White plaques in the oral cavity


  • Case 1_1012 Derm Look

  • Case 2

Case #1

A woman, aged 56 years, under care for treatment of angular cheilitis, presented to the dermatology clinic after noticing white plaques on her bilateral buccal mucosa. The lesions were asymptomatic. Application of clotrimazole 1% cream, which was given at a prior appointment for treatment of the angular cheilitis, had provided no relief. No other skin or vulvovaginal lesions were reported. Social history was negative for alcohol or tobacco use. Physical examination was significant for lacy-white plaques on bilateral buccal mucosa.

Case #2

A man in his early 50s presented with complaints of an asymptomatic white patch on his left ventral tongue. The lesion had been present for six months and did not appear to be increasing in size. No prior or current trauma was associated with the lesion. Social history was notable for a history of tobacco use. On physical examination, a well-defined and homogenous white plaque with erythema at the proximal border was appreciated on the left ventral tongue. There was no induration of the lesion or cervical lymphadenopathy.

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Case #1: Lichen planus In 1869, British physician Erasmus Wilson first described lichen planus (LP).1 Wilson likely derived the after observing that the skin lesions were flat in appearance (planus is the Latin word for flat) and looked similar to...

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Case #1: Lichen planus

In 1869, British physician Erasmus Wilson first described lichen planus (LP).1 Wilson likely derived the after observing that the skin lesions were flat in appearance (planus is the Latin word for flat) and looked similar to lichens, primitive plants composed of symbiotic algae and fungi.

LP is a common, chronic, inflammatory dermatologic disease. Cutaneous LP is used to describe lesions that affect the skin, whereas oral lichen planus (OLP) is the term used to describe lesions that primarily affect the tongue and oral mucosa. OLP affects approximately 1% to 4% of the adult population and typically develops between age 30 years and age 60 years. There is no overt racial predisposition, but women may be affected twice as often as men. OLP may be the only manifestation of the disease; however, OLP can also be observed in up to 75% of patients with cutaneous LP.2 Interestingly, only 10% to 20% of patients whose initial presentation is that of OLP will go on to develop cutaneous LP.2

Although the etiology remains unknown, an increasing amount of evidence suggests that LP is caused by auto­immune T-cell mediated damage to basal keratinocytes. Such exogenous agents as viruses, medications, and contact allergens may cause an alteration in the antigenicity of epidermal cells. This alteration leads to an inflammatory reaction that causes T cells to migrate from the circulation into a particular skin site. These T cells then function to eliminate abnormal keratinocytes, which are altered by these exogenous agents. Such autoaggressive reactions can then lead to a situation in which T cells initially responding to self-antigens modified by exogenous agents subsequently become cross-reactive with self-epitopes. Therefore, these T cells chronically respond to self-epitopes, leading to a perpetuated autoimmune attack.

Of the many exogenous antigens, viruses—especially the hepatitis C virus (HCV)—are thought to play a major role in the development of LP. OLP is the form that is most commonly viewed as a manifestation of HCV infection. In one study, HCV RNA was detected in 93% of OLP lesions.3

Such contact allergens as gold, mercury, and palladium are commonly used in dental restorations, and easy penetration of these metals through damaged mucosa may exacerbate or induce lesions of OLP. Patch testing should be considered in patients with OLP, especially if the lesions are in close contact with amalgam fillings.

Strangely, while approximately 95% of individuals with a positive patch test had improvement of their OLP after removal of the sensitizing metal, 75% of individuals with a negative patch test also reported improvement.2 Finally, cutaneous eruptions that mimic LP (clinically and histologically) have been linked to a variety of medications.

OLP favors the buccal mucosa, tongue, and gingival tissue. Clinically, there are seven different subtypes of OLP; reticular, pigmented, atrophic, erosive, papular, bullous, and plaque-type. Patients may exhibit one or several forms, with the reticular and erosive subtypes being the most common presentations. Reticular OLP is characterized by white linear plaques that are most commonly seen forming a lacelike pattern (Wickham’s striae). These lesions are usually asymptomatic, tend to wax and wane, and are typically found bilaterally on the posterior buccal mucosa.

In contrast, the lesions of erosive OLP are often symptomatic, with patients complaining of mild to severe burning pain. Clinically, atrophic erythematous plaques are seen with varying degrees of central ulceration. When lesions are restricted to the gingival mucosa, the reaction pattern is termed desquamative gingivitis.

Cutaneous LP lesions are characterized by hyperkeratosis, wedge-shaped hypergranulosis, irregular acanthosis with a “sawtooth” appearance, liquefactive degeneration of the basal cell layer, and a lymphocytic lichenoid infiltrate. Lesions of OLP often show parakeratosis rather than hyperkeratosis, and the epidermis is usually atrophic or ulcerated. Direct immunofluorescence (DIF) reveals shaggy deposits of fibrinogen at the dermal-epidermal junction with occasional granular deposits of immunoglobulin (Ig) M or linear deposits of C3 and/or IgG. While the DIF findings are characteristic of LP, immunofluorescent studies are not necessary in classic cases.

Reticular OLP may be confused with the localized form of discoid lupus erythematosus, which is characterized by white plaques with an erythematous halo. White sponge nevus and leukoplakia are common white lesions in the oral cavity that may also mimic reticular OLP.

In cases of erosive OLP or desquamative ginigivitis, biopsy specimens should be obtained for light microscopic and immunofluorescent studies of perilesional tissue because pemphigus vulgaris and mucous membrane pemphigoid may demonstrate a similar clinical presentation. Erythroplasia and carcinomas must also be histologically differentiated from OLP.

Because of its asymptomatic nature, reticular OLP does not usually need treatment and commonly undergoes spontaneous remission approximately five years after onset.4 Erosive OLP rarely resolves spontaneously and can cause significant discomfort. First-line treatment often includes a strong topical corticosteroid (fluocinonide, betamethasone, clobetasol gel) applied several times a day. Tacrolimus (Hecoria, Prograf) 0.1% ointment has also been found to be effective in reducing the symptoms of OLP. Most lesions tend to resolve within one to two weeks but will undoubtedly recur. For more recalcitrant cases, consider oral prednisone, cyclosporine, or retinoids.

Patients should be encouraged to eliminate alcohol and tobacco, eat a nutritious diet, and perform regular self-examinations to evaluate for change within the lesions. Individuals with OLP have a slightly increased risk of oral squamous cell carcinoma and should be followed regularly by a health-care provider.

Since the patient in this case was asymptomatic, no treatment was initiated. A screen for hepatitis C was negative. She continues to be followed in the dermatology clinic to monitor for disease progression.

CASE #2: Oral leukoplakia

Oral leukoplakia (OL) is strictly a clinical term and does not imply a specific histopathologic disease process. OL is considered a diagnosis of exclusion that is given after all other entities that appear as white plaques in the mouth have been ruled out. While it is not associated with a specific histopathologic diagnosis, it is considered by most to be a precancerous lesion. Approximately 1% to 5% of the U.S. adult population has OL, and males are twice as likely to be affected by the disease as females. Typical age of onset is older than 30 years, with a peak incidence older than age 50 years.

While the etiology of OL remains unknown, there is a strong association with tobacco use, UV radiation, and candidiasis. Tobacco use seems to be the most common cause, with approximately 80% of OL patients being tobacco users. Those who are heavy smokers have more lesions and larger lesions than do light smokers. In addition, many who stop smoking either have resolution or improvement of the leukoplakia within the first year of cessation.5 People who use smokeless tobacco products produce a distinctive white oral plaque called tobacco pouch keratosis, which is not considered a true OL. Some believe that the use of alcohol may be a risk factor for developing OL, while others believe that alcohol consumption may lead to grayish buccal mucosal plaques, which are not considered a true OL. OL caused by UV radiation is often found on the lower lip vermilion in transplant or immunocompromised patients.

Candida is a known pathogen associated with the production of a thick white and erythematous plaque on the oral mucosa, which is termed candidal leukoplakia. Biopsies of these lesions may show dysplastic or hyperplastic changes. It is unknown whether Candida induces these changes within the epithelium or preferentially infects previously altered epithelium. The dysplasia often resolves or improves after antifungal treatment. Physical trauma or chronic irritation to the oral mucosa may lead to a thickened hyperkeratotic white plaque known as frictional keratosis. Although clinically similar to leukoplakia, the lesion is thought to be a normal hyperplastic response (like a callus) and is not considered precancerous.

OL most commonly appears as a homogenous or non-homogenous white plaque. The former is the more common variant, often appearing as a smooth white plaque with well-demarcated borders. The surface may appear translucent, fissured, or wrinkled, and lesions are typically soft and flat. Non-homogenous (speckled or granular) lesions of OL develop more surface irregularities. When the surface becomes so irregular that it develops sharp or blunt projections, the condition is termed verruciform leukoplakia.

Approximately 70% of OLs are found on the lip vermilion, gingiva, and buccal mucosa. More than 90% of OLs that show dysplasia or undergo malignant transformation are non-homogenous lesions that are found on the lip vermilion, tongue and floor of the mouth. Clinical features alone are not sufficient to determine malignant versus premalignant lesions, so a biopsy with histologic examination is mandatory.

Lesions of OL will typically demonstrate such benign features as hyperkeratosis and acanthosis.5 Various degrees of dysplasia may also be seen. Mild epithelial dysplasia is characterized by alterations that are limited to the basal and parabasal layers. Moderate epithelial dysplasia is characterized by dysplastic changes that extend to the midpoint of the spinous layer. Severe epithelial dysplasia demonstrates atypical cells that involve most of the epithelial thickness. Carcinoma in situ is the term used when the dysplastic changes involve the entire thickness of the epithelium.

Lichen planus, morsicatio (chronic cheek nibbling), frictional keratosis, tobacco pouch keratosis, nicotine stomatitis, leukoedema, and white sponge nevus all can be mistaken for OL. Careful clinical and histologic examination can help to differentiate between these disorders.

Because of the malignant nature of OL, a biopsy specimen in the most severe region of the lesion is mandatory. If no dysplasia or mild dysplasia is present at a low-risk site, then the decision is often made to clinically evaluate the lesion every six months and discontinue any potentially carcinogenic habits. Approximately 4% of OL patients will eventually develop carcinoma.6 If there is moderate or severe dysplasia, lesions may be removed with surgical excision, laser ablation, cryosurgery, or electrocautery. Long-term follow-up after removal is necessary because recurrences are frequent.

In this case, a biopsy of the lesion was performed, revealing hyperkeratosis, acanthosis, and mild dysplasia. The man was advised to discontinue tobacco use and is being followed in the clinic every six months to monitor for malignant transformation.

Kerri Robbins, MD, is a resident in the Department of Dermatology at Baylor College of Medicine in Houston. Damjan Jutricis a second-year dental student at The University of Texas School of Dentistry, also in Houston.


  1. Boyd AS, Neldner KH. Lichen planus. J Am Acad Dermatol. 1991;25:593-619.
  2. Bolognia JL, Jorizzo JL, Rapini RP eds. Dermatology. 3rd ed. St. Louis, Mo.: Elsevier-Mosby; 2012: 159, 167-168, 170, and 1049-1050.
  3. Nagao Y, Kameyama T, Sata M. Hepatitis C virus RNA detection in oral lichen planus tissue. Am J Gastroenterol. 1998;93:850.
  4. Mignogna MD, Lo Muzio L, Lo Russo L, et al. Oral lichen planus: ­different clinical features in HCV-positive and HCV-negative patients. Int J Dermatol. 2000;39:134-139.
  5. van der Waal I, Schepman KP, van der Meij EH, Smeele LE. Oral leukoplakia: a clinicopathological review. Oral Oncol. 1997;33:291-301.
  6. Einhorn J, Wersall J. Incidence of oral carcinoma in patients with leukoplakia of the oral mucosa. Cancer. 1967;20:2189-2193.
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