1 White Lesions
White lesions of the oral mucosa are a multifactorial group of disorders, the color of which is produced by the scattering of light through an altered epithelial surface. These lesions are classified into two groups: (1) attached to the oral mucosa and (2) scraped off from the oral mucosa. The diagnosis and differential diagnosis of oral white lesions should be made on the basis of the medical history, clinical features, and laboratory tests.
| Leukoplakia | Fordyce’s Granules |
| Hairy Leukoplakia | Leukoedema |
| Lichen Planus | White Sponge Nevus |
| Lichenoid Reactions | Dyskeratosis Congenita |
| Linea Alba | Pachyonychia Congenita |
| Nicotinic Stomatitis | Focal Palmoplantar and Oral Mucosa Hyperkeratosis Syndrome |
| Cigarette Smoker’s Lip Lesions | |
| Uremic Stomatitis | Mucosal Horn |
| Cinnamon Contact Stomatitis | Papilloma |
| Chemical Burn | Verrucous Carcinoma |
| Candidiasis | Squamous Cell Carcinoma |
| Chronic Biting | Skin and Mucosal Grafts |
| Material Alba of the Gingiva | |
| Epithelial Peeling |
1.1 Leukoplakia
Definition: Leukoplakia is a clinical term without any histologic significance. It is defined as a white patch or plaque that cannot be scrapped off and cannot be characterized, clinically and histologically, as any other disease entity. Leukoplakia is the most common potentially malignant disorder (precancerous lesion) and is characterized by biological heterogenicity.
Etiology: The exact etiology remains unknown. Smoking and alcohol consumption are the main environmental causative factors, followed by human papillomavirus (HPV) types 16 and 18, Candida species, chronic local friction, etc.
Clinical features: Based on the clinical criteria, leukoplakia is classified into two main groups: (1) homogeneous (common-low risk) and (2) nonhomogeneous, which is subdivided into speckled or nodular (less common-high risk) and verrucous (rare-high risk) forms. Clinically, homogeneous form is characterized by a, thin, flat uniform white plaque (▶ Fig. 1.1 and ▶ Fig. 1.2). The speckled form is characterized by a red surface with multiple, small, white macules or nodules (▶ Fig. 1.3 and ▶ Fig. 1.4). Verrucous form presents as an exophytic, irregular, wrinkled or corrugated white plaque (▶ Fig. 1.5). Proliferative verrucous leukoplakia is a subtype of verrucous form, which is characterized by multifocal location, tendency to recur, is usually HPV positive, and has a high rate of malignant transformation. The total risk of malignant transformation of leukoplakia varies between 3 and 6% independent of the form. The buccal mucosa and commissures, tongue, floor of the mouth, gingiva, and lower lip are more frequently affected. The lateral border of the tongue and the floor of the mouth represent areas of high risk for malignant transformation.
Laboratory tests: Biopsy and histopathologic examination must be done to determine the risk of malignant transformation of oral leukoplakia. The oral clinicians should remember that the histologic results represent exclusively the site of biopsy taken in a specific time frame and do not have a long-term value.
Differential diagnosis: Lichen planus, lichenoid reaction, hairy leukoplakia, cinnamon contact stomatitis, nicotinic stomatitis, candidiasis, chronic biting, chemical burn, leukoedema, uremic stomatitis, lupus erythematosus, white sponge nevus, dyskeratosis congenita, pachyonychia congenita, skin, and mucosal grafts.
Treatment: The treatment of choice is surgical excision and smoking cessation. Electrosurgery and laser may also be used as alternative procedures. A follow-up program every 6 months for 3 to 5 years is recommended.
Fig. 1.1 Homogeneous leukoplakia on the upper gingiva.
Fig. 1.2 Homogenous leukoplakia on the floor of the mouth.
Fig. 1.3 Speckled leukoplakia on the buccal mucosa.
Fig. 1.4 Speckled leukoplakia on the buccal mucosa.
Fig. 1.5 Verrucous leukoplakia on the dorsum of the tongue.
1.2 Hairy Leukoplakia
Definition: Hairy leukoplakia was, during the pre-ART (antiretroviral therapy) era, one of the most common (20–30%) and characteristic lesions of human immunodeficiency virus (HIV) infection, while currently it appears less often. In HIV-infected patients, hairy leukoplakia develops when the CD4 count is less than 500 cells/mm3. In addition, it can also appear in immunosuppressed patients mainly after organ transplantation.
Etiology: The lesion is caused by Epstein–Barr virus.
Clinical features: Clinically, hairy leukoplakia presents as a white, asymptomatic, often elevated and unremovable patch. The lesion is almost always found bilaterally on the lateral margins of the tongue, and may spread to the dorsum and the ventral surface (▶ Fig. 1.6). Characteristically, the surface of the lesion is corrugated with a vertical orientation to the long axis of the tongue. However, smooth and flat lesions may also be seen. The lesion is not potentially malignant (precancerous).
Laboratory tests: Histologic examination, in situ hybridization, polymerase chain reaction, and electron microscopy are useful diagnostic tests.
Differential diagnosis: Leukoplakia, cinnamon contact stomatitis, uremic stomatitis, lichen planus, candidiasis, chemical burn, frictional keratosis, leukoedema, and lupus erythematosus.
Treatment: Usually, no treatment is required. However, in extent and severe cases acyclovir or valaciclovir or famciclovir can be used with success.
Fig. 1.6 Oral hairy leukoplakia.
1.3 Lichen Planus
Definition: Lichen planus is a relatively common, chronic inflammatory disease of the oral mucosa, skin, genital mucosa, nails, and hair.
Etiology: The exact etiology is not well known. However, T-cell-mediated immune reaction against components of epithelial basal cells may be involved.
Clinical features: Clinically, oral lichen planus classically presents with small white papules that coalesce, forming a network of lines usually in a symmetrical pattern (Wickman’s striae). Six forms of oral lichen planus are recognized: the reticular and erosive or ulcerative that are common (▶ Fig. 1.7
