3. Dental caries is an irreversible microbial disease of the calcified
tissues of teeth ,characterized by demineralization of inorganic
portion & destruction of organic substance of the tooth, which
often leads to cavitation.
The word caries is derived from the Latin word meaning ‘rot ‘ or
‘decay’.
4. Dentinal caries may be considered as a disease of modern
civilization, since prehistoric man rarely suffered from this form
of tooth destruction.
Arthropologic studies of Von Lenhossek revealed that
dolichocephalic skulls of men from pre –neolithic period (1200
B C) did not exhibit caries, but skulls from brachycephalic man
of neolithic period (1200 -3000 BC) contained carious tooth.
5. •Isolated population that had not acquired dietary habits of modern ,
industrialized man, retained a relative freedom from caries.
•In East Greenland native prevailed everywhere except at trading
ports where imported food was available . Pederson (1938) reported
that 4.3% males living in isolated settlement of Angmagssalik had
caries , as compared to 43.2% of comparable eskimo population living
at a trading ports.
•On western parts of Greenland ,where contact with European
technology was greatest, the percentage of male eskimos with caries
was 31.8% .
6. WHO records a global DMFT of 1.61 for 12 year old in 2004,a
reduction of .13% as compared to a DMFT of 1.7 in year 2001
WHO reported a DMFT score of 3.94 for India bin 2003
In India , data from the National Oral Health Survey (2002 -
2003) states that in children aged 12 years old the caries
prevalence was 53.8% & the mean DMFT was 1.8 , where it
was 80.2 & 5.4 in 35 -44 year age of group.In 65-74 yr age
group , the prevalence was 85% & mean DMFT was 14.9.
7. D the mean number of decayed teeth with untreated carious lesions
M the mean number of teeth which have been extracted and are
therefore missing
F the mean number of filled teeth
DMF(T) to denote decayed, missing, and filled teeth
DMF(S) to denote decayed, missing, and filled surfaces in permanent
teeth
dmf(t) dmf(s) similar indices for the primary dentition
8.
9. A )EARLY THEORIES
Legend of worms
The earliest reference to tooth decay is probably from the
ancient Sumerian text known as ‘legend of worms’.
It was discovered on a clay tablet , excavated from ancient city
within Mesopotamian area, which dates about 5000B.C.
The idea that caries is caused by worms was universal as it is
evident from the writings of homer who made a reference to
worms as the cause of tooth ache.
10. HUMORAL THEORY
Advocated by Greek physicians , who proposed that caries is
caused by internal actions of acids & corroding humors & an
imbalance in these humors resulted in disease.
The four elemental humors are blood, phlegm, black & yellow
bile.
VITAL THEORY
This theory was advanced towards end of 18th century which
postulated that tooth decay originated like bone gangrene , from
within tooth itself.
11. CHEMICAL (ACID ) THEORY
Robertson (1835) proposed that decay was caused by acid
formed by fermentation of food particles around teeth.
PARASITIC THEORY
In 1843, Erdl described filamentous parasites in the membrane
remain from teeth.
Findus in 1847 , also observed filamentous organism in enamel
cuticle& in carious lesion.
Dubos 1945 postulated that microorganism can have toxic
effect on tissue.
12. It was put forwarded by American Scientist W D Miller, states
that caries is caused by acid produced by microorganism.
He hypothesized that dental decay is chemoparisitic process;
consisting of 2 stages:
a) Decalcification of enamel & dentin as a primary step.
b) Followed by dissolution of softened residue.
13. Significant observation of W D Miller
Oral microorganism
Dietary CHO
Acid
Tooth enamel
Dental caries
14. Demerits
Unable to explain the predilection of specific sites.
Does not explain why some population are caries free.
Does not explain the phenomenon of arrested caries.
15.
16. Stephan showed that within 24 mnts of rinsing with a solution
of glucose / sucrose, plaque pH is reduced from about 6.5 – 5 &
gradually returns to the original value within approximately
40 mnts.
This is known as Stephan's curve.
17. In 1947 Gottlieb Organic/protein elements of tooth are initial
pathway of invasion of microorganism.
Enamel lamellae as pathway for microorganism in progress of
caries.
18. PROTEOLYSIS CHELATION THEORY
In 1955 Schatz and Martin proposes that some of the products
of bacterial action on enamel ,dentin and food and salivary
constituents can form chelates with calcium .A chelate is a
complex between an ion and two or more groups of complexing
compound. Since chelates can be formed at neutral or alkaline
PH the theory suggested that demineralization of the enamel
could arise without acid formation.
19. AUTO IMMUNE THEORY
In this theory, it is suggested that 'forbidden clones' of
lymphocytes attack target cells (odontoblasts) rendering the
tooth vulnerable to caries attack.
20. According to anatomical site of the lesion
• Pit and fissure caries
• Smooth surface caries
buccal and lingual surface caries
proximal surface
Based on severity and progression
• Rampant caries
• Nursing caries
• Radiation caries
21. Based on part of tooth structure involved
• Enamel caries
incipient caries
linear enamel caries(odontoclasia)
• Dentinal caries
• Cemental caries
based on activity
• Primary caries
• Secondary caries
• Residual caries
• Arrested caries
22.
23. ETIOLOGIC FACTORS IN DENTAL
CARIES
microorganisms
Host
&
tooth
substrate
time
caries
The four circle diagrammatically
represent the parameters involved in the
carious process. All four factors must be
acting concurrently (overlapping of the
circles) for caries to occur.
24. Dental caries is a multifactorial disease in which there is an
interaction between three principle factors.
a) A susceptible host tissue
b) Micro flora with a cariogenic potential
c) A suitable local substrate
26. TOOTH
The morphologic characteristics of tooth have been suggested as
influencing the initiation of dental caries
Presence of deep,narrow,occlusal fissures or buccal and lingual
pits tend to trap food, bacteria or debris
Tooth position may play a role in dental caries, teeth which are
malaligned,out of position, rotated may be difficult to cleanse
and tends to favor to accumulation of food and debris.
27. SALIVA
It plays role in increasing the cariogenic effect on the teeth and
as well it has the buffering action.
Saliva has a cleansing effect also.
A number of enzymes are isolated from the saliva, Ptyalin or
Amylase is responsible for degradation of starch.
28. pH of saliva is determined mainly by the bicarbonate
concentration.
pH increases with flow rate.
Salivary components contributing to the ability of saliva to
neutralize acid are salivary phosphate, salivary
proteins, ammonia, urea.
29. Viscosity of saliva is due to the mucin content.
Some workers found out that high caries incidence is associated
with a thick mucinous saliva.
In addition it has antibacterial properties & has
lactoperoxidases, lysozyme, lactiferrin, & igA.
30. The quantity of saliva secreted normally is 700-800 ml/day.
The quantity of saliva may influence caries incidence as is
especially evident in cases of salivary hypoplasia & in
xerostomia.
32. B.MICROFLORA WITH CARIOGENIC POTENTIAL
Role of microorganisms in caries
Microorganisms are a prerequisite for caries initiation
The ability to produce acid is a prerequisite for caries
induction, but not all acidogenic organisms are cariogenic.
Mainly the bacteria are Streptococcus Mutans,and
streptococcus sobrinus collectively known mutans
streptococci(MS)
35. C. A SUITABLE LOCAL SUBSTRATE-DIET
DIET is defined as the types and amounts of food eaten daily by
an individual
NUTRITION is defined as the sum of the processes by which an
individual takes in and utilizes food.
Physical properties of food and cariogenicity
The physical properties of food may be significant by
affecting food retention ,food clearance ,solubility and oral
hygiene.
36. Physical nature of diet
The diet of primitive man consisted of a great deal of
roughage ,which cleanses the teeth of adherent debris during
mastication.in the modern diet soft refined food tends to cling
tenaciously to the teeth and are not removed because of lack of
roughage.
Carbohydrate content of diet
Fermentable carbohydrates are on of the most important
cause of causing dental caries.
Increase in the intake of refined carbohydrates are directly
proportional in causing the dental caries
37. Vitamin content of diet
Vit. A &D is necessary for the development of the teeth.
Vit K has the capacity of enzyme inhibiting activity in the
carbohydrate degradation cycle.
Vit B complex ,Vit B6 has been proposed as an anticaries agent
Calcium and phosphorous dietary intake
Disturbance in calcium and phosphorous metabolism during
the period of tooth formation may result in severe enamel
hypoplasia and defects of the dentin.
Fluoride content of diet
some researchers believe that topical fluorides are more
important compared to systemic fluoride.
38. 1. VIPEHOLM STUDY
By Gustaffson et al in 1954, & summarized by Davies in
1955.
Purpose of study ;
To find out
1) Does an increase in carbohydrate intake cause an increase
in caries?
2) Does an increase in carbohydrate intake produce a decrease
in caries?
39. The institutional diet was nutritious , but contained little
sugar, with no provision for between meal snacks.
The experimental design divided inmates into 1 control & 6
experimental groups.
1) A control group
2) A sucrose group
3) A bread group
4) A chocolate group
5) A caramel group
6) An 8 toffee group
7) A 24 toffee group
40. 1. An increase in carbohydrate diet definitely increase the caries
activity.
2. The risk of caries is greater if the sugar is consumed in the form that
will retained on the surfaces of teeth.
3. The risk of sugar increasing caries activity is greatest, if the sugar is
consumed between meals.
4. Upon the withdrawal of the sugar rich foods , the increased caries
activity disappears.
41. 1. The groups were made up from the patients in individual
wards with no possibility of matching the age or initial caries
status.
2. The patient were mentally challenged & did not always
follow the instructions correctly.
3. The dietary regimes of the various groups were changed in
consistent pattern.
4. It is considered unethical to alter diet experimentally in
directions likely to increase disease.
42. By Sullivan & Haris Harris -1963
The dental status of children between 7 to 14 yrs of age residing
at hopewood house, New south wales was studied
longitudinally for 10 yrs.
All lived in a strict natural diet , with exception of occasional
serving of egg yolk, was entirely vegetable in nature & largely
raw.
At the end ot ten year, 13 year old children had a mean DMFT
per child of 1.6.The corresponding general was 10.7
43. The study was carried out by Turku , Finland.
Aim of the study
To compare the cariogenicity of sucrose, fructose & xylitol
Findings of the study
After 1 year,
Sucrose & fructose had equal carigenicity whereas xylitol
produced almost no caries
44. By second year;
Caries had continued to increase in the sucrose group but remain
unchanged in the fructose, whereas xylitol produced almost no
caries
Xylitol was non cariogenic.
45. It is caused by the remarkably reduced levels of hepatic
fructose- 1 – phosphate aldolase, which splits fructose -1-
phosphate into two three-carbon fragments to be further
metabolized.
The ingestion of food containing sucrose / fructose causes
symptoms of nausea, vomiting, malaise ,tremor & even coma
due to fructosemia.
46. 1. Sugar in solutions produces significantly less caries than solid
sugar.
2. Coarse particles of sugar are less cariogenic than fine
particles.
3. Post eruptive maturation of teeth is greatly reduced in a high
sugar environment.
4. Addition of fluoride to the diet / drinking water causes
reduction of caries.
5. The sugar alcohols, xylitol & mannitol have no ability to
initiate or support caries.
6. Phosphate addition of diet result in major reduction of caries.
47.
48. The approach to preventing the development of dental caries is
to establish & maintain good oral hygiene, optimize systemic &
eliminate prolonged exposure to simple sugars in the diet.
Primary preventive measures are aimed at reducing the
occurrence of new cases of caries in population.
Secondary prevention aims at reducing the prevalence of caries.
Tertiary prevention involves a treatment phase aimed at
maximum limitation of disability & maximum rehabilitation.
49. Levels of
prevention
PRIMARY SECONDARY TERTIARY
Preventive services Health
promotion
Specific
protection
Early diagnosis &
prompt treatment
Disability
limitation
Rehabilitation
Services provided by
individual
-Diet planning
-Demand for
preventive
services
-fluoride
application
-ingestion of
flrdated water
-oral hygiene
practice
Self examination &
refferl utilization of
dental services.
Utilization of
dental services.
Utilization of
dental services
Services provided by
the community
-Dental health
education
programme
-Promotion of
research efforts.
_Community
school water
fluoridation
-school fluoride
mouth rinse
-school sealant
prgm
Screening &
Refferl
Provision of dental
services
Provision of
dental services
Provision of
dental services
Services provided by -patient
education
-plaque control
-Diet counseling
-Topical applctn
of fluoride.
-pit & fissure
sealant
-caries activity
test
-prompt treatment of
incipient lesion
-simple restorative
dentistry.
-pulp capping
Complex
restorative
dentistry
-Pulpotomy
-RCT
-Extraction
-Removable &
fixed
prosthodontics.
-Minor tooth
treatment .
-Implants.
50.
51. Vaccine is an immuno – biological substance designed to
produce specific protection against a given disease.
The concept of vaccination against dental caries was
strengthened because of;
The transmissible & infectious nature of dental caries.
The discovery & understanding of the secretory immune system.
52. It entails the introduction of a foreign molecule into the body,
which causes the body itself to generate immunity against the
target.
This immunity comes frum the T cell & the B cellwith their
antibodies.
Artificial active immunization is a process where the microbe
are injected into the person so that they develop antibodies &
become immune.
53. It is a process whereby pre-made elements of the immune
system, such as antibodies are transferred to a person, & the
body doesn’t have to create these elements itself.
It can be naturally acquired when antibodies are being
transferred from mother to fetus during pregnancy.
54.
55. Risk is defined as the probability that some harmful event will
occur.
The importance of properly predicting the occurrence of lesion is
obvious as targeted preventive actions can be directed to those
persons having a high risk for caries & scares resources can be
properly utilized.
56. Assessment is highly indicated in populations where a large
portion is caries –free, but some individual are still highly caries
active.
Where resources are available to take care of these targeted
persons.
57. There are several factors & charectistics that accompany the
development of an increased number of carious lesions, which
are helpful in caries risk assessment.
Risk Indicators
1. They are circumstances , which may indicate increased caries
risk,
58. Examples :
• Socially deprived, no work, bad economy.
• Low knowledge, low educational of parents.
• No regular dental check up.
2. Factors related to general health which may indicate increased
caries risk,
Examples :
• General diseases
• Various handicaps
59. 3. Epidemiological factors, which may indicate high caries risk,
Examples :
• Living in high DMF country
• Living in high DMF area
• Member of high DMF family
60. 4 . Clinical findings which may indicate increased caries risk;
Example ;
• Newly erupted teeth
• Exposed root surfaces
• Crowded teeth
61. These factor may, depending on the dose & duration, indicate
high or lower risk for caries.
For eg: a large amount of plaque indicates high risk only if
present for a longer period of time.
62.
63. It is a graphic model proposed by Bratthall D (1996)
It illustrates the interaction b/w various factors such as
diet, bacteria & host susceptibility
This illustrate the fact that caries can be controlled by several
means.
64. ‘Caries risk’ is the term which indicate how much
demineralization of cavities will occur in the future.
The risk is expressed as ‘ % chance to avoid cavities’
A low % indicate high caries risk.
High % indicate low caries risk.
In addition to diet , bacteria & susceptibility a fourth factor
circumstances is also included.
Chance to avoid of caries must be b/w 0 – 100%.it cannot be –
ve or more than 100%.
65.
66. Advantage;
1. Affordable
2. User friendly
3. Easy to understand
4. Tool to motivate patient
5. Serve as a support for clinical discussion when selecting
preventive strategies for patient.
67. Since dental caries is a highly prevalent disease control of caries is a
concern of all the people.
For a developing country like India, the focus should be on assessing
the caries risk & identifying those individuals at high risk to develop
caries.
Preventive measures can then be targeted at this group thereby not
only reducing the economic burden of the restorative care but also
eliminating pain & improving the overall quality of life.
