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LEUKOPLAKIA

Guided by- Submitted by:

Dr. Priyanka Rastogi (HOD) Anisha Saikia


Dr. Sachin Kumar Roll No. 5
Dr. Rudra Bhardwaj BDS IIIrd year
CONTENTS
• Introduction
• Etiology
• Classification of Leukoplakia
• Homogenous Leukoplakia
• Non-homogenous Leukoplakia
• Clinical Features of Leukoplakia
• Common sites, Appearance, Surface, Colour
• Histopathological Features
• Treatment
• BIBLIOGRAPHY
INTRODUCTION
• Oral leukoplakia is defined by the WHO as “a whitish patch
or plaque which cannot be scrapped off, which is not
characterised clinically or pathologically as any other
disease & is not associated with any other physical/ chemical
agents other than the use of tobacco.”- (WHO 1996)
• Leukoplakia generally refers to a firmly attached white patch
on a mucous membrane which is associated with an increased
risk of cancer. The edges of the lesion are typically abrupt
and the lesion changes with time. Advanced forms may
develop red patches. There are generally no other symptoms.
This lesion generally occurs within the mouth.
ETIOLOGY
• LOCAL FACTORS-
1. TOBACCO
It refers to the dried leaves of nicotina tobaccum.
• It is widely used in two forms-

• Smokeless tobacco-
Chewable tobacco, snuff
• Smoking Tobacco-
Cigar, cigarette, bidi, pipe
• When tobacco is chewed , various chemical constituents leach out
such as nicotine, pyridine, picoline which leads to alkaline pH of
saliva.
• Their alkaline pH is 8.2-9.3 which act as local irritants and are
related to alterations of mucosa.
• This damage results in sub lethal cell injury within deeper layers
of oral epithelium. This induces oral hyperplasia.
• Smoking tobacco is harmful as this contains polycyclic
hydrocarbons and Beta-naphthalamine, nitrosamines, co, nicotine
which acts as source of irritation.
• Heat also plays a major role. Heat induces alteration in tissues
inducing reddening and stippling of mucosal surfaces.
2. ALCOHOL
It causes irritation and burning sensation of oral mucosa.
It facilitates the entry of carcinogens into exposed cells and this alters
the oral epithelium and its metabolism

3. CHRONIC IRRITATION
Continuous trauma or local irritation in the oral cavity is suspected as
a causative agent for leukoplakia.
Sources of irritation / trauma may be- malocclusion, ill fitting
dentures, sharp and broken tooth, hot spicy food.
REGIONAL/ SYSTEMIC FACTORS-

• - Syphilis- white patches are seen on tongue in secondary


syphilis.
• Spirochete- the causative agent for syphilis has predilection
for actively mobile tissuesof tongue.
• The shrinkage of lingual muusculature may also occur
resulting in a wrinkled surface and extremely susceptible to
oral irritation and leukoplakia may develop.
CLASSIFICATION OF LEUKOPLAKIA
• Leukoplakia is divided broadly into two main categories-

A. HOMOGENOUS LEUKOPLAKIA

B. NON-HOMOGENOUS LEUKOPLAKIA

i. Nodular or speckled Leukoplakia


ii. Verrucous Leukoplakia
iii. Erythroleukoplakia
iv. Proliferative Verrucous Leukoplakia
HOMOGENOUS LEUKOPLAKIA
Refers to usually well defined white patch localized/ extensive
that is slightly elevated and has a fissure wrinkled/ corrugated
surface. On palpation these lesion may feel leathery to dry
cracked mud like.
NON-HOMOGENOUS LEUKOPLAKIA
• I. NODULAR/ SPECKLED LEUKOPLAKIA
• It is granular/ non homogenous.
• It refers to a mixed red and white lesion in which keratotic
white
nodules/ patches are distributed over a atrophic erythematous
background.

Nodular
Leukoplakia
• II. VERRUCOUS LEUKOPLAKIA
• -It is the term used to describe the presence of thick,
white
• lesions with papillary surface in the oral cavity.
• - These lesions are heavily keratinised.
• - Some of these lesions exhibit an exophytic growth
pattern.

Verrucous
Leukoplakia
• III. PROLIFERATIVE/ VERRUCOUS
LEUKOPLAKIA
• It is an extensive papillary/ verrucoid white plaque
that tend to slowly involve multiple mucosal sites
in the oral cavity and which may transform into
squamous cell carcinoma over a period of many
years.

Proliferative
Verrucous
Leukoplakia
• IV. ERYTHROLEUKOPLAKIA
• Erythroleukoplakia is a non homogenous lesion of mixed white
• (keratotic) and red (atrophic) colour.
• Erythroplakia is an entirely red patch that cannot be attributed to
any other cause.
• Erythroleukoplakia can therefore be considered a variant of either
• leukoplakia or leukoplakia since its appearance is midway between.

Erythroleukoplakia
• IDIOPATHIC LEUKOPLAKIA

• No underlying cause has been found.


• Such lesions are termed as idiopathic (cryptogenic) leukoplakia.

Idiopathic
Leukoplakia
CLINICAL FEATURES OF LEUKOPLAKIA-
• Occurs more commonly in older age groups, i.e., 35-45 yrs above.
• Males are more affected than females.

• COMMON SITES-

• Buccal mucosa, commisures are more commonly involved.


• Lip lesions are more common in men (smoking).
• Tongue lesions are more common in women.
• Other sites involved are tongue, palate, alveolar ridge, floor of the
mouth, soft palate.
APPEARANCE-
• The extent of involvement may vary from small, well localised,
irregular patches to diffused lesions involving considerable portion
of oral mucosa.
• Patches of leukoplakia may vary from non palpable, faintly
translucent, white area to thick fissured papillomatous indurated
lesions.
SURFACE-
Lesion is often finely wrinkled in appearance & may feel rough on
palpation.
COLOUR-
White/ yellowish white
HISTOPATHOLOGICAL
FEATURES
• Keratinized pattern-
• There occur keratinization of mucosal epithelium that is normally non
keratinized.
• Microscopically leukoplakia is characterised by thickened keratin layer
of surface epithelium (hyperkeratosis) with/ without spinous layer
(acanthosis).
• The keratin layer may consist of parakeratin (hyperkeratosis),
orthokeratin(hyperorthokeratosis) or combination of both.
• Verrucous leukoplakia has papillary/ pointed surface projection varying
keratin, thickness, broad or blunted rete ridges.
• With time the condition progresses to a papillary exophytic proliferation
that is similar to localised lesions of verrucous leukoplakia.
• In later stages, this papillary proliferation exhibit down growth of well
differentiated squamous epithelium with broad blunt rete ridges.
• In final stages, the invading epithelium becomes less differentiated transforming
into full fledged squamous cell carcinoma.
• The histological alteration of dysplastic epithelial cell are similar to those of
squamous cell carcinoma & may include the following-
• Enlarged nucleus and cells
• Large & prominent nucleus
• Increased nuclearcytoplasmic ratio
• Increased mitotic activity
• Loss of polarity
• Bulbous & tear shaped rete ridges
• Keratin/ epithelial pearl
• Loss of typical epithelial cell cohesiveness
• Histomorphological alterations-
• Epithelial dysplasia-a.mild c.severe
• b.moderate d. carcinoma in situ
TREATMENT
• A biopsy is mandatory and will guide the course of treatment.
• Counsel the patient to terminate the cause.
• Definitive treatment involves surgical excision,although cryosurgery
and laser ablation.
• Total excision is aggresively recommended when microscopic
dysplasia is identified.
• Use of anti oxidant nutrients and vitamin have not been reproducibly
effective in management.
• Combination doses of vitamin A, C & beta kerotines, analogues of
vit. A & diets that are high in antioxidants & cell growth suppressor
proteins ( fruits & vegetables).
SUMMARY
• Leukoplakia is a mouth condition involving thickened white
patches on the mucous membranes of the mouth, gums or
tongue.
• It is most often caused by smoking or other types of tobacco
use.
• Leukoplakia is divided into homogenous and non homogenous
type which has further subtypes.
• If leukoplakia is mild it often goes away, but; it is a
precancerous condition, so it should not be taken lightly.
CONCLUSION
• Although it’s important not to panic about the impending risk
of oral cancer when you have leukoplakia, the risk factor
should be addressed as soon as possible such as quitting
smoking, chewing tobacco, drinking or exposure to other
irritants.
• Leukoplakia is often a warning sign that a person should make
healthy lifestyle adjustments.
• At it’s worst it is a serious condition that requires immediate
medical treatment.
BIBLIOGRAPHY
• Shafer’s Textbook of Oral Pathology

• Oral and Maxillofacial Pathology by Brad W.


Neville

• Burket’s Oral Medicine

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