Discipline : “ Preventive Dentistry” Programme of lectures: – 7 lectures + 7 lectures

1. Discipline : “ Preventive Dentistry” Programme of lectures: – 7 lectures + 7 lectures Textbooks for self-study are: - Norman O. Harris, Primary Preventive Dentistry, 6th Ed. (2004); 7th ed.(2009) - Hardy Limeback , Comprehensive Preventive Dentistry, 2012 Exam : after 7th semester - in January 2015. Exam consists : 1 written question from the syllabus and test ( multiple choice), all in one day.

2. Etiology and pathogenesis of dental caries. Prof.d-r R.Kabaktchieva- 2014

3. The three general disease categories of focus in dentistry are : • dental decay, • periodontal disease, • oral cancer.

4. Dentistry in the past has been treatment oriented,but we are witnessing an interestprevention.

5. It is obviously better to prevent the disease inthe first place, than treat it once it has happened.

6. The goals of preventive dentistry are to avoid disease altogether.

7. Maintaining a disease-free state canresult from primary prevention. • When lifestyle changesare made early on, the risk for developing dental diseaseare minimized. Lifestyle changes • – less carbohydrates • – better oral hygiene • – improved nutrition • – better education

8. MID- minimal intervention dentistry • Secondary prevention(reverse, arrestincipient caries) and early intervention(MID &“PreventiveResins”) can be used to reverse the initiation of disease. • An outcome of good health can still beachieved, when incipient enamel lesions are reversed before cavities form.

9. ! • Far too often though, dentists spend most of their time treating dentaldisease in an endless cycle of repeat restorations, which leads……to tooth loss.

10. The goal of primary prevention is never to have had any kind of dental disease.

11. Dental decay (dental caries): global patterns Fig. Global prevalence of caries from World War II to present. The relative decline in caries, was represented by DMFT (decayed, missing, filled teeth) Are also shownother factors that have contributed to the decline in caries worldwide (labeled a to j) Comprehensive Preventive Dentistry- H. Limeback

12. Тhe prevalence of caries haschanged over the decades. • In every developedcountry, there has been a steady decline in dental decay. • Experts believe, that it wasprimarily the introduction of fluoride therapies afterthe 1960s that had a huge impact on dental decay rates.

13. To know how to prevent , need to know disease, its etiology and pathogenesis

14. Etiology and Pathogenesis of Dental Caries In dealing with disease, “prevention is better than a cure.”

15. Definition • Dental caries is a dietary carbohydrate-modified bacterial infectious disease with saliva as a critical regulator. • It is the most common chronic infectious disease of childhood

16. Contemporary definition : • Tooth decay is localized progressive disease, whose character consists in the destruction of tooth structures mainly under the influence of metabolic products of the oral microflora; • Each level of decomposition is clinically differentiated.

17. Caries process takes place in the biofilm on the tooth surface . Carious lesionis the result of carious process developing between the microbial biofilm and tooth structure The metabolic activity of the microorganisms in the biofilm is invisible to the clinician, but carious lesion that is a result of this activity is clinically apparent. Kidd

18. Caries Factors Must have a tooth, plaque bacteria, fermentable carbohydrate, saliva, and enough time in order for a carious lesion to develop . Caries results when all of the factorsthat contribute to caries overlap. (red color, center). Several factors influencing each component, (seethe diagram,) affect the rate and severity of the caries. diagram The classic Venne diagram of caries.

19. This is a convenient analogy to understand and is an offshoot of the classic Venn diagram ( firstintroduced by Keyes (1962).

20. The role of microorganisms

21. Caries is an infectious disease that is actually transmissible, usually when the mother infected with S. mutans, infects her infant when the child’s first teeth appear in the oral cavity (Kulkarni et al. 1989).

22. Dental caries does not occur in a sterile mouth. (no mouth can ever be made sterile) • The conditions in the oral cavity are ideal for the growth of bacteria that metabolize sugar to acids. • The oral cavity is generally a warm place, at body temperature (37°C) encouraging the growth of bacteria.

23. Non-specific Plaque Hypothesis • Microorganisms in dental caries first observed by van Leeuwenhoek in 1683 • W.D. Miller – University of Berlin 1890 – considered all bacteria in mouth were potentially cariogenic – hence, non-specific plaque theory • Acid production by bacteria considered responsible for breakdown of tooth

24. Specific Plaque Hypothesis 1924 – Clarke isolated a streptococcus species from a cavity in a child The bacteria underwent some changes as the culture aged – Clarke named it Streptococcus mutans for “mutation”

25. Mutans streptococci • 1960 – Keyes “rediscovered” S. mutans • He demonstrated that: • specific microorganisms were responsible for caries • caries was transmissible • Later, the responsible bacteria were found to comprise seven distinct species – only mutans and sobrinus are associated with caries in humans

26. Characteristics of MS • Ecological niche: human oral cavity • “Intentionally designed … to be a cariogenic organism” (Coykendall 1976) • Cariogenic properties • ability to produce acid (acidogenicity) • ability to withstand acid conditions (aciduricity) • ability to adhere to teeth

27. Characteristics of MS • Metabolism yields: • acids, primarily lactic, from a variety of sugars • extracellular polyglucose, called glucan, which creates irreversible attachment (from sucrose metabolism only) • MS is responsible for initiation of caries • MS is a necessary, but not solely sufficient, factor for dental caries

28. Acquisition of MS by Infants • MS colonize oral cavity after eruption of teeth – require hard, non-desquamating surface; • Some believe in “window of infectivity“ that relievs on virgin tooth surfaces for initial colonization; • Second “window may open” when permanent dentition erupts

29. Acquisition of MS by Infants MS is poor competitor for colonization – once stable biofilm is in place, ability for MS to colonize is reduced Infants who acquire sanguis early have less MS mitis sanguis mutans Birth 11 8 19 26 33 mos. 1

30. Transmission of MS • Vertical transmission • Source is usually mother • Fidelity is >70% • Transmission may occur at birth, but MS reside in low numbers in reservoirs such as tonsils or dorsum of tongue

31. Other Microorganisms • Lactobacilli sp. • found in large numbers in some children • considered opportunistic, not initiators • numbers in cavity increase after DEJ invaded • lactobacilli are good indicators of total carbohydrate intake

32. Etiology - Diet • Hopewood House (Australia) 1947 – 52 determine • diets devoid of sugar and white flour- extremely low dental caries prevalence • Vipeholm (Sweden) 1945 – 52determined • effects of frequency of sugar consumption • effects of consistency (retentiveness) of sugar • sugar at meals vs. in between meals

33. Lessons from Vipeholm(Sweden) • Sugar consumption at meals– slight increase in caries; • Sugar between meals– marked increase in caries; • Sugar in sticky candies– greatest caries activity; • Caries activity differs among individuals • Caries activity declines with withdrawal of sugar-rich foods

34. The role of dietary sugars Not all sugars are cariogenic.

35. The more common dietary sugars are presented.The cariogenic potential of carbohydrates are presented too. The sugars with the most cariogenicity are sucrose and glucose (red). Other carbohydrates (maltose, lactose, fructose, and starch) are less cariogenic. The sugar alcohols, such as sorbitol and mannitol, are the least cariogenic (yellow) Xylitol haseven been shown to be anticariogenic (green).

36. The disaccharide sucrose and the monosaccharide glucose ( a component of sucrose), are most cariogenic. • Frequent ingestion, can cause severe damage to the tooth.

37. There is no question that carbohydrates are the main etiological reason for the development of caries. • One of the strategies in prevention of caries is to limit access to the more cariogenic sugars and substitute them with the anti-cariogentic ones. • Not only does their conversion to acid result in enamel dissolution, but they also encourage the growth of more virulent cariogenic bacteria.

38. Sucrose • Glucose + fructose • extracellular polyglucose, • glucan, (from sucrose metabolism only) • creates irreversible attachment plaque bacteria metabolized by fructan + glucan

39. Glucan • Water soluble • Extracellular “glue” • Enables adhesion to tooth • reduced susceptibility to mechanical disruption • Inhibits diffusion properties of plaque • reduces buffering capacity of saliva • inhibits transport of acid away from tooth

40. Role of Other Sugars • Fructose and glucose are as effective as sucrose in their ability to cause a pH drop; • Fructose is nearly equal to sucrose in cariogenicity; • Raw starch causes only a small drop in plaque pH

41. Role of Refined Starch • Soluble starch and refined starch can be broken down by salivary amylase into sugars • These refined carbohydrates cause a variable pH drop that may be as large as that caused by sucrose

42. The supragingival bacteria are dominated with streptococci and lactobacilli that can lower the plaque pH and induce decalcifications white spot lesions.

43. Figure shows an illustration of dental plaque at the gingival margin. (1) The enamel (e) has plaque biofilm (b) growing at the border of the inflamed gingival (g). (2) Same plaque at closer look. There is a ‘white spot’ lesion (w) developing at the margin of the gingiva, and brown calculus (c) developing in the sulcus attached to the tooth. (3) Close-up view of plaque. Biofilm bacteria, which consists of several species of bacteria (cocci, rods, motile spirochetes), organic material (salivary proteins) and organic matter secreted by the bacteria (yellow-stained)

44. The plaque that is responsible for caries is generally located supragingivally and is acidogenic.

45. People who consume sugars frequently in their diet increase the levels of streptococci and lactobacilli • The two bacteria species thought to be responsible for caries. • These bacteria continue to thrive as the pH drops. • If the plaque is not removed, eventually, the enamel starts to decalcify and an incipient ‘white spot’ lesion ensues.

46. Figure .The enamel white spot lesion at the mesial contact zone of the first maxillary right molar . These white-spot lesions are sometimes filled by dentists but can be remineralized.

47. Repeated glucose rinses encourages SM and LB growth when plaque acid is not controlled Fluoride at high concentrations inhibits SM , but not LB !!! Xylitol had inhibitory properties for both cariogenic and periodontal bacteria. Marsh (1994) was able to show, that feeding of bacteria a meal of glucose can encourage the growth of cariogenic bacteria when the pH is allowed to drop .

48. The demineralization–remineralizationbalance in caries • The plaque thickness dominated by cariogenic bacteria, can effectively keep the saliva from reaching the enamel surface. • In addition, the more plaque there is, the more acid is produced. • These acids have a longer time to penetrate into the enamel under thick biofilm - This allows the tooth to demineralize!!!! • If the saliva reaches the acids they are washed away and neutralized by the salivary buffers - This allows the tooth to remineralize.

49. The cycle repeats itself over and over with every sweet snack and meal containing fermentable sugars Caries occurs when the frequency of sugar exposure during the day is high.

50. The repeated cycle of ‘sugar attacks.’