Epidemiology of oral cancer

Epidemiology of oral cancer

• 1.
  EPIDEMIOLOGY OF Dept. Of PublicHealth Dentistry PCDS & RC
• 2.
  LEARNING OBJECTIVES ▸ Globalscenario of oral cancer ▸ Spectrum of oral cancer in India ▸ Distribution and Measurement of Oral Cancer ▸ Trends ▸ Etiology and risk factors ▸ Classification of oral cancers ▸ Clinical presentations ▸ Diagnosis ▸ Treatment ▸ Prevention and Control ▸ Role of dentist
• 3.
  Oral Cancer, AlsoKnown As Mouth Cancer, Is A Type Of Head And Neck Cancer And Is Any Cancerous Tissue Growth Located In The Oral Cavity. Wikipedia
• 4.
  AN INTERMEDIATE CLINICALSTATE WITH INCREASED CANCER RISK, WHICH CAN BE RECOGNIZED AND TREATED, OBVIOUSLY WITH A MUCH BETTER PROGNOSIS THAN A FULL BLOWN MALIGNANCY. ORAL PRECANCER
• 5.
  DEFINITION 4 CHARACTERISTICS ▸ CLONALITY: Cancer originates from genetic changes in single cell which proliferates to form a clone of malignant cells. ▸ AUTONOMY : Growth is not properly regulated by the normal biochemical and physical influences in environment. ▸ ANAPLASIA : There is a lack of normal, co-ordinated cell differentiation. ▸ METASTASIS : Cancer cells develop capacity for discontinuous growth and dissemination to other parts of body.
• 6.
  GLOBAL SCENARIO :CANCER ▸ Developed countries : SECOND Most common cause of death. ▸ Acc. to WHO report 2004- cancer accounted for 7.1 million deaths. ▸ Highest among Men.
• 7.
  TEXT ▸ 6th Mostcommon cause of cancer related death. ▸ 1-10 cases per 1,00,000 population. ▸ TONGUE - most common intra oral site. •Denmark, France, Germany, •Scotland, central and eastern Europe GLOBAL SCENARIO : ORAL CANCER
• 8.
  TEXTSPECTRUM OF ORALCANCER IN INDIA ▸ HIGHEST incidence of oral cancer in world. ▸ 12% of all cancers in Men. ▸ 8% of all cancers in Women. ▸ Half million cases of cancer added every year. ▸ Of these 1/3rd is Oral Cancer = 5 lakh cases at a given time. ▸ Linked with tobacco habit.
• 9.
  HEAD AND NECKCANCERS
• 10.
  ICD-9 : 140-149 ICD-10: C00-C14 International Classification of Disease system of WHO.
• 11.
  EPIDEMIOLOGICAL TRIAD OFORAL CANCER
• 12.
  1. Gender :Males > Women 2. Age
 mean age of occurrence : 50-70years 3. Race
 Increased incidence in chinese ancestry, American blacks. 4. Genetic characteristics
 genetic mutations 3q, 4q, 6q, 8q, 11q, 18q in asso with tobacco use. 5. Socio economic status
 affects those with Lower SES. 6. Education
 lower education attainment - greater risk. 7. Occupation
 exposure to carcinogens - leather industry, oil, textiles, coal mines. 8. Lifestyle
 vitamin deficiencies, Tobacco users - greater risk
• 13.
  1. BIOLOGICAL FACTORS humanpapilloma virus - associated with cancers 2. CHEMICAL Habit of tobacco with lime bhopal gas tragedy - exposure to methyl isocyanate (carcinogen) 3. MECHANICAL chronic irritation of mucosa - sharp cusps of teeth, ill fitting dentures.
• 14.
  1. UV RADIATION -Solar radiation is carcinogenic - skin cancers (basal cell carcinoma, SCC). - Lower lip affected due to sunlight exposure.
• 15.
  TEXT DISTRIBUTION OFORAL CANCER ▸ Incidence increases with age. ▸ With advancing age, certain sequenced alterations in biochemical/biophysical processes of aging cells with a particular aging predisposition undergo and accumulate mutations, resulting in carcinogenic transformations. ▸ 96% oral cancer is diagnosed in persons >40years. ▸ 50% oral cancer is diagnosed in persons >65years. ▸ Average age at time of diagnosis : 63 years. ▸ Recent evidence : frequent occurrence in younger persons. AGE DISTRIBUTION
• 16.
  TEXT DISTRIBUTION OFORAL CANCER ▸ In industrialized countries MEN are affected twice as women. (Due to high risk factors- tobacco, alcohol, sunlight.) ▸ Incidence of Tongue cancer : Women > Men ▸ Ratio of Male to Female diagnosed with oral cancer is 2:1. GENDER DISTRIBUTION
• 17.
  TEXT DISTRIBUTION OFORAL CANCER ▸ Strong influences due to social and cultural practices. ▸ Continuation by immigrants from high- incidence regions to other parts results in high cancer incidence in immigrant communities. ▸ Black Americans experience more pharyngeal cancers than their white counterparts. ETHNIC VARIATIONS
• 18.
  DISTRIBUTION OF ORALCANCER ▸ Lip cancer - more common in fair skinned races, particularly in rural areas and in men who work outdoors. ▸ Intraoral cancers in Western countries - Lateral borders of tongue and floor of mouth. ▸ Hard palate and dorsum of tongue - lowest risk. ▸ In high risk areas of South Asia - Buccal, Retromolar and commissural mucosae are most prone. SITE DISTRIBUTION
• 19.
  TRENDS ▸ In urbanparts of high incidence regions, such as 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, combined with smokeless tobacco products.
• 20.
  ETIOLOGY AND RISKFACTORS
• 21.
  Multifactorial Etiology ESTABLISHED RISKFACTORS 1. Smoking Tobacco 2. Chewing Tobacco 3. Chewing betel quid (paan) 4. Heavy consumption of alcohol 5. Presence of a potentially malignant oral lesion OTHER CONTRIBUTORY OR PREDISPOSING FACTORS 1. Dietary deficiency (vit A, C, E, iron) 2. Familial or genetic predisposition 3. Virus infections (Human papilloma virus) 4. Sunlight (lip cancer) 5. Candida albicans infection 6. Immune deficiency 7. Environmental exposure 8. Dental trauma
• 22.
  TOBACCO HISTORY : Christopher Columbus- a gift of strange dry leaves. India - pipe called tobago was placed in nostrils 1st Commercial plantation in USA - Virginia 1612. 19-20th century : dental snuff was said to relieve toothache, bleeding gums, preserve and whiten teeth and prevent decay. 40-45% of smokers (Males) - Bidi, In urban areas - Cigarretes. 9% in rural areas - chewing tobacco Orissa HIGHEST. 31% of tobacco grown in India is used for manufacture of cigarretes. “REVERSE SMOKING” - Females in AP - Air is supplied to burning zone through unlighted end of cigarrete.
• 23.
  TOBACCO PREPARATIONS PLANT- NICOTIANA SMOKED TOBACCO 1. Bidi : 0.2-0.3gm of sundried tobacco flakes are hand rolled in a rectangular piece of temburni/tendu. Nicotine content : 1.7-3mg, tar : 45-50mg. 2. Chillum : long conical clay pipe used for smoking tobacco. 3. Chutta/Cigar : cylindrical coarsest prepared cheroot with cured tobacco. 4. Cigarretes : 1gm of cured tobacco covered with paper. Flavored, aromatic. Nicotine : 1-1.4mg, Tar : 19-27mg. Filter Length= 12mm 5. Dhumti : Rolled leaf tobacco is used inside leaf of jackfruit tree. Used for Reverse smoking. 6. Hookah : (water pipe) Used in places with strong Moghul cultural influence. 7. Hookli : clay pipe SMOKELESS TOBACCO 1. Khaini :powdered sundried tobacco, slaked lime -paste mixture used with arecanut. 2. Mainpuri tobacco : tobacco, slaked lime, arecanut, camphor, cloves. Prevalent in U.P. High prevalence of oral cancer, leukoplakia. 3. Mawa: thin shavings of arecanut, tobacco, slaked lime wrapped in cellophane paper. 4. Mishri : roasting tobacco on hot metal plate. Used with catechu. 5. Paan : betel leaf. 6. Snuff 7. Zarda 8. Gutka 9. Pan Masala 10. Gudakhu
• 24.
  CONSTITUENTS OF TOBACCO ‣NICOTINE : most toxic of all poisons. Addictive effect is due to its capacity to trigger release of Dopamine - asso. with feeling of pleasure. It enables formation of tobacco specific Nitrosamines - potent carcinogens. ‣ TAR : The particulate matter inhaled while smoking. Sticky brown substance. Benzopyrene -a carcinogen is found in tar. ‣ CARBON MONOXIDE : interferes with uptake of oxygen by lungs. Devt. of Coronary heart disease. ‣ NITROGEN OXIDES : lung damage - emphysema ‣ HYDROGEN CYANIDE : deleterious effect on lungs ‣ METALS : Ni, As. Cd, Cr, Pb - asso. with cancer ‣ RADIOACTIVE COMPOUNDS : Polonium-210, Potassium-40 : Carcinogens
• 25.
  HEALTH CONSEQUENCES OFTOBACCO ‣ Major contributor to oral disease. Slows wound healing, promoted periodontal disease, halitosis, oral infections. ‣ Cancer of oral cavity, pharynx, larynx, esophagus, stomach, uterine cervix, lungs. ‣ Cardiovascular disease ‣ Chronic obstructive lung disease, emphysema, chronic bronchitis. ‣ Second hand smoke - Worsening of asthma, poor lung funtion. ‣ Major risk factor for TB ‣ Pregnant women exposed to smoke may deliver lower weight babies, stillborn babies, congenital cleft lip and palate, ‣ Men - reduced fertility and sexual impotence.
• 26.
  FAMILIAL AND GENETICPREDISPOSITION IMMUNOSUPPRESSION ‣ Polymorphisms in GST genes, CYP genes, Cytochrome P-450 system. ‣ Genetic predisposition is small. ‣ Individuals with HIV/AIDS are at higher risk of neoplasms ‣ Kaposi’s Sarcoma ‣ Lymphomas ‣ Oral hairy leukoplakia
• 27.
  OCCUPATION AND RISKOF ORAL CANCER ‣ EFFECT OF SOLAR RADIATION ‣ Outdoor workers are at greater risk for LIP cancer. ‣ Due to long term exposure to UV light ‣ EFFECT OF ATMOSPHERIC POLLUTION ‣ Mean sulphur dioxide and smoke concentration are positively correlated with SCC of larynx. ‣ Fossil-fuel combustion - pharyngeal cancers
• 28.
  VIRUSES AND ORALCANCER ‣ 15% of human cancers may have etiological relationship to viral infections. ‣ Human Papilloma Viruses (HPV) - high oncogenic risk. ‣ HPV-6,11,16 - Papilloma, Leukoplakia ‣ HPV- 16, 18, 6, 2, 57 - SCC. ‣ Ebstein Barr Virus (EBV) - Nasopharyngeal CA, Lymphomas ‣ HHV-8: Kaposi’s Sarcoma. ‣ DNA oncogenic virus is SV40.
• 29.
  CLASSIFICATION OF ORAL CANCER
• 30.
  TEXTACCORDING TO SITE ▸ALVEOBUCCAL SULCUS : Most common. More in Men. Asso. with quid placement. ▸ LIP : in elderly men. Lower lip>upper lip ▸ TONGUE : 25-50% of all oral cancers. ▸ GINGIVA : Chronic irritation is a suspected cause. ▸ FLOOR OF MOUTH : 15% of oral cancers. Pipe/cigar smoking. ▸ PALATE : Not very common. Seen with reverse smoking.
• 31.
  TEXT BENIGN ANDMALIGNANT •Benign tumours of epithelial origin •Papilloma •Squamous acanthoma •Keratoacanthoma •Pigmented cellular naevus •Premalignant lesions & conditions of epithelial origin •Leucoplakia •Erythroplakia •Oral submucous fibrosis •Lichen planus •Malignant tumors of epithelial tissue origin •Basal cell carcinoma •Adenoid squamous cell carcinoma •Malignant melanoma ‣ Begin tumors of connective tissue origin •Fibroma •Peripheral ossifying fibroma •Haemangioma •Lymphangioma •Chondroma •Osteoma ‣ Malignant tumors of connective tissue origin • Fibrosarcoma • Chondrosarcoma • Ewing's sarcoma • Osteosarcoma • Malignant lymphoma • Hodgkin's disease
• 32.
  TEXT CLINICAL PRESENTATIONSOF ORAL CANCER ▸ More than 90% of oral cancers are Squamous Cell CA. ▸ 10% are salivary gland tumors, lymphomas, sarcoma etc. ‣ ULCER : any ulcer of mucosa, that fails to heal within 2 weeks. ‣ INDURATION ‣ FUNGATION : growth of tissues to produce elevated cauliflower surface or lump. ‣ FIXATION of mucosa to underlying tissues. ‣ TOOTH mobility with no apparent reason. ‣ PAIN/PARAESTHESIA with no apparent cause. ‣ DYSPHAGIA ‣ WHITE/RED PATCHES of mucosa ‣ LYMPHADENOPATHY
• 33.
  TEXT PRECANCEROUS ▸ PRECANCEROUSLESIONS : ▸ Leukoplakia ▸ Erythroplakia ▸ Smoker’s Palate ▸ PRECANCEROUS CONDITIONS : ▸ OSMF ▸ Lichen Planus
• 34.
  TNM STAGING
• 35.
  DIAGNOSIS OF ORALCANCER‣ BIOPSY ‣ EXFOLIATIVE CYTOLOGY ‣ TOLUIDINE BLUE STAINING ‣ COMPUTED TOMOGRAPHY SCAN ‣ ULTRASOUND ‣ MAGNETIC RESONANCE IMAGING
• 36.
  TREATMENT OF ORALCANCER ‣ PREVENTION AND CONTROL OF CANCER - HEALTH EDUCATION ‣ SECONDARY PREVENTION ‣ TERTIARY PREVENTION
• 37.
  TEXT PRIMARY PREVENTION ▸Mainly focuses on Modifying Habits. ▸ Educational programs, warning signals, importance of checkup, oral hygiene, diet etc. ▸ 3 well known approaches : ▸ REGULATORY APPROACH ▸ SERVICE APPROACH ▸ EDUCATIONAL APPROACH
• 38.
  TEXT ▸ Cigarette Act1975 has made it necessary to print warnings on cigarette packets. ▸ National Cancer Control Program 1985 ▸ 2003 - ‘Cigarette and other Tobacco products Act’ - prohibit advertisement for regulation of trade. REGULATORY APPROACH SERVICE APPROACH ▸ Active search for disease among apparently healthy people is a fundamental aspect of prevention. ▸ This is embodied in screening.
• 39.
  TEXT EDUCATIONAL APPROACH ▸Hold a vital role in prevention and early detection of cases. ▸ Screening and examination are elements of dental practice routine. ▸ Dentists are in ideal position to counsel patients. ▸ Influence to adopt a tobacco free lifestyle. ▸ Can speak with authority in the community. ▸ Can be effective advocates for tobacco control in community. ROLE OF DENTIST
• 40.
  TEXT TOBACCO INTERVENTION GUIDELINESFOR TOBACCO CESSATION : 5 A’s ▸ ASK 
 Check for oral sign to know if patient is using tobacco. ▸ ADVISE
 Advise to stay away, affirm non-use, congratulate those who quit. ▸ ASSESS
 patients readiness to quit. Assess level of dependence. ▸ ASSIST
 Set a firm quit date, support from family and friends, reduce tobacco, anticipate challenges. ▸ ARRANGE
 for follow ups. Revisits, telephone contact etc.
• 41.
  TEXT PHARMACOTHERAPY ▸ NICOTINE REPLACEMENTTHERAPIES (NRTs)
 Nicotine Gum
 Nicotine Patch
 Nicotine Inhaler
 Nicotine Nasal Spray
 Nicotine Lozenges ▸ ANTIDEPRESSANTS
 Buproprion SR
 Selegeline
 Clonidine
 Nortryptiline
• 42.
  TEXT COUNSELLING THOSE UNWILLINGTO QUIT : 5 R’s ▸ Relevance of quitting ▸ Risks of continuing tobacco ▸ Rewards of quitting ▸ Roadblocks to quitting ▸ Repeat these at each visit
• 43.
  TEXT ▸ SCREENING ▸ EARLYDETECTION AND REFERRAL ▸ Community level early detection programs by primary health care givers should be taken to detect precancerous lesions and to educate them against tobacco use. SECONDARY PREVENTION
• 44.
  TEXT ▸ SURGERY ▸ RADIOTHERAPY ▸CHEMOTHERAPY TERTIARY PREVENTION
• 45.
  TEXT CONCLUSION ▸ Dentistand other health personnel have a responsibility to assist patients in minimizing risk factors, through effective health education. ▸ Oral cancer can be reasonably detected and diagnosed in early stages through a 5 min thorough examination. • National - international health authorities, research institutions, non-governmental organizations and civil society to strengthen their efforts for the effective control and prevention of oral cancer.
• 46.
  TEXT Thank you Dr. AashnaDhingra PG Dept. of Public Health Dentistry