Dental caries

Dental caries - microbiology, etiology

1. Dental caries Sohail PGT: 1 st yr Dept of pedodontics SVS Institute of Dental Sciences. 1

2. Contents Introduction History Definitions Etiology Microbiology Classification Histopathology 2 Part - 1 Part - 2

3. Introduction The word caries is derived from Latin, meaning “rot or decay” BENJAMIN FRANKLIN stated that: “HOT things, sharp things, sweet things, cold things rot the teeth and make them look like old things”. Dental caries is a multifactorial disease requiring the presence of a susceptible host, cariogenic microflora and a diet conducive to enamel demineralization. 3

4. ► Dental caries or tooth decay is one of the most common of all disorders, second only to common cold. ► The first study about dental caries was published in 1870 and has continued uninterrupted to the present. ► Some isolated populations like Eskimos, some African natives, and inhabitants of rural India are “immune” to dental caries because they are not exposed to western food habits. 4

5. 5 Historical overview of concepts in understanding dental caries

6. Evidences of dental lesions compatible with caries have been observed In Paleozoic fishes (570-250 million years) Mesozoic herbivores dinosaurs (245-65 million years) Pleistocenic animals (1.6-0.01 million). Caries has also been detected in bears and other wild animals and it is common in domestic animals 6 (Pinto & Exteberria , 2001; Palamra et al., 1981), ( Gorrel , 2006; Shklair , 1981; Wiggs & Lobprise , 1997).

7. Homo rhodesiensis cranium 7 A fossil found in 1921 in Broken Hill, Northern Rhodesia (Zambia) The specimen shows extensive dental caries and coronal destruction. Except for five teeth, all the rest is affected by rampant caries and several crowns were almost completely destroyed.

8. 10,000 B.C 8 In the Mediterranean region, Arabia and India the increase of caries began early between the 7th and 5th millennium BC. In Nautufians from the Levant region, the phase of hunter gatherers (10,500-8300 BC) shows 6.4% of caries frequency whereas Neolithic populations(8300-5500 BC) show 6.7% ( Eshed et al., 2006). In the Indo region the caries frequency range between 1.4-1.8% in the earliest populations, but in the site of Harappa (5000 BP, Pakistan) from the Early Bronze Age the caries frequency is 12% ( Lukacs , 1992, 1996)

9. 1728- Pierre Fauchard , a French physician, wrote “Le Chirurgien Dentiste .” Fauchard rejected the tooth worm theory of dental caries. Instead, he described enamel hypoplasia as “an erosion of the enamel” and recommended that hypoplastic areas be smoothed using files 9

10. The Restorative Era: 1850–Present At the International Medical Congress held in London in 1881, Miller and Underwood proposed that dental caries development was dependent on the presence and proliferation of “organisms.” (Searle F 1884, Barrett W 1885) 10

11. In 1881, Dr. W. D. Miller presented the results of his experiments (Miller W 1883) Bacteria produced the acids that led to the demineralization of enamel and dentin. He also noted that bacteria did not need to be present in enamel or dentin to initiate demineralization. Miller’s research led to a storm of debate and controversy. 11

12. Environmentalists won over those who argued that the structure of teeth play a major role in the caries process (Johnson CN 1918). The nutrition-caries hypothesis was partially discredited by the finding that populations who were malnourished had lower caries prevalence than those who were well nourished ( Massler M, Schour I 1947). By the mid-1920’s 12

13. Also discrediting that hypothesis were findings from the Vipeholm Dental Caries Study, ‘frequent consumption of sugar increases the risk of developing dental caries’ ( Gustafsson B, et al 1954). Mellanby (1934)- reviewed on literature of caries and noted that incidence was invariably less in primitive races than in modern man. 13

14. Definition(s): 14 “Microbial disease of the calcified tissues of the teeth, characterized by demineralization of the calcified tissues and destruction of the organic substance of the teeth” -Shafer “An infectious microbiological disease of the teeth that results in localized dissolution and destruction of calcified tissues” - Sturdevant “A localized post eruptive pathological process of external origin involving softening of the hard tissue and proceeding to the formation of a cavity” -WHO

15. ICDAS Definition: 15 DENTAL CARIES: Is the localized destruction of susceptible dental hard tissue by acidic by-products from bacterial fermentation of dietary carbohydrates. It is a bacterial driven, generally chronic, site-specific, multifactorial, dynamic disease process that results from the imbalance in the physiologic equilibrium between the tooth mineral and the plaque fluid; that is, when the pH drop results in net mineral loss over time. The International Caries Detection And Assessment System (ICDAS II)and the International Association For Dental Research. Available at: https://www.icdas.org. Accessed February, 2010.

16. THEORIES OF DENTAL CARIES 16

17. 17 There was no universally accepted opinion of the etiology of dental caries, and various theories have been proposed. Early theories Endogenous theories Exogenous theories

18. The legend of the worm 18

19. 19 Endogenous theories:

20. Vital theory : 20 Proposed by Hippocrates, Celsus , Galen and Auicenna . A vital theory of tooth decay was advanced towards the end of the 18 th century which postulated that tooth decay originated like bone gangrene, from within the tooth itself .

21. Exogenous theories: 21 Chemical (acid) theory: In 17 th and 18 th century, there emerged, the concept that teeth were destroyed by acid formed in the oral cavity. The acid implicated were inorganic like sulfuric, nitric, citric acids formed by decomposition of food in saliva. Robertson (1835) proposed that dental decay was caused by acid formed by fermentation of food particles around teeth.

22. 22 Dubos (1954) postulated that microorganisms (animal culae ) can have toxic and destructive effects on tissue. Early microscopic observation of scrapings from teeth and of the carious lesions by Antoni Van Leeuwenhoek (1632-1723) indicated that microorganisms were associated with the carious process. In 1843, Erld described filamentous parasites in the membrane removed from teeth. A few years later in 1847 Ficinus , a physician also observed filamentous organisms in the enamel cuticle (surface protein membrane of teeth) and in carious lesions. Parasitic (septic) theory:

23. Endogenous theories: Millers chemicoparasitic theory Proteolytic theory Proteolytic chelation theory Sucrose chelation theory 23

24. Miller’s chemicoparasitic theory: 24

25. 25 The essential features of Miller’s work which helped in developing the chemicoparasitic theory are: That microorganisms of the mouth, by secretion of enzymes or by their own metabolism, degrade the fermentable carbohydrate food material so as to form acids. The chief acids formed are those associated with fermentation, namely lactic, butyric, acetic, formic, succinic and other acids. Carbohydrates food material lodged between and on surfaces of teeth is the source of the acid which demineralizes the lime salts of the tooth.

26. 26 Miller summarized his theory as follows: Dental decay is a chemoparasitic process consists of 2 stages: decalcification or softening of the tissues and dissolution of the softened residue.

27. 27 Limitations Did not explain sub-surface demineralization Failed to justify rampant caries Did not explain caries in impacted tooth Phenomenon of arrested caries is not explained Smooth surface caries is not accounted in this theory

28. PROTEOLYTIC ENZYMES PROTEOLYTIC THEORY : Organic Inorganic 28 Gottlieb (1947) Friable and Nuckells (1947) and Pincus (1950). Acidogenic bacteria

29. PROTEOLYSIS-CHELATION THEORY : Schatz and Martin in 1955. PROTEOLYTIC ENZYMES CHELATION Organic Inorganic 29

30. 30 Egglers – Lura (1967) proposed that sucrose itself can cause dissolution of enamel by forming an ionized calcium saccharate . Calcium saccharates and calcium complexing intermediaries requires inorganic phosphate which is subsequently removed from the enamel by phosphorylating enzymes. Sucrose chelation theory-

31. 31 The most widely accepted theory till date continues to be the acidogenic theory put forth by Miller with recent addition. This can be explained by Keye’s triad which has been modified into a tetrad. Current concept :

32. Tooth Substrate Microorganism KEYE’S TRIAD ( 1960 ) Caries 32

33. Caries CARIES TETRAD ( Newburn -1982 ) 33

34. 34

35. THE HOST : - The tooth - Salivary factors - Muscular activity - Habits - Group suceptibility - Age - Environment THE MICROORGANISMS : - Bacterial plaque THE MEDIUM : - Diet Contributing factors to the caries process: 35

36. 36 Morphology and position A susceptible host is one of the factors required for caries to occur. Host factor :  Tooth

37. 37 Certain surfaces of a tooth are more prone to decay. Eg : In mandibular I molar the most prone areas in order are occlusal, buccal, mesial, distal and lingual.

38. These differences in decay rates of various surfaces on the same tooth are in part due to morphology, example lingual groove of maxillary incisors. 38

39. POSITION OF TOOTH IN THE ARCH: Malaligned ( buccally / lingually placed) Out of position Rotations. 39

40. 40 Armstrong et al - relation of caries to the chemical composition of teeth No differences were found in the calcium, phosphorous, magnesium and carbonate contents of enamel from sound and carious teeth. Significant differences in fluoride content of sound and carious teeth however have been reported by these same workers. They have found the fluoride content of enamel and dentin from Sound teeth 410ppm and 873ppm but Carious teeth 139ppm and 223ppm only. Composition of the tooth:

41. 41 Surface enamel is more resistant to caries than sub surface enamel. - Brudevold et al Surface enamel is highly mineralized and tends to accumulate greater quantities of fluoride, zinc, lead and iron than sub surface enamel .

42. 42 Role of saliva-

43. 43 99% - H2O. 1% - a) Inorganic – Main K, Na, Ca , Cu, HCO3- and inorganic phosphate. Others :b)Organic : Fluoride, sulfate, thiocyanate iodide and magnesium. Carbohydrates – glucose. Lipids – Cholesterol, lecillinin . Nitrogen –ammonia, nitrites, urea and amino acids. Miscellaneous – peroxide. Enzymes – carbohydrates (Amylase maltose), proteases trypsin Oxidases (catalase, oxidase) Composition of saliva:

44. 44 Daily volume - 0.5 – 1 litre secreted of which 90%- major salivary glands. 10%- minor salivary glands. 50%produced during chewing and 2-10% during sleep Salivary secretion rate- Normal unstimulated/resting - 0.3-0.5ml/min. Normal stimulated - 1-2ml/min. Secretion of saliva:

45. Role of saliva as a modifying factor in dental caries: 45 The principle properties of saliva that protect the teeth against caries: Dilution and clearance of dietary sugars. Neutralization and buffering of the acids in plaque. Supply of ions for remineralization . Both endogenous and exogenous antiplaque and antimicrobial factors.

46. 46 A number of antibacterial factors such as lysozyme, lactoperoxidase , lactoferrin and immunoglobulin A are present in saliva. Lysozyme : This has the property of cleaning the cell wall of certain microorganisms, thereby causing their lysis . Lactoperoxidase: (milk, tears, saliva):Known to be inhibitory towards streptococci and lactobacilli. They oxidize thiocyanate in the presence of hydrogen peroxide. Lactoferrin : Strong ion-binding capacity thereby removing bacterial iron and making it unavailable to the bacteria. Antimicrobial properties of saliva:

47. 47 Immunoglobins (IgA) It is the predominant immunoglobin present in saliva secretory IgA is an effective agglutinin. It inhibits adherence and prevents colonization of mucosal surfaces of teeth by organisms facilitating their disposal by swallowing. Other salivary protein with protective penetration. a) Glycoproteins: Depending on their linkage Mucinous Serous

48. CHEMICAL NATURE OF THE TOOTH : % F , Ca , Sn CARIES SUSCEPTIBILITY 48

49. CARIES BIOFILM Microbiology & histopathology of dental caries 49

50. Biofilm and the carious process 50

51. Dental plaque biofilm Dental plaque is a structurally and functionally organized biofilm . Dental plaque has been defined as the diverse community of micro-organisms found on a tooth surface as a biofilm embedded in a matrix of polymers of host and bacterial origin. ( Marsh 2004.) 51

52. Quorum sensing 52 Regulation of expression of specific genes through the accumulation of signaling compounds that mediate Intercellular communication Mediated by a competence stimulating Peptide (CSP) in S.mutans . Csp is directly involved in biofilm Formation This quorum sensing system also functions to regulate acid tolerance in S.mutans Biofilms.

53. Plaque sites Fissure plaque-mainly mutans streptococci Smooth surface plaque Approximal plaque –mainly G+ve rods esp. Actinomyces spp. 53

54. Oral biofilm formation 54

55. Development of dental plaque 55

56. 56

57. Current hypotheses to explain role of bacteria in the etiology of caries 57

58. Specific plaque hypothesis Proposed that out of the diverse collection of species present in plaque only a relatively small number were directly involved in causing disease. (Loesche,1976). Benefit: focusing studies on the control of specific microbial targets . Association of mutans streptococci with dental caries is not unique. 58

59. Non-specific plaque hypothesis Proposed that disease is the outcome of the overall activity of the total plaque microflora. In this way, a heterogenous mix of microorganisms could play a role in disease. 59

60. Ecological plaque hypothesis –key features 60

61. 61

62. Relatively unaffected, SUBSURFACE DEMINERALIZATION seen Special properties of enamel, with greater mineralization-not accepted Higher fluoride content Greater amount of insoluble protein Protection by pellicle/plaque- remineralization Moreno model-Ca & Phosphate that diffuse from subsurface are precipitated in outer surface layer (DCNA 1999) 62

63. pH 6.8 6.0 5.5 5.0 4.5 4.0 3.5 3.0 8.0 6.8 6.0 5.5 5.0 4.5 4.0 3.5 3.0 Critical pH of HA Demineralisation- remineralisation cycle Critical pH of FA D HA dissolves Ca,HPO42 OH FA form R FA HA, FA dissolves H + exhausted/ neutralized H + + po 4 HPO 4 2- Saliva and plaque HA, FA form calculus Re/demineralisation caries erosion 63

64. Diet and dental caries 64

65. Definitions : Cariogenic foods : are those that contain fermentable substrates that can be metabolized by oral bacteria to cause a decrease in plaque pH < 5.5 and result in demineralization of tooth enamel and ultimately caries . The Cariogenic Potential – “ a foods ability to foster caries in humans under conditions conducive to caries formation”. 65

66. 1.TYPE: 1A. Carbohydrates: 66

67. Carbohydrate nomenclature : Monosaccharides : Glucose (dextrose ) Fructose( fruit sugar ) Galactose Invert Sugar(1:1 glucose and fructose) Disaccharides: Sucrose (table sugar) Maltose Lactose (milk sugar) Trehalose (mushroom sugar) Natural and manufacured oligosaccharides. Polysaccharides(>10 units) Starch Ref : D.T.Zero . Sugars- The Arch Criminal? Caries Res 2004;38:277-285. 67

68. 1D. Form of carbohydrate : 68

69. 1D. Form of carbohydrate : Directly related to Adhesiveness ( sticky) of the foods . Form effects the length of time that teeth are exposed to sugar-containing foods . And there is high retention for foods which are adhesive . Ref:1. Robert c. Caldwell. Physical Properties of Foods and Their Caries-Producing Potential. J Dent Res Supplement to No. 6 , Vol 49 1970 2. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 69

70. Ref:1. Robert c. Caldwell. Physical Properties of Foods and Their Caries-Producing Potential. J Dent Res Supplement to No. 6 , Vol 49 1970 70

71. 1D. Form of carbohydrate : Further suggested that chemical composition of the food is possibly more significant than physical parameters from the standpoint of cariogenicity . Interplay of physical and chemical factors influences food carcinogenicity. Ref:1. Robert c. Caldwell. Physical Properties of Foods and Their Caries-Producing Potential. J Dent Res Supplement to No. 6 , Vol 49 1970 71

72. Position of carbohydrate in a meal sequence. 72

73. 1E. Position of carbohydrate in a meal sequence. Position of a food product with in a meal sequence or a snack can alter its cariogenic properties. For e.g. both cheese and peanuts have shown to reduce the acid reduction after the previous intake of sucrose – containing foods . Cheese – stimulates saliva , releases calcium , and tyramine increases salivation. Ref: 1. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 2. D.A.M. Geddes. Diet Pattern and Caries. Adv Dent Res 8(2):221-224, July, 1994. 73

74. Rugg -Gunn et al 1981 studied the position of sugar containing items in the sequence of foods was investigated in a test breakfast consisting of three items – soft – boiled egg, crisp bread and butter , and a cup of sugared coffee. If the sugared coffee was taken before or between the non – acidogenic or slowly fermented items, the acidogenicity was reduced. However the greatest reduction in acidogenicity was obtained when the sugared coffee was taken throughout the meal . Ref: 1. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 2. D.A.M. Geddes. Diet Pattern and Caries. Adv Dent Res 8(2):221-224, July, 1994. 74

75. Combination of Carbohydrates. 75

76. 1F.Combination of Carbohydrates. Starches can increase the cariogenic properties of sugar if they are consumed at the same time. The stickiness of starch enhances the retention time of sugar as well as the clearance rate , resulting in a prolonged pH fall. Ref: 1. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 76

77. 1Aa. Sugars : 77

78. 1Aa. Sugars : Technically the term applies to two classifications of carbohydrates. 1. Free form monosaccharides. 2. Disaccharides. Ref : 1. Norman O. Harris, Fraklin Gracia-Godoy.Primary Preventive Dentistry.6 th edition , 2004, Pearson Prentice Hall. 2. D.T.Zero . Sugars- The Arch Criminal? Caries Res 2004;38:277-285. 78

79. 1Aa. Sugars : Sucrose arch criminal of dental caries - : Sole substrate in synthesis of extracellular (water-soluble and water- insoluble) glucans mediated by microbial glycosyl transferases . - glucans - major component of the structural intermicrobial matrix of dental plaque. - enhances ability of mutans streptococci to accumulate on smooth surfaces of teeth. Ref : 1.D.T.Zero. Sugars- The Arch Criminal? Caries Res 2004;38:277-285 2. Norman O. Harris, Fraklin Gracia-Godoy.Primary Preventive Dentistry.6 th edition , 2004, Pearson Prentice Hall. 79

80. 1Aa. Sugars : Sucrose arch criminal of dental caries - : Review by Zero in 2004 showed that sucrose was more cariogenic than other dietary sugars in rat caries model : -strain of streptococcus mutans -generally associated with smooth surface caries Ref : 1.D.T.Zero. Sugars- The Arch Criminal? Caries Res 2004;38:277-285 2. Norman O. Harris, Fraklin Gracia-Godoy.Primary Preventive Dentistry.6 th edition , 2004, Pearson Prentice Hall. 80

81. Classic evidence from humans supporting the role of sugar in dental caries : D.T.Zero . Sugars- The Arch Criminal? Caries Res 2004;38:277-285. 81

82. HUMAN CLINICAL STUDIES: The Vipeholm studies: The Vipeholm study ( Gustaffson et al 1954) is probably the biggest example study in the field of dental caries ever undertaken . 436 inmates of vipeholm hospital – Sweden. 82

83. Does increase in carbohydrate intake cause increase in dental caries..?? If So..?? 1.)Is the caries activity influenced by Ingestion of non sticky sugars at meals Ingestion of sticky sugars at meals Ingestion of sticky sugars in between meals 2.) Does decrease in sugar intake reduce the incidence of caries.? 83 Purpose of the study

84. There was one control group and six experimental groups. Dental examination system was developed. Five bite-wing films were taken annually, together with models and photographs. Caries was diagnosed 84 Method

85. Control group: 60 males - avg age group of 34.9 yrs Low carbohydrate, high fat diet free from refined sugar (For 2 years) 85 Caries activity – suppressed After 2 years Ordinary diet – 110 gms of sugar (at meal times) Small but significant rise in caries

86. 86 57 males – 300 gms of sugar solution at meals for 2 yrs and later reduced to 75 gms SUCROSE GROUP : No significant increase in caries BREAD GROUP: 41 males and 42 females Sweet bread with 50 gms of sugar once per day (2 yrs ) no caries 4 portions of sweet bread during 4 meals Significant increase in caries

87. 87 CHOCOLATE GROUP: 47 males – 300 gms of sugar solution at meals (first 2 years) Reduced to 110 gms supplemented with 65 gms of milk chocolate between meals (next 2 yrs ) Result: caries increment was low in first two years and increased in later 2 years. CARAMEL GROUP: First 2 years – control group of 62 males Next 2 years – 22 caramels daily in 2 portions between meals. Fifth year – withdrawal of caramel Result: increase of caries incidence followed by fall

88. 88 8 toffee group: 40 males First year – low carbohydrate Second year – 8 toffees daily (during meals) marked rise in caries increment 24 toffee group: 48 males – 24 toffees in between meals for 3 rd and 4 th years Withdrawal of toffees – 5 th year Result: greatest increase in caries during 3 rd and 4 th years followed by decline in 5 th year

89. Conclusion of the study: Increase in sugar definitely increases caries activity Risk is greater if consumed in form that stays on tooth surface for longer time Increased risk if consumed between meals Upon withdrawal the risk gradually decreases Increase in clearance time of sugar increases caries activity 89

90. Studies on groups of people eating low amounts of sugar: Hopewood house is a home in rural New South Wales, Australia housing about 80 children of low socio-economic back ground. Dental examinations were conducted annually between 1947 and 1962 and thorough dietary surveys were made (Sullivan and Harris 1963). The dental surveys revealed a very low prevalence and severity of dental caries, much lower than children of the same age and socio-economic back-ground attending state schools in South Wales, who were examined using the same methods. 90 Hopewood house study

91. Spartan diet: strict natural diet with occasional egg serving Entire vegetable and raw Absence of meat and sugar were significant features of this study. Meals: vitamin concentrates, nuts and honey(rarely) End of 10 years: 13 yr old children had mean dmft of 1.6 per child 91

92. The Turku sugar studies: The object was to study the effect on dental caries increment of nearly total substitution of sucrose in a normal diet with either fructose or xylitol. The 125 subjects were allocated to 3 groups-sucrose (S), fructose (F), and Xylitol (X). The caries examination was conducted Two standardized bite-wing radiographs were taken Both precavitation and cavitation lesions were recorded, for both primary and secondary caries. 92

93. Sugar and sugar containing foods were provided free during the two-year study. All subjects were asked to avoid sweet fruits such as dried figs, raisins, and dates, since the sugars in these foods could not be substituted. The increments in the F and S groups being approximately equal at the end of the first year but during the second year the development of the S group caries increment continued at the same rate while virtually no increase was observed in the F group. Little caries occurred in the X group and that which developed was cancelled out by the healing of precavitation lesions by the 24 th month, resulting in a zero or near zero two-year increment. 93

94. While the X diet was clearly less cariogenic than the S or F diet, it cannot be concluded that the F diet was less cariogenic than the S diet. Results of serum analyses and liver-function tests indicated that Xylitol or fructose did not alter metabolic parameters of liver function compared with a normal sucrose diet. 94 RESULTS

95. 1Ad. High – fructose corn syrup(HFCS) . Produced mainly for economic reasons for use in beverages. Chemically similar to invert sugar (50% fructose plus 50% glucose. HFCS and invert sugar do not cause any production of extracellular polysaccharides in the oral cavity. Cariogenecity of invert sugar 20-25% less than that of sucrose . Ref: 1. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 95

96. 96 Sugars in medicines.

97. 1Ae.Sugars in medicines. Medicines such as cough drops , throat lozenges , vitamin preparations and antibiotic syrups. 70% sugar. Consumption of these several times a day , often before bedtime results in a fall in pH of plaque. Ref: 1. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 97

98. 1Ae.Sugars in medicines. They pose a threat to the dental health especially of children.. Thus sugar formulations containing artificial sweeteners should be encouraged - Sorbitol , hydrogenated glucose syrups ( lycasin ) and saccharin used Ref: 1. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 98

99. 1B.Total sugar consumption: 99

100. 1B.Total sugar consumption: The relationship between total sugar consumed and dental caries is strong. A study done by Sreenby et al in 1982. Data on the prevalence of dental caries for 6- and 12-year-old children in, respectively, 23 and 47 nations. For the 12 year-old-children there is a significant positive correlation between the per capita availability of sugar and dental caries. Ref: 1.Sreebny LM. Sugar availability, sugar consumption and dental caries. Community Dent Oral Epidemiol . 1982 Feb;10(1):1-7. 100

101. 1B.Total sugar consumption: WHO suggested that the availability, and presumably the ingestion, of 50 g of sugar per day may represent an outer limit of "safe" or "acceptable" sugar consumption in regard to dental caries. 101

102. 1B.Total sugar consumption: The World Health Organization and Committee on Medical Aspects of Food Policy ( COMA ). Recommended that free or non-milk extrinsic sugars intake should be below 10% of total energy intake. Strongly implicated sugars as the main causative factor in dental caries. Ref: 1.Sheiham A. Why free sugars consumption should be below 15 kg per person per year in industrialised countries: the dental evidence. Br Dent J. 1991 Jul 20;171(2):63-5. 102

103. 1B.Total sugar consumption: The dose-response curve for sugar and caries is approximately sigmoid (S-shaped). At levels of sugar consumption below 10 kg/person/year the incidence of caries is acceptably low. Beyond 15 kg the incidence increases more rapidly. Ref: 1.Sheiham A. Why free sugars consumption should be below 15 kg per person per year in industrialised countries: the dental evidence. Br Dent J. 1991 Jul 20;171(2):63-5. 103

104. 1C.Intake pattern. 104

105. 1C.Intake pattern. Most studies point at frequency of eating as being of greater etiological importance for caries than the total sugar consumption . Frequency refers to the number of times per day certain foods are eaten . Ref: 1. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 2. D.A.M. Geddes. Diet Pattern and Caries. Adv Dent Res 8(2):221-224, July, 1994. 105

106. 1C.Intake pattern. High intake frequency increases the overall length of time that the teeth are exposed to sugar containing foods . Primary evidence : Vipeholm study - Gustafsson et al 1954 Ref: 1. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 2. D.A.M. Geddes. Diet Pattern and Caries. Adv Dent Res 8(2):221-224, July, 1994. 106

107. Influence of other foods on the relationship between sugar and caries : 107

108. 1G.Influence of other foods on the relationship between sugar and caries : 1. Fluoride : During frequent administration , fluoride accumulates in dental plaque and has shown to influence the sugar caries relationship, both as free ions in the plaque fluid and in bound intracellular matrix . Total fluoride concentration 5-10 ng/mg on a wet weight basis. Ref: 1. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 108

109. 1G.Influence of other foods on the relationship between sugar and caries :Flouride Cutress et al conducted a study in 1995 – with sucrose, 5% and 10% , supplemented with between 0 and 5 ppm fluoride (F). It was found that enamel demineralization was inversely related to the F concentration in the range 2 to 5 ppm, for both 5% and 10% sucrose. Cutress et al also concluded that introduction of flouride has shifted the sugar/caries sigmoid curve to the right , increasing the safe margin of sugar intake . Ref:1. T.W. Cutress et al. Effects of fluoride-supplemented sucrose on experimental dental caries and dental plaque ph. Adv Dent Res 9(1):14-20, February, 1995 109

110. Ref: D.T.Zero. Sugars- The Arch Criminal? Caries Res 2004;38:277-285 110

111. 1Ab. Starches. A review by Lingstrom et al suggested aspects of starchy foods consumption, deserving greater attention: - bioavailability of starches in processed foods. - their retentive properties. -also in relation to sugars present (starches as co- cariogens ). - their consumption frequency. - the effect of hyposalivation on their cariogenicity . - their impact on root caries. Ref :Lingström P, van Houte J, Kashket SFood starches and dental caries. Crit Rev Oral Biol Med. 2000;11(3):366-80 111

112. 1B.Type : Other Minerals Selenium is associated with a higher prevalence of caries – excessive selenium disrupts the formation of the enamel matrix and subsequent mineralization of the tooth. Zinc – increases susceptibility to caries if present during tooth formation . Ref: 1. w.h . bowen . food components and caries. adv dent res 8(2):215-220, july , 1994 2. carole a. Palmer, Diet and Nutrition in Oral Health.Julie Levin Alexander, 2003. 112

113. Other factors in diet : Last item taken in an episode of meal would have the greatest influence on subsequent plaque Ph. If the meal also includes items which do not contain such carbohydrate, then the sequence and timing of eating periods may influence plaque acidogenecity . If food item is a good sialogogue , the saliva stimulated by the subject eating such an item will be available to neutralise plaque acid . Ref: 1. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 2. D.A.M. Geddes. Diet Pattern and Caries. Adv Dent Res 8(2):221-224, July, 1994. 113

114. Critical pH- 114 The critical pH is the pH at which environment of the enamel becomes unsaturated and in addition that pH at which sufficiently high concentration of un ionized acid are present to ensure the inward diffusion of enough acid to extend to inner lesion. On total depletion of these compounds, the pH can fall below the critical value of 5.5, at which the aqueous phase becomes undersaturated with respect to hydroxyapatite.

115. 115 Critical pH values- -Enamel - 5.2 - 5.5 - Dentin - 6.0 - Cementum - 6.7 - Fluorapetite -4.5

116. Stephans curve : 116

117. 117

118. 118

119. ORAL MICROBIOME 119

120. Types of predominant Microflora: 120 Oral streptococci Irrespective of the age of plaque and the diet, the predominant organisms are gram - positive cocci of the genus streptococcus which form about 50% of the total colony forming units. These streptococci have been divided into various groups based on their colonial morphology and physiological characteristics. Oral streptococci have been isolated on mitis-salivaries agar a selective medium that permits isolation from mixed flora.

121. Pathogenic properties of cariogenic bacteria Rapid transport of fermentable sugar and their conversion to acids Production of Extracellular Polysachharides and Intracellular Polysaccarides Ability to maintain sugar metabolism under extreme environmental conditions 121

122. Criteria for Cariogenicity An organism must acidogenic An organism must be aciduric An organism must exhibit tropism for teeth An organism must utilize refined sugar (sucrose) ( Newburn , 1983) 122

123. The caries culprits The main microorganism involved in the initial caries process is S. mutans . S. sobrunis and lactobacillus are also involved, but must have s. mutans present to colonize. Lactobacillus produces lactic acid at higher concentrations 123

124. The Mutans Streptococcus Species Serotype Source S. mutans c,e,f Human S. sobrinus d,g,h Human S. cricetus a Sometimes human, mostly rats and hamsters S. rattus b Sometimes humans, mostly rats S. downei h Macaque monkey S. macacae c Macaque monkey S. ferus c Rats 124

125. Microorganisms found in various types of carious lesions Pit and fissures s.mutans , s.sanguis,lactobacillus sp.actinomyces Smooth surface caries s.mutans , s.salivarius Root caries Actinomyces viscosus , A.naeslundii , s.mutans , s.sanguis,s.salivarius Deep dentinal caries Lactobacillus sp, Actinomyces viscosus , A.naeslundii 125

126. Streptococcus mutans In 1924 Clarke isolated a streptococcus that predominated in many human carious lesions and he named streptococcus mutans because of its varying morphology . They are non motile , catalase -negative, gram –positive cocci in short or medium chains . On mitis-salivarius agar they grow as highly convex to pulvinate (cushion –shaped)colonies. These colonies are opaque ;the surface resembles frosted glass. 126

127. When cultured with sucrose they form insoluble Polysaccharides. This property of forming insoluble extra cellular polysaccharides from sucrose is regarded as an important characteristic contributing to the caries –inducing properties of s.mutans . Mutants of s.mutans ,which lack the ability to synthesize insoluble glucans or to stick to glass surfaces, do not cause smooth surface caries. 127

128. Streptococcus mutans exhibits several important properties ; 1) synthesizes insoluble polysaccharides from sucrose 2) homo fermentative lactic acid former . 3) colonizes on tooth surfaces 4) more aciduric than other Streptococci 128

129. 129

130. The Oral Steptococci and Disease S. mutans (dental caries) S. sanguis (gingivitis) viridans Streptococci (bacteremia, endocarditis) 130

131. VIRULENCE FACTORS Aciduric (Produces lactic Acid ) Acid tolerance Produces insoluble glucans ; ECP: 1. Glucans ( dextrans ) sticky insoluble ; 2. Levans ( fructans ) energy ICP: Energy sources inside Strep; Accumulation of intracellular amylopectin -like polysaccharides (carbon/energy reserve) Adherence: S. mutans cells binds to salivary components in the pellicles. 131

132. How does Strep mutans attach to teeth and cause caries? 132

133. Attachment of S.mutans on teeth Initial attachment of S. mutans to tooth pellicle (mediated by adhesin ). Sucrose is broken down into fructose and glucose by glucosyltransferases (GTFs). Glucose is stored as a glucan polymer (dextran). Fructose and glucose are both metabolized, resulting in lactic acid accumulation. S. mutans accumulates as glucosyltansferases (GTFs) adhere to glucans produced by other bacteria in plaque. 133

134. Streptococcus sobrinus S. sobrinus is thought to enhance caries initiation ,progression and development. Prevalence is more closely associated with high caries activity than that of S. mutans . It has a higher acidogenic capacity compared to S mutans . It is unable to synthesize IPS . Requires sucrose for attachment and growth in plaque. 134

135. Streptococcus sanguis . 135 This is one of the predominant groups of streptococci colonizing on the teeth. Formerly it was called streptococcus s. b. e because of its involvement in sub acute bacterial endocarditis. Caries from this strain occurs primarily in sulci and is significantly less extensive than S. mutans . On blood agar S. sanguis causes (green) hemolysis.

136. Streptococci Salivarius 136 They have been found in the plaque, throat, nasopharynx and oral mucosa, but their natural habitat in the dorsum of the tongue. In humans they have only a minor degree of cariogenic significance.

137.   Lactobacilli are gram positive ,non spore –forming rods that generally grow best under micro aerophilic conditions. Isolation and enumeration of oral lactobacilli have been facilitated by use of selective agar medium which suppresses the growth of other oral organisms by its low pH (5.4) . Lactobacilli are found mostly as transients in the mouth of infants . Lactobacilli represents about 1% of the oral flora . L. casei and L fermentum are the most common oral species. The population of oral lactobacilli is influenced by dietary habits. A favorite habitat of lactobacilli is in the dentin of deep carious lesions. ORAL LACTOBACILLI 137

138. LACTOBACILLUS 138

139. Lactobacilli, have been reported in the oral cavity ever since Miller enunciated the chemo parasitic theory. In 1925, Bunting and his collaborators claimed that bacillus Acidophilus was the specific etiological factor responsible for the initiation of caries. Subsequent investigators have isolated other types of lactobacilli besides L. acidophilus in saliva, plaque, and carious lesions. LACTOBACILLI AND ITS ROLE IN CARIES. 139

140. Oral actinomyces Actinomyces is a gram positive , nonmotile ,non-spore-forming organisms occurring as rods and filaments that vary considering in length . Filaments are usually long and slender and are branching . The species that have been found in the oral cavity are: Facultative anaerobic anaerobic   A. naeslundii A . israelii A. viscosus Actinomyces meyeri A. odontolyticus 140

141. ORAL ACTINOMYCES 141

142. All species of Actinomyces ferment glucose, producing mostly lactic acid ,lesser amounts of acidic and succinic acid ,and traces of formic acid. Most interest has centered on A.viscosus and A naeslundii because of their ability to induce root caries, fissure caries ,and periodontal destruction when inoculated into gnotobiotic rats. 142

143. Actinomyes is a good plaque former ,capable of adhering to wires and forming tenacious deposits on the teeth. It is the most common group of microorganisms isolated from the subgingival microflora and from plaque of human root surfaces caries. It is found in the supragingival plaque of all children and comprises about 50 % of all cells present . A naeslundii predominates in the tongue ,salivary flora ,and in the plaque of young children ,while plaque from teenagers and adults has a higher proportions of A viscosus . 143

144. End of part-1 . Thank you. 144

145. 145

146. 146

147. Genetics and dental caries… J Evid Based Dent Pract . 2003 Dec; 3(4): 185–189. Evidence of a contribution of genetic factors to dental caries risk Walter A. Bretz , Patricia Corby , Nicholas Schork , and Thomas C. Hart 147 Subjects: The literature was searched for evidence of a contribution of genetic factors to increased or decreased risk for dental caries. A search for global evidence of caries heritability was carried out using twin studies. Next, separate searches were carried out for evidence of heritability for 3 potential mechanisms associated with caries risk that included variation in the quality of the dental hard tissues, variation in host immune response, and variation in sugar metabolism

148. CONCLUSIONS Twin studies provide the opportunity to dissect the relative contribution of genetics and environment on dental caries variation. Accordingly, these studies can often suggest, but not prove, biological inheritance. Current evidence supports the notion that there is an inherited variation in enamel development that is associated with increased occurrence of dental caries. At present, these results are limited to specific populations with overt recognizable syndromes. Evidence is presented that immune complex genes may modulate the presence of enamel defects and colonization of cariogenic bacteria 148

149. ANALYSIS Twin studies of dental caries have shown that genetic and environmental factors play significant roles. However, estimates of heritability from the reports reviewed display considerable variability, no doubt, caused by differences in statistical analysis models, age, gender, sample size, origin of cohorts and measurement of dental caries phenotype. In addition, cohort and case-control studies linking a particular gene to dental caries are too few and these studies often neglect the role of environmental factors on dental caries development that could interact with genetic factors to induce disease 149

150. Dental caries – part 2 Contents Classification Histopathology 150

151. 151 CLASSIFICATION:

152. According to location: Primary caries Caries of pit and fissure origin Caries of enamel smooth surface origin Backward caries Forward caries Residual caries Root surface caries Secondary (recurrent) caries 152

153. 153 According to extent: a. Incipient (reversible) caries b. Cavitated (irreversible) caries

154. 154 According to hard tissue affected: a. Enamel b. Dentin c. Cementum   Others: Primary caries & secondary caries Nursing caries Radiation caries Rampant caries

155. 155 ACCORDING TO LOCATION: Primary caries: Primary caries is the original carious lesion of the tooth. Accordingly 3 morphologic types of primary caries are evident in clinical observations. Type I – pit & fissure and occlusal surfaces. Type II – Smooth surfaces of which there are 2 variants interproximal and cervical / gingival. Root surface caries.

156. 156 These caries can form in the regions of pits and fissures Usually resulting from imperfect coalescence of the developmental enamel lobes. Such caries are not so clinically noticeable until the forces of mastication fracture the increasing amount of unsupported enamel . Type I / Pit and fissure caries :

157. 157 Limited to the – Occlusal surfaces of molars and premolars - Buccal pits of molars - Lingual surfaces of maxillary anterior teeth Poor self cleansing features Usually occurs before smooth surface caries Clinically - Black or brown in color - Slightly soft consistency - “Catch” the tip of a fine explorer

158. Caries of enamel smooth surface origin: 158 Smooth surface caries does not begin as an enamel defect, but rather in a smooth area of the enamel surface that is habitually unclean and is thereby continually or usually covered by plaque.

159. Progression 159

160. 160 Forward caries: Forward caries is wherever the caries cone in enamel is larger or atleast the same size as in dentine.

161. Backward caries: 161 When the spread of caries along the DEJ exceeds the caries in the contiguous enamel, caries extends into this enamel from the junction and is termed as backward caries.

162. Recurrent caries (secondary caries): 162 It occurs at the junction of a restoration and the tooth and may progress, under the restoration. It is termed as recurrent caries. This condition usually indicates that microleakage is present- -due to poor cavity preparation, -faulty restoration or a combination of these factors .

163. Root surface caries: 163 These kind of caries originate in the dentinal root portion of a tooth. It is predominantly found in the dentitions of older age groups with significant gingival recession and exposed root surfaces. It initiates on the surface of mineralized dentin and cementum which have greater organic content. For this reason, bacterial flora causing root caries is also different from flora causing smooth surface caries.

164. Linear enamel caries : 164 This is an atypical form of dental caries called linear enamel caries. The lesions predominate on the labial surfaces of the anterior maxillary teeth on the region of the neonatal line. Lesion is crescent shape Increase caries susceptibility of posterior teeth. Recent evidence suggests that neonatal line forms due to transient hypocalcemia , a normal feature of the neonatal period

165. Odontoclasia : 165 Variant of linear enamel caries Results in gross destruction of the labial surfaces of incisor teeth Cause may be an inherent structural defect

166. EARLY CHILDHOOD CARIES 166

167. Early childhood caries “A suddenly appearing, widespread, rapid burrowing type of caries, resulting in early involvement of the pulp and affecting those teeth usually regarded as immune to ordinary decay.” - Massler A complex disease involving maxillary primary incisors within a month after eruption and spread rapidly to involve other primary teeth. -Davies (1988) 167

168. CLASSIFICATION 168

169. NURSING CARIES A unique pattern of dental decay in young children due to prolonged and improper nursing/feeding habit. -Winter et al, 1966 169

170. 170

171. CLINICAL FEATURES 171

172. Mandibular anterior teeth are usually spared because of: Protection by tongue Cleansing action of saliva due to presence of the orifice of the duct of sublingual glands very close to lower incisors. 172

173. PROGRESSION OF THE LESION 173

174. NURSING CARIES RAMPANT CARIES 174

175. NURSING CARIES RAMPANT CARIES 175

176. 176 Complication of radiation therapy of oral cancer lesion Radiation induced xerostomia produces caries conducive environment Carious lesion develops as early as 3 months after onset of xerostomia May be caused by other factors like salivary gland tumors, autoimmune diseases, prolong illness Radiation caries:

177. Adolescent caries: 177 Acute caries attack at 11-18 years of age Lesion in teeth and surfaces that are relatively immune to caries Small opening in enamel with extensive undermining Rapid clinical course Little or no secondary dentin formation

178. Arrested caries: 178 Caries which becomes static or stationary and does not show any tendency for progression Both dentitions are affected Lesion appears as large open cavity with lack of food retention Superficially softened and decalcified dentin gets burnished and has brown stained polished appearance - “Eburnation of dentin

179. 179 Senile Caries Caries activity that spurts up during the old age. They are located exclusively on the root surfaces of the teeth. Also seen in association with partial denture clasps. Causes: gingival recession, decreased salivary secretion, poor oral hygiene.  

180. Occult Caries / Hidden Caries 180 Not clinically diagnosed, but detected only on radiograph. Seen in persons with low caries index suggestive of increased fluoride exposure. Also called as fluoride bombs or fluoride syndrome

181. CERVICAL BURNOUT 181

182. 182 G.V.Black’s Classification   Class-I: - Caries on the occlusal surfaces of molars and premolars - Occlusal 2/3 of the buccal and lingual surfaces of molars - Lingual surfaces of the anterior teeth Class-II: - lesions found on the proximal surfaces of molars and premolars Class-III: - lesions found on the proximal surfaces of anterior teeth, but do not involve the incisal angle

183. 183 Class-IV: - lesions found on the proximal surfaces of anterior teeth and involving incisal angle Class-V: - lesions found on the gingival third of the facial and lingual surfaces of anterior and posterior teeth. Class-VI: - were not included in Black’s classification - Proposed by Siomon - Lesions on the incisal edge and cusp tips of the teeth  

184. 184 ACCORDING TO EXTENT

185. 185 ICDAS classification

186. Root caries (New in ICDAS II) E = Excluded root surfaces (no gingival recession) 0 = Sound (no caries or restoration) 1 = Non- cavitated carious root surface— soft or leathery 2 = Non- cavitated carious root surface— hard and glossy 3 = Cavitated (greater than 0.5mm in depth) carious root surface— soft or leathery 4 = Cavitated (greater than 0.5mm in depth) carious root surface—hard and gloss 6 = Extensive cavity: an extensive cavity involves at least half of a tooth surface and possibly reaching the pulp. 7 = Filled root with no caries 186

187. 9 = Used for the following conditions 97 = Tooth extracted because of caries (tooth surfaces will be coded 97) 98 = Tooth extracted for reasons other than caries (all tooth surfaces coded 98) 99 = Unerupted (tooth surfaces coded 99) 187

188. The shared vision for the International Caries Detection and Assessment System is now that: it employs an evidence-based and preventively oriented approach, is a detection and assessment system classifying stages of the caries process, is for use in dental education, clinical practice, research and public health, provides all stakeholders with a common caries language, has evolved to comprise a number of approved, compatible ‘formats’, supports decision-making at both individual and public health levels and has generated the International Caries Classification and Management System, to enable improved long-term caries outcomes. 188

189. 189

190. 190 88

191. 191

192. 192

193. 193

194. 194

195. HISTOPATHOLOGY 195

196. 196

197. 197

198. Knowledge Of macroscopic features: detection & diagnosis of caries Of shape of lesion: cavity preparation Characteristics: Chronic disease Not self-limiting Cavity formation subclinical Total destruction Light microscopy Enamel lesion Mineral loss (signs, symptoms) visible Time Electron microscopy 198

199. Dental Caries Enamel Caries Dentin Caries Cementum Caries (Root caries) Smooth surface caries Pit and fissure caries 199

200. Speed of lesion formation Incipient caries to clinical caries: 18 ± 6 months Peak rate for incidence of caries: 2-4 yrs ( avg 3yrs) after eruption Poor oral hygiene, excess sucrose: 3 weeks Radiation induced Xerostomia: 3 months Occlusal caries require less time than smooth surface 200

201. Basic structure of enamel 201

202. Estimating mineral loss Clinical considerations Refractive indices of Hydroxyapatite, water and air Histological considerations Microradiography Polarized light microscopy 202

203. ENAMEL CARIES MACROSCOPIC FEATURES: White spot lesion Opaque, chalky white Surface features-SEM ( Thylstrup , 1994) : Deepened & irregular Tomes processes pits Irregular cracks & fissures Widened intercrystalline spaces Fractures of perikymata edges Microcavities 203

204. Brown spot lesion Sites Occlusal surfaces: Fissure morphology ( Newbrun , 1989) Starts at both sides of fissure wall 204

205. MICROSCOPIC FEATURES: Triangular/wedge in shape Divided into 4 zones Can be viewed in Plain transmitted light Polarized light-clearer picture 205

206. Histological features of early enamel caries 206 Loss of inter-rod substance prominent enamel-rods Appearance of transverse striations of enamel rods due to segmental demineralization Accentuation of incremental striae of Retzius

207. H/F of Advanced enamel caries 207 Classified on the basis of pore volume and mounting media used Zone 1 – Translucent zone Zone 2 – Dark zone Zone 3 – Body of lesion Zone 4 – Surface zone These zones are from the dentin towards the outer enamel surface

208. ZONE 1: TRANSLUSCENT ZONE At the advancing front- 5 -100 µm Seen with quinoline Pore volume: 1% Not always present, sometimes near lateral part 208

209. ZONE 2: THE DARK ZONE More constant feature-90-95% lesions Pore volume -2-4% Why is it called dark zone? 2 theories for small pores 209

210. ZONE 3: THE BODY OF THE LESION Largest zone Pore vol : 5% at periphery, 25% in centre Appears translucent in quinoline and dark with water Striae of retzius well marked old./chronic lesions: bands of well mineralized tissue Bacteria in between prisms (rods) 210

211. ZONE 4: THE SURFACE ZONE 20-50 µm Pore vol : 1% Negatively birefringence in water Importance: serves as barrier to bacterial invasion 211

212. Smooth surface caries The earliest manifestation of incipient enamel caries is the appearance of an area of decalcification , beneath the dental plaque, which resembles a smooth chalky white area. There is loss of interprismatic substance, with increased prominence and roughening of the ends of the enamel rods. White spot lesion 212

213. 213

214. Accentuation of incremental striae of Retzius . As deeper layers of enamel are involved it forms a cone shaped lesion with the apex toward the DEJ and the base toward the surface of the tooth. Eventual loss of continuity of enamel surface –feels rough to explorer tip. 214

215. Pit and fissure caries Fissures are diverse in shape and size Carious lesion starts at both side of fissure rather than at the base, penetrating nearly perpendicular to the DEJ. Lesion is cone-shaped with base towards dentine and apex towards enamel surface 215

216. 216

217. Progression of enamel lesion Caries dissolution along the rods Highest degree of tissue porosity is along “Central Traverse” Oldest part-along CT, lesion spreads laterally along the surface 217

218. Central defects of crystals-hollow hexagons As dissolution increases, disorganization of crystal arrangement, invasion of bacteria 218

219. Ultrastructural changes in enamel caries Destruction of crystals at borders & within the prism Arcade like defects bounded by rows of resistant crystals- “caries crystals” More dissolution in heads and less in tails 219

220. Remineralization/arrest Enamel most susceptible to caries during & after eruption 1 st molar:12-14 months 2 nd molar:14-18 months Premolars:1-2 months-less prone {Backer-Dirks (1966)} 220

221. Mechanism of arrest of non- cavitated lesions: Maintains original crystalline framework Etched crystallites serve as nucleating agents Wear & polishing of the partly dissolved external surface-regain of surface hardness Remineralized area: brown or black spots Mechanism Cavitated lesions can also be arrested with proper plaque control ( thylstrup ) New mechanism of remineralization : CPP-ACP 221

222. Clinical significance of enamel caries 222

223. CARIES OF DENTIN Begins with the natural spread of the process along the DEJ and rapid involvement of the dentinal tubules. The dentinal tubules act as tracts leading to the pulp (path for micro-organisms). Caries advances more rapidly as dentin provides much less resistance to acid attack . Early Dentinal Changes: -initial penetration of the dentin by caries  dentinal sclerosis, -calcification of dentinal tubules and sealing off from further penetration by micro-organisms, -more prominent in slow chronic caries. Dentinal sclerosis 223

224. DENTINAL CARIES Progression of enamel caries to dentin: 5.4% from 11 – 22 yrs ( Mejare et al, 1999) MACROSCOPIC CHANGES: Lateral spread along DEJ Cone shaped-apex towards the pulp Affected dentin-Brown or black in colour 224

225. MICROSCOPIC CHANGES: (mechanism) Caries advancement proceeds through 3 stages Acids demineralize the dentin Organic matter degenerates Loss of structural integrity & bacterial invasion 1 st mild stimuli –defense reaction of dentin-tubular sclerosis/TRANSPARENT ZONE Dentin demineralization-when lesion reaches DEJ Arrest of caries Cavitation of dentin-bacterial invasion 225

226. 226 Zone of Decomposed dentin Zone of Bacterial invasion Zone of Demineralisation Zone of Dentinal sclerosis Zone of Fatty degeneration Retreating Odontoblastic process INFECTED DENTIN AFFECTED DENTIN Dentinal caries

227. Behind the transparent sclerotic zone, decalcification of dentin appears. In the earliest stages, when only few tubules are involved, microorganisms may be found penetrating the tubules  Pioneer Bacteria. 227

228. This initial decalcification involves the walls allowing them to distend as the tubules are packed with microorganisms. Each tubule is seen to be packed with pure forms of bacteria, eg ., one tubule packed with coccal forms the other tubule with bacilli. 228

229. As the microorganisms proceed further they are distanced from the carbohydrates substrate that was needed for the initiation of the caries. Thus the high protein content of dentin must favour the growth of the microorganisms. Therefore proteolytic organisms might appear to predominate in the deeper caries of dentin while acidophilic forms are more prominent in early caries. 229

230. Advanced Dentinal Changes ; -decalcification of walls, confluence of the dentinal tubules, tiny “liquefaction foci”, described by Miller are formed by the focal coalescing and breakdown of dentinal tubules. These are ovoid areas of destruction parallel to the course of the tubules which filled with necrotic debris and increase in size by expanding. The adjacent tubules are distorted and their course is bent due to this expansion. 230

231. The destruction of dentin by decalcification and then proteolysis occurs in numerous focal areas- leading to a necrotic mass of dentin of a leathery consistency. Clefts present in the carious dentin that extends at right angles to the dentinal tubules, accounts for the peeling off of dentin in layers while excavating. 231

232. Shape of the lesion is triangular with the apex towards the pulp and the base towards the enamel. Zone 1; Zone of Fatty Degeneration of Tome’s Fibers,(next to pulp) -due to degeneration of the odontoblastic process. This occurs before sclerotic dentin is formed and makes the tubules impermeable. Zone 2; Zone of dentinal sclerosis, -deposition of Ca salts in the tubules. Zone 3; Zone of decalcification of dentin Zone 4; Zone of bacterial invasion Zone 5; Zone of decomposed dentin due to acids and enzymes. 232

233. ZONE OF FATTY DEGENERATION: Of the Tomes fibres -stained by Sudan red Importance: Fat contributes to impermeability of dentinal tubules Maybe a predisposing factor favouring sclerosis Innermost layer of dentinal caries towards pulp Due to deposition of fatty tissue in odontoblastic processes Seen usually in rapidly progressing caries No crystals or bacteria in lumen of tubules Intertubular dentin  normal 233

234. ZONE OF TUBULAR SCLEROSIS: Reaction of vital dentinal tubules & pulp Seals off tubules to further penetration by bacteria Mineralization process-2 types Hydroxyapatite crystals & large rhomboidal crystals ( whitlockite ) Transluscent appearance- transluscent /transparent dentin As the microorganisms cause destruction to dentin, initially there is an attempt to stop the advancement of caries by depositing the minerals. There is a deposition of mineral in intertubular dentin. Zone is called “transparent zone” Odontoblasts also start depositing dentin. At the periphery of sclerotic dentin, dead tracts are present. 234

235. ZONE OF BACTERIAL INVASION Initially tubules with single type of bacteria Liquefaction foci-beadings, varicosities, moth-eaten, rosaries Decalcification is by bacterial acid diffusion Very narrow zone, softer than normal dentin Further loss of minerals from inter tubular dentin Large crystals within lumen of dentinal tubules 235

236. ZONE OF DEMINERALIZATION Narrow zone Occlusion of tubules Softer than normal dentin Few microorganisms in the tubules – “pioneer bacteria” 236

237. 237 Zone of Decomposed Dentin / Infected Dentin Outermost zone, large scale destruction of dentin Foci of Miller join together Areas of dentin decomposition, occur perpendicular to dentinal tubules  “Transverse Clefts” Mechanism of formation of Clefts - not known May follow course of incremental lines or May result from coalescence of liquefaction of adjacent tubules Also may rise by extensive proteolytic activity along interconnecting lateral branches of odontoblastic processes Bacteria shift from dentinal tubules to the peri & inter tubular dentin

238. Zone of Decalcification with Bacterial Invasion / Turbid Dentin Initially only few tubules are involved & micro-orgs also less These are acidogenic , pioneer bacteria (initiators), present long before lesion is clinically detected Bacteria multiply within tubules & are seen in advancing front of lesion Walls of tubules are thin & when micro-orgs penetrate, they cause irregularities/distensions of walls  ROSARY BEAD appearance Later, bacteria have proteolytic activity, areas of proteolysis appear as spaces containing necrotic material & bacteria These areas  “Liquefaction Foci of Miller”. These areas vary in number & are parallel to dentinal tubules 238

239. TO SUMMARIZE: 239

240. Other features In slowly advancing lesions Sclerotic dentin-very hard, shiny Hypermineralized – radioopaque In moderately advancing lesions Dead tracts Reparative/reactionary dentin Pulp stones In rapidly advancing lesions Abscess, necrosis of pulp 240

241. Zones of dentin (sturdevant) ZONES OF DENTIN: Zone 1: normal dentin Zone 2: subtransparent dentin Zone 3: transparent dentin Zone 4: turbid dentin Zone 5: infected dentin AFFECTED DENTIN INFECTED DENTIN Caries detector – basic fuschin / 1% acid red ( Fusayama , 1979) 241

242. Secondary / Reactionary dentin 242 Protective mechanism to protect pulp Develops as a result of localized, non-specific irritation to odontoblasts Hyper mineralized,less number of dentinal tubules having irregular & torturous course

243. ROOT CARIES Occurs in older individuals where root/cementum is exposed Microorganisms penetrate along the clefts, sharpey’s fibres Delamination occurs along incremental lines Brush like appearance Radioopaque surface layer seen Dentinal tubular reactions 243

244. Root Caries Root caries as defined by HAZEN, is a soft, progressive lesion that is found anywhere on the root surface that has lost its connective tissue attachment and is exposed to the environment. -the root surface must be exposed to the oral environment before caries can develop here. -Plaque and micro-organisms are essential for the cause and progression of the lesion, mostly Actinomyces , -micro-organisms invade the cementum either along the Sharpey’s fibers or between the bundles of fibers. 244

245. 245 -spread laterally, since cementum is formed in concentric layers. -after decalcification of cementum, destruction of matrix occurs similar to dentin with ultimate softening and destruction of this tissue. -invasion of micro-organisms into the dentinal tunbules , finally leading to pulp involvement. -the rate is slower due to fewer dentinal tubules than crown area

246. 246 Histopathology: Outer surface of cementum – hyper mineralized, thus more caries resistant Resistance due to Reprecipitation of minerals from within Precipitation of minerals from Plaque Clefts formed, through which bacteria penetrate & cause tooth structure destruction Penetration occurs along course of Sharpey's fibers Once cementum completely exposed & destroyed, underlying dentin is involved

247. A tooth surface without caries. The first signs of demineralization. The enamel surface has broken down. A filling has been made but the demineralization has not been stopped. The demineralization proceeds and undermines the tooth. The tooth has fractured. 247

248. Conclusion : Dental caries should be considered as a consequence of ecologically driven imbalances of oral microbial biofilms. An appreciation of ecological principles will enable a more holistic approach to be taken in caries control. A better understanding of the process of biofilm formation ,its genetic regulation is necessary to the development of novel strategies for oral disease prevention and control. 248

249. Conclusion : Among the multifactorial etiology of dental caries diet plays an important role in the occurrence of dental caries. This seminar intended to provide an overview of the evidence for an association between diet and dental caries which has already been established and documented by a series of studies. But the information available regarding the association of diet and dental caries under the Indian context and the effect of rapid changes in urbanization and economic development on the Indian diet is sparse and needs further research. 249

250. Conclusion : The way ahead should be considered under 2 aspects: 1. The extrapolation of the data to the India diet and conditions. 2. The task of diet changes which requires lifestyle changes that would be challenging to bring about and thus should be an important focus area for dental public health programs/ approaches in any setting for different age groups and populations. 250

251. References : Cariology – Newbrun . Murray J.J. et al. The prevention of oral disease. 4 th Ed. Shafer. A textbook of Oral Pathology. 4 th Ed. S.S.Hiremath.Textbook of Preventive & Community Dentistry. Per Axelsson . Diagnosis and Risk Prediction of Dental Caries. 2000, Quintessence Publishing Co. Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease and its Management . Blackwell Munksgaard 2003. 251

252. References : T.W. Cutress et al. Effects of fluoride-supplemented sucrose on experimental dental caries and dental plaque ph. Adv Dent Res 9(1):14-20, February, 1995 . Lingström P, van Houte J, Kashket SFood starches and dental caries. Crit Rev Oral Biol Med. 2000;11(3):366-80 . Brian A. et al . Sugar Consumption and Caries Risk:A Systematic Review. Journal of Dental Education . October 2001. Volume 65, No.10 252

253. References : Gordon Nikiforuk . Understanding Dental Caries.Karger Publishers. D.T.Zero . Sugars- The Arch Criminal? Caries Res 2004;38:277-285 . Norman O. Harris, Fraklin Gracia-Godoy.Primary Preventive Dentistry.6 th edition , 2004, Pearson Prentice Hall.. Carole A. Palmer, Diet and Nutrition in Oral Health.Julie Levin Alexander, 2003. 253

254. References : Marsh P. Dental plaque as a biofilm and a microbial community-implications for health and disease. BMC Oral Health 2006,6:S14. Thomas H.J et al .Managing the complexity of a dynamic biofilm. JADA, 2006;Vol.137;10s-15s. Scheie A.A &Peterson F.C.The Biofilm concept:consequences for future prophylaxis of oral diseases? Crit Rev Oral Biol Med 15(1):4-12 (2004) 254

255. Questions asked in NTRUHS examination : Balanced diet in prevention of dental caries – 20 M – APR 2015 Early childhood caries – 7 M – 2011 Diet counselling – 2011 and 2013 for 7M and 20M Cariogenecity – 2003 Rampant caries – 2003 Bacteriological role in caries – 2002 Diet for healthy teeth – 2001 Genetics and dental caries- 2001. 255