Epidemiology Of Dental Caries - PowerPoint PPT Presentation

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Epidemiology Of Dental Caries

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  1. Epidemiology Of Dental Caries

  2. Epidemiology of dental caries

  3. Dental Caries • Dental caries is an ancient disease; paleontological evidence shows that it has troubled humans from the time that agriculture replaced hunting as the principal source of food.

  4. Low Caries incidence existed in Ancient Man • Examination of ancient skulls shows that:

  5. Low caries incidence in the ancient man is due to diet which was : • Comparatively low in carbohydrates. • Natural (unrefined) diet. • Coarse & not fully prepared or cooked.

  6. Pattern Of Ancient Dental Caries • The pattern of ancient caries as revealed by lesions in ancient skulls was mostly cervical or root caries and coronal caries was relatively uncommon. • Coronal caries seemed to start in the occlusal fissures but developed no further because the rate of attrition was faster than the rate of progression.

  7. Pattern Of Ancient Dental Cariescont. • The ancient pattern of dental caries was replaced in the 17th century by a new pattern where a lesion begins in fissured surfaces and develops later on proximal surfaces. • This pattern took place in the industrialized nations as a result of the increased use of sucrose as sugars became more available.

  8. Current globaldistribution During most of the 20th century, dental caries pattern was : • Highprevalenceindeveloped countries& higher socioeconomic group. • Lowprevalence in developing countries with less economic development. Caries was referred to as “a disease of civilization.”

  9. Global Distribution • The most obvious reason for this historical pattern is diet; the high level of consumption of refined carbohydrates in developed countries in contrast to diets low in fermentable carbohydrates in poorer societies where hunting and farming are the main source of food.

  10. Explanation of this pattern is : diet • High level of consumption of refined carbohydrates in developed countries led to increase in cariogenic bacteria. • Diet low in fermentable carbohydrates in developing countries surviving on farming &hunting lower level of cariogenic bacteria.

  11. By the late 20th century, cariespatternwas changing in two ways: 1- Sharp rising in caries prevalenceand severity in most developingcountries especially urban areas. 2- Marked reduction among children & young adults in developed countries.

  12. In both developed and developing countries , there are distinct variations in caries experience from one country to another and from region to another within The same Country.

  13. The decline of caries is attributed to: • Use of fluoridated tooth paste. • Fluoridation of water supplies. • The use of fissure sealants. • Implementation of preventive programs • better access to health care • better living conditions. • Change of sugar consumption, although the change is not substantial.

  14. Global Distributioncont. upward trend of caries in many developing countries is related to: • The absence of widespread caries preventive strategy. • Increasing consumption of sugar containing products.

  15. Variation of caries within the mouth: • The distribution pattern of dental caries closely follows that of plaque. Thus, the sites in the mouth which are most prone to caries are those where plaque accumulates.

  16. These sites are: 1. The fissures in the occlusal surfaces of molars. 2. The proximal areas. 3. The marginal area between the tooth and the gingiva.

  17. I- Types of dental caries 1)Pit & fissure caries: • It is the first to appear in the mouth. • Pits &fissure surfaces constitute the most susceptible surfaces in the mouth.

  18. 2) Proximal caries: • It is the next to appear in the mouth. • It is related to plaque accumulation in the non-self cleansing areas (beneath the contact points).

  19. 3) Cervical caries • Is the third type of dental caries that occurs uniformly throughout life. • It is related to progressive changes in the free gingival margin,poor oral hygiene & decreased salivary flow (xerostomia) • ,.

  20. 4) Root caries: • Occurs usually in old age (60 y<). • Root surfaces become exposed by gingival recession in advancing age. • These exposed areas provide perfect areas for plaque accumulation.

  21. II-Susceptibility of different teeth • Dental caries in the human mouth is usually distributed in a bilateral symmetry.

  22. Susceptibility Of Different Teeth • According to the pioneering Hagerstown studies (1937), the rank order of susceptibility of teeth to caries was listed as follows:

  23. Mandibular 1st & 2nd molars 1 Max. 1st & 2nd molars 2 Mand. 2nd,max. 1st & 2nd premolars max. central & lateral incisors. 3 Max. canines & mand. 1st premolars 4 Mand. Central& lateral Incisors & canines. 5

  24. Determinants & risk factors dental caries

  25. Dental Caries • It is the disease of calcified tissues. • It is a maltifactorial disease in which the following risk factors play role in its causation process: • Agent: Microorganisms • Host: Personal and tooth risk factors. • Environment: Dietary, and oral hygiene related risk factors.

  26. Host Environmental Agent 1- Age. 2- Gender. 3- Race. 4- Genetic &familial. 5- Role of saliva. 6- Nutrition 7-Systemic diseases and drugs. 1-Flouride. 2-diet. 3-Social factors. 1-Streptococcus mutans. 2- Lactobacilli. 3- Actinomyces.

  27. Microbial agent • Dental caries is a bacterial disease. • Regardless of any other factor, caries does not occur in the absence of bacteria.

  28. Agent Factors of Dental CariesMicroorganisms • Mainly Streptococcus mutans are responsible for initial development of dental caries with contribution of other species such as: • Lactobacillus acidophilus • Lactobacillus casei • Streptococcus salivarius • Strpetococcus milleri • Streptococcus sanguis • Actinomycis (root caries)

  29. Strept. Mutans has the ability to: • 1- Implantation on tooth surface by synthesis of adhesive extra- cellular polysaccharides (glucans) from sucrose which they use to stick and colonize on tooth surface.

  30. 2-Store intra-cellular polysaccharides which act as a transient reserves of fermentable carbohydrates. • 3-Fermentation of dietary carbohydrates as an energy source for its metabolic activity and produces lactic acid.

  31. Streptococcus mutans

  32. Lactobacillicould be considered as secondary contributors for the process. • They generally constitute less than 1% of the plaque microbiota.

  33. Their number is often increased in caries active plaque because they grow well under acid condition. • Lactobacilli are more a consequence than a cause of caries initiation.

  34. The host Risk Factors • 1- Age. • 2- Gender. • 3- Race. • 4- Genetic & familial. • 5- Role of saliva. 6- Nutrition • 7-Systemic diseases and drugs.

  35. Age Caries wasconsidered a childhood disease because all susceptible tooth surfaces become carious during early child years and few carious lesions are affected during adulthood.

  36. Age • In communities with lower attack rate, young people reach adulthood with most surfaces caries free and caries attack spread out more throughout life.

  37. Age • Caries increases progressively by age, and the increase is more slowly during adult years • This is due to: • Most of the susceptible surfaces are likely to have been attacked by that time. • The build up fluoride in outer layers of enamel over time.

  38. After age of 60 years, caries increases again because of root caries.

  39. Gender • It is observed that caries prevalence is higher in females than in males of the same age.

  40. Females generally demonstrate higher DMF scores than males probably due to : • The earlier tooth eruption in females; their teeth are at risk for a longer time. • Females visit the dentist more frequently (treatment factor). The impact of these determinant, however has not been well quantified.

  41. Race • Early studies, observed that some races as those in Africa & India, had high degree of caries resistance than “Europeans”. • Recently, the concept of racial differences have been faded, andthe evidence reveals that the global differences are the result of environment..

  42. Race • This was supported by the fact that these racial groups, once thought to be resistant to caries (Africans and Indians), quickly developed the disease when they moved to areas with different cultural and dietary patterns. • The variation in caries prevalence is the result of environmental ratherthan they are of racial attributes.

  43. Familial & genetic pattern • Dental caries has long ago shown to be grouped according to families. • Members of the same household were found to be alike in their caries pattern than between unrelated groups of individuals.

  44. Such familial tendency may be due to: 1- Interfamilial bacterialtransmission, especially from mother to baby. 2- similarity in dietary & oral hygiene habits. OR, 3-Genetic factor: as inheritance of tooth structure (deep narrow pits & fissures) or special arch form (irregularities & crowding).

  45. Socioeconomic status • It is a measure of the individual’ background; education, income, occupation, and attitudes and values. • It is inversely related to the status of many disease. • It is a powerful determinant of caries status in any community.

  46. Socioeconomic status • Earlier studies found that higher SES groups had higher DMFscores than those in the lower SES groups. • Details of DMF scores showed that lower SES groups hadhigher values forDandM, lower for F. • Whereas, the increased number of filled teeth (F) raised the DMF index among the high SES groups “treatment factor”.

  47. The difference between social groups is due to increased number of filled teeth (F) that raised the whole DMF index among high SES groups “treatment factor”.

  48. Socioeconomic Status (SES): • With the reported caries decline, the DMF values of the higher SES groups became considerably below those in the lower SES group. • The inverse relationship between caries status and SES have been reported from Britain and elsewhere in Europe. • The same was reported in Africa.

  49. Nutrition • Nutrition refers to the absorption of nutrients and their utilization by the body cells for structural and functional efficiency. • Nutrition can act only through the systemic route through influencing the host during tooth development.

  50. Nutrition and Dental Caries • There is some evidence that chronic malnourishment during development periods in a poor society may predispose to caries. • No relation between nutritional adequacy and DMF scores could be find. • Vitamin D deficiency may cause enamel hypoplasia. • Selenium: Is a cariogenic trace element when consumed during tooth developmental period .