الله الرحمن الرحيم مسب - Delta Univ
Transcript of الله الرحمن الرحيم مسب - Delta Univ
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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