Dental caries is a common chronic dental disease caused by demineralization of tooth structure by acid produced by bacteria in dental plaque. Key factors for dental caries are the host, cariogenic bacteria such as Streptococcus mutans, and fermentable carbohydrates in the diet. Prevention strategies aim to reduce the cariogenic potential of the oral environment through measures like fluoride use, dietary modification, and plaque control. Treatment depends on the severity and activity of the carious lesion.

1. DENTAL CARIES

2. Dental caries and periodontal diseases
are probably the most common
chronic dental diseases in the world.

3. DEFINITION (DENTAL CARIES)
Dental caries is a multifactorial
microbial infectious disease
characterized by demineralization of
the inorganic and destruction of the
organic substance of the tooth.

4. ETIOLOGY OF CARIES-
No universally accepted opinion of etiology
of dental caries.
3 theories have evolved:
(1) Acidogenic theory (Miller’s chemico-
parasitic theory)
(2) Proteolytic theory
(3) Proteolysis-chelation theory

5. (1) Acidogenic theory (Miller’s
chemico-parasitic theory) :
,
W.D. Miller stated that, “Dental decay is a
chemico-parasitic process consisting of two
stages, the decalcification of enamel, which
results in its total destruction and
decalcification of dentin, as a preliminary stage
followed by dissolution of the softened residue.
The acid which affects the primary
decalcification is derived from the fermentation
of starches and sugar lodged in the retaining
centres of the teeth.”

6. ROLE OF CARBOHYDRATES :
The cariogenicity of dietery carbohydrate
varies with –
(1) Frequency of ingestion : > frequency -
>caries
(2) Physical form :> Sticky, solid
carbohydrates - > caries, >Liquid
carbohyrates - < caries.
(3) Other food constituents : Meals > in
fats, proteins or salts, < oral retentiveness of
carbohydrates.

7. ROLE OF MICRO-ORGANISMS AND
DENTAL PLAQUE :
Bacteriological studies have helped to
clarify the role of micro-organisms in the
etiology of dental caries. Most commonly
Lactobacillus, Streptococcus mutans, and
Actinomyces species are associated with
dental caries. Certain micro-organisms –
Initiation of caries Certain micro-organisms
– Influence progression of caries. Micro-
organisms are located in the complex biofilm
overlying the tooth surface termed as dental
plaque.

8. ROLE OF ACIDS :
The enzymatic breakdown of carbohydrates
(sugar), results in the formation of
acids, chiefly lactic acid.
Localization of acids in dental plaque serves
a major role in dental caries.
Carbohydrates+Enzymes----Acids(lactic acid)

9. (2) The Proteolytic theory :
Another theory was proposed which claims
that the organic portion of the tooth is
attacked first with lytic enzymes.
This leaves the inorganic portion without a
matrix support causing it to be washed away
creating cavities.

10. ( 3) The Proteolysis-Chelation
theory (Schatz’s theory):
This theory states that the bacterial attack
on the enamel, initiated by keratinolytic
microorganisms, results in breakdown of
protein and other organic components of
enamel, chiefly keratin. This results in the
formation of substances which may form
soluble chelates with mineralized component
of tooth and thereby decalcify enamel at a
neutral or even alkaline pH. This theory
states that initial attack of dental caries is
on organic and inorganic portion of enamel
simultaneously.

11. Each of these theories fails to explain all
ramifications of the disease, but all three
agree on the following :
For dental caries there must be :
(1) Host
(2) Flora
(3) Substrate

12. KEYE’S RING
SALIVA

13. (1) Host –
It encompasses :
Tooth
(composition, location,morphological
characteristics),
Age,
Muscular activity,
Habits,
Group susceptibility and
Environment.

14. (2) Flora
Consists of micro-organisms which are
brought in the contact of the tooth via
plaque.
Micro-organisms mainly associated are –
(1)Streptococci (S.
mutans, S.salivarius, S.mitis, S.sanguis, S.so
brinus)
(2) Lactobacilli (L. acidophillus)- secondary
invaders
(3) Actinomyces, Veillonella

15. (3) Substrate (Diet) :
Third factor in initiation and progression of
caries.
Physical and chemical characteristics of
diet determine the relative caries activity.
(a) Physical characteristics – Solid, fibrous
food, then <caries.
(b)Chemical characteristics –
Monosaccharides and dissaccharides more
detrimental then polysaccharides.
Sucrose – most detrimental followed by
fructose, lactose, galactose and glucose.
>Fluoride - <caries.
>Calcium and phosphate - <caries.
> Vitamins(A, Bcomplex, C, D) <caries.

16. SALIVA :
Primary means to exert control over the oral
flora.
Normal oral flora – beneficial to the host.
Functions of saliva which maintain normal
oral flora and tooth surface integrity –
*Bacterial clearance
* Direct antibacterial activity
*Buffering capacity
* Remineralization

17. DR G.V.BLACK’S CLASSIFICATION
FOR DENTAL CARIES

23. CLINICAL CLASSIFICATION OF
DENTAL CARIES :
(A) According to the location on
individual tooth :
(1) Pit and fissure caries
(2) Smooth surface caries
(3) Root caries/Senile caries

24. PITS AND FISSURE CARIES,
SMOOTH SURFACE CARIES,
ROOT SURFACE CARIES

25. PIT AND FISSURE AND SMOOTH SURFACE CARIES

26. ROOT CARIES (SENILE CARIES)

27. (B) According to the rapidity of the
process :
(1) Acute/Rampant caries
(2) Chronic caries

28. ACUTE CARIES (RAMPANT) CHRONIC CARIES

29. C) According to whether the lesion is a
new one attacking a previously intact
surface or whether it is occuring
around the margins of a restoration :
(1) Primary caries
(2) Secondary/Recurrent caries

30. PRIMARY AND SECONDARY CARIES

31. SECONDARY CARIES

32. (D) According to the pathway of dental
caries :
(1) Forward caries
(2) Backward caries

33. (E) According to the number of the
tooth surfaces involved :
(1) Simple caries
(2) Compound caries
(3) Complex caries

35. (F) Residual caries
(G) Occult caries
(H) Arrested caries

37. PATHOPHYSIOLOGY OF CARIES :
Micro organisms mainly S. mutans and
lactobacilli in plaque
!
Sucrose or other substrate
!
Acid production, mainly lactic acid
!
Acid from plaque overcomes buffering
capacity of salivary bicarbonate
!
pH is lowered
!

38. When pH<5.5-critical pH and remains at
tooth surface for 20-50 minutes
!
tooth mineral acts as buffer and loses Ca
and phosphate ions into plaque
!
this buffering capacity maintains local pH 5.0
!
At pH 5.0, surface remains
intact, subsurface mineral is lost Initial
carious
lesion (incipient caries)
!

39. Incipient lesion may be reversed by
remineralization
!
When subsurface demineralization becomes
extensive
!
tooth surface collapses
!
Cavities (Caries)

40. DIAGNOSIS OF CARIES :
(1) Patient history
(2) Visual examination
(3) Explorers
(4) Radiographs
(5) Dental floss/tape
(6) Separation of teeth
(7) Ammoniated silver nitrate
(8) Caries detecting solutions/dyes
(9) Digital fiber-optic transillumination

41. (10) White light endoscopy
(11) Endoscopically filtered fluorescence
(12) Electroconductivity measurements
(13) Quantitative laser fluorescence
(14) Direct digital radiology –digital
radiographs, xeroradiography
(15) Caries detection using laser
fluorescence (diagnodent)
(16) Optical coherence tomography
(17) CO2 laser
(18) Magnetic Resonance Microimaging
(MRM)

42. PREVENTION OF DENTAL CARIES
(METHODS) :
(1) Increasing the resistance of tooth
structure to demineralization
(2) Modification of diet
(3) Plaque control

43. (1) Increasing resistance of tooth
structure to demineralization :
(a) Fluoride exposure –
Systemic fluorides:
Public water fluoridation (1
ppm), fluoride tablets(1mg NaF or
MgF), fluoridated table salt (90mg F/kg
or 200 mg NaF/kg
and fluoridated milk

44. Topical fluorides :
-Fluoride agents applied professsionally –
sodium fluoride (2%), Stannous fluoride
(8%), Acidulated phosphate fluoride gel
(1.23%)
- fluoride mouthrises
- fluoride dentrifices
- fluoride containing prophylaxis pastes
- fluoride varnishes

45. (b) Use of pits and fissure sealants
c) Remineralization

46. (2) Prevention of caries by
modification of diet :
(a) Limitation of sucrose consumption to
mealtimes
(b) Replacement of sucrose by other
sweeteners in foods (Sweeteners like
sorbitol, lycasin, xylitol)
c) Addition of caries-inhibiting agents to
foods (Fluoride, calcium, phosphates, vitamin
K, fatty acids etc.)

47. (3) Prevention of caries by plaque
control :
(1) Mechanical method
(toothbrushing, flossing)
(2) Chemical methods
(antibiotics, chlorhexidine and other
antiseptics(quaternary ammonium
compounds, vitamin c), fluorides)
(3) Immunological method
(oral, systemic, active
gingivosalivary, passive dental immunization)

48. MECHANICAL PLAQUE CONTROL

49. CHEMICAL PLAQUE CONTROL (CHLORHEXIDINE MOUTHWASH)

50. TREATMENT :
(1) NORMAL LESIONS :
No treatment required
1 year clinical examination
(2) HYPOCALCIFIED ENAMEL
(DEVELOPMENTAL WHITE SPOTS):
Treatment is elective, for esthetics, restore
defects
1 year clinical examination

51. (3) INCIPIENT ENAMEL LESIONS :
Bitewing radiographs indicated
(demineralized white spots)
Seal defective pits and fissures as indicated
3 months evaluation – oral flora, MS
count, progression of white spots, presence
of cavitations

52. (4) POSSIBLE CAVITATED LESIONS (ACTIVE
CARIES )
Bitewing radiographs indicated
Restorative treatment indicated
3 months evaluation as incipient lesions and
pulpal response
(5) ARRESTED CARIES
No active new cavitations
Treatment is elective, for esthetics, restore
defects 1-year clinical examination

53. THANK YOU