Oral Frictional Hyperkeratosis

Oral hyperkeratinization, defined as the excessive formation of tenaciously attached keratin in the mouth, may be associated with various clinical conditions; however, this article focuses on the oral hyperkeratinization that results from friction (ie, oral frictional hyperkeratosis). Friction in the oral cavity may result in the development of clinically observable white patches.The diagnosis of oral frictional hyperkeratosisis is typically based on a detailed clinical examination and the finding of an oral habit or some other agent that has produced chronic, low-grade irritation of the mucosa.

Various names have been used to describe particular examples of frictional keratosis. These include frictional keratosis arising from excessive force while brushing the teeth (toothbrush keratosis); the constant rubbing of the tongue against the teeth (tongue-thrust keratosis); constant sucking, pressure, and irritation of the teeth against the buccal mucosa along the plane of occlusion (linea alba); and the chronic habit of biting the cheek (morsicatio buccarum, cheek-bite keratosis), tongue (morsicatio linguarum), or lip (morsicatio labiorum, lip-bite keratosis). ^[1] Injuries to the oral mucosa caused by items such as pens, toothpicks, or fingernails may result in frictional keratosis.

Signs and symptoms

Most patients with frictional keratosis have no symptoms, with the exception of those with aggressive cheek- and lip-biting habits. Some individuals who repeatedly traumatize the tissues may experience tenderness, swelling, and a burning sensation. Typically, the lesions of frictional keratosis appear as distinct, focal, and translucent-to-opaque white asymptomatic patches with sharply delineated borders. One of the more common presentations is the linea alba (white line; see the image below).

White line observed on cheek is level with biting plane of teeth. Wear on occlusal surfaces of molar teeth suggests habit of bruxism. Image from Catherine M Flaitz, DDS, and Alfredo Aguirre, DDS.

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Diagnosis

The first step in the identification of white patches suspected of being associated with physical trauma is to use a 2- × 2-in. sterile gauze to wipe off the lesion or lesions. If the patch is not easily wiped off, this finding suggests hyperkeratinization. If any doubt exists about a particular lesion or if residual keratotic foci persist despite the removal of the causative factor, then a biopsy is indicated. ^[2]

Treatment

Any frictional irritant should be removed. Biting, sucking, or chewing habits should be discontinued, and fractured or rough tooth surfaces or irregularly fitting dentures or other appliances should be corrected.

The oral mucosa is lined by stratified squamous epithelium and has topographic differences that correlate with physical demands or a higher degree of specialization. For example, the epithelium lining the floor of the mouth, the ventral side of the tongue, the buccal mucosa, and the soft palate is nonkeratinized; however, the epithelium associated with the gingiva and hard palate is usually keratinized. The dorsal surface of the tongue is also keratinized, but it is referred to as specialized mucosa because of the presence of papillae. The dorsum of the tongue, the hard palate, and the gingival tissues are keratinized to enable better response to masticatory demands.

Hyperkeratinization (excessive formation of tenaciously attached keratin) may be present in a variety of clinical conditions, including genetic, physiologic, inflammatory, immunologic, premalignant, and malignant conditions. The change may result from a local insult, including chemical, thermal, or physical irritants. As the name indicates, oral frictional hyperkeratosis is the oral hyperkeratinization that results from friction.

Friction in the oral cavity may result in the development of clinically observable white patches. The white patches of frictional keratosis that develop in the oral cavity represent a chronic low-grade mechanical process that is analogous to the formation of a callus on the skin. The most common local factors involved in this process are as follows:

• Tissue chewing (mainly on the buccal mucosa or lips)
• Ill-fitting or irregularly surfaced removable dental prostheses (dentures)
• Fractured or malposed teeth
• Poorly adapted dental restorations
• Orthodontic appliances,
• Improper toothbrushing
• Constant mastication on edentulous alveolar ridges

The constant irritation stimulates the production of excessive keratin, with subsequent changes in the thickness and the color of the involved mucosa. ^[3]

In most patients with frictional keratosis, the cause is easily identified. An oral habit of cheek biting, cheek chewing, tongue thrusting, or mucosal sucking can often be identified as the cause if the site of the lesion is carefully examined in relation to the occlusal plane.

An ill-fitting, rough, or broken removable dental prosthesis or orthodontic appliance or a fractured or irregular tooth surface frequently affects the adjacent soft tissues. Occasionally, a frictional keratosis lesion may develop as a result of the constant rubbing of an external object, such as a tobacco pipe; a musical instrument; or, perhaps, a worker's tool, which, for convenience, is held in the mouth for long periods. Another cause may be manipulation of the tissues with long fingernails, which may shred the mucosa.

Improper use of toothbrushes and other oral hygiene aids can affect the attached gingival tissues. (See the image below.)

Oral frictional hyperkeratosis of attached maxillary gingiva from inappropriate toothbrushing technique. Image from Catherine M Flaitz, DDS, and Alfredo Aguirre, DDS.

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Irritation from masticatory function may cause frictional keratosis when the alveolar mucosa and retromolar pad bear the stresses of eating. When lesions occur at these sites, they are referred to as alveolar ridge calluses. ^[4]  (See the image below.) Benign alveolar ridge keratosis occurs chiefly in patients aged between 40 and 80 years, with a 2:1 male predilection. More than one third of patients have complete or partial edentulism. ^[5]

Oral frictional hyperkeratosis of retromolar pad is also referred to as ridge callus. This lesion is caused by masticatory irritation. Image from Catherine M Flaitz, DDS, and Alfredo Aguirre, DDS.

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Pregnancy may significantly increase the risk for cheek biting. ^[6]  In rare cases, the overuse of topical anesthetics, overuse of antiseptic mouth rinses, or oromucosal delivery of medications (eg, cannabis) can cause keratosis from chemical irritation. ^[7]  Identification of such habits depends on obtaining a thorough history.

US and international statistics

Few large epidemiologic studies documenting the prevalence of various oral lesions, including oral frictional keratosis, have been published. The most comprehensive survey on the prevalence of oral mucosal lesions is the Third National Health and Nutrition Examination Survey (NHANES III). ^[8] Oral examinations were performed on 17,235 noninstitutionalized civilian adults. Cheek and lip biting had a point prevalence of 3.05% and ranked third in oral lesion prevalence, while frictional keratosis had a point prevalence of 2.67% and ranked fourth.

In the same national survey, when 10,030 children aged between 2 and 17 years were evaluated, the point prevalence was 1.89% for cheek and lip biting and 0.26% for frictional keratosis. ^[9]  The reported prevalence of frictional keratosis in children and adolescents has ranged from 0.26% to 5.3% in various published series. ^[10]

In another extensive survey of 23,616 White American adults from Minnesota that evaluated a wide range of oral lesions, the number of cases of cheek-biting keratosis was 1.2 per 1000 individuals. ^[11] This study did not differentiate frictional keratosis from leukoplakic lesions and thus could not determine the prevalence of frictional keratosis alone.

Linea alba is a common mucosal variation that is rarely singled out as a specific entity in prevalence studies. In a limited study of young men, 13% had this mucosal alteration. ^[12]

In a Danish study of 20,333 people aged 15 years or older, the prevalences of cheek and lip biting and frictional keratosis were slightly higher than those reported in the US studies ^[13] : 5.1% for cheek and lip biting and 5.5% for frictional keratosis. Similarly, the prevalence of  frictional keratosis in a small study sample of Kenyan adults was 5.5%. ^[14] In a study from Slovenia, the prevalence was 2.7% for cheek and lip biting and 2.2% for frictional keratosis. ^[15] In a study of Turkish adolescents, linea alba was the second most common lesion, with a prevalence of 5.3%. ^[16]

When studies were limited to individuals seeking care in oral medicine clinics, a wider frequency of occurrence was noted. In a limited study of patients treated at a dental school in Spain, the rate was 11.5% for frictional keratosis, 10.7% for linea alba, and 6.8% for cheek biting. ^[17] In a study from a dental school in India, frictional keratosis was the most commonly detected oral lesion detected (5.8% of patients). ^[18] When referred hospitalized and clinic patients were evaluated in an Australian oral medicine clinic, hyperkeratotic lesions, including tobacco-induced lesions, were documented in 11.6% of the hospitalized patients and 10.3% of the clinic patients. ^[19]

In a large study (N = 23,785) of patients attending a Mexican dental school clinic, frictional keratosis was the third most common oral mucosal finding (prevalence, 32 cases per 1000 patients), and cheek-biting lesions were the fifth most common (21.7 cases per 1000 patients). ^[20]

Age-, sex-, and race-related demographics

Oral frictional keratosis affects persons from a wide range of ages, and contributing factors determine which age group is more commonly affected. Overall, oral frictional keratosis lesions are more common in adults.

In general, frictional keratosis has no known sex predilection, except for cheek and lip biting, which have been shown to be more prevalent in women. ^[1]

No racial predilection has been established.

The prognosis for frictional keratosis is excellent. Resolution is usually accomplished when the frictional element is eliminated. Most lesions resolve in 1-3 weeks following the removal of the causative factor.

Frictional keratosis and its variants do not cause symptoms and are benign mucosal lesions that remain localized with no associated mortality or morbidity.

Patients should be encouraged to stop any habit that may be implicated with this lesion. If the putative traumatic factors are eliminated and no resolution of the lesions ensues, the patient should be advised that a biopsy is indicated.