Volume 1, Issue 1


An Update of Evaluation of Common Oral Lesions

October 12, 2009

A family practitioner may see a variety of oral conditions daily during physical examination of patients and may be called upon to identify the oral pathology and provide care or referral for care of oral disease. There are many superficial mucosal lesions, masses and tumors that affect the oral cavity that may be commonly seen. The size and location, surface appearance and texture, duration of the lesion and associated pain, should be noted during examination. Further, forming a differential diagnosis of oral disease requires knowledge of the pathogenesis and characteristics of oral disease and proper treatment. In informing patients of the diagnosis, the medical professional should be comfortable discussing the prognosis of the diagnosed condition. Of course, the most common oral diseases caused by bacteria, dental caries and periodontal disease, should prompt referral to a general dentist for treatment. There are a dozen other common conditions of the oral and paraoral region, however, that may be first diagnosed by a family practitioner. These conditions from most prevalent to least prevalent include denture and recurrent aphthous stomatitis, hyperkeratosis, candidiasis and angular cheilitis, oral nevi, leukoedema, benign migratory glossitis, squamous cell carcimona, acute necrotizing ulcerative gingivitis, lichen planus and herpes labialis are among the most prevalent observed in the U.S. population. Treatment may range from use of topical ointment to referral to an oral and maxillofacial surgeon for biopsy. Interdisciplinary care is often necessary for proper treatment of patients presenting with these common oral lesions.

The prevalence of oral lesions has been reported in a variety of select populations such as those performed with school children, Army recruits and institutionalized patients.1 However, few published studies exist on prevalence of oral lesions in adults in the United States that has been extrapolated from available data. Axéll reported on oral lesions in 1976 among a random sample of 20, 333 Swedish adults with the finding that recurrent apthous ulcers (17.70 percent), recurrent herpes labialis (17.38) and denture stomatitis (16.02 percent) were the most common conditions observed over a two year period.2 Geographic tongue was also seen commonly in 8.57 percent of those sampled. In the U.S., The Third National Health and Nutrition Examination Survey (19881994), NHANES III, reported on 17,235 civilian, noninstitutionalized adults, age 17 and older. 4 801 participants (27.9 percent) were observed to have 6,003 clinically detectable lesions. The examiners were dentists who were trained to identify and record oral conditions for the study. The broad categories of lesions reported included those caused by trauma and the wearing of denture appliances (stomatitis, hyperplasia, ulcers, inflammation and angular cheilitis) and tobacco use (smokeless tobacco and nicotine stomatitis).

The most prevalent lesion reported was the amalgam tattoo which was identified in 3.30 percent of those studied. An amalgam tattoo is staining of the oral mucosa most often resulting from silver impregnated into the tissue during restoration of a carious tooth. Following closely, the second most common condition, observed in 3.05 percent of those studied, morsicatio buccarum, results from a hyperkeratosis of the buccal or cheek mucosa which is pinched between the upper and lower dentition during biting. Similar appearing white lesions resulting from traumatic hyperkeratosis were seen intraorally in 2.67 percent of the population sampled. Denture wearers and people who used smokeless tobacco had the highest likelihood of having leukoplakia: a white lesion of the oral cavity that could not be removed by rubbing that was of unknown etiology. The prevalence of lesions of the oral and paraoral cavity vary with covariants including gender, age, racial and ethnic background as well as habits such as the use of tobacco products, the wearing of dentures and appliances and immunologic status which influence the likelihood of developing oral disease.

Based on analysis of the NHANES III study, Shulman, et al., projected that 28.24 percent of the U.S. population examined had at least one clinically observable oral lesion with the hard palate the most common site (25.9 percent). The gingival, lip and dorsum of the tongue were the next most common sites that lesions were found. Also, Shulman, et al., compared four different categories of tobacco users and found that lesions of the lips, mucosa, tongue and commissures were more common than in nontobacco product users.3

Tobacco users were almost four times as likely to have an oral lesion than those who had never used tobacco products.

US Population

from Shulman, et al., J Am Dent Assoc 2004; 135; 1281

Denture and Recurrent Aphthous Stomatitis

Recurrent aphthous stomatitis sometimes called "canker sores," is a common ulcerative condition of the mouth. Its prevalence in the U.S. may be as high as 20%.4 The condition is characterized by the presence painful oral ulcers. By definition it is a recurring condition and may involve buccal, labial, tongue, hard and soft palate mucosal surfaces. Ulcers are usually shallow, covered by gray, yellow or white plaques and are accompanied by surrounding erythema.


RAS can be quite painful thus inferring with food intake and occasionally with speech in some patients. Etiology of this condition is unknown, however strong genetic predisposition is observed.5 Family history of RAS is common. Some recognized precipitating factors include local trauma (such as dentures, orthodontic braces, toothbrush abrasion, etc.), salivary gland dysfunction, stress, local infections, nutritional deficiencies, GI disorders, systemic disorders, food allergy or hypersensitivity, hormonal fluctuations, and exposure to certain chemicals (for example, sodium lauryl sulfate, a chemical used in many toothpastes).6

RAS occasionally can be associated with certain systemic conditions. Some examples are HIV infection, Behcet’s syndrome, inflammatory bowel disease, celiac disease. There are three main types of RAS: minor, major and herpetiform, with minor form being most common one. Minor aphthous ulcers are less than 10 mm in diameter and usually heal spontaneously in 1014 days. Major aphthous ulcers (also called Sutton’s disease) are greater than 10 mm in diameter, may take up to 30 days or more to heal, and may leave scars.7 Usually, major ulcers first appear after puberty. Herpetiform ulcers are multiple, clustered, 1to 3mm lesions that may coalesce into plaques. These usually heal in 710 days. They are not related to herpes virus and basically differ from the minor form by the number of lesions. When approaching the patient with RAS the initial treatment goals include decreasing the number of ulcers, decreasing pain, and at times reducing frequency.8 Most patients with minor aphthae require no treatment or only periodic topical therapy. Commonly used therapies include topical corticosteroids, such as fluocinonide gel (Lidex) and triamcinolone acetonide with carboxymethylcellulose paste (Kenalog in Orabase). However, much of the evidence in support of these treatments is from small, incompletely blinded trials, and thus their effectiveness is uncertain.9

Chlorhexidine gluconate (Peridex) mouthwash decreases the severity of an episode but does not reduce the incidence of ulcers. Amlexanox 5% paste (Aphthasol) may promote healing and lessen pain. In severe or constantly recurring cases, systemic therapy with agents such as thalidomide (Thalomid) may be necessary. Because of the risk of serious adverse effects and its offlabel status, thalidomide generally is reserved for severe cases such as those associated with HIV infection.10 A biopsy should be considered for solitary or multiple ulcers that last more than three weeks. Immunostaining is mandatory if a mucocutaneous disorder is suspected. The need for additional analyses, such as serologic tests for rheumatologic disease, cultures or other specific tests for infectious agents (such as herpes simplex virus, cytomegalovirus, or HIV), and evaluation for gastrointestinal disease, should be guided by the presence of features suggestive of these disorders.11


Leukoplakia is a term that applies to any white plaque or patch that does not fit the profile of any other disease and is therefore a diagnosis of exclusion. Other potential lesions must be ruled out before a diagnosis of leukoplakia can be justified. Often times, leukoplakia is considered to be a precancerous or premalignant lesion, and it usually affects people over the age of 40, with a strong male predilection. There is also a close association among smoking and leukoplakia. Leukoplakia lesions are typically found on the lip vermillion, buccal mucosa, and gingiva and may have a translucent, fissured, wrinkled, soft, and flat appearance.


The hyperkeratosis associated with leukoplakia is derived from the thickened keratin layer on the surface epithelium, which is visible microscopically. The keratin layer may consist of parakeratin, orthokeratin, or both, and this differentiation may help determine further classification of the leukoplakia in question. Leukoplakia may or may not show dysplastic changes upon microscopic examination. If dysplastic changes exist, the severity is determined based on the layers of epithelium involved. Mild is limited to the basal and parabasal layers. Moderate involves the basal to the midportion of the spinous layer. Severe epithelial dyplasia incorporates changes from te basal layer to a point above the midline of the epithelium. When involving the entire epithelium, however, the term carcinoma in situ is used. In carcinoma in situ, the lesion appears precisely like squamous cell carcinoma, with the exception that there has not been any invasion, thereby preventing metastasis.

Leukoplakia must be diagnosed by biopsy, and the specimen should be taken from the area showing the most change, or the most severe. A leukoplakia lesion with moderate dysplasia should, if possible, be completely removed, either by surgical excision, electrocautery, laser ablation, or cryosurgery. Leukoplakia without dysplasia or with less severe dysplasia should be monitored and conservatively treated, with consideration to such actions as smoking cessation. Cessation of smoking may cause the lesion to shrink in size or disappear. If the lesion grows larger or shows increase in severity, additional biopsy should be performed. Transformation from leukoplakia to a cancerous lesion may occur anywhere from months to decades after initial appearance of a leukoplakia lesion, but typically within a range of two to four years.


Candidiasis is a fungal infection caused by the organism Candida albicans. Candidiasis is the most common oral fungal infection in humans and is often times present intraorally in 3050% of people without clinical manifestation. In patients over 60 years old, C. albicans is found in almost 60% of dentate people. There are several types of candidiasis, and the three main factors that contribute to these different types of infection are:

1) the patient’s immune status

2) the status of the patient’s oral mucosa

3) the strain of C. albicans In order to help identify and diagnose this infection, this section will help identify the clinical patterns of candidiasis, and the recommended treatment modalities currently available. Pseudomembranous candidiasis is more commonly known as “thrush,” and it is characterized by removable white plaques, a burning sensation, and a foul taste. Plaques commonly occur on the buccal mucosa, tongue, and the palate. Erythematous candidiasis presents as red macular lesions that evoke a burning sensation, and these occur on the posterior hard palate, buccal mucosa, and the dorsum of the tongue.


Central papillary atrophy, otherwise known as median rhomboid glossitis, exhibits red, atrophic mucosal areas, usually on the midline posterior dorsal surface of the tongue, and tends to be asymptomatic. Chronic multifocal candidiasis also presents as a red lesion, but often with removable white plaques, and it may present either with a burning sensation or without symptoms. This infection can typically be seen on the posterior palate, the posterior dorsal tongue, and on the angles of the mouth. Angular chelitis occurs at the angles of the mouth and often causes a raw, irritated feeling that creates a red, fissured appearance.

Denture stomatitis has been synonymously known as both chronic atrophic candidiasis and denture sore mouth, and it presents as a red, asymptomatic lesion that is confined to the palate in denturebearing areas. Hyperplastic candidiasis, also known as candidal leukoplakia, is characterized by white plaques that are not removable and are mostly asymptomatic, occurring on the anterior buccal mucosa. Mucocutaneous candidiasis presents on the tongue, the palate, and the buccal mucosa, with both white plaques as well as reddish areas. The white plaques may or may not be removable. Endocrinecandidiasis syndromes usually consist of white, nonremovable plaques occurring on the tongue, palate, and buccal mucosa. The diagnosis of candidiasis is usually made based on the clinical signs combined with cytologic studies, although culture studies may not be possible in an office setting. A culture can be obtained by rubbing a cotton swab over the lesion and then placing the specimen on Sabouraud’s agar medium.

Candidiasis can be treated by a number of antifungal medications. Nystatin, a polyene agent, must be used multiple times on a daily basis as either a suspension or a lozenge. Nystatin can also be combined with triamcinolone acetonide cream or ointment and applied topically to the angular chelitis form of candidiasis. Similar to Nystatin, Clotrimazole must also be taken several times a day in order to be effective. Clotrimazole is and imidazole agent, and it may also be applied topically to treat angular chelitis. Another imidazole agent is ketoconazole, which may be taken in a single daily dose. Ketoconazole, however, is hepatotoxic and is associated with drug interactions with macrolide antibiotics, possibly causing cardiac arrhythmias. Ketoconazole is not recommended as the first line of defense for routine candidiasis. Most recently approved are the triazole class of antifungal medications, which include fluconazole and itraconazole. Both drugs have similar efficacy to clotrimazole and may have significant drug interactions with a number of medications. These agents may be taken once a day. Iodoquinol has antifungal properties and may be effective in the treatment of angular chelitis when combined with a cream or corticosteoid. If treatment does not resolve with antifungal therapy, a biopsy may be warranted to determine if there is another underlying condition responsible. If infection recurs, thought should be given to possible immunosupression of the patient, and a proper and thorough workup should be performed.

Oral Nevus

Oral nevus is a generic term that includes malformations of the skin and mucosa that may be congenital or developmental. Acquired melanocytic nevus, commonly known as a mole, is the most common type and results from proliferation of cells from the neural crest or nevus cells. Nevus cells have the ability to produce melanin. Most acquired melanocytic nevi develop before 35 years of age.

Prevalence is higher in Caucasians than in other racial backgrounds. Nevi occur in several clinical stages with distinct histopathologic features. The junctional nevus is a demarcated brown or black macule, typically less than 6 mm in diameter. Nevus cells may proliferate over many years to produce an elevated, soft papule with a smooth surface known as a compound nevus.12

Over time, the surface texture of the nevus may become papillomatous and hair follicles may arise from the center of the nevus. Nevi usually remain less than 6 mm in diameter and may in later life decrease in size. There are other types of developmental nevi that may be observed during clinical exam including epidermal nevi, nevus sebaceous, basal cell nevus, white sponge nevus and intramucosal melanocytic nevus. In one percent of newborns in the U.S., congenital malanocytic nevi may be present with 15% of these lesions noted in the head and neck area.13 Treatment of these lesions is usually for cosmetic reasons. However, 3 to 15% of large congenital nevi may undergo malignant transformation into melanoma.14 Large lesions should be excised when possible through conservative excision. A rare condition of patients with multiple large nevi results in central nervous system melanotic neoplasms, miningeal melanosis or melanoma.15 All patients with multiple large nevi that are not excised should have careful, regular followup examinations.

Intermucosal venus

Intermucosal Nevus


Leukoedema is a very common condition of unknown origin that occurs in the oral mucosa. It is characterized by diffuse, grayishwhite wrinkles or streaks that cannot be removed but which do disappear upon stretching the cheek. Leukoedema occurs far more commonly in blacks than whites, and it may be a variation of normal mucosa, rather than a disease. Changes in mucosal pigmentation may make leukoedema easier to identify in blacks than whites. Smoking may cause this condition to become more evident upon examination. Leukoedema requires no treatment, as it is a benign lesion.


Benign migratory glossitis

Benign migratory glossitis or geographic tongue also known as erythema migrans, is usually an asymptomatic inflammatory disorder of unknown etiology that affects the epithelium of the tongue. Estimated prevalence is about 2 percent, according to some studies.16 Local loss of filiform papillae leads to ulcerlike lesions that rapidly change the color and size. Lesions have central erythema and may display yellowishwhite borders. Histopathologic findings parallel the clinical appearance and may have a psoriasiform pattern. The condition is characterized by exacerbations and remissions and the lesions may have a migrating pattern.17 The most commonly suggested associations are atrophy and psoriasis. Some investigators have suggested that benign migratory glossitis is an oral manifestation of psoriasis18 . There are numerous case reports of successful treatments of refractory benign migratory glossitis with systemic immunosuppressive therapy, such as cyclosporine, further strengthening the proposed immunological etiology of this condition.

Benign migratory glossitis

In most cases, patients do not require treatment other than reassurance about the benign nature of the disorder. However, occasionally patients do complain of pain when eating.

Several treatment modalities exist including topical steroids, zinc supplements, and topical anesthetic rinses. None of these treatments has been proven to be uniformly effective19 Another notable condition is known as geographic tongue in which areas of atrophy of the filiform papillae are interspersed in patches with normal fungiform papillae. These areas are separated by white lines of hypertrophied filiform papillae. The patches may wander or remain static. The condition usually appears early in life and is of obscure etiology but requires no intervention except for meticulous cleaning of the tongue to prevent colonization of deep ridges with candida.

Squamous Cell Carcinoma

Squamous cell carcinoma comprises about 94% of all oral malignancies, and the cause if multifactorial. Multiple extrinsic and intrinsic factors have been identified, such as tobacco, alcohol, syphyillis, sunlight, radiation, immunosuppression, malnutrition, iron deficiency anemia, vitamin A deficiency, or presence of a precancerous lesion, such as leukoplakia. Oral squamous cell carcinoma typically has one of the following presentations:

Exophytic (massforming, fungating, papillary, verruciform) Endophytic (invasive, burrowing, ulcerated) Leukoplakic (white patch) Erythroplakic (red patch) Erythroleukoplakic (red and white patch)

The most common sites of occurrence for oral squamous cell carcinoma are the posterior lateral and ventral surface of the tongue. In males the floor of the mouth is affected with equal frequency, while in females the occurrence is diminished. Other possible locations for oral squamous cell carinoma are the soft palate, gingiva, buccal mucosa, labial mucosa, and hard palate.

Squamos Cell Carcinoma

The tongue comprises over half of all intraoral cancers in the United States, with twothirds of these lesions appearing as painless, firm masses or ulcerations or the posterior tongue. The floor of the mouth accounts for 35% of all intraoral carcinomas and appears to most likely derive from preexisting leukoplakia or erythroplakia. Gingival and alveolar carcinomas are usually painless as well, and these lesions tend to be found in the posterior mandible. Carcinomas of the oropharynx and soft palate tend to be more closely associated with increased size and metastasis due to the patient being unaware of its existence and thus delaying detection and diagnosis.

Oral squamous cell carcinoma is quantified by using the tumornodemetastasis (TNM) classification system that is used for the majority of human carcinomas. Treatment for intraoral squamous cell carcinoma is dependent on its clinical stage and can be treated by surgical excision, radiation therapy, or both. Chemotherapy agents are used as an adjunctive treatment, sometimes reducing the size of a tumor, but never increasing survival rates. Patients with a small intraoral squamous cell carcinoma should choose a single treatment modality, while those with larger or metastasized lesions should consider combination therapy. Survival rate depends on the stage of the cancer. The 5year diseasefree rate for intraoral cancer is 76% for stage I and II, 41% for stage III, and 9% when at stage IV.

Acute necrotizing ulcerative gingivitis

Acute necrotizing ulcerative gingivitis also known by the colloquial term trench mouth is an acute infectious gingivitis. The term trench mouth was coined in World War I when ANUG was common among trenchbound soldiers. It is characterized by punched out lesions of the interdental papillae and sometimes accompanied by a gingival edema. ANUG is associated with local pain, spontaneous bleeding or in response to minimal trauma, alterations in taste and a foul breath. Systemic signs of infections such as fever and malaise may be present.

Acute necrotizing ulcerative gingivitis

ANUG is caused by acute infection of the gingiva with organisms such as Prevotella intermedia, alphahemolytic streptococci, Actinomyces species, or any of a number of different oral spirochetes. ANUG may result in accelerated destruction of affected tissues, as well as local or systemic spread of infection. If it progresses into the local soft tissues of the mouth, it may result in noma or cancrum oris. It is most often seen in smokers and correlates highly with the amount of tobacco used per day. ANUG may also occur in immunocompromised patients during chemotherapy Treatment for patients with ANUG includes antibiotics, NSAIDs, and topical anesthetics for pain relief. Saline rinses as well as oral rinses with 3% hydrogen peroxide are utilized as well as part of a treatment plan.

Lichen Planus

Oral lichen planus is an inflammatory condition that affects 1 to 2 percent of adults in the U.S. Etiology is unknown, by immunemediated CD8+ cytotoxic Tcell induced apoptosis of epithelial cells is believed to be a causative factor. The condition predominates in adults older than 40 years with females affected more often than males in a ratio of 1.4 : 1. Two forms of lichen planus are known: reticular and erosive. The reticular form has bilateral, asymptomatic, white, lacy striations known as Wickham’s striae. Papules may also be present of the posterior buccal mucosa. Erosive lichen planus results in erythematous, painful ulcers which are often surrounded by white, lacy, radiating patterns of striae. Generalized erythema and ulceration of the gingival may also occur.

Lichen Planus

Reticular lichen planus is readily identified but often the erosive form requires biopsy for diagnosis. Topical corticosteroid gels such as fluocinonide and corticosteroid mouth rinses my be prescribed to patients. Controversy exists regarding the association with oral cancer and therefore, periodic followup examination is indicated for patients with oral lichen planus.

Herpes Labialis

Oral infections with herpes simples virus (HSV) may occur in infancy. The condition is usually asymptomatic and is not associated with significant morbidity. The initial infection may be painful with an acute outbreak of oral vesicles that coalesce in erythematous ulcerations. The gingiva is always involved. Other mucosal sites and the vermillion of the lips and perioral region may be affected. Other findings include lymphadenopathy, fever, chills and anorexia and irritability. The virus lingers, usually in the Trigeminal Ganglion, and may later reactivate during times of stress or depressed immune system response. During later reactivation, the virus may cause lesions of the labial mucosa or cold sores. Known triggers for the activation of the latent virus particles include ultraviolet light, fatigue, stress and menstruation.20 Lesions may affect 15 to 45 percent of the U.S. population. The appearance is usually of welllocalized clusters of small vesicles along the vermillion of the lip and adjacent skin. The course of the infection includes appearance, rupture, ulceration and crusting of the lesions within 24 to 48 hours. Healing occurs spontaneously in 7 to 10 days.

Herpes Labialis

Treatment of herpes labialis includes orally administered antiviral agents, acyclovir (Zovirax) or valacyclovir (Valtrex) which may reduce the course of the infection when initiated at the initial onset or prodrome of the infection. Treatment with topical 1% penciclovir cream (Denavir) may also reduce the healing time and is palliative throughout the course of the infection. Only a slight reduction in the course of the infection occurs with these agents. Some patients may have frequent episodes and should be treated prophylactically with antiviral medicatioins as should those patients who suffer from postherpetic erythema multiforme. Recurrent herpetic infections should not be treated with corticosteroids.

Many common oral lesions may be encountered by the family practice physician during examination of patients. Through careful history taking and complete oral examination, oral pathology may be recognized and diagnosed. Many conditions, such as recurrent apthough stomatitis may reflect a nutritional deficiency. Other systemic conditions such as autoimmune disorders and human immunodeficiency virus, HIV infection may manifest first as lesions of the oral cavity. Other conditions such as poor oral hygiene, tobacco and alcohol use or poorly fitting denture prosthesis may contribute to the presence of the oral lesion. The family practitioner who is aware of common oral entities, contributing factors and treatment modalities will be the first to recognize and treat the common lesions of the oral cavity.

1 The Prevalence of Oral Mucosal Lesions in U.S. Adults: Data from the Third National Health and Nutrition Examination Survey, 1988 – 1994, Shulman, J.D., Beach, M., RiveraHidalgo, F., J Am Dent Assoc 2004; 135;1279

2 Axéll T. A prevalence study of oral mucosal lesions in an adult Swedish population. Odont Revy 1976; 27 (suppl 26):1103.

3 Shulman, et al., J Am Dent Assoc 2004; 135; 1281

4 Gonsalves WC, Chi AC, Neville, BW. Common oral lesions: part I. Superficial mucosal lesions. Am Fam Physician 2007;75:5017.

5 McBride DR. Management of Aphtous Ulcers. Am Fam Physician 2000;62:14954,160.

6 Femiano F, Lanza A, Buonaiuto C, Gombos F, Nunziata M, Piccolo S, Cirillo N. Guidelines for diagnosis and management of aphthous stomatitis. Pediatr Infect Dis J. 2007 Aug;26(8):72832

7 Scully C. Clinical practice. Aphthous ulceration. N. Engl. J. Med. 355 (2): 165–72.

8 Barrons RW. Treatment strategies for recurrent oral aphtous ulcers. Am J Health Syst Pharm. 2001 Jan 1;58(1):4150.

9 Jurge S, Kuffer R, Scully C, Porter SR. Recurrent aphthous stomatitis. Oral Dis. 2006 Jan;12(1):121. Published Online: 23 Dec 2005

10 Plewa MC, Earl BJ, Dobson JE. Aphtous Ulcers. Emedicine.com. Accessed 1 Aug 2008

11 University of Texas at Austin, School of Nursing, Family Nurse Practitioner Program. Recommendations for the Diagnosis and Management of Recurrent Aphthous Stomatitis, Austin, TX, University of Texas at Austin, School of Nursing; 2003, May.

12 Neville, B., Damm, D., Allen, C., Bouquot, J., Oral and Maxillofacial Pathology, Third Edition, Saunders, Elsevier., St. Louis, Missouri, 2009., p. 383.

13 Neville, et al., p. 385.

14 Neville, et.al., p. 385.

15 Neville, et. al., p. 385386.

16 Shulman JD, Carpenter WM, Prevalence and risk factors associated with geographic tongue among US adults. Oral Dis. 2006 Jul;12(4):3816

17 Assimakopoulos D, Patrikakos G, Fotika C, Elisaf M. Benign migratory glossitis or geographic tongue: an enigmatic oral lesion. Am J Med. 2002; 113(9):7515 (ISSN: 00029343)

18 Abe M, Sogabe Y, Syuto T, Ishibuchi H, Yokoyama Y, Ishikawa O. Successful treatment with cyclosporin administration for persistent benign migratory glossitis. Journal of Dermatology. 2007; 34:340343

19 Sigal MJ. Mock D. Symptomatic benign migratory glossitis: report of two cases and literature review. Pediatric Dentistry. 1992:14:3926.

20 Gonsalves, Wanda C., Chi, Angela C., Neville, Brad W., Common Oral Lesions: Part I. Superficial Mucosal Lesions. American Family Physician, February 15, 2007, vol. 75, no. 4., p. 503