Hume- “caries is essentially a progressive loss by acid dissolution of the apatite component of the enamel then the dentin or of the cementum then dentin.” According to location: Pit or Fissure caries Smooth Surface caries According to rapidity: Acute Chronic Arrested According to occurrence: Primary (Virgin) caries Secondary (Recurrent) caries According to the site of occurrence: Enamel caries Cemental caries. Acidogenic [ Miller’s Chemico-parasitic] theory. Proteolytic theory. Proteolysis- chelation theory.

1. DENTAL CARIES
DR AMITHA G , BDS, MDS
ORAL AND MAXILLOFACIAL PATHOLOGY

2. CLINICAL FEATURES
• Young girls > boys.Young girls > boys.
• Maxillary arch > Mandibular arch.Maxillary arch > Mandibular arch.
• Maxillary & mandibular 1Maxillary & mandibular 1stst
molars are the most susceptiblemolars are the most susceptible
individual teeth.individual teeth.
• Mandibular incisors are the most resistant.Mandibular incisors are the most resistant.
• Occlusal lesion is the most prevalent type of lesion in bothOcclusal lesion is the most prevalent type of lesion in both
deciduous & permanent teeth.deciduous & permanent teeth.

3. The sequence in which teeth are affectedThe sequence in which teeth are affected
•Upper & lower 1Upper & lower 1stst
molarsmolars
•Upper & lower 2Upper & lower 2ndnd
molarsmolars
•Upper 2Upper 2ndnd
premolarpremolar
•Upper 1Upper 1stst
premolar & lower 2premolar & lower 2ndnd
premolarpremolar
•Upper central & lateral incisorsUpper central & lateral incisors
•Lower incisors & canines.Lower incisors & canines.

4. DEFINITION
Hume- “caries is essentially a progressive loss by acidHume- “caries is essentially a progressive loss by acid
dissolution of the apatite component of the enamel thendissolution of the apatite component of the enamel then
the dentin or of the cementum then dentin.”the dentin or of the cementum then dentin.”

5. CLASSIFICATION OF DENTAL CARIES
According to location:
•Pit or Fissure caries
•Smooth Surface caries
According to rapidity:
•Acute
•Chronic
•Arrested

6. According to occurrence:
•Primary (Virgin) caries
•Secondary (Recurrent) caries
According to the site of occurrence:
•Enamel caries
•Cemental caries.

7. PIT &FISSURE CARIES
• Developmental pits & fissures of the teeth.
• Occlusal surface of molars & premolars.
• Buccal & lingual surface of the molars.
• Lingual surface of the maxillary incisors.
• Fissures with high steep walls & narrow
• Bases are most prone to develop caries.

8. • Brown or black & slightly soft.
• Enamel at border appears opaque, bluish white.
• Lateral spread of caries at DEJ.
• Extensive penetration into dentinal tubules.
• Overhanging enamel- Large cavity with small opening.
• Slowly progressive.

9. SMOOTH SURFACE CARIES
• Proximal surface of the teeth.
• Gingival third of buccal & lingual surfaces.
• Usually preceded by the formation of a
• dental plaque.
• Begins just below the contact point.

10. • Faint white opaque enamel, yellow or brown pigmentation.
• Bluish white surrounding area.
• Small area of penetration- rapidly progressive.
• Open shallow cavity- slowly progressive.

11. ACUTE DENTAL CARIES
• Rapid clinical course.
• Early pulp involvement.
• Children & young adults.
• Small area of penetration
• Light yellow dentin.

12. RAMPANT CARIES
• Acute fulminating type.
• Simultaneous involvement of multiple number of teeth, in
multiple surfaces.
• Early involvement of pulp.
• Common age groups: 4-8 yrs & 11-19 yrs

13. NURSING BOTTLE CARIES
• Baby bottle syndrome/ Bottle mouth syndrome.
• Deciduous teeth.
• Prolonged use of milk or fruit juices by the nursing
bottle.
• Breast feeding.
• Wide spread distribution of deciduous teeth.
• Most commonly affected : 4 maxillary incisors
followed by 1st molars & cuspids.
• Absence of caries in mandibular incisors.

14. CHRONIC DENTAL CARIES
• Slowly progressive.
• Common in adults.
• Large opening.
• Deep brown dentin.
• Less undermining enamel.

15. ARRESTED CARIES
• Progression is ceased.
• Usually occurs when a carious cavity becomes
wide open.
• Hard, black or brown colored dentinal
• Surface at it’s base. [ Eburnated Dentin]

16. RECURRENT CARIES
• Around the margins of a defective restoration.
• Due to inadequate extension of an original restoration or
fracture of a restoration.

17. FORWARD CARIES
Carious lesion progresses unidirectionally from the enamel to the
dentin & pulp.
BACKWARD CARIES
Undermined dentinal caries progresses from the dentin towards
the enamel surface.
RADIATION CARIES
In patients receiving large doses of radiation for the treatment of
malignant lesions.
Cervical areas of teeth.

18. ROOT CARIES
• Both cementum & dentin are involved.
• Slowly progressing chronic lesion.
• Saucer shaped cavity.
• Invades along the direction of the sharpey’s fibers.
• Initial lesions clefts in the cementum.
• Microorganisms eventually penetrate along the clefts
leading to stepwise destruction of the cementum..

19. CONTRIBUTING FACTORS IN DENTAL CARIES
• MULTIFACTORIAL DISEASEMULTIFACTORIAL DISEASE
TOOTHTOOTH
1. Composition1. Composition
2. Morphologic characteristics.2. Morphologic characteristics.
3. Position.3. Position.

20. B.B. SALIVASALIVA
1. Composition1. Composition
- Inorganic- Inorganic
- Organic- Organic
2. pH2. pH
3. Quantity3. Quantity
4. Viscosity4. Viscosity
5. Antibacterial factors.5. Antibacterial factors.
C. DIET. DIET
1. Physical factors- Quality of diet.1. Physical factors- Quality of diet.
2. Local factors2. Local factors
- carbohydrate content- carbohydrate content
- vitamin content- vitamin content
- fluoride content- fluoride content

21. TOOTH FACTOR:TOOTH FACTOR:
1.1. Composition:Composition:
Surface enamel is more resistant to caries than subsurfaceSurface enamel is more resistant to caries than subsurface
enamel.enamel.
2.2. Morphologic Characteristics:Morphologic Characteristics:
* Enamel hypoplasia predisposes to the development of caries.* Enamel hypoplasia predisposes to the development of caries.
* Presence of deep, narrow occlusal fissures or buccal or lingual* Presence of deep, narrow occlusal fissures or buccal or lingual
pits.pits.
3.3. Tooth position:Tooth position:
* Mal aligned* Mal aligned
* Out of position* Out of position
* Rotated teeth* Rotated teeth

22. SALIVA FACTORSSALIVA FACTORS
• Calcium & phosphate content of the saliva is low in cariesCalcium & phosphate content of the saliva is low in caries
active persons.active persons.
• Ammonia content of caries susceptible persons areAmmonia content of caries susceptible persons are
comparatively less than caries resistant persons.comparatively less than caries resistant persons.

23. Salivary enzymes:Salivary enzymes:
• AmylaseAmylase
• PtyalinPtyalin
High amylotic activity is associated with low caries [ Few studies]High amylotic activity is associated with low caries [ Few studies]
pH of saliva:pH of saliva:
Quantity of saliva: flow = cariesQuantity of saliva: flow = caries
* Xerostomia* Xerostomia
* Sjogren’s syndrome* Sjogren’s syndrome

24. Viscosity:Viscosity:
High caries incidence is associated with thick mucinous saliva.High caries incidence is associated with thick mucinous saliva.
Antibacterial properties of saliva:Antibacterial properties of saliva:
- Lysozyme- Lysozyme
- Salivary peroxidase & thiocyanate- Salivary peroxidase & thiocyanate
- Salivary IgA- Salivary IgA

25. DIET FACTORS:DIET FACTORS:
PHYSICAL NATURE:PHYSICAL NATURE:
* Soft refined food- caries* Soft refined food- caries
* More carbohydrate content* More carbohydrate content

26. VITAMIN CONTENT:VITAMIN CONTENT:
Vitamin D:Vitamin D:
Infantile ricketsInfantile rickets
Alteration in tooth structureAlteration in tooth structure
Tooth more susceptible to cariesTooth more susceptible to caries
Evidence indicates that vitamin D supplements may reduce the dentalEvidence indicates that vitamin D supplements may reduce the dental
caries incident.caries incident.
• Vitamin B 6 (Pyridoxine) – Anticarious?Vitamin B 6 (Pyridoxine) – Anticarious?
- Promotes the non carious microflora- Promotes the non carious microflora

27. Calcium & phosphorus intake:Calcium & phosphorus intake:
Disturbance in Ca & P metabolism during tooth formationDisturbance in Ca & P metabolism during tooth formation
Enamel hypoplasia & defect in the dentineEnamel hypoplasia & defect in the dentine
Susceptible to cariesSusceptible to caries
Fluoride content of dietFluoride content of diet
Selenium & Vanadium:Selenium & Vanadium:
* Selenium- caries incidence* Selenium- caries incidence
* Vanadium- caries incidence* Vanadium- caries incidence

28. SYSTEMIC FACTORS:SYSTEMIC FACTORS:
•Heredity
•Racial factors

29. THEORIES:THEORIES:
• Acidogenic [ Miller’s Chemico-parasitic] theory.Acidogenic [ Miller’s Chemico-parasitic] theory.
• Proteolytic theory.Proteolytic theory.
• Proteolysis- chelation theory.Proteolysis- chelation theory.

30. 1.1. Chemoparasitic theory [ Acidogenic theory]:Chemoparasitic theory [ Acidogenic theory]:
- W. D. Miller (1882)- W. D. Miller (1882)
““ Dental decay is a chemo-parasitic process consisting of 2 stages.Dental decay is a chemo-parasitic process consisting of 2 stages.
The decalcification of enamel, which results in it’s totalThe decalcification of enamel, which results in it’s total
destruction, & then decalcification of dentin, as a preliminarydestruction, & then decalcification of dentin, as a preliminary
stage.stage.
Followed by dissolution of softened residue.Followed by dissolution of softened residue.
The acids which affects this primary decalcification is derivedThe acids which affects this primary decalcification is derived
from fermentation of starches & sugars lodged in the retainingfrom fermentation of starches & sugars lodged in the retaining
centers of teeth.”centers of teeth.”

31. Miller concluded that no single species of microorganismMiller concluded that no single species of microorganism
caused caries, but rather that the process was mediated bycaused caries, but rather that the process was mediated by
oral microorganisms capable of producing acid and digestingoral microorganisms capable of producing acid and digesting
proteins.proteins.

32. 22. Proteolytic Theory:. Proteolytic Theory:  Gottlieb (1944)Gottlieb (1944)
• Organic portion has a major role in caries.Organic portion has a major role in caries.
• ““The organic component is most vulnerable & is attacked byThe organic component is most vulnerable & is attacked by
hydrolytic enzymes of microorganisms. This precedes the loss ofhydrolytic enzymes of microorganisms. This precedes the loss of
inorganic phase”.inorganic phase”.
• Initial action was due to proteolytic enzymes attacking the lamellae,Initial action was due to proteolytic enzymes attacking the lamellae,
rodsheath, tufts & walls of the dentinal tubules & he suggested thatrodsheath, tufts & walls of the dentinal tubules & he suggested that
coccus probably staphylococcus aureus, was involved because ofcoccus probably staphylococcus aureus, was involved because of
the yellow pigmentation that he considered pathognomic of dentalthe yellow pigmentation that he considered pathognomic of dental
caries.caries.

33. • Acid alone produce chalky enamel but not true caries.Acid alone produce chalky enamel but not true caries.
• He found that bacteria enters enamel through the enamelHe found that bacteria enters enamel through the enamel
lamellae.lamellae.
Pincus (1949) modified the theory.Pincus (1949) modified the theory.
• Gram negative bacilli are capable of producing enzyme ‘sulfatase’.Gram negative bacilli are capable of producing enzyme ‘sulfatase’.
This enzyme releases sulfuric acid from the mucoprotein thenThis enzyme releases sulfuric acid from the mucoprotein then
dissolves enamel.dissolves enamel.

34. 3. Proteolytic - chelation theory:3. Proteolytic - chelation theory: Shartz.
Chelating agent is a molecule capable of seizing & holding a metal ion
& forming a heterocyclic ring.
In Bacterial destruction of teeth the initial attack is essentially on
organic components of enamel. The breakdown product of this
organic matter have chelating properties & thereby dissolve the
minerals in the enamel.

35. • Both, inorganic & organic constituents of enamel are simultaneously
demolished.
• The bacterial attack on the enamel initiated by the keratinolytic
microorganisms, consists breakdown of the protein & other organic
components of enamel, chiefly keratin. This results in the formation
of substances which may form soluble chelates with the mineralized
component of the tooth & thereby decalcify the enamel.

36. • Enamel also contains other organic component besides keratin,
such as mucopolysaccharides, lipid & citrate, which may be
susceptible to bacterial attack & act as chelators.

37. HISTOPATHOLOGY OF DENTAL CARIES
SMOOTH SURFACE CARIES:SMOOTH SURFACE CARIES:
Early Enamel caries:Early Enamel caries:
•Area of decalcification beneath the dental plaque.Area of decalcification beneath the dental plaque.
•Loss of inter rod substance.Loss of inter rod substance.
•Roughening of the ends of the enamel rods.Roughening of the ends of the enamel rods.
•Appearance of transverse striations.Appearance of transverse striations.
•Cone shaped lesion with apex towards DEJ & the base toward theCone shaped lesion with apex towards DEJ & the base toward the
surface of tooth.surface of tooth.

38. Advanced Enamel Caries:Advanced Enamel Caries:
Before complete disintegration of the enamel, several zones can beBefore complete disintegration of the enamel, several zones can be
distinguished.distinguished.
I.I. ZONE 1 (Translucent Zone):ZONE 1 (Translucent Zone):
• Zone is slightly more porous than sound enamel.Zone is slightly more porous than sound enamel.
• Pore volume of 1% as compared to .1% in sound enamel.Pore volume of 1% as compared to .1% in sound enamel.
• Earliest change in enamel at the advancing front of the lesion.Earliest change in enamel at the advancing front of the lesion.

39. ZONE 2 [ Dark Zone]: { Positive zone}ZONE 2 [ Dark Zone]: { Positive zone}
• Adjacent & superficial to the zone 1.Adjacent & superficial to the zone 1.
• Appear dark brown in ground section in transmitted lightAppear dark brown in ground section in transmitted light
• Formed as a result of demineralization.Formed as a result of demineralization.
• An average reduction of 6 % of mineral per unit volume.An average reduction of 6 % of mineral per unit volume.

40. ZONE 3 : [ BODY OF THE LESION ]ZONE 3 : [ BODY OF THE LESION ]
• Largest zone.Largest zone.
• Forms the inner periphery of the whole lesion.Forms the inner periphery of the whole lesion.
• 24% mineral loss per unit volume24% mineral loss per unit volume
• Zone of +ve birefringenceZone of +ve birefringence
• Pore volume 5 to 25 %.Pore volume 5 to 25 %.

41. ZONE 4 : [ SURFACE ZONE ]ZONE 4 : [ SURFACE ZONE ]
•Relatively unaffected.Relatively unaffected.
•Pore volume of less than 5%Pore volume of less than 5%
•Zone of –ve birefringenceZone of –ve birefringence
•1% to 10% mineral loss1% to 10% mineral loss

42. PIT & FISSURE CARIES
• Similar to smooth surface caries.Similar to smooth surface caries.
• Caries follows the direction of the enamel rods.Caries follows the direction of the enamel rods.
• Cone shaped lesion with its apex at the outer surface & its baseCone shaped lesion with its apex at the outer surface & its base
towards the DEJ.towards the DEJ.
• More undermining enamel.More undermining enamel.

43. ULTRASTRUCTUREULTRASTRUCTURE
• Scattered destruction of individual apatite crystals both withinScattered destruction of individual apatite crystals both within
the enamel prisms and at their borders.the enamel prisms and at their borders.
• Crystals become irregular and also decrease in size.Crystals become irregular and also decrease in size.
• Bacterial colonies seen within the prism structure.Bacterial colonies seen within the prism structure.

44. CARIES OF THE DENTINCARIES OF THE DENTIN::
• Carious lesion spreads laterally along the DEJ and follows theCarious lesion spreads laterally along the DEJ and follows the
direction.direction.
• Cone shaped lesion with its base at the DEJ and the apex pointingCone shaped lesion with its base at the DEJ and the apex pointing
towards the pulp.towards the pulp.

45. ADVANCED DENTINAL CHANGESADVANCED DENTINAL CHANGES
• Thickening and swelling of the Sheath of Neumann at irregularThickening and swelling of the Sheath of Neumann at irregular
intervals.intervals.
• Increase in the diameter of the dentinal tubules.Increase in the diameter of the dentinal tubules.
• Liquefaction foci (described by Miller)- Focal coalescence &Liquefaction foci (described by Miller)- Focal coalescence &
breakdown of dentinal tubules.breakdown of dentinal tubules.
• Ovoid area of destruction parallel to the course of tubules andOvoid area of destruction parallel to the course of tubules and
filled with necrotic debris.filled with necrotic debris.

46. VARIOUS ZONES OF CARIOUS DENTINVARIOUS ZONES OF CARIOUS DENTIN
• Zone 1: Zone of fatty degeneration.Zone 1: Zone of fatty degeneration.
• Zone 2: ~ Zone of dentinal sclerosis.Zone 2: ~ Zone of dentinal sclerosis.
~ Deposition of calcium salts in the~ Deposition of calcium salts in the
dentinal tubules.dentinal tubules.
• Zone 3: ~ Narrow zone.Zone 3: ~ Narrow zone.
~Zone of decalcification.~Zone of decalcification.
• Zone 4: ~Zone of bacterial invasion.Zone 4: ~Zone of bacterial invasion.
~Liquefaction foci.~Liquefaction foci.
~Dentinal clefts.~Dentinal clefts.
• Zone 5: Decomposed dentin.Zone 5: Decomposed dentin.

47. CARIES ACTIVITY TEST
• To detect the presence of oral conditions associated with increasedTo detect the presence of oral conditions associated with increased
risk of caries.risk of caries.
• To determine the need for caries control measures.To determine the need for caries control measures.
• As an indicator of patient cooperation.As an indicator of patient cooperation.
• To aid in the determination of prognosis.To aid in the determination of prognosis.

48. SNYDER TEST:SNYDER TEST:
• Measures the ability of salivary microorganisms to produce organicMeasures the ability of salivary microorganisms to produce organic
acids from a carbohydrate medium.acids from a carbohydrate medium.
• Glucose Agar media containing indicator dye is used for this test.Glucose Agar media containing indicator dye is used for this test.
The indicator dye changes from green to yellow in the range of pHThe indicator dye changes from green to yellow in the range of pH
between 5.4 & 3.8.between 5.4 & 3.8.
• Paraffin stimulated saliva (0.2ml) is added into the medium and thenParaffin stimulated saliva (0.2ml) is added into the medium and then
it is incubated at 37 C for 72 hrs. Now the rate of color change of theit is incubated at 37 C for 72 hrs. Now the rate of color change of the
medium from green to yellow is indicative of the degree of cariesmedium from green to yellow is indicative of the degree of caries
activity.activity.

49. RESULTSRESULTS
•Colour change within 24 hrs – High caries susceptibility.Colour change within 24 hrs – High caries susceptibility.
•Within 48 hrs – Definite caries susceptibility.Within 48 hrs – Definite caries susceptibility.
•Within 72 hrs – Limited caries susceptibility.Within 72 hrs – Limited caries susceptibility.
•No color change – Caries immune.No color change – Caries immune.

50. SALIVARY REDUCTASE TESTSALIVARY REDUCTASE TEST
• Measures the activity of Reductase enzyme present in the salivaryMeasures the activity of Reductase enzyme present in the salivary
bacteria.bacteria.
• Paraffin-stimulated saliva is collected in a plastic container and anParaffin-stimulated saliva is collected in a plastic container and an
indicator dye “Diazoresorcinol” is added to it which colours salivaindicator dye “Diazoresorcinol” is added to it which colours saliva
blue.blue.
• Reductase enzymes liberated by the cariogenic bacteria causesReductase enzymes liberated by the cariogenic bacteria causes
colour change in the medium from blue to other colours whichcolour change in the medium from blue to other colours which
indicates “Conduciveness”.indicates “Conduciveness”.

51. RESULTSRESULTS
• No change in colour in 15 mins – Non conducive.No change in colour in 15 mins – Non conducive.
• Blue to Orchid in 15 mins – Slightly conducive.Blue to Orchid in 15 mins – Slightly conducive.
• Blue to Red in 15 mins – Moderately conducive.Blue to Red in 15 mins – Moderately conducive.
• Blue to red immediately – Highly conducive.Blue to red immediately – Highly conducive.
• Blue to colorless in 15 mins – Extremely conduciveBlue to colorless in 15 mins – Extremely conducive..

52. SALIVARY BUFFERING CAPACITYSALIVARY BUFFERING CAPACITY
• Chair side test to measure the buffering capacity of the saliva.Chair side test to measure the buffering capacity of the saliva.
• Kit contains a small vial of weak HCl & a colour indicator chart.Kit contains a small vial of weak HCl & a colour indicator chart.
• 1ml saliva is put into the acid solution, its pH will raise gradually1ml saliva is put into the acid solution, its pH will raise gradually
depending upon the buffering capacity of the saliva and this changedepending upon the buffering capacity of the saliva and this change
of pH is measured by the accompanying colour chart.of pH is measured by the accompanying colour chart.

53. RESULTS:RESULTS:
Normal buffering capacity – pH 5 to 7.Normal buffering capacity – pH 5 to 7.
Low buffering capacity – pH 4 or less.Low buffering capacity – pH 4 or less.

54. MICROBIOLOGICAL TESTMICROBIOLOGICAL TEST
• LACTOBACILLUS COUNT.LACTOBACILLUS COUNT.
• STREPTOCOCCUS MUTANS.STREPTOCOCCUS MUTANS.
Two samples of paraffin-stimulated saliva (1ml each) are collectedTwo samples of paraffin-stimulated saliva (1ml each) are collected
from the patients, these are diluted 10 times. Each is cultivated infrom the patients, these are diluted 10 times. Each is cultivated in
two different special mediatwo different special media
• Rogosa’s agar medium for Lactobacillus acidophilus.Rogosa’s agar medium for Lactobacillus acidophilus.
• Mitis Salivarius agar medium for Streptococcus mutans.Mitis Salivarius agar medium for Streptococcus mutans.

55. After incubation, the no. of colonies that developed inAfter incubation, the no. of colonies that developed in
two separate media are counted and then multiplied bytwo separate media are counted and then multiplied by
10 to estimate the no. of bacteria in 1ml of saliva.10 to estimate the no. of bacteria in 1ml of saliva.
10,00,000 S.mutans10,00,000 S.mutans
1,00,000 L.acidophillus High susceptibility.1,00,000 L.acidophillus High susceptibility.
1,00,000 S.mutans1,00,000 S.mutans
1,000 L.acidophillus Less susceptibility.1,000 L.acidophillus Less susceptibility.

56. CARIES VACCINE
• Dental caries fulfills the criteria of an infectious disease and
possibility of preventing it by vaccination has been persuaded.
• The rationale is that immunization with streptococcus mutans
should induce an immune response which might prevent the dental
caries in the following ways:

57. • It will prevent the ability of the microorganisms to colonize on toIt will prevent the ability of the microorganisms to colonize on to
the tooth surface.the tooth surface.
• It can alter the pattern of polysaccharide metabolism by theIt can alter the pattern of polysaccharide metabolism by the
bacteria & there by reduce their adhering capacity on to the toothbacteria & there by reduce their adhering capacity on to the tooth
surface.surface.
• It can reduce the ability of microorganisms to produce acids.It can reduce the ability of microorganisms to produce acids.
• The caries vaccines, if developed, should be given at the age of 6The caries vaccines, if developed, should be given at the age of 6
months, before the eruption of the deciduous teeth.months, before the eruption of the deciduous teeth.

58. CARIES MANAGEMENT
• To remove all infected tissue and its replacement with someTo remove all infected tissue and its replacement with some
resistant material to obliterate the cavity and restore the naturalresistant material to obliterate the cavity and restore the natural
form of the tooth.form of the tooth.
• Removal of all decayed enamel and dentin.Removal of all decayed enamel and dentin.
• Protection of the pulp.Protection of the pulp.
• Placing a water tight restoration.Placing a water tight restoration.
• Restoration of the original form of the tooth.Restoration of the original form of the tooth.

59. MICROBIOLOGY OF DENTAL CARIES.MICROBIOLOGY OF DENTAL CARIES.
EVIDENCE OF BACTERIAL ROLE IN DENTAL CARIES.
• Germ free animals do not develop dental caries.Germ free animals do not develop dental caries.
• Antibiotics fed to animals are effective in reducing incidence &Antibiotics fed to animals are effective in reducing incidence &
severity of dental caries.severity of dental caries.
• Totally unerupted teeth do not develop caries.Totally unerupted teeth do not develop caries.
• Oral bacteria can demineralize enamel & dentin in vitro.Oral bacteria can demineralize enamel & dentin in vitro.
• Microorganisms have been histologically demonstrated in invadingMicroorganisms have been histologically demonstrated in invading
carious dentin and enamel.carious dentin and enamel.
• Organisms responsible for initiation of dental caries is specificOrganisms responsible for initiation of dental caries is specific
strains of Streptococcus mutans.strains of Streptococcus mutans.

60. ESSENTIAL PROPERTIES OF CARIOGENIC BACTERIA
• Acidogenic.Acidogenic.
• Able to produce a pH low enough to demineralize tooth structure.Able to produce a pH low enough to demineralize tooth structure.
• Able to survive & continue to produce acid low pH.Able to survive & continue to produce acid low pH.
• Possess attachment mechanism for firm adhesion to smooth toothPossess attachment mechanism for firm adhesion to smooth tooth
surface.surface.

61. STREPTOCOCCUS MUTANSSTREPTOCOCCUS MUTANS
• It produces lactic acid from sucrose.It produces lactic acid from sucrose.
• It can live at pH as low as 4.2.It can live at pH as low as 4.2.
• It produces large amounts of extracellular, sticky & insoluble glucanIt produces large amounts of extracellular, sticky & insoluble glucan
plaque matrix.plaque matrix.
• Adheres to pellicle.Adheres to pellicle.

62. THANK YOU