Background
Nicotinic stomatitis (smoker's palate), a lesion of the palatal mucosa, has been described in the literature since 1926. In 1941, Thoma named the lesion stomatitis nicotine because it is almost exclusively observed in individuals who smoke tobacco. [1] The name is a misnomer because it is not the nicotine that causes the lesion, but the concentrated heat stream of smoke from tobacco products. [2, 3] These mucosal changes are most often observed in pipe and reverse cigarette smokers and less often in cigarette and cigar smokers. Generally, it is asymptomatic or mildly irritating. Patients typically report that they are either unaware of the lesion or have had it for many years without changes. See the image below.

Rawal et al reported two cases of patients using marijuana with oral manifestations. They observed nicotine stomatitis–like lesions in addition to gingival hyperplasia and uvulitis. [4] The heat from smoking marijuana causing minor salivary gland inflammation theoretically should produce similar lesions as tobacco smoking.
Pathophysiology
Nicotine stomatitis affects the oral mucosa of the hard palate posterior to the rugae and the adjacent soft palate. [5, 6] . Lesions are not seen on the anterior hard palate since there are no minor salivary glands present where the rugae are present. The red orifices of the lesions are inflamed salivary gland ducts, as shown in the image below.
Etiology
Nicotine stomatitis has been associated with pipe, cigarette, and cigar smoking, and, rarely, with chronic ingestion of high-temperature liquids or other irritants. The mechanism of action is heat and chemical irritation from a tobacco product that acts as a local irritant, stimulating a reactive process, including inflammation, hyperplasia, and epithelial keratinization. Dentures often protect the palate from these irritants in patients who wear them.
Epidemiology
Frequency
United States
The incidence of nicotinic stomatitis in the United States is unknown. However, approximately 40 million Americans smoke. [7]
International
A large study in Saudi Arabia showed that 29.6% of all smokers had nicotine stomatitis and that 60% of pipe smokers had nicotinic stomatitis. See also studies of smokers in India, [8] Turin, [9] and China. [10]
Race
The appearance of nicotine stomatitis is related directly to the population that smokes tobacco products.
Sex
Men and women who smoke tobacco products are affected equally by nicotinic stomatitis. Women smoke pipes less often than men; therefore, nicotinic stomatitis is less prevalent in women.
Age
Nicotinic stomatitis is related to duration, intensity, and types of smoking and is not related to the age of the smoker. [11]
Prognosis
Nicotine stomatitis is generally a reversible lesion once the irritant is removed. The prognosis for nicotinic stomatitis is excellent. Although nicotine stomatitis is caused by smoking tobacco products, it is generally not associated with dysplastic or malignant changes. [12] Essentially, it has the same malignant potential as normal hard and soft palate. [13] The exception to this is in individuals who reverse smoke. Reverse smoking is common in some parts of the Caribbean and Southeast Asia. The concentrated heat and chemicals increase the potential for malignant change. [14] Nicotine stomatitis is an indicator of heavy smoking tobacco use. Careful oral examination in these patients is needed since these patients may have a higher risk for premalignant and malignant mucosal lesions on other oral mucosal surfaces. [15]
Patient Education
Educate patients with nicotinic stomatitis concerning the dangers of tobacco use. Many cigar and pipe smokers believe that they are not at risk for cancer because they do not inhale.
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Classic nicotine stomatitis. Note the speckled white and red appearance from the hyperkeratosis and minor salivary gland openings.
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Fissured appearance of nicotine stomatitis. Notice the gingival-palatal areas where a partial denture protects the mucosa from the heat and smoke.
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Nicotine stomatitis in a reverse smoker. Notice the increased hyperkeratosis, hyperplasia, and swelling of minor salivary glands.
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Inflamed salivary gland ducts in nicotine stomatitis.