Lecture 6 - White Lesions Flashcards Preview

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5 Reasons a lesion may appear white

1. Plaque covering mucosa 2. Hyperkeratosis (thick keratin layer) 3. Hyperplasia (thick spinous layer) 4. Fluid accumulation in epithelium 5. Epithelium alteration


Three main groups of white lesions

Developmental Inflammatory Cancer / dysplasia


Developmental White Lesions

Leukoedema White spongy nevus Dyskeratosis congenita


Inflammatory White Lesions

Frictional Infectious Autoimmune Tobacco-related


Cancerous or Dysplastic White Lesions

Dysplastic leukoplakia Verrucous leukoplakia Proliferative leukoplakia Squamous Cell Carcinoma



Opalescent, milky, white film that disappears when mucosa is stretched Usually asymptomatic BIlateral on buccal mucosa No tx needed More prevalent in blacks More severe in smokers


Leukoedema Histologic Findings

Intracellular edema of spinous layer Acanthosis Parakeratosis Broad/elongated rete ridges


White Spongy Nevus

Genetic skin disorder High penetrance, autosomal dominant Defect in normal keratinization of the epithelium Develops in childhood or adolescence Benign - no tx needed


White Spongy Nevus Histologic Findings

Hyperparakeratosis Acanthosis Basketweave appearance Clearing of cytoplasm in spinous layer **Peri-nuclear eosinophilic condensation in superficial epithelium


Hereditary benign intraepithelial dyskeratosis (Witkop - Von Sallmann syndrome)

Genetic, very rare, autosomal dominant Predominantly in tri-racial area of N. Carolina (Native American, white, black) Lesions develop in childhood No tx for oral plaques, refer to opthamologist


White Spongy Nevus Appearance

Bilateral, symmetric lesions Thick, spongy texture Buccal mucosa, lip, alveolar ridge, soft palate, or floor of mouth


Hereditary benign intraepithelial dyskeratosis (Witkop - Von Sallmann syndrome) Clinical Findings

Affects ORAL MUCOSA and CONJUNCTIVA of eyes Oral lesions: -Thick, corrugated, white plaques (similar to white spongy nevus) -Floor of mouth and lateral tongue Occular lesions: -Opaque, gelatinous plaques -Tearing, photophobia -Worse in spring -Can lead to blindness


Hereditary benign intraepithelial dyskeratosis (Witkop - Von Sallmann syndrome) Histologic Findings

Hyperparakeratosis Acanthosis "Cell-within-a-cell" - dyskeratotic process


Dyskeratosis Congenita Pathology

Mutation disrupts normal maintenance of telomerase (determines cellular longevity) Lesions may undergo malignant transformation (SCC) 70% of pts develop aplastic anemia


Dyskeratosis Congenita Clinical Findings

Triad: -reticular skin hyperpigmentation -nail dystrophy -tongue/buccal mucosal bullae (-> pre-malignant/malignant leukoplakia) Can also see rapidly progressive perio disease or cognitive delays


Dyskeratosis Congenita Histologic Findings

Oral lesions have hyperorthokeratosis with epithelia atrophy, which can progress into dysplasia and SCC


Dyskeratosis Congenita Treatment

FATAL DISEASE Severely affect patients live ~32yrs Careful oral examinations for malignant transformation Careful monitoring for aplastic anemia (may need BM transplant)


Pachyonychia Congenita Types

Jadassohn-Lewandowsky Type Jackson-Lawler Type


Pachyonychia Congenita Jackson-Lawler Type

Nails dramatically affected No oral lesions Why do we need to know this? Seriously Mutated keratin 17 gene


Pachyonychia Congenita

Rare autosomal dominant Less than 200 cases ever VERY VERY RARE you will never see this Why are we learning this? No tx, nails fall off


Pachyonychia Congenita Jadassohn-Lewandowsky Type

Probably named after the only two people to have this Mutated keratin 16 gene Hyperkeratinaceous nails - pinched, tube-shaped, nail falls off Hyperkeratosis - callous-like palmar/plantar surfaces Hyperhidrosis (increased sweating) Painful blisters on soles of feet Oral lesions - thick, white plaques on tongue lateral margins and dorsal surface