Nicotine Stomatitis (Smoker's Palate)

Updated: Feb 15, 2022
Author: James E Cade, DDS, FACD; Chief Editor: Jeff Burgess, DDS, MSD 


Practice Essentials

Nicotine 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. The condition has also been noted in electronic cigarette users.[4]  Generally, nicotine stomatitis 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.

The mechanism of action of nicotine stomatitis (smoker's palate) 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.

(See the image below.)

Classic nicotine stomatitis. Note the speckled whi Classic nicotine stomatitis. Note the speckled white and red appearance from the hyperkeratosis and minor salivary gland openings.

Rawal et al reported 2 cases of patients using marijuana with oral manifestations. They observed nicotine stomatitis–like lesions in addition to gingival hyperplasia and uvulitis.[5]  The heat from smoking marijuana causing minor salivary gland inflammation theoretically should produce similar lesions as tobacco smoking.

Nicotine stomatitis first becomes visible as a reddened area and slowly progresses to a white, thickened, and fissured appearance. The palate has numerous minor salivary glands. They become swollen and the orifices become prominent, giving the tissue a speckled white and red appearance. Patients with nicotine stomatitis are usually asymptomatic. An association of nicotine stomatitis with human papillomavirus (HPV) infection, alcohol intake, genetics, and diet are unknown.[6]

Nicotine stomatitis affects the oral mucosa of the hard palate posterior to the rugae and the adjacent soft palate.[7, 8] . 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.

Inflamed salivary gland ducts in nicotine stomatit Inflamed salivary gland ducts in nicotine stomatitis.

If unable to make the diagnosis of nicotine stomatitis by clinical appearance or if the lesion does not resolve after cessation of smoking, perform a 5-mm punch biopsy or scalpel biopsy. A biopsy is also indicated in a patient with a symptomatic lesion, even if it appears consistent with a benign smoker’s palate, or if the patient reports that he or she is a reverse smoker.

Histologically, nicotine stomatitis lesions appear acanthotic and hyperkeratotic, with some mild-to-moderate chronic inflammation. The epithelium of the minor salivary ducts often shows squamous metaplasia. 


The incidence of nicotine stomatitis in the United States is unknown. However, approximately 40 million Americans smoke.[9]  A large study in Saudi Arabia showed that 29.6% of all smokers had nicotine stomatitis and that 60% of pipe smokers had nicotine stomatitis. There also have been studies of smokers in India,[10] Turin,[11] and China.[12]

The appearance of nicotine stomatitis is related directly to the population that smokes tobacco products. Men and women who smoke tobacco products are affected equally by nicotine stomatitis. Women smoke pipes less often than men; therefore, nicotine stomatitis is less prevalent in women. Nicotine stomatitis is related to duration, intensity, and types of smoking and is not related to the age of the smoker.[13]


Nicotine stomatitis is generally a reversible lesion once the irritant is removed. The prognosis for nicotine stomatitis is excellent. Although nicotine stomatitis is caused by smoking tobacco products, it is generally not associated with dysplastic or malignant changes.[14] Essentially, it has the same malignant potential as normal hard and soft palate.[15] 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.[16] 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.[17]



Physical Examination

Lesions of nicotine stomatitis are exclusively found on the palatal mucosa. They have a white cobblestone appearance, often with a red dot in the center of the cobblestone. The nicotine stomatitis lesion cannot be wiped off and can have some fissuring. Nicotine stomatitis is primarily limited to the posterior hard palate and less often to the adjacent soft palate.

(See the images below.)

Fissured appearance of nicotine stomatitis. Notice Fissured appearance of nicotine stomatitis. Notice the gingival-palatal areas where a partial denture protects the mucosa from the heat and smoke.
Nicotine stomatitis in a reverse smoker. Notice th Nicotine stomatitis in a reverse smoker. Notice the increased hyperkeratosis, hyperplasia, and swelling of minor salivary glands.




Medical Care

The only definitive treatment for nicotine stomatitis is smoking cessation. Myung et al reported from a meta-analysis of randomized, controlled trials that sufficient clinical evidence exists to support the use of computer- and Internet-based smoking cessation programs in adults who smoke.[18]

If any of the smoking-cessation medications appear to be effective, continue medications in conjunction with support groups. The most effective long-term smoking-cessation results are observed in patients who are members of support groups.

It has been suggested that resveratrol, a polyphenol medication, could prevent or treat oral inflammatory lesions, including nicotine stomatitis.[19]

If a patient is interested in stopping the tobacco habit, a referral to a comprehensive smoking-cessation program is indicated. This program should include peer-group sessions.[20, 21]

To prevent nicotinic stomatitis lesions and other more serious tobacco-induced lesions in the oral cavity, counsel patients on the dangers of tobacco use. Once they understand the need to stop using tobacco products, make a referral to a comprehensive tobacco-cessation program.

Monitor patients with nicotine stomatitis. If after smoking cessation the lesion does not resolve, further investigation is warranted.



Medication Summary

Medical therapy for nicotine stomatitis is directed at smoking cessation.[22, 23]  Varenicline decreases the stimulatory effect from consuming nicotine products by blocking nicotine receptors.[24, 25]

Nicotine substitutes

Class Summary

Nicotine substitutes are available as a transdermal patch, gum, an inhaler, or nasal spray.

Nicotine transdermal system (Nicotrol, NicoDerm CQ, Habitrol)

The nicotine transdermal system works best when used in conjunction with a support program (eg, counseling, group therapy, behavioral therapy).

Antidepressant agents

Class Summary

These are used in conjunction with a support group and/or behavioral counseling.

Bupropion (Zyban)

Bupropion inhibits neuronal dopamine reuptake in addition to being a weak blocker of serotonin and norepinephrine reuptake.

Nicotinic acetylcholine receptor partial agonists

Class Summary

Nicotinic acetylcholine receptor partial agonists bind to nicotine receptors and elicit mild nicotine central effects to ease withdrawal symptoms.

Varenicline (Chantix)

Varenicline is a partial agonist selective for alpha4, beta2 nicotinic acetylcholine receptors. Its action is thought to result from activity at a nicotinic receptor subtype, where its binding produces agonist activity while simultaneously preventing nicotine binding. Agonistic activity is significantly lower than nicotine. It also elicits moderate affinity for 5-HT3 receptors. Maximum plasma concentrations occur within 3-4 hours after oral administration. Following regular dosing, a steady state reached within 4 days.