AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Background

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. In contrast, 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 FK 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 or lip biting (cheek- or lip-bite keratosis).¹

Pathophysiology

The white patches of FK 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.

Frequency

United States

Few large epidemiologic studies documenting the prevalence of various oral lesions, including oral FK, 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 FK had a point prevalence of 2.67% and ranked fourth.² 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 FK.³
• 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.⁴ In this same study, FK was not differentiated from leukoplakic lesions, so the prevalence of FK 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.⁵

International

In a Danish study of 20,333 people aged 15 years and older, the prevalences of cheek and lip biting and FK were slightly higher than those reported in the US studies.⁶ The prevalence for cheek and lip biting was 5.1%, and the prevalence for FK was 5.5%. Similarly, the prevalence for FK from a small study sample⁷ of Kenyan adults was 5.5%. In Slovenia, the prevalence was 2.7% for cheek and lip biting and 2.2% for FK.⁸ In a limited study of patients treated at a dental school in Spain, the rate was 11.5% for FK, 10.7% for linea alba, and 6.8% for cheek biting.⁹

Mortality/Morbidity

FK 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 this condition.

Sex

In general, FK has no known sex predilection, except for cheek biting and lip biting, which are twice as prevalent in women compared with men.

Age

Oral FK affects persons from a wide range of ages, and contributing factors determine which age group is more commonly affected. The exception is cheek biting and lip biting, which are detected 3 times more often after age 35 years.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

History

• Most patients with FK 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 FK 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 have 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, mouthguards, occlusal splints, or removable full or partial dental prostheses.
• In rare examples, individuals may give a history of picking the oral mucosa with long fingernails or some other external object.

Physical

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 FK 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 features of FK is the linea alba (white line). This feature manifests as a horizontal thickening of the buccal mucosa along the line of the teeth, the occlusal line. It is thought to result from chronic cheek biting or sucking of these tissues (see Media File 1 and Media File 3).
• • 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 Media File 1). 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 Media File 2).
• 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 Media Files 4-5), 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.
• 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 Media File 6).
• An FK lesion may be elevated from the surface, and patients may find that they develop the habit of nibbling further at these thickened mucosal sites. Media File 4 shows an FK lesion that displays marked keratinization. The patient admitted to nibbling at the thickened mucosa (see Media File 5), which, in turn, made it thicker and easier to feel and, therefore, encouraged further nibbling.
• 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.

Causes

In most patients with FK, 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, an FK 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 (see Media File 6).
• Irritation from masticatory function may cause FK when the alveolar mucosa and retromolar pad bear the stresses of eating (see Media File 8).
• The identification of such habits depends on obtaining a thorough history.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Other Problems to be Considered

Hairy leukoplakia
Leukoedema
Actinic cheilitis
Lupus erythematosus
White sponge nevus

Several conditions should be included in the differential diagnosis of FK in both children and adults.^{10, 11} Occasionally, plaquelike lesions of lichen planus and lupus erythematosus may resemble areas of FK. Chemical burns and acute pseudomembranous candidiasis may have the same clinical appearance as FK; however, these white areas can be easily wiped off with gauze because they consist of necrotic epithelium (in the case of superficial chemical burns) or fungal colonies (in the case of acute pseudomembranous candidiasis). Sheets or clustered aggregates of Fordyce granules and scars may resemble FK because of their yellowish-white, submucosal appearance. In these examples, the surface mucosa is smooth.

Consider genokeratosis, such as white sponge nevus, hereditary benign intraepithelial dyskeratosis, and pachyonychia congenita, when the lesions are multifocal. These 3 autosomal dominant conditions appear in young persons. In white sponge nevus, the hyperkeratinization is restricted to the oral cavity, the esophagus, the anus, and the vagina. In hereditary benign intraepithelial dyskeratosis, gelatinous plaques manifest in the ocular conjunctiva. In pachyonychia congenita, the fingernails exhibit koilonychia

White patches associated with smoking and smokeless tobacco can be clinically indistinguishable from FK. Clinical information regarding tobacco and smokeless tobacco use is essential for differentiating these conditions. Some examples of tobacco-related keratoses are caused by thermal and chemical irritation, while other keratotic lesions represent a precancerous entity. For this reason, differentiating between lesions from smoking or smokeless tobacco and FK is important because their prognoses may be different from that associated with FK, which has an excellent prognosis.

An uncommon but important adherent white lesion typically found on the lateral border of the tongue is hairy leukoplakia. This shaggy white plaque is caused by the Epstein-Barr virus and is associated with immunosuppression, including an oral manifestation of HIV infection.

Leukoplakia is a clinical term reserved for white lesions that cannot be characterized as any other disease (ie, FK, smokeless tobacco lesion, candidiasis, hairy leukoplakia, white sponge nevus). The term leukoplakia conveys a more sinister prognosis and may be associated with premalignant or malignant epithelial changes.

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Procedures

• 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 FK 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 FK 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 FK lesion, by definition, shows increased keratin on the surface, which makes the harvesting of the intermediate layer and basal cells much more difficult.
  • A 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
  • Importantly, note 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.

Histologic Findings

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 gingival tissues often display parakeratosis.

FK shows hyperkeratinization (either hyperorthokeratinization or hyperparakeratinization) and acanthosis as the main microscopic features of the surface epithelium (see Media Files 9-10). 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 prickle 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. FK is a clinical term that conveys the cause and effect of the condition.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical Care

• 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.

Consultations

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.

Diet

The patient's diet is typically not of concern unless the FK 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.

FOLLOW-UP

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Further Outpatient Care

• The patient should receive follow-up care to ensure the frictional area is resolving.

Deterrence/Prevention

• 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 FK.
• Wearing an occlusal splint may be useful for decreasing or eliminating cheek and lip biting.

Complications

• No significant complications are associated with FK. 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 ulcerating the tissues because of this chronic habit.¹²

Prognosis

• The prognosis for FK 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.

Patient Education

• 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.

MISCELLANEOUS

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical/Legal Pitfalls

• Failure to make a definitive diagnosis and to rule out epithelial dysplasia or neoplasia if a clinically diagnosed FK lesion does not resolve is a serious potential pitfall.

ACKNOWLEDGMENTS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Alan Drinnan, MB, ChB, FDS, DDS, to the development and writing of this article.

MULTIMEDIA

Section 10 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Media file 1:  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 Aquirre, DDS.
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Media file 2:  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 Aquirre, DDS.
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Media file 3:  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 Aquirre, DDS.
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Media file 4:  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 (same patient as in Media File 5). Courtesy of Catherine M. Flaitz, DDS and Alfredo Aquirre, DDS.
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Media file 5:  Anterior rough surface area at the occlusal plane of the teeth (same patient as in Media File 4). Courtesy of Catherine M. Flaitz, DDS and Alfredo Aquirre, DDS.
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Media file 6:  Oral frictional hyperkeratosis of the lateral border of the tongue from chronic biting habit. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aquirre, DDS.
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Media file 7:  Oral frictional hyperkeratosis of the attached maxillary gingiva from inappropriate toothbrushing technique. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aquirre, DDS.
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Media file 8:  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 Aquirre, DDS.
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Media file 9:  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 Aquirre, DDS.
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Media file 10:  High-power view of the surface keratin layer and a prominent granular cell layer. Courtesy of Catherine M. Flaitz, DDS and Alfredo Aquirre, DDS.
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REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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3. Shulman JD. Prevalence of oral mucosal lesions in children and youths in the USA. Int J Paediatr Dent. Mar 2005;15(2):89-97. [Medline].
4. Bouquot JE, Gorlin RJ. Leukoplakia, lichen planus, and other oral keratoses in 23,616 white Americans over the age of 35 years. Oral Surg Oral Med Oral Pathol. Apr 1986;61(4):373-81. [Medline].
5. Kashani HG, Mackenzie IC, Kerber PE. Cytology of linea alba using a filter imprint technique. Clin Prev Dent. 1980;2:21-4.
6. Axell T. Occurrence of leukoplakia and some other oral white lesions among 20,333 adult Swedish people. Community Dent Oral Epidemiol. Feb 1987;15(1):46-51. [Medline].
7. Macigo FG, Mwaniki DL, Guthua SW. Prevalence of oral mucosal lesions in a Kenyan population with special reference to oral leukoplakia. East Afr Med J. Dec 1995;72(12):778-82. [Medline].
8. Kovac-Kovacic M, Skaleric U. The prevalence of oral mucosal lesions in a population in Ljubljana, Slovenia. J Oral Pathol Med. Aug 2000;29(7):331-5. [Medline].
9. Martinez Diaz-Canel AI, Garcia-Pola Vallejo MJ. Epidemiological study of oral mucosa pathology in patients of the Oviedo School of Stomatology. Med Oral. Jan-Feb 2002;7(1):4-9, 10-6. [Medline].
10. Flaitz CM. Differential diagnosis of oral mucosal lesions in children and adolescents. Adv Dermatol. 2000;16:39-78; discussion 79. [Medline].
11. Coleman GC, Flaitz CM, Vincent SD. Differential diagnosis of oral soft tissue lesions. Tex Dent J. Jun 2002;119(6):484-8, 490-2, 494-503. [Medline].
12. Flaitz CM, Felefli S. Complications of an unrecognized cheek biting habit following a dental visit. Pediatr Dent. Nov-Dec 2000;22(6):511-2. [Medline].

Article Last Updated: Oct 5, 2006