Pocket Atlas of Oral Diseases. George Laskaris
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Fig. 1.26 Pseudomembranous candidiasis on the palate.
Fig. 1.27 Hyperplastic candidiasis on the lateral border of the tongue.
Fig. 1.28 Candida endocrinopathy syndrome, multifocal lesions on the tongue.
1.12 Chronic Biting
Definition: Chronic biting of the oral mucosa or maceration can be a relatively common chronic habit with a psychological background.
Etiology: The patients repeatedly bite the oral mucosa, pull it between the teeth, and detach the superficial epithelial layers.
Clinical features: Clinically, chronic biting appears as a localized or diffused irregular whitish lesion of small furrows, with desquamation of the epithelium (▶ Fig. 1.29 and ▶ Fig. 1.30). Rarely, petechiae and superficial erosions may be seen. The buccal mucosa, the lateral margins of the tongue, and the labial mucosa are the sites of predilection. Usually, the lesions are bilateral. The diagnosis is exclusively based on the history and clinical features.
Differential diagnosis: Leukoedema, candidiasis, cinnamon contact stomatitis, uremic stomatitis, chemical burn, leukoplakia, hairy leukoplakia, lichen planus, and white sponge nevus.
Treatment: Usually no treatment is required. However, patients should be recommended to stop the habit.
Fig. 1.29 Extensive chronic biting of the lateral border of the tongue.
Fig. 1.30 Localized chronic biting of the lateral border of the tongue.
1.13 Materia Alba of the Gingiva
Definition: Materia alba may be seen along the vestibular surface of the attached gingiva in patients with poor oral hygiene and is common along the dentogingival margin.
Etiology: It is caused by the accumulation of food debris, dead epithelial cells, and bacteria.
Clinical features: Materia alba appears as a soft, whitish plaque that is easily detached after slight pressure (▶ Fig. 1.31). The diagnosis is exclusively made clinically.
Differential diagnosis: Candidiasis, leukoplakia, cinnamon contact stomatitis, and chemical burn.
Treatment: Good oral hygiene.
Fig. 1.31 Materia alba deposition on the alveolar mucosa of the maxilla.
1.14 Fordyce’s Granules
Definition: Fordyce’s granules are ectopic sebaceous glands in the oral mucosa.
Etiology: Developmental. It is a normal anatomical variation.
Clinical features: Clinically, Fordyce’s granules appear as multiple small, asymptomatic, slightly raised, whitish-yellow well-circumscribed spots that rarely coalesce, forming plaques (▶ Fig. 1.32 and ▶ Fig. 1.33). The vermilion border of the upper lip, commissures, buccal mucosa, and the retromolar region, usually in a symmetrical bilateral pattern, are the sites of predilection. Characteristically, the granules become more evident when the mucosa is stretched. The diagnosis is exclusively based on the clinical features.
Differential diagnosis: Candidiasis, lichen planus, and leukoplakia.
Treatment: No treatment is required.
Fig. 1.32 Fordyce’s granules in the buccal mucosa.
Fig. 1.33 Sizeable Fordyce’s granule of the upper lip.
1.15 Leukoedema
Definition: Leukoedema is a common normal anatomical variation.
Etiology: It is caused by the increased thickness of the epithelium and intracellular edema of the spinous layer cells.
Clinical features: Clinically, the oral mucosa presents as opalescent or grayish-white with a slightly wrinkled surface, which characteristically disappears when the mucosa is everted and stretched (▶ Fig. 1.34 and ▶ Fig. 1.35). Leukoedema has a normal consistency on palpation. It usually occurs bilaterally on the buccal mucosa, and rarely on the lateral aspects of the tongue and lips. The diagnosis is exclusively made on clinical grounds.
Differential diagnosis: Chronic biting, candidiasis, lichen planus, leukoplakia, hairy leukoplakia, cinnamon contact stomatitis, white sponge nevus, and hereditary benign intraepithelial dyskeratosis.
Treatment: No treatment is required.
Fig. 1.34 Leukoedema of the buccal mucosa.
Fig. 1.35 Leukoedema of the tongue.
1.16 White Sponge Nevus
Definition: White sponge nevus or Cannon’s disease is a relatively rare genetic disease.
Etiology: Genetic. It is inherited as an autosomal dominant trait and mutation in the genes encoding keratin 4 and 13.
Clinical features: Clinically, it appears as bilateral asymptomatic, white or gray-white thick, lesions with multiple furrows and a spongy texture (▶ Fig. 1.36). The buccal mucosa, tongue, floor of the mouth, soft palate, and labial mucosa are the most commonly affected sites, although lesions may also develop in the vaginal, rectal, nasal, and laryngeal mucosa. The diagnosis is based on the history, clinical features, and histologic examination.
Laboratory tests: Biopsy and histologic examination.
Differential diagnosis: Leukoedema, chronic biting, leukoplakia, dyskeratosis congenita, pachyonychia congenita, focal palmoplantar and oral mucosa hyperkeratosis syndrome, and hereditary benign intraepithelial dyskeratosis.
Treatment: No treatment is required.
Fig. 1.36 White sponge nevus,