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 better respond 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. This article focuses on the oral hyperkeratinization that results from friction. Friction (the constant rubbing of 2 surfaces against one another) in the oral cavity may result in the development of clinically observable white patches.
Various names have been used to describe particular examples of frictional keratosis (FK). 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); the constant sucking, pressure, and irritation of the teeth against the buccal mucosa along the plane of occlusion (linea alba); and the habit of chronic cheek, tongue, or lip biting (cheek- or lip-bite keratosis).[1] Injuries to the oral mucosa, using items such as a pen, toothpicks, or fingernails, may result in frictional keratosis.
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 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, and constant mastication on edentulous alveolar ridges. The constant irritation stimulates the production of excessive keratin, with a subsequent change in the thickness and the color of the involved mucosa.[2]
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). 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.[3] In the same national survey, when 10,030 children aged 2-17 years were evaluated, the point prevalence for cheek and lip biting was 1.89% and 0.26% for frictional keratosis.[4]
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 cases per 1000 individuals.[5] In this same study, frictional keratosis was not differentiated from leukoplakic lesions, so the prevalence of frictional keratosis alone cannot be determined.
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.[6]
International
In a Danish study of 20,333 people aged 15 years and older, the prevalences of cheek and lip biting and frictional keratosis were slightly higher than those reported in the US studies.[7] The prevalence for cheek and lip biting was 5.1%, and the prevalence for frictional keratosis was 5.5%. Similarly, the prevalence for frictional keratosis from a small study sample[8] of Kenyan adults was 5.5%. In Slovenia, the prevalence was 2.7% for cheek and lip biting and 2.2% for frictional keratosis.[9] In a study of Turkish adolescents, linea alba was the second most common lesion, with a prevalence of 5.3%.[10]
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.[11] In an India dental school study, frictional keratosis was the most common oral lesion detected, occurring in 5.8% of the patients.[12] 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.[13]
The largest study of 23,785 patients, attending a Mexican dental school clinic, found frictional keratosis to be the third most common oral mucosal finding, with a prevalence rate of 32 cases per 1000 patients, while cheek-biting lesions were ranked fifth, or 21.7 cases per 1000 patients.[14]
Mortality/Morbidity
Frictional keratosis and its variants do not cause symptoms and are benign mucosal lesions that remain localized with no associated mortality or morbidity.
Race
No racial predilection seems apparent for oral frictional keratosis.
Sex
In general, frictional keratosis has no known sex predilection, except for cheek biting and lip biting, which are twice as prevalent in women compared with men.[1]
Age
Oral frictional keratosis affects persons from a wide range of ages, and contributing factors determine which age group is more commonly affected. In general, oral frictional keratosis lesions are more common in adults.
Most patients with frictional keratosis are free of symptoms, with the exception of those with aggressive cheek and lip biting habits. In some individuals who repeatedly traumatize the tissues, tenderness, swelling, and a burning sensation may be presenting symptoms.
Patients with persistent cheek and lip biting habits tend to have increased stress and psychologic disorders.
A patient may notice a thickening or roughness of the involved mucosal site, or frictional keratosis may be discovered as an incidental finding during a routine oral examination.
Individuals with a cheek and lip biting habit often report they are able to remove thin strands or tags of mucosa from the involved site.
Patients may report that they are aware of sucking the mucosa or thrusting their tongue against their teeth. Some patients report that their cheeks and tongue feel swollen. Occasionally, the affected fungiform papillae in persons with a tongue biting or thrusting habit may be tender and sometimes associated with a burning sensation.
When the gingival tissues are involved, patients may report using a medium- or hard-bristled toothbrush or other oral hygiene aids.
In some instances, patients give a history of wearing orthodontic appliances or removable full or partial dental prostheses that may traumatize the soft tissues.[15] Occasionally, ill-fitting or broken mouthguards or occlusal splints irritate the oral mucosa, resulting in frictional keratosis.
Sucking on the cheeks, lips, or sides of the tongue may be a habit to relieve the discomfort from temporomandibular disorder or burning mouth syndrome. Forceful or aberrant nutritional sucking on the nipple of the bottle or breast may result in calluses on the lips of infants.
In rare examples, individuals may give a history of picking the oral mucosa with long fingernails or some other external object.
The first step in the identification of white patches suspected of being associated with physical trauma is to use a 2 X 2-inch sterile gauze to wipe off the lesion or lesions. If the patch is not easily wiped off, this suggests the presence of hyperkeratinization.
The lips, the lateral margins of the tongue, the buccal mucosa (mainly along the occlusal line), and the edentulous alveolar ridges are the most common sites to find frictional keratosis and its variants.
Typically, the lesions appear as distinct, focal, and translucent-to-opaque white asymptomatic patches with sharply delineated borders. The surface of a lesion may appear irregular and feel rough to the tongue.
Slight variations in the clinical presentation are directly related to the nature and the source of the physical trauma.
One of the more common presentations of frictional keratosis is the linea alba (white line). This feature manifests as a horizontal thickening of the buccal mucosa along the occlusal line of the teeth. Linea alba is thought to result from chronic cheek biting or sucking of these tissues (see images below).
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The white line observed on the cheek is level with the biting plane of the teeth. The wear on the occlusal surfaces of the molar teeth suggests that t....
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This wider area of roughened mucosa is typical of those produced by the habit of cheek biting or nibbling. Courtesy of Catherine M. Flaitz, DDS and Al....
See the list below:
In one patient, the surface of the last molar tooth showed considerable occlusal wear, which is evidence that the patient had the habit of grinding his teeth (see first image above). This habit most probably led to the biting of the cheek mucosa.
Occasionally, the line reflects the irregularity of the adjacent teeth and has a somewhat scalloped appearance (see image below).
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Prominent linea alba with evidence of cheek biting. The white line shows a slightly scalloped appearance, which correlates with the buccal surfaces of....
Occasionally, the frictional line is somewhat more diffuse, and this type of change is more likely to be associated with the habit of cheek chewing, also known as morsicatio buccarum (see images below), rather than the occasional accidental friction of teeth against the mucosa during the normal eating process. These white patches are associated with either a conscious or an unconscious chronic oral habit.
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This frictional keratotic line shows a roughened surface. A thicker patch of mucosa is at the anterior end (under the tongue blade edge). This area is....
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Anterior rough surface area at the occlusal plane of the teeth. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
The effects of the habit of chronic biting may also manifest on the anterior and lateral borders of the tongue and appear as white, shaggy or mildly wrinkled plaques (see image below).
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Oral frictional hyperkeratosis of the lateral border of the tongue from chronic biting habit. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre....
A frictional keratosis lesion may be elevated from the surface, and patients may find that they develop the habit of nibbling further at these thickened mucosal sites. The first image below shows a frictional keratosis lesion that displays marked keratinization. The patient admitted to nibbling at the thickened mucosa (see second image below), which, in turn, made it thicker and easier to feel and, therefore, encouraged further nibbling.
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This frictional keratotic line shows a roughened surface. A thicker patch of mucosa is at the anterior end (under the tongue blade edge). This area is....
View Image
Anterior rough surface area at the occlusal plane of the teeth. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Occasionally, patchy erythema with or without petechiae is observed with recent trauma to the site.
Lesions associated with a tongue thrusting habit often demonstrate prominent crenations of the lateral tongue. In addition, the affected fungiform papillae may be red and enlarged from the chronic irritation.
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 relationship 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 toothbrushing and other oral hygiene aids affect the attached gingival tissues.
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Oral frictional hyperkeratosis of the attached maxillary gingiva from inappropriate toothbrushing technique. Courtesy of Catherine M. Flaitz, DDS and ....
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.[16]
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Oral frictional hyperkeratosis of the retromolar pad is also referred to as a ridge callus. This lesion is caused by masticatory irritation. Courtesy ....
Pregnancy may significantly increase the risk for cheek biting.[17]
In rare cases, the overuse of topical anesthetics, overuse of antiseptic mouthrinses, or oromucosal delivery of medications (eg, cannabis) causes keratosis from chemical irritation.[18]
The identification of such habits depends on obtaining a thorough history.
In some cases, the clinical presentation of oral frictional keratosis mimics potentially malignant oral lesions and oral cancer. New optical visualization devices have been developed as an adjunctive aid to a conventional clinical examination for differentiating between benign and malignant mucosal disorders.[23] These optical devices include the use of autofluorescence, multispectral fluorescence and reflectance, diffused white light with acetic acid rinse, and chemiluminescence with acetic acid rinse.[24] At the present time, well-designed clinical trials are not available to confirm the value of these devices for improved specificity and sensitivity in a general patient population.[24]
The diagnosis of frictional hyperkeratinization is typically made based on a detailed clinical examination and the finding of an oral habit or some other agent that has produced the chronic, low-grade irritation of the mucosa. In patients in whom the clinical evidence for frictional keratosis is equivocal or the appearance of the lesion is atypical, a biopsy of the tissue is indicated.
Premalignant and malignant conditions of the oral cavity most often appear benign, and using the clinical history and examination findings alone does not ensure the precise histologic nature of any oral lesion. In most cases, removal of the chronic irritation reverses frictional keratosis in 1-3 weeks.
If any doubt exists concerning a particular lesion or if residual keratotic foci persist despite the removal of the causative factor, then a biopsy is indicated. Most often, this should be a conventional scalpel biopsy.
The use of exfoliative cytology for the collection of cells is not usually appropriate because the frictional keratosis lesion, by definition, shows increased keratin on the surface, which makes the harvesting of the intermediate layer and basal cells much more difficult.
A oral brush biopsy may be used; however, because the thick surface layer of keratin is a barrier, moderate pressure must be applied in order to ensure that an adequate sampling of basal cells is obtained
Important to note is that a definitive diagnosis cannot be obtained from an oral brush biopsy specimen. Only a scalpel biopsy can provide an accurate diagnosis of the white lesion in question.
The oral mucosa is lined by stratified squamous epithelium that exhibits topographical differences correlated with specific 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 usually nonkeratinized; however, the gingiva and hard palate are keratinized.
Frictional keratosis shows hyperkeratinization (either hyperorthokeratinization or hyperparakeratinization) and acanthosis as the main microscopic features of the surface epithelium (see images below).
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Low-power view of stratified squamous epithelium with marked hyperkeratinization, acanthosis, and a prominent granular cell layer. Courtesy of Catheri....
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High-power view of the surface keratin layer and a prominent granular cell layer. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
The epithelial surface may be smooth, corrugated, or ragged, with multiple keratin projections. Bacterial colonies are frequently found attached to the surface when it is irregular or shaggy. Often, a prominent granular cell layer is present. Occasionally, vacuolated cells can be seen in the upper spinous cell layer, especially in patients with cheek-biting keratosis. The underlying dense, fibrous connective tissue may demonstrate a patchy chronic inflammatory infiltrate. The terms focal keratosis or focal hyperkeratosis are frequently used for the histopathologic diagnosis. Frictional keratosis is a clinical term that conveys the cause and effect of the condition.
The most important management protocol includes the following:
Establish a diagnosis.
Be sure that any frictional irritant is 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.
Observe and monitor the patient to be certain that the frictional area is resolving in a timely fashion. In general, the patient should be reevaluated in 2-3 weeks for signs of lesion regression or resolution.
In the absence of resolution, even when the cause has been eliminated, obtain a biopsy specimen of the tissue to confirm that no dysplastic or neoplastic change is present.
Consultation with a dentist, an oral and maxillofacial surgeon, an oral and maxillofacial pathologist, a dermatologist, or otolaryngologist may be indicated if a lesion does not resolve after elimination of the suspected irritant. For aggressive cheek and lip biting habits, a psychological evaluation may be appropriate.
The patient's diet is typically not of concern unless the frictional keratosis is a result of constant chewing of hard foods against an edentulous ridge. The patient should be encouraged to eat on the dentate side, if possible, to avoid trauma to the alveolar mucosa during mastication.
Removing the frictional irritant resolves the condition. Irritants include tissue chewing or sucking, ill-fitting or irregularly surfaced dentures, jagged teeth, poorly adapted dental restorations, and constant mastication on edentulous alveolar ridges.
If dental prostheses fit poorly or are broken, relining or fabricating new removable partial and full dentures decreases the development of frictional keratosis.
Wearing an occlusal splint may be useful for decreasing or eliminating cheek and lip biting.
No significant complications are associated with frictional keratosis. This reactive lesion has no propensity for malignant transformation.
The risk of mutilating the buccal and labial mucosa following local anesthesia for dental treatment is increased, especially in children with lesions due to cheek biting. Both the child and the parent should be warned of the potential complication of unconsciously traumatizing the tissues because of this chronic habit.[25]
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.
Encourage patients 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, advise the patient that a biopsy is indicated.
Jose Luis Tapia, DDS, Assistant Professor, Department of Oral Diagnostic Sciences, State University of New York at Buffalo
Disclosure: Nothing to disclose.
Coauthor(s)
Alfredo Aguirre, DDS, MS, Director of Advanced Oral and Maxillofacial Pathology Training Program, Professor, Department of Oral Diagnostic Sciences, State University of New York at Buffalo
Disclosure: Nothing to disclose.
Specialty Editors
Michael J Wells, MD, FAAD, Dermatologic/Mohs Surgeon, The Surgery Center at Plano Dermatology
Disclosure: Nothing to disclose.
Drore Eisen, MD, DDS, Consulting Staff, Dermatology of Southwest Ohio
Disclosure: Nothing to disclose.
Chief Editor
William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
Additional Contributors
Daniel J Hogan, MD, Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center
Disclosure: Nothing to disclose.
Acknowledgements
Catherine M Flaitz, DDS, MS Professor of Oral and Maxillofacial Pathology and Pediatric Dentistry, Department of Diagnostic and Biomedical Sciences, University of Texas Health Sciences Center at Houston School of Dentistry
Catherine M Flaitz, DDS, MS is a member of the following medical societies: American Academy of Oral and Maxillofacial Pathology, American Academy of Oral Medicine, American Academy of Pediatric Dentistry, American Dental Association, International Association for Dental Research, and International Association of Oral Pathologists
Disclosure: Trimira, LLC Clinical contract for study Co-investigator on clinical grant; Trimira, LLC Honoraria Speaking and teaching; GC America Clinical contract for study Co-investigator on clinical grant; Forward Science LLC Device evaluation Product evaluation for school use
References
Neville BW, Damm DD, Allen CM, Bouquot JE. Physical and Chemical Injuries. Oral and Maxillofacial Pathology. 3rd ed. St. Louis, Mo: WB Saunders; 2009. 285-329.
Martinez Diaz-Canel AI, Garcia-Pola Vallejo MJ. Epidemiological study of oral mucosa pathology in patients of the Oviedo School of Stomatology. Med Oral. 2002 Jan-Feb. 7(1):4-9, 10-6.
The white line observed on the cheek is level with the biting plane of the teeth. The wear on the occlusal surfaces of the molar teeth suggests that the patient had a habit of bruxism. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
This wider area of roughened mucosa is typical of those produced by the habit of cheek biting or nibbling. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Prominent linea alba with evidence of cheek biting. The white line shows a slightly scalloped appearance, which correlates with the buccal surfaces of the teeth against which the mucosa is rubbed. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
This frictional keratotic line shows a roughened surface. A thicker patch of mucosa is at the anterior end (under the tongue blade edge). This area is exactly level with the occlusal plane and was being chewed constantly by the patient. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Anterior rough surface area at the occlusal plane of the teeth. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Oral frictional hyperkeratosis of the lateral border of the tongue from chronic biting habit. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
This frictional keratotic line shows a roughened surface. A thicker patch of mucosa is at the anterior end (under the tongue blade edge). This area is exactly level with the occlusal plane and was being chewed constantly by the patient. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Anterior rough surface area at the occlusal plane of the teeth. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Oral frictional hyperkeratosis of the attached maxillary gingiva from inappropriate toothbrushing technique. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Oral frictional hyperkeratosis of the retromolar pad is also referred to as a ridge callus. This lesion is caused by masticatory irritation. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Low-power view of stratified squamous epithelium with marked hyperkeratinization, acanthosis, and a prominent granular cell layer. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
High-power view of the surface keratin layer and a prominent granular cell layer. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
The white line observed on the cheek is level with the biting plane of the teeth. The wear on the occlusal surfaces of the molar teeth suggests that the patient had a habit of bruxism. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Prominent linea alba with evidence of cheek biting. The white line shows a slightly scalloped appearance, which correlates with the buccal surfaces of the teeth against which the mucosa is rubbed. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
This wider area of roughened mucosa is typical of those produced by the habit of cheek biting or nibbling. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
This frictional keratotic line shows a roughened surface. A thicker patch of mucosa is at the anterior end (under the tongue blade edge). This area is exactly level with the occlusal plane and was being chewed constantly by the patient. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Anterior rough surface area at the occlusal plane of the teeth. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Oral frictional hyperkeratosis of the lateral border of the tongue from chronic biting habit. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Oral frictional hyperkeratosis of the attached maxillary gingiva from inappropriate toothbrushing technique. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Oral frictional hyperkeratosis of the retromolar pad is also referred to as a ridge callus. This lesion is caused by masticatory irritation. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
Low-power view of stratified squamous epithelium with marked hyperkeratinization, acanthosis, and a prominent granular cell layer. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
High-power view of the surface keratin layer and a prominent granular cell layer. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aguirre, DDS.
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