This document provides an overview of dental caries epidemiology and etiology. It begins with definitions of epidemiology and dental caries. It then covers classification of dental caries, global and Indian scenarios, and studies conducted in Rajasthan, India. Theories of caries etiology are discussed, from early theories to current concepts. Epidemiological and etiologic factors are described, including diet, indices used to measure caries, and the histopathology of dental caries. Trace elements associated with caries prevalence are mentioned. The document concludes with a discussion of dietary studies related to caries.

1. 1

2. PRESENTED BY-
Ira Solanki
(final year BDS)
GUIDED BY-
DR. Anupama Gaur
Dr. Abhishek Sharma
Dr. Sonia Pareek
Dr. Sudhanshu Sanadhya
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3. CONTENTS
 Introduction
 Definition
 Classification
 Global Scenario
 Indian scenario
 Rajasthan studies
 Theories of caries etiology
 Current concept of dental caries
 Epidemiological factors of dental caries
 Etiologic factors
 Dietary studies
 Indices for dental caries
 Histopathology of dental caries
 prevention
 Conclusion
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4. INTRODUCTION
 The word caries is derived from Latin , meaning “rot” or decay. It is similar
to the Greek word “Ker” meaning death.
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5. DEFINITION
 Epidemiology is defined as “ The study of distribution and determinants
of health-related states or events in specified populations , and the
application of this study to the control of health related problems.”
(John M.Last,1988)
 Dental caries is defined as “irreversible microbial disease of the calcified
tissues of the tooth characterised by demineralisation of inorganic portion
and destruction of the organic substances of the tooth”
(Shafer)
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6. CLASSIFICATION OF DENTAL CARIES
OCCURRENCE
INCIPIENT RECURRENT RESIDUAL
SPEED
ACUTE CHRONIC
LOCATION
PIT AND
FISSURE
SMOOTH
SURFACE
ROOT
SURFACE
DIRECTION
FORWAD
CARIES
BACKWARD
CARIES
AGE
EARLY
CHILDHOOD
CARIES
ADOLESCENT
CARIES
SENILE
CARIES
SURFACE
SIMPLE
COMPOUD-
TWO SURFACE
COMPLEX-
MORE THAN
TWO SUFACE
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7. 7
WHO SYSTEM
D1- clinically detected
enamel lesions with
intact (non cavitated)
D2-clinically
detectable cavities
limited to enamel
D3- clinically
detectable cavities in
dentin
D4- lesions extending
into the pulp

8. CARIES IN
PREHISTORIC MAN
 Dental caries may be considered a disease of modern civilization, since
prehistoric man was rarely affected from dental caries.
 There is no evidence of dental caries in the relatively very few teeth
found in skull fragments of our earliest known ancestors,
pithecanthropus.
 Anthropologic studies of Von Lenhossek revealed that the
Dolicocephalic skulls of men from Pre-Neolithic periods (12,000 BC)
did not exhibit dental caries, but skulls from Brachycephalic man of the
Neolithic periods (12,000-3000 BC) contained carious teeth.
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9. GLOBAL SCENARIO
 Dental caries is still a major health problem in most industrialized countries,
affecting 60-90% of school children & vast majority of adults.
 It is most prevalent oral disease in several Asian and Latin American
countries, while it appears to be less common and less severe in most African
countries.
 The WHO records a global DMFT of 1.61 for 12 year old in 2004, a reduction
of 0.13 as compared to a DMFT of 1.74 in the year 2001.
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10. INDIAN SCENARIO
 WHO reported a DMFT score of 3.94 for India in 2003.
 In India, data from the National Oral Health Survey (2002-2003) states
that
AGE
GROUP
CARIES
PREVALENCE
DMFT
12 years 53.8% 1.8
35-44 year 80.2% 5.4
65-74year 85% 14.9
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11. INDIAN STUDIES
AUTHORS YEAR POPULATION FINDINGS
Day & Tandon 1940 756 subjects aged 5-18
yrs. in Lahore
Point prevalence= 94.04
The mean deft= 0.23
Chaudhury &
chawla
1957 2991, 5-16 years old
children in Lucknow
deft= 11.1
DMFT= 1.9
Dutta 1965 1424 children aged 6-121
years in Calcutta
DMFT/deft= 1.17
Mehta 1977 1160 children 5-6 yrs old
in Behrampur, Orissa
Point prevalence= 60.4
Ashwini Rao,
Sequeira SP, Peter S
1999 2902 school children
aged between 5 and 12
years in Karnataka
Caries prevalence 76.9%
Mean DMFT= 0.78
Mean deft= 3.48
Das JK, Sahoo PK,
Bhuyan SK, sahoo
SK
2002 1257 school children
aged 5,8,11&15 years in
Cuttack, Orissa
Point prevalence = 64.3%
Average DMFT = 2.38
Dhar v, jain A, Van
Dyke TE, Kohli A.
2007 1587 school children
aged 5-14 years in
Udaipur
Caries prevalence= 46.75%
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12. RAJASTHAN STUDIES
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 Performed by Pradhuman verma, Kanika Gupta, suruchi jhuneja
 They divided Rajasthan into 5 geographical zone- Shri Ganganagar,
Jaisalmer, Udaipur, Ajmer and Bharatpur.
 Examined 1125 adult subjects aged 25 to 44 years.
 RESULTS

13. FEW STUDIES IN OTHER RAJASTAN CITIES
13
Authors Area involved Population Prevalence
Navin anand,
harsh vardan
dubey & Rahul
gupta
Bharatpur city 12-15 years old
1400 children (700
private & 700
govt.)
In govt. school
children- 53%
Private school
children- 47%
Vikram khare, Ajit
koshy, p J rani,
Anil agarwal
Udaipur city 883 orphanages In primary teeth-
49.6%
In permanent
teeth – 41%

14. THEORIES OF CARIES ETIOLOGY
I.EARLY THEORIES OF CARIES FORMATION-
A. THE LEGEND OF THE WORM- In past, dental caries was thought to
be caused by living worms inside the tooth structure.
II. ENDOGENOUS THEORIES-
A. HOMORAL THEORY- According to Galen An imbalance between the
humors(blood, phlegm, black bile and yellow bile) of body caused tooth
decay.
B. VITAL THEORY- was advanced towards the end of the 18th century,
Tooth decay originated from within the tooth itself, like a bone
gangrene.
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15. III.EXOGENOUS THEORIES
A. CHEMICAL (ACID) THEORY- On the basis of findings of Robertson
(1835), this theory proposed that tooth decay was caused by the
fermentation of food particles around the teeth.
B. PARASITIC (SEPTIC) THEORY-
 By Antoni Von Leeuwenhock (1632-1723)- that microorganisms were
associated with the carious process.
 In 1843,Erdl- filamentous parasite in the membrane removed from the
teeth.
 In 1847,Ficinus- observed a filamentous organisms in the enamel cuticle &
in carious lesions.
 In1954, Dubos- microorganisms can have toxic effects on tissue.
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16. C. ACIDOGENIC THEORY- Proposed by W.D.Miller in 1890. According to
this theory-
• Sugar(carbohydrates) + bacteria = makes acid (mainly lactic acid)
• Acid attacks the healthy tooth & make it carious.
 STEPHAN CURVE: within 2-4 minutes of rinsing with solution of glucose
or sucrose, plaque pH is reduced from about 6.5-5 and gradually returns
to original value within approx. 40 min. this is graphically plotted as the
“Stephan's curve”
16

17. D. PROTEOLYSIS THEORY- Gottileb(1947) Proteolytic enzyme liberated by
cariogenic bacteria  destruction of the organic matrix  detachment of
inorganic crystals from one another  collapse of whole structure 
CAVITATION
E. PROTEOLYSIS CHELATION THEORY- originated by Schatz & Martin in
1955. Product of bacterial action + enamel/dentin/salivary constituents 
chelates with calcium. Chelate can be formed at neutral/alkaline pH
Demineralization could arise without acid formation.
IV. OTHER THEORIES OF CARIES ETIOLOGY-
A. AUTOIMMUNE THEORY- Burch & Jackson in 1966 suggested that
genes, partly inherited and partly mutational, determine whether a site on a
tooth is at risk.
17

18. CURRENT CONCEPT OF DENTAL
CARIES
TOOTH
FLORASUBSTRATE
CARIOUS
Flow rate pH
Time
18

19. EPIDEMIOLOGICAL FACTORS OF DENTAL
CARIES
AGENT HOST
ENVIRONMENT
Geographic variation
Fluoride
Trace elements
Urbanization
Social factors
19

20. TEETH POSITION-
Teeth which are rotated, malalinged or out of position may be
difficult to clean and tends to favour accumulation of food and
debris.
This in sesceptible persons, would be sufficient to cause caries
in tooth
Alteration of tooth structure
by disturbance in formation or
in calcification
MORPHOLOGY-
Presence of deep, narrow occlusal
fissures or buccal & lingual pits
TEETH
20

21. SALIVA
 The fact that teeth are in constant contact with and bathed in saliva
would suggest that this fact could profoundly influence the state of
oral health of a person.
 One of the most important function of saliva is its role in removal of
micro flora & food debris from the mouth.
Quantity of saliva- normal: 700-800ml/day
Salivary gland aplasia and xerostomia in which salivary flow may be
entirely lacking results in rampant caries
Viscosity of saliva: high caries incidence is associated with thick
Mucinous saliva
Antibacterial properties of saliva: Lactoperoxidase :Lactoferrin
: Lysozyme :IgA
21

22.  Other salivary components with protective function-
Proline rich proteins- mucin and glycoprotein.
 Salivary pH- determined mainly by the bicarbonate
concentration
Salivary pH increases with flow rate
Salivary buffers increase pH of saliva in the oral cavity
22

23. HOST FACTORS
 RACE- Africa & India, had high degree of caries resistance than
“Europeans”.
The global differences are the result of environment.
 AGE- previously caries was considered ‘essentially a
disease of childhood’. Caries increases progressively
by age and the increase is more slowly during adult years.
 SEX- caries prevalence female > male
root caries prevalence males > females
 FAMILIAL HEREDITARY- “good or bad teeth run in
family” due to bacterial transmission, dietary
and oral hygiene habits genetic factors
23

24.  EMOTIONAL DISTURBANCE- period of stress have been
associated with high caries incidence,
Due to decreased salivary flow.
 DIET AND NUTRITION- physical nature of diet
- carbohydrates content of diet
- vitamin content in diet
 SOCIOECONOMIC STATUS- SES ∞ 1
status of many diseases
caries is nowadays, considered to be a “disease of poverty” or
“social behavioural disease”.
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25. AGENT FACTORS
 MICROFLORA- microorganisms are a prerequisite for caries
initiation.
mainly the bacteria are- Streptococcus Mutans ,
Strep.sanguis, Strep.Salivaius, Strep.milleri, lactobacillus,
Actinomyces viscous and Actinomyces naeslundii (root caries)
 DIET- It is taken as under host, agent and environment.
food and beverages taken by individual serve as substrates for
fermentation by the plaque micro flora.
25

26. TRACE ELEMENTS AND DENTAL
CARIES
26
 Caries low prevalence was
associated with- raising conc.
Of Ca, Mg and Mo
 High prevalence- Cu, Fe, Mn
 Strong inverse relationship-
Sr, Ba, K, Mg, Ca and Li
.

27. DIETARY STUDIES ON CONTROL HUMAN
POPULATIONS
I.VIPEHOLM STUDY – described by Gustaffson et al in 1954,
summarized by Davies in 1955.
Mental institution at the Vipeholm hospital near Lund, Sweden.
 Purpose- to determine the effects of frequency and quantity of sugar
intake on the formation of caries
 Conclusion- physical form of carbohydrates(stickiness, oral clearance time
frequency of intake) much more important in cariogenicity than the total
amount.
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28. Increase in caries activity due to-
28

29. II.HOPEWOOD HOUSE STUDY -
 Strictly institutional diet- occasional serving of egg yolk
- diet-vegetable in nature and largely raw.
- the absence of meat and a rigid restriction of refined carbohydrates.
- meal supplemented by vitamin concentrates and occasional serving of nuts
and honey.
- fluoride content of water and food was insignificant and no tea was
consumed.
7-14 yrs.
age
children
Hope wood
house, Bowral,
New South
Wales
Australia
Longitudinally
studied for 10
years
29

30. Results of hopewood House study-
 At the end of 10 years  13 years old had DMFT mean 1.6/child
 General population  13 years old mean DMFT 10.7
 53% children at the hope wood house  caries free
 0.4% children of state children  caries free
 Hope wood house children’s oral hygiene was poor, calculus + gingivitis
more prevalent in 75% of children.
 Conclusion- In institutionalized children at least dental caries can be
reduced by carbohydrate restricted diet without the beneficial effects
of fluoride and in the presence of unfavorable oral hygiene.
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31. III.TURKU SUGAR STUDIES-
Aim: To study the effects of the chronic consumption of sucrose, fructose and
xylitol on dental caries.
2 years study of 125 young adults
125 young adults 
Sucrose group – 35 people
Fructose group – 38 people
Xylitol group – 52 people
Sucrose & fructose had equal cariogenicity whereas xylitol produced
almost no caries
Caries continued to increase in the sucrose group, remained unchanged
in the fructose group and produced almost no change in xylitol group
After 1
year
By the
2nd year
31

32. IV.HEREDITARY FRUCTOSE INTOLERANCE (HFI)-
Newbrun in 1969 tabulated the caries prevalence of 31 persons with HFI
and found that the dental caries prevalence was extremely low.
32

33. INDICES FOR DENTAL CARIES
33
MOST COMMONLY
USED
DMFT
DMFS
def
dmf
OTHER DENTAL
CARIES INDICES
STONE’S INDEX
1949
CARIES SEVERITY
INDEX
1960
CZECHOSLOVAKI
AN CARIES INDEX
1956
CARIES
SUSCEPTIBILITY
TEST 1961
D-M-F SURFACE
PERCENTAGE
INDEX 1963
MOLLER’S INDEX
1966

34. HISTOPATHOLOGY OF DENTAL
CARIES
• Deepest zone lies at the advancing front of enamel lesion
• More porous than normal enamel
• Pores are larger than normal enamel. Pore volume 1%
• Appears structureless
TRANSLLUCENT
ZONE
• Located just superficial to the translucent zone.
• Darkness is due to the excessive demineralization of the enamel.
• Rapidly advancing caries narrower zone.
• Slowly advancing zone wider
• Pore volume 2-4% . This zone reveals degree of remineralization of
carious lesion
DARK
ZONE
• Zone is situated between the dark zone & surface layer of enamel
• Represents area of greatest demineralization.
• Pore volume 5-6%
BODY OF LESION
• When examined by the polarizing light appears relatively unaffected,
it may be due to the surface remineralization by the salivary mineral
ions
SURFACE ZONE
ZONES OF ENAMEL CARIES 34

35. Normal
zone
• Innermost layer of carious dentin. Dentinal tubules appears normal.
• No crystals in the lumen of the tubules. No bacteria in the tubules
• Intertubular dentin has normal cross banded collagen.
• Fatty degeneration of the Tome’s process
Sub
transpar
ent
zone
• Deposition of very fine crystal structures within the dentinal tubules
• Superficial layer show area of demineralization & damage of odontogenic process
• No bacteria in the tubules; dentin is capable of remineralization.
Transpar
ent zone
• Outermost zone
• Characterized by complete destruction of dentinal tubules.
• In this the entire dentinal structure become destroyed & cavitation begins from dntino enamel
junction.
Turbid
zone
• Marked by widening & distortion of dentinal tubules.
• Microorganisms are found
• Denaturation of collage fibers also takes place.
• Zone cannot undergoes self repair or remineralization.
Infected
zone
• Zone appears as transparent because of decalcification of dentin
• It is softer than normal dentin ; no bacteria in the tubules.
• This zone is capable of repair & remineralization
ZONES OF DENTINAL CARIES
35

36. 36
ENAMEL
CARIES
DENTINAL
CARIES

37. PREVENTION
37

38. CONCLUSION
 Dental caries is still a considerable burden largely in developing world
and to a lesser extent in developed world.
 Nevertheless continuous and significant presence of dental caries in
population & with its prime determinants is operating in relatively large
number of populations.
 Further exploration using epidemiology as a tool in our country will
certainly throw a light in understanding and management of dental
caries.
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39. REFERENCES
 Essential of preventive and community dentistry
5th edition - Soben peter
 A textbook of public health dentistry- C M marya
 Textbook of preventive and community dentistry-
S S Hiremath
 Textbook of Oralpathology Shafer
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