Dental Caries


Introduction History Definitions Epidemiology Classification Carious process Concepts of caries development


Plaque Host factors-tooth ,saliva factorsSubstrate Socioeconomic factors Summary References


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. 


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.

characterized by demineralization of the inorganic portion and destruction of organic portion of the tooth.Definitions   Dental caries is a microbial disease of the calcified tissues. (Sturdevant) . (Shafer) Dental caries is an infectious microbiologic disease of the teeth that results in localized dissolution and destruction of the calcified tissues.

(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.

. refined carbohydrates. soft drinks and snacks has been shown to increase the frequency of caries.EPIDEMIOLOGY   Prehistoric man skulls-very infrequent caries. Exposure to processed foods. skullsattributed to rough coarse nature of food consumed.

Polarization of caries . Increasing prevalence of caries in less developed countries.Epidemiology    Decline in caries prevalence in developed countries.

A cumulative index.    Most common epidemiologic measure of caries is evaluation of measure of permanent teeth that are diseased. over- . missing or filled (DMF) Either reported as no of teeth (DMFT) or no of surfaces (DMFS) affected. But over-estimates the prevalence of caries.

Geographical differences   More remote areas of world with less access to refined foods shows decreased incidence of caries. Caries often rightly called Disease of the civilization .

. 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.Family differences    More caries rate seen in siblings of individuals with high caries rates & less incidence seen in siblings of caries immune individuals.

. Attributed to earlier eruption of teeth in girls because of early growth spurt.Gender    Girls show high caries incidence than boys of same age till early teens. 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 surface of second molars & distal surface of second premolars. Mesial & distal surface of maxillary first premolars Distal surface of canines & Mesial surface of mandibular first premolars Approximal surface of maxillary incisors .

Extent . STURDEVANT Based on .CLASSIFICATION I.Location .Rate of progression .

Backward caries e. Caries of enamel smooth surface origin d. Caries of pit and fissure origin c. Residual caries g. Root surface caries h. Secondary (recurrent) caries . Forward caries f. Primary caries b.According to location: a.

Cavitated (irreversible) caries  According to rate of progression: a. Incipient (reversible) caries b. Chronic (slow or arrested) caries . Acute (rampant) caries b. According to extent: a.

Rampant caries . Cementum Others: a. Root surface caries According to hard tissue affected: a. Nursing caries c. Pit and fissure caries b.inter proximal. Smooth surface caries. Deciduous (A-T) (Ab.II. DCNA: According to tooth type: a. Primary caries & secondary caries b. Dentin c. cervical cariesc. Radiation caries d. Enamel b. Permanent (1-32) (1According to anatomic site a.

Morphology (anatomical site ) 2. Chronology (age patterns) . Dynamics (severity and rate of progression) 3.GORDAN Based on 1.III.

Recurrent caries e. Incipient caries c. According to morphology: a. Xerostomia induced caries (radiation caries) . Rampant caries b. Arrested caries d. Occlusal pit and fissure and smooth surface caries b. Linear enamel caries (Odontoclasia)  According to rate of progression: a. Root caries c.

.caries on the occlusal surfaces of molars and premolars .restorations on proximal surfaces of IIposterior teeth. Class III.Black·s classification of tooth preparation    ClassClass-I: .restorations on anterior teeth that do not IIIinvolve the incisal angles. Class II.occlusal 2/3 of the buccal and lingual surfaces of molars .lingual surfaces of the anterior teeth.

   Class IV. proposed by Siomon .Restorations on anterior teeth that IVinvolve the incisal angles.restorations on incisal edge of anterior VIteeth or the occlusal cusp heights of posterior teeth. Class V.Restorations on all gingival third of Vfacial or lingual surfaces of all teeth (except pit and fissure lesions) Class VI.

.1. Simple caries: one surface is involved Compound caries: two surfaces are involved Complex caries: three or caries: more surfaces are involved 2. 3.

.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.

Site 2. such as cingula pits on anterior teeth. 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. .Approximal enamel immediately below 2contact areas with adjacent teeth Site 3.pits.

Minimal involvement of the dentin but 1beyond treatment by remineralization alone.According to the size   Size 1. 2following cavity preparation. . remaining enamel is sound. Size 2.moderate involvement of dentin. well supported by dentin and unlikely to fail under normal occlusal load.

.enlarged beyond moderate.  Size 3. 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.extensive caries with bulk loss of tooth 4structure. The cavity needs to be further designed to provide support and protection to the remaining tooth structure. Size 4.


5mm in depth)  Pigmentation: variable. Light tan to brown . rough can be penetrated with a Dental Explorer  Surface defect (<0. Light tan to brown Grade II (shallow)  Surface texture: Soft.Classification of root caries Grade I ( Incipient)  Surface texture: Soft. can be penetrated with a Dental Explorer  No surface defect  Pigmentation: variable. irregular.

 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.5mm in depth): no pulpal involvement  Pigmentation: variable. Light tan to brown From Billings (1986)  .Grade III (Cavitation)  Surface texture: Soft.

247-254 .32.Ekstrand classification   Three criteria used in the classification Visual. 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

lingual surfaces of maxillary anterior teeth Poor self cleansing features Usually occurs before smooth surface caries Clinically .black or brown in color .buccal pits of molars .PIT AND FISSURE CARIES       Limited to the ± occlusal surfaces of molars and premolars .³catch´ the tip of a fine explorer Adjacent enamel appears bluish white ³Internal Caries´ .slightly soft consistency .

ClinicallyClinically. point.proximal surfaces of the teeth . Usually initiate just below the contact point.Smooth Surface Caries  Develops on . Adjacent enamel appears bluish white.gingival third of the buccal and lingual surfaces (cervical caries) Preceded by the formation of dental plaque.     .initially as faint white opacity or yellow brown pigmented area.

Cervical Caries Appears as crescent shaped lesion. cavity.  Almost always an open cavity. lesion.  May extend proximally.  Lack of oral hygiene on the part of patient.  .

Backward Caries  Lateral spread of the lesion along the DEJ exceeds the caries in the contiguous enamel. caries extends into this enamel from the junction. .

Forward Caries  Caries cone in enamel is larger or at least the same size as that in dentin .

prepared enamel wall   .present at DEJ .Residual Caries Caries that remains in a completed cavity preparation  Not acceptable if .

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. .

 Odontoclasia: .variant of linear enamel caries .cause may be an inherent structural defect .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  .

 Slowly progressive lesion that involves pulp much later  .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.

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´ .

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. prolong illness . autoimmune diseases.

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

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

 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 .

3. Composition:  Surface vs subsurface enamel .

DIET  1. 4. 3. 2. 6. 5. Carbohydrate is a cariogenic diet Cariogenicity is based on Physical nature Chemical nature Mode of intake Clearance rate Frequency of intake Other dietary factors .

PLAQUE AND MICROORGANISMS PLAQUE:  The concept about dental plaque was first proposed by Williams in 1897  Consist of .calcium and phosphate .desquamated epithelial cells .microorganisms .mucin component.salivary component.

Should be able to synthesize extracellular glucans. micro organisms should have following properties: 1. Should have the capacity to store sucrose. . 5.To produce caries. Should be acedogenic. 4. 2. Should be aceduric. 3. Should posses attachment mechanism.

2. Veillonellae . Pioneer / primary bacteria ± initiate caries  S.1.mutans (smooth surface caries)  Lactobacillus acidophilus (pit & fissure caries)  Actinomyces (root surface caries) Invaders / secondary bacteria  Staphylococcus.

it can produce low pH (acidogenic) acidogenic) 2. can metabolize sucrose to synthesize glucan and fructan ( attachment mechanism ) 5. it can survive in low pH (acidouric) 3. utilize sucrose at a faster rate than other bacteria 4.Streptococci mutans:  Chief etiological agent in dental caries disease 1. it can store intracellular glycogen amylopectin type polysaccharides that act as a reservoir of substrate and prolongs its metabolic activity .

Other Bacteria  Lactobacillus acidophilus   Found in carious dentin & saliva of persons with high caries activity Release lactic acid Found esp. in root caries Acidogenic Attachment to tooth by glycoprotein called Lectin  Actinomyces    .

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 .

6.5.5 pHCaries immune.5 pHCaries active.5 to 5.Plaque pH:    Critical pH. pH.8 pH- STEPHEN¶S CURVE . pH.

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 . Below this value the inorganic constituents dissolve . more phosphate ions leave the solid apatite phase. With conc. of H+ ions.

and once the supply of fermentable nutrients is exhausted.STEPHAN CURVE Approximately twenty minutes after ingestion of sucrose. . the bacterial will cease to produce acids and the plaque pH will gradually return to a slightly alkaline resting level.

3. SALIVA: Flow rate Viscosity Buffering capacity Amount of saliva Components of saliva:  Bicarbonates  AntiAnti-bacterial agents  Ig-A Ig Salivary urea and bicarbonates . 4. 2.MINOR FACTORS I. 1.

II. Thus if they are deficient. removal of lodged food III. hypoplasia of teeth is seen. Dietary factor       Diet containing Phosphates decreases caries Proteins & fat also prevents or decreases caries. 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. teeth more prone to caries Fibrous food help in cleansing of teeth.

HISTOPATHOLOGY Important for: 1. Studied under:  Light microscope  Electron microscope  Polarized microscope . Research purpose 2. To know the changes taking place in dental caries  Not important for diagnosis.

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 .


1%) Zone cant be easily identified clinically / radiographically . appear clear due to mounting media which enters these big pores making them look clear/bright Pore volume is 1%. which is more than normal (0.Translucent Zone     Is deepest & forms advancing front of lesion Not seen always. seen in 50% of cases. When seen.

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    .Dark zone / positive zone  Dark zone as mounting media cant penetrate this zone. Positive zone as it is always present Pore volume ± 2-4%. 2 types of pores seen here large & small Initially only large pores.

Dark zone / positive zone .

between dark & surface zone Greater amount of demineralization taking place. Pore size ± 5-25% 5% variation is near periphery. 25% at center Prominent striae of Retzius due to demineralization of inorganic minerals Contains apatite crystals larger than that found in normal enamel .Body of the lesion      Largest zone.

Body of the lesion .

appears radio-opaque radio Unaffected despite subsurface demineralization. may be due to:  surface remineralization by salivary ions  More amount of fluoride .Surface Zone Quite intact.

Dentinal Caries  Once lesion spreads to DEJ. Zones start from pulpal side towards dentinal side . there is lateral spread of caries  Surface enamel gets unsupported enamel rods enamel # greater cavitation   Zones of dentinal caries.

4. .1. 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. 5. 3.

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    .

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. . At the periphery of sclerotic 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.

Further loss of minerals from inter tubular dentin Large crystals within lumen of dentinal tubules . softer than normal dentin zone.Zone of Decalcification without Bacterial Invasion / Transparent Dentin     Decalcification is by bacterial acid diffusion Very narrow zone.

pioneer bacteria (initiators). before lesion is clinically detected  Bacteria multiply within tubules & are seen in advancing front of lesion . present long (initiators).Zone of Decalcification with Bacterial Invasion / Turbid Dentin   Initially only few tubules are involved & micro-orgs also less microThese are acidogenic.

    Walls of tubules are thin & when micro-orgs micropenetrate. bacteria have proteolytic activity. they cause irregularities/distensions of walls ROSARY BEAD appearance Later. areas of proteolysis appear as spaces containing necrotic material & bacteria These areas ³Liquefaction Foci of Miller´. These areas vary in number & are parallel to dentinal tubules .

Zone of Decomposed Dentin / Infected Dentin  Outermost zone. occur perpendicular to dentinal tubules ³Transverse Clefts´ . large scale destruction of dentin   Foci of Miller join together Areas of dentin decomposition.

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 . Mechanism of formation of Clefts .

Secondary / Reactionary dentin   Protective mechanism to protect pulp Develops as a result of localized. non-specific irritation to nonodontoblasts  Hyper mineralized. 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.

   Clefts formed. through which bacteria penetrate & cause tooth structure destruction Penetration occurs along course of Sharpey's fibers Once cementum completely exposed & destroyed. underlying dentin is involved .

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

Makinen 1975 studiesHereditary fructose intolerance-Newbrun 1969 intoleranceHopewood house-Sullivan & Harris houseVon der Fehr et al(1970) and Loe et al(1972) .Human longitudinal interventional studies 1) 2) 3) 4) 5) Vipeholm studies-Gustaffson et al 1954 studiesTurku sugar studies-Schenin.

. 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.

5) .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.

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 .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.

Increase in caries activity varies widely between individuals .  In subjects with poor oral hygiene. caries develops despite avoidance of sugar.

125 young adults divided into 3 groups.fructose -38. xylitol-52 xylitolEvaluated by two standardized bitewing radiographs on each side of mouth . studiesMakinen 1975      Done in Turku.Turku sugar studies-Schenin. Finland (1972-1974) (1972Done to study effect of dental caries in almost total substitution of sucrose with fructose or xylitol. Sucrose -35.

Fructose was as cariogenic as sucrose in 1st 12 months but became less cariogenic at end of 24 months.  Results ²dramatic reduction in caries prevalence was seen after two yrs of xylitol consumption. .

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 .

Australia. New South Wales. DMFT index score was 1. At end of 10 yr period. .Hopewood house-Sullivan & Harris house   Study was done on institutionalized children aged 3-14 3yrs residing at Hopewood house. Bowral. The meals were supplemented by vitamin concentrates and occasional serving of nuts and honey. The main feature was absence of meat and rigid restriction of refined carbohydrates.1 just 10% of the score of other state schools in Australia.

But the resistance is not permanent. 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.   As the children grew older and moved out of Hopewood house. .

PREVENTION OF DENTAL CARIES ´An ounce of prevention is worth a pound of dental cureµ. -Old Dental Public Health Proverb .

3. Limiting pathogen growth & metabolism Increasing resistance of tooth surface to demineralization Caries control methods which include operative procedures 2.AIMS OF PREVENTION  AIMS OF PREVENTION (Sturdevant): 1. .


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  .

shallow fissures . protein-extruding interferenceproteinATPase. 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.

NUTRITIONAL MEASURES  Diet counseling  restriction of refined carbohydrates  Phosphated diets  Calcium phosphate rich diet.  Sugar substitutes  NonNon-caloric sweeteners-aspartame. saccharine sweeteners- .

MECHANICAL MEASURES          Dental prophylaxis Tooth brushing Mouth rinsing Dental floss Oral irrigators Detergent foods Chewing gum Pit & fissure sealants Preventive resin restorations .

acquired pellicle). A good understanding of the caries process can help in formulation of better diagnosis.Summary     Dental caries is an oral infection. saliva. diet.prevention and treatment of dental caries. Dental caries has a multi-factorial causation involving the interaction of host factors (tooth surface. . and dental plaque (biofilm). Besides these other modifying factors like socioeconomic status and behavioral patterns also greatly influence the caries process in a complex manner.

Soben Peter -2nd edition .References 1) Sturdevant's Art and Science of Operative 2) 3) 4) 5) DentistryDentistry-5th edition Cariology Ernest Newbrun. The biologic basis of dental caries-Lewis cariesMenaker Essentials of Preventive and Community dentistrydentistry.3rd edition NewbrunDiagnosis & Risk prediction of dental cariescariesPer Axelsson.

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