Risk factors and prevention strategies of oral cancer

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RISK FACTORS AND PREVENTION STRATEGIES OF ORAL CANCER IN INDIAN SCENARIO

ByDr. Priyanka SharmaIII Year MDSDepartment of Public Health Dentistry

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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

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INTRODUCTION- A grim picture of oral cancer in India and global scenario

- Global and Indian trends of oral cancer

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• 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

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• 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.


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• 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: AIIMSIANS, Modified: July 25, 2015 14:55 ISTNDTV

ANOTHER REPORT

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• 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: ExpertIDA secretary general, International Bussiness times, July 21, 2014 15:39 IST

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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.


9• 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.


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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.


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• 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.


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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.

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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.

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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

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Estimated new cases Estimated deaths



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Estimated new cases Estimated deaths

1,30,90074,500

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Gender More developed areas Less developed areasIncidence Mortality Incidence Mortality

ASR Cumulative

risk, % (Aged

birth to 74

years)

ASR Cumulative

risk, % (Aged

birth to 74

years)

ASR Cumulative

risk, % (Aged

birth to 74

years)

ASR Cumulative

risk, % (Aged

birth to 74

years)MALES2012

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 mortality2. 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.

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• 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

19INDIAN CANCER PATTERN

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

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International Agency for Research on Cancer, WHO estimation.

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• 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

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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.

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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.

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• 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).

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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."

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• 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.

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• 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

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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

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• “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)

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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.

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(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

http://en.wikipedia.org/wiki/ICD-10_Chapter_C

http://apps.who.int/classifications/icd10/browse/2010/en#/C00

http://en.wikipedia.org/wiki/Oral_cancer





















http://en.wikipedia.org/wiki/Head_and_neck_cancer












http://en.wikipedia.org/wiki/Nasopharyngeal_carcinoma











TYPES OF CANCER• Classification of Benign tumors of jawA. Epithelial tissue Papilloma KeratocanthomaB.Fibrous connective tissue Fibroma Giant cell fibroma MyxomaC.Cartilage tissue Chondroma Chondroblastoma

D. Adipose tissueLipomaE. BoneOsteomaOsteoblastomaF. Vascular tissue Hemangioma LymphangiomaG. Neural tissue NeurofibromaH. Salivary gland tumor Adenoma Warthin’s tumor

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Classification of malignant tumor of jawA. Epithelial tissue Squamous cell carcinoma Basal cell carcinoma Verrucous carcinomaB. Fibrous connective tissue FibrosarcomaC. Cartilage tissue Chondrosarcoma

D. Adipose tissueLiposarcomaE. BoneOsteosarcomaEwing sarcomaF. Vascular tissue AngiosarcomaG. Neural tissue NeurofibrosarcomaH. Salivary gland tumor Adenocarcinoma

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Premalignant lesions Premalignant conditions

Leukoplakia Oral submucous fibrosisErythroplakia 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 relateda. Tobacco associated lesions• Leukoplakia • Tobacco pouch keratosis• Stomatitis palatine nicotinib. Betel nut associated• Oral submucous fibrosisc. Sanguinaria-associated keratosis

2. Non-habit related

• Actinic cheilosis

• Chronic candidiasisCertain 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 trauma2. Lichenoid reactions3. Poor oral hygiene4. Chronic infections• Chronic bacterial infections• Chronic viral infections• Chronic fungal infections5. 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 syndrome2. Diskeratosis congenita3. Epidermolysis bullosa4. White sponge nevus5. Darier’s disease6. 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 LESIONLeukoplakia:- 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.

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CLASSIFICATIONI. Acc to clinical description Homogenous Non homogenousII. Acc to etiology Tobacco induced Non tobacco inducedIII. Acc to risk development for future High risk Low risk Intermediate risk

IV. Acc to histology Dysplastic Non-dysplastic

V. Acc to extent Localizeddiffuse

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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

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• 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.

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• 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

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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

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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 irritationPhenols – burning sensationAlkaloid – fibroblast proliferation and collagen synthesis

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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

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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.

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SQUAMOUS CELL CARCINOMAEpidermoid 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, swallowingLymphatic spread

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

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TNM SYSTEM OF TUMOR STAGING

STAGE GROUPING

Stage I – T1N0MO

Stage II – T2N0M0

Stage III – T3N0M0T1 or T2 or T3N1M0

Stage IV – T4N0 or N1M0Any T, N2 or N3M0Any T, any N, M1

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RISK FACTORS FOR ORAL CANCER

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


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EPIDEMIOLOGICAL TRIAD

HOST

ENVIRONMENTALAGENT

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I. HOST FACTOR1. AGE2. SEX3. RACE 4. CUSTOMS AND HABITS5. NUTRITION AND DIET6. GENETIC PREDISPOSITION7. OCCUPATION.

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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 initiatorsdecreased 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

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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

• 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 IndiaOral cancerLung

International agency for research on cancer (WHO)

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INDIAN STATISTICS FOR 2002- 2003

Age Oral cancer prevalence (%)

Leukoplakia prevalence (%)

5 years 0.1 0.212 years 0.1 0.215 years 0.5 0.235-44 years 0.6 2.165-74 years 0.7 3.2

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REGISTRIES, 1964Males per 1 lakhs Registry Females per 1

lakhs16.7 Bombay 914.9 Poona 9.413 Madras 12.610.2 Bangalore 17.2

• 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.

68Sunny 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

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• 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

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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.

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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

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• 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

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• 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.


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• 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.

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• 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.

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• 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.

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• 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.

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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

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• 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

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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.


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• 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.


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• 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.


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• 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.*

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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.

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• 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.

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• 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.

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• 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.


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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


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

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II. AGENT FACTOR

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1. Tobacco2. Biological * Virus * Fungal infection.3. Mechanical4. Chemical5. Nutritional

John J; Textbook of preventive dentistry; 2nd edition

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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.

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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.

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In National Oral Health Survey and Fluoride mapping (2002- 2003)

In 35-44 year oldsAbout 23 percent males and more in urban

area reported smoking tobaccoNature of smoking :-45% more male and more in rural had the

habit of smoking bidis21% more males and more in urban had the

habit of smoking cigarettes.

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• 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

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• 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).


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• 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.*


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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.

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• 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

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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.


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• 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.


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3. Chutta- * Also called cigar, * Air cured, fermented tobacco used in modern

factories. * Chutta are small cigars made of heavily boiled tobacco.


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• 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. Chadda RK and Sengupta SN. Tobacco use by Indian adolescents Tobacco Induced Diseases 2002; 1(2):111–119

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• 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.


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HOOKLI • Clay pipe of short stem – 7-10 cm with a mouth piece

and bowl• Commonly used in Bhavnagar district of Gujrat.

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REVERSE SMOKING SQUAMOUS CELL CARCINOMA

Reverse smoking :- (Carcinoma palate, more in Andhra).Tissues vulnerable- lips, gums, tongue, cheeks, palate.

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• 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

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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).

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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/

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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.


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• 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 cancerHepatocellular cancerStill birthHeart disease


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• 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

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• 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)


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• 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.

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• 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.

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• 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

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• 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 mechanisms. Mutagenesis 2004;9(4):251-262

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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.

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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.


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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.


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4. Mishri

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


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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.


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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

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CONSTITUENTS OF TOBACCO

CONSTITUENTS ADVERSE EFFECTSPoly aromatic hydro carbon Carcinogenesis.Nicotine Potential carcinogenic agentPhenol Ganglionic stimulation

and depressionsTumor promotion.

Benzopyrene Tumor promotionIrritation

Carbon mono oxide Impaired oxygen transport and repair.

Formaldehyde Toxicity to cilia and irritation.Nitrosamine Potential carcinogenic agent.

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.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

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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.Johnson N. Tobacco Use and Oral Cancer: A Global Perspective. Journal of Dental Education 2001; 65(4): 328-339

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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

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• 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)

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• Tongue commonest site.• Smoking, alcohol, irradiation

are co-factors.• Role of viruses as initiators

cannot be ruled out.

HIV - Squamous Cell Carcinoma

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Candidiasis - Associated with leukoplakia.


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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.Johnson N. Tobacco Use and Oral Cancer: A Global Perspective. Journal of Dental Education 2001; 65(4): 328-339

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III. ENVIRONMENTAL FACTORS

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• 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.

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• 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

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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

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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

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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.

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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

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TOLUIDINE BLUE STAIN • It is used as an extra tool for the

identification of patients suspected with oral cancer lesions

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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.

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ULTRASOUND • It uses high frequency sound waves to

create an image of the internal organs.

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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.

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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).

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• 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.

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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

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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 informatione) Active involvement of oral health professionalsf) Training of primary health care worker in

screeningg) Access to health facilities and provision of

system for early detection and intervention.

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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

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• 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.

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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.

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PREVENTION AND CONTROL

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

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1. REGULATORY APPROACH.

• 1590- First governmental edict against tobacco was derived in Japan.

• 1604- King James of England increased tax on tobacco by 400% .

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• 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.

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

REGULATORY/ LEGISLATIVE MEASURES171

• 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.

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STARS N TOBACCO!!!

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.

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For early detection – Self examinationToludine Blue Vital Staining Other techniques used are – Biopsy Techniques.Exfoliative Cytology.

Sikri V, Sikri P. Community Dentistry. 2010. CBS Publishers.

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3. Educational Approach

• Dentist See harmful effectsCounsel child and youth patientsSpend more time with patientsTreat women of childbearing ageBuild patient’s interest in quittingSpeak with authority in community.

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• Danger signalsAny persistent scaly white patchAny lesion which increase in sizeNon healing ulcerNon healing extraction socketFacial asymmetryOral numbness or pain during jaw movements.

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• Guide to Counselling for tobacco cessation (5 A’s)Ask Advise AssessAssistArrange • Use of PharmacotherapyNicotine replacement therapyAntidepressants (Selegeline, Clonidine)

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• Counselling those unwilling to quit:-Relevance of quittingRisk of continuing tobacco useRewards of quittingRoadblocks to quittingRepeat these at each visit

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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.

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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

http://ocf.org.in/professional/IncidenceAndPrevalence.aspx/

http://ocf.org.in/professional/IncidenceAndPrevalence.aspx/

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http://www.iarc.fr/en/publications/list/bb/

• 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.

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• 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

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• 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.

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• 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.

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• 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

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• 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 mechanisms. Mutagenesis 2004;9(4):251-262

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Health & Medicine

Risk factors and prevention strategies of oral cancer