Dental Caries

Contents
      

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) Proteolysis theory. Schatz & Martin(1955) Proteolysis chelation theory.

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. (Shafer) Dental caries is an infectious microbiologic disease of the teeth that results in localized dissolution and destruction of the calcified tissues. (Sturdevant)

Dental caries is defined as a progressive, irreversible multifactorial in nature affecting the calcified tissues of teeth, characterized by demineralization of the inorganic portion and destruction of organic portion of the tooth. (Soben peter)

EPIDEMIOLOGY


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

Epidemiology


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

 

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

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

Family differences


 

More caries rate seen in siblings of individuals with high caries rates & less incidence seen in siblings of caries immune individuals. Children of high caries incident parents shows higher caries incidence. Attributed mainly to genetic factors such as tooth morphology, salivary flow rate and also to dietary habits and oral hygiene habits of the family.

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.

Age


Even at age six around 20% of the children have caries incidence in their permanent dentition. Most frequently involved is the first permanent molar (six yr molar)

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

CLASSIFICATION
I.

STURDEVANT Based on - Location - Extent - Rate of progression

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

According to extent: a. Incipient (reversible) caries b. Cavitated (irreversible) caries

According to rate of progression: a. Acute (rampant) caries b. Chronic (slow or arrested) caries

II. DCNA:
According to tooth type:

a. Deciduous (A-T) (Ab. Permanent (1-32) (1According to anatomic site

a. Pit and fissure caries b. Smooth surface caries- inter proximal, cervical cariesc. Root surface caries
According to hard tissue affected:

a. Enamel b. Dentin c. Cementum

Others:

a. Primary caries & secondary caries b. Nursing caries c. Radiation caries d. Rampant caries

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

According to morphology: a. Occlusal pit and fissure and smooth surface caries b. Root caries c. Linear enamel caries (Odontoclasia)

According to rate of progression: a. Rampant caries b. Incipient caries c. Arrested caries d. Recurrent caries e. Xerostomia induced caries (radiation caries)

Blacks classification of tooth preparation



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

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

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 Lesions into the pulp.

Mounts classification
 

 

According to site and size of the lesion Site 1- pits,fissures and enamel defects on 1occlusal surfaces of posterior teeth or other smooth surfaces, such as cingula pits on anterior teeth. Site 2- Approximal enamel immediately below 2contact areas with adjacent teeth Site 3- the cervical third of the crown or 3following gingival recession, the exposed root surface.

According to the size



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

Size 3- enlarged beyond moderate. 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. Size 4- extensive caries with bulk loss of tooth 4structure.

Classification of root caries

Grade I ( Incipient)  Surface texture: Soft, can be penetrated with a Dental Explorer  No surface defect  Pigmentation: variable; Light tan to brown Grade II (shallow)  Surface texture: Soft, irregular, rough can be penetrated with a Dental Explorer  Surface defect (<0.5mm in depth)  Pigmentation: variable; Light tan to brown

Grade III (Cavitation)  Surface texture: Soft, can be penetrated with a Dental Explorer  Surface defect: Cavitation present (> 0.5mm in depth): no pulpal involvement  Pigmentation: variable; Light tan to brown  Grade IV (pulpal)  Deeply penetrating lesion with pulpal or root canal involvement.  Pigmentation: variable; Light tan to brown From Billings (1986)


Ekstrand classification
 

Three criteria used in the classification Visual, Radiographic and Histological examinations

Caries research1998;32;247-254

Visual examination
0 No or slight change in enamel translucency after prolonged air drying(>5 sec) 1 Opacity (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 Localized 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

PIT AND FISSURE CARIES



  

 

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

Smooth Surface Caries



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

  

Cervical Caries
Appears as crescent shaped lesion. lesion.  May extend proximally.  Almost always an open cavity. cavity.  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

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

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 caries reversibility or consolidation 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 - results in gross destruction of the labial surfaces of incisor teeth - cause may be an inherent structural defect

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 Eburnation 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, autoimmune diseases, prolong illness

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. clasps.  Causes: gingival recession, decreased salivary secretion, poor oral hygiene.


Occult Caries / Hidden Caries



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

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. 2. 3. 4. 5. 6.

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 - salivary component- mucin component- desquamated epithelial cells - microorganisms - calcium and phosphate

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

1.

2.

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

Streptococci mutans:


Chief etiological agent in dental caries disease 1. it can produce low pH (acidogenic) acidogenic) 2. it can survive in low pH (acidouric) 3. utilize sucrose at a faster rate than other bacteria 4. can metabolize sucrose to synthesize glucan and fructan ( attachment mechanism ) 5. 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

Plaque pH:
  

Critical pH- 5.5 pHCaries active, pH- 5 to 5.5 pHCaries immune, pH- 6.8 pH-

STEPHENS CURVE

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. Below this value the inorganic constituents dissolve . With conc. of H+ ions, more phosphate ions leave the solid apatite phase. Above this pH the remineralization takes place

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.

MINOR FACTORS
I. 1. 2. 3. 4.

SALIVA: Flow rate Viscosity Buffering capacity Amount of saliva

Components of saliva:  Bicarbonates  AntiAnti-bacterial agents  Ig-A Ig Salivary urea and bicarbonates

II. Dietary factor

    

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

III. Hereditary factors:

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

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. When seen, 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 (0.1%) Zone cant be easily identified clinically / radiographically

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, 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

Body of the lesion

 

 

Largest 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

Surface Zone
Quite intact, appears radio-opaque radio

Unaffected despite subsurface demineralization; may be due to:



surface remineralization by salivary ions

More amount of fluoride

Dentinal Caries


Once lesion spreads to DEJ, 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

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.

3.

4.

5.

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, initially there is an attempt to stop the advancement of caries by depositing the minerals. There is a deposition of mineral in intertubular dentin. Zone is called transparent zone Odontoblasts are also start depositing dentin. At the periphery of sclerotic dentin, dead tracts are present.

Zone of Decalcification without Bacterial Invasion / Transparent Dentin

   

Decalcification is by bacterial acid diffusion Very narrow zone, softer than normal dentin zone, Further loss of minerals from inter tubular dentin Large crystals within lumen of dentinal tubules

Zone of Decalcification with Bacterial Invasion / Turbid Dentin

 

Initially only few tubules are involved & micro-orgs also less microThese are acidogenic, pioneer bacteria (initiators), present long (initiators), before lesion is clinically detected

Bacteria multiply within tubules & are seen in advancing front of lesion

 

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

Zone of Decomposed Dentin / Infected Dentin



Outermost zone, large scale destruction of dentin

 

Foci of Miller join together Areas of dentin decomposition, occur perpendicular to dentinal tubules Transverse Clefts

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

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

Root Caries / Cemental Caries

Histopathology:


Outer surface of cementum hyper mineralized, thus more caries resistant Resistance due to  Reprecipitation of minerals from within  Precipitation of minerals from Plaque

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

Microorganisms found in various types of carious lesions

Pit and fissures S.mutans, S.mutans, S.sanguis,lactobacillus sp.actinomyces S.mutans, S.mutans, S.salivarius Actinomyces viscosus, A.naeslundii, s.mutans, A.naeslundii, s.mutans, s.sanguis,s.salivarius Lactobacillus sp, sp, Actinomyces viscosus, A.naeslundii

Smooth surface caries Root caries

Deep dentinal caries

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)

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, Sweden. It was done to determine the relation between caries and sugar consumption The experimental design divided inmates into 7 groups.

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.
1)

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

Turku sugar studies-Schenin, studiesMakinen 1975

 

  

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

Results dramatic 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

Hopewood house-Sullivan & Harris house

Study was done on institutionalized children aged 3-14 3yrs residing at Hopewood house, Bowral, New South Wales, Australia. The main feature was absence of meat and rigid restriction of refined carbohydrates. The meals were supplemented by vitamin concentrates and occasional serving of nuts and honey. At end of 10 yr period, DMFT index score was 1.1 just 10% of the score of other state schools in Australia.

As the children grew older and moved out of Hopewood house,they no longer adhered to the original diet and there was a steep increase in DMFT index again. 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. But the resistance is not permanent.

PREVENTION OF DENTAL CARIES

An

ounce of prevention is worth a pound of dental cure.

-Old Dental Public Health Proverb

AIMS OF PREVENTION


AIMS OF PREVENTION (Sturdevant):

1.

Limiting pathogen growth & metabolism Increasing resistance of tooth surface to demineralization Caries control methods which include operative procedures

2.

3.

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, protein-extruding interferenceproteinATPase, sugar transport


Modification in tooth morphology



Smaller, shallow fissures

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

Summary
 

Dental caries is an oral infection. Dental caries has a multi-factorial causation involving the interaction of host factors (tooth surface, saliva, acquired pellicle), diet, 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. A good understanding of the caries process can help in formulation of better diagnosis,prevention and treatment of dental caries.

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