White Lesions Flashcards
Leukoedema
Hereditary Condition
mild opacification of the buccal mucosa of unknown etiology. The opaque changes dissipate when stretched. In rare cases textural changes can be seen
Epithelium is perakeratotic and acanthotic with intracellular edema of the spinous cells.
DD: white sponge nevus, hereditary benign intraepithelial dyskeratosis, cheek biting, lichen planus (differentiated microscopically)
No treatment but biopsy should be performed if diagnosis is in question
White Sponge Nevus (Cannon’s Disease)
Asymptomatic, folded, white lesion in several mucosal sites. Lesions tend to be thickened and have a spongy consistency, typically bilateral and symmetric, and appears typically pre-puberty.
Microscopically the epithelium is thickened, with marked spongiosis, acanthosis, and parakeratosis. perinuclear eosinophilic condensation of cytoplasm is characteristic of prickle cells.
DD: hereditary benign epithelial dyskeratosis, lichen planus, lichenoid drug reaction, lupus erythematosus, cheek chewing, candidiasis.
No treatment necessary after biopsy
Hereditary Benign Intraepithelial Dyskeratosis
rare hereditary condition. Early Onset, bulbar conjunctivitis, conjunctival plaques, and oral white lesions.
Oral lesions are soft, asymptomatic, white folds and plaques of spongy mucosa, usually in the buccal and labial mucosa and labial commisures, and floor of the mouth, and lateral surfaces of the tongue. Typically begin in the first year of life.
Histopathologically, epithelial hyperplasia and acanthosis with intracellular edema.
No treatmetn is necessary
Hereditary, does not disappear when stretched, biopsy to confirm, may also involve conjunctiva
White sponge Nevus and hereditary benign intraepithelial dyskeratosis
Look for bilateral white reticulations (striae), erosions, atrophy, and associated skin lesions, Biopsy
Lichen Planus
Look for white lesions, asymmetrical, in contrast with new drug history
Lichenoid drug reaction
White shaggy lesions along occlusal plane or trauma sites
Cheek Chewing
Delicate radiating straie. usually unilateral Biopsy
Lupus Erythematosus
Look for predisposing factors, can rub off, responds to antifungal therapy
Candidiasis
Follicular Keratosis
autosomal dominant disorder occurring between age 6-20. most have skin lesions, the oral lesions are small, skin-colored papular lesions, symmetrically distributed over the skin that parallel the oral lesions. Typically small, whitish papules, producing a cobbelstone appearance.
Histopathology: suprabasal lacunae containing acanthotic epithelial cells, basal layer proliferation below the lacunae, formation of vertical clefts that show a lining of parakeratotic and dyskeratotic cells, and the presence of specific benign dyskeratotic cells.
Treatment: topical corticosteroids and vitamin A, but long term therapy is tolerated poorly.
Focal (frictional) hyperkeratosis
a white lesions related to chronic fubbing or friction, causing a hyperkeratotic white lesion. commonly traumatized areas such as lips and lateral margin of the tongue, buccal mucosa, and edentulous alveolar ridges.
Histopathology: hyperkeratosis
Diagnosed by careful history, and removing the source should resolve the lesion or reduce in intensity over time. Biopsy if in doubt.
No treatment required, patient to control the habit.
Determine cause (ill fitting dentures, trauma), biopsy
Frictional Keratosis
White lesion of unknown origin. Assess risk factors and biopsy
Dysplasia, in situ carcinoma, SSC
History of aspirin or other agent application to site of lesion, food injury
Burn (chemical or food)
Lateral borders of tongue, irregular surface architecture, often bilateral, frequently with immunosuppression. Biopsy
Hairy Leukoplakia
White lesions associated with smokeless tobacco
clinical results in development of white patches in the labial mucosa with a slight increase in malignant potential. acceleration of periodontal disease and dental abrasion are common.
Histopathology: slight to moderate perakeratosis. Superficial epithelium may demonstrate vacuolization or edema. occasional epithelial dysplasia.
Discontinuation of smokeless tobacco will frequently improve lesions. Persistent lesions should be biopsied.
Nicotine Stomatitis
Palatal mucosa responds with an erythematous change followed by keratinization. Red dots surrounded by white keratotic rings appear, which is inflammation surrounding the minor salivary glands.
Histopathology characterized by epithelial hyperplasia and hyperkeratosis.
Denture can frequently block the formation. Low risk of dysplasia but an indicator for frequency of smoking
Hairy Leukoplakia
an unusual lesion along the lateral margins of the tongue, related to an Epstein-Barr virus in immunosupressed individuals (HIV, organ transplant)
Well demarcated white lesion that varies in architecture from flat and plaque like to papillary/filiform, or a corrugated lesion. May be unilateral or bilateral.
Histopathology: Viral inclusions and/or peripheral displacement of chromatin with a smudgy nucleus is evident
DD: idiopathic leukoplakia, frictional hyperkeratosis, and leukoplakia associated with tobacco use
no treatment available, other than address immunosupression.
Hairy Tongue
sometimes caused by broad-spectrum antibiotics and systemic corticosteriods, or peroxide mouth rinse in some cases.
Asymptomatic hyperplasia of the filiform papillae, resulting in a thick matted surface that traps bacteria, fungi, cellular debris, and foreign material.
Histopathology: elongated filiform papillae, with clusters of microorganisms and fungi.
identify abx of mouth rinse, brushing with baking soda or tongue scraper can reduce.
Dentifrice-Associated Slough
Superficial white slough of the buccal mucosa, typically that easily wipes away. Associated with sanguinaria, resolves with discontinuation of the toothpaste/mouth rinse
Actinic Cheilitis
Accelerated tissue degeneration of the vermilion of the lips. potentially pre-malignant condition.
the vermilion of ht elips takes on an atrophic, pale gray, glossy appearance. Slightly firm, bilatral swelling is common.
Histopathology: epitheium is typically atrophic and may show epithelial dysplasia. Basophilic changes in the submucosa
Treatment: Lip protection is indicated, with the use of lip balm containing a sunscreen agent indicated. Biopsy if ulceration persists (wedge excisional biopsy)
Idiopathic Leukoplakia
A white patch or plaque that cannot be rubbed off and cannot be characterized clinically as any other disease (excludes lichen planus, candidiasis, leukoedema, WSN, and frictional keratosis). Biopsy is mandatory to establish definitive diagnosis.
Aproximately 5% are malignant at time of biopsy, and 5% of the remainder will become malignant.
THe floor of the mouth has few of these but a high percentage of dysplasia, carcinoma insitu, or invasive carcinoma.
Some have red zones (erythroleukoplakia) and are more frequently malignant.
DD: if lesion can be removed then it is a pseudomembrane, fungus colony, or debris. If bilateral then hereditary conditions, cheek chewing and lichen planus and lupus eruthematosis. Concomitant cutaneous lesions indicate the latter two. Frictional or tobacco associated should be considered. Hairly leukoplakia and geographic tongue.
Geographic Tongue
seen in 2% of US population, young non-smokers. Atrophic patches surrounded by elevated keratotic margins. It is more common with a fissured tongue possibly due to secondary fungal infection.
Most are asympatomatic but some report irritation or tenderness to spicy foods or alcohol.
Histopathology: Filliform papillae are atrophic, with hyperkeratosis and acanthosis at the margins.
DD: generally clinical appearance is diagnostic, but biopsy may be required for an equivocal case, such as candidiasis, leukoplakia, lichen planus, and lupus erythematosus
No treatment required, but keeping the oral cavity clean with baking soda mouth rinse can help. Topical steroids with an antifungal can help
Lichen Planus
Chronic mucocutaneous disease of unknown cause. 0.2-2% of population
Bilateral white lesions, occasionally with associated ulcers. Generally considered to be an immunologic process. Possibly preceded by dental materials, stress, drugs, infectious agents.
THe disease follows several steps: initiating factor/event, focal release of regulatory cytokines, upregulation of vascular adhesion molecules, recruitment of T cells, and cytotoxicity of basak keratninocytes mediated by T cells.
most common type is characterized by numerous interlacing white keratotic lines or striae that produce an annular or lacy pattern. The plaque form resembles leukoplakia clinically with a multifocal distribution, primarily on dorsum of tongue and buccal mucosa. Erythematous form has red patches with very fine white striae, where the central area of the lesion is ulcerated. A fibrinous plaque or pseudomembrane covers the ulcer.
Histopathology: hyperkratosis, basal layer vacuolization with apoptotic keratinocytes, and lymphophagocytic infiltrate at the epithelium-connective tissue interface. Sawtooth rete ridge pattern can be seen.
DD: lichenoid drug reaction, lupus erythematosus, white sponge nevus, hairy leukoplakia, cheek chewing, graft-versus-host disease, and candidiasis. Idiopathic leukoplakia or SSC could be considered. Erosive forms must be differentiated from cicatrical pemphigoid, pemphigus vulgaris, chronic LE, contact hypersensitivitym and chronic candidiasis.
Corticosteroids are the most useful treatment, topically appied, but do not cure.
There is a low risk of malignant transformation, usually with the erosive forms.
