Dental caries etiology, theories and prevention

a detailed presentation on dental caries, etiology of dental caries , various theories and preventive measures to be taken to prevent dental caries

1. DENTAL CARIES: ETIOLOGY,THEORIES AND PREVENTION Presented by, Dr. Geethanjali.R 1st year post graduate student Department of conservative dentistry and endodontics 1

2. CONTENTS DEFINITION CLASSIFICATION OF DENTAL CARIES DEMINERALIZATION-REMINERALIZATION CYCLE CARIES BALANCE CONCEPT ETIOLOGY THEORIES OF DENTAL CARIES PREVENTION OF DENTAL CARIES 2

3. DEFINITION According to WHO, caries is defined as a localized post eruptive, pathological process of external origin involving softening of the hard tooth tissue and proceeding to the formation of a cavity. Dental caries is defined as a multifactorial, transmissible, Infectious oral disease caused primarily by the complex interaction of cariogenic oral flora (biofilm) with fermentable dietary carbohydrates on the tooth surface over time ( Sturdevant ) Dental Caries is an irreversible microbial disease of the calcified tissues of the teeth, characterized by de-mineralization of the inorganic portion and destruction of the organic substance of the tooth which often leads to cavitation ( shafer 1993) 3

4. CLASSIFICATION According to location 1.Pit and fissure caries 2.Smooth surface caries 3.Root caries According to clinical management strategy 1.Initial caries lesion/non cavitated caries lesion/white spot lesion 2.Cavitated caries lesion 4

5. According to rate of activity 1.Active caries lesion -moderate caries lesion -advanced (deep) caries lesion 2.Inactive caries lesion 3.Rampant caries 5

6. According to occurrence 1.Primary caries 2.Secondary caries 3.Residual caries According to depth of lesion 1.Enamel caries 2.Dentin caries 6

7. Based on extent of caries 1.Incipient caries 2.Cavitated caries Based on pathway of caries spread within the tooth 1.Forward caries 2.backward caries 7

8. G.V Black’s classification 8

9. STURDEVANT’S Classification 9

10. Graham mount’s classification(1998) 10

11. DEMINERALIZATION-REMINERALIZATION BALANCE KEYES-JORDAN DIAGRAM TEETH - BIOFILM - CONSUMING CARBOHYDRATES 11

12. CARIES BALANCE CONCEPT ( featherstone) The balance between demineralization and remineralisation depends upon - pathologic factors (those favouring demineralization) - protective factors (those favouring remineralization) 12

13. Demineralization-Remineralization cycle ACID PRODUCTION- Cariogenic bacteria in biofilm metabolize refined carbohydrates for energy and produce organic acid by-products CRITICAL BIOFILM pH- These organic acids can lower the pH of biofilm to critical level ( 5.5 for enamel and 6.5 for dentin ) DEMINERALIZATION - The low pH drives calcium and phosphate from the tooth to the biofilm in an attempt to reach equilibrium. REMINERALIZATION - when the pH in biofilm returns neutral and the concentration of soluble calcium and phosphate is supersaturated , mineral can be added back to partially demineralized enamel 13

14. Dental caries is a disease that is dependent on the complex inter-relationships between the following critical parameters: PRIMARY FACTORS: 1.Biofilm 2.Tooth habitat 3.Diet 4.Saliva 5.Time 14 ETIOLOGY

15. MODIFYING FACTORS: 1.Age 2.Sex 3.Race 4.Hereditary 5.Systemic health 6.Occupation 7.Geographic area 15

16. BIOFILM Dental plaque is a term used to describe the soft, tenacious film accumulating on the surface of teeth. ( sturdevant’s operative dentistry-2 nd south asia edition) Biofilm is defined as a microbiologically derived community, characterized by cells which are irreversibly attached to substrate or interface or with each other , embedded in matrix of extracellular polymeric substances that they have produced and exhibit an altered phenotype with respect to growth rate and gene transcription. 16

17. Salient attributes of dental biofilm 1. Biofilm is composed mostly of bacteria, their by-products, extracellular matrix and water. 2.Accumulation of biofilm on teeth is a highly organized and ordered sequence of events. 3. Teeth normally have a biofilm community dominated by streptococcus sanguis and streptococcus mitis. 4.Mature plaque biofilm are capable of rapid anaerobic metabolism of any available carbohydrates. 17

18. Hedgehog formation 18

19. COMPONENTS OF BIOFILM: INORGANIC : Calcium, phosphorous and fluoride are more in biofilm than in saliva ORGANIC : carbohydrate such as glycans and fructans , proteins are derived from saliva and lipids including endotoxins from gram negative bacteria. 19

20. DEVELOPMENT OF BIOFILM: 1. FORMATION OF PELLICLE : Different bacteria reversibly or irreversibly attach to tooth surface resulting in formation of enamel pellicle which act as foundation for multilayered biofilm 2. COLONIZATION OF BACTERIA : The bacteria starts dividing and form microcolonies. 3. MATURATION OF BIOFILM : In two weeks, the plaque becomes more mature 20

21. Acquired pellicle is defined as a homogenous, membranous, acellular film that covers the tooth surface and frequently form the interface between the tooth, dental plaque and calculus. ( SCHLUGER) The pellicle consists of salivary glycoproteins, enzymes and immunoglobulins Functions -protect the enamel -reduce friction between teeth -provide a matrix for remineralization 21

22. There are three major hypothesis for etiology 1.The specific plaque hypothesis 2.The nonspecific plaque hypothesis 3.The ecological plaque hypothesis The specific plaque hypothesis states that only a few specific species, such as streptococcus mutans and streptococcus sobrinus are involved in disease 22

23. The nonspecific plaque hypothesis states that the outcome of caries is the overall activity of the total plaque microflora. The ecological plaque hypothesis ( Philip D.marsh 1994 ) suggests caries is a result of shift in the balance of the resident microflora driven by changes in local environmental conditions. 23

24. TOOTH HABITAT The tooth habitat favorable for harboring pathogenic biofilm are 1. pits and fissures -they provide excellent mechanical shelter for organisms and harbor a community dominated by s.sanguis and other streptococci. 24

25. 2. Smooth enamel surfaces -The proximal enamel surfaces immediately gingival to the contact area are the second most susceptible areas to dental caries lesions. These area are free from salivary flow ,effect of mastication and tongue movements 25

26. 3. Root surfaces - the proximal root surfaces , particularly near the cementoenamel junction (CEJ) is unaffected by action of hygiene procedures. caries lesions originating on root have a comparatively rapid progressive, often asymptomatic , they are closer to pulp and are difficult to restore, 26

27. 4. sub-gingival areas -The facial or lingual root surfaces when exposed to oral environment (due to gingival recession) are often neglected in hygiene procedures. The enamel surface of a newly erupted tooth is highly susceptible to caries because of increased carbonate content of enamel crystals. Any deficiencies of vitamin A and D, minerals like calcium, phosphorus and fluorides during tooth development predispose to caries 27

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30. Streptococcus mutans : 1.Isolated by Clarke ( 1924 ) 2.catalase negative, gram positive cocci 3.cariogenic strains contain lysogenic bacteriophage 4.It polymerize glucose and fructose moieties of sucrose to glycans and fructans 30

31. lactobacilli 1. gram positive non spore forming rods 2.acidogenic and aciduric 3.produce lactic acid oral actinomyces 1.gram positive filamentous organisms 2. A.naesulundi and viscosus-facultative anaerobes A.isreli and odontolyticus-strict anaerobes 31

32. DIET High frequency exposure of fermentable carbohydrates such as sucrose may be the most important factor in producing cariogenic biofilm and caries lesion Dietary sucrose has two important detrimental effects on how biofilm affects caries; 1. frequent ingestion of foods containing sucrose provides a change in biofilm from noncariogenic to cariogenic biofilm 2.mature biofilm exposed frequently to sucrose rapidly metabolizes it into organic acids, resulting in a profound and prolonged decline in pH 32

33. Other factors that also affect are: i . Type of carbohydrate (monosaccharides, disaccharides or polysaccharides) ii. Frequency of intake iii. Time of stagnation It has been established that sugar given in solution form, is much less capable of producing caries than the same amount of sugar incorporated in food . Also, caries activity is higher when sugar is administered in the form of sticky food, which tends to remain on the surface of teeth. 33

34. Following factors of diet are responsible for dental caries: i. Roughness ii. Palatability iii. Eating and drinking pattern iv. Retention and clearance of diet v. Age 34

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36. Stephan curve 36 It describe the change in pH occurring within dental plaque when it is subjected to cariogenic food The relationship of the shape of stephan curve to critical pH can be used to asses the relative cariogenicity of foods

37. SALIVA BACTERIAL CLEARANCE - Adults produce 1-1.5L of saliva a day, it lubricates oral tissues and bathes teeth and the biofilm -The flushing effect of this salivary flow by itself is adequate to remove virtually all microorganisms not adherent to an oral surface 37

38. DIRECT ANTIBACTERIAL ACTIVITY - Lysozyme, lactoperoxidase , lactoferrin and agglutinins are salivary proteins that possess antibacterial activity -The caries susceptibility in healthy individuals is more related to the quantity of saliva . Individuals with decreased salivary production may have significantly higher caries susceptibility 38

39. BUFFER CAPACITY According to Neil (1978). The normal range of buffer capacity in saliva is 3-30mg/100ml The benefit of buffering is to reduce the potential for acid formation 39 -primary buffer: Bicarbonate ion concentration -additional buffers: urea and sialin

40. REMINERALIZATION Saliva contains statherin , a proline-rich peptide that stabilizes calcium and phosphate ions and prevents excessive deposition of these ions on teeth Under normal conditions the critical pH is 5.5, below this value, the inorganic material of tooth may dissolve. 40

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42. Time The time period during which all the three factors ie . tooth, microorganisms and substrate are acting jointly should be adequate to produce acidic pH which is critical for dissolution of enamel to produce a carious lesion. It takes around two hours to return the pH to normal and remineralise the tooth surface through the buffering capacity of saliva. 42

43. Modifying factors 1. Age : Young age and old age are more prone to caries 2. Sex: Females are more susceptible to caries due to early eruption of teeth 3. Race : It may relate to their cultural and dietary influences 4. Hereditary : Due to genetic, caries may be inherited from parents especially from mothers. Children are usually colonized with strains of streptococcus mutans identical to strains carried by their mothers 43

44. 5. Systemic health : Any condition which predisposes to poor oral hygiene like Sjogren’s syndrome, diabetes mellitus, patients undergoing radiotherapy and chemotherapy 6. Occupation : Where frequent food sampling is required are associated with increased risk for caries like bakery workers, workers in confectionary industry etc. 7. Geographic area : In regions where there is high phosphate content of food and water and where there is adequate fluoridation of water, cavity is diminished 44

45. 45 THEORIES OF DENTAL CARIES

46. 46 Worm theory Early theory Humor theory Vital theory Endogenous theories Chemical theory Parasitic theory Acidogenic theory Proteolytic theory Proteolysis chelation theory Sucrose chelation theory Exogenous theories

47. Worm theory The earliest reference of tooth decay appeared around 14th century B.C. According to concept of that time, the cause of caries was thought to be invasion of ‘worms’ into teeth . The association of systemic disease and teeth was probably obtained from writings of a physician around 668 B.C. 47

48. Humor theory Galen hypothesized that the dental caries was produced by the action of acids along with corroding humors The four humors that were thought to maintain the body health included blood, phlegm, black bile and yellow bile caused dental caries due to imbalance between these factors 48

49. Vital theory Towards the end of 18th century,it was postulated that tooth decay orginated from within the tooth itself like bone gangrene 49

50. Chemical theory Robertson (1835) Acids formed by fermentation of food particles cause dental decay. The exact nature of acids and the exact mechanism of their formation were not known. Different postulates were suggested; 1. Putrefaction of protein gave rise to ammonia, which was subsequently oxidized to nitric acid. 2. The food was decomposed to sulphuric acid. Till then, the activity of bacteria was not recognized. 50

51. Parasitic or septic theory Erdl (1843) Filamentous parasites ( denticolae ) in the membrane of tooth surfaces. Dental caries was thought to develop as a result of infiltration and decomposition of enamel cuticle (surface protein membrane on the enamel) 51

52. Acidogenic theory Willought D miller in 1890 Dental decay is a chemico -parasite process consisting of two stages,the decalcification of enamel and dissolution of the softened residue of the enamel and dentin -on coronal surface - Streptococcus mutans -on root surface- Actinomyces viscosus -Lactobacillus acidophillus count is more in saliva shows active carious lesion 52

53. He was of the view that micro-organisms of the oral cavity, by secretion of enzymes or by their own metabolites degrade the carbohydrates into acids . The acids formed were lactic acid, butyric acid, etc. The acid demineralize the enamel surface. After the disintegration of enamel, the organisms along with acids penetrate dentinal tubules leading to dissolution of dentin. The proteolytic enzymes finally digest the organic part. (Textbook of operative dentistry by vimal k sikri - 4 th edition) 53

54. Miller suggested that no single species of micro-organisms were capable of producing acids and digesting proteins. His work was confirmed by the facts: • Acid was present in the deeper carious lesions. • Several micro-organisms of oral cavity were capable of producing acids. • Lactic acid was identified in carbohydrate saliva combined mixtures. Different micro-organisms had the potential to invade enamel and dentin. 54

55. Drawbacks • The caries on the smooth surfaces of teeth. Particular type of micro-organism could not be isolated, which is responsible for particular acid. The phenomenon of arrested caries. Certain populations exhibit less caries despite of consuming enough carbohydrates. Caries of un-erupted/impacted teeth. The carious dentin, if left under a filling continues to decay. (Textbook of operative dentistry by vimal k sikri - 4 th edition) 55

56. Proteolytic theory HEIDER,BODECKER (1948) Gottlieb (1944) was of the view that the initial action is due to the proteolytic enzymes attacking the lamellae, rod sheaths, tufts and walls of tubules etc , i.e. all organic components. Caries is initiated at a slightly alkaline pH produced by the proteolytic activity liquefying the organic matrix of enamel. After the dissolution of organic part, these salts are dissolved subsequently by acidogenic bacteria. Predominantly by Staphylococci. 56

57. Pincus (1949) The initial process in caries was the proteolytic breakdown of the dental cuticle. The organic membrane was found on the teeth followed by destruction of the prism sheaths. The loosened prisms then fell out mechanically. The Nasmyth’s membrane and the enamel proteins (mucoproteins), which are acted upon by the sulphatase enzyme of the bacilli yield sulphuric acid. 57

58. Drawbacks • Enamel is a highly mineralized tissue. Though enamel contains 1.0 to 1.5% organic matrix out of which 0.6% is protein, initiation of caries with breakdown of this small percentage of protein is highly questionable. • The sulphatases of gram-negative bacilli which are considered to dissolve the mucoitin sulfate of enamel have not been found in abundance in experimental studies. • This theory lacks experimental support 58

59. Proteolysis chelation theory Schatz et.al. (1957) T he microbial degradation of organic component by proteolysis followed by dissolution of inorganic part by the process of chelation lead to caries Chelation is the process in which there is complexing of the metal ions to form complex substance through covalent bond. Bacteria attack on enamel is initiated by keratinolytic microorganisms . This causes the breakdown of the protein chiefly keratin, resulting in formation of soluble chelates which decalcify enamel at neutral pH Enamel contains mucopolysaccharides,lipids and citrate which are susceptible to bacterial attack and act as chelators 59

60. 60 This theory states that inorganic and organic portions of enamel are attacked simultaneously and it occur independent of pH of the medium

61. Drawbacks • Since the enamel contains very little amount of organic component(4%), can such dissolution produce sufficient amount of chelates to disintegrate the rest of inorganic enamel (96.6%), is doubtful. • Although chelation is an accepted biological phenomenon, its role in caries initiation is yet to be established. 61

62. Sucrose chelation theory Egglers -Lura (1967) Sucrose itself and not the acid derived can cause dissolution of enamel by forming an ionized calcium saccharate The theory states that calcium saccharates and calcium complexing intermediatries require inorganic phosphate, which is subsequently removed from the enamel by phosphoryalating enzymes 62

63. Auto-immunity theory In this theory, it was suggested that 'forbidden clones' of lymphocytes attack the target cells (odontoblast) rendering the tooth vulnerable to caries attack 63

64. Levine's theory Levine (1977) The chemical relationship of enamel,plaque and factors which determine the movement of minerals from saliva/ plaque to enamel and vice versa is termed as see-saw mechanism. The demineralization and remineralization of enamel is a continuous process. If in a given interval of time, more ions leave the enamel than enter, then there is a net demineralization, which amounts to the start of the carious process. The passage of ions is not a one way process and that ions are constantly being exchanged between enamel and plaque 64

65. The three most important factors are: -If the pH falls below the critical pH, during carbohydrate intake, mineral ions are liberated from the hydroxyapatite crystals of the enamel surface and diffuse into plaque. Later, the salivary buffers neutralize the acid. Here , the plaque is supersaturated with ions . Some of the ions are lost and others are deposited onto the enamel. With such repeated episodes, overall demineralization occurs which may lead to caries -If free calcium and phosphate ions are higher in the saliva there would be a greater tendency of ions to move from plaque to enamel . Reverse would be true if ion concentration in saliva is low. -Fluoride favors movement of ions from plaque to enamel. Fluoride concentration, as low as 5.0 ppm ,can tilt the ‘see-saw’ in enamel’s favor. 65

66. Systemic Theory It highlights on body’s own inflammatory response and disturbance of oxidant-antioxidant balance that lead to caries. It states that in dental caries, the acidic environment erodes the enamel and triggers an inflammatory response in the dentin layer of the tooth. Similar periodontal disease, where bacterial toxins initiate the body’s own matrix metalloproteinases (MMPs) to break down the periodontium, the collagen matrix of the dentin is lysed by endogenous MMPs such as collagenase. Both dental caries stimulated by acid and periodontal disease stimulated by bacterial toxins share a common pathway of oral bacteria initiating a host inflammatory response. 66

67. Dentinal fluid flow is regulated by the endocrine portion of the parotid gland, which receives signals from the hypothalamus, Minimizing the effect of free radicals on the hypothalamus with antioxidants can avoid down-regulation of the parotid hormone, maintaining centrifugal dentinal fluid flow. Excessive MMPs release causing carious process is prevented, and dentinogenesis is enhanced. 67

68. PREVENTION OF DENTAL CARIES 68

69. The primary goal of a caries prevention program are 1.To modulate the biofilm into a nonpathogenic biofilm 2.To create an environment conducive to remineralization 69

70. Levels of prevention Primary prevention: actions taken prior to the onset of disease, which removes the possibility that the disease will ever occur By plaque control program, caries activity test, patient's education, topical application, pit and fissure sealants Secondary prevention: limits the progression and extent of the disease at early stage as possible by preventive resin restoration pulp capping Tertiary prevention: limits the extent of disabilities once a disease has caused any functional limitations by complex restorative dentistry 70

71. methods to reduce demineralizing factors 1.dietary measures 2.methods to improve oral hygiene 3.chemical measures methods to increase protective factors 1.methods to improve flow,quantity and quality of saliva 2.chemicals altering the tooth surface -fluoride,iodides, zinc chloride, silver nitrate ,bisbiguanides 3.application of remineralizing agents 4.use of sealent 71

72. Clinical consideration in caries prevention GENERAL HEALTH 1.patients undergoing radiation or chemotherapy treatment have significantly decreased immunocompetence and are at risk for increased caries 2. medically compromised patients should be examined for changes in plaque index, salivary analysis, oral mucosa ,gingiva and teeth 3.Of the systemic diseases, the greatest risk for caries is with rheumatoid conditions especially sjogren's syndrome. 72

73. DIET Frequent ingestion of foods containing sucrose provides a stronger potential for colonization by mutans streptococci enhancing the potential of the biofilm rampant caries on interproximal surfaces may point diet as main causative factor whereas rampant caries in cervical and interproximal areas may point to diet and hygiene as causative factors 73

74. use of sugar substitutes like xylitol and sorbitol low caloric sweeteners like aspartame, saccharin and cyclomate is useful to prevent caries fats: It form a protective barrier on enamel or carbohydrate surface so that it becomes less available for bacteria cheese also increases the salivary flow, increases pH and promotes clearance of sugar 74

75. ORAL HYGIENE 1.Dental prophylaxis 2.Tooth brushing 3.Interdental cleaning oral prophylaxis: Careful polishing of roughened smooth surface and correction of faulty restoration decreases the formation of bacterial plaque and there by reducing the development of new carious lesion 75

76. Tooth brushing : Bass technique is most recommended as it emphasizes sulcular placement of bristles while in periodontal cases, sulcular technique with vibratory motion is preferred. I nterdental cleaning aids: -D ental floss. -Wooden sticks. -Interdental brushes 76

77. Disclosing agents They are solutions, tablets or wafers containing a red dye like erythrosin . when applied on tooth surfaces with cotton swab or diluted in mouthwashes they can stain the bacterial plaque. Disclosing agents are used after tooth brushing to improve plaque control measures. 77

78. FLUORIDES Mechanism of action: Presence of fluoride ions in oral cavity precipitates fluorapatite into tooth structur e from the calcium and phosphate ions present in saliva. fluorapatite makes enamel more resistant to caries attack fluoride interferes with bacterial enzymatic process by inhibiting glucose uptake by bacterial cell, thus prevents formation of extracellular polysaccharides which helps in bacterial adhesion 78

79. Public water supply fluoridation Ideal concentration for public water supply fluoridation is 1 ppm. children with developing permanent teeth benefit the most. School water fluoridation The optimum fluoride level for school water is 4.5 to 5.5 ppm as water consumption is less frequent during limited hours in school 79

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81. Professional application of fluoride 2 % sodium fluoride contains 9200 ppm fluoride. It is preferred in composite restoration as APF etches glass filler particles of composite. stannous fluoride (8%) sodium fluoride varnish (5%) Duraflor is the most widely accepted vehicle of choice and the most cost effective means for fluoride delivery to people - for high risk- 3months -moderate risk-6 months -low risk-not indicated Duraphat (2.26% F) -sodium fluoride in organic lacquer Fluoroprotectote (0.7% F)- diflurosilicane in polyurthane lacque and chloroform 81

82. The fluoride varnish deposits large amount of fluoride on enamel surface. calcium fluoride precipitates on the surface, and often fluorapatite is formed. The high concentration of surface fluoride may provide as reservoir of fluoride which promotes remineralization . Acidulated phosphate fluoride gel (1.23%) It has 3.5 pH and contains 12,300 ppm fluoride . It is made from sodium fluoride and 0.1M phosphoric acid. 82

83. Silver diamine fluoride ( SDF 38%) It is a topical solution used as a caries arresting and anti-hypersensitivity agent Both silver and fluoride play active roles in their mechanisms of arresting caries development and treatment of tooth hypersensitivity The main drawback is that with precipitation of silver, the carious dentin becomes stained black 83

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85. Self administered fluoride Fluoride mouth rinses : They have an additive effect (20%) when used in conjunction with topical or systemic fluoride treatment 1. High dose (0.2% F) -Low frequency rinses- used in supervised weekly rinsing programs based in public schools. 2. Low dose (0.05% F)- High frequency rinses- used by individual patients at home. 85

86. Fluoridated dentifrices Stannous fluoride, sodium fluoride, sodium monoflurophosphate are seen in dentifrices 1000-1450 ppm- for low risk patients and it generally contain 0.32% sodium fluoride (1450 ppm) 5000 ppm- for moderately risk or high risk patients and it contain 1.1% sodium fluoride (5000 ppm) 86

87. Sealant It fill pits and fissures with a resin based polymer. They eliminate the geometry that harbors bacteria and to prevent nutrients reaching bacteria in the base of the pit and fissure complete penetration of the sealant is not necessary, it is possible to occlude only the neck region of fissures and produce clinically acceptable results. caries free pits and fissure and incipient lesions in enamel not extending to the DEJ are the sites recommended for treatment with sealant 87

88. Resin infiltration It is a new technique and alternative to sealant It is used for treating lesions extending into enamel or outer third of dentin It includes lesion pores with low-viscosity light curing resins in order to create diffusion barrier and arrest caries progression 88

89. saliva Diluting the acid produced in plaque biofilm washing the acid away buffering the produced acid assisting in remineralization due to presence of calcium, phosphorous and fluoride 89

90. chemical agents chlorhexidine : The traditional use of CHX in mouthwash, varnish or both along with fluoride toothpaste. Toothpaste free from sodium laurel sulphate which causes foaming action is not to be used as it inhibit the ability of chlorhexidine to reduce biofilm formation 0.12% mouth rinse at bedtime for 2 weeks reduces streptococcus mutans activity 1% gel or 40% varnish professionally applied once a week for several week reduces caries in high risk patients. 90

91. xylitol : It is usually recommended to chew 2 pieces of xylitol gum containing a total of 1g xylitol 3-6 min after eating As mutan streptococci cannot ferment xylitol, acid is not produced , chewing any sugar free gum after meal reduces acidogenicity of the biofilm as chewing stimulates salivary flow, which improves buffering action 91

92. Anticariogenic effect of xylitol -It reduces plaque formation -It inhibits enamel demineralization -It has direct effect on S.mutans -Increases salivary flow -Nonfermentable -It increases concentration of aminoacids which neutralize the plaque acidity 92

93. Urea and ammonium compounds : ureas on degradation releases ammonia , neutralizes the acids and interferes with bacterial growth Nitrofurans : They have both bacteriostatic and bactericidal action on gram positive and gram negative organisms Glutaraldehyde: T wo minutes of daily application of glutaraldehyde reduces mineral loss in dentin caries due to -collagen fixation -reduced diffusion of ions out of carious lesion -antibacterial action of glutaraldehyde Iodine : It has strong antimicrobial effect 93

94. Remineralizing agents They are required to rapidly precipitate on partially demineralized tooth structure and transform into a more stable, less acid-soluble apatite than hard tissue replaced For optimum remineralization, the agent must also be able to diffuse into the pellicle covered enamel surface. Commonly used agents are calcium glycerophosphate and calcium lactate, dicalcium phosphate dihydrate(DCPD),calcium carbonate,casein phosphopeptide ( CPP) and amorphous calcium-phosphate(ACP) complexes 94

95. Calcium and Phosphate compounds casein phosphopeptide (CPP) is a milk derived protein that binds to tooth's biofilm and is used to stabilize amorphous calcium phosphate (ACP) ACP is a reactive and soluble calcium phosphate compound that releases calcium and phosphate ions to convert to apatite and remineralize the enamel when it comes in contact with saliva remineralization products use CPP as a vehicle and maintains a supersaturation state of ACP at or near the tooth surface. 95

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97. Probiotics The fundamental concept is to inoculate the oral cavity with bacteria that will compete with cariogenic bacteria and eventually replace them when attached, probiotic bacteria can produce bacteriocins ( eg,hydrogen peroxide and reuterin ) that hamper and inhibit growth of a variety of bacteria. probiotic bacteria stimulate the specific and nonspecific immune response through activation of T cells and production of cytokines that mediates the inflammatory process. 97

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99. Restorations Old restorations that are rough and plaque retentive should be smoothened and polished or replaced Restoration defects such as overhangings , open proximal contacts and defective contours contribute to plaque formation and retention 99

100. 100 Recent methods of caries prevention

101. Genetic modalities in caries prevention Genes for enzyme glycosyl transferase were decoded,resulting new strains of S.mutans which lacked the capability to produce lactic acid responsible for caries genetically modified foods: F oods containing antagonist peptides against glycosyl transferase genetically modified organisms : A new strain of s.mutans has been created which lacks lactodehydrogenase gene , thus unable to produce lactic acid. Lactobacillus zeae : They are modified bacteria which produce antibodies so as to attach to surface of S.mutans resulting in their death. Probiotic approach : S.mutan strain is modified to increase the production of enzyme urease . This urease converts urea into ammonia which helps in remineralization. 101

102. CARIES VACCINE Rationale of caries vaccine is that immunization with S.mutans should induce an immune response so as to prevent organisms from colonizing the tooth surface and thus prevent carious decay Vaccine should be given before eruption of deciduous teeth so as to achieve maximum benefits General public should be well exposed to vaccine 102

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104. Drawbacks in development of caries vaccine Since complete etiology is not known,100% effectiveness is not possible Even with same level and type of S.mutans , variation in severity of disease occur Cross reactivity of S.mutans cell antigens is seen in heart muscles Lack of immunological competence can result in lack of response to S mutans 104

105. Caries solvent It is a natural endoprotein enzyme based gel formulation for non invasive and non traumatic removal of infected dentin from carious lesion. The technique involves the application of this gel to cause a selective softening of carious dentin and facilitate removal by gentle excavation thus allowing maximum preservation of healthy dental structure. 105

106. Lasers Treatment with lasers can reduce the rate of subsurface demineralization in enamel Erbium family ( Er:YAG , Er:YSGG ) are lasers of choice and most efficient for enamel, dentin caries removal Laser treatment particularly in combination with topical fluoride application increases resistance against caries, desensitization of hypersensitive dentin and improve seal under composite resin. Co2-laser = caries reduction up to 82.7% Er:YAG laser= reduction in surface lesion depth Nd:YAG-laser (with duraphat ) = caries inhibition 106

107. Polymeric coatings A thin, polymeric coating over tooth surfaces which would increase the resistance of tooth to dental caries. 107

108. Passive immunization Monoclonal antibodies have been prepared that can prevent adhesion of streptococcus mutans to tooth surfaces . After eradication of existing S.mutans from the patients mouth by using chlorhexidine, these antibodies can be applied to teeth so that recolonization by streptococcus mutans can be prevented 108

109. REFERENCES sturdevant's operative dentistry- 2 nd south asia edition Studevant’s operative dentistry- 5 th edition Textbook of operative dentistry by Nisha garg-3 rd edition Textbook of operative dentistry by vimal k sikri - 4 th edition clinical operative dentistry- 3 rd edition by ramya raghu 109

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