Nicotine Stomatitis

Nicotine Stomatitis

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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.

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.

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.

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]

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 nicotinic stomatitis. Women smoke pipes less often than men; therefore, nicotinic stomatitis is less prevalent in women.

Nicotinic stomatitis is related to duration, intensity, and types of smoking and is not related to the age of the smoker. [11]

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]

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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dos Santos RB, Katz J. Nicotinic stomatitis: positive correlation with heat in maté tea drinks and smoking. Quintessence Int. 2009 Jul-Aug. 40(7):537-40. [Medline].

Rawal SY, Tatakis DN, Tipton DA. Periodontal and oral manifestations of marijuana use. J Tenn Dent Assoc. 2012 Fall-Winter. 92 (2):26-31; quiz 31-2. [Medline].

Vellappally S, Fiala Z, Smejkalova J, Jacob V, Somanathan R. Smoking related systemic and oral diseases. Acta Medica (Hradec Kralove). 2007. 50(3):161-6. [Medline].

Samatha Y, Sankar AJ, Ganapathy KS, Srinivas K, Ankineedu D, Choudary AL. Clinicopathologic evaluation of lesions associated with tobacco usage. J Contemp Dent Pract. 2014 Jul 1. 15 (4):466-72. [Medline].

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Mathew AL, Pai KM, Sholapurkar AA, Vengal M. The prevalence of oral mucosal lesions in patients visiting a dental school in Southern India. Indian J Dent Res. 2008 Apr-Jun. 19(2):99-103. [Medline].

Pentenero M, Broccoletti R, Carbone M, Conrotto D, Gandolfo S. The prevalence of oral mucosal lesions in adults from the Turin area. Oral Dis. 2008 May. 14(4):356-66. [Medline].

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Neville BW, Damm DD, Allen CM, Chi AC. Epithelial Pathology. Oral and Maxillofacial Pathology. 4th ed. Philadelphia, Pa: Saunders; 2016. 331-421.

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Myung SK, McDonnell DD, Kazinets G, Seo HG, Moskowitz JM. Effects of Web- and computer-based smoking cessation programs: meta-analysis of randomized controlled trials. Arch Intern Med. 2009 May 25. 169(10):929-37. [Medline].

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James E Cade, DDS Associate Professor, Chair, Department of Oral Diagnostic Sciences, Meharry Medical College School of Dentistry; Private Practice, Honeycutt Family Dentistry

James E Cade, DDS is a member of the following medical societies: American Academy of Oral and Maxillofacial Pathology, American Academy of Oral Medicine, American Dental Association

Disclosure: Nothing to disclose.

David F Butler, MD Former Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for MOHS Surgery, Association of Military Dermatologists, Phi Beta Kappa

Disclosure: Nothing to disclose.

Drore Eisen, MD, DDS Consulting Staff, Dermatology of Southwest Ohio

Drore Eisen, MD, DDS is a member of the following medical societies: American Academy of Dermatology, American Academy of Oral Medicine, American Dental Association

Disclosure: Nothing to disclose.

Jeff Burgess, DDS, MSD (Retired) Clinical Assistant Professor, Department of Oral Medicine, University of Washington School of Dental Medicine; (Retired) Attending in Pain Center, University of Washington Medical Center; (Retired) Private Practice in Hawaii and Washington; Director, Oral Care Research Associates

Disclosure: Nothing to disclose.

Marjan Garmyn, MD, PhD Professor, Faculty of Medicine, Katholieke Universiteit Leuven, Belgium; Chair and Adjunct Head, Department of Dermatology, University of Leuven, Belgium

Disclosure: Nothing to disclose.

Sol Silverman, DDS, MA, DipABOM Professor Emeritus, Department of Orofacial Sciences, University of California at San Francisco

Sol Silverman, DDS, MA, DipABOM is a member of the following medical societies: American Academy of Oral Medicine, American Dental Association

Disclosure: Nothing to disclose.

Dana Gelman Keiles, DMD Assistant Clinical Professor, Department of Stomatology, University of California at San Francisco

Dana Gelman Keiles, DMD is a member of the following medical societies: American Academy of Oral Medicine, American Dental Association

Disclosure: Nothing to disclose.

Nicotine Stomatitis

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