epidemiology of dental caries - public health dentistry
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- 2. PRESENTED BY- Ira Solanki (final year BDS) GUIDED BY- DR. Anupama Gaur Dr. Abhishek Sharma Dr. Sonia Pareek Dr. Sudhanshu Sanadhya 2
- 3. CONTENTS Introduction Definition Classification Global Scenario Indian scenario Rajasthan studies Theories of caries etiology Current concept of dental caries Epidemiological factors of dental caries Etiologic factors Dietary studies Indices for dental caries Histopathology of dental caries prevention Conclusion 3
- 4. INTRODUCTION The word caries is derived from Latin , meaning “rot” or decay. It is similar to the Greek word “Ker” meaning death. 4
- 5. DEFINITION Epidemiology is defined as “ The study of distribution and determinants of health-related states or events in specified populations , and the application of this study to the control of health related problems.” (John M.Last,1988) Dental caries is defined as “irreversible microbial disease of the calcified tissues of the tooth characterised by demineralisation of inorganic portion and destruction of the organic substances of the tooth” (Shafer) 5
- 6. CLASSIFICATION OF DENTAL CARIES OCCURRENCE INCIPIENT RECURRENT RESIDUAL SPEED ACUTE CHRONIC LOCATION PIT AND FISSURE SMOOTH SURFACE ROOT SURFACE DIRECTION FORWAD CARIES BACKWARD CARIES AGE EARLY CHILDHOOD CARIES ADOLESCENT CARIES SENILE CARIES SURFACE SIMPLE COMPOUD- TWO SURFACE COMPLEX- MORE THAN TWO SUFACE 6
- 7. 7 WHO SYSTEM D1- clinically detected enamel lesions with intact (non cavitated) D2-clinically detectable cavities limited to enamel D3- clinically detectable cavities in dentin D4- lesions extending into the pulp
- 8. CARIES IN PREHISTORIC MAN Dental caries may be considered a disease of modern civilization, since prehistoric man was rarely affected from dental caries. There is no evidence of dental caries in the relatively very few teeth found in skull fragments of our earliest known ancestors, pithecanthropus. Anthropologic studies of Von Lenhossek revealed that the Dolicocephalic skulls of men from Pre-Neolithic periods (12,000 BC) did not exhibit dental caries, but skulls from Brachycephalic man of the Neolithic periods (12,000-3000 BC) contained carious teeth. 8
- 9. GLOBAL SCENARIO Dental caries is still a major health problem in most industrialized countries, affecting 60-90% of school children & vast majority of adults. It is most prevalent oral disease in several Asian and Latin American countries, while it appears to be less common and less severe in most African countries. The WHO records a global DMFT of 1.61 for 12 year old in 2004, a reduction of 0.13 as compared to a DMFT of 1.74 in the year 2001. 9
- 10. INDIAN SCENARIO WHO reported a DMFT score of 3.94 for India in 2003. In India, data from the National Oral Health Survey (2002-2003) states that AGE GROUP CARIES PREVALENCE DMFT 12 years 53.8% 1.8 35-44 year 80.2% 5.4 65-74year 85% 14.9 10
- 11. INDIAN STUDIES AUTHORS YEAR POPULATION FINDINGS Day & Tandon 1940 756 subjects aged 5-18 yrs. in Lahore Point prevalence= 94.04 The mean deft= 0.23 Chaudhury & chawla 1957 2991, 5-16 years old children in Lucknow deft= 11.1 DMFT= 1.9 Dutta 1965 1424 children aged 6-121 years in Calcutta DMFT/deft= 1.17 Mehta 1977 1160 children 5-6 yrs old in Behrampur, Orissa Point prevalence= 60.4 Ashwini Rao, Sequeira SP, Peter S 1999 2902 school children aged between 5 and 12 years in Karnataka Caries prevalence 76.9% Mean DMFT= 0.78 Mean deft= 3.48 Das JK, Sahoo PK, Bhuyan SK, sahoo SK 2002 1257 school children aged 5,8,11&15 years in Cuttack, Orissa Point prevalence = 64.3% Average DMFT = 2.38 Dhar v, jain A, Van Dyke TE, Kohli A. 2007 1587 school children aged 5-14 years in Udaipur Caries prevalence= 46.75% 11
- 12. RAJASTHAN STUDIES 12 Performed by Pradhuman verma, Kanika Gupta, suruchi jhuneja They divided Rajasthan into 5 geographical zone- Shri Ganganagar, Jaisalmer, Udaipur, Ajmer and Bharatpur. Examined 1125 adult subjects aged 25 to 44 years. RESULTS
- 13. FEW STUDIES IN OTHER RAJASTAN CITIES 13 Authors Area involved Population Prevalence Navin anand, harsh vardan dubey & Rahul gupta Bharatpur city 12-15 years old 1400 children (700 private & 700 govt.) In govt. school children- 53% Private school children- 47% Vikram khare, Ajit koshy, p J rani, Anil agarwal Udaipur city 883 orphanages In primary teeth- 49.6% In permanent teeth – 41%
- 14. THEORIES OF CARIES ETIOLOGY I.EARLY THEORIES OF CARIES FORMATION- A. THE LEGEND OF THE WORM- In past, dental caries was thought to be caused by living worms inside the tooth structure. II. ENDOGENOUS THEORIES- A. HOMORAL THEORY- According to Galen An imbalance between the humors(blood, phlegm, black bile and yellow bile) of body caused tooth decay. B. VITAL THEORY- was advanced towards the end of the 18th century, Tooth decay originated from within the tooth itself, like a bone gangrene. 14
- 15. III.EXOGENOUS THEORIES A. CHEMICAL (ACID) THEORY- On the basis of findings of Robertson (1835), this theory proposed that tooth decay was caused by the fermentation of food particles around the teeth. B. PARASITIC (SEPTIC) THEORY- By Antoni Von Leeuwenhock (1632-1723)- that microorganisms were associated with the carious process. In 1843,Erdl- filamentous parasite in the membrane removed from the teeth. In 1847,Ficinus- observed a filamentous organisms in the enamel cuticle & in carious lesions. In1954, Dubos- microorganisms can have toxic effects on tissue. 15
- 16. C. ACIDOGENIC THEORY- Proposed by W.D.Miller in 1890. According to this theory- • Sugar(carbohydrates) + bacteria = makes acid (mainly lactic acid) • Acid attacks the healthy tooth & make it carious. STEPHAN CURVE: within 2-4 minutes of rinsing with solution of glucose or sucrose, plaque pH is reduced from about 6.5-5 and gradually returns to original value within approx. 40 min. this is graphically plotted as the “Stephan's curve” 16
- 17. D. PROTEOLYSIS THEORY- Gottileb(1947) Proteolytic enzyme liberated by cariogenic bacteria destruction of the organic matrix detachment of inorganic crystals from one another collapse of whole structure CAVITATION E. PROTEOLYSIS CHELATION THEORY- originated by Schatz & Martin in 1955. Product of bacterial action + enamel/dentin/salivary constituents chelates with calcium. Chelate can be formed at neutral/alkaline pH Demineralization could arise without acid formation. IV. OTHER THEORIES OF CARIES ETIOLOGY- A. AUTOIMMUNE THEORY- Burch & Jackson in 1966 suggested that genes, partly inherited and partly mutational, determine whether a site on a tooth is at risk. 17
- 18. CURRENT CONCEPT OF DENTAL CARIES TOOTH FLORASUBSTRATE CARIOUS Flow rate pH Time 18
- 19. EPIDEMIOLOGICAL FACTORS OF DENTAL CARIES AGENT HOST ENVIRONMENT Geographic variation Fluoride Trace elements Urbanization Social factors 19
- 20. TEETH POSITION- Teeth which are rotated, malalinged or out of position may be difficult to clean and tends to favour accumulation of food and debris. This in sesceptible persons, would be sufficient to cause caries in tooth Alteration of tooth structure by disturbance in formation or in calcification MORPHOLOGY- Presence of deep, narrow occlusal fissures or buccal & lingual pits TEETH 20
- 21. SALIVA The fact that teeth are in constant contact with and bathed in saliva would suggest that this fact could profoundly influence the state of oral health of a person. One of the most important function of saliva is its role in removal of micro flora & food debris from the mouth. Quantity of saliva- normal: 700-800ml/day Salivary gland aplasia and xerostomia in which salivary flow may be entirely lacking results in rampant caries Viscosity of saliva: high caries incidence is associated with thick Mucinous saliva Antibacterial properties of saliva: Lactoperoxidase :Lactoferrin : Lysozyme :IgA 21
- 22. Other salivary components with protective function- Proline rich proteins- mucin and glycoprotein. Salivary pH- determined mainly by the bicarbonate concentration Salivary pH increases with flow rate Salivary buffers increase pH of saliva in the oral cavity 22
- 23. HOST FACTORS RACE- Africa & India, had high degree of caries resistance than “Europeans”. The global differences are the result of environment. AGE- previously caries was considered ‘essentially a disease of childhood’. Caries increases progressively by age and the increase is more slowly during adult years. SEX- caries prevalence female > male root caries prevalence males > females FAMILIAL HEREDITARY- “good or bad teeth run in family” due to bacterial transmission, dietary and oral hygiene habits genetic factors 23
- 24. EMOTIONAL DISTURBANCE- period of stress have been associated with high caries incidence, Due to decreased salivary flow. DIET AND NUTRITION- physical nature of diet - carbohydrates content of diet - vitamin content in diet SOCIOECONOMIC STATUS- SES ∞ 1 status of many diseases caries is nowadays, considered to be a “disease of poverty” or “social behavioural disease”. 24
- 25. AGENT FACTORS MICROFLORA- microorganisms are a prerequisite for caries initiation. mainly the bacteria are- Streptococcus Mutans , Strep.sanguis, Strep.Salivaius, Strep.milleri, lactobacillus, Actinomyces viscous and Actinomyces naeslundii (root caries) DIET- It is taken as under host, agent and environment. food and beverages taken by individual serve as substrates for fermentation by the plaque micro flora. 25
- 26. TRACE ELEMENTS AND DENTAL CARIES 26 Caries low prevalence was associated with- raising conc. Of Ca, Mg and Mo High prevalence- Cu, Fe, Mn Strong inverse relationship- Sr, Ba, K, Mg, Ca and Li .
- 27. DIETARY STUDIES ON CONTROL HUMAN POPULATIONS I.VIPEHOLM STUDY – described by Gustaffson et al in 1954, summarized by Davies in 1955. Mental institution at the Vipeholm hospital near Lund, Sweden. Purpose- to determine the effects of frequency and quantity of sugar intake on the formation of caries Conclusion- physical form of carbohydrates(stickiness, oral clearance time frequency of intake) much more important in cariogenicity than the total amount. 27
- 28. Increase in caries activity due to- 28
- 29. II.HOPEWOOD HOUSE STUDY - Strictly institutional diet- occasional serving of egg yolk - diet-vegetable in nature and largely raw. - the absence of meat and a rigid restriction of refined carbohydrates. - meal supplemented by vitamin concentrates and occasional serving of nuts and honey. - fluoride content of water and food was insignificant and no tea was consumed. 7-14 yrs. age children Hope wood house, Bowral, New South Wales Australia Longitudinally studied for 10 years 29
- 30. Results of hopewood House study- At the end of 10 years 13 years old had DMFT mean 1.6/child General population 13 years old mean DMFT 10.7 53% children at the hope wood house caries free 0.4% children of state children caries free Hope wood house children’s oral hygiene was poor, calculus + gingivitis more prevalent in 75% of children. Conclusion- In institutionalized children at least dental caries can be reduced by carbohydrate restricted diet without the beneficial effects of fluoride and in the presence of unfavorable oral hygiene. 30
- 31. III.TURKU SUGAR STUDIES- Aim: To study the effects of the chronic consumption of sucrose, fructose and xylitol on dental caries. 2 years study of 125 young adults 125 young adults Sucrose group – 35 people Fructose group – 38 people Xylitol group – 52 people Sucrose & fructose had equal cariogenicity whereas xylitol produced almost no caries Caries continued to increase in the sucrose group, remained unchanged in the fructose group and produced almost no change in xylitol group After 1 year By the 2nd year 31
- 32. IV.HEREDITARY FRUCTOSE INTOLERANCE (HFI)- Newbrun in 1969 tabulated the caries prevalence of 31 persons with HFI and found that the dental caries prevalence was extremely low. 32
- 33. INDICES FOR DENTAL CARIES 33 MOST COMMONLY USED DMFT DMFS def dmf OTHER DENTAL CARIES INDICES STONE’S INDEX 1949 CARIES SEVERITY INDEX 1960 CZECHOSLOVAKI AN CARIES INDEX 1956 CARIES SUSCEPTIBILITY TEST 1961 D-M-F SURFACE PERCENTAGE INDEX 1963 MOLLER’S INDEX 1966
- 34. HISTOPATHOLOGY OF DENTAL CARIES • Deepest zone lies at the advancing front of enamel lesion • More porous than normal enamel • Pores are larger than normal enamel. Pore volume 1% • Appears structureless TRANSLLUCENT ZONE • Located just superficial to the translucent zone. • Darkness is due to the excessive demineralization of the enamel. • Rapidly advancing caries narrower zone. • Slowly advancing zone wider • Pore volume 2-4% . This zone reveals degree of remineralization of carious lesion DARK ZONE • Zone is situated between the dark zone & surface layer of enamel • Represents area of greatest demineralization. • Pore volume 5-6% BODY OF LESION • When examined by the polarizing light appears relatively unaffected, it may be due to the surface remineralization by the salivary mineral ions SURFACE ZONE ZONES OF ENAMEL CARIES 34
- 35. Normal zone • Innermost layer of carious dentin. Dentinal tubules appears normal. • No crystals in the lumen of the tubules. No bacteria in the tubules • Intertubular dentin has normal cross banded collagen. • Fatty degeneration of the Tome’s process Sub transpar ent zone • Deposition of very fine crystal structures within the dentinal tubules • Superficial layer show area of demineralization & damage of odontogenic process • No bacteria in the tubules; dentin is capable of remineralization. Transpar ent zone • Outermost zone • Characterized by complete destruction of dentinal tubules. • In this the entire dentinal structure become destroyed & cavitation begins from dntino enamel junction. Turbid zone • Marked by widening & distortion of dentinal tubules. • Microorganisms are found • Denaturation of collage fibers also takes place. • Zone cannot undergoes self repair or remineralization. Infected zone • Zone appears as transparent because of decalcification of dentin • It is softer than normal dentin ; no bacteria in the tubules. • This zone is capable of repair & remineralization ZONES OF DENTINAL CARIES 35
- 37. PREVENTION 37
- 38. CONCLUSION Dental caries is still a considerable burden largely in developing world and to a lesser extent in developed world. Nevertheless continuous and significant presence of dental caries in population & with its prime determinants is operating in relatively large number of populations. Further exploration using epidemiology as a tool in our country will certainly throw a light in understanding and management of dental caries. 38
- 39. REFERENCES Essential of preventive and community dentistry 5th edition - Soben peter A textbook of public health dentistry- C M marya Textbook of preventive and community dentistry- S S Hiremath Textbook of Oralpathology Shafer 39
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Editor's Notes
- #10: Various studies conducted in different countries at different time periods have given evidence that a substantial decrease in caries prevalence in the last decade has been found among western countries whereas in case of developing and underdeveloped countries, prevalence of caries seems to be increasing.