CHAPTER 15. Benign chronic white mucosal lesions
The appearance of most mucosal white lesions is due to hyperkeratosis; any excess keratin, becoming sodden with saliva, appears white. Apart from the lingual filiform papillae, visible keratinisation of any significant degree is abnormal in the mouth.
Chronic mucosal white plaques have sometimes been termed leukoplakias. This term literally means no more than a white plaque but, in the past, was widely but mistakenly regarded as implying premalignancy. However, only a small minority of white patches are premalignant (Ch. 16). The majority, without malignant potential, are discussed here (Table 15.1).
White sponge naevus
Chronic mucocutaneous candidosis
Oral keratosis of renal failure
LEUKOEDEMA → Summary p. 278
Leukoedema is a bilateral, diffuse, translucent greyish thickening, particularly of the buccal mucosa. It is a variation of normal, present in 90% of blacks and variable numbers of whites.
Histologically, there is thickening of the epithelium with intracellular oedema of the spinous layer.
Treatment is unnecessary but reassurance may be required.
White patches can be caused by prolonged mild abrasion of the mucous membrane by such irritants as a sharp tooth, cheek biting or dentures.
At first, the patches are pale and translucent (Fig. 15.1), but later become dense and white, sometimes with a rough surface. Habitual cheek biting causes an area of buccal mucosa to appear patchily red and white with a rough surface (Fig. 15.2).
The epithelium is moderately hyperplastic with a prominent granular cell layer and thick hyperkeratosis but no dysplasia (Fig. 15.3). There are often scattered chronic inflammatory cells in the corium.
Removal of the irritant causes the patch quickly to disappear. Biopsy is necessary only if the patch persists. Frictional keratosis is completely benign and there is no evidence that continued minor trauma alone has any carcinogenic potential.
FORDYCE’S GRANULES → Summary p. 278
Sebaceous glands are present in the oral mucosa in at least 80% of adults, particularly the elderly. They grow in size with age and appear in the oral mucosa as soft, symmetrically distributed, creamy spots a few millimetres in diameter, particularly in older persons (Fig. 15.4). The buccal mucosa is the main site, but sometimes the lips and, rarely, even the tongue are involved.
These glands are sometimes mistaken for disease, but patients can be reassured that they are of no significance. If a biopsy is carried out, it shows a normal sebaceous gland with two or three lobules (Fig. 15.5).
PIPE SMOKER’S KERATOSIS (‘STOMATITIS NICOTINA’) → Summary p. 277
Smoker’s keratosis is seen among heavy, long-term pipe smokers and some cigar smokers.
The appearances are distinctive in that the palate is affected, but any part protected by a denture is spared. Changes are then seen only on the soft palate.
The lesion has two components – hyperkeratosis and inflammatory swelling of minor mucous glands. Either may predominate, but typically, white thickening of the palatal mucosa is associated with small umbilicated swellings with red centres (Fig. 15.6). The white plaque is sometimes distinctly tessellated (pavement-like).
The white areas show hyperorthokeratosis and acanthosis with a variable inflammatory infiltrate beneath. The diagnostic feature is the swollen, inflamed mucous glands with hyperkeratosis extending up to the duct orifice (Fig. 15.7).
The clinical appearances, history and ease of management are so distinctive that biopsy should not be necessary. If the patient can be persuaded to stop smoking the lesion resolves within weeks.
Key features are summarised Box 15.1.
• Affects mucosa exposed to smoke (mainly the hard palate)
• Areas protected by denture unaffected
• Palate is white (keratotic) with umbilicated swellings with red centres (inflamed mucous glands)
• Responds rapidly to abstinence from pipe smoking
• Statistically, a raised risk of oral cancer but not in the hyperkeratinised (palatal) area (Ch. 16)
Epidemiological evidence suggests that pipe smoking raises the risk of cancer, but when oral cancer develops in association with pipe smoking, it typically appears not in the keratotic area on the palate (one of the least common sites for cancer) but low down in the mouth, often in the lingual retromolar region. This may be the result of carcinogens pooling and having their maximal effect in drainage areas of the mouth. It also suggests that there are different causes for the hyperkeratosis and any carcinomatous change.