Dental caries is caused by bacteria in the mouth that metabolize carbohydrates, producing acids that demineralize tooth enamel and dentin. It progresses through stages from early subsurface lesions to cavity formation and bacterial invasion. Risk factors include diet, oral hygiene, tooth composition, and saliva. Treatment involves preventing demineralization through fluoride, controlling plaque and bacteria, and restoring teeth through fillings or other methods.

1. Dental Caries

2. Contents
DEFINITION OF DENTAL CARIES
ETIOLOGY
CLINICAL FEATURES
HISTOPATHOLOGY
DIAGNOSIS
TREATMENT

3. Definition
Dental caries is an irreversible microbial
disease of the calcified tissues of the
teeth,characterized by demineralization of the
inorganic portion and the destruction of the
organic substance of the tooth.

4. Etiology

5. Etiology
EARLY THEORIES
The legend of worms
Endogenous theory
Chemical theory
Parasitic theory
MODERN THEORIES
Miller’s theory
Proteolytic theory
Proteolysis chelation theory

6. MILLER’S CHEMICO PARASITIC THEORY
Acidogenic theory
Theory: Caries is caused by micro-organisms of the mouth.
Two Stages:
Decalcification of enamel and dentin
Dissolution of softened tissue

7. ROLE OF CARBOHYDRATES
Bacteria+Sugar+Teeth Organic acids Caries

8. ROLE OF MICROORGANISMS
Pits and fissure
s.mutans
s.sanguis
Smooth surface
s.mutans
s.salivarius
Root surface
A.viscous
A.naeslundii
Deep dentinal
Lactobacilli species

9. ROLE OF ACIDS
Acidsdemineralises tooth surface
↓
S.mutans,lactobacillus(ferment Sugars)
↓
Lactic acid,butyric acid,propionic acid
↓
Decrease ph in saliva
↓
Critical ph <5.5
↓
Removal of calcium

10. STEPHAN CURVE

11. ROLE OF DENTAL PLAQUE
Plaque is the soft,
unmineralised bacterial
deposit which forms on teeth
and prostheses.
Composition salivary
components such as mucin,
desquamated epithelial cells
and microorganism
Plaque shields the bacteria
from saliva acid formation
occurs
Plaque containing acidogenic
s.mutansexposed to dietary
sucroseproduce
acidsdemineralise the
enamel

12. PROTEOLYTIC THEORY
Theory: Organic or protein elements of tooth as initial pathway of invasion
by microorganisms
ENAMEL LAMELLAE  pathway for infection

13. GOTTLIEB, DIAMOND& APPLEBAUM
Initial stage
Yellow pigmentation
Due to pigment production by proteolytic organisms

14. SUB THEORIES
“SULPHATASE THEORY” by PINCUS
“Microorganisms
↓
produce sulphatase
↓
degrade sulphated mucopolysaccharides
↓
Sulphuric acid production
↓
Causes destruction of inorganic portion of teeth
↓
Destruction of organic portion
↓
By product
↓
Destruct inorganic portion

15. SUB THEORIES
FRIESBIE proposed that
“ proteolytic process involves depolymerisation
and liquefaction of organic matrix of enamel”
MANLEY and HARDWICK proposed that there are two types of caries
lesion
ONE TYPE  “Enamel lamellae attack enamel involve dentin before there
is clinical evidence of caries”
OTHER TYPE “No enamel lamellae, prior to invasion of microorganisms,
alteration of enamel through decalcification of enamel by acids formed by
bacteria overlying enamel”

16. SUB THEORIES
DRAWBACKS:
No evidence that initial attack on enamel is proteolytic
Experimental studies show caries even in absence of
proteolytic organisms

17. PROTEOLYTIC CHELATION THEORY
Postulated by: SCHATZ
Bacterial attack
On the organic components of enamel
Break down products form soluble
CHELATES with mineralized
component of teeth
Decalcify enamel at neutral or
alkaline pH

18. CURRENT CONCEPTS OF CARIES ETIOLOGY

19. FACTORS
HOST
FACTORS
COMPONENTS
TOOTH
 COMPOSTION
MORPHOLOGIC CHARACTERISTICS
POSITION
SALIVA
COMPOSITION
QUANTITY
VISCOSITY
ANTIBACTERIAL FACTORS
DIET  CARBOHYDRATES
SYSTEMIC
CONDITIONS

20. HOST
TOOTH
 COMPOSITION OF TOOTH
Structure & composition of a tooth determines initiation and rate of
progression of caries.

21. HOST
 MORPHOLOGIC
CHARACTERISTICS
The most susceptible teeth
are mandibular 1st molars
followed by maxillary 1st ,
mandibular and maxillary 2nd
molars
 POSITION
Malaligned, rotated or otherwise
abnormally situated teeth can be
difficult to cleanse and are
likely to trap food debris and
bacteria

22. SALIVA
• Functions
• Composition –Calcium
and phosphate
• pH- 5.5
• Quantity – Salivary gland
aplasia and Xerostomia
• Viscosity – Associated
with high caries incidence
• Antibacterial properties –
Lysozyme,lactoferrin,IgA,etc

23. SUBSTRATE
ROLE OF CARBOHYDRATES
Fermentable dietary carbohydrates:
•Glucose
•Fructose
•Sucrose (most potent) etc.
Fermentable dietary carbohydrate
due to their low molecular weight gets
rapidly diffused into the plaque &
hence are easily available for fermentation
pH of plaque falls to 4.5-5 within 1-3 mins. & it takes another 10-30 mins. To
return to neutrality
When sucrose is replaced by sorbitol or xylitol (non fermentable) caries
formation is greatly reduced

24. DENTAL PLAQUE
Plaque defined as a soft, unmineralized, bacterial deposit or
biofilm which forms on teeth and dental prostheses
• Considered as a contributing factor for initiation of caries.
COMPOSITION:
Water – 80%
Solids – 20%
Dry weight of plaque composed of
Bacterial & Salivary proteins – 50%
Carbohydrates & Lipids - 25%
Inorganic ions, mainly Ca++ & Po4--- - 10%
CLASSIFICATION:
Supra gingival and Sub gingival

25. CLINICAL FEATURES
Classified based on
A. Norphology on anatomical site
1.Pit & fisseure caries
• Occlusion surface of molars and premolars
• Palatale surface of maxillary incisors
2.Smooth surface caries
Develops on Proxilmal surface of the teeth Or on the gingival
third of the buccal and lingual surfaces

26. CLINICAL FEATURES
B. RATE OF CARIOUS PROGRESSION
1. Acute dental caries
Caries which runs a rapid clinics course and early pulp involvement
Initial entrance of lesion is small while rapid spread of process produce large
Internal excavation Pain is more apt to be a feature of acute caries
2. Chronic dental caries
Which progresses slowly and tends to involve pulp much later
Initial entrance is invariably larger
Pain is not a common feature Because secondary denti n protects pulp

27. C.Based on Chronology
1. Infancy( rampant caries)
characterized by sudden rapid uncontrollable destruction of teeth affecting surfaces of
a teeth That are relatively caries free.
often in , primary dentition of young children / permanent dentition of teenagers.
Dietary factors affecting oral substrate and oral flora and factors affecting saliva are
significant.
2. Nursing bottle caries ( baby bottle syndrome)
unfortunate form of rampant caries
affecting deciduous teeth
Bottle Feeding
Breast Feeding
Sugar or honey sweetened Pacifiers
Adolescent Caries
Acute caries attacking 11-15 yrs of age is usually Characterized as Adolescent Caries
seen in tooth surface that are relatively immune to caries
CLINICAL FEATURES

28. D. BASED ON NATURE OF ATTACK
1. Primary Caries
New lesion occurs on previously intact tooth surface
2. Secondary Caries / Recurrent Caries
around the margins of restoration
CLINICAL FEATURES

29. CLINICAL FEATURES
OTHER THAN THIS , CARIES SEEN ARE
1. Radiation caries
Development of rampant caries in patients undergoing radiation therapy in head and
back is referred as radiation caries
Differs from other by involving cusp tips incisal edges and cervical areas
2.Arrested Caries
Caries which become static and shows no tendency to further progression
Deciduous and permanent dentitions are both affected
3.Cervical Caries
special type of tooth decay characterized by destruction of bone at cervical margin
of tooth
disease progresses very rapidly and affecting nerve canals
4. Linear enamel caries
occurs in neonatal line of maxillary anterior teeth
line represent metabolic defect Such as hypocalcemia or trauma at birth leading to
gross destruction of labial surface

30. CLINICAL FEATURES
DIAGNOSIS
Radiographic Diagnosis
1.Radiograph may reveal 50% more cavities than found by visual examination.
2.Interproximal various lesion is easily recognised and appears in early lesion as
small , triangular radiolucent area of enamel
INFRARED LASER FLUORESCENCE
Detection and qualification of dental caries of occlusal and smooth surface
DIGITAL IMAGING FIBEROPTIC TRANSILLUMINATION
• advanced teeth used in clinical use
• used to detect caries in proxial surface of posterior teeth
QUANTITATIVE LIGHT FLUORESCENCE
Tool for quantitative assessment of dental caries lesion , dental plaque , bacterial
activity, staining , calculus, etc.

31. HISTOPATHOLOGY OF CARIES
 Caries process in enamel progresses through following stages
A. Early Submicroscopic lesion
B. Phase of nonbacterial enamel crystal destruction
C. Cavity Formation
D. Bacterial invasion of enamel
* C & D Occur almost simultaneously
HISTOPATHOLOGY OF CARIES- ENAMEL

32. HISTOPATHOLOGY OF CARIES
•Earliest visible changes are seen as a chalky
white spot on the tooth just adjacent to contact
point.
•Electron microscopic study reveals the early
changes as loss of inter rod enamel,
accentuation of striae of retzius and penikymata
EARLY LESION- SMOOTH SURFACE

33. HISTOPATHOLOGY OF CARIES
•As caries progresses ,the lesion of smooth surface
caries has a distinctive conical shape with its base
towards enamel surface and apex towards DEJ
•This conical lesion when observed in a light
microscope reveals four different one as seen from
deepest advancing zone first
1. Translucent Zone 2. Dark Zone
3. Body of lesion 4. Surface Zone

34. HISTOPATHOLOGY OF CARIES

35. HISTOPATHOLOGY OF CARIES
HISTOPATHOLOGY OF CARIES- ENAMEL
The initial ( non infected )lesion in dentin forms
beneath enamel before any cavity has formed.
Even though acids formed from fermentation of
carbohydrate substrate diffuse into dentin, they leave
the organic matrix intact.
Once bacteria penetrate enamel , they spread
laterally along DEJ and attack dentin over a wide
area.

36. HISTOPATHOLOGY OF CARIES

37. HISTOPATHOLOGY OF CARIES
HISTOPATHOLOGY OF CARIES- DENTIN (ADVANCWE CHANGES)

38. HISTOPATHOLOGY OF CARIES

39. HISTOPATHOLOGY OF CARIES
ZONES OF DENTAL CARIES
5
4
3
2
1

40. TREATMENT
Suggested method of control are :
1. Chemical measures
2. Nutritional measures
3. Mechanical measure
CHEMICAL MEASURES
The chemical substance includes
 Alter the tooth surface ke tooth structure
Interfere with carbohydrate degradation
 Interfere with bacterial growth and metabolism

41. TREATMENT
Substance which alter tooth surface :
FLUORINE: Most promising
FLUORINE administration :
A. Communal water supply
B. Topical application
Fluoridation of water absolute safe method and
highly beneficial.
0.7-1.0 ppm is optimum for health

42. TREATMENT
Topical Application :
1.sodium fluoride 2. fluoride dentifrices
3. stannous fluoride 4. fluoride mouthwashes
Bio - bigunanides: chlorboxidine and alexidine topical antiplaque
agents
Silver Nitrate : zinc chloride are also topical application

43. TREATMENT
DEGRADATION
Vitamin K :
prevent acid formation
Sarcoside : Two promising enzyme inhibitors were:
• Sodium N- Lauroyl Sarcosinate
• Sodium dehydroacetate
Reduce enamel solubility in acid presence.

44. TREATMENT
MECHANISM:
Inhibits coenzyme of enolase system.
Inhibiting convertion 2- phosphoglyceric acid to phosphoyruvic acid.
Thus preventing carbohydrate degradation
FLUORINE + hydroxyapatite Fluorapatite ( less acid labile)

45. TREATMENT
Substance which interfere with Bacterial Growth:
Urea and Ammonium Compounds
 chlorophyll
 nitro furans
Penicillin
Other antibiotics :
1.Erythromycin 2 tetracycline
3 Kanamycin 4 Vanomycin

46. TREATMENT
PLAQUE CONTROL AGENTS:
They control formation of plaque
NUTRITIONAL METHODS:
•Fluoride supplements
•Reduced intake of carbohydrate intake
Phosphates Diets:
Phosphate diets have major role in reducing cariogenic activity.

47. MECHANICAL MEASURES
Oral Prophylaxis
Tooth Brushing
Mouth rinsing
Dental Floss
Chewing gum

48. MECHANICAL MEASURES
PIT AND FISSURE SEALANTS
A dental procedure done to reduce cavities protecting the vulnerable pits
and fissures
Placed on children’s teeth.
Materials used

49. CARIES ACTIVITY TESTS
DEFINITION:
Caries activity test is defined as increment of active lesions
over a slated period of time.
TESTS:
 Lactobacillus colony test
 Colorimetric synder test
 Swab test
 Salivary s.mutans level test
 S.mutans dip slide method
 Buffer capacity test
 Enamel solubility test
 Salivary reductase test