JIDAM
CASE REVIEW
eISSN 2582 - 0559
“An Official Journal of IDA - Madras Branch”©2019.
Available online
FINDING LEUKOPLAKIA: THE DENTIST’S
WINDOW OF OPPORTUNITY
Dr. K. Raghavendhar Karthik, Dr. Poornima Karthik
Radiant smile care,
General Dental Practitioner, Chennai, Tamilnadu, India
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ABSTRACT
Website: jidam.idamadras.com
India has the dubious distinction in accounting for
almost half of all oral cancer cases in the world .
Ironically, out of all cancers, Oral Squamous cell
carcinoma (OSCC) is one of the most preventable
cancers that occur in people where the patient
simply has to make a definite life style choice (to
use or not to use tobacco) to reduce the risk of its
occurrence. General Dentist can play an important
role in prevention and in early recognition of signs
Address for Correspondence:
and prompt referral of patients. This review will focus
particularly on early identification of Leukoplakia in
Dr. K. Raghavendhar Karthik
dental practice and is an update about the influence of
90, Perumal Koil Street, Saidapet West,
internal and external environmental factors associated
Chennai
with pre cancer stage, recognizing the clinical
e-mail id: radiantsmilecare@gmail.com
spectrum of Leukoplakia for identifying individuals
at greater risk and provide suggestions for instituting
a realistic plan for clinical follow up and performing
opportunistic screening.
KEY WORDS: Oral Potentially malignant disorders,
Leukoplakia, Pre-Cancer screening, opportunistic
screening.
Received
: 24.08.2019
Accepted
: 17.09.2019
Published
: 27.09.2019
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JIDAM/Volume:6/Issue:3/Pages 95 - 101/July-September 2019
Karthik et al : Finding Leukoplakia: the Dentist’s Window of Opportunity
INTRODUCTION:
•
Influence of internal and external environmental
factors associated with pre cancer stage.
The current challenge with regards to Oral
•
Recognizing the clinical spectrum of Leukoplakia
Squamous cell carcinoma (OSCC) in India is not
and to identify individuals at greater risk.
only its increasing incidence or the dismal long term
survival after treatment, but the fact that people
•
Instituting a realistic plan for clinical follow up
continue to put themselves at risk through smoking,
and perform Opportunistic screening.
chewing tobacco and drinking alcohol. And all of
INTERNAL & EXTERNAL FACTORS FOR
this continues to happen despite the public being
OPMD’S:
educated in various platforms, health care workers
creating awareness in rallies and campaigns and the
Cancer is a genetic disease where the genetic
government placing regulations and ban of sale of
mutations may be spontaneous or acquired. Acquired
chewable tobacco products in few states in India.
mutations are associated with etiological factors that
India is the third largest tobacco producer and
cause DNA damage. These factors are traditionally
second largest consumer of tobacco worldwide.1 The
classified as initiators
(inaugurating the genetic
epidemiological burden and demographic disaster
event) and promoters
(propels the genetic event
caused by OSCC in India is well known to dentists
forward) 7.
and even other health care providers. The five year
survival for oral Squamous cell carcinoma from
Tobacco (Smoking and Smokeless):
the time of diagnosis has not improved remarkably,
primarily because majority of patients are diagnosed
Tobacco use is the single most
at higher clinical stages of the disease that jeopardizes
important preventable risk factor for cancer8.
the outcome and survival 2.
Smoking tobacco includes products like bidi,
manufactured cigarette, hand-rolled cigarette,
This situation suggests that both the dentists
pipe, cigar, hukkah, water-pipe, chutta, dhumti and
and/or patients are failing to recognize early mucosal
chillum. Studies consistently show a dose response
changes that indicate oral cancer development and are
relationship with increased incidence of OSCC
evading timely clinical evaluation of such changes 3.
related to frequency and duration of smoking.
Interestingly, with regards to OSCC, in 90% of cases,
Smokeless tobacco is available courtesy products
there is always a preceding stage or precursor stage
like betel quid with tobacco, khaini, gutka and these
of disease that exists for a variable and extended
are consumed by chewing. Other smokeless tobacco
period of time before transforming in to OSCC 4.
products, such as mishri, gul, bajjar and gudakhu, are
Practically not all cases of pre-malignancy transform
applied to teeth and gums while snuff is inhaled. In
to malignancy. Usage of the prefix “Pre” implies
India, prevalence of the use of smokeless tobacco is
that there is a definitive consequence of the disorder
much higher (21.4%) than that of tobacco smoking
to transform in to malignancy. So, Oral Potentially
(10.7%)
1.
Malignant Disorders (OPMD) is an umbrella term
used to predict risk of cancer in the lesion/condition
Most smokeless tobacco products consumed
at the time of diagnosis or in the future. And
in Indian sub continent are unregulated such as Paan
this is depicted as a percentage 5. Given the ready
(mixture of betel leaf, lime, tobacco, catechu, areca
anatomic access of oral cavity to visual and tactile
nut); Zarda
(powdered tobacco and slaked lime
examination, detecting OPMD’s before they become
that is rubbed on gums) seems to account for the
early carcinoma should not be very difficult for the
predominance of buccal and gingival carcinoma in
General Dentist 6.
India 9.
OBJECTIVES:
Smokeless tobacco exhibits different risk for
different brands and preparations. This is attributable
This review will focus particularly on early
to presence/absence of additives, flavoring agents,
identification of Leukoplakia in dental practice and
modifiers, etc that enhance the carcinogenic
is an update about the following aspects of OPMD’s
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Karthik et al : Finding Leukoplakia: the Dentist’s Window of Opportunity
potential3.
OSCC in patients below 40 years with no tobacco/
alcohol use has been increasing in recent years
Even non tobacco containing chewable
and may be attributed to genetic susceptibility.
products like Pan masala containing areca is
Individuals with underlying defects in key genes/
considered a risk as, recently, Areca has been
molecules that maintain homeostasis are predisposed
upgraded to a Group
1 carcinogen. There is
to develop OSCC when exposed to initiating and
sufficient evidence in humans for the carcinogenicity
promoting agents. Inherently deficient functions
of betel quid without added tobacco as it can cause
in DNA repair; Cell cycle regulation; Apoptosis;
cancers of the oral cavity 10.
Immune surveillance may predispose to OSCC 16.
Any history of tobacco or areca use, past/
Also, mitochondrial DNA appears to be a
present must be viewed as a potential risk for OPMD
source of maternal genetic susceptibility for Tongue
and OSCC8.
OSCC 17.
Alcohol:
Chronic Mechanical Irritation:
Alcohol is a well recognized promoter
The usual example of sharp tooth as a risk
of carcinogenesis in OSCC. Ethanol potentiates
factor appears to have come back to prominence as
the effect of tobacco. The effect is addictive and
a factor that predisposes to OSCC due to persistent
multiplicative in heavy drinkers. Dehydration effect
chronic inflammation18.
of alcohol renders mucosa vulnerable to carcinogens
in tobacco11.
OPMD- CLINICAL SPECTRUM:
Ethanol is oxidized to acetaldehyde.
Clinically visible pre cancerous mucosal
Acetaldehyde associated with the consumption
changes are frequently observed at sites of future
of alcoholic beverages is carcinogenic to humans
tumor presentation. Similar appearing lesions are
(Group 1 carcinogen) 12.
found surrounding the periphery of actual tumor for a
few millimeters. So, clinically visible pre cancerous
Human Papilloma Virus (HPV):
lesions demonstrate a risk for cancer development.
These recognized mucosal lesions are usually
HPV is a epitheliotropic DNA virus with two
described as Leukoplakia, Erythroplakia, or erythro-
varieties: High risk (HPV type 16 and 18) and Low
leukoplakia. Whether any of the above mentioned
risk. High risk HPV is associated with oro-pharyngeal
lesions harbor potential for progression to OSCC is
and base of tongue OSCC especially in non-smokers
indicated only by histopathology which is the gold
and nondrinkers and young individuals13.
standard for diagnosis 4.
Few population studies are suggesting that
Leukoplakia
possible change in sexual practices, multiple oral sex
partners may predispose to HPV associated OSCC 13,
The old dictum, all Leukoplakic lesions are
14.
white, but all white lesions are NOT Leukoplakia
is a useful guide in recognizing Leukoplakia.
WHO (2017) Head and Neck Tumor book
Leukoplakia is white non-scrapable mucosal patch
has reclassified OSCC based on HPV etiology
or plaque that cannot be attributed clinically to any
adding HPV associated OSCC and Oro pharyngeal
other diagnosable condition”.
squamous cell carcinoma15.
Lesion which is diagnostically ambiguous
Genetic Susceptibility:
strictly on clinical grounds can be designated as
Leukoplakia. If a dentist is able to recognize a
It is well known that only a fraction of
white lesion as specific definable white lesions,
smokers and drinkers develop OSCC. Incidence of
such as Linea Alba, Frictional keratosis, Morsicatio
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JIDAM/Volume:6/Issue:3/Pages 95 - 101/July-September 2019
Karthik et al : Finding Leukoplakia: the Dentist’s Window of Opportunity
buccorum, Leukoedema, Lichen planus, etc then
High Risk Group 19
the term Leukoplakia cannot be used.
•
All non-homogenous leukoplakias.
A white non scrapable lesion on cancer
•
Homogenous leukoplakia more than 2cm2 in size.
prone sites where there is no obvious or
identifiable source of friction is classic example
•
Homogeneous leukoplakia on the floor of the mouth,
of Leukoplakia. In patients with known history of
the soft palate or the tongue regardless of size.
exposure to carcinogen, a clinically indeterminate
•
Homogeneous leukoplakia regardless of size in a
white lesion irrespective of location may be
patient without any known risk factors (“idiopathic”
regarded as Leukoplakia5.
leukoplakia).
Thus the designation Leukoplakia is
•
Homogeneous leukoplakia involving multiple sites.
reserved for use as an exclusively provisional
•
Leukoplakia of any size in immuno-compromised
diagnosis than a definitive diagnosis.
patient.
Leukoplakia- Clinical types:
Low Risk Group 19 :
Leukoplakia is clinically classified as
Homogenous and Non- homogenous (Ulcerated,
Homogeneous leukoplakia less than 2cm2 in size
Nodular, Verrucous variants) that commonly occur
on the buccal mucosa, commisure and lips in a patient
in the site of buccal mucosa, alveolar mucosa, floor
with known risk factors.
of mouth, tongue, lips and palate 5.
Flow chart for the clinical diagnosis of leukoplakia 19
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JIDAM/Volume:6/Issue:3/Pages 95 - 101/July-September 2019
Karthik et al : Finding Leukoplakia: the Dentist’s Window of Opportunity
Flow chart for the management of leukoplakia 19
After
representative
biopsy
and
OPPORTUNISTIC SCREENING:
histopathological examination, the clinical diagnosis
of Leukoplakia MUST be replaced with a definitive
In OPMD, the epithelial tissue acquires
histopathological diagnosis. There can never be an
genotypic alteration long before it is visible
h/p diagnosis of Leukoplakia. The following h/p
clinically as a mucosal abnormality. So the mucosa
diagnosis is possible 3:
appears deceptively clinically normal. This is a great
limitation of standard oral examination. The biology
•
Benign hyperkeratosis (most common)
of this process itself likely attributes to the dentist’s
failure to identify suspicious lesions as early as
•
Epithelial dysplasia
possible3.
This need for earlier detection has fuelled the
•
Squamous cell carcinoma.
demand for Oppurtunistic screening. The dentist must
Recently it was recommended that a two
grab every opportunity to evaluate the oral cavity for
tiered binary system for classifying dysplasia can
OPMD’s when patient comes for any of the dental
be followed (LOW GRADE and HIGH GRADE) in
needs 21. It is cost effective, and does not require
the place of mild, moderate, severe dysplasia. Such a
special time, place, event planning or preparation of
classification is useful for the dentist to draw a more
the patient. It can be done in a regular dental practice
meaningful, patient centric, treatment plan as well as
setting solely by one provider itself, irrespective of
follow up plan 20.
the speciality. There is implied consent by the patient
and hence less apprehension in screening process 22.
Irrespective of grade of dysplasia, the
It is useful in all three levels of prevention.
h/p diagnosis should alert the dentist there is a
Primary Prevention: Oppurtunistic screening can
recognised risk and so clinical vigilance and follow
be done for every patient irrespective of presence
up is mandatory. Even a low grade dysplasia can
of habits. If relevant, the dentist must identify the
transform to malignancy over a period of time 3.
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JIDAM/Volume:6/Issue:3/Pages 95 - 101/July-September 2019
Karthik et al : Finding Leukoplakia: the Dentist’s Window of Opportunity
patient with habit of tobacco and alcohol usage. It
comparison. Cancer Epidemiol. 2018 Apr;53:27-
is essential to educate about life style modifications
34
and counsel on good hygiene and nutrition. For
3.
Natarajan E, Eisenberg E. Contemporary
those patients needing help in quitting the habits the
concepts in the diagnosis of oral cancer
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and precancer.Dent Clin North Am.
2011
Secondary Prevention: It is not always easy for
Jan;55(1):63-88.
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4.
Slaughter DP, Southwick HW, Smejkal W.
patients with habits, screening should be done at
Field cancerization in oral stratified squamous
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origin. cancer 1953 sep; 6(5):963-8
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Warnakulasuriya S, Johnson NW, van der Waal
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FINANCIAL SUPPORT AND
SPONSORSHIP:
uploads/2018/06/mono100E-10.pdf
Nil
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TR, Krutchkoff DJ, Eisenberg E, Kosis D,
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CONFLICTS OF INTEREST:
to oral epithelial dysplasia. Cancer Epidemiol
Biomarkers Prev. 1996 Oct;5(10):769-77.
There are no conflicts of interest.
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