Dental Caries.pptx

Dental Caries- Dr.Archana Mukunda

1. DENTAL CARIES DR Archana Mukunda Reader Dept of Oral Pathology Royal Dental College

2. Human tooth is unique made of both mineralized and soft tissue Enamel- hardest non vital tissue Dentin- hardest vital tissue Pulp- specialized connective tissue which contains odontoblasts which form dentin throughout life

3. Each tooth is composed of unique regional diversity of anatomy, chemistry, sensory physiology, and mineral and organic components that constantly change throughout life Loss of tooth structure can be due to a. Microbial- Dental caries b. Non-microbial - attrition, abrasion, erosion

4. The word CARIES was derived from the Latin word meaning DECAY or ROT. a disease of modern civilization, prehistoric man rarely suffered from Dental caries. The rate of caries remained low through the Prehistoric era Periodic increases in caries prevalence occurred when Sugar cane became more accessible to the Western world.

5. Definition Dental caries is an irreversible microbial disease of the calcified tissues of the teeth,characterised by demineralisation of the inorganic portion and destruction of the organic substance of the tooth,which often leads to cavitation .

6. Factors affecting caries prevalence Age: more in children Race: Less in blacks & more in whites Familial: Higher in mono zygotic twins than dizygotic twins Sex: More in permanent teeth of females More in deciduous teeth of males

7. Etiology-the early theories Most disease was attributed to the presence of unseen demons in the body or to an insult that was caused against a particular god magic or witch craft - Ruffer   Legend of worms stated that dental caries occurred from worms like any other disease

8. Etiology-the early theories   Humoral theory : balance between 4 humour a) b lood, (b) phlegm, chemically. (c) black bile, and (d) yellow bile determines mental & physical health and imbalance causes disease. Vital theory : Hippocrates (460–357 BC) suggested that caries originated from tooth itself due to normal predisposition of tooth to filth accumulation and hence corroding action by the same

9. Etiology-the early theories Aristotle (384–322 BC) observed a relationship of eating sweets with dental caries ; soft & sweet figs cause damage to teeth Chemical theory : Parmly (1820) caries is caused by external factor & not internal. Robertson in 1935 showed that acid formation by fermentation of food caused caries

10. Etiology-the early theories Parasitic theory : Erdl in 1843 was the 1 st to related micro organism and caries who showed filamenetous organisms from membrane on tooth Ficnus in 1847 called the tooth related micro organism as denticolae

11. Newer theories Miller’s chemicoparasitic or the acidogenic theory Proteolytic theory Proteolysis-chelation theory Sucrose chelation theory

12. W.D Miller’s chemicoparasitic or the acidogenic theory-1882 Caries is caused by acids produced by variety of microorganisms of the mouth It is a chemoparasitic process consisting of two stages- decalcification of enamel and dentin(preliminary stage) and decalcification of the softened residue(subsequent stage) Acids resulting in primary decalcificaion is produced by the fermentation of starches and sugar from the retaining centers of teeth

13. W.D Miller’s chemicoparasitic or the acidogenic theory-1882 Caries is caused by acids produced by microorganisms of the mouth. DC is a chemoparasitic process consisting of two stages- decalcification of enamel and dentin(preliminary stage) and decalcification of the softened residue(subsequent stage) Acids resulting in primary decalcificaion is produced by the fermentation of starches and sugar from the retaining centers of teeth.

14. W.D Miller’s chemicoparasitic or the acidogenic theory-1882 Caries is caused by acids produced by microorganisms of the mouth. DC is a chemoparasitic process consisting of two stages- decalcification of enamel and dentin(preliminary stage) and decalcification of the softened residue(subsequent stage) Acids resulting in primary decalcificaion is produced by the fermentation of starches and sugar from the retaining centers of teeth.

15. Keyes triad

16. Role of Micro organisms Enamel caries- streptococcous mutans, sanguis, mitis, salivarius, sobrinus Dentinal caries- Lactobacillus acidophillus Root caries- Actinomyces viscosus, maeslundii, israelli, odontolyticus

17. Role of Carbohydrates Refined diet containing fermentable carbohydrates Dietary carbohydrate is involved and not salivary carbohydrate Cariogenicity depends on Frequency of ingestion physical form chemical composition route of administration presence of other food constituents

18. BACTERIA+SUGARS+TEETH  ORGANIC ACIDS CARIES

19. Role of Acids Bacteria degrades carbohydrate to form acids Lactic acid is the chiefly formed acids Other acids formed in small amounts are butyric acid, succinic acid, propionic acid, ethanol, acetic acid etc Homofermentative- which form 90% or more lactic acid eg streptococci & lactobacillus Heterofermentative- form mixture of acids

20. Accumulation of acid is greater by S mutans than other strains Actinomyces are gram + rods anaerobic conditions is homolactic in Co 2 presence is heterolactic

21. Streptococcus mutans : Gram + cocci arranged as chains, isolated by Clark in 1924 Are actively involved in caries initiation are highly localized on the surfaces of the teeth and their abundance in the plaque is highest over initial lesions their level of colonization within the plaque is increased by sucrose consumption They do not colonize in mouth prior to the eruption of teeth and after disappearance of teeth

22. they synthesize insoluble macro-molecules from sucrose that advance their attachment to the teeth Sucrose transport inside the cell is associated with direct phosphorylation by glycolytic pathway glucose – Glucans Sucorse Fructose- Fructans Fructosyl transferase Glycosyl transferase

23. Glucans ( mutans & dextrans)- is insoluble, extracellular adhesive fibrillar polymer moe resistant to enzymatic attack, which helps in accumulation of S mutans Fructans- Soluble , serves as a reservoir of fermentable sugars for oral bacteria They form highly negatively charged lipotechoic acid an extra cellular polymer contributing to adhesiveness

24. They store intracellular glycogen called amylopectin Both intracellular & extracellular polysaccahrides act as reservior prolonging glycolysis beyond meal time They contain enzyme invertase which is activated by inorganic phosphate to degrade sucrose into glucose & fructose

25. They form insoluble polysaccharides, more aciduric, homo fermentative than other oral streptococci Lactobacilli are gram + rods, anaerobic grows best at low pH; are aciophillic & aciduric S mutans provide favorable acid enviornment for growth of lactobacilli L casei & L acidophilus are homofermentators L fermentum & L brevis are heteroferementators

26. They are mainly responsible for caries progression as they cannot adhere to the tooth surface Found more in deep dentinal caries

27. Lactobacilli Streptococci

28. Role of dental plaque Tooth surface cannot shed like oral epithelium Pellicle- salivary glycoprotein adsorbed onto tooth surface ; acts as double sided adhesive tape Plaque – pellicle + bacteria Dental plaque or microcosm = mucin, desquamated epi cells, micro organism Tenacious thin film accumulated on surfaces not constantly cleansed for 24-48hrs

29. Bacteria & teeth have negatively charged surfaces but are attracted by Vander waals forces which is weak The polymers present on the surface of the bacteria help in attaching the bacteria to the tooth surface by ionic, hydro phobic or hydrogen bonds Techoic acid present in the cell wall may form bridges with calcium ions onto pellicle surface

30. Bacteria have specific receptors called adhesins which bind to specific receptors on pellicle Adhesins which bind to sugar are called lectins Hydroxyapatite crystal in tooth = saliva is seen in equillibrium In neutral pH, HA crystals dissolve to release calcium, phosphate and hydroxyl ions the saliva is supersaturated with calcium, phosphate and hydroxyl ions which is deposited back onto tooth

31. In acidic pH saliva is under saturated with phosphate ions so HA crystals are dissolved from tooth to re saturate saliva The ‘critical pH’ is the pH at which a solution is just saturated with respect to a particular mineral. For the HA crystal, it is approximately 5.5–6 , below which the enamel disintegrates. Critical pH for FA is 4.5

32. Streptococcus sobrinus produces a virulence-associated immunomodulatory protein (VIP) called enolase which suppresses the host-specific immune response It differs from S mutans > requires sucrose for attachment and growth in plaque > lacks adhesins required for sucrose independent attachment ; hence can grow on smooth surface

33. Draw backs of theory Unable to explain specific site predilection Initiation of smooth surface caries Concept of dental plaque was later added in 1897 by William’s Does not explain why some population is caries free The occurrence of arrested caries

34. PROTEOLYTIC THEORY The evidence given by the acidogenic theory was considerable but it was not conclusive, and alternative explanation was given in the form of proteolytic theory by Gottlieb and Gottlieb 1944 . Workers like “ Heider, Bodecker (1878)and Abbott (1879) contributed considerably to this theory

35. Protelytic enzymes produced by the bacteria destroy the organic matrix of enamel thereby loosening the apatite crystal Hypocalcified structures in enamel like enamel lamelle and enamel rods as thought to be path ways for the advancing microorganisms

36. It has been established that enamel contains 0.56 % of organic matter of which 0.18% is keratin and 0.17 % is a soluble protein Microorganisms invade the enamel lamelle and the acid produced by the bacteria's causes damage to the organic pathways in advance Yellowish pigment produced by the proteolytic bacteria’s was only possible in the presence of dietary carbohydrates.

37. Draw backs of the theory It couldn’t provide sufficient evidences to support the claim that the initial attack on enamel is proteolytic It is not possible to produce caries in vitro using proteolytic agents Proteolytic enzymes produced in plaque are capable of producing periodontal disease However , this theory is still helpful in explaining the progression of a more advanced carious lesion.

38. PROTEOLYSIS CHELATION THEORY Some of the minor flaws of the acidogenic and the proteolytic theory were addressed in the proteolysis chelation theory This theory was put forward by Schatz 1955 and his co-workers

39. CHELATION It is a process in which there is complexing of the metal ions to form complex substance through coordinate covalent bond which results in: poorly dissociated /or weakly ionized compound

40. Hemoglobin in which 4 pyrrole nuclei are linked to iron by a similar bond Chelation is independent of the pH of the medium. keratinolytic microorganisms attack enamel resulting in the breakdown of the protein chiefly keratin and results in the formation of soluble chelates which decalcify enamel even at neutral pH Mucopolysaccarides may also act as secondary chelators

41. Sucrose chelation theory Was proposed by Lura in 1967 High content of sucrose in the oral cavity results in formation of complex substance like calcium saccharate by the action of phosphorylating enzymes by bacteria These substances causes release of calcium and phosphorous from enamel

42. Autoimmune theory Proposed by Burch and Jackson 1970 Genes partly inherited and partly mutated determine whether a site on tooth is at high risk or low risk Odontoblasts may be the target in caries, which may change the resistance of enamel to acid attack rejected theory based on epidemiology

43. Sulfatase theory Proposed by Pincus et al in 1950 Bacteria in plaque producing sulfatase enzyme hydrolyse mucotin sulfate of enamel and chondrotin sulfate of dentin This results in formation of sulfuric acid which decalcifies The amount of mucotin sulfate in enamel is very less and not available for degradation

44. Caries susceptibility incidence of the teeth Upper and lower 6s  95% Upper and lower 7s  75% Upper 5s  45% Upper 4s and lower 5s  35% Upper 1s and 2s  30% Upper 3s and lower 4s  10% Lower 1s ,2s and s  3%

45. CLINICAL FEATURES Chalky white spot on surface of tooth; indicates area of demineralization (350-500µ); reversible The lesion may become brown as demineralization progresses and turns into a cavity; irreversible The affected part of tooth is soft to touch Once caries reaches DEJ symptoms such as sensitivity or pain can be felt Some times caries can be arrested and appear brown and shiny

46. CLINICAL CLASSIFICATION OF CARIES Based on anatomical site -pit and fissure caries -smooth surface caries -linear enamel caries -cervical caries -root caries Based on rapidity of caries progression -acute dental caries -chronic dental caries

47. Based on age -infancy/nursing bottle caries -adolescent caries Based on whether it is new or recurrent -primary/virgin caries -secondary/recurrent caries

48. Pit and Fissure caries Occlusal surfaces of molars and premolars Buccal and lingual surfaces of molars, lingual surface of maxillary incisors Among children, pit and fissure caries represent 90% of all dental caries As the decay progresses, caries in enamel nearest the surface of the tooth spreads gradually deeper Once the caries reaches the dentin at the DEJ, the decay quickly spreads laterally

49. Within the dentin, the decay follows a triangle pattern that points to the tooth's pulp This pattern of decay is typically described as two triangles (one triangle in enamel, and another in dentin) with their bases conjoined to each other at the DEJ. This base-to-base pattern is typical of pit and fissure caries, unlike smooth-surface caries (where base and apex of the two triangles join).

50. Smooth surface caries Proximal caries, also called interproximal caries, form on the smooth surfaces between adjacent teeth below contact area May occur on gingival 3 rd of buccal & lingual surfaces of any other smooth tooth surface

51. NURSING BOTTLE CARIES Baby Bottle syndrome, bottle mouth syndrome, nursing caries, bottle caries, infant caries, early childhood caries etc Occurs as a result of inappropriate feeding of children A form of rampant caries affecting the deciduous dentition

52. Etiology Prolonged use of nursing bottle containing juice, milk, milk formula, or any other liquid sweetened with fermentable carbohydrates. Prolonged breast feeding, sugar or honey sweetened pacifiers The stagnation of fluid in the neck of anterior teeth leads to fermentation of the carbohydrate which produces acid causing caries

53. Causes wide spread destruction of deciduous teeth, usually the maxillary incisors followed by 1 st molar then cuspid Caries does not affect the mandibular teeth as they are covered by tongue

54. ROOT CARIES Root caries is defined by Hazen as a soft, progressive lesion that is found anywhere on the root surface that has lost connective tissue attachment and is exposed to the oral environment Earlier referred to as cemental caries Predominant in the elderly usually occur when the root surfaces have been exposed due to gingival recession

55. When the gingiva is healthy, root caries is unlikely to develop because the root surfaces are not as accessible to bacterial plaque. The root surface is more vulnerable to the demineralization process than enamel because cementum begins to demineralize at 6.7 pH, which is higher than enamel's critical pH Regardless, it is easier to arrest the progression of root caries than enamel caries because roots have a greater reuptake of fluoride than enamel.

56. Root caries is most likely to be found on facial surfaces, then interproximal surfaces, then lingual surfaces. Mandibular molars are the most common location to find root caries, followed by mandibular premolars, maxillary anteriors , maxillary posteriors, and mandibular anteriors .

57. Rampant caries Rampant caries signifies advanced or severe decay on multiple surfaces of many teeth Rampant caries may be seen in individuals with xerostomia, poor oral hygiene, stimulant use (due to drug-induced dry mouth), and/or large sugar intake.

58. If rampant caries is a result of previous radiation to the head and neck, it may be described as radiation-induced caries Problems can also be caused by the self destruction of roots and whole tooth resorption when new teeth erupt or later from unknown causes

59. Radiation caries Form of rampant caries occuring in patients undergoing radiation therapy of head & neck Xerostomia , increase in viscosity & low pH of saliva Causes brown or black discoloration of crown or disintegrating the crown as irregularly shaped discolored stump or complete amputation of neck of tooth

60. Acute caries Runs a rapid clinical course & results in early pulp involvement Seen in children & young adults- as dentinal tubules are open & show no sclerosis The caries is so rapid that there is little or no time for reparative dentin deposition

61. The initial entry is small & rapid spread at DEJ , large involvement of dentin with large internal excavation Lesions are light yellow in color Is usually associated with pain

62. Chronic caries That form of caries which progresses slowly and tends to involve pulp much later than acute caries The entrance to the lesion is almost invariably larger than that of acute caries Common in adults; appears dark brown in color Allows sufficient time for both dentinal sclerosis and secondary dentin deposition

63. Arrested caries - describes as a lesion which becomes static without further progression

64. Affects both dentitions Occurs in large open cavities with lack of food retention and in which the superficially softened and decalcified dentin is gradually burnished until it takes on a brown stained, polished, appearance and is hard This is called eburnation of dentin

65. Sclerosis of dentinal tubules and secondary dentin formation occurs Another form seen on proximal surfaces of teeth in which adjacent teeth have been extracted, revealing a brown stained area at or just below contact point

66. Recurrent caries Recurrent caries, also described as secondary, are caries that appears at a location with a previous history of caries. This is frequently found on the margins of fillings and other dental restorations.

67. Histopathology of dental caries

68. As the enamel loses minerals, and dental caries progresses, the enamel develop several distinct zones, visible under a light microscope. From the deepest layer of the enamel to the enamel surface, the identified areas are the: Zone 1-translucent zone Zone 2-dark zone Zone 3-body of the lesion Zone 4-surface zone

69. TRANSLUCENT ZONE Zone of Initial demineralization More porous than the normal enamel; pore volume is 1% These pores are larger than the normal enamel. Chemical analysis show that there is a fall in the magnesium and carbonate content as compared to the normal enamel Zone may not always present

70. In this zone , pores or voids form along the enamel prism(rod) boundaries (due to easy H+ ion penetration) It appears structureless when perfused with quinolone solution (having refractive index comparable to that of enamel) and seen with polarized light ( hence translucent )

71. Dark zone Called as positive zone This zone contains 2-4% by volume pores Does not transmit polarized light Smaller air filled pores make the region opaque as quinoline cannot enter into smaller pores

72. The smaller size of the pores may form a sieve like structure preventing escape of minerals helping in remineralization

73. Body of the Lesion This zone has pore volume of 5% periphery -25% center It contains appetite crystals larger than the normal enamel more of an effort for the remineralization but by the further attack there is further dissolution of the mineral Thus this is the zone of maximum demineralization

74. Surface zone This is about 40 micrometer thick Relatively unaffected by caries Pore volume less than 5% Radiopaque Hypermineralized

75. Smooth surface caries

76. Smooth surface caries Early macroscopic changes - An area of decalcification - White spot - Brown spot Early microscopic changes - Accentuation of Striae of Retzius - Accentuation of perikymata

77. Pit & Fissure caries

78. Zones of dentinal caries Zone 1 - zone of fatty degeneration of Tome’s fibres Zone 2- zone of dentinal sclerosis characterised by deposition of calcium salts in dentinal tubules Zone 3- zone of decalcification of dentin,a narrow zone ,preceding bacterial invasion Zone 4- zone of bacterial invasion of decalcified but intact dentin Zone 5- zone of decomposed dentin

79. Zone 1: zone of fatty degeneration of Tomes’ fiber the most advancing front of dentinal caries characterized by the presence of a layer of fat globules ; hence stains red with the stain, sudan red significance: 1) fat layer leads to impermiability of the dentinal tubules (DT) – trying to prevent further invasion of carious lesion 2) favors sclerosis of dentin in zone 2.

80. Zone 2: zone of dentinal sclerosis layer of sclerotic dentin which appears white in transmitted light calcification of DT as a reaction of vital pulp and vital dentin to carious invasion , so as to prevent further penetration of microorganisms formation of this zone is minimal in rapidly progressing caries, and prominent in slow caries

81. Zone 3: zone of decalcification of dentin this zone lies above the zone of sclerotic dentin initial decalcification of only the walls of the DT presence of PIONEER BACTERIA - first of the microorganisms penetrating DT before there is any clinical evidence of caries Bacteria present in individual DT are in pure form (i.e. either completely cocci or completely bacilli; not in mixed form)

82. Zone 4: zone of microbial invasion Is a layer above zone 3 Characterized by the presence of microorganisms in early stage of caries- acidogenic microorganisms in deeper layer- proteolytic microorganisms replace acidogenic bacteria supports the hypothesis that initiation (by acidogenic bacteria) and progression ( by proteolytic microorganisms ) are 2 distinct processes in caries development

83. During initiation phase- in the early stage when caries is not deep , acidogenic bacteria predominant which utilizes carbohydrate for their metabolism Later in progression phase – as the caries goes deeper , less and less of carbohydrate substrate available , hence acidogenic bacteria are replaced by proteolytic microorganisms which uses dentinal protein for their metabolism

84. Zone 5: zone of decomposed dentin Most superficial zone of early dentinal caries no recognizable structure in decomposed dentin collagen and minerals seem to be absent great number bacteria dispersed in this decomposed granular matter Diameter of dentinal tubules increases as it is packed with bacteria

85. Focal coalescence & breakdown of few dentinal tubules form tiny liquefactive foci – a ovoid area of destruction parallel to dentinal tubules filled with necrotic debri This produces compression & distortion of DT & their course in bent around liquefactive focus Numerous focal areas coalesce & give leathery consistency to necrotic mass of dentin

86. Transverse clefts are seen in this necrotic dentin extending at right angles to dentinal tubules Occurs due to extension of carious process along lateral branches of tubules These clefts are seen parallel to the contour lines of dentin This allows peeling away dentin in layers with a hand instrument

87. Thickening of dentinal tubules

88. Liquefactive foci

89. Transverse cleft

90. ROLE OF FLUORIDES IN DENTAL CARIES

91. Fluoride is the ionic form of the element fluorine, the 13th most abundant element in the earth's crust Fluoride is negatively charged and combines with positive ions (e.g., calcium or sodium) to form stable compounds (e.g., calcium fluoride or sodium fluoride) In humans, fluoride is mainly associated with calcified tissues (i.e., bones and teeth) because of its high affinity for calcium

92. Fluoride reduces the incidence of dental caries and slows or reverses the progression of existing lesions Fluoride concentrated in plaque and saliva inhibits the demineralization of sound enamel and enhances the remineralization (i.e., recovery) of demineralized enamel As acids are produced by bacteria fluoride is released from plaque which takes up calcium and phosphate released by demineralization

93. Fluoride is taken up more readily in demineralized enamel than sound enamel Functions of fluoride concentrates in dental plaque and inhibits cariogenic bacteria from utilizing the carbohydrate to produce acid Also reduces adhesive polysaccharides produced by bacteria Fluorapatite crystals are more resistant to acid attack crtical pH is 4.5

94. Fluoride can be supplemented as water, salt, milk fluoridation & topical appilication Fluoride works primarily via topical mechanisms which include a. Inhibits demineralization at the crystal surfaces in the tooth b. Enhances remineralization at the crystal surfaces inhibition of bacterial enzymes

95. AIDS FOR CARIES DETECTION

96. Caries Diagnosis The primary aim of effective diagnosis and treatment planning is early detection of incipient caries and interception of carious process before significant amount of tooth destruction occurs. Various diagnosis methods are available to detect caries activity at early stages:- Identification of subsurface demineralization (inspection, radiography and dye uptake methods) Bacterial testing Assessment of environmental conditions such as pH, salivary flow and salivary buffering.

97. Visual- good in detecting lesions but does not give good results for non cavitated caries Visual & Tactile- probe or explorer is used along with visual- may lack preventive X- rays- is a vital tool to detect occult proximal caries and depth of the lesion

98. Explorer Dental floss Radiographs

99. Fiber-optic transillumination test (FOTI)- This device is based on the principle of light scattering Light is scattered more in a carious tissue than in a non-carious tissue, it is observed as a dark shadow against a light background 1 st used for detection of anterior proximal lesions now used for posterior proximal lesions

100. Transillumination Digital imaging

101. Digital imaging fiber-optic transillumination ( DIFOTI ) The device works on the same principle of light scattering, but the human eyes are replaced by CCD intraoral camera to capture the image and instantly project in the monitor Laser/Light-induced fluorescence Diagnodent - sound enamel & dentin and carious lesion have auto fluorescence due to presence of chromophores ; The difference in the fluorescing capacity of the sound tooth and the carious lesion can be recorded or observed

102. Digital Substraction radiography Diagnodent

103. Electrical caries meter (ECM)- The electrical conductivity of a normal tooth is less compared to a demineralized lesion; as electrical conductivity increases after porous enamel is filled with ionic fluid Caries detecting dyes- uses protein dye acid red Which stains the organic matrix of less mineralized dentin & differentiates between infected & non infected dentin

104. Caries detecting dyes

105. CARIES VACCINE

106. Caries vaccine is a vaccine used to prevent & protect tooth against caries S mutans is the main etiological agent hence vaccine are developed against it S mutans cell surface contains adhesins, GTFs, and glucan binding proteins (GBP). These substances are used as antigens for vaccine preparation

107. Antibodies against these antigens block adherence of S mutans onto HA crystal antibodies formed are S-IgA Antibodies in saliva (secretory immune system) or IgG or IgM (systemic immunity) In GCF its mainly S-IgA

108. Antibody with specificity for S. mutans adhesins interferes with bacterial adherence  prevent dental caries Antibody directed to GTF: interferes with activity of the enzyme and thus plaque formation Antibodies against GBP prevents ability of mutans strep to bind to glucans Antibodes against dextranase prevents convertion of glucans into glucose for glycolysis

109. Caries vaccines can be given by 1. mucosal route like oral, intranasal, tonsillar, minor salivary glands, rectal routes 2. adjuvants cholera toxin subunits monophosphoryl lipid A 3. recombinant vaccines cloned antigens recombinant vector

110. The antigen stimulate the immune system thereby producing antiobodies S Ig A

111. Problems with caries vaccine Not known how to generate long-term IgA response to antigens Studies of rodents and humans show periods of elevated IgA levels for weeks/months (would require frequent “booster” innoculations) Argument that even delayed infection of S. mutans would be beneficial since newly erupted teeth are more susceptible to cariogenic attack than teeth that had more time to mature (calcification)

112. Caries control measures Chemical Mechanical Nutritional

113. Chemical 1)Substances that alter tooth surface structure Fluorides-topical,water fluoridation,tablets,drops,dentifrices,mouthwashes Bisbiguanides-chlorhexidine Silver nitrate.zinc chloride,potassium ferrocyanide

114. 2)Substances which interferes with carbohydrates metabolism through enzymatic alteration Vitamin K Sarcoside 3)Substances which interfere with bacterial growth and metabolism Urea and ammonium compounds Chlorophyll Nitrofurans Penicillins Other antibiotics

115. Nutritional restriction of refined carbohydrates

116. Mechanical Dental prophylaxis Tooth brushing Dental flossing Detergent foods Chewing gums Pit and fissure sealants

117. Treatment The goal of treatment is to preserve tooth structures and prevent further destruction of the tooth. Dental restoration    Restorative materials include dental amalgam , composite resin , porcelain , and gold . When the decay is too extensive, there may not be enough tooth structure remaining to allow a restorative material to be placed within the tooth. Thus, a crown may be needed. This restoration appears similar to a cap and is fitted over the remainder of the natural crown of the tooth. Crowns are often made of gold, porcelain, or porcelain fused to metal.

118. In certain cases, endodontic therapy may be necessary for the restoration of a tooth. Endodontic therapy, also known as a "root canal", is recommended if the pulp in a tooth dies from infection by decay-causing bacteria or from trauma. During a root canal, the pulp of the tooth, including the nerve and vascular tissues, is removed along with decayed portions of the tooth. The canals are instrumented with endodontic files to clean and shape them, and they are then usually filled with a rubber-like material called gutta percha . The tooth is filled and a crown can be placed. Upon completion of a root canal, the tooth is now non-vital, as it is devoid of any living tissue.

119. An extraction can also serve as treatment for dental caries. The removal of the decayed tooth is performed if the tooth is too far destroyed from the decay process to effectively restore the tooth. Extractions are sometimes considered if the tooth lacks an opposing tooth or will probably cause further problems in the future, as may be the case for wisdom teeth .Extractions may also be preferred by patients unable or unwilling to undergo the expense or difficulties in restoring the tooth.

120. Caries activity and susceptibility Caries activity refers to the increment of active lesions new or recurrent over a stated period of time. Caries susceptibility refers to the inherent tendency of the host and target tissues,the tooth to be afflicted by the caries process.

121. Caries activity tests Caries susceptibility tests Lactobacillus colony test Colorimetric Snyder test Swab test Salivary streptococcus mutans level test Enamel solubility test Salivary reductase test

122. T H A N K Y O U