Lecture 6 - White Lesions Flashcards
5 Reasons a lesion may appear white
- 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
Leukoedema
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
