EPIDEMIOLOGY ,ETIOLOGY and

PREVENTION OF ORAL CANCER

ORAL CANCER

• Cancer that forms in tissues of the oral cavity (the mouth) or the oropharynx (the part of the throat at the back of the mouth). (NCI)

• Oral cancer and precancerous lesions are neoplastic conditions that are caused by local chemical or mechanical irritants or may be of unknown etiology.(WHO1987)

• Oral cancer is classified under the rubrics 140(lip),141(tongue),143(gingiva),144(floor of mouth)and145(other parts of mouth)

• According to the World Health Report 2004, cancer accounted for 7.1 million deaths in 2003, and it is estimated the overall number of new cases will rise by 50% in the next 20 years.

• Characteristics of cancer cells: Clonality

Autonomy

Anaplasia

Metastasis

• Oropharyngeal cancer is more common in developing than developed

countries.• 8th most common cancer worldwide

• Age: older age group(5th-6th decade)

• Sex: more common in men

• Incident rates Risk factors (47% of Indians aged 15yrs/> use tobacco in one form /other)

• An increased risk is seen in those who chew than those who smoke.

EPIDEMIOLOGY

Population based registered entries

Age adjusted incidence rates

MALES FEMALES

Tongue

Oral cavity

Tongue Oral cavity

Bangalore

3.5 - - 8.0

Barshi 2.2 2.4 0.6 0.9

Bhopal 8.8 7.3 - 5.1

Delhi 6.0 4.1 - -

Chennai 5.1 6.4 - 6.0

Mumbai 5.7 5.7 - 4.2

• Site: Lip cancer is most common in fair skinned races.• Intraoral- In western countries ,most commonly affects

the lateral borders of the tongue and the floor of the mouth, followed by the buccal mucosa, mandibular alveolus, retromolar region and soft palate.

• In the high-risk areas of south Asia, the buccal, retromolar and commissural mucosa are the most prone sites.

CANCER REGISTRATION IN INDIA

• Until 1964, no info on cancer occurrence in India• 1982- National Cancer Registry Program by Indian council

of medical research . # highlighting magnitude and common sites of cancer

in india # planing the National Cancer Control Program

CANCER REGISTRIES

Population based Hospital based

Bombay Chandigarh

Chennai Dibrugarh

Bhopal Trivandrum

New Delhi Bangalore

Bangalore Chennai

Barshi Mumbai

ETIOLOGY and RISK FACTORS

• multi factorial

Established Risk Factors Predisposing Factors

• Smoking tobacco Dietary deficiencies(vitamins A,

• Chewing tobacco/oral snuff C,Eand Fe)

• Chewing betel quid (paan), Faimilial or genetics especially if tobacco is included Viral infections

• Heavy consumption of alcohol Sunlight

• Precancerous lesion/condition immune suppression

Dental trauma

Host immunity Metabolis

mAngiogen

esis

Chronic inflamma

tion

Genetic susceptibi

lity

TOBACCO

DEVELOPED DEVELOPING0

100

200

300

400

500

600

700

MALESFEMALES

*WHO report on global consumption of tobacco (1U=1 million)

• most known etiological factor

• According to National Epidemiological survey of drug and alcohol conducted in 25 states in India (2002),55.8% of males aged 12-60yrs currently use tobacco.

• National Epidemiological Oral Health Survey and Fluoride Mapping of DCI (1994)- 23-24%,more males, across age groups reported smoking tobacco.

Tobacco Preparations

• Tobacco is derived from species of plant of genus Nicotina of potato family.

• Tobacco leaves flue-curing/fire-curing/sun-curing tobacco

• In india tobacco is used in various ways : Smoked tobacco - most popular, rural( Bidi-0.15g-0.25g coarsely

ground tobacco) Urban area ( Cigarette-1g finely cut

tobacco) Reverse smoking- smoked with lighted end inside mouth ,found

among females in Vishakapattanamand Srikakulam(AP) Temperature of palate-58⁰C ,it causes

palatal patches(0.12% malignant change)

Smoking habits in India

1) Bidi: 0.2-0.3g sundried tobacco flakes rolled in rectangular piece of temburni leaf. Nicotine content is 1.7-3mg and Tar is 45-50mg.2 ) Chillum : conical clay pipe used for smoking with coarsely cut

tobacco pieces and glowing charcoal3) Chutta(shruttu/cigar): cylindrical,cured tobacco wrapped in dried

tobacco leaf.4) Cigarettes: 1g suncured /artificially cured tobacco is covered with

paper and treated with sugars and flavoring agents.Nicotine content:1-1.4mg,Tar:19-27

mg5) Dhumti: rolled leaf of tobacco inside jackfruit leaf ,used in reverse

smoking 6)Gudakhu: paste of powdered tobacco,molasses and other

ingredients ( women ,Bihar)7) Hookah : tobacco smoke drawn in water in the base of hookah

( mughal culture )8) Hookli : clay pipe with mouth piece and bowl ( Gujarat )

Smokeless Tobacco

Paan chewing • most common• Uses:- aids digestion, appetite, strengthens gums, sweetens

breath, colors oral structure, alertness, induces euphoria and anti-helmenthic.

• Association of betel quid and oral cancer ( Balram, Trivandrum 1895)

Khaini• Sun-dried tobacco+slaked lime+arecanut ( Maharshtra)• Mixture placed in premolar region of mandibular groove Mainpuri tobacco • Tobacco + slaked lime + arecanut + camphor + cloves ( Uttar

Pradesh )• High prevalence of oral cancer and leukoplakia

Paan (alkaline)

pH alteration

Rough

oral mucosa

Discoloration

Lesion

Mawa• Arecanut +tobacco + slaked lime • Mixture is chewed as a ball and transferred to mandibular groove Mishri• Roasted tobacco +/- catechu Paan• Betel leaf +arecanut+ lime +catechu + cardamom + cinnamon +

coconut + cloves + sugar + tobacco wrapped in betel leaf Snuff• Air-cured and fire_cured tobacco leaves • Used orally / nasally • Bajar ( Gujarat )-twig is dipped and applied over tooth and gingiva Zarda• Colored residual tobacco leaf boiled with lime and spices

Gutka• Crushed beetel nut + tobacco + sweet flavourings Pan masala• Betel leaf + lime+ arecanut + clove + cardamom + mint +

tobacco

Constituents in Tobacco

• There are 43 known carcinogens in tobacco smoke

NICOTINE• Most toxic ( lethal dose -30-60mg)• It causes addiction by triggering dopamine that is associated with

feelings of pleasure • Physiological effects-increase HR,BP and platelet stickiness( CAD)• Carcinogenic activity :it enables formation of potent carcinogens

( nitrosamines)

TAR• Particulate matter inhaled • It condense to form sticky brown sub ( stain teeth ,fingers and

lungs tissues )• Organic(volatile/semi-volatile) + Inorganic (N2,O2,H2,CO2,CO)• Carcinogen –Benzopyrene (polycyclic aromatic compound )

CARBON MONOXIDE • Odorless , tasteless gas which interferes with uptake of O2 in

lungs and release from blood to tissues • Heavy smokers – O2 levels,15 %• CAD –myocardial oxygenation, increasing platelet stickiness,

atherosclerosis• Pregnant smokers – low weight babies due to decreased O2

NITROGEN OXIDE •Very high level •Initiate lung damage leading to emphysema

HYDROGEN CYANIDE •Direct deleterious effect on cilia in lung•Interferes with cleansing and accumulates toxins

METALS •30 metals (Ni,Cd,As,Cr,Pb)•Carcinogenic-arsenic , chromium,nickel,cadmium

RADIOACTIVE•Polonium-210 and potassium – 40•carcinogenic

Health consequences of tobacco use

• Delays oral wound healing • Promotes periodontal disease • Halitosis• Oral infections• Smoking – oropharyngeal cancer, cancer in esophagus ,stomach,

uterine cervix and lungs,cardiovascular disease,COPD,emphysem and chronic bronchitis

• Smokeless tobacco- oral and esophageal cancer ( paan)• exposure to non-smokers: respiratory infections ( women and

children )• Smoking is major risk factor for TB in India• Pregnant smokers –lower weight babies and infant with congenital

cleft lip / palate• Men-reduced fertility and sexual impotence

ALCOHOL

• Independent risk factor for oral cancer. • Synergestic effect Alcohol + Tobacco

Dehydrating effects of

alcohol

Increasing mucosal

permeability

Effects of carcinogen

s of tobacco

DIET and NUTRITION

• Plummer-Vinson syndrome , a manifestation of iron deficiency anemia attributes to carcinogenesis.

• Decreased levels of copper, zincand manganese deplete antioxidants increase tumor-enhancing free radicals

• Decreased levels of serum retinol • Ascorbic acid and Vit E prevents conversion of amines to

nitrosamines • Beta –carotene protects against cancer

( carrot,spinach,lettuce )• Red – chilli consumption increases cancer risk

OTHER FACTORS

Ultraviolet radiation :• Fair-skinned individuals are more susceptible• Imp etiology of scc of vermillion border of lip Fungal infection :• Hyphae of Candida albicans in outer epi layer in oral red and

white lesions and in oral cancer • They may be secondary invaders / risk factors • Dysplastic candidial lesions are more prone to transformation

to oral cancer Trauma and dental irritation • From jagged teeth and dentures • Poor oral hygiene

VIRAL and GENETIC FACTORS

Viruses:• Human herpes virus 1 may increase risk of oral cancer • Herpes simplex virus type 1 and HIV have been associated with

scc Genetic factors • Expression and stability of gene is affected • Loss of heterozygosity • Suppression of tumor suppressor genes : 3p (FHIT )

9p( CDKN2A )17p (TP53 )

PRECANCEROUS LESIONS and CONDITIONS

Definition Precancerous lesion 'a morphologically altered tissue in which cancer is more

likely to occur than in its apparently normal counterpart' -WHO 1978.

Precancerous condition 'the generalized state of the body, which is associated with a

significantly increased risk of cancer'- WHO 1978

LEUKOPLAKIA

Definition ‘ a predominantly white lesion of the oral mucosa that

cannot be characterized as any other definable lesion ;some oral leukoplakia will transform into cancer ‘ (Axell et al , 1996 )

• The global prevalence of leukoplakia has been reported to be about 2.6%

Etiology • Smoking• Spirits • Spices• Sharp tooth edge • Syphilis • Vit defeciency, endocrine disturbances • Virus • Blood grp A and active radiation • Related to fresh tobacco that contacts the oral mucosa

Site : buccal mucosa,commisures, tongue , alveolar mucosa ,floor of mouth , lips , gingiva , hard and soft palate

Clinical types a) Homogenous :white ,well demarcated plaque with an

identical reaction pattern throughout the entire lesion b) Non homogenous : may have patches / plaque intermixed

with red tissue elements .due to red and white areas it is also called erythroleukoplakia.

Precancerous nature : leukoplakia may be persistent ,regress spontaneously , recur/progress to oral cancer .

• Regression – 40% of cases• Malignant change – 1-20%• Lesion cracks, bleeds / erosion is present –malignant

ERYTHROPLAKIA

Definition ‘Lesions of oral mucosa that present as bright red velvety

patch which cannot be characterized clinically / pathologically as due to any condition’

• Global prevalence – 0.02-0.1%• It has been associated with reverse smoking

SMOKER’S PALATE

• Smoker’s palate / stomatitis nicotina is reaction of palatal mucosa

• Diffuse white palate numerous excrescenes having red dots , usually corresponding to minor salivary glands

• Global prevalence – 0.1-0.2%• Etiology : high temperature due to smoking

ORAL SUBMUCOUS FIBROSIS (OSMF )

• Precancerous condition • Global prevalence – 2.5 million individuals • in India – 5 % women + 2% men Etiology :• Betel nut • tobacco • Chillies• Nutritional deficiencies • Genetic susceptibility • Autoimmunity• Collagen disorders and blood grp A• Betel nut : constant irritant ,tannins ppt proteins and damage

mucosa ,phenol cause burning sensation, arecoline stimulate fibroblast proliferation and collagen synthesis

Clinical Aspects

• Characteristic : palpable fibrous bands • Site : buccal mucosa , retromolar areas and around rima oris tongue ( devoid of papillae and smooth ) • Trismus , tongue mobility reduces if affected • Initial symptoms : burning sensation aggravated by spicy food

followed by hyper salivation / dryness, blanching due to decreased vascularity

LICHEN PLANUS

Definition ‘Oral lichen planus is a chronic mucocutaneous condition in

which mucosal and skin manifestations occur independently ,concurrently / sequentially ‘

Etiology : cell-mediated ,immunologically induced destruction of basal cell layer of epithelium

Global prevalence : 0.5-2.2% GRINSPAN’S SYNDROME : predisposes to development of

scc Lichen planus

Diabetes

mellitus

Hypertension

Clinical Aspects

• Keratotic white lines that cannot be eliminated by stretching/ rubbing

Site : most – buccal mucosa Symptoms : burning sensation with pain / asymptomatic Histologic types :1. Reticular : common ,criss-crossing white striae giving white

lacey like appearance 2. Papular : initial ,small white dots, which intermingle to form

reticular type3. Plaque-like: homo well-demarcated white plaque which may /

may not be surrounded by striae 4. Erythematous : homo red area 5. Ulcerative : disabling form , ulcers surrounded by

erythematous zone displaying white striae, may have burning sensation on food intake

SQUAMOUS CELL CARCINOMA

• Can occur as carcinoma of lip , mouth , floor of mouth , buccal mucosa , gingiva , palate , maxilary sinus

Clinical features : it appears as red , white / mixed lesion , a change in surface texture / presence of mass / ulceration

• Lesion – flat / elevated / ulcerated / non ulcerated and minimally palpable / indurated

• Loss of function involving tongue – speech, swallowing and diet • Lymphatic spread –submandibular and digastric nodes , upper

cervical and remaining nodes of cervical chain

TNM SYSTEM OF TUMOR STAGING

• Anatomical extent of cancer is determined T- Size of primary tumor N-Status of cervical nodes M-Presence / absence of metastasis T — Primary tumour

TX Primary tumour cannot be assessed T0 No evidence of primary tumour Tis Carcinoma in situ T1 Tumour 2 cm or less in greatest dimension T2 Tumour more than 2 cm but not more than 4 cm in greatest dimension T3 Tumour more than 4 cm in greatest dimension T4a (lip) Tumour invades through cortical bone, inferior alveolar nerve,

floor of mouth, or skin (chin or nose) T4a (oral cavity) Tumour invades through cortical bone, into deep/extrinsic

muscle of tongue (genioglossus, hyoglossus, palatoglossus, and styloglossus), maxillary sinus, or skin of face

T4b (lip and oral cavity) Tumour invades masticator space, pterygoid plates, or skull base; or encases internal carotid artery

• N - Regional Lymph NodesNX Regional lymph nodes cannot be assessedN0 No regional lymph node metastasisN1 Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest dimensionN2 Metastasis as specified in N2a, 2b, 2c below N2a Metastasis in a single ipsilateral lymph node, more than 3 cm but not more than 6 cm in greatest dimension N2b Metastasis in multiple ipsilateral lymph nodes, none more than 6 cm in greatest dimensionN2c Metastasis in bilateral or contralateral lymph nodes, none more than 6 cm in greatest dimensionN3 Metastasis in a lymph node more than 6 cm in greatest dimension

• M – Distant metastasisMX Distant metastasis cannot be assessedM0 No distant metastasisM1 Distant metastasis

Stage 0 Tis N0 M0

Stage I T1 N0 M0

Stage II T2 N0 M0

Stage III T1, T2 N1 M0

T3 N0, N1 M0

Stage IVA T1, T2, T3 N2 M0

T4a N0, N1, N2 M0

Stage IVB Any T N3 M0

T4b Any N M0

Stage IVC Any T Any N M1

Stage Grouping

DIAGNOSTIC METHODS

Vital staining • Toluidine blue (TB) staining- simple ,inexpensive • uses a blue dye - highlight abnormal areas of mucosa. • TB - metachromatic nuclear stain( stains nuclear material of

malignant lesions but not normal mucosa) • method (a) the patient rinsing the mouth with 1% acetic acid for 20

seconds followed by a similar rinse with water twice for 20 seconds

(b) rinsing the mouth with 5-10 cc. 1% toluidine blue solution; and

(c) rinsing with 1% acetic acid solution (5 oz.) for about 1 minute followed by a water rinse.

• TB -higher sensitivity to detect carcinoma in situ (CIS) and OSCC

False- 8-10% of cases associated with keratotic lesions and the regenerating edges of ulcers and erosions.

• clinical appearance -the nuclear uptake of TB, related to genetic changes molecular changes of early carcinogenesis.

Biomarkers • molecular markers -TSG p53 protein expression, chromosomal

polysomy (DNA ploidy) and changes ( loss of heterozygozity) in chromosomes

• available markers-cell proliferation (Ki-67 antigen)and apoptosis (Bax, Bcl-2 :decreases significantly in dysplastic and early invasive lesions )

• Ki-67 expression: increases sharply in initial stages of OSCC, but significantly decreases in later

• aggressive tumor behavior and worse prognosis : E-cadherin expression,54,55 laminin and decreased tumor cell transmembrane proteo- glycan syndecan-1.5

DNA ploidy • measurement of nuclear DNA content. • measure of gross genetic damage • Aneuploidy –cancers.• Measured with automated image cytometry of nuclei obtained

from routinely processed tissue samples

Brush biopsy• uses a small nylon brush to gather cytology samples then sent

for computer scanning and analysis (Oral CDx) to identify and display individual cells

• abnormal cells from the computer display followed with a conventional incisional biopsy.

• Controversial: false negative results Optical systems • Interaction of light -changes in tissue structure and

metabolism. • Optical spectroscopy- detect changes about the histological

and biochemical characteristics of tissue.• identification of cellular and molecular abnormalities• Early detection -use of a dilute acetic acid rinse and

observation under a chemi- luminescent light • enhanced by the use of fluorescence.

Saliva-based oral cancer diagnostics• Exfoliative cell samples -to detect genetic alterations in the

oral epithelium ,to detect microsatellite alterations• Promoter hypermethylation patterns of TSG p16, O6-

methylguanine-DNA-methyltransferase and death-associated protein kinase

• messenger ribo-nucleic acid (mRNA) testing from saliva• Salivary soluble CD44 (solCD44) levels were found significantly

raised in cancer• High salivary counts - Capnocytophaga gingivalis,Prevotella

melaninogenica and Streptococcus mitis have been found in patients with OSCC

Biopsy CT scan / ultrasound / MRI

Other potential future diagnostic technologies• Laser-induced fluorescence spectroscopy • Light-induced fluorescence spectroscopy • Elastic scattering spectroscopy• Raman spectroscopy • Photoacoustic imaging • Photon fluorescence • Orthogonal polarization spectral (OPS) imaging• Quantum dots Optical coherence tomography (OCT)• Trimodal spectroscopy Doppler • Nuclear magnetic resonance spectroscopy • Chromoendoscopy • Narrow band imaging (NBI• Immunophotodiagnostic techniques

TREATMENT OF ORAL CANCER

Surgery• Surgery (including the use of lasers) involves removing just

the affected tissue. • Surgery is sometimes followed by chemotherapy or

radiotherapy treatment Non-surgical treatments• Radiotherapy• Chemotherapy - anti-cancer drugs are used to destroy cancer

cells• Biological therapy - special manufactured monoclonal

antibodies (cetuximab) are used to block areas on the surface of cancer cells that can trigger growth.

PREVENTION and CONTROL OF ORAL CANCER

LEVELS OF PREVENTI

ON

PRIMARY SECONDARY TERTIARY

PREVENTIVE SERVICES

Health promotion

Specific protection

Early diagnosis and treatment

Disability limitation

Rehabilitation

SERVICES PROVIDED

BY INDIVIDUAL

-Periodic visits to

dental clinic-Demand for preventive measures

Avoidance of known irritants

-Self examination and referral

-Utilization of dental services

Utilization of dental services

Utilization of dental services

SERVICES PROVIDED

BY THE DENTAL

COMMUNITY

-Dental health

education programs -Promotion of research

efforts -Lobby efforts

Avoidance of known irritants

-Periodic screening and referral

-Provision of dental services

Provision of dental

services

Provision of dental

services

SERVICES PROVIDED BY DENTAL PROFESSIO

NAL

Patient education

Removal of known

irritants

-complete examination -Biopsy-Complete excision

Chemotherapy-Radiotherapy-Surgery

prosthodontics-plastic surgery -speech therapy

TALUK HOSPITAL/

SUB DISTRICT HOSPITAL

Health Promotion/H

ome Care/Early

Detection/Pain

Relief/Palliative Care

DISTRICT HOSPITAL

Health Promotion/Home Care/

Early Detection/Pa

in Relief/Palliative

Care/Treatment of

common cancers

MEDICAL COLLEGE HOSPITAL

Health Promotion/H

ome Care/Early Detection/

Pain Relief/Palliati

ve Care/Treatment of

common cancers/Training ofmedical

officers/paramedical

personnel

REGIONAL CANCER CENTREHealth

Promotion/Home

Care/Early Detection/Pa

inRelief/

Palliative Care/Compr

ehensive Cancer

treatment/Organise screening

programmes/Cytology training/

Basic and applied

research/Training of all

categories ofpersonnel/

Cancer Registries/Epidemiology

The Crete Declaration on Oral Cancer Prevention 2005

• 10th International Congress on Oral Cancer which took place 19-24 April 2005 in Crete, Greece

• initiative to analyse the evidence on oral cancer and the implications for prevention and public health programmes.

• 57 countries emphasized that oral health is an integral part of general health and wellbeing.

• neglected burden of oral cancer -developing countries with low availability of prevention programmes and services for oral health.

• In particular, the following areas of work should be strengthened:

provision of systematic epidemiological information on prevalences of oral cancer and cancer risks in countries, particularly in the developing world.

promotion of research into understanding biological, behavioural and psychosocial factors in oral cancer, emphasizing the inter-relationship between oral health and general health

integrating oral cancer information into national health surveillance systems which record chronic diseases and common risk factors

dissemination of information on oral cancer, prevention and care through every possible means of communication

active involvement of oral health professionals in oral cancer prevention through control of risk factors such as tobacco, alcohol and diet

training of primary health workers in screening and provision of first-level care in oral cancer

access to health facilities and provision of systems for early detection and intervention, oral health care and health promotion for the improvement of quality of life of people affected by oral cancer.

The participants support the efforts of the WHO Oral Health Programme aiming at coordination and inter-country sharing of experiences in prevention and oral health care of people affected by oral cancer.

WHO Framework Convention On Tobacco C ontrol

For the purposes of this Convention:(a) “illicit trade” means any practice or conduct prohibited by law and

which relates to production, shipment, receipt, possession, distribution, sale or purchase including any practice or conduct intended to facilitate such activity;

(b) “regional economic integration organization” means an organization that is composed of several sovereign states, and to which its Member States have transferred competence over a range of matters, including the authority to make decisions binding on its Member States in respect of those matters

(c) “tobacco advertising and promotion” means any form of commercial communication, recommendation or action with the aim, effect or likely effect of promoting a tobacco product or tobacco use either directly or indirectly;

(d) “tobacco control” means a range of supply, demand and harm reduction strategies that aim to improve the health of a population by eliminating or reducing their consumption of tobacco products and exposure to tobacco smoke;

(e) “tobacco industry” means tobacco manufacturers, wholesale distributors and importers of tobacco products

1

(f) “tobacco products” means products entirely or partly made of the leaf tobacco as raw material which are manufactured to be used for smoking, sucking, chewing or snuffing;

(g) “tobacco sponsorship” means any form of contribution to any event, activity or individual with the aim, effect or likely effect of promoting a tobacco product or tobacco use either directly or indirectly;

Bloomberg Initiative to reduce tobacco use

• Campaign for Tobacco-Free Kids Grants management and advocacy/legal assistance.

• Centers for Disease Control and Prevention (CDC) Foundation Monitoring/surveillance.

• Johns Hopkins Bloomberg School of Public Health Education/training.

• World Health Organization - Tobacco Free Initiative (WHO/TFI) Coordination mechanism at country level

• World Lung Foundation (WLF) Grants management, global clearing house for tobacco ads.

PUBLIC HEALTH APPROACHES TO PREVENTION OF ORAL CANCER

Build Healthy Public Policy• Tighten restriction on tobacco and alcohol advertizing and

promotion• Subsidize the cost of healthier choices. e.g. fruits and

vegetables.• Improve labeling on betel quid products. Create Supportive Environment• Smoke free public spaces, e.g. cinemas• Increase availability of fresh fruits and vegetables [in school

canteen and tuck-shop]. Develop Personal Skills• Expand personal and social education in schools-life skills:

empowerment, refusal and negotiation skills. etc.• Incorporate tobacco and alcohol control within health

promoting schools.• Reorient Health Services• Expand health professionals education and training in smoking

cessation and alcohol control

• Increase numbers and range of health promotion professional, with expertize in smoking and alcohol support.

• Establish evidence-based smoking and alcohol preventive services with primary care setting

TOBACCO/SMOKING CESSATION The first step in treating tobacco use and dependence is to

identify tobacco users. Screening for current or past tobacco use will result in tour possible responses:

1. The patient uses tobacco and is now willing to make a quit attempt.

2. The patient uses tobacco but is not now willing to make a quit attempt.

3. The patient once used tobacco but has since quit. 4. The patient never regularly used tobacco.

FOR THE PATIENT WILLING TO QUIT • Given that so many tobacco users visit a dentist each year, it is

important that these dentist be prepared to intervene with tobacco users who are willing to quit. The five major steps (the "5 As") to intervention are [The SA approach]:

Ask Identify and document tobacco user about patient's habits Advice of consequence of smoking Assess willingness to quit Assist with cessation plant development Arrange for follow-up

FOR PATIENTS NOT WILLING TO QUIT (5 R method ) 1. Relevance: Provide information that has the greatest impact on the

patient’s disease status, family or social situation (e.g., children and second-hand smoke), health concerns, age or gender.2. Risks:Acute risks: shortness of breath, exacerbation of asthma, harm to pregnancy, impotence, infertility, increased blood carbon monoxide, bacterial pneumonia; increased risk for surgeryLong-term risks: heart attacks, strokes, lung and other cancers, chronic obstructive pulmonary diseases, long-term disability and need for extended careEnvironmental risks: increased risks of lung cancer and heart disease in spouses; higher rate of smoking by children of tobacco users; increased risk of low birth weight babies, SIDS, asthma, middle ear disease, and respiratory infections in children of smokers

3. Rewards: Highlight benefits most relevant to the patient, such as

better health, improved sense of taste and smell, money saved, good example for children, more physically fit, and reduced wrinkling and aging of skin.4. Roadblocks:

Ask the patient to identify barriers to quitting, such as withdrawal symptoms, fear of failure, weight gain, lack of support and depression. Note elements of cessation treatment, such as problem solving or pharmacotherapy.5. Repetition:

Repeat the motivational intervention each time the patient has an office visit. Let the patient know that most people make repeated attempts to quit before they are finally successful.

CONCLUSION

‘ No tobacco day ‘ is observed on 31st May to highlight the adverse effect of tobacco on health .It has been estimated that a majority of cancer death worldwide are due to tobacco.

Oral cancer is easily accessible for diagnosis . These factors coupled with finding that oral cancer is generally preceded by precancerous lesions provides an excellent opportunity for early detection and control