This document discusses different types of white lesions of the oral cavity. It covers hereditary lesions like oral epithelial naevus, leukoedema, pachyonychia congenita, and dyskeratosis congenita. It also discusses traumatic lesions caused by mechanical, chemical, or thermal injury. Infective lesions covered include candidiasis and hairy leukoplakia. Dermatological conditions discussed are lichen planus and lupus erythematosus. Neoplastic lesions of carcinoma-in-situ and squamous cell carcinoma are also mentioned. Idiopathic leukoplakia is categorized separately. Each lesion is described clinically and histologically.
13. Oral Epithelial Naevus (White Sponge Naevus):
AD
Mutation in genes of keratin 4 or 13.
Clinically:
Asymptomatic
Whitish, soft
Irregularly thickened
Usually bilateral (all OM)
The gingival margin and
dorsum of the tongue are
almost never affected
20. Pachyonychia Congenita:
AD
Extreme thickening of nails (≈ birth)
Palmoplantar hyperkeratosis & hyperhidrosis
White patches on D or LBT or BM
Hist: ≈ WSN
21.
22. Dyskeratosis Congenita:
? Mode of inheritance
Pigmentation of skin
Dystrophic nails
Destructive periodontitis
Hyperkeratosis of oral & other MMS
Premalignant
23. Tylosis:
AD
Palmoplantar hyperkeratosis
Esophageal Ca in later life
± Oral hyperkeratosis
24. Hereditary Benign Intraepithelial Dyskeratosis:
AD (North Carolina)
Conjunctival plaques → blindness
Oral white folds and plaques
Hist:
Acanthosis &
premature keratinization
25. Follicular Keratosis (Darier’s disease):
AD & sporadic
Face, trunk, ears & scalp: ↑ k papules (coalesce & infected)
Orally: Small whitish papules on K mucosa
Hist:
Hyperk
Suprabasal clefts
Dyskeratotic cells
The presentation intraorally is almost always bilateral and symmetric and usually appears early in life, typically before puberty.
The conjunctival mucosa is usually spared, but mucosa of the esophagus, anus, vulva, and vagina maybe affected.
Deep indentations or groves may be seen to extend from the surface almost to the basal layer, but the lower portions of the epithelium are otherwise not involved.
In cytological smears occasional cells will have condensed eosinophilic cytoplasm immediately surrounding the nucleus. characteristic perinuclear condensation of keratin
Should the affected individual stop using tobacco products, the lesion will likely become less pronounced.
Intracellular edema is not pathognomonic for white sponge nevus. Leukoedema is another developmental phenomenon with childhood onset and abundant superficial epithelial cells with edema. It typically lacks the parakeratosis and vertical groves of white sponge nevus, but there are times when the only viable means of distinguishing between the two is to stretch the affected mucosa; leukoedema tends to diminish or disappear when this is done, while no change is seen in white sponge nevus or other look-alike lesions.
In general, frictional keratosis has no known sex predilection, except for cheek biting and lip biting, which are twice as prevalent in women compared with men.
The use of exfoliative cytology for the collection of cells is not usually appropriate because the frictional keratosis lesion, by definition, shows increased keratin on the surface, which makes the harvesting of the intermediate layer and basal cells much more difficult.
A oral brush biopsy may be used; however, because the thick surface layer of keratin is a barrier, moderate pressure must be applied in order to ensure that an adequate sampling of basal cells is obtained