eMedicine Specialties > Dermatology > Diseases of the Oral Mucosa

Oral Frictional Hyperkeratosis: Differential Diagnoses & Workup

Author: Catherine M Flaitz, DDS, MS, Professor of Oral and Maxillofacial Pathology and Pediatric Dentistry, Department of Diagnostic Sciences, University of Texas Health Sciences Center at Houston, Dental Branch
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; Jose Luis Tapia, DDS, MS, Assistant Professor, Department of Oral Diagnostic Sciences, State University of New York at Buffalo
Contributor Information and Disclosures

Updated: Jul 27, 2009

Differential Diagnoses

Other Problems to Be Considered

Hairy leukoplakia
Leukoedema
Actinic cheilitis
Lupus erythematosus
White sponge nevus
Contact stomatitis

Several conditions should be included in the differential diagnosis of frictional keratosis in both children and adults.^16,17,18 Occasionally, plaquelike lesions of lichen planus and lupus erythematosus may resemble areas of frictional keratosis. Chemical burns and acute pseudomembranous candidiasis may have the same clinical appearance as frictional keratosis; 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 frictional keratosis 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 subungual hyperkeratosis.

White patches associated with smoking and smokeless tobacco can be clinically indistinguishable from frictional keratosis. 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 frictional keratosis is important because their prognoses may be different from that associated with frictional keratosis, which has an excellent prognosis. Also see Smokeless Tobacco Lesions.

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 infection and is associated with immunosuppression resulting from HIV infection. Similarly, the long-term use of topical steroids to treat chronic ulcerative conditions (ie, mucous membrane pemphigoid, erosive lichen planus) may result in the formation of white patches on the lateral borders of the tongue that are indistinguishable from hairy leukoplakia.

Leukoplakia is a clinical term reserved for white lesions that cannot be characterized clinically or pathologically as any other disease (ie, frictional keratosis, lichen planus, candidiasis, hairy leukoplakia, white sponge nevus). Leukoplakia may be associated with premalignant or malignant epithelial changes.

Contact stomatitis associated with the use of artificially flavored cinnamon products (eg, gum, candy, toothpaste, mouthwashes, dental floss) may present as a white patch that may resemble frictional keratosis. However, pain and burning are common symptoms in contact stomatitis.¹⁹

Workup

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 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
  • 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 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 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 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.

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