Keratoses leukoplakias white lesions

leukoplakias are chronic white (kcratotic) mucosal plaques which are not due to any identifiable disease. The term is purely clinical and has no histological implications, but histology' is necessary to cxcludc malignancy or other diseases. Most leukoplakias arc not premalignant but red lesions (erythroplasias; pp. 95 96) are frequently precancerous or invasive carcinoma.

Terminology Oral white plaques share many histological features, and idiopathic forms are often not distinguishable histologically from those with defined causes such as frictional keratosis, but may show dysplasia microscopically. Features of oral white lesions include the following in varying combinations:

Microscopy • Hyper(ortho)keratosis—a superficial eosinophilic layer of dead epithelial squamcs under which there is a layer of epithelial cells containing basophilic granules of prekeratin (Fig. 155).

• Parakeratosis—the surface consists of effete epithelial cells containing shrunken, pyknotic, basophilic nuclei with no underlying granular cell layer (Figs 156 & 157).

• Acanthosis—hyperplasia of the prickle cell layer usually wiih loss of the normally regular profile of the rete ridges (Fig. 156).

• Epithelial atrophy—thinning usually with loss of the rete ridges of the epithelium (Fig. 158).

• Dysplasia (sec pp. 93-94) may be associated with keratosis but there is no consistent relationship.

White Sponge Nevus

Fig. 157 Parakeratosis: detail. fig. 158 Hyperorthoteratosis and epithelial atrophy.

Fig. 157 Parakeratosis: detail. fig. 158 Hyperorthoteratosis and epithelial atrophy.

White sponge naevus

Aetiology and Hereditary (autosomal dominant) disorder producing pathology soft, white thickening of the oral mucosa. The condition is asymptomatic (may not be noticed until adulthood), but tags of protruding epithelium may be chewed off or detached, producing an irregular surface. The whole of the oral mucosa may be affected to variable degree.

Microscopy Typically regular acanthosis with widespread intracellular oedema extending particularly in the plaque where prominent cell membranes give a 'basket-weave' appearance (Figs 159 & 160). The surface is typically irregular. Inflammatory infiltrate is absent from the corium (Fig. 161).

The diagnosis should be confirmed by biopsy, especially if the family history is uninformative. Reassurance can then be given.

Frictional Keratosis
fig. 159 White sponge naevus

fig. 160 White spooge naevus: oedematous epithelial cells.

Frictional Keratosis
fig. 161 White sponge naevus: partial detachment of plaque.

Frictional keratosis

This shows non-spccific keratosis microscopically (Fig. 162) and is distinguishable only by clinical evidence of mechanical trauma and resolution with removal of the irritant.

Smoker's keratosis

This results from heavy long-term pipe smoking, is therefore seen mainly in men, and affects the palate.

Pathology The keratosis is non-specific but there is characteristically inflammation and swelling of the palatal mucous glands producing red umbilicatcd swellings (Fig. 163).

Syphilitic leukoplakia

A feature of the tertiary stage of syphilis but rarely seen now. It typically affects the dorsum of the tongue and there is a high risk of malignant changc.

Microscopy Features of epithelial keratosis arc not specific but dysplasia or malignant changc may be evident (Fig. 164).

A characteristic syphilitic inflammatory response (endarteritis (Fig. 165), plasma ccll infiltrate and occasionally granuloma formation) may be seen deeply, but diagnosis is essentially serological.

Tertiary Syphilis

Rg. 162 Frictional keratosis.

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Rg. 162 Frictional keratosis.

Rg. 163 Smoker's keratosis: swollen palatal salivary tissue.

Smokers KeratosisFrictional Keratosis Tongue

Rg. 164 Syphiitic leukoplakia with mild dysplasia.

fig. 165 Endarteritis beneath syphilitic leiAoplakia.

Acute candidosis (thrush; 'pseudomembranous' candidosis)

Aetiology Thrush is the typical acute infection of mucous membranes by Candida albicans. It implies underlying immunodeficiency, e.g. neonates; HIV infection; prolonged broad spectrum antimicrobial, immunosuppressive and cytotoxic treatment or debilitating illness.

Clinically, thrush forms soft friable, creamy flecks or plaques that wipe off easily revealing intact but erythematous epithelium. A Gram-stained smear shows many Gram-positive hyphae of C. albicans and inflammatory cells (Fig. 166).

Microscopy The plaque of thrush is due to epithelial hyperplasia—it is not a pseudomembrane (adherent slough). The epithelial cells of the plaque are separated by inflammatory exudate (hence it is friable) including many neutrophils.

The inflammatory infiltrate is most dense, forming microabscesses, at the surface of the prickle cell layer and provides the plane of cleavage that allows the plaque to be wiped off. PAS staining will demonstrate hyphae of C. albicans growing downwards through the epithelial cells to the surface of the spinous cell layer (Fig. 168). Deeply, there is acanthosis with long, slender downgrowths of epithelium, and an inflammatory infiltrate in the lamina propria (Fig. 167).

Treatment Thrush frequently responds well to topical antifungals such as nystatin or amphotericin but in severe immunodeficiency (e.g. HIV infection) fluconazole may be needed.

Hyphae Gram Stain
Fig. 166 Thrush: tangled hyphae in smear. Fig. 167 Thrush: plaque. (PAS.) (Gram stain.)
Oral Thrush Aids Patients
Rg. 168 Thrush: hyphae in plaque. (High power; PAS.)

Chronic candidosis (candidal leukoplakia)

Uncommon, persistent candidal infection usually of middle-age or over but may occasionally be seen in patients with HIV infection, who may develop any type of oral candidosis. Clinically, chronic candidal plaques may be homogeneous or speckled in charactcr.

Microscopy Production of parakeratotic plaque. Hyphac grow through plaque to the spinous layer (Figs 169 & 170). Plaque is infiltrated by moderate numbers of leukocytes and beads of oedema. The deeper epithelium is acanthotic, sometimes grossly so (Fig. 171), and sometimes dysplastic.

Chronic mucocutaneous candidosis syndromes

All are rare but comprise leukoplakia-like oral candidosis associated with variable skin and nail involvement, and sometimes systemic disorders. There is a limited defect of cellular immunity in about 60% of patients but no special susceptibility to systemic candidosis. One variant is associated with endocrine deficiencies, particularly primary hypoparathyroidism and Addison's disease (Candida endocrinopathy syndrome).

Microscopy As for isolated chronic candidosis (see l'igs 169-171).

Denture-induced erythematous candidosis

Most common under an upper denture where hyphae of C. albicans proliferate in the interface between denture base and mucosa, which is cut off from local defenses. Diffuse candidal erythema is also seen in xerostomia.

In HIV infection C. albicans can cause red mucosal macules (erythematous candidosis).

Microscopy Hyphac arc superficial to the epithelium and not seen in sections. The epithelium is spongiotic, acanthotic and infiltrated by chronic inflammatory cells.

Hairy leukoplakia

See pages 143-144.

Oral Hairy Leukoplakia

Fig. 169 Chronic candidosis: hyphae invading parakeratotic plaque. (PAS.)

Red And White Leukoplakia

Fig. 171 Chronic candidosis: plaque and gross acanthosis.

Fig. 169 Chronic candidosis: hyphae invading parakeratotic plaque. (PAS.)

fig. 170 Chronic candidosis: hyphae and inflammatory infiltrate in plaque.

Fig. 171 Chronic candidosis: plaque and gross acanthosis.

Dysplasia (epithelial atypia; dyskeratosis)

Dysplasia is abnormal maturation and differentiation of the epithelium, as seen in carcinomas and also in leukoplakias, when it is usually an indication of premalignancy. The following features arc seen in varying combinations:

Microscopy • Hyperchromatism and alteration of the nuclcar cytoplasmic ratio. The nuclei arc abnormally large in relation to the area of cytoplasm and arc more heavily basophilic. Nucleoli may be more prominent or numerous. Nuclcar plcomorphism (irregularly shaped nuclei) is often associated (Fig. 172).

• Individual, deep ccll kcratinization (dyskeratosis). Individual cells within the prickle ccll layer develop intracytoplasmic keratin and become eosinophilic (Fig. 173).

• I^>ss of polarity. The basal ccll layer loses its normal orderly arrangement and the cclls lie irregularly at angles to one another (Figs 173 & 174).

• Mitoses. These may be seen superficially among the spinous cells and are of sinister import, particularly if abnormal.

• Other features. Loss of intercellular adhcrcncc with fluid-filled spaces appearing between the epithelial cells (Fig. 174) and drop-shaped (bulbous) rctc ridges are sometimes associated with dysplasia. Hyperkeratosis and/or acanthosis may or may not be associated.

Severe dysplasia with cellular abnormalities extending through the full thickness of the epithelium (lop-to-bottom change) is sometimes termed carcinoma-in-situ (Fig. 175), i.e. the cellular abnormalities of carcinoma arc present but there is no invasion.

Dysplasia Loss Polarity

Fig. 173 Dysplasia with deep cell keratinization: hyperchromatism and loss of polarity.

fig. 172 Mild to moderate dysplasia with hyperchromatism and hyperkeratosis.

Fig. 173 Dysplasia with deep cell keratinization: hyperchromatism and loss of polarity.

Dysplasia Hyperchromatism

Fig. 175 Severe dysplasia Itop-to-bottom change, carcinoma-in-situ).

fig. 174 Dysplasia: loss of intercellular adherence.

Fig. 175 Severe dysplasia Itop-to-bottom change, carcinoma-in-situ).

Erythroplasia ('erythroplakia')

This is a clinical term for chronic red lesions (i.e. hyperkeratosis is absent). They do not form raised plaques but are typically level with, or depressed below, the surrounding mucosa and typically show severe dysplasia (Fig. 176) or early carcinoma.

Early carcinoma

In addition to dysplastic leukoplakias, some early carcinomas, before ulccrating, produce keratin on the surface and appear as innocent white lesions.

There is invasive squamous cell carcinoma replacing the normal epithelial surfacc and an overlying parakcraiinizcd plaque (Fig. 177).

Squamous cell papilloma

A common, benign lesion characterized by fine, finger-likc papillae, giving it a characteristic warn' appearancc clinically. HPV (particularly types 6 and 11) may be implicated, but cytological signs of viral infection are not evident histologically. Oral viral warts resemble papillomas clinically, but show viral changes and inclusion bodies.

A central branching core of vascular connective tissue extends into the papillae. The latter arc covered by hyperplastic stratified squamous epithelium which maybe keratinized (Fig. 178). The papilloma then appears white.

Excision is curative.




Syphilis The Tongue Microscopy
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