A thermally induced keratosis of the hard palate in especially pipe smokers and in a lesser extent in cigar or heavy cigarette smokers. Nicotine stomatitis is a response to heat and not to the chemicals in tobacco, which explains that it does not have a premalignant character. Especially pipe smoking induces the lesion, probably because pipe smoking generates more heat on the palate than the other forms of smoking.
Reverse smoking, as practiced in South American and Southeast Asian countries, with the burning end held inside the mouth, produces a more or less similar clinical picture. However, this lesion has a significant potential to develop dysplasia or carcinoma.
The use of electronic cigarettes (EC) has rapidly gained popularity. Stomatitis nicotina seems to occur more often in EC-smokers than in smokers of regular cigarettes, possibly due to the combination of nicotine, heat, and fine particles of flavors (Bardellini et al. 2018). EC smoking also induces a higher prevalence of smoker’s melanosis, hairy tongue, and hyperplastic candidiasis.
Incidence: Stomatitis nicotina was once a common entity; due to a decrease in pipe and cigar smoking, the lesion decreased in prevalence. However, due to the introduction of electronic cigarettes, the entity may increase again.
Age: Persons affected are mostly older than 45 years.
Sex: Mostly men.
Site: Stomatitis nicotina is located on the hard palate.
Treatment: Smoking cessation.
Outcome: It is a completely reversible condition, independent of the duration of the lesion, within 1 or 2 weeks after cessation of smoking.
Hyperkeratosis and acanthosis of the palatal squamous epithelium are present with chronic inflammation of the subepithelial connective tissue and mucous glands. The excretory ducts show squamous hyperplasia and metaplasia due to the chronic inflammatory infiltrate.