Leukoplakia1/cosmetic dentistry courses

INDIAN DENTAL ACADEMY
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INTRODUCTION :-
Cancer is a major cause of disease and death throughout the world.
Oropharyngeal cancer is the most common cancer worldwide in
men.
The death rate from oral cancer has increased more than fivefold
since the early 1960S, due mainly to a rapid increase of tobacco
and alcohol.
Tobacco and alcohol use as well as diet have been implicated in the
large increase in oral cancer mortality. Of these, tobacco and alcohol
are identified as major risk factors, but interaction and/or summation
of all factors may play a role.

Cancer is a disorder involving multiple alterations of the genome
progressively accumulated during a protracted period, the overall
effects of which surpasses the inherent reparative ability of the cell.
In the course of its progression, visible physical changes are taking
place at the cellular level (atypia) and at the resultant tissue level
(dysplasia).
 These alterations include genetic changes. epigenetic changes,
surface alterations, and alterations in intercellular interactions.
The sum total of these physical and morphological alterations are of
diagnostic and prognostic relevance and is designated as
'precancerous' changes

Virtually all oral squamous cell carcinomas arise from a premalignant
precursor .
 Oral pathologists use the term epithelial dysplasia to indicated
microscopic features in a biopsy specimen that are associated with a
risk of malignant change and then assign a grade of severity.
 There is good correlation between higher grades of dysplasia and
increasing risk of cancer but less so with the lower grades.

PRECANCEROUS LESION :-
A morphologically altered tissue in which cancer is more likely to
occur than in its apparently normal counterpart (WHO 1972).
Examples of precancerous lesions are leukoplakia and erythroplakia.
PRECANCEROUS CONDITION :-
A generalized state associated with a significantly increased risk of
cancer. Examples of precancerous conditions arc sidcropenic
dysphagia, sub mucous fibrosis and possibly, lichen planus.

It is now known that even clinically normal appearing mucosa in a
patient harboring precancerous lesion may have dysplasia on contra
lateral anatomic site or molecular aberration in other oral mucosal
sites suggestive of a pathway to malignant transformation.
So cancer could subsequently arise in apparently normal tissue.
[S. Warnakulasuria, Newell. W. Johnson, I . Van der wall ; Nomenclature and
classification of potentially malignant disorder of the oral mucosa. J oral pathol med
(2007) 36 : 575-580.]

A more recent WHO workshop recommended
abandoning the distinction between the terms
"potentially malignant lesions" and "potentially
malignant conditions" and to use the term "potentially
malignant disorders" instead.

Dysplasia :- It includes the following
Uncoordinated cellular proliferation .
Loss in the uniformity of the individual cells, as well as a loss in their
architectural orientation.
Pleomorphism (variation in size and shape)
Hyper chromatic nuclei.
 Nuclear: cytoplasmic ratio increases from 1:4 to 1:1, at the expense
of the cytoplasmic volume.
Increased mitosis.
Usual proliferative organization of the epithelium is lost and is
replaced by a disorderly arranged cells.

"Dysplasia is reversible, When the underlying inciting stimulus is
removed, the dysplastic alterations revert to normal".
The line of demarcation when the cell surpass the point of no return
is rather faint and the underlying mechanism poorly defined. In short,
dysplasia giving rise to neoplasia is akin to the cellular changes in
response to a noxious stimulus.
As it is evident, it transverses the stage of cellular adaptation,
reversible damage, and finally irreversible cell death

When a susceptive cell is exposed to a carcinogen it probably tries
to adapt to it, depending on the extent and duration of stimuli.
When the irritant persists, the epithelium shows features of cellular
atrophy, again a well characterized feature of adaptation (atrophy).
 At a later stage, when the stages of adaptation and reversible cell
damage surpass, the cells progressively slip into a stage of
irreversible cell damage: manifesting either as cell death or
neoplastic transformation.

Cytological and architectural features of oral epithelial
dysplasia :-
Cellular changes:
Abnormal variation in nuclear size and shape (anisonucleosis and
pleomorphism)
Abnormal variation in cell size and shape (anisocytosis and
pleomorphism)
Increased nuclear/cytoplasmic ratio
Enlarged nuclei and cells
Hyperchromatic nuclei
Increased mitotic figures
Abnormal mitotic figures (abnormal in shape or location)
Increased number and size of nucleoli

Architectural (Tissue) changes:
Loss of polarity
Disordered maturation from basal to squamous cells
Increased cellular density
Basal cell hyperplasia
Dyskeratosis (premature keratinization and keratin pearls deep in
epithelium)
Bulbous drop shaped rete pegs
Secondary extensions (nodules) on rete tips

Leukoplakia (Leukokeratosis)
Schwimmer coined the term "leukoplakia“
(Schwimmer, E. Die idiopathischen Schleimhautplauques der Mundhohle (Leukoplakia
buccalis). Arch Dermat Syph 9:611-570, 1877. )
The World Health Organization first defined oral leukoplakia as a
white patch or plaque that could not be characterized clinically or
pathologically as any other disease; therefore, lichen planus,
candidiasis, and white sponge nevus were excluded.
 At the 1983 international seminar, the current definition was
composed:
 Leukoplakia is a whitish patch or plaque that cannot be
characterized clinically or pathologically as any other disease, and is
associated the use of tobacco.

The term originates from two Greek words leuko – white and plakia -
patch
Leukoplakia denotes a diagnosis based on exclusion criteria.
 It represents an area localized in distribution, hyperkeratotic in
nature, and white in appearance due to wetting of the keratotic patch
while in contact with saliva.
 It should be stressed that the diagnosis of leukoplakia denotes
mainly, that (a) the mucosa is irritated by either mechanical,
chemical or galvanic means and (b) the mucosa is trying to adapt to
the noxious stimuli by undergoing hyperkeratinisation of its surface.
So it is irrational to consider it as a disease entity.

EPIDEMIOLOGY
The prevalence of this lesion in Ernakulum District,
Kerala, India was 17 per 1000; it was higher (61 per
1000) among people with mixed habits.
(R Rajendran, Oral leukoplakia (Leukokeratosis):
Compilation of facts and figures: Oral Maxillofacial Pathol :2004 ; Vol.8,58-68).
And
(Prakash C. Gupta, James E. Hammer; Control of Tobacco- Related Cancers and other
Diseases; Proceedings of an International Symposium, January 15-19, 1990, Tata Institute
of Fundamental Research, Bombay)

CAUSES :- Leukoplakia has a multifactorial etiology
 Chronic irritation((eg, chronic trauma from a sharp or broken tooth or from mastication
may cause keratosis)), smoking, tobacco, alcohol, and chewing betel Quid. Pipe
smokers have a risk of having Leukoplakia.
 Hairy leukoplakia is caused by the infection of Epstein Barr virus (EBV), Candida
albicans, human papilloma virus (type 16).
 People having HIV or AIDS are prone to hairy leukoplakia.
 Ultraviolet radiation.(actinic cheilitis / farmers lip).
 Chemicals (eg, sanguinaria)
 Immune defects: Leukoplakias appear to be more common in transplant patients
 Idiopathic

It was thought that the candida is merely growing in an altered
epithelium which has a strong susceptibility to transform into
carcinoma.
But now it has been proved that certain strains of Candida produce
carcinogenic nitrosamines.
AGE :-
Leukoplakia mostly affects elderly people within the age group of 50
to 70 years.

Nada ,Marija Bokor, Dejan Vuèko,I vana ; Presence of Candida albicans in potentially
malignant oral mucosal lesions : Arch Oncol 2004;12(1):51-4.

CLASSIFICATION :-
According to Clinical Appearance :-
 Homogenous : completely white lesion
• Flat : smooth surface.
• Corrugated : like beach.
• Pumice like.
• Wrinkled : cracked mud surface.
 Non homogenous :
• Nodular / speckled : characterized by white specks or nodules on
erytematous base.
• Verrucous : slow growing papillary proliferation.
• Ulcerated
• Erythroplakia.

 According to Etiology :-
 Tobacco induced
 Non tobacco induced
According to Extent :-
 Localized
 Diffuse
According to site :-
 High risk sites : (gingivo-buccal/ labial sulcus, Commisures, lateral or
ventral surface of tongue, floor of mouth, soft palate)
 Low risk sites :- (dorsum of tongue, hard palate)
 Intermediate : ( other sites of oral mucosa)

Clinical classification
(Teruo Amagasa, Saito K : Clinical classification of oral leukoplakia. Japan J Oral Surg
23 : 89-96, 1977)
Type I :- Flat white patch or plaque without red
component.
Type II :- Flat white patch or plaque with erosion or red
component.
Type III :- Slightly elevated or raised white patch or
plaque.
Type IV :- Marked elevated or raised white patch or
plaque.

Type I
Type II
Type III
Type IVwww.indiandentalacademy.com

A B C
HSTOPATOLOGICAL CLASSIFCATION OF ORAL LEUKOPLAKIA
4-11% malig. Potent. 20-35% malig. Potent.no malig. Potent.

Staging of Leukoplakia :-
 Three parameters are used:-
size (denoted by ‘L’)
• L1 - size less than 2 cm.
• L2 - 2-4 cm.
• L3 - more than 4 cm.
• Lx - size is not specified.
Clinical aspect denoted by (‘C’)
• C1 - homogenous.
• C2 - non homogenous
• Cx - not specified.

Pathological features (‘p’)
• P1 - no dysplasia.
• P2 - mild dysplasia.
• P3 - moderate dysplasia.
• P4 - severe dysplasia.
• Px - not specified.

CLINICAL FEATURES
Age/sex :- occurs commonly in older age group i.e. 35-45 yrs and
above. Males are affected more than females. 1% of males prior to
30 years of age have lesions and 8% of males older than 70 yrs of
age are affected. some studies have found it to occur about five
years earlier than cancer.
Prevalence in India is 0.2-4.9 %.
Common sites :- In descending order of frequency of involvement
• Commisures
• Buccal mucosa
• Lips
• Tongue
• Palate, alveolar ridge
• Floor of mouth
• Soft palate
• Gingiva

Appearance :- May vary from small well- localized, irregular
patches to diffuse lesion involving considerable portion of oral
mucosa.
Patch of leukoplakia may vary from non palpable, faintly translucent,
white area to thick fissured papillomatous indurated lesion.
Surface :- Smooth, finely wrinkled or rough on palpation.
ebbing tide type.
Colour :- White or yellowish white or brownish (tobacco stains)
Symptoms:- Feeling of increased thickness of oral mucosa. And
some may complaint of burning sensation.
Preleukoplakia :- Low grade or mild reaction of mucosa appearing as
grayish white lesion but not completely white with
indistinct borders blending with normal mucosa
and is preferably designated thin leukoplakia.
 (Prakash C. Gupta, James E. Hammer; Control of Tobacco- Related Cancers and other Diseases; Proceedings
of an International Symposium, January 15-19, 1990, Tata Institute of Fundamental Research, Bombay, Oral
health consequences of tobacco use : 100-101.)

This thin leukoplakia would be a Phase I leukoplakia (prevalance
2.4%).
Thin leukoplakia may disappear / continue unchanged, but as time
progresses as many as 2/3 of such plaques extend slowly laterally
and acquire a distinctly white appearance .
 They may become leathery to palpation and fissures may deepen,
but there should be only a few, if any, localized nodules or surface
projections if they are to be given the next most "severe" diagnosis:
Phase II leukoplakia (homogeneous or thick, smooth, perhaps
fissured leukoplakia).
 Most Phase II lesions remain indefinitely in this Phase but some,
perhaps as many as one-third, regress or disappear and a few
become even more severe.

They develop surface irregularities of a nodular or granular nature,
hence are referred to as granular or nodular leukoplakia .
Occasionally, pointed projections develop on the surface and may be
so numerous that the resulting lesions are called verrucous
leukoplakia.
Both types are Phase III lesions with similar prognoses.

Phase III leukoplakias may become dysplastic, even invasive, with
no change whatsoever in the clinical appearance.
Multiple circular or oval patches of nonblanching redness or
"erythroplakia" begin appearing in scattered areas which represent
sites in which epithelial cells are so immature that they are no longer
able to produce keratin.
 These intermixed red-and-white Phase IV lesions
(erythroleukoplakia, speckled leukoplakia, nonhomogeneous
leukoplakia), are the most worrisome form of the disease and carry
an extremely high risk of malignant transformation.

Oral hairy leukoplakia (OHL) was first observed in 1981 and reported
in 1984 as a common, benign, asymptomatic, white, non-removable
lesion of the lateral borders of the tongue and buccal mucosa in
patients with HIV infection and AIDS, (non-premalignant keratosis and is
not a true leukoplakia. It is, rather, a keratin hyperplasia presumably induced by the
Epstein-Barr virus and is perhaps better termed "oral HIV keratosis".)
 The lesion is rare in the healthy population. In patients with HIV
infection, when laboratory estimates are not available, OHL may be a
useful clinical marker of the presence, severity and progression of
HIV disease.
OHL has been observed in immunodeficient patients with other
causes of immunosuppression (chemotherapy, long term steroid
use, organ transplantation).

Thus, it is regarded as a clinical marker of impaired immune status,
in general, and its appearance should prompt the clinician to carry
out further investigations in order to establish the underlying cause of
immunosuppression. The lesion is not premalignant in nature
OHL has an intimate etiologic relationship with Epstein-Barr virus
(EBV) which replicates floridly within the lesion. Thus, in addition to
its clinical significance, OHL has a unique biologic importance
offering a unique in vivo research model for the study of the Epstein-
Barr virus.
The differential diagnosis should include idiopathic leukoplakia,
smoker's keratosis, frictional keratosis, hyperplasic candidiasis,
lichen planus

Hairy leukoplakia of the border of the tongue
Hairy leukoplakia, histological aspect,
showing hyperparakeratosis and pyknic
cell nuclei (koilocytosis) indicating
presence of virus (courtesy: prof JJ
Pindborg, Copenhagen)

Treatment
OHL is usually symptomless and has no known premalignant
potential,
topical retinoid, topical podophyllin, surgical excision and
cryotherapy, Antifungal therapy may lead to some reduction in the
extent of the lesion . but does not eradicate the infection.
Oral acyclovir 200 mg 4 times daily for Epstein Barr virus infection
shows regression
 but none prevent the recurrence of the lesion after therapy.

HOMOGENOUS LEUKOPLAKIA
Accounts for 84% of cases and also called as leukoplakia simplex
Localized, extensive with consistent pattern through out with white or
yellowish white in color (red component is absent)
Surface may be describe as corrugated, wrinkled or papillomatous
surface characterized by raised plaque formation consisting of single
or group of plaques varying in size with irregular edges .
Generally seen in pipe smokers and betel quid chewers, and 1 to7%
of cases undergo malignant transformation.

ULCERATED LEUKOPLAKIA
Accounts for 13 % of cases
Characterized by red areas which at times exhibit yellowish areas of
fibrin giving appearance of ulceration.
Generally associated with pigmentation of varying intensity on
periphery of lesion.(most of the times due to heat produced due to
smoking).
NODULAR LEUKOPLAKIA :- (leukoplakia erosiva /
speckled)
Mixed red and white lesion is seen with small keratotic nodules are
scattered
Nodules may be pinhead sized or even larger.
High malignant potential.(4-15%)

Granular leukoplakia Early or thin leukoplakia.
Proliferative Verrucous leukoplakia

Speckled leukoplakia. Homogenous type
Leukoplakia, Verrucous variant Commissural leukoplakia

Frictional leukoplakia Reticular Lichen Planus
Presumed to be Leukoplakia
Erosive Lichen Planus Presumed to be Erythroleukoplakia

Leukoplakia of ventral surface of tongue
Leukoplakia of floor of mouthwww.indiandentalacademy.com

VERRUCOUS LEUKOPLAKIA
Also called as leukoplakia verrucosa. Characterized by slow
growing verrucous proliferation above mucosal surface.
Buccal mucosa, alveolar mucosa, tongue floor of mouth and lips are
most common sites.
It is white lesion with multiple papillary projection that may be heavily
keratinized.
Initially it is slow growing, persistent and irreversible.
 In course of time erythematous component may develop and later
may become exophytic and wart like and transform the lesion that is
clinically and microscopically identical to verrucous carcinoma or sq.
cell carcinoma.(4-15% malignant potential)
Oral florid papillomatosis :- Extensive lesion of verrucous leukoplakia
.

MALIGNANT POTENTIAL
It is development of oral cancer from pre-existing leukoplakia.
Occurs in 0.3 to10% of cases.
When associated with habits shows higher rate of transformation as
compared to others.
In buccal mucosa and Commisures region 108% malignant
transformation occurs.
In lip and tongue 16% to 38% malignant transformation occurs.
Nodular leukoplakia has got higher rate of malignant transformation.
Idiopathic leukoplakia and Candida associated leukoplakia also
come under high group.

Features responsible for malignant transformation
Persistence of lesion for several years.
Female patient.
Lesions on floor of mouth and base of tongue.
Erosive lesions.
Combination of above factors.
[Carcinomas arising from leukoplakia
usually occur 2-4 years after the onset of the white plaque, but may
occur decades later. Transformation does not appear to be
dependent on the age of the affected patient.]
.

SQUAMOUS CELL CARCINOMA

Prognosis :-
Fair to poor.
Regression is higher when tobacco habit is discontinued.
Lesions of long duration have a greater risk of malignant
transformation than those of short duration.
The older a leukoplakia the worse is its prognosis.

DIFFERENTIAL DIAGNOSIS
Lichen planus
Chemical burn
White sponge nevus
Discoid lupus erythematous
Leukoedema
Hairy leukoplakia
Psoriasis
Cheek biting lesion
Electro galvanic white lesion
Alveolar ridge keratosis

Frictional ridge keratosis. Rough, white change
of the edentulous area of the alveolar ridge
represents a frictional hyperkeratosis because
this area receives irritation during mastication.
This should not be mistaken for true leukoplakia,
and biopsy is not indicated
Aspirin burn

Diagnostic procedures:-
1. Elimination of possible cause:-
The clinician should first try to rule out any of
the definable white lesions before accepting a definitive clinical
diagnosis of leukoplakia.
1. The biopsy :-
Taking biopsy in leukoplakia should be the standard
rule. If treatment consists of C02 - laser evaporation, it is
mandatory to have a biopsy taken prior to such treatment.
In non-homogeneous leukoplakia, biopsy should be
taken at the site of symptoms, if present, or at a site of redness or
induration.

Diagnostic methods other than histological
examination, such as the use of toluidine blue staining or Lugol's
iodine,autofluroscence, vizilite and exfoliative cytology are of value
when dealing with leukoplakia.
Computer-assisted, oral brush biopsy is a detection tool providing
evidence of cellular abnormalities in precancerous and cancerous
lesions.
Highly specialized, network-based, image-processing system
specifically designed to detect oral epithelial precancerous and
cancerous cells, the pathologist can detect as few as 1 or 2
abnormal individual cells in several hundred thousand cells.

MANAGEMENT :-
Elimination of etiologic factor –
As many as 30% of leukoplakia can regress if habits are stopped
Prohibition of smoking
Selective cuspal grinding and extraction of broken tooth
Replace faulty metal restoration and metal bridge
Elimination of other etiologic factor like alcohol, viral infection.
Leukoplakia not exhibiting dysplasia are not excised but follow up
after every 6 months is recommended.
Conservative treatment –
Antifungal :- for candidiasis (for 2weeks).
Vitamin A therapy -(protective effect on epi.)
4000 IU orally, parentally (daily req.)
Therapeutic dose 75000 – 300000 IU for 3 months

13-cis-retinoic acid (synthetic analogue of vitA) – 1.5-2 mg/kg BW for
3 months, of relapse occurs 0.5 mg/kg BW for 9 months given.
Anti-oxidants :- β-carotene an be beneficial.
SURGICAL:-
Conventional surgery :- excision with safe margins. It should be
deep and wide. Sliding mucosal flap is used to cover the defect.
Cryosurgery:- Cryosurgery involves local freezing of tissues for their
controlled destruction or removal. Various cryogens used are Nitrous
oxide (-75°C), Carbon-dioxide snow (-79°C) and liquid Nitrogen (-
196°C).
Cryoprobe applied for 1 min, followed by 5 min withdrawal and this is
repeated for 2-3 times until desired results are achieved.
Contraindication -patients on immunosuppressive drugs, allergic to
cold temperatures, cold intolerance.

Advantages:-
1. No anaesthesia is required.
2. No hospitalization is necessary.
3. Multiple lesions can be treated at the same time.
4. Good for small local cancer recurrences.
5. It is a no touch technique, hence beneficial while treating HIV
POSITIVE cases.
Complication :-
1. Hyper pigmentation
2. Hypertrophic scars
Fulguration (electrocautery and electrosurgery)
1. Destruction of tissues by high voltage of electric current
2. Coagulate lesion and easy control of hemorrhage.

Disadvantages :-
1. Hazards of explosion
2. Need of profound anesthesia
3. Slow healing, pain and scarring.
Most electrosurgical units work at frequencies
just below the AM radio frequency band.
The electrical resistance of human tissue helps
convert this electrical energy into molecular energy, which causes
denaturation of intracellular and extracellular proteins, resulting in
coagulation or desiccation effects.
Raising intracellular water above the boiling
point causes cell membrane rupture to produce a cutting effect.

Two forms of electrosurgery: (A) Electrodessication with an active electrode tip
touching the skin and showing penetration of planned tissue damage. (B)
Fulguration with sparking from electrode to tissue. Treatment area is more
superficial than A

Electro section :-
1. In electro section, the electrode is used to cut tissue.
2. An electrode tip in the shape of a fine needle, wire loop, diamond,
ellipse, or triangle
3. It is advanced slowly through the tissue, causing a steam envelope
to advance around the tip and producing a smooth cutting effect with
little sense of pressure against the tissue by the operator.
4. Electro section is a biterminal technique because it requires two
electrodes.
Complications :-
1. Burns
2. Shocks
3. Pacemaker problems
4. Transmission of infection

Lasers :- (light amplification by stimulated emission of radiation)
Co2 lasers are most commonly used as they have high affinity for
tissues wth water and minimum penetration depth(0.2-0.8mm)
Contains – CO2, nitrogen and helium gases.
Used in biopsy, removal of lesion.
Photodynamic therapy (PDT) :-
PDT uses laser, combined with a light-sensitive drug (sometimes
called a photosensitizing agent) to destroy cancer cells
Photosensitizing agent makes cells more sensitive to light. Once in
the body, the drug is attracted to cancer cells. It does not do
anything until it is exposed to a particular type of light.

When the light is directed at the area of the cancer, the drug is
activated and the cancer cells are destroyed. Some healthy, normal
cells in the body will also be affected by PDT, although these cells
will usually heal after the treatment.
[The aim of PDT for advanced cancer is
usually to reduce symptoms by shrinking the tumor. In this situation
PDT cannot cure a cancer]
To date, the U.S. Food and Drug Administration (FDA) has approved
the photosensitizing agent called porfimer sodium, or Photofrin,
Visudyne,and LS11.

Recurrence and/or malignanT transformation of oral leukoplakia
have occasionally been observed following laser surgery. It is
reported that the rate of recurrence was 7.7-38.1%, while malignant
transformation was 2.6-9%.
Laser excision is suitable for leukoplakia cases on non-keratinized
epithelia (i.e., the tongue and buccal mucosa)
It has been proved that laser surgery is an excellent procedure for
oral leukoplakia.
Long term follow up after removal is important as recurrence are
frequent (granular or Verruciform recur rate 83% )

Patient Education is of paramount importance.
A diet rich in fresh fruits and vegetables may help
prevent cancer.
There should be complete ban on advertisement and
promotion on tobacco and its products.
Special attention to public education.
Separation of smokers from non smokers by complete
ban on smoking in public places, hospitals, theatres, etc,.

CONCLUSION
Tobacco smoking/ smokelss tobacco and betel-quid
chewing are detrimental to oral health, as they are strongly
associated with oral leukoplakia, oral cancer, and other
mucosal pathologies.
Prevention is found to be feasible and
effective by timely diagnosis and management of oral
Precancerous lesions without immediate result but
definitely give dividend in long term.

REFERENCES :-
Teruo Amagasa, Masashi Yamashiro and Hitoshi Ishikawa:Oral
Leukoplakia Related to Malignant Transformation.
Oral Science International, Vol. 3, No. 2 ,45-55 (2006).
Teruo Amagasa, Saito K : Clinical classification of oral leukoplakia.
Japan J Oral Surg 23 : 89-96, 1977.
Silverman, S., Gorsky, M., Lozada, F. Oral leukoplakia and
malignant transformation. A follow-up study of 257 patients. Cancer
53:563-568, 1984.

 Greenspan, J.S., Greenspan, D. Oral hairy leukoplakia: diagnosis
and management. Oral Surg 67:396-403, 1989.
S. Warnakulasuria, Newell. W. Johnson, I . Van der wall ;
Nomenclature and classification of potentially malignant disorder of
the oral mucosa. J oral pathol med (2007) 36 : 575-580.
Mehta FS, Pindborg JJ, Gupta PC, Daftary DK(1969). Epidemiologic
and histologic study of oral cancer and leukoplakia among 50,915
villagers in India. Cancer 24:832-849
R Rajendran, Oral leukoplakia (Leukokeratosis): Compilation of facts
and figures: Oral Maxillofacial Pathol :2004 ; Vol.8,58-68

Junnosuke Ishii, Takahide Komori. Management of Oral Leukoplakia
by Laser Surgery: Relation between Recurrence and Malignant
Transformation and Clinic pathological Features: Journal of Clinical
Laser Medicine & Surgery. February 1, 2004, 22(1): 27-33.
Nada Vuckovi, marija Bokor-brati, Dejan Vuckovi, Ivana picuri :
Presence of Candida albicans in potentially malignant oral mucosal
lesions ; Arch Oncol 2004;12(1):51-4.
Brad W. Neville, Douglas D. Damm: Oral and Maxillofacial
Pathology, chapter 10; Epithelial Pathology, 2nd
edition; 337-340,
Saunders Publicatiion.

Prakash C. Gupta, James E. Hammer; Control of Tobacco- Related
Cancers and other Diseases; Proceedings of an International
Symposium, January 15-19, 1990, Tata Institute of Fundamental
Research, Bombay.
BARRY L. HAINER, RICHARD B. USATINE, Electrosurgery for the
Skin: journal of American Academy of Family Physician, oct 1 (2002)

Thank
you

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