Risk factors and prevention strategies of oral cancer

RISK FACTORS AND
PREVENTION STRATEGIES
OF ORAL CANCER IN
INDIAN SCENARIO
By
Dr. Priyanka Sharma
III Year MDS
Department of Public Health Dentistry
1

CONTENT
• INTRODUCTION
• TERMINOLOGIES
• CLASSIFICATION OF ORAL CANCER
• CLINICAL PRESENTATION OF ORAL LESIONS
• RISK FACTORS - EPIDEMIOLOGICAL TRIAD
• DIAGNOSTIC TOOLS
• PREVENTION AND CONTROL OF ORAL CANCER
• CONCLUSION
• REFERENCES
2

INTRODUCTION
- A grim picture of oral cancer in India and global scenario
- Global and Indian trends of oral cancer
3

• Cancer has overtaken heart disease as the world's top killer in
2011. According to a study by World Health Organization (WHO),
part of a trend that more than double global cancer cases and
deaths will occur by 2030.
• Cancer diagnoses around the world have steadily been rising and
are expected to hit 12 million this year. Global cancer deaths are
expected to reach 7.9 million, according to the new report by
WHO.
• That means new cancer cases will likely mushroom to 27 million
annually by 2030, with deaths hitting 17 million.
"Incidence & Prevalence of Oral cancer“ May 2015. Oral Cancer Foundation
4

• Annually, over 3,00,000 new cases of oral cancer are
diagnosed all over the world where the majority are
diagnosed in the advanced stages III or IV.
• Such data make the oral cancer an important public health
matter which is responsible for 3% to 10% of cancer
mortality worldwide.
5

• According to AIIMS, over 25 percent of the total cancer
patients in India suffer from oral and throat cancers. The
average age group suffering from oral cancers in India has
dwindled from 55 years to 35 years.
• It is estimated that nearly 275 million people in India are
addicted to tobacco and the unhealthy habit is expected to
claim 1.5 million lives annually by the year 2020.
Oral Cancer Accounts for 25% of All Cancer Cases: AIIMS
IANS, Modified: July 25, 2015 14:55 IST
NDTV
ANOTHER REPORT
6

• Earlier, a report released by the Public Health Foundation of
India (PHFI) showed that India spent ₹1,04,500 crore for
managing tobacco-related diseases in 2011.
• Oral cancer claims a significant number of lives in India.
Every six hours at least one person loses battle with the
deadly disease.
Oral Cancer Deaths Up in India: Expert
IDA secretary general, International Bussiness times,
July 21, 2014 15:39 IST
7

GIST- THE INDIAN SCENARIO
• Oral cancer is the most common cancer in India; as 4 in 10 of all cancers are
oral cancers.
• Annually 130,000 people succumb to oral cancer in India which translates into
approximately 14 deaths per hour.
• The reason for high prevalence of oral cancer in India is primarily because
tobacco is consumed in the form of gutka, quid, snuff or misri. Rising tobacco
use in India, where 40 per cent of the world's smokers live has contributed to
this trend.
• In comparison, in US oral cancer represents approximately 13% of all cancers
thereby translating into 30,000 new cases every year.
8

• Recently, a trend has been observed towards increased incidence of oral
cancer among young adults. This increase in incidence is only observed in
patients with tongue cancer.
• In fact, in India, 60-80% of patients are present with advanced disease as
compared to 40% in developed countries. Early detection would not only
improve the cure rate, but it would also lower the cost and morbidity
associated with treatment.
• Increasing prevalence of oral submucous fibrosis, especially in younger
individuals, caused by gutka, an industrially manufactured food item has
been seen. The above facts state that, cancer cases in general, are
increasing in India and it is high time that planners, social activists and
government give adequate stress for prevention, early diagnosis, treatment
and rehabilitation of these populations.
9

THE GLOBAL SCENARIO
• There is a wide variation in the incidence and mortality rates of oral cancer in different
regions around the world.
• Highest rates are reported in South Asian countries such as India and Sri Lanka.
• The Indian sub-continent accounts for one-third of the world burden.
• The incidence and mortality from oral cancer is rising in several regions of Europe,
Taiwan, Japan and Australia.
• Every year in Europe, around 100,800 people are diagnosed with head and neck
cancer and almost 40,000 die from the disease.
• In the USA alone, 30,000 Americans are diagnosed with oral or pharyngeal cancer
each year. About 90 percent of head and neck cancers are of the squamous cell
variety.
10

• Oral or oropharyngeal cancer is the eleventh most common cancer worldwide
with over 300,000 new cases annually.
• Tobacco use, including smokeless tobacco and excessive alcohol consumption
are estimated to account for about 90% of oral cancers.
• Usually cancer begins with white patches, leukoplakia or red patches,
erythroplakia, associated with risk factors such as tobacco or/and alcohol.
• Tobacco users – smoked, chewing or both – developed most oral lesions with
an annual incidence rate ranging from 5.2/1,000 to 30.2/1,000, whereas non-
user develop the fewest oral lesions ranging from 0.6/1,000.
• An increasing number of young people are being affected and 25% of the
cases have no associated risk factors.
11

GLOBAL TRENDS OF ORAL
CANCER
• Based on GLOBOCAN estimates, about 14.1 million new cancer cases and 8.2 million
deaths occurred in 2012 worldwide.
• Over the years, the burden has shifted to less developed countries, which currently
account for about 57% of cases and 65% of cancer deaths worldwide.
• Although incidence rates for all cancers combined are nearly twice as high in more
developed than in less developed countries in both males and females, mortality rates
are only 8% to 15% higher in more developed countries.
• This disparity reflects regional differences in the mix of cancers, which is affected by risk
factors and detection practices, and/or the availability of treatment.
12

Estimated Number of New Cancer Cases in 21 World Areas, 2012.
*Region estimates do not sum to the worldwide estimate due to calculation method.
Source: GLOBOCAN 2012.
13

ESTIMATED NEW CANCER CASES AND DEATHS WORLDWIDE FOR LEADING CANCER
SITES BY LEVEL OF ECONOMIC DEVELOPMENT, 2008. SOURCE: GLOBOCAN 2008.
Ahmedin Jemal et al, Global Cancer Statistics, CA CANCER J CLIN 2011;61:69–90
14

Estimated new cases Estimated deaths
15

Estimated new cases Estimated deaths
1,30,900
74,500
16

Gender More developed areas Less developed areas
Incidence Mortality Incidence Mortality
ASR Cumulati
ve risk,
% (Aged
birth to
74 years)
ASR Cumulati
ve risk,
% (Aged
birth to
74 years)
ASR Cumulati
ve risk,
% (Aged
birth to
74 years)
ASR Cumulati
ve risk,
% (Aged
birth to
74 years)
MALES
2012
7.0 0.8 2.3 0.3 5.0 0.6 2.8 0.3
2008 6.9 0.8 2.3 0.3 4.6 0.5 2.7 0.3
Females
2012
2.6 0.3 0.6 0.1 2.5 0.3 1.4 0.2
2008 2.4 0.3 0.6 0.1 2.6 0.3 1.5 0.2
1. Less developed areas had slightly more incidence and mortality
2. With increase in years there was a slight increase in incidence
and mortality in both the areas.
ASR- Age standardized rate -
Summary measure of the rate that
a population would have if it had a
standard age structure.
CR- Probability or risk of
individuals dying from the disease
during a specified period of time.
17

• Trends in oral cancer incidence are not uniform in the world.
• For example, there is an increasing trend in oral cavity and tongue cancer incidence in men and
women in North and Eastern Europe, Asia, China, and India.
• Declining rates are seen in men in France and Italy; however, rates for oral and tongue cancer are
increasing in women in France, Germany, the UK, and Japan.
• In South America the rates are stable for men and increasing for women.
• The incidence of cancer of the oral cavity and pharynx in the United States has been declining in
men since 1975 and in women since 1980, although recent studies have shown that the incidence
is increasing for those cancers related to human papillomavirus (HPV) infection (ACS 2010).
• Changes in alcohol and tobacco consumption may modify trends in oral cancer incidence and
mortality.
• Death rates in the United States from oral cavity and pharynx cancer have decreased by more than
2% per year since 1980 in men and since 1990 in women (ACS 2010) and is probably related to
changes in tobacco and alcohol consumption
18

INDIAN CANCER PATTERN
`Nair K et al, Cancer: Current scenario, intervention strategies and projections for 2015
19

20

21

International Agency for Research on Cancer, WHO
estimation.
22

• India has one of the highest incidence in the world.
• Oral cancer rank no.1 in males and 3 in females.
• 12% in males and 8% in females of all cancers.
• Urban part in highest incidence regions like Mumbai there may be fall in
oral cancer which could be attributed to change from pan chewing and
bidi smoking to smoking of manufactured cigarettes.
• The rising trend of tongue cancer in young men in western countries is
thought to be due to marked increase in alcohol consumption, perhaps
combined with increase use of smokeless tobacco products especially in
USA.
Textbook of community dentistry, S.S.Hiremath
23

HENCE….
• The study of tumors of the oral cavity and adjacent
structures constitutes an important phase of dentistry
because of the role which the dentist plays in the diagnosis
and treatment of these lesions.
• Although tumors constitute only a small number of the
pathologic conditions seen by the dentist, they are of great
significance since they have the potential ability to
jeopardize the health and longevity of the patient.
24

TERMINOLOGIES
• A tumor, by definition, is simply a swelling of the tissue in the
strict sense, the word does not imply a neoplastic process.
• Many of the lesions sometimes discussed as tumors only
because they are manifested as swellings; they are in no way
actually related to true neoplasms.
25

• Neoplasia is a poorly understood biological phenomenon which, in
some instances, cannot be clearly differentiated from other
processes or tissue reactions.
• A neoplasm can be defined as an abnormal mass of tissue, the
growth of which exceeds and is uncoordinated with that of the
normal tissues and persists in the same excessive manner after
cessation of the stimuli which evoked the change (Willis 1952).
26

According to the National Cancer Institute,
• "A tumor is an abnormal mass of tissue that results when cells divide more than
they should or do not die when they should.
• Tumors may be benign (not cancer), or malignant (cancer). Also called
neoplasm.
• Cancer is a term for diseases in which abnormal cells divide without control
and can invade nearby tissues. Cancer cells can also spread to other parts of
the body through the blood and lymph systems. There are several main types
of cancer.
• Carcinoma is a cancer that begins in the skin or in tissues that line or cover
internal organs.
• Sarcoma is a cancer that begins in bone, cartilage, fat, muscle, blood vessels, or
other connective or supportive tissue."
27

• Oral precancer – An intermediate clinical state with increased
cancer risk, which can be recognized and treated with a much
better prognosis than a full blown cancer.
• Premalignant lesion – Morphologically altered tissue in which
cancer is more likely to develop than its apparently normal
counterpart.
• Premalignant condition – A generalized state associated with
significantly increased risk of cancer.
28

• Oncogenes – genes which can cause malignant transformation
when inappropriately expressed, because of mutation,
amplification or rearrangement.
• Suppressor genes – act by inhibiting cell growth.
• Any malignancy that arise from oral tissue (head and neck) – Oral
Cancer
29

In a World Health Organization (WHO) Workshop, held in 2005
• The term ‘‘potentially malignant” was preferred above
‘‘premalignant” or ‘‘precancerous”; furthermore, it has been
recommended to abandon the traditional distinction between
potentially malignant lesions and potentially malignant conditions
and to use the term ‘‘potentially malignant disorders” instead.
OPMD/PMD
30

• “It is a group of disorders of varying etiologies, usually tobacco
characterized by mutagen associated, spontaneous or hereditary
alterations or mutations in the genetic material of oral epithelial cells with
or without clinical and histo-morphological alterations that may lead to
oral squamous cell carcinoma transformation”.
(Oral potentially malignant disorders: Precising the deﬁnition)
- Oral Oncology journal (2012)
31

CLASSIFICATION
• There are various classifications of oral cancer.
1. International Classification of disease (WHO – 10th version )
Here oral cancer is classified under the rubics C00-C14.
32

(C00) Malignant neoplasm of lip
(C01) Malignant neoplasm of base of tongue
(C02) Malignant neoplasm of other and unspecified parts of tongue
(C03) Malignant neoplasm of gum
(C04) Malignant neoplasm of floor of mouth
(C05) Malignant neoplasm of palate
(C06) Malignant neoplasm of other and unspecified parts of mouth
(C07) Malignant neoplasm of parotid gland
(C08) Malignant neoplasm of other and unspecified major salivary glands
(C09) Malignant neoplasm of tonsil
(C10) Malignant neoplasm of oropharynx
(C11) Malignant neoplasm of nasopharynx
(C12) Malignant neoplasm of piriform sinus
(C13) Malignant neoplasm of hypopharynx
(C14) Malignant neoplasm of other and ill-defined sites in the lip, oral cavity and pharynx
International Statistical Classification of Diseases
and Related Health Problems, WHO,10th revisión
33

TYPES OF CANCER
• Classification of Benign tumors of jaw
A. Epithelial tissue
 Papilloma
 Keratocanthoma
B.Fibrous connective tissue
 Fibroma
 Giant cell fibroma
 Myxoma
C.Cartilage tissue
 Chondroma
 Chondroblastoma
D. Adipose tissue
Lipoma
E. Bone
Osteoma
Osteoblastoma
F. Vascular tissue
 Hemangioma
 Lymphangioma
G. Neural tissue
 Neurofibroma
H. Salivary gland tumor
 Adenoma
 Warthin’s tumor
34

Classification of malignant tumor of jaw
A. Epithelial tissue
 Squamous cell carcinoma
 Basal cell carcinoma
 Verrucous carcinoma
B. Fibrous connective tissue
 Fibrosarcoma
C. Cartilage tissue
 Chondrosarcoma
D. Adipose tissue
Liposarcoma
E. Bone
Osteosarcoma
Ewing sarcoma
F. Vascular tissue
 Angiosarcoma
G. Neural tissue
 Neurofibrosarcoma
H. Salivary gland tumor
 Adenocarcinoma
35

36
Premalignant lesions Premalignant conditions
Leukoplakia Oral submucous fibrosis
Erythroplakia Oral lichen planus
Leukokeratosis nicotina palatinae Actinic keratosis
Candidiasis Syphilis
Carcinoma in situ Discoid lupus erythematosus
Sideropenic dysphagia

NEW CLASSIFICATION FOR ORAL
POTENTIALLY MALIGNANT DISORDERS
SARODE, SARODE, KARMARKAR, TUPKARI(Ref - Oral Oncology xxx, 2011)
CLASSIFIED OPMD INTO 4 GROUPS:
Group I:
Morphologically altered tissue in which external factor is responsible for the etiology
and malignant transformation.
Group II:
Morphologically altered tissue in which chronic inflammation is responsible for
malignant transformation (chronic inflammation mediated carcinogenesis).
Group III:
Inherited disorders that do not necessarily alter the clinical appearance of local
tissue but are associated with a greater than normal risk of PMD or malignant
transformation.
Group IV:
No clinically evident lesion but oral cavity is susceptible to Oral squamous cell
carcinoma.

Group I: Morphologically altered tissue in which external factor is responsible for the
etiology and malignant transformation.
1. Habit related
a. Tobacco associated lesions
• Leukoplakia
• Tobacco pouch keratosis
• Stomatitis palatine nicotini
b. Betel nut associated
• Oral submucous fibrosis
c. Sanguinaria-associated keratosis
2. Non-habit related
• Actinic cheilosis
• Chronic candidiasis
Certain strains of Candida have been shown to produce nitrosamines a chemical
carcinogen (external factor) and hence, candidiasis is included under Group I.

Group II: Morphologically altered tissue in which chronic inflammation is responsible for
malignant transformation (chronic inflammation mediated carcinogenesis).
Group II a. Chronic inflammation caused by internal derangement.
• 1. Lichen planus
• 2. Discoid lupus erythematosus
Group II b: Chronic inflammation caused by external factors.
1. Chronic mucosal trauma
2. Lichenoid reactions
3. Poor oral hygiene
4. Chronic infections
• Chronic bacterial infections
• Chronic viral infections
• Chronic fungal infections
5. Other pathologies associated with prolonged untreated chronic inflammation of the oral
cavity.

• Group III: Inherited disorders that do not necessarily alter the clinical appearance of local
tissue but are associated with a greater than normal risk of PMD or malignant
transformation.
1. Inherited cancer syndromes
• Xeroderma pigmentosum
• Ataxia telangiectasia
• Fanconi’s anemia
• Li Fraumeni syndrome
2. Diskeratosis congenita
3. Epidermolysis bullosa
4. White sponge nevus
5. Darier’s disease
6. Hailey–Hailey disease

Group IV: No clinically evident lesion but oral cavity is susceptible to
Oral squamous cell carcinoma.
1. Immunosupression
• AIDS
• Immunosupression therapy (for malignancy or organ
transplant)
2. Alcohol consumption and abuse
3. Nutritional deficiency
• Sideropenic dysphagia
• Deficiency of micronutrients

PRECANCEROUS LESION
 Leukoplakia:-
 A raised white part of oral mucosa measuring 5 mm or more which cannot be scrapped
off and which cannot be attributed to any other diagnosable disease.
• Etiopathgogenesis:-
 Local factors
Smoking, Alcohol, Chronic irritation, Candidiasis
 Systemic factors
Syphilis, Vit def, Hormones, Drugs
 Site – buccal mucosa, lip, floor of mouth, gingiva, soft and hard palate.
 Precancerous nature – persistent, regress spontaneously and progress to oral cancer.
42

CLASSIFICATION
I. Acc to clinical description
 Homogenous
 Non homogenous
II. Acc to etiology
 Tobacco induced
 Non tobacco induced
III. Acc to risk development for future
 High risk
 Low risk
 Intermediate risk
IV. Acc to histology
 Dysplastic
 Non-dysplastic
V. Acc to extent
Localized
diffuse
43

 Regression in 40% of cases
 Cracks, bleeding, redness and area of erosion – turning
malignant
 1-20% become malignant – 1 to 30 years.
 Lesion over 1 cm – high risk
44

45
• The highest rate of transformation was reported
for nodular homogenous erythematous base
leukoplakia a rate of 16 per percent per year.-
Gupta et al 1989.

46
• Silverman has reported that leukoplakia in non
smokers referred to sometimes as idiopathic
leukoplakia exhibit a higher rate of malignant
transformation than in smokers 16%.

Erythroplakia
 Red lesion of oral mucosa that cannot be characterized
as any other definable lesion.
 Red eroded area with demarcation against normal
appearing mucosa.
 Associated with reverse smoking
47

Smoker’s palate
 Common reaction of palatal mucosa to smoking.
 Stomatitis nicotina
 Lesion – diffuse white palate with numerous
excrescence having central red dots.
 High temperature and chemical compositions
48

PRECANCEROUS CONDITION
Oral sub mucous fibrosis
 Betel nut with or without tobacco, chillies, nutritional deficiency,
genetic susceptibility, autoimmunity and collagen disorder.
 Betel nut cause:-
Constant irritation
Phenols – burning sensation
Alkaloid – fibroblast proliferation and collagen synthesis
49

 Palpable fibrous bands
 Buccal mucosa, retromolar area, rima oris
 Tongue affected become devoid of papilae , smooth
 Mobility (protrusion ) impaired
 Opening of mouth restricted
 Burning sensation – hypo-salivation or dryness of
mouth
50

 Lichen planus
 It is a chronic mucocutaneous condition in which the skin and mucosal
manifestations can occur independently, concurrently or sequentially.(Wickham’s
striae)
 Cell mediated, immunologically induced degeneration of basal cell layer of the
epithelium.
 Oral lichen planus, diabetes mellitus and hypertension – Grinspan syndrome
 Site – buccal mucosa
 Asymptomatic
 Types – reticular, papular, plaque like, erythematous, ulcerative.
51

SQUAMOUS CELL CARCINOMAEpidermoid carcinoma
Carcinoma of lip, tongue, floor of mouth, buccal mucosa,
palate, maxillary sinus, gingiva.
Red white or mixed red and white lesion, change in surface
texture or presence of mass or ulceration.
Lesion may be flat or elevated.
Loss of function – speech, diet, swallowing
Lymphatic spread
52

• Carcinoma of floor of mouth
• Carcinoma of buccal mucosa
• Carcinoma of labial mucosa
• Carcinoma of palate
53

TNM SYSTEM OF TUMOR STAGING
STAGE GROUPING
Stage I – T1N0MO
Stage II – T2N0M0
Stage III – T3N0M0
T1 or T2 or T3N1M0
Stage IV – T4N0 or
N1M0
Any T, N2 or N3M0
Any T, any N, M1
55

RISK FACTORS FOR ORAL CANCER
57

7’S OF ORAL CANCER
• Smoking
• Spirit
• Spices
• Sepsis
• Sunlight
• Sharp tooth
• Syphilis
58

59

EPIDEMIOLOGICAL TRIAD
HOST
ENVIRONMENTALAGENT
60

I. HOST FACTOR
1. AGE
2. SEX
3. RACE
4. CUSTOMS AND HABITS
5. NUTRITION AND DIET
6. GENETIC PREDISPOSITION
7. OCCUPATION.
61

1. AGE
• Seen predominantly in older age group.
• Studies have shown maximum prevalence in 5th 6th decade .
• Increase in older age group may be due to
prolong exposure to initiators
decreased immunological surveillance.
Pulino B F B,2, Santos J F M, Pastore G P, Filho G P C, Pereira R A. Oral cancer: potentially malignant
lesions and statistics of diagnosed cases in the municipality of Santo André-SP. J Health Sci Inst.
2011;29(4):231-4
62

2. SEX
• MALES MORE AFFECTED.
• In South East Asia- leading cancer in males.
• Incidence range of oral cancer in men from 1 to 10 cases per
1,00,000
GLOBAL DATA ON INCIDENCE OF ORAL CANCER BY WHO 2005
63

• Age standardized incidence rate per 100,000 populations
ranges from 0.7 in China to 4.6 in Thailand and 12.6 in India.
• The two most fatal cancer in men in India
Oral cancer
Lung
International agency for research on cancer (WHO)
64

INDIAN STATISTICS FOR 2002-
2003
Age Oral cancer
prevalence (%)
Leukoplakia
prevalence (%)
5 years 0.1 0.2
12 years 0.1 0.2
15 years 0.5 0.2
35-44 years 0.6 2.1
65-74 years 0.7 3.2
66

REGISTRIES, 1964
Males per 1 lakhs Registry Females per 1
lakhs
16.7 Bombay 9
14.9 Poona 9.4
13 Madras 12.6
10.2 Bangalore 17.2
67

• 9670 oral cancers (8.2% of all neoplasms)
• Data taken from Bombay Population Based Cancer Registry
during the 15 year period from 1986 to 2000.
• Results : 6577(10.7%) males and 3093 (5.4%) females.
• Decreasing trend 1.70% yearly.
• Reason : decrease in the usage of pan and tobacco.
68
Sunny Lizzy et al 2004. Oral Cancers in Mumbai, India:
a Fifteen Years Perspective with Respect to Incidence
Trend and Cumulative Risk.

3. RACE
• White develop lip melanoma more frequently
than black races
• For the oral cavity as a whole, NH black males
have the highest age-adjusted incidence rate
(AAIR) for oral cancer (4.86/100 000), followed
by NH whites males (4.71/100 000).
Lihua Liu et al. Oral squamous cell carcinoma incidence by subsite
among diverse racial and ethnic populations in California. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 2008;105:470-80
69

• The Oral cancer incidence rate for Hispanics is
much lower than that of the NH whites or
blacks (2.52/100 000 men, 1.38/100 000
women). *
Daniel M Saman.A review of the epidemiology of oral and pharyngeal
carcinoma: update Head & Neck Oncology 2012: 4:1
70

4. CUSTOMS AND HABITS
• Use of tobacco on global scale is the major cause of oral cancer.
• Reverse smoking – palate cancer
• Tobacco chewing, pan chewing – floor of mouth and buccal mucosa
cancer
• In India about 200 million people use tobacco in some form or the other
e.g.- 70 % smoke bidi
10 % smoke cigarettes
20 % use smoke less tobacco.
72

Alcohol
• Causes postulated :-
• Dehydrating effect makes mucosa vulnerable
to carcinogens (nitrosamines and hydrocarbons)
• Most heavy drinkers also are smokers
• (synergistic effect of alcohol and tobacco).
S.K.S. Kumar, R.B. Zain. Aetiology and Risk factors for Oral Cancer – A Brief
Overview. Annal Dent Univ Malaya 2004; 11: 41–50
73

• Ethanol is shown to increase the permeability of oral
mucosa.*
• For instance, concentrations of ethanol of 25% and
above significantly increased the permeability of
porcine oral mucosa to nitrosonornicotine (NNN)
• The major metabolite of alcohol is acetaldehyde whose
transformation is mainly carried out by the enzyme
alcohol dehydrogenase (ADH).
S.K.S. Kumar, R.B. Zain. Aetiology and Risk factors for Oral Cancer – A
Brief Overview. Annal Dent Univ Malaya 2004; 11: 41–50
74

• Accumulation of acetaldehyde can occur due to
increased activity of alcohol dehydrogenase
(ADH) enzyme activity.
• ADH type-3 genotypes cause rapid oxidation of
alcohol to acetaldehyde and these individuals
are predisposed to oral cancer.
75

76
• In India alcohol drinking does not emerge as a
strong risk factor, as the risks reported for
alcohol consumers were relatively much lower
than those for tobacco smokers and chewers.
Notani (1985) Sankarnarayanan (1990)

• A recent report (2012) prepared by experts of National
Institute of Health and Family Welfare (NIHFW) to study the
harmful effects of gutka specified clearly that India alone
accounted for 86 per cent of the total oral cancer figure
across the world.
77

• Health Ministry now banking on the successful
implementation of the 2011 notification which banned the
use of tobacco in gutkha by describing gutkha as a food
product and saying that food products cannot contain
nicotine.
78

• Food Safety Commissioners across states have, however,
reported the fact that chewing tobacco industry is trying to
tweak the law by selling gutkha and tobacco in separate
packs.
79

• In India, tobacco alone is responsible for 1.5 lakh cancers, 4.2
million heart diseases, 3.7 million lung diseases every year.
• The Health Ministry's own statistics show that over 65 per cent of
cancers in India can be attributed to tobacco use.
80

BETEL QUID CHEWING
• Betel quid chewing with different ingredients is
the most common habit in Southeast Asia
especially in the Indian subcontinent. Betel quid
(also referred to as paan) usually contains betel-
leaf (leaf of Piper betel vine), areca nut, slaked
lime and tobacco.
Johnson N. Tobacco Use and Oral Cancer: A Global Perspective. Journal
of Dental Education 2001; 65(4): 328-339
81

• Slaked lime – lowers pH.
• Chewing betel quid without tobacco is also carcinogenic to
humans and areca nut, a common component of many
chewing habits is carcinogenic to humans.
Johnson N. Tobacco Use and Oral Cancer: A Global Perspective. Journal of
Dental Education 2001; 65(4): 328-339
82

4. NUTRITION AND DIET
• Related to low intake of fruits and vegetables.
• Suppressive agents:-indoles, flavonoids, isothiocyanates,
terpenes, rutin and phenolic anti-oxidants.
• Low dietary/serum vitamin A associated pre-cancers /
cancers.
• Vitamin C blocks conversion of nitrites to nitrosamines.
• Iron deficiency anaemia –part of Plummer-Vinson
syndrome – associated with carcinoma tongue.
84

• The earliest evidence was that of the iron deficiency
caused Plummer-Vinson syndrome which led to the
development of oral cancer in Swedish women. It was
believed that patients with this syndrome also had
deficiencies of vitamins B and C
• In Europe, diet has been accounted for 10-15% of oral
cancer cases. More frequent consumption of fruit and
vegetables, particularly of carrots, fresh tomatoes and
green peppers were associated with reduced risk of oral
and pharyngeal cancer.
85

• Fish, vegetable oil, olive oil, bread, cereals,
legumes, protein, fat, fresh meat, chicken, liver,
shrimp, lobster and fiber – protective effect.
• Associated with higher risk of oral cancer
namely processed meats, cakes and desserts,
butter, eggs, soups, red meat, salted meat,
cheese, pulses, pasta or rice, millet and corn
bread.
S.K.S. Kumar, R.B. Zain. Aetiology and Risk factors for Oral Cancer – A Brief
Overview. Annal Dent Univ Malaya 2004; 11: 41–50
86

• Micronutrients - vitamins A (retinol), C (ascorbic
acid) and E (α-tocopherol), carotenoids (β-
carotene), potassium and selenium. *
• Β carotene, retinol, retinoids, vitamin C (ascorbic
acid) and vitamin E (α-tocopherol) are
antioxidants.*
87

88
CASE CONTROL STUDIES
• Several major case control studies have been reported
from the western countries. One of the largest case
control study was reported from the US on 871 cases
and 979 control, frequency matched for age and sex.-
McLaughlin et al 1988.
• Meat, fish, grains and dairy products showed no
association with the risk in females, where as in males,
meat and dairy products increased and fish decreased
the risk.

89
• However fruits in general including citrus fruits and dark yellow
fruits decreased the risk in both the sexes
• Marshall et al (1996) reported that low intake of vitamins C and
A was associated with doubling of the risk.
• Lavecchia et al (1994) of the sixteen food items studied eggs,
cold meat, fish , bread / pasta, butter , margarine and oil
showed no association however a protective effect was seen
with cheese, carrots, green vegetables and fresh fruits, milk and
meat.

90
• A single case control study exploring the association of
individual food items has been reported from India
region of high incidence or oral pharyngeal cancer –
Notani and Jayant.
• This study was based on cancers in males at a large
referral hospital, and compared the diet of cancer cases
with two groups of controls, hospital and community.

91
• An exhaustive review of epidemiological evidence on
the relationship between nutrition and oral cancer
published recently Marshall and Boyle 1996 discussed
the limitations of dietary case control studies.

5. GENETIC FACTORS.
• Some evidence shown by some studies conducted
shows familial and genetic predisposition to oral
cancer.
• Genetic polymorphisms in the genes coding for
the enzymes (P450 enzymes, xenometabolising
enzymes: XMEs) responsible for tobacco
carcinogen metabolism are suspected to play key
role.
92

6. OCCUPATION
• Occupational risks, namely exposure to excessive solar
radiation/ ultraviolet light is known to cause lip cancers.
• UV rays also causes actinic cheilitis which may
transform to oral squamous cell carcinomas.
• Sulfur dioxide, asbestos, pesticide exposures and mists
from strong inorganic acids, burning of fossil fuels have
been known to cause cancers of posterior mouth,
pharynx and larynx
93

• Outdoor workers like farmers, fishermen,
foresters, and postal delivery workers are at risk
of lip cancer from ultraviolet light.
94

1. Tobacco
2. Biological
* Virus
* Fungal infection.
3. Mechanical
4. Chemical
5. Nutritional
John J; Textbook of preventive dentistry; 2nd edition
96

1. TOBACCO
• Christopher Columbus reported a gift of strange
dry leaves from a native of San Salvador.
• Ceremonial and medicinal purpose.
• Frair Roman Columbus in 1493 carried a supply of
tobacco back to Portugal and the practice of
sniffing started to spread.
• First commercial plantation of tobacco was in
Virginia (USA) in 1612.
Peter S. Essentials Of Preventive And Community Dentistry. 4th Edition 2010.
Arya Publications.
97

 In India tobacco was introduced in late 16th and 17th century by the
Portugese traders.
 Symbol of aristocracy – introduction of hookah during Moghul rule.
 In 1776, British East India Company – cash crop
 Used as
Smoking.
Chewing.
Snuff.
Peter S. Essentials Of Preventive And Community Dentistry. 4th Edition
2010. Arya Publications.
98

In National Oral Health Survey and Fluoride mapping
(2002- 2003)
In 35-44 year olds
About 23 percent males and more in urban
area reported smoking tobacco
Nature of smoking :-
45% more male and more in rural had the habit
of smoking bidis
21% more males and more in urban had the
habit of smoking cigarettes.
99

• Tobacco use and especially smoking is a male-
dominated phenomenon among children and
adolescents in India.
• This is unlike the West, where its distribution is
equal among both genders.
Chadda RK and Sengupta SN. Tobacco use by Indian adolescents Tobacco
Induced Diseases 2002; 1(2):111–119
100

• In some countries like China, Fiji, Jordan and Venezuela,
smoking is rather more common among females.
• In India, the use of smokeless tobacco has become popular
during the last few decades (1960-2000).
101

• A decline in tobacco use, as evident in the USA
and some European countries, does not seem
to be observed in near future in India.*
Chadda RK and Sengupta SN. Tobacco use by Indian adolescents
Tobacco Induced Diseases 2002; 1(2):111–119
102

103
SMOKELESS TOBACCO
• The use of smokeless tobacco is an important cause of oral
cancer, particularly in India and its evidence is largely
derived from case control studies.
• The reported risks of developing oral cancer in chewers are
2-4 times higher as compared to those with no tobacco
habits.
Jussawall and Deshpande 1971, Notani and Jayant 1987,
Sankaranarayanan et al Nandakumar et al 1990.

104
• Smokeless tobacco, whether of the chewing variety
or snuff, masheri contain several carcinogens of
which tobacco specific nitrosamines are the most
significant .
Brunnemann and Hoffman 1992, Bhide et al 1989.

Smoking:-
bidi, cigarette, cigar, chutta, pipe, chilum, hukka
105

1. BIDI-
* Most popular form of tobacco in India.
* 0.2-0.3 g of sun dried tobacco flakes
are hand rolled in rectangular piece of
tembu leaves and tied with a thread.
Nicotine Content-
1.7-3 mg.
Tar content – 45-50 mg.
106

107
• Bidis contain a much higher concentration of toxic
agents like tar, nicotine, a carbon monoxide,
hydrogen cyanide, phenols and benzopyrene as
compared to locally manufactured cigarettes, as well
as US cigarettes.
Hoffman et al 1974, Pakhale 1990.

2. Chillum-
* Straight 10 -14 cm clay pipe.
* Held vertically and pebble present at
one end to prevent tobacco from
entering the mouth.
* Filled with coarsely cut tobacco
pieces and a glowing charcoal is kept
at top.
108

3. Chutta-
* Also called cigar,
* Air cured, fermented tobacco used in modern factories.
* Chutta are small cigars made of
heavily boiled tobacco.
109

110
• Pipe and cigar smokers have also been reported to
be at a higher risk for oral cancer as compared to
non smoker. Pipe smoker are particularly at a higher
risk for cancer of the lip.
Keller, A.Z. (1970) Cellular types, survival, race, nativity, occupations, habits and
associated diseases in the pathogenesis of lip cancers. Am. J. Epidemiol., 91, 486–
499.

4. Cigarettes-
* 1 gm of tobacco cured in sun or
artificial heat is covered with paper.
* Tobacco is treated with variety of
sugars, flavoring agents and
aromatic ingredients.
* Nicotine content- 1- 1.4 mg
* Tar content- 19 -27 mg.
111

112
• It has been demonstrated that the risk of oral/
pharyngeal cancers associated with cigarette
smoking decreases sharply with cessation of the
habit and reaches the risk of level of non smokers
after ten years of quitting. Blot et al 1988

5. Hookah-
* Also called water pipe or hubble
bubble.
* Tobacco smoke is drawn through
water in base of hookah which cools
and filters the smoke.
113

HOOKLI
• Clay pipe of short stem – 7-10 cm with a mouth piece and
bowl
• Commonly used in Bhavnagar district of Gujrat.
114

REVERSE SMOKING SQUAMOUS CELL CARCINOMA
Reverse smoking :- (Carcinoma palate, more in Andhra).
Tissues vulnerable- lips, gums, tongue, cheeks, palate.
115

116
• The relationship between reverse smoking with the
burning end inside the mouth, and palatal cancer is well
established in India Reddy et al 1982.
• In western countries the effect of cigarette smoking has
usually been studied along with alcohol drinking with
respect to cancer of the oral cavity and pharynx.
Rothman and Keller 1972, Blot et al 1988, Tuyns et al 1988,
Franceschi et al 1990, La Blot et al

117
ATTRIBUTABLE RISK
• For the Indian population the proportion attributable to
tobacco use both smoking and chewing has been
estimated to vary form 61 percent to 70 % (81% for
males and 36% for females) for oral cancer.
Notani PN, Jayant K. Role of diet in upper aerodigestive tract cancers. Nutr
Cancer 1987;10:103–13.

Chewing:-
Chronic irritation causes precancerous & cancerous lesions at
contact site ( betel quid,mainpuri tobacco ,mawa, mishri,
zarda, and khaini).
118

BETEL NUT/ARECA NUT
• Betel Nut or Areca Nut is the nut of the Areca Palm
tree, which is chewed either alone or in combination
with the Betel Leaf and Slaked lime.
• Areca nut is the fourth commonest psycho-active
substance used by the humankind. *
Arecapedia. Available from https://sites.google.com/site/quitnut/
119

Different preparations:
• Paan, Vettalai paaku, Surti, Pan Masala (even marketed
as mouth freshner), Gutkha, Supari, Khaini, Naswaar,
Zardaa, Mawa, Mishri, Pin Lang, Buyo, Gudaku, Lao-hwa
(Taiwan), Mainpuri, Tamol, etc.
Contents:
• Betel quid contains Areca nut, Betel leaf, and Slaked
lime and may contain tobacco, catechu, spices,
sweeteners and essences.
121

• Areca nut: contains Alkaloids like arecoline, arecaidine,
guvacine and guvacoline, polyphenols (Flavonols and
tannins) and Betel nut specific nitrosamines (mainly Saffrole)
as its main constituents.
Effects:-
OSMF (Oral submucous fibrosis)
White patch (leukolplakia, erythroplakia)
Oral cancer
Hepatocellular cancer
Still birth
Heart disease
Arecapedia. Available from
https://sites.google.com/site/quitnut/
122

• Slaked lime or Chuna aids in the Cancer causing property
of Areca nut by:
Resulting in increase in Alkalinity thereby helping in action
of the carcinogens in Areca nut
Causing caustic damage to the oral tissues making them
more susceptible to the cancerous agents
123

• Catechu is an astringent, reddish-brown
substance which is often smeared on the betel
leaf used to wrap the ingredients of betel quid.
Two main types of catechu may be used
depending on the tree or shrub from which the
catechu has been extracted (Acacia catechu,
Uncaria Gambier)
124

• Chewing areca nut has been proven to cause cancer in a
dose dependent manner. Risk of cancer increases with the
frequency and duration of chewing. It commonly results
in Oral submucous fibrosis which most times progresses to
cancer, specially on continuing chewing of the areca nut.
125

• Digestive properties of Betel quid are due to the
increase in Salivation and stimulation of smooth
muscles caused by Areca nut. However, it is associated
with an increased incidence of Peptic ulcers.
• Consumption of a single Betel Quid or a single sachet
of Pan masala or Ghutka increases the risk of Oral pre-
cancer.
• As betel nut (supari) ripens, its tanin content decreases
but all form of areca nut are carcinogenic.
126

• Oral Cancers from chewing Areca nut preparations are
almost always preceded by Pre-cancer lesions.
• Pan masala, Mawa, Ghutka and such preparations have
resulted in Oral Submucous Fibrosis (OSF) in 2-3 yrs of
chewing
• Betel Quid has shown to give rise to OSF in 8-11 yrs of
chewing
• Oral Submucous Fibrosis has a Malignant potential of 7.6
– 95%
• Leukoplakia has a malignant potential of 2 – 12%
• Erythroplakia has a malignant potential of 15 – 40 %
Nair U. Alert for an epidemic of oral cancer due to use of the betel quid
substitutes gutkha and pan masala: a review of agents and causative
mechanisms. Mutagenesis 2004;9(4):251-262
127

• Addiction to Pan Masala and its like
preparations is greater prevalent in younger
age groups on account of the low cost, easy
availability, misleading advertising, artificial
flavouring and attractive packaging. It is
popular amongst children and adolescents.
Nair U. Alert for an epidemic of oral cancer due to use of the betel quid
substitutes gutkha and pan masala: a review of agents and causative
128

PREPARATIONS OF ARECA
NUT
1. Khaini-
* Powdered sun dried tobacco, slake lime
paste mixture.
* Placed in mouth and chewed.
* Wide spread use in – Maharashtra and
many North Indian states.
* Ingredients are mixed with thumb to make
the mixture alkaline and is placed in
premolar region of mandible.
129

2. Mainpuri tobacco
• Ingredients are – tobacco ,slake lime, finely cut areca nut ,
camphor and cloves.
• About 7% of villages in UP use this form of tobacco.
130

3. Mawa
• Preparation containing thin shaving of areca nut with addition of
tobacco and slake lime.
• Packet rubbed vigorously to mix the contents and the mixture is
chewed till becomes softer after which it is transferred to the
mandibular groove.
131

4. Mishri
* Prepared by roasting tobacco on hot metal
plate until it is uniformly black.
• It is then powdered.
• Used primarily to clean teeth.
132

5. Paan
• History of over 2000 years.
• Refers to betel leaf (from piper betel wine) itself
and often to the quid.
• Quid also contains- areca nut, aniseed, catechu
(kattha gambir), cardamom, cinnamon, coconut,
sugar, tobacco wrapped in betel leaf.
133

Snuff :-
• Known to cause cancers
• Finely powdered air-cured and fire cured tobacco
leaves.
• It may be dry or moist.
• Used orally or nasally
• Bajjar is dry snuff – 14% women in Gujrat
134

CONSTITUENTS OF
TOBACCO
CONSTITUENTS ADVERSE EFFECTS
Poly aromatic hydro carbon Carcinogenesis.
Nicotine Potential carcinogenic agent
Phenol Ganglionic stimulation
and depressions
Tumor promotion.
Benzopyrene Tumor promotion
Irritation
Carbon mono oxide Impaired oxygen transport and
repair.
Formaldehyde Toxicity to cilia and irritation.
Nitrosamine Potential carcinogenic agent.
135

2. MECHANICAL
Dentures/ poor oral hygiene/ jagged teeth/ fillings.
Denture Material not shown to be carcinogenic.
Poor oral hygiene- fails to clean tobacco from the oral cavity.
Micro organism – from dental plaque may contribute to
chemical carcinogenesis by elaboration of toxins.
136

3. BILOLOGICAL
Viruses
(a) Herpes viruses :- HSV Type-1, EBV, Human Herpes Virus-6 and
Human Herpes Virus-8 ,all associated.
No conclusive evidence for cause and effect relationship
(only suspected )
Maximum suspicion on HHV-8.
(b) Papilloma viruses :- HPV-16 and HPV-18 associated. They play
role in neoplastic transformation from pre-cancer to cancer.
HPV-16 found in proliferative verrucous leukoplakia.
137

138
VIRUSES
• Saranath 1999 has reported that
Oral cancer :25-50% prevalence of EBV
Premalignant lesions 0-13%
Normal mucosa : 4 - 28%.
• HPV 16 was detected in higher proportion of oral
lesions compared to oral cancer cases probably
impling its importance in early events of
carcinogenesis D’costa et al, Saranath.1999

139
• Their activations can be through several pathways and could
well be influenced by the presence of other co factors.
• Herpes simplex virus type I and the human immuno
deficiency virus have been associated with squamous cell
carcinoma.
• An increase in oral cancer has been observed in workers of
leather, cotton and woolen textile industries.

More aggressive and
lethal.
HIV - Kaposi’s Sarcoma (KS)
140

• Tongue commonest site.
• Smoking, alcohol, irradiation are co-
factors.
• Role of viruses as initiators cannot
be ruled out.
HIV - Squamous Cell Carcinoma
141

Candidiasis - Associated with leukoplakia.
142

4. CHEMICAL
• Arsenic, Dyes, nickel, Aromatic amines
5. NUTRITIONAL
• Precarcinogens in food – Saccharin and Aflatoxin
• Increased consumption of fat
• Deficiency of folic acid
• Protein deficiency
• Increased consumption of red chilly powder
• Decrease in vit C, Vegetables.
143

III. ENVIRONMENTAL FACTORS
144

• Ultra-violet radiation.
• Excessive exposure associated with cancer lips.
• Occupations like- farming, fishing, forestry etc are at risk due
to prolong exposure.
• Countries near tropics and equator where air is cleaner and
UV rays are not trapped cancers can account for about 60%
of all oral cancers.
145

• Air pollution.
• Oral cancers are associated with aromatic
hydrocarbons present in polluted air.
Automobiles and factories gases
• Water and air contaminated by toxins of industries - cancer
146

REGISTERIES OF ORAL CANCER IN INDIA
• Cancer registration – 1982 through initiation of
National Cancer Registry Program (NCRP) by
Indian Council of Medical Research.
• Males in Bhopal have the highest age adjusted
incidence rates of cancer of tongue. (8.8 per
100,000)
• Similarly rate of oral cancer of oral cavity in both
males and females in all urban registeries are
among the highest in the world.
Ramnath Takiar. Projections of Number of Cancer Cases in India (2010-2020)
by Cancer Groups Asian Pacific J Cancer Prev, 11, 1045-1049
147

149
DIAGNOSIS OF ORAL CANCER
In addition to complete medical history and
physical examination, diagnostics procedures for
oral cancer may include the following:
• Biopsy
• Exfoliative cytology
• Toludine blue staining
• Computed tomography scan
• Ultrasound
• Magnetic resonance imaging

150
BRUSH BIOPSY OF ORAL
CANCER
• It is a procedure in which tissue samples are
removed (with a needle or during surgery) from
the body for examination under a microscope
to determine if cancer or other abnormal cells
are present.

151
EXFOLIATIVE CYTOLOGY
• Histologic examination of surface cells scraped
from a suspected lesion with a tongue blade.
• Accuracy is highly variable, weak in detecting
premalignant lesion
• False positive and false negative are common

152
TOLUIDINE BLUE STAIN
• It is used as an extra tool for the identification
of patients suspected with oral cancer lesions

154
COMPUTED TOMOGRAPHY
SCAN (CTSCAN)
• It uses a combination of radiography and
computer technology to produce cross
sectional images both horizontally and vertically
of the body.
• It shows a detailed images of any part of the
body, including bones, muscles, fat and organs.

155
ULTRASOUND
• It uses high frequency sound waves to create an
image of the internal organs.

156
MAGNETIC RESONANCE
IMAGING
• It uses a combination of large magnets,
radiofrequencies, and a computer to produce
detailed images of organs and structures within
the body.

157
USE OF MICRO NUCLEI
• Since the formation of micronuclei in the eukaryote cells is an end
point of chromosomal damage or segregation errors (Geard et al
1990) the presence of micronuclei reflects a genotoxicor
carcinogenic exposure.
• Due to its association with chromosomal aberrations, micronuclei
have been used since 1937 as an indicator of genotoxic exposure,
based on the radiation studies conducted by Brenneke and Mather
(Heddle etal. 1983).

158
• The assay is reliable and technically easy to
perform. The direct correlation between the
micronuclei formation and genomic damage
make the micronuclei assay an efficient
alteration to the metaphase analysis (Fenech
1990)

GLOBAL INITIATIVE IN
PREVENTION OF ORAL CANCER
• The crete declaration on oral cancer prevention
2005
• WHO Framework convention on tobacco
control
• Bloomberg initiative to reduce tobacco control.
159

CRETE DECLARATION
• 10th International Congress on Oral Cancer organized
by the Hellenic Cancer Society, International Congress
on Oral Cancer, Hellenic Association for treatment of
maxillofacial cancer and WHO was held from 19-24
April 2005 in Crete, Greece.
• 57 countries
• Areas strengthened should be:-
a)Provision of systemic epidemiological information on
prevalence of oral cancer and cancer risk specially in
developing countries.
Peterson P E. Strengthening the prevention of oral cancer: the WHO
perspective.Community Dent Oral Epidemiol 2005; 33: 397–9
160

b) Promotion of research (biological, behavioral and
psychosocial factors of oral cancer)
c) Integrating oral cancer information into national
health surveillance system.
d) Dissemination of information
e) Active involvement of oral health professionals
f) Training of primary health care worker in screening
g) Access to health facilities and provision of system
for early detection and intervention.
161

WHO FRAMEWORK
CONVENTION ON TOBACCO
CONTROL
• WHO FCTC treaty opened – 16th to 22 June
2003.
• 168 signatories.
• most widely embraced treaties in UN history.
• Member states – strive in good faith to ratify,
accept or approve it and show political
commitment not to undermine the objective set
out in it.
• Into force – 27 Feb 2005
162

• Cross border effect, trade liberization and direct
foreign investment
• Global marketing, promotion and sponsership
and international movement of contraband and
counterfeit cigarettes.
• Assert importance of –
Demand reduction strategies.
Supply reduction provisions.
163

BLOOMBERG INITIATIVE TO
REDUCE TOBACCO CONTROL.
(2006)
• This initiative funded by Bloomberg
philanthropies, is 2 year contribution of US$125
million by Michael R Bloomberg for global
tobacco control.
• In 15 developing countries (Bangladesh, Brazil,
China, Egypt, India, Indonesia, Pakistan, Poland,
Thialand)
• 5 key partner organisation.
164

• Approaches to Public Health.
1. Regulatory Approach.
2. Service Approach.
3. Educational Approach.
168

1. REGULATORY APPROACH.
• 1590- First governmental edict against
tobacco was derived in Japan.
• 1604- King James of England increased tax
on tobacco by 400% .
169

• 1975- In India Cigarette Act 1975 made it
necessary to print warnings on
cigarette packets.
- In India 2003 , prohibition of smoking in public places came
into force.
170

Ban tobacco and alcohol use
Ensure adequate legislation
Ensure warnings on products sold
Increase cost
Avoid glorification of products through
advertisements.
REGULATORY/ LEGISLATIVE MEASURES
171

• In India Cigarette Act in 1975
• National Cancer Control Program in 1985
• IN 2003, Indian Parliament passed ‘Cigarette
and other Tobacco product act to prohibit the
advertisement of and to provide for the
regulation of trade and production, supply and
distribution of cigarettes and other products.
172

2. SERVICE APPROACH
• Services provided by the professionals.-
• In order to be suitable for screening certain criteria have to be
met
* Disease is serious yet treatable in early
stages.
* Facilities for diagnosis and treatment
exists.
* Natural history of disease is known.
* Screening tool is inexpensive and safe.
174

For early detection –
 Self examination
Toludine Blue Vital Staining
Other techniques used are –
Biopsy Techniques.
Exfoliative Cytology.
Sikri V, Sikri P. Community Dentistry. 2010. CBS Publishers.
175

3. Educational Approach
• Dentist
See harmful effects
Counsel child and youth patients
Spend more time with patients
Treat women of childbearing age
Build patient’s interest in quitting
Speak with authority in community.
176

• Danger signals
Any persistent scaly white patch
Any lesion which increase in size
Non healing ulcer
Non healing extraction socket
Facial asymmetry
Oral numbness or pain during jaw movements.
177

• Guide to Counselling for tobacco cessation (5 A’s)
Ask
Advise
Assess
Assist
Arrange
• Use of Pharmacotherapy
Nicotine replacement therapy
Antidepressants (Selegeline, Clonidine)
178

• Counselling those unwilling to quit:-
Relevance of quitting
Risk of continuing tobacco use
Rewards of quitting
Roadblocks to quitting
Repeat these at each visit
179

CONCLUSION
• Several risk factors are implicated in the development
of oral cancer of which the most common and
established are tobacco smoking and betel quid
chewing.
• Hence, it is important for the public and the clinicians
to be completely aware of the risk factors for oral
cancer and it is prudent for dentists to look carefully for
early signs of oral cancer while routine examination of
the oral cavity especially in patients with history of
known risk factors.
182

REFERENCES
• http://ocf.org.in/professional/IncidenceAndPrevalence.aspx/
• http://www.iarc.fr/en/publications/list/bb/
• Isaäc van der Waal. Potentially malignant disorders of the oral and
oropharyngeal mucosa; terminology, classification and present
concepts of management. Oral Oncology. Article in press.
• Grace Bradley and Iona Leong. Chapter 4. Oral cancer. Book of
comprehensive dentistry.
• Textbook of community dentistry, S.S.Hiremath 2007 – 2nd edition.
• World Health organization site.
• M. Krishnan Nair, Cherian Varghese, R. Swaminathan. Cancer: Current
Scenario, Intervention Strategies And Projections For 2015. NCMH
Background Papers·burden Of Disease In India
183

• Peter S. Essentials Of Preventive And
Community Dentistry. 4th Edition 2010. Arya
Publications.
• Marya CM. A Textbook Of Public Health
Dentistry. 1st Edition 2011. Jaypee Publications.
• John J; Textbook of preventive dentistry; 2nd
edition
• Ghom A G.Textbook of oral medicine. Jaypee
publications.
184

• Pulino B F B,2, Santos J F M, Pastore G P, Filho G
P C, Pereira R A. Oral cancer: potentially
malignant lesions and statistics of diagnosed
cases in the municipality of Santo André-SP. J
Health Sci Inst. 2011;29(4):231-4
• Peterson P E. Oral cancer prevention and
control – The approach of the World Health
Organization. Oral Oncol (2008): 1-7
185

• Takiar. Projections of Number of Cancer Cases in
India (2010-2020) by Cancer Groups. Asian Pacific
J Cancer Prev, 11, 1045-1049
• Kumar S. K.S , Zain R.B. Aetiology and Risk factors
for Oral Cancer – A Brief Overview. Annal Dent
Univ Malaya 2004; 11: 41–50.
• Saman D M. A review of the epidemiology of oral
and pharyngeal carcinoma: update. Head & Neck
Oncology 2012, 4:1
186

• Liu L. Oral squamous cell carcinoma incidence by
subsite among diverse racial and ethnic
populations in California. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 2008;105:470-80
• Peterson P E. Strengthening the prevention of oral
cancer: the WHO perspective.Community Dent Oral
Epidemiol 2005; 33: 397–9
• Global data on incidence of oral cancer . WHO
2005,2008,2012.
187

• Dikshit R. et al. Cancer mortality in India: a
nationally representative survey. The Lancet, Early
Online Publication, 28 March 2012
doi:10.1016/S0140-6736(12)60358-4
• Chadda RK and Sengupta SN. Tobacco use by
Indian adolescents Tobacco Induced Diseases
2002; 1(2):111–119
• National oral health survey and fluoride mapping
2002-2003, India
188

• Johnson N. Tobacco Use and Oral Cancer: A
Global Perspective. Journal of Dental Education
2001; 65(4): 328-339
• Nair U. Alert for an epidemic of oral cancer due
to use of the betel quid substitutes gutkha and
pan masala: a review of agents and causative
189

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