This presentation aims to explain the history of dental caries, the theories of dental caries and delves into each etiological factor in depth- Microflora, diet, saliva, tooth, dental plaque, time and some systemic factors. also talks about the dietary studies and caries relation

1. DENTAL CARIES-
HISTORY &
ETIOLOGY
D R H R I S H I T A
M D S - 1

2. Definition
Dental caries is an irreversible microbial disease of the calcified tissues of the
teeth, characterized by demineralization of the inorganic portion and
destruction of the organic substance of the tooth, which often leads to
cavitation- Shafer,1993

3. History
-Dental Caries seen in
brachycephalic skulls of
Neolithic period (12,000-3,000
BC)
-Caries found at or just below
the contact area
-More caries at the CEJ
-By 17th Century, Increase in
total caries experience seen
-Caries in primitive population
was a lot lesser than the
modern societies (Mellanby,
1934)
-Increase in caries incidence
was seen due to shift of diet
from raw foods to more
carbohydrates and refined
sugars (Larsen, 1997)
Caries In
Modern
Society
Caries In
Prehistoric
Man

4. Theories of dental caries
Early Theories
1.-Legend of worms
Endogenous
Theories
1.-Humoral Theory
2.-Vital Theory
Exogenous Theories
-Chemical Theory
-Parasitic Theory
-Millers Chemico-parasitic theory
-Proteolytic Theory
-Proteolysis Chelation Theory

5. Legend of Worms
5000 BC
Originates from Sumerian text and was discovered in
the Euphrates Valley
According to them, decay occurred due to worms
Most universally accepted theory of that time with
evidence from other places across the globe

6. Humoral Theory
Proposed by Greeks
All diseases were attributed to imbalance between four
humors
According to Hippocrates and Aristotle stagnated food
in teeth interacted with the humors and produced
decay

7. Vital theory
Developed in the 18th century
Attributed caries to originate within the tooth itself like bone gangrene
Failed to explain what change had occurred within the tooth for initiation of caries

8. Chemical Theory
Parmly in 1819
According to him caries was caused due to a chemical substance that acted on
putrefied food particles in teeth
Robertson in 1835 stated that caries is caused due to acid formed by fermented
food particles around teeth
Did not highlight the role of microbes

9. Parasitic theory
Proposed in 1843 by Erdl and later by Antonie Leeuwenhock
 Found filamentous microbes that resembles parasites in the scrapings removed
from teeth which were observed under microscope
Did not tell about the origin of these parasites and the role of food

10. Miller’s Chemo-parasitic theory
Susceptible
host
Food accumulation
Fermentable
carbohydrates
Acid Production
Demineralization
followed by dissolution

11. Proteolytic Theory
Proposed by Gottlieb in 1944 & Gottlieb, Diamond, Applebaum in 1946
According to them organic or protein elements of enamel are initial pathways of invasion
by microbes
Dental caries were histologically characterized by pigmentation, a phenomenon
associated with proteolysis
Regarded Staphylococcus aureus to be mainly responsible

12. Proteolysis Chelation Theory
Proposed by Schatz et al in 1955
According to this theory, bacteria first attack on organic matter of enamel which
leads to destruction of enamel and the byproducts of the destruction have
chelating properties by virtue of which they cause demineralization of enamel

13. Caries Balance Theory
Protective Factors Pathological Factors
Remineralization Demineralization

14. Keye’s Triad
SUBSTRATE HOST
MICROFLORA

15. Caries Tetrad
SUBSTRAT
E
TIME
HOST MICROFLORA

16. Current
Concept
SUBSTRATE
TIME
TOOTH
SALIVA
SALIVA
INCOME
EDUCATION
ATTITUDE SOCIAL
CLASS
MICROFLORA

17. Microflora and Dental Caries

18. Historical Studies
Miller demonstrated the presence of microbes in dentinal tubules of carious teeth
mainly cocci and leptothrix
1900- Goadby- Isolated gram positive bacillus from carious dentin and termed as
B. necrodentalis. Later he changed his view that streptococci are involved
1922- Mcintosh, James, Lazorous-Barlow- Microbes are capable of lowering the
pH to the degree that enamel is softened

19.  1924-Clarke isolated Streptococcus mutans from teeth that were found in initial
stage dental caries
 1925- Bunting and Parmelee reported the bacillary forms in the initial lesions of
caries similar to those described earlier and they termed as B. acidophilus
 Bunting, Nickerson and Hard observed that B. acidophilus was absent in
caries immune individuals while was present in caries susceptible individuals
 1942-Floresta studied saliva from carious and non carious individuals, Aciduric
streptococci and staphylococci were isolates

20. Several organisms have been found to induce dental caries when used as
monocontaminants in gnotobiotic ( germ-free) rats –
1. Streptococci group-
o Streptococcus mutans
o Streptococcus salivarius
o Streptococcus milleri
o Streptococcus mitior
o Streptococcus oralis
o Streptococcus sanguis
2. Peptostreptococcus intermedius
3. Lactobacillus acidophillus
4. Lactobacillus casei
5. Actinomyces viscous
6. Actinomyces naeslundii

21. Type of caries Micro-organism Humans
Pit and fissure S. mutans
S. sanguis
Lactobacillus species
Actinomyces species
Very significant
Uncertain
Very significant
By chance
Smooth surface S. mutans
S. salivarius
Very significant
By chance
Root surface A.viscous
A.naelsundii
S. mutans
S. sanguis
Very Significant
Very Significant
Significant
By chance
Deep dentinal caries Lactobacillus species
A.naelsundii
Other filamentous rounds
Very Significant
Very significant
Very significant

22. Lactobacilli
Gram-positive
 Non spore forming rods
Microaerophilic conditions
Homofermenters- L. casei and L. acidophilus
Heterofermenters- L. fermentum and L. brewes
Acidogenic and aciduric- Can multiply in low pH of plaque and dental caries
Amount of acid produced by Lactobacilli is insignificant compared to the acid
produced by other organisms
 Also, their increased amount in plaque and saliva does not necessarily establish their
causative role. Hence, they can be considered as secondary invaders

23. Oral Actinomyces
Gram positive
 Filamentous organisms
Facultative Anaerobes- A. naelsundii and A. viscosus
Strict Anaerobes- A. isarelii and A. odontolyticus
They have been isolated in large amounts from the roots of decayed human teeth
A. viscosus are acidogenic bacteria
They have intracellular polysaccharide stores
They also form extracellular levans and heteropolysaccharides consisting of hexose and
hexosamine

24. Veillonella
Gram-negative cocci
These organisms lack key enzymes involved in glycolysis and HMP shunt and thus
do not utilize sugars as energy source
Veillonella uses lactic acid and converts it to propionic acid and other weak acids
 This converts stronger lactic acid with pKa 3.08 to a less dissociated acid of pKa in
4.7 range
Reported as anti-cariogenic

25. Streptococcus mutans
Gram-positive cocci forming short to medium chains
Facultatively anaerobic, Catalase negative
S. Mutans synthesizes insoluble polysaccharides from sucrose
Cariogenic properties:
oFerments sucrose, Homofermenters of lactose
oColonizes on tooth surfaces
oMore aciduric than other Streptococci

26. Mechanism
of action

27. Streptococcus sanguis
Present in plaque obtained from both carious and non
carious sites
Caries from this strain mostly occur in occlusal pits and
fissures
Low cariogenicity than S. mutans

28. Streptococcus salivarius
 Found in tongue, throat and in saliva but not high
numbers in dental plaque
 Attaches more to the epithelial surfaces than
hard tissues
 Produces copious amounts of the water soluble
polymer of fructose called levans

29. Role Of Dental Plaque

30.  Dental Plaque is a specific but highly
variable structural entity, resulting from
sequential colonization of microorganisms
on tooth surfaces, restorations & other
parts of oral cavity, composed of salivary
components like mucin, desquamated
epithelial cells, debris & microorganisms, all
embedded in extracellular gelatinous
matrix- (WHO 1961)
 Acquired pellicle: It is the form of
glycoprotein that is derived from saliva and
is adsorbed on tooth surface
 It is on this component of plaque that
bacterial colonization takes place

31. Historical Studies
 Bibby (1940) and his associates studied the characteristics of different strains of
filamentous organisms isolated from dental plaque and noted their ability to
adhere to tooth surface
 Blaney (1942) and his associates pointed out that the time required for definite
cavitation on intact enamel representing early caries was several months
 Hemmes and his associates (1946) stated that dental plaque was most likely the
starting point for earliest enamel caries. They examined plaques from teeth of
numerous children which became carious throughout the investigation
o Presence of aciduric streptococci was 86%
o Presence of lactobacilli in 57% individuals, increase in lactobacilli count
according to the progress of dental caries

32.  Most investigations of micro-organism of the dental plaque have concluded that three
basic groups of micro-organisms predominate :
o Streptococcus
o Actinomyces
o Veillonella
o S. mutans
o S. salivarius
o S. milleri
o S. mitior
o S. sanguis
o A. viscosus
o A. naelsundii
o A. isarelii
o Rothia
dentocariosa
o V. parvula
o V. alcalescenes

33. Mechanism of plaque formation
Adhesion Proliferation Microcolonies
Association Biofilm
Formation
Growth or
maturation

35. Role Of pH Of Dental Plaque
Carbohydrates permeating dental plaque are degraded rapidly (Stephan,
1940)
Average pH in caries free person- 7.1
 Average pH in extremely caries active person- 5.5
Lowest pH varied from 4.6-4.1
Stephan studied the pH of dental plaque after rinsing with 10% sucrose
solution
Within 2.5 minutes the pH dropped to 4.5-5.0 and gradually returned to
original pH level in 1-2 hours. The plaque pH on the caries free group did
not fall below 5.0 in half of the cases

36.  At critical pH 5.5, tooth minerals act
as buffers. They loose calcium and
phosphorous into the plaque,
initially helping to maintain the pH to
5.5. When pH falls below 5.0,
subsurface demineralization is
inevitable- Incipient caries
 When pH lowers further, surface
demineralisation of enamel occurs

37. Non-specific plaque hypothesis
Based on the work of Black (1884) and Miller (1980)
Quantity of plaque determined the pathogenicity without discriminating between
the levels of virulence of bacteria
Theilade (1986) added that the host has the capacity to detoxify the bacterial
products (e.g salivary neutralizing acids) and disease would only develop if this
threshold is surpassed
The conclusion was that if any plaque has an equal potential to cause disease, the
best way of disease prevention would be non-specific mechanical removal of as
much plaque as possible by e.g., tooth brushing or tooth picking

38. Specific Plaque Hypothesis
Loesche and Nafe, 1973
States that only certain plaque is pathogenic, its pathogenicity depend on the
presence of or increase in specific microorganisms
However, the theory couldn’t explain why caries occurred even in the absence
of these bacteria, albeit to a lesser degree
Despite this, the hypothesis was useful in diagnosis and treatment, associating
caries with such truly cariogenic bacteria as Streptococcus mutans and the
Lactobacilli species

39. Ecological Plaque Hypothesis
Philips D. Marsh (1994)

40. Saliva and Dental Caries

41. Water (99.5%)
Saliva
Solids
Inorganic Substances Gases
Organic Substances
1. Oxygen
2. CO2
3. Nitrogen
1. Sodium
2. Calcium
3. Potassium
4. Bicarbonate
5. Bromide
6. Chloride
7. Fluoride
8. Phosphate
Other Organic
Substances
Enzymes
1. Amylase
2. Maltase
3. Lingual Lipase
4. Lysosyme
5. Phosphatase
6. Carbonic Anhydrase
7. Kallikrein
8. Lactoperoxidase
9. Lactoferrin
1. Mucin
2. Albumin
3. Proline Rich Proteins
4. IgA
5. Blood Group Ags
6. Free Amino Acids
7. Non Protein nitrogenous
substances- Urea, Uric
Acid, Creatinine
Composition

42. Calcium & Phosphate Concentrations
Enamel consists of crystalline hydroxyapatite
These complexes usually dissociate as the pH drops and result in free
active concentration of ions
Calcium and phosphate in saliva form an important natural defense
mechanism against dissolution of teeth
When the saliva is unsaturated (less Ca and P)- demineralization occurs
When the saliva is supersaturated (more Ca and P)- mineral precipitates
Normally, saliva is supersaturated in comparison to enamel apatite, so
mineral precipitation occurs

43. pH of Saliva
Normal pH of saliva - 6.2 to 7.6
Saliva plays a critical role in remineralization-demineralization process
Critical pH of saliva – 5.5
The pH at which any particular saliva ceases to be saturated with calcium and
phosphate is referred to as the 'critical pH'

44. Buffering Capacity Of Saliva
In saliva, the chief buffer systems are bicarbonate carbonic acid (HCO3
-/H2CO3, pKl
= 6.1) and phosphate (HPO4 or H2PO4, pK2 = 6.8)
The bicarbonate in saliva is able to diffuse into the dental plaque to neutralize the
acid formed from carbohydrate by the microorganisms
The higher the flow rate, the greater will be its buffering capacity
Within active carious lesions, a pH gradient exists. The deep advancing edges of
such lesions were more acidic than the shallower layers
In enlarged and exposed cavities, the pH was closer to neutrality, probably
because of better access to saliva

45. Quantity Of Saliva
A restriction in salivary flow leads to exacerbation of dental caries, as the
removal of bacteria and food debris from the mouth is reduced
Salivary gland aplasia and Xerostomia

46. Flow Rate Of Saliva
Unstimulated saliva - 0.3–0.4 ml/minute
Stimulated saliva - 0.5 ml per gland in 5 minutes
Xerostomia – less than 0.1ml/min
Significant increase in caries

47. Viscosity of Saliva
High viscosity of saliva is due to high quantity of mucin content
Sometimes, High caries index has been seen in individuals with highly viscous
saliva
Numerous cases have been reported where patients were caries free in spite of
having highly viscous saliva (Miller)

48. Tooth Factors and Dental Caries

49. Composition
Caries Resistance- Surface enamel>Subsurface Enamel
Fluoride Content- Sound enamel > Carious enamel
Surface of enamel is lower in CO2 , dissolves slower in acids, contains less
water and has more inorganic material than subsurface enamel
Decrease in density and permeability and increase in nitrogen and fluoride
content, occur with age- Post eruptive ‘maturation’ process

50. Morphological Characteristics
Deep, narrow occlusal fissures Buccal or Lingual pits

51. Nagano Classification

52. Susceptible Teeth & Surfaces
Occlusal>Buccal>Mesial>Distal>Lingual
Occlusal>Mesial>Lingual>Buccal>distal
Lingual>Labial

53. Position of Teeth & Proximal Contacts
Caries initiate just below contact
point/area
Contact areas are more susceptible to
caries than contact points
Mal-aligned teeth are more susceptible
to caries
Rotated / Malaligned teeth exhibit greater
contact areas

54. Diet and Dental caries

55. Diet
Diet is defined as the type & the amounts of food eaten by an
individual- FDA, 1994
Physical form of Diet Nature of Diet
Nutrition
Nutrition is defined as the sum of processes by which individual
takes and utilizes food- FDA,1994

56. History
Relationship of sucrose to the prevalence of dental caries can be found in many
epidemiological studies
The prevalence of caries on isolated islands such as Australia, New Zealand,
Trista da Cunha etc. was found to be lower before introduction of the European
diet containing high carbohydrates, mainly sugars
Europe and Japan have demonstrated the drastic reduction in dental caries during
war times food restrictions , due to reduction of sugars, syrup and all sugar
products

57.  Cumulative dental decay
prevalence, expressed as DMFT,
in children of ages 11-12 was
charted against the corresponding
annual per capita sugar utilization
data (1959) for 18 countries and
state of Hawaii, from the food and
Agriculture Organization of the
United Nations (Dr. T. Marthaler)

58. Physical Form of Diet
Diet of primitive man consisted of great deal of roughage compared to the diet of a
modern man which consists of refined food
Mechanical cleansing by masticatory forces is noticed to reduce the number of
culturable microbes and the amount of plaque which tenaciously clings to the tooth
surface
 The effect of dietary restriction on the L. acidophilus index in 1250 rampant caries
affected individuals and 265 caries free individuals was studied. Replacement of
refined dietary carbohydrates with meat, eggs, vegetables, milk and milk based
products helped to reduce the index by 82% and clinical evidence of extensive arrest
of caries (Beck et al, 1994)

59. Role of Carbohydrates
TOTAL SUGARS
INTRINSIC SUGARS
Sugar molecules inside the cells
eg fresh fruits and vegetables
EXTRINTIC SUGARS
Sugar molecules outside
the cell
MILK SUGARS NON-MILK EXTRINSIC
SUGARS
CAUSE NO HARM HARMFUL

60. Sucrose : Arch criminal of dental
caries
 Sucrose is a substrate for production of extracellular polysaccharides (fructan
and glucan) and insoluble matrix polysaccharides (mutans)
 Sucrose favours colonization by oral micro-organisms and increases the
stickiness of plaque allowing it to adhere in larger quantities to the teeth
 A combination of soluble starch and sucrose is expected to be a more powerful
caries risk factor because of increased retention of food which prolongs the
clearance time of sugar

61. Carbohydrate
substrates
Sucrose Starch
Extracellular
Polysaccharides (glucan,
fructan & others)
Dental Plaque
Biofilm adherence
Maltose
Lactic Acid
Enamel
Dissolution
Amylase
Glucosyl-
transferase

62. Frequency Of Intake
Rather than the amount of carbohydrates taken by an individual, the
number of times affects the caries experience more
Individuals with habit of eating in between meals have higher caries
incidence than individuals who eat sweets with their meals
This occurs because each time a drop in pH occurs that leads to
demineralization

63. WHO Recommendations
Sugar intake of <10 % of total energy intake for prevention of caries
Intake of sugars should be limited to 15-20 kg/person/year (40-55g per day) in
presence of fluoride and <15 kg/person/year (<40g per day ) in absence of
fluorides
Frequency of foods that contain sugar should be limited to maximum four times
a day

64. Role of Lipids
The medium chain fatty acids and their salts have antibacterial properties at low pH
They serve as anionic surfactants and uncouple substrate transport and oxidative
phosphorylation from electron transport in bacteria
Mouthwash containing potassium non-anoate has been studied and found to reduce
the rate of dental caries by reducing the production of acidogenic bacteria

65. Role of Vitamins
VITAMIN A: Vitamin A deficiency shows developmental disturbances in teeth
VITAMIN D:
o Children with rickets have shown higher experience of dental caries
o Deficiency of Vitamin D may contribute to Enamel hypoplasia
o Studies reveal that people with Vitamin D supplements showed lower caries incidence
VITAMIN B: Vitamin B6 (pyridoxine) has been proposed as an anticaries agent as it
selectively alters the microflora in the oral cavity promoting the growth of non-
cariogenic plaque

66. Trace Elements in Diet
Calcium and Phosphorous disturbances in the dietary intake does not affect dental
caries experiences
Nizel and Harris experimented on laboratory rodents to demonstrate that
phosphates were cariostatic. Their effectiveness depends on the anions and cations
with which they are combine according to the food they are fed with
Selenium is observed to be cariogenic, Vandium is observed to be anticariogenic
The fluoride content of diet has been examined by numerous workers. But it was
found that the dietary fluoride was not as important as the fluoride of drinking water
as, dietary fluoride become unavailable after metabolism

67. Anticariogenic & Cariostatic Food
FOOD COMPONENT
FIBROUS PLANT FOODS (eg
Apple)
o Increases salivary flow
o Rich in tannins (anti adhesive property)
BERRIES o Rich in flavanoids (anti adhesive properties)
o Phenols (damage bacterial cell wall)
UNREFINED CEREALS AND NUTS
(eg Peanuts, Groundnuts)
o Polyphenols (Reduces enamel solubility)
CHEESE o Rich in casein, whey, calcium & phosphorus (prevents demineralization)
o Tyramine fatty acids (Increase salivary flow & pH of plaque)
YOGURT o Protein content is high
o Rich in Calcium, phosphorus & casein
GARLIC o Inhibits growth of bacteria- Streptococcus & Bacillus
COFFEE o Rich in polyphenols
BLACK TEA o Rich in polyphenols and fluorides

68. Dietary Studies on Controlled Human
population
Vipeholm Study
Hopewood House study
Turku Sugar Study
Hereditary Fructose Intolerance study
Tristan Da Cunha Study

69. Vipeholm Study (1946-1951)
 Described by Gustaffson et al in 1954,
summarized by Davies in 1955
 It was a five year investigation carried out
in 436 adults from Vipeholm hospital in
Lund, Sweden, an institution for mentally
challenged
 Purpose- It was done to find out the effect
of carbohydrates (amount, frequency and
nature) on dental caries

70. 1)CONTROL GROUP
 60 males
 Low carbs, high fat diet for 2
years followed by addition of
110g sugar to one meal for
next 3 years
 Small, but significant in
caries 4)CARAMEL GROUP
 62 males
 22 caramels daily in 2 portions
between meals in 3rd year, 22
caramels in 4 portions between
meals in 4th year
 In the 5th year caramels replaced
by isocaloric fat
 Fall in caries increment
3)BREAD GROUP
 41 males, 42 females
 345g sweet bread given once
daily with afternoon coffee for
first 2 years, followed by 4
portions of sweet bread with all
4 meals for next 3 years
 Increase in Caries index
2)SUCROSE GROUP
 75 males
 300g sucrose solution at meal
times, which was reduced to
75g in last 2 years
 No significant increase in
caries
5)CHOCOLATE GROUP
 47 males
 300g sucrose solution at meal
times for first 2 years reduced to
110g in the next 2 years &
supplemented by 65g chocolate
milk between meals
 Increase in caries incidence
6)8 TOFFEE GROUP
 40 males
 High fat. Low carbs diet in the first
year, 8 toffees with lunch and
breakfast in the second year and 8
toffees in between meals in the
subsequent years
 Significant increase in the caries
7)24 TOFFEE GROUP
 48 males
 24 toffees between meals in the
third and fourth year followed by
withdrawal of toffees in the fifth
year
 Significant drop in caries index in
the fifth year

71. Conclusion of Vipeholm Study
 Increase in the carbohydrate amount definitely increases the caries activity
 The risk of caries is greater if carbohydrates are retained of tooth surface
 The risk of sugars increasing caries activity is greater if sugar is consumed
between meals
 Upon withdrawal of sugar rich foods, increased caries activity rapidly
disappears
 The increase in the clearance time increases the risk of dental caries
 Physical form of sugars is more important than the amount

72. Hopewood House study
Sullivan and Harris in 1958, Harris in 1963
Dental status of children between 7-14 years of age residing at Hopewood house,
Bowral, South Wales was studied longitudinally for 10 years
Subjects were strictly kept on natural diet, no meat, no refined carbohydrates, with
occasional serving of egg yolk. Meals were supplemented by Vitamins, nuts and
sweetening agents such as honey
At the end of 13 years the children had a mean DMFT of 1.6 compared to the DMFT
of state school which was averaged at 10.7
53 % subjects were caries free compared to only 0.4 % caries free children of state
school

73. Turku Sugar Study
Scheinin and Makinen, 1975 in Turku, Finland
Compared the cariogenicity of sucrose, fructose and xylitol
In the two year feeding study, 125 young adults (average age of 27.6) were divided in
3 groups according to their own preferences:
35- Sucrose group 38- Fructose Group 52- Xylitol
Results: After one year, sucrose and fructose had equal caries incidence with xylitol
individuals showing no caries activity
In the second year, caries activity continued to increase in the sucrose group,
was unchanged in fructose group, whereas xylitol produced almost no caries
Conclusions : Fructose is less cariogenic than sucrose. Xylitol was non cariogenic

74. Hereditary Fructose Intolerance Study
 Newbrun in 1969 tabulated that caries prevalence of 31 persons with HFI and found
that caries prevalence was extremely low
Tristan da Cunha Study
 Study done on the habitants of remote South Atlantic Island before and after refined
carbohydrates and packed food was available
 Results :
YEAR PREVALENCE OF CARIES
1932 0%
1937 0%
1962 50 %
1966 80%

75. Time Factor & Dental Caries

76. Shift in microflora can occur over a fairly short period but a significant amount of time
is needed for demineralization to lead to the development of white spot/ carious
lesions
Acid production does not instantly trigger tooth decay and in early stages
remineralization can restore enamel
The longer the interaction of the dietary sucrose and the cariogenic microbes in the
plaque, the more deleterious is the effect of acid on the dissolution of tooth mineral

77. Systemic Factors & Dental Caries

78. Hereditary
When a family lives in the same locality, caries susceptibility in children is similar to
their parents who had grown up in similar conditions (GV Black, 1899)
Racial tendency for high caries or low caries incidence (sometimes) appears to
follow hereditary pattern but local factors may easily alter this tendency
May be mediated through inheritance of tooth form or structure, which predisposes
to caries immunity or susceptibility

79. Pregnancy & Lactation
Evidence showed increase in caries incidence during or post pregnancy
Studies showed that increase in caries incidence was due to negligence
of oral care

80. Conclusion
Dental caries is a disease with complex etiology and more studies will be
needed to develop strategies against the etiological factors
The presently alarming rate of dental caries is due to the change in diet,
by addition of fermentable sugars
For a developing country like India the assessment of caries risk
individuals is important so that preventive measures can be targeted at
this group

81. References
Cariology : Newburn E. 3rd edition
Shafers: Textbook of oral pathology, 7th edition
Soben Peter: Essentials of Public Health Dentistry, 5th edition

82. Thank You