D of keratotic white lesions

DIFFERENTIAL DIAGNOSIS
OF KERATOTIC WHITE
LESION

presented by :-

Y.PRIYANKA RAO

Saturday 11 June 2011 1

INTRODUCTION.

CLASSIFICATION.

DIFFERENTIAL DIAGNOSIS OF
KERATOTIC WHITE LESIONS.

CONCLUSION.

REFERENCES.


INTRODUCTION
DEFINITION:-

Any condition that increases the thickness of the epithelium causes it to
appear white by increasing the distance to the vascular bed.

CAUSES:-

it is due to the hyperkeratosis ; any excess keratin ,
becoming sodden with saliva appears white.

hyperplasia of epithelium.

marked intracellular edema.

much microvesicular formation in the prickle cell
layer.


CLASSIFICATION :-
A) keratotic white lesions :-

white sponge nevus.
leukoedema.
hereditary benign intraepithelial dyskeratosis.
dyskeratosis congenita.

linea alba(white line).
FOCAL (frictional) keratosis & cheek biting.
smokeless tobacco-induced keratosis.
nicotine stomatitis.

oral hairy leukoplakia.
mucous patches.
Candidiasis.

benign migratory glossitis & mucositis.

KERATOTIC WHITE LESIONS

HEREDITARY
WHITE LESION

WHITE SPONGE
NEVUS


white sponge nevus:-
(familial white folded gingivostomatitis)
ETIOLOGY:-
1) It is a developmental anomaly .

2) Inherited as an autosomal dominant trait , caused by
mutation in keratin genes.
CLINICAL FEATURES:-
1)Affected mucosa is white,soft & irregularly thickened
white folded appearance.

2)Usually bilateral.

3)No defined borders.

4)Edges fade imperceptibly into normal tissue.


WHITE SPONGE NEVUS


differential diagnosis:-
Leukoedema:- It is only opalescent & white sponge has
rough granular & lethargic appearance.

Leukoplakia:- It occurs over 40 years of age & not
disseminated throughout the oral cavity. white sponge
nevus occur soon after birth or atleast by puberty &
widely distributed over the oral mucous membrane.

Hereditary benign intraepithelial dyskeratosis:- Involves
buccal, labial mucosa,lateral tongue , floor of the
mouth,the gingiva & palate ,along with conjuctiva .
Occular lesions manifest during the first year of life.

Pachyonychia congentia:- Presence of nail anomalies as
well as skin lesions.


LEUKOEDEMA.


LEUKOEDEMA
ETIOLOGY:-
USE OF TOBACCO.
PH OF SALIVA.
ORAL BACTERIAL INFECTION.
SYPHILIS OR GALVANIC IRRITATION.
CLINICAL FEATURES :-
1) ASYMPTOMATIC

2) FREQUENTLY ON BUCCAL MUCOSA , LABIAL MUCOSA &
SOFT PALATE.

3) BILATERAL , DIFFUSE , TRANSLUCENT GRAYISH-WHITE
THICKENING.

4) IT DISAPPEARS OR FADES UPON STRETCHING THE
MUCOSA.


LEUKOEDEMA

Leukoedema with a faint white
diffuse ﬁlmy appearance
and mild wrinkling of the
mucosa.

DIFFERENTIAL DIAGNOSIS:-
1 )LEUKOPLAKIA:-
A) LEUKOEDEMA HAS FAINT MILKY APPEARANCE, FOLDED & WRINKLED
PATTERN AS COMPARED TO DEFINITE WHITENESS OF LEUKOPLAKIA.
B) CANNOT ELIMINATE BY STRETCHING.

2 )CHEEK BITING LESION:-
A) FOUND BILATERALLY ON POSTERIOR BUCCAL MUCOSA ALONG THE PLANE
OF OCCLUSION.
B) ASSOCIATED WITH TRAUMA.
C) ROUGHNESS OR SMALL TAGS OF TISSUE THAT THEY ACTUALLY TEAR FREE
FROM THE SURFACE.

3) WHITE SPONGE NEVUS:-
A) LEUKOEDEMA IS A FAINT , WHITE, DIFFUSE ,FILMY APPEARANCE AND MILD
WRINKLES OF MUCOSA.
B) FADES OFF ON STRETCHING OF THE MUCOSA.
C) WHERE AS WSN DOESNT FADES OFF ON STRETCHING .

4) DYSKERATOSIS HEREDITARY BENIGN
INTRAEPITHELIAL:-
A) SAME AS WSN .
B) IT HAS TYPICAL MICROSCOPIC FEATURE.


REACTIVE/INFLAMMATORY WHITE
LESION

FRICTIONAL (TRAUMATIC)
KERATOSIS & CHEEK BITING.


FRICTIONAL(traumatic)KERATOSIS &
CHEEK BITING:-

Definition:- defined as “ a white plaque with rough & frayed
surface that is clearly related to an identifiable source of
mechanical irritation that will usually resolve on elimination
of the irritant.”
ETIOLOGY:-
1)prolonged mild abrasion of the mucous membrane such as ;
a)irritant due to sharp cusp & edges of broken tooth.
b) cheek biting (or) maladjusted dentures.
CLINICAL FEATURES:-
SITES:- Most common sites are lip and buccal mucosa.

APPEARANCE:- At first appears;pale and translucent ,
later become dense and white.


CHEEK BITING


Sometimes mimic dysplastic leukoplakia.

Isolated white patch with identified local irritant.


LINEA ALBA.

LINEA ALBA:-
“A horizontal streak on the buccal mucosa at the
level of occlusal plane extending from the
commissure to the posterior teeth.”

ETIOLOGY:-
Associated with pressure ,frictional irritation , or sucking
trauma from the facial surfaces of the teeth.

CLINICAL FEATURES:-
Usually present bilaterally.

More prominent in individuals with reduced overjet of the
posterior teeth.

often scalloped and restricted to dentulous areas.


LINEA ALBA:-

A HORIZONTAL
STREAK AT
THE LEVEL
OCCLUSAL
PLANE.


smokeless tobacco-induced
keratosis.

smokeless tobacco-induced keratosis.
Habitually chewing tobacco leaves or dipping snuff results in the
development of a well-recognized white mucosal lesion in the area of
tobacco contact, called smokeless tobacco keratosis,snuff dipper’s
keratosis, or tobacco pouch keratosis

CLINICAL FEATURES:-
Development of root surface caries .

Increased amount of gingival recession with periodontal destruction in the
immediate area of contact.

The most common area of involvement is the anterior mandibular vestibule
followed by the posterior vestibule.

Surface of the mucosa appears gray or gray-white & is granular, wrinkled &
translucent.

stretched mucosa appears fissured or rippled & a “pouch” is usually
present.

The white pouch may become leathery or nodular in long term heavy users.

Snuff pouch with a white wrinkled
White leathery nodular tobacco pouch
mucosal surface.

Differential Diagnosis
• Leukoplakia (idiopathic)
• Mucosal burn (chemical/thermal)

Snuff pouch showing extensive
periodontal tissue
destruction and a thickened area
of leukoplakia.

NICOTINE STOMATITIS.

NICOTINE STOMATITIS
A speciﬁc white lesion that develops on the hard and
soft palate in heavy cigarette, pipe, and cigar
smokers.

CLINICAL FEATURES:-
The palatal mucosa becomes diffusely gray or white.

Numerous slightly elevated papules with punctate red
centers that represent inﬂamed & metaplastically altered
minor salivary gland ducts are noted.

Nicotine stomatitis with diffuse
white change in the
palatal mucosa, along with
elevated papules with red centers.


INFECTIOUS WHITE LESIONS.


ORAL HAIRY LEUKOPLAKIA


ORAL HAIRY LEUKOPLAKIA:-

Oral hairy leukoplakia is a corrugated white lesion that usually
occurs on the lateral or ventral surfaces of the tongue in patients
with severe immunodeﬁciency.

ETIOLOGY:-
1)The most common disease associated with oral hairy leukoplakia is
HIV infection.

2)Epstein-Barr virus (EBV) is implicated as the causative agent in oral
hairy leukoplakia.
CLINICAL FEATURES:-
1)Oral hairy leukoplakia most commonly involves the lateral border of
the tongue but may extend to the ventral or dorsal surfaces.

2)Usually corrugated and may have a shaggy or frayed appearance,
mimicking lesions caused by tongue chewing.

3)It may also present as a plaquelike lesion and is often bilateral.


Mandibular vestibular lesion

Typical white corrugated leukoplakia in the
maxillary vestibule, associated with
sanguinaria use.

Bilateral linear
leukoplakic lesions on
the dorsolateral tongue,
suggestive of oral hairy
leukoplakia.



1)It is important to differentiate this lesion from other clinically
similar entities such as
Hyperplastic candidiasis:- These patients develop similar lesions around the nails
and other skin sites or alternatively develop only isolated oral lesions.
lichen planus.
lupus erythematosus.
WSN .
idiopathic leukoplakia.

2)Since oral hairy leukoplakia is considered to be highly predictive
of the development of AIDS, differentiation from other lesions is
critical.


CANDIDIASIS:-
Classiﬁcation of Oral Candidiasis:-
Acute
Pseudomembranous
Atrophic (erythematous)
Antibiotic stomatitis
Chronic
Atrophic
Denture sore mouth
Angular cheilitis
Median rhomboid glossitis
Hypertrophic/hyperplastic
Candidal leukoplakia
Papillary hyperplasia of the palate (see denture sore mouth)
Median rhomboid glossitis (nodular)
Multifocal
Mucocutaneous
Syndrome associated
Familial +/– endocrine candidiasis syndrome
Myositis (thymoma associated)
Localized
Generalized (diffuse)
Immunocompromise (HIV) associated


ETIOLOGY:-
1)Candidiasis is the most common oral fungal infection
caused by candida albicans.
2) Associated with predisposing factors: most commonly,
immunosuppression, diabetes mellitus, antibiotic use, or
xerostomia (due to lack of protective effects of saliva).

CLINICAL FEATURES:-
1)The pseudomembranous and
hyperplastic type of candidiasis present as white lesions of pseudomembranous
the oral cavity. candidiasis.
2)Pseudomembranous candidiasis, also
known as thrush is characterized by adherent white
plaques resembling curdled milk.
3) Scraping the white lesion can remove the plaques.
4)The hyperplastic candidiasis or candidal leukoplakia
presents as non-scrapable white patch usually located on
the anterior buccal mucosa .
1)Hyperplastic candidiasis cannot be clinically
distinguished from leukoplakia.
2)The diagnosis is conﬁrmed by the presence of candidal
hyphae in the lesions and resolution of the lesion after hyperplastic candidiasis:-
antifungal therapy.

ORAL LICHEN PLANUS
“Oral lichen planus (OLP) is a common chronic immunologic inﬂammatory
mucocutaneous disorder that varies in appearance from keratotic (reticular or
plaquelike) to erythematous and ulcerative.”

Etiology:-
The etiology of lichen planus involves a cell-mediated immunologically induced
degeneration of the basal cell layer of the epithelium.

Clinical and microscopic changes that are consistent with OLP will often occur in
response to a variety of agents (eg, drugs, chemicals, metals, and foods).When these
manifestations take place, they arereferred to as “lichenoid” reactions.

Reticular lichen planus of the buccal
mucosa.

Clinical features:-
The fifth decade of life.

A female predominance.

The buccal mucosa is the most common site.

OLP is classified as :-
1) reticular (lacelike keratotic mucosal configurations),
2)atrophic (keratotic changes combined with mucosal erythema),
3) erosive (pseudomembrane-covered ulcerations combined with keratosis and erythema) .
4) bullous (vesiculobullous presentation combined with reticular or erosive

Reticular form consists of slightly elevated fine whitish lines (Wickham’s striae) that produce
either a lacelike pattern or a patern of fine radiating lines or annular lesions.

This is the most common and most readily recognized form of lichen planus patterns.

Whitish elevated lesions, or papules, usually measuring 0.5 to 1.0 mm in diameter, may be seen
on the well-keratinized areas of the oral mucosa


Bullous lichen planus is rare .

Atrophic lichen planus presents as inﬂamed areas of
the oral mucosacovered by thinned red-appearing
epithelium.

Erosive lesions probably develop as a complication of
the atrophic processwhen the thin epithelium is Erosive lichen planus of the tongue.
abraded or ulcerated.

Papular, plaquelike, atrophic, and erosive lesions are
very frequently accompanied by reticular lesions.

The keratotic white lines cannot be eliminated by
either stretching the mucosa or rubbing.

Atrophic, erosive, and bullous forms are generally
associated with pain.
Atrophic lichen planus of the gingiva.


Verruciform leukoplakia:-The surface is excessively keratinized by parakeratin,
orthokeratin, or a combination . On mucosal surfaces which are normally heavily
keratinized, this keratin hyperplasia may represent more than half of the entire epithelial
thickness and may show short, pointed surface projections .

Discoid and systemic lupus erythematosus :- May present with oral keratotic and
ulcerative lesions which are clinically identical to lichen planus .Have broader
dimension.Flaky & feathery appearance of lupus lesion.

Candidiasis:- Pseudomembrane can be rubbed off in case of candidiasis.

Pemphigus:- Characteristic white striation of lichen planus are usually evident.the
absence of immunoglobulin or complement reactivity, to rule out other autoimmune
disorders such as pemphigoid and lupus erythematosus.

Graft-vs-host disease:- The lymphocytic band in GVHD is usually more sparse and less
well-deﬁned than that of idiopathic lichen planus, and marked ﬁbrosis of subepithelial
stroma is common in long-standing cases. Subepithelial blistering is rare except during
acute stage disease, in which case skin involvement is quite likely and greatly aids in the
diagnosis.

LEUKOPLAKIA
Leukoplakia is a white oral precancerous lesion with a recognizable risk for malignant
transformation.
DEFINITION:- “A predominantly white lesion of oral mucosa that cannot be
characterized as any other deﬁnable lesion.”

ETIOLOGY
TOBACCO.
ALCOHOL.
SANGUINARIA.
ULTRAVIOLET RADIATION.
MICRO-ORGANISMS.
TRAUMA .

Hyperkeratosis of
the palate in a
heavy pipe
smoker
appears as an
area of
leukoplakia


CLINICAL FEATURES:-
occurs in adults older than 50 years of age.

Leukoplakia lesions are found on the buccal
mucosa, vermilion border of the lower lip,
and gingiva & tongue.
SUBTYPES:-
Mild lesions appear slightly elevated gray -
white plaques.

Thicker lesions (homogenous) extend
laterally & becomes leathery & ﬁssures
deepen & appear distinctly white.

Granular or nodular leukoplakia-increase
surface irregularities.

Verrucous or verruciform leukoplakia- sharp/ Buccal leukoplakia and an adjacent
blunt projections. verrucous carcinoma.

Proliferative verrucous leukoplakia-
characteristically ,development of multiple
keratotic plaques with roughened surface
projections.


Thick white plaque on the lateral
border of tongue represents
verrucous leukoplakia. The
small ulcerated lesion anterior
to the white bumpy lesion is a
squamous cell carcinoma

Proliferative verrucous
leukoplakia of the ﬂoor of the
mouth and of the lip. In this form
of leukoplakia, the risk for
malignant transformation is very
high.


LICHEN PLANUS :- OFTEN OCCURRENCE OF MULTIPLE LESIONS &
PRESENCE OF WICKHAM’S STRIAE.

SYPHILITIC MUCUS PATCHES:- FEATURES LIKE SPLIT PAPULE OR
CONDYLOMA LATUM MAY BE PRESENT.

WHITE SPONGE NEVUS:- OCCURS SOON AFTER BIRTH OR ATLEAST
PUBERTY.WIDELY DISTRIBUTED OVER THE ORAL MUCOUS
MEMBRANE.

DISCOID LUPUS ERYTHEMATOUS:- CENTRAL ATROPHIC AREA WITH
SMALL WHITE DOT AND SLIGHTLY ELEVATED BORDER ZONE OR
RADIATIING WHITE STRIAE.

HAIRY LEUKOPLAKIA:- CORRUGATED LEUKOPLAKIC LESION
OCCURS LATERALLY AND VENTRAL SURFACE OF TONGUE .

CHEEK BITING:- CAREFUL HISTORY ELICITS THE CAUSE AND
PROMOTES PROPER DIAGNOSIS.

NICOTINE STOMATITIS:- WHITE PALATAL
ALTERATIONS,HYPERPLASTIC RESPONSE TO THE HEAT GENERATED
BY TOBACCO SMOKING.

CONCLUSION:-
1) White lesions of the oral cavity can range from genetic
disorders like white spongy nevus to potentially malignant
disorders like leukoplakia.

2) Differentiating these lesions histologically are extremely
important as the treatment and prognosis
is highly variable.


REFERENCES:-

1) WOOD & GAOZ.

2) SHAFERS.

3) NEVILLE.

4) CAWSON.

5) INTERNET PICTURES.


THANK YOU


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