Dental caries is caused by bacteria in dental plaque that produce acids which demineralize tooth structure. The most common bacteria involved are Streptococcus mutans and Lactobacilli. There are several theories for how dental caries progresses, but it is now accepted that acids produced by bacteria lower the pH and cause the enamel and dentin to demineralize. Dental caries can affect the pits and fissures of teeth, smooth surfaces, or root surfaces. It is classified based on location, rate of progression, extent of damage, and other factors. Histologically, dental caries progresses through zones in enamel and dentin as the mineral content is reduced by acid attacks from bacteria.

1. DENTAL CARIES
Preparedby- ShreejaNair

2.  Definition: Dental caries is an infectious microbiologic disease of the
teeth that results in localized dissolution and destruction of the
calcifiedtissues.
 Carious lesions occur only under a mass of bacteria capable of
producing a sufficiently acidicenvironment to demineralize tooth
structure.

3.  Organisms that cause caries are cariogenic.
 Thedegreeto which a tooth is likely to becomecarious is described as its
cariogenicity potential.

4. Organisms responsible
1. Streptococcus mutans (MS)
2. Lactobacilli
 MSare associated withtheonset of caries.
 Lactobacilliare associated withactive progression of cavitated
lesions.

5. Typeof caries Microorganism
Pit and Fissure S. Mutans
S. Sanguis
Lactobacillus species
Actinomycesspecies
Smooth Surface S. Mutans
S. Salivarius
Root surfaces A. Viscosus
A. Naeslundii
S. Mutans
S. Sanguis
Deep dentinal caries Lactobacillus species
A. Naeslundii
Other filamentous rods

6. THEORIES OFDENTALCARIES

7. 1. ChemicoparasiticTheory
(Miller W.D 1890 )
 This states that oral bacteria actsonsugars to release acidsthat
demineralize the inorganicportion of enamel, resulting inthe
development of dental caries.

8. 2. Proteolytictheory
(Bodekar C.F.1948)
 This theory states theorganiccomponent of the enamel is first
brokendownby proteolyticenzymes, openingup pathwaysfor
bacteria to attackthe enamel by other processes such as by acidor
chelation.

9. 3. Chelationtheory
(ShatzAet al1957)
 This states that the enamel is demineralized by chelatingagents at
neutral pH.Protein breakdownproducts and lacticacidare some
chelatingagents present innature.
 This is the most accepted theory.
 The factors responsible for this delicate balanceare:
 pHofplaque.
 Calciumandphosphateionconcentrationattheinterfacebetween
enamelandplaque.
 Fluorideionconcentration.

10. Etiologic agentsof caries

11. Pathogenic bacterialplaque
 Bacterialplaque:The soft, translucent, andtenaciously adherent
material accumulatingonthe surface of teeth is commonly called
bacterial plaque.
 The accumulationof plaqueonteeth is a highly organizedand
ordered sequence of events.
 Caries causes damageby demineralized andthe dissolution of tooth
structure, resulting from:
1. AhighlylocalizeddecreaseinthepHattheplaque-toothinterface.
2. Toothdemineralization.

12. Dentalplaqueon toothsurface.

13. Factors affecting
I. PRIMARY FACTORS
1. Tooth
2. Dentalplaque
3. Diet
4. Time
II. MODIFYING FACTORS
1. Saliva
2. Systemichealth
3. Sex
4. Heredity
5. Race
6. Geographic environment
7. Occupation

15. CLINICALCHARACTERISTICSOF LESION

16.  The characteristics vary with the natureof surface onwhichthe
lesions develops.
 There are 3 different clinicalsites:
1. Pitsandfissures.
2. Smoothenamelsurfaces.
3. Rootsurface.

17. Dental caries
Cementum
caries Enamel caries
Smooth
surface caries
Pit and fissure
caries
Dentine caries

18. 1. Pits and fissures.
 Bacteria rapidly colonizethepits andfissures andform a “bacterial
plug.”
 They:
1. endblindly.
2. opennear thedentin.
3. penetrateentirelythroughenamel.
 Incross section : invertedV with narrow entrance and
progressively widerarea of involvementcloserto theDEJ.

19. LS showing caries on occlusal surface.

20. 2. Smooth enamelsurfaces.
 The smoothenamel surfaces of teeth are less favorable site for
plaque attachment.
 Lesions have abroad area of originand aconicalor pointed
extension towardDEJ.
 Cross section : V shaped witha widearea of origin and the apex
of the vdirectedtowards DEJ.

21. LS showing initiation and progression of caries on interproximal surfaces.

22. 3. Rootsurfaces.
 Root surfaces are rougher thanenamel and readily allowsplaque
formation.
 Cementum coveringthe root surface is extremely thin and provides
little resistance to caries attack.
 Cross section: U shapedwith less welldefined margins .

23. Histopathology ofcaries

24. Enamelcaries
 Histology ofenamel:
 Accordingtochelationtheorythemovementofionsthroughcarious
enamelcanresultinaciddissolutionoftheunderlyingdentinbefore
actualcavitationoftheenamelsurface.
 Cariespreferentiallyattacksthecoresoftherodsandthemore
permeablestriaeofRetzius,whichpromoteslateral spreadingand
underminingoftheadjacentenamel.

25.  Clinical& histologicalcharacteristicsof enamelcaries:
 Anearlyenamellesionseenunderpolarizedlightreveals4distinctzones
ofmineralization.
1. Translucentzone
2. Darkzone
3. Bodyof lesion
4. Surface zone

26.  This is the deepest zone
whichrepresents the
advancingfront of the
enamel caries.
 This zone is translucent due
to demineralizationwhich
creates a structureless
appearanceof the enamel.
 This lies deeper to the bodyof
the lesion andit represents
some remineralization.
1. Translucent zone Darkzone

27.  This is the largest portion of
enamel caries.
 It is poorlymineralized.
 The striae of Retzius are well
marked.
 The caries spreads alongthe
striae of Retzius and
interprismatic areas and then
attacksthe prism cores.
 Bacteria are present inthis
zone.
 This outermost zone is
relatively unaffected by caries
attack.
 It is well mineralized by
replacement ionsfrom
plaque and saliva.
Bodyoflesion Surfacezone

31. Dentinalcaries
 Histology ofdentin:
 Caries of the dentinbegins with the spread of
process along the DEJ.
 There is a rapidinvolvement of great numbers
of dentinaltubules whichacts as a tract leading
to dental pulpalong with the microorganisms.

32.  Clinical& histologicalcharacteristicsof dentin caries:
 Progressionofcariesindentinisdifferentfromprogressioninthe
overlyingenamelbecauseofthestructuraldifferenceofdentin.
 Episodesofpainmay befeltwhichisduetostimulationofunderlying
pulp.
 Cariesadvancementindentinproceedsthrough3changes.
1. Weakorganicacidsdemineralizethe dentin.
2. Collagendegeneratesand dissolves.
3. Lossof structuralintegrityfollowedby invasionof bacteria.

33.  5differentzonesare observed:
1. Normaldentin
2. Subtransparentdentin
3. Transparentdentin
4. Turbiddentin
5. Infecteddentin

34.  The deepest zone of carious
dentinis normal withnormal
collagen, odontoblastic
processes andintertubular
dentin.
 The intertubular dentin is
demineralized , odontoblastic
processes are damagedand
fine crystals are seen inthe
lumenof dentinal tubules.
 No bacteria is foundin this
zone.
Normaldentin Subtransparentdentin

35.  Superficial to the
subtransparent layer.
 Softer thannormal dentin
and exhibits mineral loss in
theintertubular dentin.
 No bacteria is seen and the
collagencross-linking is
intact.
 Capableof remineralization.
 Next superficiallayer.
 Dentinal tubules arewidenedand
distorted due tobacterial
penetration.
 There is considerable
demineralizationand collagenis
irreversiblydenatured.
 This zone is incapable of
remineralizationand must be
removed.
Transparent dentin Turbid dentin

36.  Outermost zone.
 It has decomposed dentin
with destruction of dentinal
tubules andcollagen.
 A highconcentration of
bacteria are seen.
 This zone has to be removed
to prevent thespread of the
infection.
Infecteddentin

38. Histopathology of Dental Caries
Enamel Caries Dentin Caries

39. Radiograph showing cariesin dentin

40. Classificationof caries

41. BASED ON LOCATION
1. Pit andfissure caries
2. Smooth surface caries
3. Root surface caries

42. BASEDON RATE OFPROGRESSION
1. Acute / rampant caries
 Rapidlyinvadingcariesinvolvingseveral teeth.
 Appearssoftor lightcolored.
 Ifunattendedcausesearlypulpinvolvement.
2. Chroniccaries
 Slowlyprogressing,longstandingcaries.
 Hard consistencyanddark colored.
3. Arrested caries
 Sometimesochroniccariouslesioncanbecomearresteddueto
changeinlocalenvironment.

43. BASEDON EXTENT OF CARIES
1. Incipient caries
 Firstevidenceofcariesactivityinenamel.
 DemineralizedenamelnotextendedtoDEJ.
 Enamelsurfaceishard andstillintact.
 Can beremineralized.
2. Cavitatedcaries
 Carieshasspreadbeyondenamelintodentin.
 Enamelisbrokendownandremineralizationisnotpossible.

44. BASEDON NEW OR RECURRENT
1. Initial/primary caries
 Firstattackofcariesontooth.
2. Recurrent /secondary caries
 Cariesseenaroundthemarginsofrestoration.
 Occursduetomicroleakageandother favorableconditions.

45. BASEDON PATHWAYOF CARIESSPREAD
1. Forward caries
 Whenever the caries cone in enamel is larger or the same size as
that in dentin its referred to asforward caries.
2. Backwardcaries
 Whenever the spread of caries along the DEJ exceeds the caries
cone in enamel, the caries extends into enamel from the junction.
 Spread of caries isin backward direction.

46. FORWARDCARIES BACKWARDCARIES

47. BASED ON NO.OF TOOTH SURFACES INVOLVED
1. Simple caries
 Involving1surface.
2. Compoundcaries
 Involving2surfaces.
3. Complexcaries
 Involving3 ormoresurfaces.

48. BASEDONWHETHERCARIESIS COMPLETELY
REMOVEDOR NOT
 Residual caries
 Cariesthatremainsinthepreparedcavityevenafter therestorationis
completed.
 Thismay beleftbehindeitherbyaccident,neglector intension.

49. BASEDON AGE OFPERSON
1. Nursing bottle caries
 Duringearlyinfancy,bottlefedbabiesdeveloprapidlyspreading
caries.
 Usuallymaxillaryincisors.
2. Adolescent caries
 Acutecariesseeninadultsduetodietaryhabits.
3. Senile caries
 Cariesoccurringinelderlyinvolvingrootsurfaces.
 Duetogingivalrecessionandpoororalhygiene.

50. BASEDON TOOTH SURFACESINVOLVED
1. O occlusal surface.
2. M mesial surface.
3. D distal surface.
4. F facialsurface.
5. B buccal surface.
6. L lingualsurface.

51. WHO SYSTEM
1. D1clinicallydetectable enamel lesions with intact
surfaces.
2. D2clinicallydetectable cavities limited to enamel.
3. D3clinicallydetectable cavities in dentin.
4. D4lesions extending into the pulp.

52. GRAHAMMOUNT’S CLASSIFICATION
Cavitysite Size 1 Size 2 Size 3 Size 4
Minimal Moderate Enlarged Extensive
Site 1
Pit and fissure
1.1 1.2 1.3 1.4
Site 2
Approximal surface/ contact
surface
2.1 2.2 2.3 2.4
Site 3
Cervical region
3.1 3.2 3.3 3.4

53. BASED ONRESTORATION
(G.V.BLACK CLASSIFICATION)
1. Class I caries
2. ClassII caries
3. ClassIIIcaries
4. Class IVcaries
5. ClassV caries
6. ClassVI caries

55. CLASSI CAVITYPERPARATION
 Restorations on occlusal surfaces of premolars and molars
 Occlusal 2/3rd of facial and lingual surfaces of molars
 Lingual surfaces of maxillaryincisors.

56. CLASSII CAVITYPERPARATION
 Restorations on proximal surfaces of posterior teeth.

57. CLASSIII CAVITYPERPARATION
 Restorations on proximal surfaces of anterior teeth that do not involve incisal angle.

58. CLASSIV CAVITYPERPARATION
 Restorations on proximal surfaces of anterior teeth that involve incisal edge.

59. CLASSV CAVITYPERPARATION
 Restorations on gingival 1/3rd of facial or lingualsurfaces of all teeth.

60. CLASSVI CAVITYPERPARATION
 Restorations on incisal edge of anterior teeth or occlusal cusp heights of posterior teeth.