Dental CariesContents Introduction History Definitions Epidemiology Classification Carious process Concepts of caries development Plaque Host factors-tooth ,saliva factorsSubstrate Socioeconomic factors Summary References Introduction Dental caries is the most common chronic disease (5 billion people worldwide) It is costly in terms of time and work hours lost, money spent. In addition the expense incurred in education of health professional required to cope with this disease in terms of prevention, treatment and oral rehabilitation. HISTORY Aristotle, Hippocrates and Shakespeare have all written on dental caries in their writings. Some theories put forward are the Worm theory, Vital theory etc. L. S. Parmly (1819)-first contributed to current (1819)understanding of caries mechanism Emil Magitot experimented using Pasteur findings. He produced artificial carious lesions in extracted teeth. W.D.Miller (1890) Chemo parasitic theory. Gottlieb (1941) ² Proteolysis theory. Schatz & Martin(1955) ²Proteolysis chelation theory. (Sturdevant) . (Shafer) Dental caries is an infectious microbiologic disease of the teeth that results in localized dissolution and destruction of the calcified tissues.Definitions Dental caries is a microbial disease of the calcified tissues. characterized by demineralization of the inorganic portion and destruction of organic portion of the tooth. (Soben peter) . characterized by demineralization of the inorganic portion and destruction of organic portion of the tooth. irreversible multifactorial in nature affecting the calcified tissues of teeth. Dental caries is defined as a progressive. . Exposure to processed foods.EPIDEMIOLOGY Prehistoric man skulls-very infrequent caries. refined carbohydrates. skullsattributed to rough coarse nature of food consumed. soft drinks and snacks has been shown to increase the frequency of caries. Polarization of caries . Increasing prevalence of caries in less developed countries.Epidemiology Decline in caries prevalence in developed countries. But over-estimates the prevalence of caries. missing or filled (DMF) Either reported as no of teeth (DMFT) or no of surfaces (DMFS) affected. A cumulative index. over- . Most common epidemiologic measure of caries is evaluation of measure of permanent teeth that are diseased. Caries often rightly called Disease of the civilization .Geographical differences More remote areas of world with less access to refined foods shows decreased incidence of caries. Family differences More caries rate seen in siblings of individuals with high caries rates & less incidence seen in siblings of caries immune individuals. salivary flow rate and also to dietary habits and oral hygiene habits of the family. Children of high caries incident parents shows higher caries incidence. . Attributed mainly to genetic factors such as tooth morphology. Gender Girls show high caries incidence than boys of same age till early teens. Attributed to earlier eruption of teeth in girls because of early growth spurt. Significant as teeth are maximally susceptible to caries immediately after eruption. . Most frequently involved is the first permanent molar (six yr molar) .Age Even at age six around 20% of the children have caries incidence in their permanent dentition. Caries susceptibility in permanent dentition 1) 2) 3) 4) 5) 6) Sites ranked in decreasing order of occurrence Fissure of the molars Mesial & distal surface of first molars. Mesial & distal surface of maxillary first premolars Distal surface of canines & Mesial surface of mandibular first premolars Approximal surface of maxillary incisors . Mesial surface of second molars & distal surface of second premolars. CLASSIFICATION I. STURDEVANT Based on .Location .Extent .Rate of progression . Primary caries b.According to location: a. Caries of enamel smooth surface origin d. Root surface caries h. Secondary (recurrent) caries . Forward caries f. Caries of pit and fissure origin c. Residual caries g. Backward caries e. Incipient (reversible) caries b. Chronic (slow or arrested) caries . Cavitated (irreversible) caries According to rate of progression: a. According to extent: a. Acute (rampant) caries b. Smooth surface caries. DCNA: According to tooth type: a. Dentin c. cervical cariesc. Enamel b.II. Permanent (1-32) (1According to anatomic site a. Primary caries & secondary caries b. Deciduous (A-T) (Ab. Cementum Others: a. Root surface caries According to hard tissue affected: a.inter proximal. Radiation caries d. Pit and fissure caries b. Nursing caries c. Rampant caries . GORDAN Based on 1. Morphology (anatomical site ) 2. Chronology (age patterns) . Dynamics (severity and rate of progression) 3.III. Root caries c. Rampant caries b. Arrested caries d. Xerostomia induced caries (radiation caries) . Incipient caries c. Occlusal pit and fissure and smooth surface caries b. According to morphology: a. Linear enamel caries (Odontoclasia) According to rate of progression: a. Recurrent caries e. caries on the occlusal surfaces of molars and premolars . . Class III.occlusal 2/3 of the buccal and lingual surfaces of molars . Class II.lingual surfaces of the anterior teeth.Black·s classification of tooth preparation ClassClass-I: .restorations on anterior teeth that do not IIIinvolve the incisal angles.restorations on proximal surfaces of IIposterior teeth. restorations on incisal edge of anterior VIteeth or the occlusal cusp heights of posterior teeth. Class IV. Class V. proposed by Siomon .Restorations on anterior teeth that IVinvolve the incisal angles.Restorations on all gingival third of Vfacial or lingual surfaces of all teeth (except pit and fissure lesions) Class VI. Simple caries: one surface is involved Compound caries: two surfaces are involved Complex caries: three or caries: more surfaces are involved 2. 3. .1. WHO classification The shape and the depth of the carious lesion can be scored on a 4 point scale D1 -Clinically detectable enamel lesions with intact (non cavitated) surfaces D2 -Clinically detectable cavities limited to enamel D 3 -Clinically detectable lesions in dentin (with and without cavitation of dentin) D 4 ² Lesions into the pulp. . pits. the exposed root surface.fissures and enamel defects on 1occlusal surfaces of posterior teeth or other smooth surfaces.Mounts classification According to site and size of the lesion Site 1.the cervical third of the crown or 3following gingival recession. Site 2. such as cingula pits on anterior teeth. .Approximal enamel immediately below 2contact areas with adjacent teeth Site 3. well supported by dentin and unlikely to fail under normal occlusal load.According to the size Size 1. . Size 2.Minimal involvement of the dentin but 1beyond treatment by remineralization alone.moderate involvement of dentin. remaining enamel is sound. 2following cavity preparation. Remaining 3tooth structure is weakened to the extent that cusps or incisal edges are split or likely to fail if left exposed to occlusal or incisal load. The cavity needs to be further designed to provide support and protection to the remaining tooth structure.extensive caries with bulk loss of tooth 4structure. . Size 3.enlarged beyond moderate. Size 4. . 5mm in depth) Pigmentation: variable. rough can be penetrated with a Dental Explorer Surface defect (<0. irregular. Light tan to brown Grade II (shallow) Surface texture: Soft. can be penetrated with a Dental Explorer No surface defect Pigmentation: variable. Light tan to brown .Classification of root caries Grade I ( Incipient) Surface texture: Soft. Pigmentation: variable. can be penetrated with a Dental Explorer Surface defect: Cavitation present (> 0. Light tan to brown Grade IV (pulpal) Deeply penetrating lesion with pulpal or root canal involvement. Light tan to brown From Billings (1986) .5mm in depth): no pulpal involvement Pigmentation: variable.Grade III (Cavitation) Surface texture: Soft. Ekstrand classification Three criteria used in the classification Visual.32.247-254 . Radiographic and Histological examinations Caries research1998. Visual examination 0 ²No or slight change in enamel translucency after prolonged air drying(>5 sec) 1 ²Opacity (white) hardly visible on the wet surface but distinctly on the wet surface after air drying. 1 a- Opacity (brown) hardly visible on the wet surface but adistinctly on the wet surface after air drying. 2- Opacity (white) distinctly visible without air drying. 2a- Opacity (brown) distinctly visible without air drying. 2a3 ²Localized enamel breakdown in opaque or discoloured enamel and /or greyish discolouration from underlying dentin. 4- Cavitation in opaque or discoloured enamel exposing the underlying dentin. Radiographic examination 0- No radioluscency visible 1- Radioluscency visible in the enamel 2- Radioluscency visible in the dentin but restricted to the outer third of the dentin 3- Radioluscency extending to middle third of the dentin 4- Radioluscency in the pulpal third of the dentin Histological examination 0- No enamel demineralization or a narrow surface zone of opacity (edge phenomenon) 1- Enamel demineralization limited to outer 50% of 50% enamel layer 2- Demineralization involving between 50% of the enamel 50% and1 and1/3rd of dentin 3- Demineralization involving middle1/3rd of dentin middle1 4- Demineralization involving inner 1/3rd of dentin buccal pits of molars .³catch´ the tip of a fine explorer Adjacent enamel appears bluish white ³Internal Caries´ .black or brown in color .slightly soft consistency .lingual surfaces of maxillary anterior teeth Poor self cleansing features Usually occurs before smooth surface caries Clinically .PIT AND FISSURE CARIES Limited to the ± occlusal surfaces of molars and premolars . gingival third of the buccal and lingual surfaces (cervical caries) Preceded by the formation of dental plaque.Smooth Surface Caries Develops on . . Adjacent enamel appears bluish white.proximal surfaces of the teeth . Usually initiate just below the contact point. point.initially as faint white opacity or yellow brown pigmented area. ClinicallyClinically. Lack of oral hygiene on the part of patient. Almost always an open cavity. May extend proximally. . cavity. lesion.Cervical Caries Appears as crescent shaped lesion. caries extends into this enamel from the junction. .Backward Caries Lateral spread of the lesion along the DEJ exceeds the caries in the contiguous enamel. Forward Caries Caries cone in enamel is larger or at least the same size as that in dentin . Residual Caries Caries that remains in a completed cavity preparation Not acceptable if .prepared enamel wall .present at DEJ . Root Surface Caries In old age patients Initiates at the surface of a mineralized dentin and Cementum which have greater organic content Usually have rapid clinical course Recurrent (secondary) caries: Occurs at the junction of the restoration and the cavosurface of the enamel May extend beneath the restoration Indicates unusual susceptibility to caries attack, poor cavity preparation, defective restoration. Also indicates presence of microleakage. Incipient (reversible) caries: First evidence of caries activity in enamel Clinically as white opaque region Subsurface demineralization has occurred but no cavitation May take up extrinsic stains May undergo remineralizationremineralizationcalled as ³caries reversibility´ or ³consolidation´ of early enamel carious lesion .Cavitated (irreversible) caries: Lesion that has advanced into dentin with broken surface Remineralization is not possible Treatment include cavity preparation and restoring with suitable material. .Linear enamel caries (odontoclasia): Atypical form of dental caries in primary dentition Lesion predominates on the labial surface of the maxillary anterior teeth in the region of neonatal zone Lesion is crescent shape Increase caries susceptibility of posterior teeth. cause may be an inherent structural defect .variant of linear enamel caries . Odontoclasia: .results in gross destruction of the labial surfaces of incisor teeth . Acute dental caries: Rapid clinical course resulting in early pulp involvement Frequently in children and young adults Entry of lesion remains small while rapid spread along the DEJ Clinically appears light yellow in colour Pain is often present . Chronic dental caries Common in adults Large entrance of the lesion Dentin is stained deep brown Moderate lateral spread of caries at DEJ Pain is not a common clinical finding. Slowly progressive lesion that involves pulp much later . Rampant caries: Sudden and rapid onset and almost uncontrollable destruction of teeth Involves teeth that are ordinarily caries free (mandibular incisors) Ten or more new increments of carious lesion in one year . Nursing Bottle (Infancy or Soother) Caries Rapidly progressing caries affecting primary dentition usually during first 2 years of life 4 maxillary anterior are affected first If unchecked. maxillary and mandibular molars may also get involved Lower anterior are spared (characteristic feature) . Adolescent caries: Acute caries attack at 11-18 years 11of age Lesion in teeth and surfaces that are relatively immune to caries Small opening in enamel with extensive undermining Rapid clinical course Little or no secondary dentin formation . Arrested caries: Caries which becomes static or stationary and does not show any tendency for progression Almost exclusively occurs on occlusal surfaces Both dentitions are affected Lesion appears as large open cavity with lack of food retention Superficially softened and decalcified dentin gets burnished and has brown stained polished appearance ³Eburnation of dentin´ . prolong illness .Xerostomia induced caries (radiation caries) Complication of radiation therapy of oral cancer lesion Radiation induced xerostomia produces caries conducive environment Carious lesion develops as early as 3 months after onset of xerostomia May be caused by other factors like salivary gland tumors. autoimmune diseases. They are located exclusively on the root surfaces of the teeth. clasps. decreased salivary secretion. Also seen in association with partial denture clasps. .Senile Caries Caries activity that spurts up during the old age. poor oral hygiene. Causes: gingival recession. but detected only on radiograph. Also called as fluoride bombs or fluoride syndrome .Occult Caries / Hidden Caries Not clinically diagnosed. Seen in persons with low caries index suggestive of increased fluoride exposure. Limitations Did not explain sub-surface subdemineralization Failed to justify rampant caries Did not explain caries in impacted tooth Phenomenon of arrested caries is not explained Smooth surface caries is not accounted in this theory . TEETH Morphology: Accentuated pits and fissures Enamel hypoplasia Mottled enamel BuccoBucco-lingual width of carious teeth Position: Malpositioned teeth Rotated teeth . Composition: Surface vs subsurface enamel .3. 3. 6. 2. Carbohydrate is a cariogenic diet Cariogenicity is based on Physical nature Chemical nature Mode of intake Clearance rate Frequency of intake Other dietary factors . 4.DIET 1. 5. microorganisms .PLAQUE AND MICROORGANISMS PLAQUE: The concept about dental plaque was first proposed by Williams in 1897 Consist of .mucin component.salivary component.desquamated epithelial cells .calcium and phosphate . Should be acedogenic. micro organisms should have following properties: 1. 4. 2. Should have the capacity to store sucrose.To produce caries. . Should be able to synthesize extracellular glucans. 5. 3. Should be aceduric. Should posses attachment mechanism. Pioneer / primary bacteria ± initiate caries S.mutans (smooth surface caries) Lactobacillus acidophilus (pit & fissure caries) Actinomyces (root surface caries) Invaders / secondary bacteria Staphylococcus.1. Veillonellae . 2. Streptococci mutans: Chief etiological agent in dental caries disease 1. utilize sucrose at a faster rate than other bacteria 4. it can store intracellular glycogen amylopectin type polysaccharides that act as a reservoir of substrate and prolongs its metabolic activity . it can survive in low pH (acidouric) 3. can metabolize sucrose to synthesize glucan and fructan ( attachment mechanism ) 5. it can produce low pH (acidogenic) acidogenic) 2. in root caries Acidogenic Attachment to tooth by glycoprotein called Lectin Actinomyces .Other Bacteria Lactobacillus acidophilus Found in carious dentin & saliva of persons with high caries activity Release lactic acid Found esp. Acids produced are a) Lactic acid b) Acetic acid c) Butyric acid d) Propionic acid e) Traces of formic acid Lactic acid is the strongest acid . 5 pHCaries immune.8 pH- STEPHEN¶S CURVE . pH. pH.Plaque pH: Critical pH.5.6.5 pHCaries active.5 to 5. Concept of critical pH pH at which any particular saliva ceases to be saturated with calcium and phosphorus ions is referred to as critical pH. Above this pH the remineralization takes place . of H+ ions. more phosphate ions leave the solid apatite phase. Below this value the inorganic constituents dissolve . With conc. STEPHAN CURVE Approximately twenty minutes after ingestion of sucrose. . and once the supply of fermentable nutrients is exhausted. the bacterial will cease to produce acids and the plaque pH will gradually return to a slightly alkaline resting level. 1. 2. 4. SALIVA: Flow rate Viscosity Buffering capacity Amount of saliva Components of saliva: Bicarbonates AntiAnti-bacterial agents Ig-A Ig Salivary urea and bicarbonates .MINOR FACTORS I. 3. teeth more prone to caries Fibrous food help in cleansing of teeth. hypoplasia of teeth is seen. removal of lodged food III. Hereditary factors: . as they prevent attachment of carbohydrates to tooth Trace elements of Vanadium & Molybdenum decreases caries Selenium increases risk of caries Vitamin A & B are important in formation of hard tissues.II. Thus if they are deficient. Dietary factor Diet containing Phosphates decreases caries Proteins & fat also prevents or decreases caries. To know the changes taking place in dental caries Not important for diagnosis.HISTOPATHOLOGY Important for: 1. Studied under: Light microscope Electron microscope Polarized microscope . Research purpose 2. Histological Features of early enamel caries Loss of inter-rod substance interprominent enamel-rods enamelAppearance of transverse striations of enamel rods due to segmental demineralization Accentuation of incremental striae of Retzius . Preferential loss of Interprismatic Substance . Histological Features of Advanced enamel caries Classified on the basis of pore volume and mounting media used Zone 1 ± Translucent zone Zone 2 ± Dark zone Zone 3 ± Body of lesion Zone 4 ± Surface zone These zones are from the dentin towards the outer enamel surface . NORMAL ENAMEL DEJ SURFACE LAYER BODY OF THE LESION DARK ZONE TRANSLUSCENTZONE . Translucent Zone Is deepest & forms advancing front of lesion Not seen always. seen in 50% of cases.1%) Zone cant be easily identified clinically / radiographically . When seen. which is more than normal (0. appear clear due to mounting media which enters these big pores making them look clear/bright Pore volume is 1%. later change to micro-pores. This microchange mainly due to demineralization occurring in deeper areas which release ions & there is remineralization of superficial areas This zone is narrower in rapidly advancing caries & wider in slowly advancing caries . Positive zone as it is always present Pore volume ± 2-4%.Dark zone / positive zone Dark zone as mounting media cant penetrate this zone. 2 types of pores seen here large & small Initially only large pores. Dark zone / positive zone . Body of the lesion Largest zone. between dark & surface zone Greater amount of demineralization taking place. 25% at center Prominent striae of Retzius due to demineralization of inorganic minerals Contains apatite crystals larger than that found in normal enamel . Pore size ± 5-25% 5% variation is near periphery. Body of the lesion . Surface Zone Quite intact. may be due to: surface remineralization by salivary ions More amount of fluoride . appears radio-opaque radio Unaffected despite subsurface demineralization. there is lateral spread of caries Surface enamel gets unsupported enamel rods enamel # greater cavitation Zones of dentinal caries. Zones start from pulpal side towards dentinal side .Dentinal Caries Once lesion spreads to DEJ. 4. 5. . Zone of Fatty Degeneration of Tomes¶ process Zone of Sclerosis Zone of Decalcification without Bacterial Invasion Zone of Decalcification with Bacterial Invasion Zone of Decomposed Dentin / Infected dentin 2. 3.1. DENTINAL CARIES Zone of Decomposed dentin Zone of Bacterial invasion Zone of Dentinal sclerosis Zone of Demineralisation Zone of Fatty degener ation Retreating Odontoblastic process INFECTED DENTIN AFFECTED DENTIN . Fatty Degeneration of Tomes¶ Process Innermost layer of dentinal caries towards pulp Due to deposition of fatty tissue in odontoblastic processes Seen usually in rapidly progressing caries No crystals or bacteria in lumen of tubules Intertubular dentin normal . At the periphery of sclerotic dentin.Zone of Sclerosis/Sub-Transparent Sclerosis/SubDentin As the microorganisms cause destruction to dentin. dead tracts are present. Zone is called ³transparent zone´ Odontoblasts are also start depositing dentin. There is a deposition of mineral in intertubular dentin. . initially there is an attempt to stop the advancement of caries by depositing the minerals. Zone of Decalcification without Bacterial Invasion / Transparent Dentin Decalcification is by bacterial acid diffusion Very narrow zone. Further loss of minerals from inter tubular dentin Large crystals within lumen of dentinal tubules . softer than normal dentin zone. present long (initiators). before lesion is clinically detected Bacteria multiply within tubules & are seen in advancing front of lesion .Zone of Decalcification with Bacterial Invasion / Turbid Dentin Initially only few tubules are involved & micro-orgs also less microThese are acidogenic. pioneer bacteria (initiators). bacteria have proteolytic activity. These areas vary in number & are parallel to dentinal tubules . areas of proteolysis appear as spaces containing necrotic material & bacteria These areas ³Liquefaction Foci of Miller´. Walls of tubules are thin & when micro-orgs micropenetrate. they cause irregularities/distensions of walls ROSARY BEAD appearance Later. occur perpendicular to dentinal tubules ³Transverse Clefts´ .Zone of Decomposed Dentin / Infected Dentin Outermost zone. large scale destruction of dentin Foci of Miller join together Areas of dentin decomposition. Mechanism of formation of Clefts .not known May follow course of incremental lines or May result from coalescence of liquefaction of adjacent tubules Also may rise by extensive proteolytic activity along interconnecting lateral branches of odontoblastic processes Bacteria shift from dentinal tubules to the peri & inter tubular dentin . non-specific irritation to nonodontoblasts Hyper mineralized.Secondary / Reactionary dentin Protective mechanism to protect pulp Develops as a result of localized. less number of dentinal tubules having irregular & torturous course . thus more caries resistant Resistance due to Reprecipitation of minerals from within Precipitation of minerals from Plaque .Root Caries / Cemental Caries Histopathology: Outer surface of cementum ± hyper mineralized. underlying dentin is involved . Clefts formed. through which bacteria penetrate & cause tooth structure destruction Penetration occurs along course of Sharpey's fibers Once cementum completely exposed & destroyed. Actinomyces viscosus. A. S. sp.sanguis. A.Microorganisms found in various types of carious lesions Pit and fissures S.s.salivarius Lactobacillus sp. S. S.mutans.mutans.actinomyces S. S.lactobacillus sp.mutans. s.mutans.naeslundii. A.mutans.salivarius Actinomyces viscosus.sanguis. s.naeslundii Smooth surface caries Root caries Deep dentinal caries .mutans. s.naeslundii. Human longitudinal interventional studies 1) 2) 3) 4) 5) Vipeholm studies-Gustaffson et al 1954 studiesTurku sugar studies-Schenin. Makinen 1975 studiesHereditary fructose intolerance-Newbrun 1969 intoleranceHopewood house-Sullivan & Harris houseVon der Fehr et al(1970) and Loe et al(1972) . . It was done to determine the relation between caries and sugar consumption The experimental design divided inmates into 7 groups. Sweden.Vipeholm studies-Gustaffson et al studies1954 Five yr interventional study by Gustaffson et al on 436 inmates in a mental institution in Vipeholm district hospital. 1) .Experimental groups Control group-low sugar diet only at meals group2) Sucrose group-high sugar mostly in drinks with groupmeals 3) Bread group-received sugar intake half or equal groupto normal in sweetened bread at meals 4) Caramel group-22 sticky candies in two groupportions at meals or 4 portions between meals. 8 toffee group-8 toffees in two portions at groupmeals or 4 portions between meals 6) 24 toffee group-24 toffees at their pleasure groupthroughout the day 7) Chocolate group-given milk chocolates in 4 groupportions between meals. 5) . Conclusions Consumption of sugar is associated with only slight increase in caries incidence if ingestion is limited to meal times(4 times a day) In subjects with poor oral hygiene. consumption of sugar both b/w meals & at meals is associated with marked increase in caries incidence Caries activity subsides once sugar rich foods are withdrawn from diet . In subjects with poor oral hygiene. caries develops despite avoidance of sugar. Increase in caries activity varies widely between individuals . xylitol-52 xylitolEvaluated by two standardized bitewing radiographs on each side of mouth . Finland (1972-1974) (1972Done to study effect of dental caries in almost total substitution of sucrose with fructose or xylitol.Turku sugar studies-Schenin. 125 young adults divided into 3 groups. Sucrose -35. studiesMakinen 1975 Done in Turku.fructose -38. Results ²dramatic reduction in caries prevalence was seen after two yrs of xylitol consumption. Fructose was as cariogenic as sucrose in 1st 12 months but became less cariogenic at end of 24 months. . Turku sugar studies 7 6 5 4 3 2 1 0 0 2 4 6 8 10 12 14 16 18 20 22 24 Mont Sucr s ruct s lit l . At end of 10 yr period. The main feature was absence of meat and rigid restriction of refined carbohydrates. . New South Wales. DMFT index score was 1.Hopewood house-Sullivan & Harris house Study was done on institutionalized children aged 3-14 3yrs residing at Hopewood house.1 just 10% of the score of other state schools in Australia. The meals were supplemented by vitamin concentrates and occasional serving of nuts and honey. Australia. Bowral. As the children grew older and moved out of Hopewood house. Thus this study demonstrated that dental caries can be reduced by restricted diet even in absence of beneficial effects of fluoride and unfavorable oral hygiene. .they no longer adhered to the original diet and there was a steep increase in DMFT index again. But the resistance is not permanent. -Old Dental Public Health Proverb .PREVENTION OF DENTAL CARIES ´An ounce of prevention is worth a pound of dental cureµ. AIMS OF PREVENTION AIMS OF PREVENTION (Sturdevant): 1. 3. . Limiting pathogen growth & metabolism Increasing resistance of tooth surface to demineralization Caries control methods which include operative procedures 2. CLASSIFICATION OF METHODS FOR PREVENTION According to SHAFER: . CHEMICAL MEASURES Substances which alter tooth surface/structure Fluorine Bis-biguanides Bis Silver nitrate Zinc chloride & potassium ferrocyanide Interfere with carbohydrate degradation through enzymatic alterations Vitamin K Sarcoside . Interfere with bacterial growth & metabolism Urea & ammonium compounds Chlorophylls Nitrofurans Penicillins Other antibiotics Caries vaccine Ozone technology . Mechanism Of Action Of Fluorides Increased enamel resistance/reduction in enamel resistance/reduction solubility Formation of fluorapatite Increased rate of post eruptive maturation Deposition of minerals in hypomineralized areas Remineralization of incipient lesions Enhances remineralization rate Larger crystals are formed . Inhibition of demineralization Well formed surface layer also seen Interference with plaque microorganisms High conc-bacteriocidal conc Low concentration-bacteriostatic concentration Enzymatic interference-enolase. sugar transport Modification in tooth morphology Smaller. shallow fissures . protein-extruding interferenceproteinATPase. NUTRITIONAL MEASURES Diet counseling restriction of refined carbohydrates Phosphated diets Calcium phosphate rich diet. saccharine sweeteners- . Sugar substitutes NonNon-caloric sweeteners-aspartame. MECHANICAL MEASURES Dental prophylaxis Tooth brushing Mouth rinsing Dental floss Oral irrigators Detergent foods Chewing gum Pit & fissure sealants Preventive resin restorations . acquired pellicle). Besides these other modifying factors like socioeconomic status and behavioral patterns also greatly influence the caries process in a complex manner. diet. saliva.prevention and treatment of dental caries. . A good understanding of the caries process can help in formulation of better diagnosis. Dental caries has a multi-factorial causation involving the interaction of host factors (tooth surface.Summary Dental caries is an oral infection. and dental plaque (biofilm). The biologic basis of dental caries-Lewis cariesMenaker Essentials of Preventive and Community dentistrydentistry.3rd edition NewbrunDiagnosis & Risk prediction of dental cariescariesPer Axelsson.Soben Peter -2nd edition .References 1) Sturdevant's Art and Science of Operative 2) 3) 4) 5) DentistryDentistry-5th edition Cariology Ernest Newbrun.