Quick Review for Patients
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Frictional keratosis is the oral counterpart of a callus on the skin. It is a common alteration, especially in areas of recurring, mild mechanical trauma or irritation from malposed teeth, dental prosthetics or patient habit, such as smokeless tobacco use (smokeless tobacco keratosis), exuberant toothbrushing with an overly firm brush (toothbrush keratosis), constant rubbing of the tongue against the teeth (tongue thrust keratosis), or the frequent clenching of the facial muscles, thereby pushing cheek and lips firmly against the dentition (chronic cheek bite keratosis, chronic lip bite keratosis). In most cases the cause is obvious, but without a known etiology the clinician is forced to presume the keratotic plaque to be leukoplakia and to manage it as a premalignancy.
Chemical keratosis may also occur as the result of the compounds in smokeless tobacco, certain toothpastes, acid medication used inappropriately (aspirin placed on the gingiva to alleviate toothache pain), and certain spices in candies or chewing gum, especially cinnamon and peppermint.
A special form of thermally/chemically-induced
keratosis is seen as a generalized whiteness of the hard palate in persons
who smoke cigars and pipes. Once a common mucosal change, this nicotine
stomatitis (nicotine palatinus, smoker's palate) has
become less common as cigar and pipe smoking have lost popularity. During the
1960s and 1970s it had a prevalence rate of 0.6/1,000 adults (Table
this lesion is a white keratotic change obviously associated with tobacco
smoking, it does not appear to have a premalignant nature, perhaps because
it develops in response to the heat rather than the chemicals of tobacco
smoke. It can also be produced by the long-term use of
extremely hot beverages. In some South American and Southeast
Asian cultures hand-rolled cigarettes and cigars are smoked with the lit
end held within the mouth. This "reverse smoking" habit produces a similar
but more pronounced palatal keratosis, called reverse smoker's palate,
which is definitely a premalignant lesion.
Frictional keratosis is usually found in teenagers and young adults of both genders. Many individuals have a thin, slightly raised white keratotic line along the occlusal plane of the buccal mucosa, often bilateral. This linea alba (Figure 1) is considered to be a variation of normal anatomy but is called frictional keratosis, chronic cheek bite keratosis or morsicatio buccarum when it becomes pronounced (Figures 2 & 3). There is usually a clenching or bruxing habit and the most severe lesions are found in persons with the habit of constantly pushing the cheeks between the teeth with a finger while gently biting on the buccal tissues. The surface of a frictional keratosis may be quite rough and irregular, and on the buccal mucosa may show a scalloped effect as the tissues take on the contours of adjacent teeth. Focal oval areas of pink mucosa may be seen, representing areas in which the patient has peeled off the thick surface keratin with his or her teeth. The resulting combination of red and white mucosa may be mistaken for the precancers granular leukoplakia or erythroleukoplakia.
A similar linear line of excess keratin may be found along the lateral edges of the tongue, often with crenations from chronically pushing the tongue against the teeth. Rounded or irregularly shaped white plaques may be seen on the anterior dorsal surface of the tongue from a chronic tongue thrust habit, and may be seen in the retromolar region because of trauma from the maxillary dentition.
Nicotine stomatitis is found in males older than 45 years of age with long-term tobacco use. The palatal mucosa becomes diffusely gray and then white, with scattered white papules with punctate red centers, representing inflamed salivary glands and ducts (Figures 4 & 5). In severe cases the palate becomes fissured and takes on the appearance of a dried lake bed.
Smokeless tobacco keratosis is a white, nonelevated plaque with a poorly demarcated periphery and usually with regular and intertwining fissures running through it (Figure 6). It occurs in the area of habitual tobacco placement and is a completely painless lesion.
Pathology and Differential Diagnosis
Acanthosis and hyperkeratosis, usually orthokeratosis, are the hallmarks of frictional keratosis. The keratin may become ragged and delaminated by the patient's habit and it is not unusual to find bacterial colonies lodged in surface irregularities. The granular cell layer is often quite prominent, a feature lacking in most other oral hyperkeratoses (Figure 7). The cells of the spinous layer often demonstrate intraepithelial edema and occasional vacuolated cells with pyknotic nuclei resemble koilocytes (Figure 8). Dysplasia is not seen in the epithelium and there is no increase in mitotic activity. There is a mild scattered chronic inflammatory cell infiltrate within underlying fibrovascular stroma.
Frictional keratosis with prominent intracellular edema and koilocyte-like cells may be difficult to distinguish from leukoedema, white-sponge nevus, smokeless tobacco keratosis, chemical keratosis, and hairy leukoplakia. The differential diagnosis of these lesions is discussed elsewhere in the present book (see the leukoedema section).
Nicotine stomatitis shows hyperkeratosis and acanthosis of palatal epithelium with scattered chronic inflammatory cells within subepithelial stroma and mucous glands (Figure 9). Squamous metaplasia and hyperplasia of excretory ducts are often seen and neutrophils may fill some ducts. The degree of epithelial hyperplasia and hyperkeratosis correlates positively with the duration and the amount of smoking. Epithelial dysplasia is rare.
Smokeless tobacco keratosis is predominantly a chemical burn, hence, the major changes are seen in the more superficial epithelium, where hyperparakeratosis may be pronounced and were the cells often show considerable intraepithelial edema (Figure 10). As the mucosa is habitually stretched during smokeless tobacco use but is not in the biopsy specimen, surface verruciform change is commonly seen as a "shrinkage" artifact. Underlying stroma usually contains small numbers of chronic inflammatory cells and minor salivary glands may show a hyalinized stroma.
Treatment and Prognosis
No treatment is required for frictional keratosis and there is no potential for malignant transformation. The patient's habit, however, may produce aching facial or tongue muscles or dysfunction of the temporomandibular joint. This may be reason to stop the habit. The white keratotic plaques will completely disappear within a few days or weeks of the elimination of the chronic trauma. Any keratosis remaining after four weeks should be considered to be true leukoplakia or another diagnosis and biopsy would be in order in order to evaluate for dysplastic epithelial cells.
Within a month or two of smoking cessation the palate affected by nicotine palatinus will usually return to normal, even when the keratosis has been present for many decades. While this is not a precancerous lesion and requires no treatment, the patient nevertheless should be encouraged to stop smoking and other high risk areas should be examined closely. Any white lesion of the palatal mucosa which persists after two months of habit cessation should be considered a true leukoplakia and managed accordingly.
The smokeless tobacco keratosis will almost always disappear within a few weeks or months or cessation of the tobacco habit. Any residual white keratosis after two months should be considered a leukoplakia and viewed with suspicion.
References (Chronologic Order)
Note: Click on underlined author's names for additional detail.
Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. Philadelphia, W. B. Saunders; 1995.
Elder D, Elenitsas R, Jaworsky C, Johnson B Jr. Lever's Histopathology of the skin, 8th edition. Philadelphia; Lippincott-Raven, 1997.
Sapp JP, Eversole LR, Wysocki GP. Contemporary oral and maxillofacial pathology. Mosby; St. Louis, 1997.
Odell EW, Morgan PR. Biopsy pathology of the oral tissues. London; Chapman & hall Medical, 1998.
Saunders WH. Nicotine stomatitis of the palate. Ann Otol Rhinol Laryngol 1958; 67:618-627.
Schwartz DL. Stomatitis nicotina of the palate: report of two cases. Oral Surg Oral Med Oral Pathol 1965; 20:306-315.
Bouquot JE, Gorlin RJ. Leukoplakia, lichen planus and other oral keratoses in 23,616 white Americans over 35 years of age. Oral Surg Oral Med Oral Pathol 1986; 61:373-381.
Rossi KM, Guggenheimer J. Thermally induced "nicotine" stomatitis. A case report. Oral Surg Oral Med Oral Pathol 1990; 70:597-599.
Salons L, Axell T, Hellden L. Occurrence
of oral mucosal lesions, the influence of tobacco habits and an estimate
of treatment time in an adult Swedish population. J Oral Pathol Med 1990;
Table 1: Gender-specific prevalence rates per 1,000 population for selected oral masses and surface alterations in U.S. adults, ranked by total frequency. Modified from Bouquot JE. Common oral lesions found during a mass screening examination. J Am Dent Assoc 1986; 112:50-57, and Bouquot JE, Gundlach KKH. Oral exophytic lesions in 23,616 white Americans over 35 years of age. Oral Surg Oral Med Oral Pathol 1986; 62:284-291.
* total examined population = 23,616 adults over 35 years of age
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