LEUKOPLAKIA

drg. Zaiviani Juniani K, Mkes

Definition
Leukoplaki is a clinical term as a chronic
mucosal white plaques ,
It is a precanceroyus lesion.

Defined as a white patch or plaque of the

oral mucosa that cannot be deatached

and cannot be identified as a lesion
belonging to a specific disease entity
The term leukoplakia describes a greyish

white patch or plaque found in the

mucous membrane of the oral cavity
(buccal mucosa, alveolar mucosa, and
lower lip. .
most often in middle-aged and older men
Etiology Predisposing
1. precise etiology of factor :
leokoplaki is still obscure.
2. Tobacco chewing or
smoking Smoking
3. Alcohol
4. Local irritations Alcohol
5. Vitamin deficiency : Vit A human
and Vit B
6. Endocrine disturbances papillomavirus
7. Candidiasis (HPV)
8. Syphilis Candida Albican
Chronic Trauma.
Other Precancerous Lesions
It is a benign, morphologically altered tissue
that has a greater than normal risk of
malignant transformation.
Leukoplakia
Erythroplakia
Erythroleukoplakia
Leukoplakia: A Premalignant or
Precancerous Lesion
Although leukoplakia is not associated with
a specific histopathologic diagnosis, it is
considered to be a premalignant lesion for
the risk of malignant transformation is
greater in a leukoplakic lesion than that
associated with normal or unaltered
mucosa.
Classification
There are three main clinical forms of oral
leukoplakia :
1. Homogeneous
2. Speckled
3. Proliferative Verrucous
 Leukoplakia: Histopathologic
Leukoplakia is characterized by a thickened
keratin layer (hyperkeratosis) with or without a
thickened spinous layer (acanthosis).
Some leukoplakias show surface hyperkeratosis
but with atrophy or thinning of the underlying
epithelium.
Variable numbers of chronic inflammatory cells
are typically noted within the underlying
connective tissue.
While most leukoplakias show no dysplasia on
biopsy, evidence of epithelial dysplasia (or
squamous cell carcinoma).
 Enlarged nuclei and cells.
Large and prominent nucleoli.
Increased nuclear-cytoplasmic ratio.
Hyperchromatic (dark-staining) nuclei.
Pleomorphic (abnormally shaped) nuclei & cells.
Dyskeratosis (premature keratinization)
mitotic activity and abnormal mitotic figures
Bulbous or teardrop-shaped rete ridges.
Loss of polarity (lack of progressive maturation

toward the surface).

Keratin or epithelial pearls.
Loss of typical epithelial cell cohesiveness.
Clinical Features
Clinical features
More common in men than women
Prevalence increases in males.

Common above 40 years of age

Common Site

1. Buccal mucosa and Alveolar mucosa

2. Tongue

3. vermilion of the lower lip.

4. Hard and soft palate

5. Floor of the mouth

6. Gingiva
that show dysplasia or carcinoma
Early/mild lesions

- usually appear as slightly elevated gray or

gray-
white plaques appear translucent,
fissured or
wrinkled and are typically soft and flat.
- usually well demarcated

If the cause (s) of the lesion are not

removedgradually become thicker and larger.
 Ultraviolet radiation vermilion of the lower
lip.
associated with actinic cheilosis.
Treponema pallidum dorsal surface of the

tongue syphilis.
Candida albicans hyperplastic/dysplastic

epithelium termed candidal leukoplakia and

candidal hyperplasia. group are lesions
termed nicotine stomatitis and frictional
keratosis.
The keratoses are readily reversible after the

elimination of the trauma or chronic irritation

Disorders of the Lips
Actinic cheilitis
Premalignant condition due
to chronic UVR exposure
Affects lower lip, initially
edematous &
erythematous, later
atrophic, white, scaly
plaque, may obliterate
vermillion border
Ulceration or induration -
biopsy to rule out
malignant transformation
histopathologic changes are presented
in the following diagram
Speckled
Red background with multiple small
white macules
Calbicans infection is often present High
risk of malignant transformation (20 30%)
Homogeneous

White, asymptomatic, Homogeneous plaque

Surface is usually smooth or wrinkled and
occasionally may be traversed by fissures
or cracks
Low risk for malignant transformation (2 ~4
%)
Most common (92- 96%)
 Proliferative Verrucous
Leukoplakia (PVL)
PVL is a special high risk form of leukoplakia.
White exophytic papillary surface
It is characterized by multiple keratotic plaques

with rough surface projections although initially

beginning as a simple flat hyperkeratosis.
to spread slowly, yet progressively.

transforms into a squamous cell carcinoma

within about 8 years.

female predilection (1:4 male to female) and

minimal association with tobacco usage.

Diagnosis
Biopsy and histopathologic examination
is the key to define the nature and the
relative risk of leukoplakia. Molecular
biological and immunohistochemical
techniques (p53 antigen. HPV 16 , 18,
33) are important for the detection of
leukoplakia in cases with high risk for
malignant transformation
Differential Diagnosis
Lichen Planus
Discoid lupus erythematosus
Candidiasis
Hairy leukoplakia
Cinnamon contact stomatitis
Uremic stomatitis
Leukodema
Chronic biting
Chemical burn
Several Genetic discases with oral keratinization
Disorders of Tongue
Orai hairy leukoplakia-
caused by Epstein-Barr
virus, presents as
asymptomatic,
corrugated, white plaques
with accentuation of
vertical folds along the
lateral borders of tongue
Predominantly seen in
HIV infection, organ
transplant recipients and
patients on
chemotherapy
Disorders of Tongue
Hairy tongue (white or black
hairy tongue) - hypertrophy of
filiform papillae resembling hair-
like projections
Associated with - heavy tobacco
use, mouth breathing, antibiotic
therapy, poor oral hygiene,
general debilitation, radiation
therapy, chronic use of bismuth
containing antacids, lack of dietary
roughage
White, yellow green, brown, or
black color is due to chromogenic
bacteria or staining from
exogenous sources
Cinnamon contact stomatitis
Uremik Stomatitis
 Erythroplakia
These are red patches found in the oral cavity
Erythroplakia not very common than Leukoplakia

There is no sex difference

Occurs in 6th and 7th decades of life

Etiology:
1. Smoking: Pipe smokers

2. Trauma

3. Dental irritation

Common Site:
. Buccal muosa,soft palate,Floor of the

mouth,Retromolar area,Tongue,Mandibular
mucosa and sulcus
Oral submucous fibrosis
This is due to fibroelastic change of oral
mucosa with epithelial atrophy leading
to stiffness of oral mucosa and causing
trismus and inability to eat.
Etiology :
Panparag , Chewing bettel nut
Vitamin B deficiency
Protein deficiency
 Types
1.Homogenous form:
Which appears as a bright red,soft,velvety lesions and

quite extensive in size

Site: Commonly found in buccal mucosa and soft palate

2. :Speckled erythroplakia
These are soft,red lesions,slightly elevated with an

irregular outline
Surface being granularThese are often referred to as

speckled leukoplakia/erythroplakia
Common Site: Anywhere in the oral cavity
3.Erythroplakia interspersed with patches of
Leukoplakia:
In this erythematous patches are not as bright as the

homogenous form
Common Site: Tongue and floor of the mouth
Oral submucous fibrosis
This is due to fibroelastic change of oral
mucosa with epithelial atrophy leading to
stiffness of oral mucosa and causing
trismus and inability to eat.
Etiology :
Panparag , Chewing bettel nut
Vitamin B deficiency
Protein deficiency
Oral submucous fibrosis
This is due to fibroelastic change of oral
mucosa with epithelial atrophy leading to
stiffness of oral mucosa and causing trismus
and inability to eat.
Etiology :
Panparag , Chewing bettel nut
Vitamin B deficiency
Protein deficiency
Management

Proper history
Prevention of the cause
Surgical excision of the small lesion
In females: supplementation of Oestrogen
Topical chemotherapy and radiation
 Clinical features:
Most common between 20-40 years of age,but can occur
in any decades of life
The disease is characterized by burning sensation of

mouth particularly when eating spicy foods.

This is accompanied by the formation of the

vesicles,ulceration or recurrent stomatitis with

excessive salivation or xerostomia
Ultimately the patient develops stiffning of certain area of

the oral mucosa with difficult in opening the mouth and

swallowing.
The fibroelastic band eventually appear on mucosa

usually involving the buccal mucosa,soft palate,lips and

tongue
Treated with Local Hydrocortisone injection and

Systemic corticosteroids
 Investigations for all premalignant
lesions:Biopsy
Treatment:Radiation therapy
Treatment : Basic
Guidelines
Improvement in oral hygiene
Elimination or discountinueation of all
presdisposing factors. Specially smoking.
Before any treatment a biopsy and
histopathologic examination is always
necessary to detect the presence or absence of
epithelial dysplasia
Molecular biologic marker profile should be
done
The size and the site of the lesions are
important in the formulation of a treatment
plan
Suggested Therapies
Surgical therapies excision is the mainstay
of the treatment of leukoplakia. Complete
removal is suggested for a homogeneous
leukoplakia with epithelial dysplasia or
without dysplasia
Carbon dioxide (CO2) Laser surgery

may be used as an alternative procedure

Cryosurgery and electrodessication are

therapeutic modalities have limited results .

 Homogeneous leukoplakia without epithelial
dysplasia may disappear or diminish in size
within 2-3 months after the patients stop
smoking, particulary if the lesions is located
on the floor of the mouth
Topical application of retinoic acid (solution

or in orabase cram or in mucoadhesive slow

release two layer tablets. Has been used the
treatment of selective cases of leukoplakia with
very limited access
Leukoplakia: Treatment and
Prognosis
first step biopsy and histologic
examination of the tissue.
Treatment depends upon moderate
epithelial dysplasia/ worse warrants
complete removal if possible.
If less severe changes is guided by
conservative eliminating tobacco use.
 dysplasia often is not excised
evaluation every 6 months is
recommended.
Biopsies if smoking continues or if

clinical changes increase in severity.

Biopsies