Leukoplakia
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.
