nicotinic stomatitis appears with redness of the palatal mucosa, which later assumes a grayish-white color. It presents with numerous small nodules with characteristic red dots 1 to 5 mm in diameter. They represent the inflamed and dilated orifices of the minor salivary grand ducts (▶ Fig. 1.17). In heavy smokers, fissures, furrows, and mucosal elevation may occur forming an irregular wrinkled surface. The palatal lesions are not potentially malignant. The diagnosis is based on the history and clinical features. Biopsy only rarely may be necessary.
Laboratory tests: Usually not required. However, a histopathologic examination is occasionally useful.
Differential diagnosis: Reverse smoker’s palate, thermal burn, chemical burn, leukoplakia, Darier’s disease, discoid lupus erythematosus, and candidiasis.
Treatment: Cessation of smoking.
Fig. 1.17 Typical nicotine stomatitis.
1.7 Cigarette Smoker’s Lip Lesions
Definition: Cigarette smoker’s lip lesions are common in heavy smokers (over of 40 cigarettes daily) of nonfiltered cigarettes.
Etiology: The lesions are due to high temperature that develops in the area during smoking.
Clinical features: Characteristically, the lesions appear on the mucosal surface of the lower lip corresponding to the site at which the cigarette is held. Clinically, the lesions appear as flat or slightly elevated, asymptomatic whitish wide lines intermixed with red striations (▶ Fig. 1.18). The lesions are not premalignant. The diagnosis is exclusively based on the history and clinical features.
Differential diagnosis: Chronic biting, chemical and thermal burn, cinnamon contact stomatitis, candidiasis, lichen planus, leukoplakia, and discoid lupus erythematosus.
Treatment: The lesions usually disappear after smoking cessation in 1 to 2 months.
Fig. 1.18 White lines of the lower lip due to heavy smoking.
1.8 Uremic Stomatitis
Definition: Uremic stomatitis is a relatively rare complication of acute or chronic renal failure.
Etiology: It is caused by increased levels of urea and other nitrogen-containing products in the peripheral blood and saliva. Uremic stomatitis usually occurs when the urea levels in the blood exceed 300 mg/100 mL. The degradation of oral urea by the enzyme urease forms free ammonia, which may damage the oral mucosa.
Clinical features: Two main forms of uremic stomatitis are recognized: (1) the ulcerative and (2) the nonulcerative. The ulcerative form is characterized by painful, superficial, and irregular ulcers of different sizes. These ulcers are covered by a white-brown or black pseudomembrane (▶ Fig. 1.19). The nonulcerative form presents with creased, thick, white projections or plaques that are painful and develop on an inflammatory base (▶ Fig. 1.20). The floor of the mouth and the tongue are more frequently affected. Hemorrhage and hematomas may also be observed. Candidiasis and other opportunistic viral and bacterial infections are common oral complications. Unpleasant taste, xerostomia, characteristic uriniferous breath odor, and a burning sensation are common symptoms. The diagnosis of uremic stomatitis is based on the medical history and clinical features, but should be confirmed by laboratory tests.
Laboratory tests: The blood and urine levels of urea should be determined for accurate diagnosis.
Differential diagnosis: Pseudomembranous candidiasis, cinnamon contact stomatitis, hairy leukoplakia, verrucous hyperplasia, verrucous leukoplakia, necrotizing ulcerative stomatitis, drug-induced stomatitis, and white sponge nevus.
Treatment: The oral lesions usually improve after 2 to 4 weeks after hemodialysis and improvement of renal function. A high level of oral hygiene, oxygen-releasing mouthwashes, and artificial saliva are recommended.
Fig. 1.19 Uremic stomatitis, ulceration covered by a necrotic black pseudomembrane on the buccal mucosa.
Fig. 1.20 Uremic stomatitis, white, elevated, creased plaques on the lateral border of the tongue.
1.9 Cinnamon Contact Stomatitis
Definition: Cinnamon contact stomatitis is a relatively common oral mucosal reaction in individuals that consume artificially flavored cinnamon-containing products.
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.
