بسم الله الرحمن الرحيم

Def.

Premalignant lesions may expose to a promoting

factor & may be induced to undergo malignant

transformation.

Carcinoma in situ displays the cytologic features of

malignancy without invasion of the basement

membrane

Premalignant lesions include:

1. Leukoplakia

2. Candidal leukoplakia

3.Erythroplakia

4.Oral Submucous filrosis.

Leukoplakia

Definition

It is a clinical term, and the lesion is

defined as a white patch or plaque, firmly

attached to the oral mucosa, that cannot be

classified as any other disease entity. It is a

precancerous lesion

Etiology

The exact etiology remains unknown.

predisposing factors

1.Tobacco

2.Alcohol

3.chronic local friction

4. Candida albicans

5. Human papilloma virus (HPV)

6.biting the cheek

7. rough, uneven teeth

8. dentures (especially if improperly fitted)

Clinical classification

1.Homogeneous (common)

2.Nodular leukoplakia

3. speckled (less common)

4. Proliferative verrucous (rare).

Clinical Features

Site: mainly on

buccal mucosa

Features: uniformly

white plaques

Prognosis: Low

malignant

transformation

potential

Features:

1.Small aggregated

hemispherical red or white

surface alterations

2. red background or

substrate

Prognosis

Stronger risk of dysplasia or

malignant potential than in

homogeneous leukoplakia

Def.

Regarded as a combination of

or a transition between

leukoplakia and erythroplakia.

It is less common

Clinical Features Site: buccal mucosa, tongue,

floor of the mouth, gingiva

S&S:

1.white flecks

2. fine nodules on an atrophic

erythematous base

Prognosis:

Stronger malignant potential

than homogeneous leukoplakia

Def.

Diffuse white and /or

papillary (“warty”) areas of

the oral mucosa resulting

from varying degrees of

epithelial hyperplasia;has

the potential to develop

into verrucous carcinoma

or well-differentiated .It is

the least common type

squamous cell carcinoma.

Prognosis:

High risk of intervening dysplasia and

carcinoma developing

High rate of recurrence and histological

progression toward carcinoma

epithelial dysplasia

Epithelial

atrophy

Cellular atypia Epithelial

dysplasia

Carcinoma in situ

Reduction in the

normal thickness of

epithelium that

involves less than the

entire thickness of

the epithelium

Atypia is

individual cellular

changes in

dysplastic

epithelium which

reflect

abnormalities in

proliferation,

maturation, and

differentiation of

epithelial cells.

A premalignant change

in epithelium

characterized by a

combination of cellular

and architectural

alterations

The most severe stage of

epithelial dysplasia,

involving the entire

thickness of the

epithelium, with the

epithelial basement

membrane remaining

intact.

1.The histological appearances reflect varying

degrees of keratosis

2.Changes in epithelial thickness

3.Epithelial dysplasia

4. Diffuse chronic inflammatory cell infiltration of

varying severity in the lamina propria.

1. Nuclear and cellular pleomorphism (Nuclei and cells show different size and shape).

2. Increase in the nuclear/cytoplasmic ratio by either area or volume.

3. Nuclear hyperchromatism (Deeply stained Nucleus).

4. Prominent nucleoli.

5. Increased and abnormal mitoses. Mitoses may be increased in number, occur higher up in epithelium than is usual (i.e. away from the basal layer

6. Distributed polarity of the basal cells or loss of cellular orientation (The cells in the basal layer have no definable long axis and the nuclei have no regular polarity. 7. Basal cell hyperplasia. The presence of several layers of cells of basaloid appearance.

8. Drop-shaped rete pegs(The rete pegs are wider at their deeper part than they are more

superficially).

9.Irregular epithelial stratification or distributed maturation. The cells no longer show a proper sequence of morphological and maturational changes as they pass from the basal layer to the surface.

10.Abnormal keratinization. Keratinization occurring below the normal keratin layer, either as individual cell keratinization with in the stratum spinosum or as disturbed maturation of groups of cells resulting in the formation of intraepithelial keratin pearls.

11-Loss or reduction of intercellular adhesion (or cohesion). This may be difficult to distinguish from intercellular oedema.

:Types

1.Mild epithelial dysplasia

2. Moderate epithelial dysplasia

3.Severe epithelial dysplasia

Alterations limited principally to the basal and parabasal

layers.

Demonstrates involvement from the basal

layer to the midportion of the spinous layer.

Demonstrates alterations from the basal layer

to above midpoint of the epithelium.

Def.

Carcinoma in situ is defined as

dysplastic epithelial cells that

extend from the basal layer to the

surface of the mucosa " top to

bottom" change.

Histopathology

1.There may or may not be a thin

layer of parakeratin on the

surface.

2. The epithelium may be

hyperplastic or atrophic.

3. the entire thickness of the

epithelium is involved

4. No invasion has occurred

despite the fact that a typical

epithelial- cell look exactly like

those of squamous cell carcinoma.

5. Keratin pearl formation is rare

in carcinoma in situ and may

indicate the presence of a focus of

invasive squamous cell carcinoma

1.Leukoplakia is generally diagnosed with an oral exam.

2. During a physical exam, your dentist can confirm if the patches

are leukoplakia.

3. Other tests may be needed to confirm the cause.

4. Biopsy ( A small tissue sample is sent to a pathologist for

diagnosis. The goal is to rule out the possibility of oral cancer).

D.D

Oral thrush is a yeast infection of the mouth. The patches it

causes are usually softer than leukoplakia patches. They may

bleed more easily.

With treatment, you may be able to prevent future patches

from developing.

Erythroplakia

Erythroplakia

Def.

Red - patch that cannot be clinically or pathologically

diagnosed as any other condition

Etiology

1.Unknown

2.epithelial dysplasia

3.Carcinoma in situ

Clinical features Age: older men (65 -74) years old

Site: floor of mouth, tongue, and soft palate

S&S: 1. asymptomatic

2. well demarcated erythematous

macule

3. plaque with a soft velvety

texture.

4. associated with an adjacent

leukoplakia ( erythroplakia).

Histopathology 1.several epithelial dysplasia

2. carcinoma in situ

3.superficially invasive squamous cell carcinoma.

4.The epithelium shows a lack of keratin production and often

is atrophic, but it may be hyperplastic.

5.This lack of keratinization, especially when combined

epithelial thinness allows the underlying microvasculature to

show through, thereby explaining the red color.

6.The underlying connective tissue often demonstrate chronic

inflammation

Differential

Diagnosis 1.Non specific mucsitis

2. Candidiasis

3. Vascular lesions

These lesions may clinically mimic Erythroplakia

Biopsy is often required to distinguish between

them

Oral submucous fibrosis

Oral submucous

fibrosis

Def.

It is a chronic progressive, diffuse firm whitish areas of

submucosal scarring usually caused by frequent and

prolonged contact with betel nut quids,tobacco,or hot chili

peppers; lesions have high-risk precancerous condition of

the oral mucosa seen primarily on the Indian and in South

East Asia.

Etiology

1. tobacco

2. betel nut quids

3. hot chili peppers

Clinical features Site: buccal mucosa retromalar area, and the soft palate

Age: young adult

S&S:1. inability to open the mouth ( trismus )

2, mucosal pain associated with spicy food.

3. The jaws may actually be inseparable in the advanced

cases.

4. Vesicles, petachiae, melanosis, xerostomia

5. Generalized oral burning sensation are usually the first

signs and symptoms .

6. The mucosa in these regions develops a blotchy marble-

like pallor and a progressive stiffness of subepithelial tissues.

7. When the tongue is involved, it becomes rather immobile

frequently diminished in size and often avoid of papillae.

Histopathology 1.submucosal deposition of extremely dense

& a vascular collagenous connective tissue

2. variable numbers of chronic inflammatory

cells.

3. Epithelial changes include hyperkeratosis

with marked epithelial atrophy.

4. Epithelial dysplasia without carcinoma is found.

Chronic hyperplastic candidosis

(candidal leukoplakia)

Chronic hyperplastic

candidosis

(candidal

leukoplakia)

A clinical form of C. albicans infection consisting of white plaques or papules

against an erythematous background containing hyphae in the parakeratin layer

of the thickened epithelium.

Etiology

1.Tobacco

2. Smoking

3. Denture wearing

4. Occlusal friction

Clinical features Site: Lesions are seen most frequently on the buccal mucosa to the

commissure of the lips

S&S: 1. Dense, opaque white patches of irregular thickness and

density with a rough or nodular surface

2. They cannot be removed by scraping,but fragments may

be detached & identification of hyphae in smears of

such material assists in the diagnosis.

3. Speckled leukoplakia (areas fo erythematous mucosa are

present within the plaque)

4. Roughly triangular

5. Often bilateral white plaques tapering posteriorly

Histopathology .1.Parakeratinized epithelium

2. Markedly hyperplastic and acanthotic

epithelium

3. Many of cells in tparakeratinizedd surface of epitheliums separated by

oedema

4.Micro-abscesses from numerous neutrophil leucocytes

5. Candidal hyphae invade the parakeratin more or less at right angles to the

surface, but never penetrate deeper into the prickle cell layers

6.Acute and chronic inflammatory cells innprickle cell layer

7. Mixed chronic inflammatory cell infiltrate lamina propria)

8. Areas of atrophic epithelium may be present within the lesion and in these

areas the superficial layers of candida infected parakeratinnmay be

missing which may be responsible for the erythematous appearance seen

clinically

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