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Epidemiology of oral diseases
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Epidemiology of oral diseases

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  • 1. Epidemiology of ORAL CANCER Epidemilogy of MALOCCLUSION Epidemiology of PERIODONTAL DISEASE Epidemiology of DENTAL CARIES
  • 2.  DEFINITION: It is defined as an indurated or ulcerated sore which may or may not be painful and is often associated with cervical lymph adenopathy EPIDEMIOLOGY OF ORAL CANCER
  • 3. EPIDEMIOLOGY 1. GEOGRAPHIC VARIATIONS: In industrialized countries 3-5% In highly developing countries 40% 2. SEX: More common in males
  • 4. 3. AGE: Usually occurs in 6th decade of life 4. SITES OF ORAL CANCER: Lateral border of tongue Labial commissure Buccal mucosa Undersurface of tonge
  • 5. HOST FACTORS 1. AGE: older age shows increased risk of CARCINOMA younger age shows increased risk ok SARCOMA 2. RACE: lip melanoma in more common in whites whereas certain odontogenic tumors are more common in blacks EPIDEMIOLOGICAL TRIAD
  • 6. 3. SEX: In females cancer of lip is common In males cancer of buccal mucosa and tongue is common 4. GENETIC FACTORS: discovery of oncogenes made it possible to identify the possible genetic and environmental factors associated with the initiation and progression on malignant tumors 5. OCCUPATION: male textile workers show increased risk of cancer of buccal cavity , larynx and pharynx.
  • 7. 6. IMMUNITY: kaposi sarcoma is more common in AIDS patient 7. SOCIAL CLASS: low income groups show increase in cancer of oral cavity 8. CUSTOMS AND HABITS: tobacco chewing, pan chewing, spicy food increases the rate of cancer of floor of mouth and buccal mucosa. Alcohol consumption also increases the chance for cancer.
  • 8. 1. BIOLOGICAL: virus (HIV,HSV) Fungus (candida) 2. CHEMICAL: arsenic, dyes, nickel, aromatic amines, chromium 3. MECHANICAL: sharp tooth, ill fitting dentures AGENT FACTORS
  • 9. 4. NUTRITIONAL: precarcinogens in food, increased consumption of fat, deficiency of folic acid, protein deficiency
  • 10. 1. WATER CONTAMINANTS: chloroform 2. AIR POLLUTION: carbon dioxide 3. GEOGRAPHIC VARIATIONS: in Netherlands buccal mucosa is most commonly affected In Switzerland lip, tongue are the sites most affected ENVIRONMENTAL FACTORS
  • 11. 4. SOLAR HEAT: prolonged exposure to sunlight causes melanoma 5. INDUSTRIALIZATION: the release of various toxins by the industries contaminates water and air which may lead to cancer
  • 12. SEQUELEA OF MALOCCLUSION Poor facial appearance Risk of caries Predisposition to periodontal disease Psychological disturbances Risk of trauma Abnormalities of function TMJ problems EPIDEMIOLOGY OF MALOCCLUSION
  • 13. EPIDEMIOLOGY Prevalence of malocclusion is estimated to be higher in developed countries as compared to developing and under developed countries Malocclusion percentage is relatively low in deciduous dentition. Incidence of normal occlusion in deciduous dentition in 51%; mixed 40%; permanent dentition 30%
  • 14. GRABERS CLASSIFICATION General factors: 1. Heredity 2. Congenital 3. Environmental (a) pre-natal (trauma, maternal diet, German measels, maternal metabolism) ETIOLOGY
  • 15. (b) Post natal ( birth injury, cerebral palsy, TMJ injury) 4. Predisposing metabolic climate and disease 1. Endocrine imbalance 2. metabolic disturbances 3. Infectious disease 5. Abnormal pressure habits and functional aberrations 1. Abnormal sucking
  • 16. (b) Thumb and finger sucking (c) Tongue thrust and tongue sucking (d) Lip and nail biting (e) Improper deglutition (f) Speech defects (g) Respiratory abnormalities (h) Tonsils and adenoids 1. Bruxism
  • 17. 7. Posture 8. Trauma and accidents LOCAL FACTORS 1. anomalies of tooth number 2. Amomalies of tooth size 3. Anomalies of tooth shape 4. Abnormal labial frenulum 5. Premature loss
  • 18. 6. Prolonged retention 7. Delayed eruption of permanent teeth 8. Abnormal eruptive path 9. Ankylosis 10. Dental caries 11. Improper dental restorations
  • 19. PERIODONTAL DISEASE IS A TERM, WHICH INCLUDES ALL PATHOLOGICAL CONDITIONS OF PERIODONTIUM i.e: GINGIVA, ALVEOLAR BONE,CEMENTUM AND PERIODONTAL LIGAMENT. EPIDEMIOLOGY OF PERIODONTAL DISEASE:
  • 20. CHANGES IN THE PERCEPTIONS OF PERIODONTAL DISEASES:  IN 1961, WHO SAID THAT GINGIVITIS LEAD TO THE DEVELOPMENT OF PERIODONTITIS. ON THE CONTRARY RESEARCH BY 1990's SHOWED: 1. SEVERE PERIODONTITIS WAS SEEN ONLY IN A SMALL PROPORTION OF POPULATION, WHEREAS MILD & MILD TO MODERATE GINGIVITIS WAS MORE COMMON. 2. GINGIVITIS N PERIODONTITIS ARE ASSOCIATED WITH BACTERIAL FLORA WHICH MAY HAVE SIMILARITIES BUT MAY ALSO DIFFER. ONLY FRACTION OF SITES AND NOT ALL SITES WITH GINGIVITIS LATER DEVELOP PERIODONTITIS. 3. PERIODONTAL DISEASE IS NOT A NATURAL CONSEQUENCE OF AGEING.
  • 21.  SOME OF THE INDICES USED IN THE STUDY OF PERIODONTAL EPIDEMIOLOGY ARE; 1. PERIODONTAL INDEX 2. PERIODONTAL DISEASE INDEX 3. PAPILLARY-MARGINAL ATTACHMENT INDEX 4. GINGIVAL INDEX 5. OHI-S 6. CPITN EPIDEMIOLOGICAL INDICES:
  • 22. • HOST FACTORS-- 1. AGE- CHRONIC DESTRUCTIV PERIODONTAL DISEASE HAS BEEN ASSOCIATED WITH AGES GREATER THAN 40. 2. SEX- MORE COMMON IN MALES. 3. RACE- BLACKS ARE MORE AFFECTED. 4. INTRA ORAL VARIATIONS- MORE SEEN IN INTERPROXIMAL AREAS THAN BUCCAL OR LINGUAL AREAS.UPPER ARCH IS MORE PRONE TO GINGIVITIS AND IS MORE SEEN IN LEFT ARCH THAN ON THE RIGHT ARCH. 5. SEVERITY OF BONE LOSS- SEVERELY AFFECTED ARE THE LOWER CENTRALS AND THE LATERALS AND UPPER MOLARS. 6. ENDOCRINE CHANGES- PUBERTY, PREGNANCY, HYPERTHYROIDISM AND PARATHYROIDISM INCREASE CHANCES OF GINGIVITIS. 7. TRAUMATIC OCCLUSION- SHARP CUSP ACTS AS 'PLUNGERS' AND LEAD TO PERIODONTITIS. 8. FOOD IMPACTION EPIDEMIOLOGICAL TRIAD:
  • 23. 9. TOOTH POSITION- IRREGULAR ALIGNMENT MAKES IT DIFFICULT TO KEEP THESE AREAS CLEAN.ROOTS MAY APPROACH CLOSE TO EACHOTHER WHICH MAY ALLOW INSUFFICIENT INTERVENING ALVEOLAR SUPPORT. 10. OCCUPATIONAL HABITS- THREAD BITING N HOLDING NAILS BETWEEN TEETH CAN PRODUCE TRAUMATIC AFFECTS ON PERIODONTIUM. 11. BRUXISM,LIP, CHEEK AND NAIL BITING CAN AFFECT ALSO. 12. USE OF TOBACCO- IT LOWERS THE TISSUE RESISTENCE IN THE ORAL CAVITY. 13. MISUSE OF TOOTHBRUSH. 14. CONCOMITANT DISEASE- ALVEOLAR BONE DESTRUCTION AND GINGIVITIS MAY BE ACCENTUATED IN Pts. WITH UNCONTOLLED DIABETES, HEAVY METAL POISONING, ACUTE MONOCYTIC LEUKEMIA AND PERNICIOUS ANEMIA. 15. INCOME AND EDUCATION
  • 24. AGENT FACTORS; 1. PLAQUE, 2. CALCULUS 1. DENTAL PLAQUE IS THE PRIMARY ETIOLOGIC FACTOR FOR PERIODONTAL DISEASE. THEY ARE SOFT DEPOSITS FORMING A BIO-FILM ADHERENT TO THE TOOTH SURFACE AND ALSO INCLUDING REMOVABLE AND FIXED RESTORATIONS. 2. CALCULUS IS AN ADHERENT CALCIFIED MASS THAT FORMS ON THE SURFACE OF NATURAL TEETH AND DENTAL PROSTHESIS. IT CONSISTS OF MINERALIZED PLAQUE.
  • 25. ENVIRONMENTAL FACTORS; 1. GEOGRAPHIC VARIATIONS- FOUND TO BE HIGH IN JORDAN,INDIA, MALAYSIA. FOUND TO BE INTERMEDIATE IN USA(BLACKS), COLUMBIA, ETHIOPIA AND ECUADOR AND LOW IN US whiteS AND PRIMITIVE ESKIMOS OF ALASKA. 2. NUTRITION- AVITAMINOSIS C, NIACIN DEFICIENCY AND VITAMIN A DEFICIENCY. 3. DEGREE OF URBANIZATION- RURAL POPULATION SEEMS TO SUFFER MORE THAN URBAN POPULATION. 4. STRESS- STRESS IS SAID TO PREDISPOSE TO ACUTE NECROTIZING ULCERATIVE GINGIVITIS AND OFTEN SEEN IN MILITARY GROUPS AND IN EXAM GOING STUDENTS.
  • 26. What is Dental Caries? Dental caries is a microbiological , reversible, infectious disease that results in dissolution and destruction of calcified tissues of the tooth. OR It is a microbial ,infectious disease which leads to demineralization of enamel and dentin followed by disintegration of their organic materials. OR It is a dynamic process (multifactorial) of episodic demineralization and demineralization occurring over time. If demineralization process predominates ,disintegration of mineral component will occur leading to cavity.
  • 27. Etiology of Dental Caries THEORIES: 1.Legend of the worm. 2.Endogenous theories.  Humoral theory.  Vital theory. 3.Exogenous theories.  Chemical(acid) theory.  Parasitic (septic) theory.  Miller’s chemicoparasitic theory.  Proteolysis theory.  Proteolysis chelation theory.
  • 28. CARIES Etiological Tetrad TOOTH Substrate Time Sugar Bacteria
  • 29. SUGARS (non-cariogenic) BACTERIA •Bulk sweeteners 1. Sorbitol 2. Mannitol •Streptococcus mutans primarily responsible-transmitted placentally in the first 30 months. • Intense sweeteners(cariogenic) 1. Saccharin 2. Aspartame •Lactobacilli Progression of Caries FERMENTABLE SUGAR + PLAQUE BACTERIA Organic acids dissolving tooth mineral Main Etiological Factors
  • 30. EPIDEMIOLOGICAL TRIAD. HOST ,AGENT ,ENVIRONMENT. HOST FACTORS AGENT FACTORS ENVIRONMENTAL FACTORS 1) Host Factors: 1. Tooth composition and morphology 2. Saliva(contents) 3. Sex 4. Race 5. Age 6. Familial heredity 7. Developmental disturbances 8. Economic status 9. Concomitant disease 10. Oral hygiene habits 1. Role of micro- organisms : are pre- requisite for caries initiation, some produce extracellular dextrans or levans,may be acidogenic. 2. Properties of cariogenic plaque. 1. Diet A. Vipeholm Study B. Hopewood House Study C. Turku Sugar study D. Seventh-Day Adventist Children Study E. Hereditary Fructose Intolerance 2. Geographic variations 3. Soil 4. Urbanization 5. Climate
  • 31. THANK YOU

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