drg.

Zaiviani Juniani K, Mkes

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
1.

2.
3.
4.

5.
6.
7.
8.

precise etiology of
leokoplaki is still
obscure.
Tobacco chewing or
smoking
Alcohol
Local irritations
Vitamin deficiency :
Vit A and Vit B
Endocrine
disturbances
Candidiasis
Syphilis

Predisposing factor :

Smoking
Alcohol
human papillomavirus
(HPV)

Candida Albican
Chronic Trauma.

It is a benign, morphologically altered tissue

that has a greater than normal risk of
malignant transformation.
Leukoplakia
Erythroplakia
Erythroleukoplakia

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.

There are three main clinical forms of oral

leukoplakia :
1. Homogeneous
2. Speckled
3. Proliferative Verrucous

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.

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 graywhite 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

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

Red background with multiple small white

macules
Calbicans infection is often present High
risk of malignant transformation (20 30%)

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%)

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.

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

Lichen Planus
Discoid lupus erythematosus
Candidiasis
Hairy leukoplakia
Cinnamon contact stomatitis
Uremic stomatitis
Leukodema
Chronic biting
Chemical burn
Several Genetic discases with oral keratinization

Orai hairy leukoplakiacaused 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

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

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

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

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

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

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

Proper history
Prevention of the cause
Surgical excision of the small lesion
In females: supplementation of Oestrogen
Topical chemotherapy and radiation

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

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

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

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