Frictional Keratosis, Contact Keratosis and Smokeless Tobacco Keratosis: Features of Reactive White Lesions of the Oral Mucosa

Abstract

White lesions of the oral cavity are quite common and can have a variety of etiologies, both benign and malignant. Although the vast majority of publications focus on leukoplakia and other potentially malignant lesions, most oral lesions that appear white are benign. This review will focus exclusively on reactive white oral lesions. Included in the discussion are frictional keratoses, irritant contact stomatitis, and smokeless tobacco keratoses. Leukoedema and hereditary genodermatoses that may enter in the clinical differential diagnoses of frictional keratoses including white sponge nevus and hereditary benign intraepithelial dyskeratosis will be reviewed. Many products can result in contact stomatitis. Dentrifice-related stomatitis, contact reactions to amalgam and cinnamon can cause keratotic lesions. Each of these lesions have microscopic findings that can assist in patient management.

Keywords: Cinnamon; Frictional keratosis; Leukoedema; Leukoplakia; Smokeless tobacco keratosis; Stomatitis.

Fig. 1

a Irregular, shaggy macerated appearance of the left buccal mucosa typical for cheek biting (morsicatio mucosae). b Photomicrograph showing marked hyperparakeratosis with a shaggy appearance with surface fissures and clefts. The epithelium is acanthotic with ballooned cells. Bacterial colonies are present on the keratin surface without an inflammatory response (H&E, magnification × 100). c Alveolar ridge keratosis presenting as a relatively discrete keratotic plaque on the retromolar pad. This is in contrast to the diffuse, ill-defined keratotic plaques seen in proliferative verrucous leukoplakia (Fig. 2a). d Histopathologic features of ridge keratosis characterized by marked hyperorthokeratosis, hypergranulosis and acanthosis. The epithelium has elongated anastomosing rete. Note the lack of inflammation (H&E, magnification × 100)

Fig. 2

a Clinical features of proliferative verrucous leukoplakia in a 76-year-old non-smoking female. White, thickened plaques with irregular, rough surface change are noted on the gingiva of the right maxilla and mandible. b Biopsy shows a corrugated or slightly papillary epithelial architecture with hyperorthokeratosis, a prominent granular cell layer but normal epithelial maturation. This histology is virtually indistinguishable from ridge keratosis (Fig. 1d) and requires clinical correlation (H&E, magnification × 100)

Fig. 3

a Leukoedema of the left buccal mucosa in a 58-year-old Black female presenting as an ill-defined opalescent filmy gray to white lesion. b When the cheek is everted and stretched the lesion diminishes. (Photographs courtesy of Dr. Kristin K. McNamara)

Fig. 4

a White sponge nevus of the right buccal mucosa in a 36-year-old Black man. Although there are clinical similarities to frictional keratoses the histology is distinct. b Photomicrograph of white sponge nevus exhibiting prominent hyperparakeratosis and acanthosis with vacuolation of the spinous cell layer. Within the spinous layer occasional cells with bright eosinophilic perinuclear condensation representing keratin tonofilaments can be observed. (H&E magnification × 100). Inset: High-power photomicrograph of exfoliative cytology with Papanicolaou staining demonstrating the eosinophilic perinuclear condensation (magnification × 400)

Fig. 5

Hereditary benign intraepithelial dyskeratosis. Low-power photomicrograph exhibiting marked parakeratosis and acanthosis. Scattered throughout the epithelium but most appreciated in the upper spinous layer are dyskeratotic cells. A mild lymphoplasmacytic infiltrate in the subepithelial lamina propria is typical. Inset: High-power photomicrograph highlights the dyskeratotic cells which have crenated or pyknotic nuclei surrounded by dense hypereosinophilic cytoplasm giving the appearance of intraepithelial dyskeratosis. (H&E magnification × 400). (Photographs courtesy of Dr. Hans Grossniklaus)

Fig. 6

a Superficial sloughing of the oral mucosa due to the use of triclosan and pyrophosphate containing toothpaste. There is peeling of the superficial keratin without any underlying erythema or erosion. Total resolution of the condition was achieved upon discontinuation of the tartar control toothpaste. b Photomicrograph demonstrates marked parakeratosis, acanthosis and intracellular edema. Intraepithelial linear clefting of the superficial parakeratin is seen. At times the superficial parakeratin is completely detached from the underlying stratified squamous epithelium or this superficial sloughing is all that is submitted for histologic examination. (H&E magnification × 100)

Fig. 7

1a Oral lichenoid contact reaction to dental amalgam presenting as areas of erythema and white plaques on the left buccal mucosa. Note the large amalgam restorations that directly contacts the affected mucosa. 1b Oral lichenoid contact reaction to dental amalgam often has a dense lymphocytic infiltrate subjacent to the epithelial cells. Perivascular inflammation in the deeper lamina propria is present, a feature not typical for oral lichen planus (H&E magnification × 40). 1c Interface mucositis in amalgam contact reactions are seen and the dense lymphocytic infiltrate can form tertiary follicles (arrow) (H&E magnification × 100). 2a Oral lichenoid contact reaction of the right buccal mucosa to cinnamon flavored chewing gum. Within 10 days of discontinuing the gum, the lesion completely resolved. 2b The microscopic features of oral lichenoid contact reaction to cinnamon show marked epithelial acanthosis and intracellular edema. A dense inflammatory cell infiltrate is seen in the superficial lamina propria and generally extends deeper into the lamina propria around vascular spaces (H&E magnification × 100). 2c Acanthosis, dyskeratotic cells and inflammatory exocytosis is seen along with interface mucositis. The inflammation unlike oral lichen planus is composed of lymphocytes, plasma cells and scattered eosinophils. However, these microscopic findings are relatively non-specific (H&E, magnification × 200)

Fig. 8

a Typical clinical presentation of an early smokeless tobacco keratosis demonstrating an area of superficial keratosis with slight wrinkling, lacking any appreciative mucosal thickening. b A more advanced lesion demonstrates obvious mucosal thickening and wrinkling of the mucosa with intervening furrows. Flecks of smokeless tobacco are present within the lesion. c Photomicrograph of smokeless tobacco keratosis shows a corrugated parakeratotic surface and epithelial acanthosis. Prominent chevron keratinization and vacuolated cells in the stratum spinosum are seen. The basal cells show nuclear hyperchromatism but no dysplasia is seen. The connective tissue lacks inflammation. (H&E, magnification × 100). d Subepithelial collagen eosinophilia that can be mistaken for amyloid is an unusual finding in smokeless tobacco keratoses. These deposits can be seen around nerves, vessels, salivary glands, and at the epithelial-stroma interface. (H&E, magnification × 100)