Oral Leukoplakia


Oral leukoplakia (OL) is a white patch or plaque that cannot be rubbed off, cannot be characterized clinically or histologically as any other condition, and is not associated with any physical or chemical causative agent except tobacco. Therefore, a process of exclusion establishes the diagnosis of the disease. In general, the term leukoplakia implies only the clinical feature of a persistent, adherent white plaque; therefore, reserve the term for idiopathic lesions when investigations fail to reveal any cause. The term carries absolutely no histologic connotation, although, inevitably, some form of disturbance of the surface epithelium is characteristic.

Follow-up studies suggest that cancer is more likely to occur in individuals with idiopathic leukoplakia than in individuals who do not have this condition. Thus, idiopathic leukoplakia is considered a premalignant lesion. [12]


The etiology of most cases of OL is unknown (idiopathic). In other cases, the initiation of the condition may depend on extrinsic local factors and/or intrinsic predisposing factors. Factors most frequently blamed for the development of idiopathic leukoplakia include tobacco use, alcohol consumption, chronic irritation, candidiasis, vitamin deficiency, endocrine disturbances, and possibly a virus.




OL occurs in fewer than 1% of individuals.


OL is considered to be potentially malignant, with a transformation rate in various studies and locations that range from 0.6 to 20%.

A long-term follow-up study by Fan et al indicated that oral leukoplakia can increase the risk of esophageal squamous cell carcinoma (ESCC). The study, in which nearly 29,584 healthy adults were enrolled, found that 2924 persons in the study developed ESCC over a 28-year follow-up period; in adults aged 52 years or younger at baseline, the hazard ratio for the disease in those with leukoplakia was 1.31. [3]


OL is more common in men than in women, with a male-to-female ratio of 2:1.


Most cases of OL occur in persons in their fifth to seventh decade of life. Approximately 80% of patients are older than 40 years.



See the list below:

  • Oral leukoplakia (OL) manifests as patches that are bright white and sharply defined. The surfaces of the patches are slightly raised above the surrounding mucosa.

  • Individuals with OL are not symptomatic.



The following three stages of OL have been described:

  • The earliest lesion is nonpalpable, faintly translucent, and has white discoloration.
  • Next, localized or diffuse, slightly elevated plaques with an irregular outline develop. These lesions are opaque white and may have a fine, granular texture.
  • In some instances, the lesions progress to thickened, white lesions, showing induration, fissuring, and ulcer formation.

Clinically, OL falls into one of the following two main groups:

  • The most common are uniformly white plaques (homogenous OL) prevalent in the buccal mucosa, which usually have low premalignant potential.
  • Far more serious is speckled or verrucous leukoplakia, which has a stronger malignant potential than homogenous leukoplakia. Speckled leukoplakia consists of white flecks or fine nodules on an atrophic erythematous base. These lesions can be regarded as a combination of or a transition between leukoplakia and erythroplasia, which is flat or depressed below the level of the surrounding mucosal red patch, is uncommon in the mouth, and carries the highest risk of malignant transformation.

The following five clinical criteria demonstrate a particularly high risk of malignant change:

  • The verrucous type is considered high risk.
  • Erosion or ulceration within the lesion is highly suggestive of malignancy.
  • The presence of a nodule indicates malignant potential.
  • A lesion that is hard in its periphery is predictive of malignant change.
  • OL of the anterior floor of the mouth and undersurface of the tongue is strongly associated with malignant potential.

A literature review by Lyu et al focused on Chinese patients indicated that other risk factors for malignant transformation of OL include female gender, age over 50 years, and nonhomogeneity of OL. [4]

In all cases, the relative risk of malignant potential is determined by the presence of epithelial dysplasia upon histological examination.


See the list below:

  • In persons who smoke, the combustion end-products brought about by burning tobacco and heat (eg, tobacco tars and resins) are irritating substances capable of producing leukoplakic alterations of the oral mucosa. Years of heavy pipe, cigar, and cigarette smoking can lead to a characteristic type of benign keratosis in the hard palate, called stomatitis nicotina. Many investigators regard this lesion as simply an anatomic variant of leukoplakia. Numerous red dots due to the inflamed and dilated orifices of salivary gland ducts are apparent throughout the whitened palatal mucosa. Later, the mucosa becomes pale because of a slight increase in keratinization. In advanced cases, the palatal tissue is keratinized more heavily, and nodules appear that are related to hyperplasia of the underlying glands, retention of saliva, and fibrosis.

  • The use of alcohol has been suggested as a possible etiology because alcohol may irritate the mucosa. Persons who habitually consume considerable quantities of alcohol usually also smoke inveterately; therefore, establishing the effects of alcohol alone is difficult.

  • Malocclusion; chronic cheek biting; ill-fitting dentures; and sharp, broken-down teeth that constantly irritate the mucosa are considered extremely important in the etiology of OL.

  • Patients who have had syphilitic glossitis have a higher prevalence of OL than individuals with a nonsyphilitic background.

  • The presence of Candida albicans, a relatively common oral fungus, has been reported to be very frequently associated with OL.

  • Deficiency of vitamins A and B has been suggested as an inciting factor in the development of OL.


Diagnostic Considerations

These include the following:

  • Leukoedema

  • Lichen planus

  • Chemical burn

  • Morsicatio buccarum (habitual cheek biting)

  • Candidosis

  • Psoriasis

  • Lupus erythematosus

  • White sponge nevus


Medical Care

Surgical excision of oral leukoplakia (OL) may be considered. Frequent clinical observation accompanied by photographic records is recommended. Because of the unpredictable behavior of dysplastic lesions, immediately obtain a biopsy on any areas that are suggestive or that change in appearance. [14Cryotherapy ablation and carbon dioxide laser ablation are also used. [15The area heals rapidly, and apparently healthy mucosa is left behind. However, uncertainty remains regarding the risk of invasive carcinomas subsequently arising in sites previously treated.


Consult an oral medicine specialist to evaluate etiologic factors and to determine the individualized treatment.


Discontinue the use of alcohol.


Physical activity is not restricted.


Medication Summary

Topical retinoids are ineffective. Systemic retinoids may be effective, but they have toxic effects. Studies that investigated the use of a high-dose induction followed by low-dose systemic isotretinoin report stabilization of the majority of lesions, a more effective response than beta-carotene in preventing malignant changes, and no toxicity. [16Recently, studies report that beta-carotene produced sustained remissions in patients with oral leukoplakia (OL), with a durable response for at least 1 year. [17Both of these drugs have been used in experimental trials and must be investigated in more depth.


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