Reactive keratotic lesions (nonleukoplakias)

Clinical findings

• This is present in up to 90% of the population and is more readily discerned in dark-skinned individuals.

• Delicate lacy, gray-white lines are present on the buccal mucosa or tongue (nonkeratinized sites) that disappear with stretching ( Fig. 10.1 A–B).

  

• Sucking pads of infants are extreme examples of this (see Fig. 10.1 C).

Etiopathogenesis and histopathologic features

Leukoedema usually results from mildly irritating substances such as smoke from tobacco products or marijuana, caustic oral rinses, or toothpaste in episodic contact with the mucosa. It is also associated with a minimally traumatic, parafunctional habit such as mucosal sucking.

• Acanthosis is always present and there is keratinocyte edema of superficial cells causing cells to be enlarged, pale, and ballooned; anucleation may be caused by plane of section and/or nuclear degeneration; cell membranes have a compact “jigsaw puzzle” appearance and keratinocytes often exhibit perinuclear halos but they do not represent koilocytes because the nuclei are not shrunken or hyperchromatic ( Fig. 10.2 ).

  

• Minimal-to-no keratin is noted, although parakeratin chevrons may be present, similar to smokeless tobacco lesions ( Fig. 10.3 ). There is minimal to no inflammation in the lamina propria because this mild injury is located superficially.

  

Differential diagnosis

• Keratinocyte edema is seen in contact irritant lesions such as in smokeless tobacco lesions, and in association with frictional/factitial keratoses, although the latter will also show marked parakeratosis or hyperkeratosis.

• Hairy leukoplakia shows chromatin condensation against the nuclear membrane and Cowdry inclusion bodies, and are positive for Epstein-Barr virus (EBV).

Management and prognosis

• No treatment is necessary for leukoedema, although patients should be educated about the causes and avoidance of the causative agent if appropriate. There is no potential for malignant transformation.

Clinical findings

• Painless, thready white tissue lies on the mucosa (usually nonkeratinized sites) which readily peels off, leaving normal underlying mucosa ( Fig. 10.4 ). Surrounding leukoedema may be seen and patients may also exhibit contact desquamative cheilitis.

  

Etiopathogenesis and histopathologic features

This condition results from caustic mouth washes high in alcohol, essential oils, or astringent content; toothpastes high in sodium lauryl sulfate or triclosan; or other contactants that are irritants to the superficial layers of the epithelium but not strong enough to cause necrosis and ulceration as aspirin would. Two brands of mouth care products associated with this condition are Listerine™ and Pro-Health™ because of high content of alcohol and essential oils. Strips of desquamated keratinocytes appear eosinophilic and degenerated or coagulated, and generally lie on the surface of the otherwise intact mucosa ( Figs. 10.5 and 10.6 ).

Management

• Resolution occurs on discontinuation of the use of the dentifrice.

Clinical findings

• More than 80% occur within the third and sixth decades of life with a 3:1 male predilection. The most common locations lie close to the biting surfaces of the teeth, namely, buccal mucosa (54%), lateral/ventral tongue (32%), and lower lip mucosa (9%, rare on upper lip mucosa); more than 50% of patients are unaware of their habit which may occur when they are asleep.

• Poorly-demarcated papules and plaques often display a shaggy, macerated, rough surface, and may be associated with areas of erythema and ulceration depending on the severity of the parafunctional chewing/nibbling habit ( Fig. 10.7 B–D).

• Chronic irritation of the mucosa against an oral appliance or other hard foreign object results in similar findings.

Etiopathogenesis and histologic features

Parafunctional habits such as raking of the teeth, prosthesis, or other foreign object against the nonkeratinized mucosa result in these benign reactive keratotic lesions with distinctive histopathology. It is important that these lesions not be signed out as merely “parakeratosis or acanthosis” but as a frictional or reactive keratosis so that they do not get relegated to the category of leukoplakia.

• Linea alba shows mostly leukoedema with variable parakeratosis ( Fig. 10.8 ).

  

• Classic lesions show mild to severe shaggy parakeratosis with slight surface corrugations and undulations. Frequently there are fissures and clefts within the parakeratin often rimmed by bacteria, but without inflammation, and candidal hyphae are infrequently seen; parakeratosis diminishes toward the lateral edges. There is acanthosis, keratinocyte edema and tapered rete ridges ( Figs. 10.9–10.11 ). Ulcers may be present and long-standing lesions show hyperkeratosis similar to benign alveolar ridge keratosis ( Fig. 10.12 ).

  
  
  
  

• Inflammation is usually absent unless an ulcer is present and there may be plasma pooling. ( Fig. 10.13 ).

  

Differential diagnosis

• Hairy leukoplakia usually shows sharp demarcation of the parakeratin from an underlying pale band of edematous keratinocytes that exhibit chromatin beading against the nuclear membrane, Cowdry inclusions, and presence of EBV in superficial keratinocytes.

• Any other papular/nodular lesion, such as a dysplasia or even a fibroma, may show overlying secondary frictional/factitial keratosis.

Management and prognosis

• Use of barrier devices to prevent patients from habitually chewing the mucosa may or may not be helpful because patients may continue to rake the mucosa against the appliance.

• Lesions have no malignant potential and do not require further management.