Leukoplakia - pediagenosis
Article Update

Wednesday, November 13, 2019


Although oral leukoplakia is often a benign reactive process, it can also represent a precancerous lesion, appearing as white plaques consisting of hyperplastic squamous epithelium, in the initial step in the malignant transformation process from hyperplasia to dysplasia and finally to squamous cell carcinoma. Over a 10-year period, 1% to 20% of leukoplakia lesions will progress to squamous cell carcinoma. There is a decreased risk of malignant transformation in areas of thick mucosa, such as the dorsum of the tongue or cheek, and an increased risk in areas of thin mucosa, such as the ventral aspect of the tongue. The prevalence of leukoplakia in the United States is less than 1% of the population. The strongest risk factor for the development of leukoplakia is tobacco use. Alcohol use, illfitting dentures, and other restorative dental appliances, age over 40, male gender, and lower socioeconomic status are also associated with an increased risk of malignant transformation. When seen in association with inflammatory conditions, it is purely an inflammatory reaction, with no risk of malignant transformation. An association between the development of leukoplakia and human papillomavirus or Candida albicans has been established. Leukoplakia on the dorsal surface of the tongue can be seen in tertiary syphilis. Iron, folate, and vitamin B12 deficiencies may result in a disruption in epithelial differentiation, increasing the risk of leukoplakia. Most lesions are asymptomatic; biopsy is required to differentiate benign from malignant disease and, in benign disease, to describe the presence, or absence, of dysplasia.


Oral proliferative verrucous leukoplakia has a different appearance of the white plaques, and it is a rare, aggressive from of leukoplakia with a higher risk of malignant transformation. The lesion is multifocal and exophytic, presenting with a wartlike appearance. Unlike oral leukoplakia, this disorder is more common in elderly women across all ethnic groups; an association with tobacco or alcohol use and human papillomavirus has not been established. Pathologic features differentiating oral proliferative verrucous leukoplakia from oral leukoplakia and other lesions of the tongue include a dense lichenoid inflammatory process, including basal vacuolar degeneration, apoptotic cells, eosinophilic bodies, and a bandlike lymphocytic infiltrate, with an exophytic warty configuration.
Oral hairy leukoplakia is one of the most common oral manifestations of HIV infection, believed to be due to infection caused by the Epstein-Barr virus. It presents most often as a white thickening of the lateral border of the tongue with vertical hairlike projections and corrugations. Although it can extend to the ventral and dorsal surfaces of the tongue, it is rarely seen in other parts of the oral cavity. Unlike oral leukoplakia or oral proliferative verrucous leukoplakia, there is no risk of malignant transformation.
Leukoplakia of the cheek is usually found parallel to the line of occlusion, sometimes extending from the corners of the mouth as a pattern of fanlike radiating lines.
A favorite site of leukoplakia is the lower lip, where a barely discernible whitish plaque (smoker’s patch) appears, which at first may be removed by rubbing but becomes more permanent and thickened with time. Leukoplakia of the palate may manifest as a diffuse grayish white discoloration or as discrete plaques or rings around the orifices of the palatal mucous glands, which, in time, may become enlarged and nodular, owing to chronic obstruction.
The diagnosis of leukoplakia requires differentiation from syphilis, thrush, carcinoma, lichen planus, and traumatic scars.
Lichen planus presents a very similar picture, although the delicacy of the lacy markings, the skin lesions, and its presence in women help to identify it and distinguish it from leukoplakia. A biopsy is most indicative although not always definitive. The histologic features of leukoplakia, including hyperkeratosis, accentuation of the stratum granulosum, and moderate dyskeratosis of the prickle cells with hyperchromatic nuclei, particularly in the cells f the basal layer, differentiate it from lichen planus.

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