10 Reactive Keratotic Lesions (Nonleukoplakias)
White lesions are some of the more commonly biopsied lesions and one of the most challenging for general pathologists and dermatopathologists. This is particularly because of confusion over nomenclature (especially over the term leukoplakia) and difficulty recognizing oral frictional keratoses, the two most common being morsicatio mucosae oris and benign alveolar ridge keratosis. There are also other frictional/reactive keratoses that are not as well defined histologically. Table 10-1 provides a list of mucosal conditions that are usually white; these are discussed subsequently and in other chapters.
When a mildly irritating substance comes in contact with the mucosa or when there is mild physical surface trauma, superficial cells become edematous and degenerate until the effects of the irritation (contacting chemical or physical irritation) are diluted, beyond which the keratinocytes appear normal. Such changes are seen in leukoedema and morsicatio mucosae oris. Smokeless tobacco lesions in particular show this effect, although over time carcinogens from tobacco may result in significantly keratotic and dysplastic lesions. Aspirin, however, is so caustic that it leads to complete destruction of the epithelial layer, resulting in ulceration and necrosis rather than a keratotic lesion, although the earliest changes may be leukoedema. Irritant contact stomatitis results in a clinical erythematous lesion with spongiosis as its main histologic feature (see Chapter 7). Correlating the histopathologic and clinical findings is key to arriving at an accurate diagnosis.
Leukodema usually results from mildly irritating fluid substances (cigarette or marijuana smoke or dentifrice) in episodic contact with the mucosa; putative failure of injured cell to maintain sodium pump leads to ingress of water.
• Keratinocyte edema of superficial cells appear pale and ballooned; absent nuclei may be due to plane of section or degeneration; cell membranes have compacted “jigsaw” puzzle appearance; deeper cells show perinuclear halos (but do not represent koilocytes because they lack other nuclear characteristics); usually, minimal-to-no keratin is noted, although keratin chevrons may be present (Figs. 10-2 and 10-3).
• Painless, thready white fragments lie on the mucosa (usually nonkeratinized sites) that easily peel off, leaving normal mucosa (Fig. 10-4); surrounding leukoedema may be seen; patients may also develop contact cheilitis.
The majority of hyperparakeratotic and hyperorthokeratotic lesions in the oral cavity are reactive, frictional keratoses. Two histologically well-defined frictional keratoses in the oral cavity are morsicatio mucosae oris (generally on the nonkeratinized mucosa) and benign alveolar ridge keratosis (lesions on the keratinized mucosa). The linea alba on the buccal mucosa is considered a variation of normal but is a severe localized leukoedema or a mild morsicatio mucosae oris (Fig. 10-7, A)
FIGURE 10-7 A, Linea alba; note slight reticulated leukoedema on either side. B, Morsicatio mucosae oris: poorly-demarcated yellowish white, macerated plaque that fades into normal mucosa. C, Morsicatio mucosae oris: white papules of right lateral tongue that fade into normal mucosa. D, Morsicatio mucosae oris of lower labial mucosa with irregular macerated papules and plaques and areas of erosion (arrow).
• Most common locations are close to the biting surfaces of the teeth, namely buccal mucosa, lateral/ventral tongue, and lower labial mucosa (rare on upper labial mucosa); more than 50% of patients are unaware of their habit (which may be nocturnal).