Leukoedema is a quite common developmental alteration of the oral mucosa which appears to be a simple variation of normal anatomy.
Similar mucosal changes have been reported in the vaginal and laryngeal mucosa.
Epidemiology of Leukoedema
When the mildest cases are included, it is seen in almost 90% of adult blacks and half of adult whites, although it presents as a much less pronounced alteration in whites.
The incidence of leukoedema increases with age in both ethnic groups up to ages 40-49 and then declines systematically. There is no sex predilection.
The occurrence of leukoedema is significantly greater in African Americans.
Symptoms of Leukoedema
Leukoedema typically appears as an asymptomatic, bilateral, white-gray, semitransparent macule of the buccal mucosa ( image ).
Few patients may show fine grooves or folds crisscrossing the macule in a lace-like pattern.
This mucosal change may begin as early as 3-5 years of age but is not usually noticeable until adolescence. By the end of the teenage years, 50% of black children demonstrate the altered mucosa.
The opalescent macule is usually poorly demarcated from surrounding mucosa and is occasionally seen on the soft palate and oral floor. When the cheeks are stretched outward, the leukoedema typically disappears. This aids to differentiate this lesion from other similar looking conditions which could be premalignant, such as leukoplakia ( image ).
Pathogenesis and Differential Diagnosis
Leukoedema is characterized by a variable intracellular edema of the superficial half of the epithelium ( image ).
The vacuolated cells are large and often have pyknotic nuclear aspect. They may extend to the basal layer and may cluster into inverted wedge-shaped regions separated by normal spinous epithelial cells. The epithelium is hyperplastic and rete ridges are often broad and elongated. Parakeratosis is commonly seen but is not pronounced unless there has been chronic trauma.
Intracellular edema is characteristic of several other oral lesions, many of which may be found on the buccal mucosa:
smokeless tobacco keratosis,
frictional keratosis (chronic cheek bite keratosis),
white sponge nevus,
The identification of etiologic habits will help in establishing a final diagnosis for smokeless tobacco keratosis and frictional keratosis.
Microscopically, these typically present with a more pronounced surface keratosis and have scattered chronic inflammatory cells within the underlying stroma.
Since leukoedema and white sponge nevus both have innocuous onsets in the childhood and teenage years, it may be impossible to distinguish between them except by the clinical "stretch test." The nevus will remain visible when the affected mucosa is stretched, while leukoedema will disappear.
Hereditary benign intraepithelial dyskeratosis (HBID, Witkop's disease) also shows pronounced intracellular edema but can be distinguished from the others by the scattered presence in the spinous layer of individually keratinized cells.
Although the etiology is unknown, it has been suggested that leukoedema develops in areas of local irritation.
It seems that nor vascular and hormonal factors are related to the development of leukoedema.
Tobacco (and cannabis) smoking and chewing are a risk factor for the development of the lesion and the whiteness and size are increased, most cases, anyway, are so subtle that they are not even formally diagnosed.
Complications and Treatment
No treatment is necessary for leukoedema. It has no malignant potential, unlike leukoplakia, and does not change significantly after 25-30 years of patient age.
Should the affected individual stop using tobacco products, the lesion will likely become less pronounced.