dental caries classifications, histopathology

1. Dental caries – part 2
• Contents
• Classification
• Histopathology
1

2. 2
Rate of
progression
Extent
Location
CLASSIFICATION:

3. According to location:
• Primary caries
• Caries of pit and fissure origin
• Caries of enamel smooth surface origin
• Backward caries
• Forward caries
• Residual caries
• Root surface caries
• Secondary (recurrent) caries
3

4. 4
According to extent:
• a. Incipient (reversible) caries
• b. Cavitated (irreversible) caries

5. 5
According to hard tissue affected:
• a. Enamel
• b. Dentin
• c. Cementum
Others:
• Primary caries & secondary caries
• Nursing caries
• Radiation caries
• Rampant caries

6. 6
ACCORDING TO LOCATION:
Primary caries:
• Primary caries is the original carious lesion of the tooth.
• Accordingly 3 morphologic types of primary caries are evident in
clinical observations.
• Type I – pit & fissure and occlusal surfaces.
• Type II – Smooth surfaces of which there are 2 variants interproximal and
cervical / gingival.
• Root surface caries.

7. 7
• These caries can form in the regions of pits and fissures
• Usually resulting from imperfect coalescence of the developmental
enamel lobes.
• Such caries are not so clinically noticeable until the forces of
mastication fracture the increasing amount of unsupported enamel.
Type I / Pit and fissure caries:

8. 8
• 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

9. Caries of enamel smooth surface origin:
9
• Smooth surface caries does not begin as an enamel defect, but
rather in a smooth area of the enamel surface that is habitually
unclean and is thereby continually or usually covered by plaque.

10. Progression
10

11. 11
Forward caries:
• Forward caries is wherever the caries cone in
enamel is larger or atleast the same size as in
dentine.

12. Backward caries:
12
• When the spread of caries along the DEJ exceeds the
caries in the contiguous enamel, caries extends into this
enamel from the junction and is termed as backward
caries.

13. Recurrent caries (secondary caries):
13
• It occurs at the junction of a restoration and the tooth and may
progress, under the restoration. It is termed as recurrent
caries.
• This condition usually indicates that microleakage is present-
-due to poor cavity preparation,
-faulty restoration or a combination of these factors.

14. Root surface caries:
14
• These kind of caries originate in the dentinal root
portion of a tooth.
• It is predominantly found in the dentitions of older
age groups with significant gingival recession and
exposed root surfaces.
• It initiates on the surface of mineralized dentin and
cementum which have greater organic content.
• For this reason, bacterial flora causing root caries is
also different from flora causing smooth surface
caries.

15. Linear enamel caries :
15
• This is an atypical form of dental caries called linear enamel
caries.
• The lesions predominate on the labial surfaces of the anterior
maxillary teeth on the region of the neonatal line.
• Lesion is crescent shape
• Increase caries susceptibility of posterior teeth.
• Recent evidence suggests that neonatal line forms due to
transient hypocalcemia, a normal feature of the neonatal period

16. Odontoclasia:
16
• Variant of linear enamel caries
• Results in gross destruction of the labial surfaces of
incisor teeth
• Cause may be an inherent structural defect

17. EARLY CHILDHOOD CARIES
17

18. Early childhood caries
• “A suddenly appearing, widespread, rapid burrowing type of caries,
resulting in early involvement of the pulp and affecting those teeth
usually regarded as immune to ordinary decay.”
-Massler
• A complex disease involving maxillary primary incisors within a
month after eruption and spread rapidly to involve other primary teeth.
-Davies (1988)
18

19. CLASSIFICATION
TYPE 1
ECC
(mild to
moderat
e)
• Carious lesions involving the molars and incisors
• Seen in 2-5 years of age
• Cause is usually a combination of cariogenic semisolid or solid
food and lack of oral hygiene
• Number of affected teeth usually increases as the cariogenic
challenge persists
TYPE 2
ECC
(moderat
e to
severe)
• Labiolingual carious lesion affecting the maxillary incisors with
or without molar caries
• Seen soon after 1st tooth erupt
• Cause is inappropriate use of feeding bottle, at-will breast
feeding or combination, poor oral hygiene
TYPE 3
ECC
(severe)
• Carious lesion involve all the teeth, including mandibular incisors.
• Usually seen in 3-5 years of age
• Cause is combination of factors and poor oral hygiene
• Rampant in nature and involves immune tooth surfaces.
19

20. NURSING CARIES
• A unique pattern of dental decay in
young children due to prolonged and
improper nursing/feeding habit.
-Winter et al, 1966
20

21. Etiological agents
in nursing bottle
caries
Pathogenic
microorganisms
Substrate
(fermentable
carbohydrates)
Host Time
Other
predisposing
factors
21

22. CLINICAL FEATURES
Mandibular molars: at later stage
Maxillary canines & 2nd molars: facial, lingual, proximal surfaces
Maxillary 1st molars: facial, lingual, occlusal, proximal surfaces
Maxillary lateral incisors: facial, lingual, mesial, distal surfaces
Maxillary central incisors: facial, lingual, mesial, distal surfaces
22

23. • Mandibular anterior teeth are usually spared because of:
I. Protection by tongue
II. Cleansing action of saliva due to presence of the
orifice of the duct of sublingual glands very close to
lower incisors.
23

24. PROGRESSION OF THE LESION
Initially, a
demineralization dull,
white area is seen along
the gum line on labial
aspect of maxillary
incisors.
These white lesions
become cavities which
involve the neck of the
tooth in a ring like
fashion
Finally, the whole
crown of the incisors is
destroyed leaving
behind brown-black
root stumps.
24

25. NURSING CARIES
Specific form of rampant caries.
Age of occurrence
In infants & toddlers
Dentition involved
Affects the primary dentition
Characteristic feature
Specific pattern is seen
Mandibular molars are not involved
RAMPANT CARIES
Acute, widespread caries with early pulpal
involvement of teeth which are usually immune
to decay.
Age of occurrence
Seen at all ages
Dentition involved
Both primary & permanent dentition
Characteristic feature
Surfaces considered immune to decay are
involved. Thus, mandibular incisors are affected
25

26. Etiology
Bottle feeding before sleep
Pacifiers dipped in honey
Prolonged at-will beast-feeding
Treatment
In early stage- topical fluoride application & education
Directed toward maintenance of the teeth till the
transition occurs
Prevention
Education of the parents
Etiology
More multifactorial with all the essential factors involved
are not just feeding practices
Frequent snacks, excessive sticky refined carbohydrates
Decreased salivary flow
Genetic background
Treatment
Require pulp therapy
Long term treatment
Prevention
Dental Health Education at a mass level involving people of
all ages
NURSING CARIES RAMPANT CARIES
26

27. 27
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
Radiation caries:

28. Adolescent caries:
28
• Acute caries attack at 11-18 years of 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

29. Arrested caries:
29
• Caries which becomes static or stationary and does not show any
tendency for progression
• 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

30. 30
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.
• Causes: gingival recession, decreased salivary secretion, poor oral
hygiene.

31. Occult Caries / Hidden Caries
31
• 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

32. CERVICAL BURNOUT
32

33. 33
G.V.Black’s Classification
Class-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: - lesions found on the proximal surfaces of molars and premolars
Class-III: - lesions found on the proximal surfaces of anterior teeth, but do
not involve the incisal angle

34. 34
• Class-IV: - lesions found on the proximal surfaces of anterior
teeth and involving incisal angle
• Class-V: - lesions found on the gingival third of the facial and
lingual surfaces of anterior and posterior teeth.
• Class-VI: - were not included in Black’s classification
- Proposed by Siomon
- Lesions on the incisal edge and cusp tips of the teeth

35. 35
ACCORDING TO EXTENT

36. 36
ICDAS classification

37. Root caries (New in ICDAS II)
• E = Excluded root surfaces (no gingival recession)
• 0 = Sound (no caries or restoration)
• 1 = Non-cavitated carious root surface— soft or leathery
• 2 = Non-cavitated carious root surface— hard and glossy
• 3 = Cavitated (greater than 0.5mm in depth) carious root surface— soft or
leathery
• 4 = Cavitated (greater than 0.5mm in depth) carious root surface—hard and
gloss
• 6 = Extensive cavity: an extensive cavity involves at least half of a tooth
surface and possibly reaching the pulp.
• 7 = Filled root with no caries 37

38. • 9 = Used for the following conditions
• 97 = Tooth extracted because of caries (tooth surfaces will be coded
97)
• 98 = Tooth extracted for reasons other than caries (all tooth surfaces
coded 98)
• 99 = Unerupted (tooth surfaces coded 99)
38

39. • The shared vision for the International Caries Detection and
Assessment System is now that:
• it employs an evidence-based and preventively oriented approach,
• is a detection and assessment system classifying stages of the caries process,
• is for use in dental education, clinical practice, research and public health,
• provides all stakeholders with a common caries language,
• has evolved to comprise a number of approved, compatible ‘formats’,
• supports decision-making at both individual and public health levels and
• has generated the International Caries Classification and Management System,
to enable improved long-term caries outcomes.
3

40. 40

41. 4188

42. 42

43. 43

44. 44

45. 45

46. HISTOPATHOLOGY
46

47. 47

48. 48

49. •Knowledge
•Of macroscopic features:
detection & diagnosis of
caries
•Of shape of lesion: cavity
preparation
•Characteristics:
•Chronic disease
•Not self-limiting
Cavity formation
subclinical
Total destruction
Light microscopy
Enamel lesion
Mineral loss
(signs, symptoms)
visible
Time
Electron microscopy
49

50. Dental Caries
Enamel Caries Dentin Caries Cementum Caries
(Root caries)
Smooth surface caries Pit and fissure caries
50

51. Speed of lesion formation
• Incipient caries to clinical caries: 18 ± 6 months
• Peak rate for incidence of caries: 2-4 yrs (avg 3yrs) after eruption
• Poor oral hygiene, excess sucrose: 3 weeks
• Radiation induced Xerostomia: 3 months
• Occlusal caries require less time than smooth surface
51

52. Basic structure of enamel
52

53. Estimating mineral loss
• Clinical considerations
• Refractive indices of Hydroxyapatite, water and air
• Histological considerations
• Microradiography
• Polarized light microscopy
53

54. ENAMEL CARIES
MACROSCOPIC FEATURES:
White spot lesion
Opaque, chalky white
Surface features-SEM (Thylstrup, 1994) :
• Deepened & irregular Tomes
processes pits
• Irregular cracks & fissures
• Widened intercrystalline spaces
• Fractures of perikymata edges
54

55. •Brown spot lesion
•Sites
•Occlusal surfaces:
•Fissure morphology (Newbrun, 1989)
•Starts at both sides of fissure wall
55

56. • MICROSCOPIC FEATURES:
• Triangular/wedge in shape
• Divided into 4 zones
• Can be viewed in
• Plain transmitted light
• Polarized light-clearer picture
56

57. Histological features of early enamel caries
57
o Loss of inter-rod substance
o prominent enamel-rods
o Appearance of transverse striations of
enamel rods due to segmental
demineralization
o Accentuation of incremental striae of
Retzius

58. H/F of Advanced enamel caries
58
• 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

59. •ZONE 1:TRANSLUSCENT ZONE
•At the advancing front- 5 -100 µm
•Seen with quinoline
•Pore volume: 1%
•Not always present, sometimes near lateral part
59

60. •ZONE 2: THE DARK ZONE
•More constant feature-90-95% lesions
•Pore volume -2-4%
•Why is it called dark zone?
•2 theories for small pores
60

61. •ZONE 3: THE BODY OF THE LESION
•Largest zone
•Pore vol: 5% at periphery, 25% in centre
•Appears translucent in quinoline and dark with water
•Striae of retzius well marked
•old./chronic lesions: bands of well mineralized tissue
•Bacteria in between prisms (rods)
61

62. •ZONE 4: THE SURFACE ZONE
•20-50 µm
•Pore vol: 1%
•Negatively birefringence in water
•Importance: serves as barrier to bacterial
invasion
62

63. Smooth surface caries
• The earliest manifestation of incipient
enamel caries is the appearance of an area
of decalcification , beneath the dental
plaque, which resembles a smooth chalky
white area.
• There is loss of interprismatic substance,
with increased prominence and roughening
of the ends of the enamel rods.
White spot lesion
63

64. 64

65. • Accentuation of incremental striae of
Retzius.
• As deeper layers of enamel are involved it
forms a cone shaped lesion with the apex
toward the DEJ and the base toward the
surface of the tooth.
• Eventual loss of continuity of enamel
surface –feels rough to explorer tip.
65

66. Pit and fissure caries
• Fissures are diverse in shape and size
• Carious lesion starts at both side of fissure
rather than at the base, penetrating nearly
perpendicular to the DEJ.
• Lesion is cone-shaped with base towards
dentine and apex towards enamel surface
66

67. 67

68. Progression of enamel lesion
•Caries dissolution along the rods
•Highest degree of tissue porosity is along “Central
Traverse”
•Oldest part-along CT, lesion spreads laterally along the
surface
68

69. •Central defects of crystals-hollow hexagons
•As dissolution increases, disorganization of
crystal arrangement, invasion of bacteria
69

70. Ultrastructural changes in enamel caries
•Destruction of crystals at borders & within the prism
•Arcade like defects bounded by rows of resistant crystals- “caries
crystals”
•More dissolution in heads and less in tails
70

71. Remineralization/arrest
•Enamel most susceptible to caries during & after
eruption
•1st molar:12-14 months
•2nd molar:14-18 months
•Premolars:1-2 months-less prone
{Backer-Dirks (1966)}
71

72. •Mechanism of arrest of non-cavitated lesions:
•Maintains original crystalline framework
•Etched crystallites serve as nucleating agents
•Wear & polishing of the partly dissolved external surface-regain of surface hardness
•Remineralized area: brown or black spots
•Mechanism
•Cavitated lesions can also be arrested with proper plaque control (thylstrup)
•New mechanism of remineralization: CPP-ACP
72

73. Clinical significance of enamel caries
73

74. CARIES OF DENTIN
Begins with the natural spread of the process along the DEJ and rapid
involvement of the dentinal tubules. The dentinal tubules act as tracts leading to
the pulp (path for micro-organisms).
Caries advances more rapidly as dentin provides much less resistance to acid attack .
Early Dentinal Changes:
-initial penetration of the dentin by caries dentinal sclerosis,
-calcification of dentinal tubules and sealing off from further penetration by
micro-organisms,
-more prominent in slow chronic caries.
Dentinal
sclerosis
74

75. DENTINAL CARIES
•Progression of enamel caries to
dentin: 5.4% from 11 – 22 yrs
(Mejare et al, 1999)
•MACROSCOPIC CHANGES:
•Lateral spread along DEJ
•Cone shaped-apex towards the pulp
•Affected dentin-Brown or black in
colour
75

76. •MICROSCOPIC CHANGES: (mechanism)
•Caries advancement proceeds through 3 stages
•Acids demineralize the dentin
•Organic matter degenerates
•Loss of structural integrity & bacterial invasion
•1st mild stimuli –defense reaction of dentin-tubular sclerosis/TRANSPARENT ZONE
•Dentin demineralization-when lesion reaches DEJ
•Arrest of caries
•Cavitation of dentin-bacterial invasion
76

77. 77
Zone of
Decomposed
dentin
Zone of
Bacterial
invasion
Zone of
Demineralisation
Zone of
Dentinal
sclerosis
Zone of
Fatty
degener
ation
Retreating
Odontoblastic
process
INFECTED DENTIN AFFECTED DENTIN
Dentinal
caries

78. • Behind the transparent sclerotic zone, decalcification of dentin
appears.
• In the earliest stages, when only few tubules are involved,
microorganisms may be found penetrating the tubules Pioneer
Bacteria.
78

79. • This initial decalcification involves
the walls allowing them to distend as
the tubules are packed with
microorganisms.
• Each tubule is seen to be packed
with pure forms of bacteria, eg., one
tubule packed with coccal forms the
other tubule with bacilli.
79

80. • As the microorganisms proceed further they are distanced from the
carbohydrates substrate that was needed for the initiation of the caries.
• Thus the high protein content of dentin must favour the growth of the
microorganisms.
• Therefore proteolytic organisms might appear to predominate in the deeper
caries of dentin while acidophilic forms are more prominent in early caries.
80

81. Advanced Dentinal Changes ;
-decalcification of walls, confluence of the dentinal tubules,
tiny “liquefaction foci”, described by Miller are formed by the focal
coalescing and breakdown of dentinal tubules.
These are ovoid areas of destruction parallel to the course of the
tubules which filled with necrotic debris and increase in size by
expanding. The adjacent tubules are distorted and their course is bent
due to this expansion.
81

82. • The destruction of dentin by decalcification and then proteolysis
occurs in numerous focal areas- leading to a necrotic mass of
dentin of a leathery consistency.
• Clefts present in the carious dentin that extends at right angles to
the dentinal tubules, accounts for the peeling off of dentin in
layers while excavating.
82

83. Shape of the lesion is triangular with the apex towards the pulp and the base towards the enamel.
Zone 1; Zone of Fatty Degeneration of Tome’s Fibers,(next to pulp)
-due to degeneration of the odontoblastic process. This occurs before sclerotic dentin is formed
and makes the tubules impermeable.
Zone 2; Zone of dentinal sclerosis,
-deposition of Ca salts in the tubules.
Zone 3; Zone of decalcification of dentin
Zone 4; Zone of bacterial invasion
Zone 5; Zone of decomposed dentin due to acids and enzymes.
83

84. ZONE OF FATTY DEGENERATION:
•Of the Tomes fibres-stained by Sudan red
•Importance:
•Fat contributes to impermeability of dentinal tubules
•Maybe a predisposing factor favouring sclerosis
• 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 84

85. •ZONE OF TUBULAR SCLEROSIS:
•Reaction of vital dentinal tubules & pulp
•Seals off tubules to further penetration by bacteria
•Mineralization process-2 types
•Hydroxyapatite crystals & large rhomboidal crystals (whitlockite)
•Transluscent appearance-transluscent/transparent dentin
• 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 also start depositing dentin.
85

86. ZONE OF BACTERIAL INVASION
•Initially tubules with single type of bacteria
•Liquefaction foci-beadings, varicosities, moth-
eaten, rosaries
• Decalcification is by bacterial acid diffusion
• Very narrow zone, softer than normal dentin
• Further loss of minerals from inter tubular dentin
• Large crystals within lumen of dentinal tubules
86

87. •ZONE OF DEMINERALIZATION
•Narrow zone
•Occlusion of tubules Softer than normal dentin
•Few microorganisms in the tubules – “pioneer bacteria”
87

88. 88
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

89. Zone of Decalcification with Bacterial Invasion / Turbid Dentin
• Initially only few tubules are involved & micro-orgs also less
• These are acidogenic, pioneer bacteria (initiators), present long before lesion
is clinically detected
• Bacteria multiply within tubules & are seen in advancing front of lesion
• Walls of tubules are thin & when micro-orgs penetrate, 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
89

90. •TO SUMMARIZE:
90

91. Other features
•In slowly advancing lesions
•Sclerotic dentin-very hard, shiny
•Hypermineralized –radioopaque
•In moderately advancing lesions
•Dead tracts
•Reparative/reactionary dentin
•Pulp stones
•In rapidly advancing lesions
•Abscess, necrosis of pulp 91

92. Zones of dentin (sturdevant)
•ZONES OF DENTIN:
•Zone 1: normal dentin
•Zone 2: subtransparent dentin
•Zone 3: transparent dentin
•Zone 4: turbid dentin
•Zone 5: infected dentin
•AFFECTED DENTIN
•INFECTED DENTIN
•Caries detector – basic fuschin/ 1% acid red (Fusayama, 1979)
92

93. Secondary / Reactionary dentin
93
• Protective mechanism to protect pulp
• Develops as a result of localized, non-specific irritation to
odontoblasts
• Hyper mineralized,less number of dentinal tubules having
irregular & torturous course

94. ROOT CARIES
•Occurs in older individuals where
root/cementum is exposed
•Microorganisms penetrate along the
clefts, sharpey’s fibres
•Delamination occurs along
incremental lines
•Brush like appearance
•Radioopaque surface layer seen
94

95. Root Caries
Root caries as defined by HAZEN, is a soft, progressive lesion that is found
anywhere on the root surface that has lost its connective tissue attachment and
is exposed to the environment.
-the root surface must be exposed to the oral environment before caries can
develop here.
-Plaque and micro-organisms are essential for the cause and progression of the
lesion, mostly Actinomyces,
-micro-organisms invade the cementum either along the Sharpey’s fibers or
between the bundles of fibers.
95

96. 96
• -spread laterally, since cementum is formed in concentric
layers.
• -after decalcification of cementum, destruction of matrix
occurs similar to dentin with ultimate softening and
destruction of this tissue.
• -invasion of micro-organisms into the dentinal tunbules,
finally leading to pulp involvement.
• -the rate is slower due to fewer dentinal tubules than crown
area

97. 97
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

98. 1. A tooth surface without caries.
2. The first signs of demineralization.
3. The enamel surface has broken down.
4. A filling has been made but the demineralization has not been stopped.
5. The demineralization proceeds and undermines the tooth.
6. The tooth has fractured.
98

99. Conclusion :
• Dental caries should be considered as a consequence of ecologically
driven imbalances of oral microbial biofilms.
• An appreciation of ecological principles will enable a more holistic
approach to be taken in caries control.
• A better understanding of the process of biofilm formation ,its genetic
regulation is necessary to the development of novel strategies for oral
disease prevention and control.
99

100. Conclusion :
• Among the multifactorial etiology of dental caries diet plays
an important role in the occurrence of dental caries. This seminar
intended to provide an overview of the evidence for an association
between diet and dental caries which has already been established
and documented by a series of studies.
• But the information available regarding the association of diet
and dental caries under the Indian context and the effect of rapid
changes in urbanization and economic development on the Indian 100

101. Conclusion :
The way ahead should be considered under 2 aspects:
1. The extrapolation of the data to the India diet and conditions.
2. The task of diet changes which requires lifestyle changes that
would be challenging to bring about and thus should be an important
focus area for dental public health programs/ approaches in any setting
for different age groups and populations.
101

102. References :
• Cariology – Newbrun.
• Murray J.J. et al. The prevention of oral disease. 4th Ed.
• Shafer. A textbook of Oral Pathology. 4th Ed.
• S.S.Hiremath.Textbook of Preventive & Community Dentistry.
• Per Axelsson . Diagnosis and Risk Prediction of Dental Caries. 2000,
Quintessence Publishing Co.
• Ole Fejerskov and Edwina A.M. Kidd. Dental Caries – The Disease
and its Management . Blackwell Munksgaard 2003.
102

103. References :
• T.W. Cutress et al. Effects of fluoride-supplemented sucrose on
experimental dental caries and dental plaque ph. Adv Dent Res
9(1):14-20, February, 1995.
• Lingström P, van Houte J, Kashket SFood starches and dental caries.
Crit Rev Oral Biol Med. 2000;11(3):366-80 .
• Brian A. et al . Sugar Consumption and Caries Risk:A Systematic
Review. Journal of Dental Education . October 2001. Volume 65,
No.10
103

104. References :
• Gordon Nikiforuk. Understanding Dental Caries.Karger Publishers.
• D.T.Zero. Sugars- The Arch Criminal? Caries Res 2004;38:277-285 .
• Norman O. Harris, Fraklin Gracia-Godoy.Primary Preventive
Dentistry.6th edition , 2004, Pearson Prentice Hall..
• Carole A. Palmer, Diet and Nutrition in Oral Health.Julie Levin
Alexander, 2003.
104

105. References :
• Marsh P. Dental plaque as a biofilm and a microbial community-
implications for health and disease. BMC Oral Health 2006,6:S14.
• Thomas H.J et al .Managing the complexity of a dynamic biofilm.
JADA, 2006;Vol.137;10s-15s.
• Scheie A.A &Peterson F.C.The Biofilm concept:consequences for
future prophylaxis of oral diseases? Crit Rev Oral Biol Med 15(1):4-
12 (2004)
105

106. Questions asked in NTRUHS examination :
• Balanced diet in prevention of dental caries – 20 M – APR 2015
• Early childhood caries – 7 M – 2011
• Diet counselling – 2011 and 2013 for 7M and 20M
• Cariogenecity – 2003
• Rampant caries – 2003
• Bacteriological role in caries – 2002
• Diet for healthy teeth – 2001
• Genetics and dental caries- 2001.
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107. • Newbrun stated that “ the dentist of future will still have to treat
caries, but unquestionably the emphasis will be on early diagnosis and
preventive intervention.”
• Times change and we change with time”.
Thank you
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