History
See the list below:
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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.
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Individuals with OL are not symptomatic.
Physical
The following three stages of OL have been described:
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The earliest lesion is nonpalpable, faintly translucent, and has white discoloration.
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Next, localized or diffuse, slightly elevated plaques with an irregular outline develop. These lesions are opaque white and may have a fine, granular texture.
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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:
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The most common are uniformly white plaques (homogenous OL) prevalent in the buccal mucosa, which usually have low premalignant potential.
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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:
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The verrucous type is considered high risk.
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Erosion or ulceration within the lesion is highly suggestive of malignancy.
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The presence of a nodule indicates malignant potential.
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A lesion that is hard in its periphery is predictive of malignant change.
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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. [11]
In all cases, the relative risk of malignant potential is determined by the presence of epithelial dysplasia upon histological examination.
Causes
See the list below:
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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.
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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.
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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.
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Patients who have had syphilitic glossitis have a higher prevalence of OL than individuals with a nonsyphilitic background.
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The presence of Candida albicans, a relatively common oral fungus, has been reported to be very frequently associated with OL.
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Deficiency of vitamins A and B has been suggested as an inciting factor in the development of OL.
