5. CARIOLOGY in conservative dentistry and endodontics .pptx

5. CARIOLOGY .pptx

1. DENTAL CARIES- HISTORY & ETIOLOGY DR. SUSHMITA RANE MDS-1 SEMINAR 5 11/7/2022

2. Definition Dental caries is an irreversible microbial disease of the calcified tissues of the teeth, characterized by demineralization of the inorganic portion and destruction of the organic substance of the tooth, which often leads to cavitation- Shafer ,1993 The word Caries is derived from the Latin word meaning ‘ Rot or decay’

3. History Caries In Modern Society Caries In Prehistoric Man

4. Legend of Worms 5000 BC- The earliest reference to tooth decay and toothache Was discovered on a clay tablet Originates from Sumerian text and was discovered in the Euphrates Valley According to them, decay occurred due to worms Most universally accepted theory of that time with evidence from other places across the globe

5. Humoral Theory Proposed by Greeks According to this theory, Imbalance between humors of the body caused decay According to Hippocrates and Aristotle stagnated food in teeth interacted with the humors and produced decay

6. Vital theory Developed in the 18 th century According to which tooth decay originated within the tooth itself, like a bone gangrene Failed to explain what change had occurred within the tooth for initiation of caries

7. Chemical Theory Parmly in 1819 According to him caries was caused due to a chemical substance that acted on putrefied food particles in teeth Robertson in 1835 stated that caries is caused due to acid formed by fermentation of food particles around the teeth Did not highlight the role of microbes

8. Parasitic theory Proposed in 1843 by Erdl and later by Antonie Leeuwenhock Found filamentous microbes that resembles parasites in the scrapings removed from teeth which were observed under microscope Did not tell about the origin of these parasites and the role of food

9. Miller’s chemo-parasitic theory Proposed by Miller in 1882 His work culminated in the hypothesis, 'Dental decay is a chemico -parasitic process consists of two stages 1 )Decalcification of enamel and dentin 2) Dissolution of the softened residue

10. Miller’s Chemo-parasitic theory ACIDOGENIC AND PROTEOLYTIC ORGANISMS SUGARS TEETH ORGANIC ACIDS DENTAL CARIES

11. Proteolytic Theory Proposed by Gottlieb in 1944 & Gottlieb, Diamond, Applebaum in 1946 According to them, organic or protein elements of enamel are initial pathways of invasion by microbes Some enamel structures are made of organic material such as enamel rods and lamellae, they act as pathways for advancing microorganisms in the progression of dental caries Dental caries were histologically characterized by pigmentation, a phenomenon associated with proteolysis Regarded Staphylococcus aureus to be mainly responsible

12. Proteolysis Chelation Theory Proposed by Schatz et al in 1955 According to this theory, bacteria first attack on organic matter of enamel Simultaneous microbial degradation of the organic components and the dissolution of the minerals of the tooth by the process known as CHELATION

13. Caries Balance Theory D emineralization

14. Autoimmune theory The autoimmune theory of dental caries suggests that a few odontoblast cells at some specific sites,within the pulp of a few specific teeth are damaged by the autoimmune mechanisms. For this reason, the defense capacity and integrity of the overlying enamel or dentin in those specific areas are compromised, and they can be the potential sites for caries development in future

15. Keye’s Triad SUBSTRATE HOST MICROFLORA

16. Caries Tetrad SUBSTRATE TIME HOST MICROFLORA

17. Current Concept SUBSTRATE TIME TOOTH SALIVA SALIVA GENDER AGE SOCIO- ECONOMIC STATUS MICROFLORA Familial and genetic pattern

18. Microflora and Dental Caries

19. Historical Studies Miller demonstrated the presence of microbes in dentinal tubules of carious teeth mainly cocci and leptothrix 1900- Goadby - Isolated gram positive bacillus from carious dentin and termed as B. necrodentalis . Later he changed his view that streptococci are involved 1922- Mcintosh, James, Lazorous -Barlow- Microbes are capable of lowering the pH to the degree that enamel is softened

20. 1924- Clarke isolated Streptococcus mutans from teeth that were found in initial stage dental caries 1925- Bunting and Parmelee reported the bacillary forms in the initial lesions of caries similar to those described earlier and they termed as B. acidophilus Bunting, Nickerson and Hard observed that B. acidophilus was absent in caries immune individuals while was present in caries susceptible individuals 1942- Floresta studied saliva from carious and non carious individuals, Aciduric streptococci and staphylococci were isolates

21. Several organisms have been found to induce dental caries when used as monocontaminants in gnotobiotic ( germ-free) rats – Streptococci group- Streptococcus mutans Streptococcus salivarius Streptococcus milleri Streptococcus mitior Streptococcus oralis Streptococcus sanguis Peptostreptococcus intermedius Lactobacillus acidophillus Lactobacillus casei Actinomyces viscous Actinomyces naeslundii

22. Type of caries Micro-organism Humans Pit and fissure S. mutans S. sanguis Lactobacillus species Actinomyces species Very significant Uncertain Very significant By chance Smooth surface S. mutans S. salivarius Very significant By chance Root surface A.viscous A.naeslundii S. mutans S. sanguis Very Significant Very Significant Significant By chance Deep dentinal caries Lactobacillus species A.naeslundii Other filamentous rounds Very Significant Very significant Very significant

23. Lactobacilli Gram-positive Non spore forming rods Microaerophilic conditions Homofermenters - L. casei and L. acidophilus Heterofermenters - L. fermentum and L. brewes Acidogenic and aciduric - Can multiply in low pH of plaque and dental caries Amount of acid produced by Lactobacilli is insignificant compared to the acid produced by other organisms Also, their increased amount in plaque and saliva does not necessarily establish their causative role. Hence, they can be considered as secondary invaders

24. Oral Actinomyces Gram positive Filamentous organisms Facultative Anaerobes- A. naeslundii and A. viscosus Strict Anaerobes- A. isarelii and A. odontolyticus They have been isolated in large amounts from the roots of decayed human teeth A. viscosus are acidogenic bacteria They have intracellular polysaccharide stores They also form extracellular levans and heteropolysaccharides consisting of hexose and hexosamine

25. Veillonella Gram-negative cocci These organisms lack key enzymes involved in glycolysis and HMP shunt and thus do not utilize sugars as energy source Veillonella uses lactic acid and converts it to propionic acid and other weak acids This converts stronger lactic acid with pKa 3.08 to a less dissociated acid of pKa in 4.7 range Reported as anti-cariogenic

26. Streptococcus mutans Gram-positive cocci forming short to medium chains Facultatively anaerobic S. Mutans synthesizes insoluble polysaccharides from sucrose Cariogenic properties: Ferments sucrose, Homofermenters of lactose Colonizes on tooth surfaces More aciduric than other Streptococci

27. Mechanism of action

28. Streptococcus sanguis Present in plaque obtained from both carious and non carious sites Caries from this strain mostly occur in occlusal pits and fissures Low cariogenicity than S. mutans

29. Streptococcus salivarius Found in tongue, throat and in saliva but not high numbers in dental plaque Attaches more to the epithelial surfaces than hard tissues Produces copious amounts of the water soluble polymer of fructose called levans

30. Role Of Dental Plaque

31. Dental Plaque is a specific but highly variable structural entity, resulting from sequential colonization of microorganisms on tooth surfaces, restorations & other parts of oral cavity, composed of salivary components like mucin, desquamated epithelial cells, debris & microorganisms, all embedded in extracellular gelatinous matrix- ( WHO 1961) Acquired pellicle : It is the form of glycoprotein that is derived from saliva and is adsorbed on tooth surface It is on this component of plaque that bacterial colonization takes place

32. Historical Studies Bibby (1940) and his associates studied the characteristics of different strains of filamentous organisms isolated from dental plaque and noted their ability to adhere to tooth surface Blaney (1942) and his associates pointed out that the time required for definite cavitation on intact enamel representing early caries was several months Hemmes and his associates (1946) stated that dental plaque was most likely the starting point for earliest enamel caries. They examined plaques from teeth of numerous children which became carious throughout the investigation Presence of aciduric streptococci was 86% Presence of lactobacilli in 57% individuals, increase in lactobacilli count according to the progress of dental caries

33. Most investigations of micro-organism of the dental plaque have concluded that three basic groups of micro-organisms predominate : Streptococcus Actinomyces Veillonella S. mutans S. salivarius S. milleri S. mitior S. sanguis A. viscosus A. naeslundii A. isarelii Rothia dentocariosa V. parvula V. alcalescenes

34. Mechanism of plaque formation

35. STEPS IN PLAQUE FORMATION

36. Role Of pH Of Dental Plaque Carbohydrates permeating dental plaque are degraded rapidly ( Stephan , 1940) Average pH in caries free person- 7.1 Average pH in extremely caries active person- 5.5 Lowest pH varied from 4.6-4.1 Stephan studied the pH of dental plaque after rinsing with 10% sucrose solution Within 2.5 minutes the pH dropped to 4.5-5.0 and gradually returned to original pH level in 1-2 hours. The plaque pH on the caries free group did not fall below 5.0 in half of the cases

37. At critical pH 5.5, tooth minerals act as buffers. They loose calcium and phosphorous into the plaque, initially helping to maintain the pH to 5.5. When pH falls below 5.0, subsurface demineralization is inevitable- Incipient caries When pH lowers further, surface demineralisation of enamel occurs

38. Non-specific plaque hypothesis Based on the work of Black (1884) and Miller (1980) Quantity of plaque determined the pathogenicity without discriminating between the levels of virulence of bacteria Theilade (1986) added that the host has the capacity to detoxify the bacterial products ( e.g salivary neutralizing acids) and disease would only develop if this threshold is surpassed The conclusion was that if any plaque has an equal potential to cause disease, the best way of disease prevention would be non-specific mechanical removal of as much plaque as possible by e.g., tooth brushing or tooth picking.

39. Specific Plaque Hypothesis Loesche and Nafe , 1973 States that only certain plaque is pathogenic, its pathogenicity depend on the presence of or increase in specific microorganisms However, the theory couldn’t explain why caries occurred even in the absence of these bacteria, though to a lesser degree Despite this, the hypothesis was useful in diagnosis and treatment, associating caries with such truly cariogenic bacteria as Streptococcus mutans and the Lactobacilli species

40. Ecological Plaque Hypothesis Philips D. Marsh (1994)

41. Saliva and Dental Caries

42. Water (99.5%) Saliva Solids Inorganic Substances Gases Organic Substances Oxygen CO 2 Nitrogen Sodium Calcium Potassium Bicarbonate Bromide Chloride Fluoride Phosphate Other Organic Substances Enzymes Amylase Maltase Lingual Lipase Lysosyme Phosphatase Carbonic Anhydrase Kallikrein Lactoperoxidase Lactoferrin Mucin Albumin Proline Rich Proteins IgA Blood Group Ags Free Amino Acids Non Protein nitrogenous substances- Urea, Uric Acid, Creatinine Composition

43. Calcium & Phosphate Concentrations The inorganic phase of enamel consists of crystalline hydroxyapatite essentially in the form of calcium and phosphate complexes of various compositions. These complexes usually dissociate as the pH drops and result in free active concentration of ions Calcium and phosphate in saliva form an important natural defense mechanism against dissolution of teeth When the saliva is unsaturated (less Ca and P)- demineralization occurs When the saliva is supersaturated (more Ca and P)- mineral precipitates

44. Under normal circumstances saliva is supersaturated with respect to enamel apatite, which not only prevents enamel from dissolving but even tends to precipitate apatite, in the surface enamel of carious lesions.

45. pH of Saliva Normal pH of saliva - 6.2 to 7.6 Saliva plays a critical role in remineralization-demineralization process Critical pH of saliva – 5.5 (but varies according to Ca and phosphate concentration) The pH at which any particular saliva ceases to be saturated with calcium and phosphate is referred to as the 'critical pH’ Below this the inorganic material of the tooth may dissolve

46. Buffering Capacity Of Saliva In saliva, the chief buffer systems are bicarbonate carbonic acid (HCO 3 - /H 2 CO 3 , pKl = 6.1) and phosphate (HPO 4 or H 2 PO 4 , pK2 = 6.8) The bicarbonate in saliva is able to diffuse into the dental plaque to neutralize the acid formed from carbohydrate by the microorganisms The higher the flow rate, the greater will be its buffering capacity In enlarged and exposed cavities, the pH was closer to neutrality, probably because of better access to saliva

47. Quantity Of Saliva A restriction in salivary flow leads to exacerbation of dental caries, as the removal of bacteria and food debris from the mouth is reduced This is especially evident in cases of salivary gland aplasia and xerostomia in which salivary flow may be entirely lacking, typically resulting in rampant dental caries.

48. Flow Rate Of Saliva Unstimulated saliva - 0.3–0.4 ml/minute Stimulated saliva - 0.5 ml per gland in 5 minutes Xerostomia – less than 0.1ml/min Significant increase in caries

49. Viscosity of Saliva High viscosity of saliva is due to high quantity of mucin content Sometimes, High caries index has been seen in individuals with highly viscous saliva Numerous cases have been reported where patients were caries free in spite of having highly viscous saliva ( Miller )

50. LOW CARIES INCIDENCE HIGH CARIES INCIDENCE High flow rate Low salivary flow rate Proper salivation Xerostomia Normal Viscosity Too high or too low viscosity Buffering capacity Lack of salivary buffering action Salivary enzymes Salivary glycoproteins may contribute to plaque formation Fluoride action Sucrose in saliva may be used up by plaque bacteria to produce caries Salivary Immunoglobulins

51. Tooth Factors and Dental Caries

52. Composition Caries Resistance- Surface enamel>Subsurface Enamel Fluoride Content- Sound enamel > Carious enamel Surface of enamel is lower in CO 2 , dissolves slower in acids, contains less water and has more inorganic material than subsurface enamel

53. Morphological Characteristics Deep, narrow occlusal fissures Buccal or Lingual pits

54. Nagano Classification

55. Position of Teeth & Proximal Contacts Caries initiate just below contact point/area Contact areas are more susceptible to caries than contact points Mal-aligned teeth are more susceptible to caries Rotated / Malaligned teeth exhibit greater contact areas

56. DIET AND DENTAL CARIES

57. History Relationship of sucrose to the prevalence of dental caries can be found in many epidemiological studies The prevalence of caries on isolated islands such as Australia, New Zealand, Trista da Cunha etc. was found to be lower before introduction of the European diet containing high carbohydrates, mainly sugars Europe and Japan have demonstrated the drastic reduction in dental caries during war times food restrictions , due to reduction of sugars, syrup and all sugar products

58. Cumulative dental decay prevalence, expressed as DMFT, in children of ages 11-12 was charted against the corresponding annual per capita sugar utilization data (1959) for 18 countries and state of Hawaii, from the food and Agriculture Organization of the United Nations ( Dr. T. Marthaler )

59. PHYSICAL FORM OF DIET Diet of the primitive man generally of raw, unrefined foods containing a great deal of roughage, which cleanses the teeth of adherent debris during the usual masticatory excursions. In addition, this primitive diet induced severe attrition of both occlusal and proximal surfaces of the teeth. This resulted in the flattening of the occlusal and proximal surfaces causing a reduction in the probability of decay In the modern diet, soft, refined foods tend to cling tenaciously to the teeth and are not removed because of the general lack of roughage. For those areas of teeth that are exposed to the excursions of food are usually immune to caries, mechanical cleansing by detergent foods may have some value in caries control.

60. The effect of dietary restriction on the L. acidophilus index in 1250 rampant caries affected individuals and 265 caries free individuals was studied. Replacement of refined dietary carbohydrates with meat, eggs, vegetables, milk and milk based products helped to reduce the index by 82% and clinical evidence of extensive arrest of caries (Beck et al, 1994)

61. Sucrose : Arch criminal of dental caries Sucrose is a substrate for production of extracellular polysaccharides ( fructan and glucan) and insoluble matrix polysaccharides ( mutans ) Sucrose favours colonization by oral micro-organisms and increases the stickiness of plaque allowing it to adhere in larger quantities to the teeth A combination of soluble starch and sucrose is expected to be a more powerful caries risk factor because of increased retention of food which prolongs the clearance time of sugar

62. Carbohydrate substrates Sucrose Starch Extracellular Polysaccharides (glucan, fructan & others) Dental Plaque Biofilm adherence Maltose Lactic Acid Enamel Dissolution Amylase Glucosyl- transferase

63. Frequency Of Intake Rather than the amount of carbohydrates taken by an individual, the number of times affects the caries experience more Individuals with habit of eating in between meals have higher caries incidence than individuals who eat sweets with their meals This occurs because each time a drop in pH occurs that leads to demineralization

64. WHO Recommendations Sugar intake of <10 % of total energy intake for prevention of caries Intake of sugars should be limited to 15-20 kg/person/year (40-55g per day) in presence of fluoride <15 kg/person/year (<40g per day ) in absence of fluorides Frequency of foods that contain sugar should be limited to maximum four times a day

65. Role of Lipids The medium chain fatty acids and their salts have antibacterial properties at low pH They serve as anionic surfactants and uncouple substrate transport and oxidative phosphorylation from electron transport in bacteria Mouthwash containing potassium non- anoate has been studied and found to reduce the rate of dental caries by reducing the production of acidogenic bacteria

66. Role of Vitamins VITAMIN A: Vitamin A deficiency shows developmental disturbances in teeth VITAMIN B: Vitamin B6 (pyridoxine) has been proposed as an anticaries agent as it selectively alters the microflora in the oral cavity promoting the growth of non-cariogenic plaque

67. VITAMIN D: Children with Rickets have shown higher experience of dental caries Deficiency of Vitamin D may contribute to Enamel hypoplasia Studies reveal that people with Vitamin D supplements showed lower caries incidence

68. Trace Elements in Diet Calcium and Phosphorous disturbances in the dietary intake does not affect dental caries experiences Nizel and Harris experimented on laboratory rodents to demonstrate that phosphates were cariostatic. Their effectiveness depends on the anions and cations with which they are combine according to the food they are fed with Selenium is observed to be cariogenic, Vandium is observed to be anticariogenic The fluoride content of diet has been examined by numerous workers. But it was found that the dietary fluoride was not as important as the fluoride of drinking water as, dietary fluoride become unavailable after metabolism

69. Anticariogenic & Cariostatic Food FOOD COMPONENT FIBROUS PLANT FOODS (eg Apple) Increases salivary flow Rich in tannins (anti adhesive property) BERRIES Rich in flavanoids (anti adhesive properties) Phenols (damage bacterial cell wall) UNREFINED CEREALS AND NUTS (eg Peanuts, Groundnuts) Polyphenols (Reduces enamel solubility) CHEESE Rich in casein, whey, calcium & phosphorus (prevents demineralization) Tyramine fatty acids (Increase salivary flow & pH of plaque) YOGURT Protein content is high Rich in Calcium, phosphorus & casein GARLIC Inhibits growth of bacteria- Streptococcus & Bacillus COFFEE Rich in polyphenols BLACK TEA Rich in polyphenols and fluorides

70. Dietary Studies on Controlled Human population Vipeholm Study Hopewood House study Turku Sugar Study Hereditary Fructose Intolerance study Tristan Da Cunha Study

71. Vipeholm Study (1946-1951) Described by Gustaffson et al in 1954, summarized by Davies in 1955 It was a five year investigation carried out in 436 adults from Vipeholm hospital in Sweden, an institution for mentally challenged Purpose- It was done to find out the effect of carbohydrates (amount, frequency and nature) on dental caries

72. 1)CONTROL GROUP 60 males Low carbs, high fat diet for 2 years followed by addition of 110g sugar to one meal for next 3 years Small, but significant in caries 4)CARAMEL GROUP 62 males 22 caramels daily in 2 portions between meals in 3 rd year, 22 caramels in 4 portions between meals in 4 th year In the 5 th year caramels replaced by isocaloric fat Fall in caries increment 3)BREAD GROUP 41 males, 42 females 345g sweet bread given once daily with afternoon coffee for first 2 years, followed by 4 portions of sweet bread with all 4 meals for next 3 years Increase in Caries index 2)SUCROSE GROUP 75 males 300g sucrose solution at meal times, which was reduced to 75g in last 2 years No significant increase in caries 5)CHOCOLATE GROUP 47 males 300g sucrose solution at meal times for first 2 years reduced to 110g in the next 2 years & supplemented by 65g chocolate milk between meals Increase in caries incidence 6)8 TOFFEE GROUP 40 males High fat. Low carbs diet in the first year, 8 toffees with lunch and breakfast in the second year and 8 toffees in between meals in the subsequent years Significant increase in the caries 7)24 TOFFEE GROUP 48 males 24 toffees between meals in the third and fourth year followed by withdrawal of toffees in the fifth year Significant drop in caries index in the fifth year

73. Conclusion of Vipeholm Study Increase in the carbohydrate amount definitely increases the caries activity The risk of caries is greater if carbohydrates are retained of tooth surface The risk of sugars increasing caries activity is greater if sugar is consumed between meals Upon withdrawal of sugar rich foods, increased caries activity rapidly disappears The increase in the clearance time increases the risk of dental caries Physical form of sugars is more important than the amount

74. Hopewood House study Sullivan and Harris in 1958, Harris in 1963 Dental status of children between 7-14 years of age residing at Hopewood house, Bowral, South Wales was studied longitudinally for 10 years Subjects were strictly kept on natural diet, no meat, no refined carbohydrates, with occasional serving of egg yolk. Meals were supplemented by Vitamins, nuts and sweetening agents such as honey At the end of 13 years the children had a mean DMFT of 1.6 compared to the DMFT of state school which was averaged at 10.7 53 % subjects were caries free compared to only 0.4 % caries free children of state school

75. Turku Sugar Study Scheinin and Makinen , 1975 in Turku, Finland Compared the cariogenicity of sucrose, fructose and xylitol In the two year feeding study, 125 young adults (average age of 27.6) were divided in 3 groups according to their own preferences: 35- Sucrose group 38- Fructose Group 52- Xylitol Results : After one year, sucrose and fructose had equal caries incidence with xylitol individuals showing no caries activity In the second year, caries activity continued to increase in the sucrose group, was unchanged in fructose group, whereas xylitol produced almost no caries Conclusions : Fructose is less cariogenic than sucrose. Xylitol was non cariogenic

76. Hereditary Fructose Intolerance Study Newbrun in 1969 tabulated that caries prevalence of 31 persons with HFI and found that caries prevalence was extremely low Tristan da Cunha Study Study done on the habitants of remote South Atlantic Island before and after refined carbohydrates and packed food was available Results : YEAR PREVALENCE OF CARIES 1932 0% 1937 0% 1962 50 % 1966 80%

77. Time Factor & Dental Caries

78. Shift in microflora can occur over a fairly short period but a significant amount of time is needed for demineralization to lead to the development of white spot/ carious lesions Acid production does not instantly trigger tooth decay and in early stages remineralization can restore enamel The longer the interaction of the dietary sucrose and the cariogenic microbes in the plaque, the more deleterious is the effect of acid on the dissolution of tooth mineral

79. Systemic Factors & Dental Caries

80. Hereditary When a family lives in the same locality, caries susceptibility in children is similar to their parents who had grown up in similar conditions ( GV Black , 1899) Racial tendency for high caries or low caries incidence (sometimes) appears to follow hereditary pattern but local factors may easily alter this tendency May be mediated through inheritance of tooth form or structure, which predisposes to caries immunity or susceptibility

81. Pregnancy & Lactation Evidence showed increase in caries incidence during or post pregnancy Studies showed that increase in caries incidence was due to negligence of oral care

82. Conclusion Dental caries is a disease with complex etiology and more studies will be needed to develop strategies against the etiological factors The presently alarming rate of dental caries is due to the change in diet, by addition of fermentable sugars For a developing country like India the assessment of caries risk individuals is important so that preventive measures can be targeted at this group

83. References Cariology : Newburn E. 3 rd edition Shafers : Textbook of oral pathology, 7 th edition Soben Peter: Essentials of Public Health Dentistry, 5 th edition

84. Thank You