EPIDEMIOLOGY OF Dental Caries.pptx

EPIDEMIOLOGY OF DENTAL
CARIES
DR ASWINI SEKAR

INTRODUCTION
 Dental caries is an infectious microbiological disease that results in localized
dissolution and destruction of calcified structures of the teeth.
 The word caries is derived from Latin word meaning “rot” or decay.
Bacterial enzyme+Fermentable carbohydrate=Acid
Acid+Enamel=Dental caries

EPIDEMIOLOGY
 Dental caries may be considered as a disease of modern civilization, since
prehistoric man was rarely affected from dental caries.
 Anthropologic studies of Von Lenhossek revealed that the dolichocephalic skulls
of men from Pre-Neolithic periods (12,000BC) did not exhibit dental caries, but
brachycephalic skulls of the neolithic period (12,000-30,000 BC) contained
carious teeth.

CURRENT TRENDS IN CARIES EXPERIENCE
 Dental caries is still a major health problem in most industrialized countries,
affecting 60-90% of school children & vast majority of adults. . It is the 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.
 In India DMFT scores for 12, 35-44 and 65-74 year age group are 1.8, 5.4 and 14.9
respectively.

 Various studies conducted in different countries at different time periods have
given evidence that a substantial decrease in caries prevalence in the last decade
has been found among western countries whereas in case of developing and
underdeveloped countries, prevalence of caries seems to be increasing.

Theories of Caries Etiology
The etiology of dental caries is a complex problem. There is no universally accepted
opinion of the etiology of dental caries.
 A. Early theories of caries:
The legend of Worm:
In the past, dental caries was thought to be caused by living worms inside the tooth
structure.(Ancient Sumerian text)
 B. Endogenous theories:
Humoral theory
According to which an imbalance between the humors of body caused tooth decay.

Vital theory:
According to which tooth decay originated from within the tooth itself, like a bone
gangrene.
 C . Exogenous Theories:
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.
Theories of Caries Etiology

 Parasitic (septic) theory:
 This was the first theory that related microorganisms with caries on a causative
basis (by ERDLE, 1843). Accordingly, it was proposed that even though caries
starts purely as a chemical process but microorganisms continued the
disintegration in both enamel and dentin.

 Miller's chemico-parasitic theory(the acidogenic theory):
 Proposed by W.D Miller(1890).
 This theory is a blend of both chemical and parasitic theory.

 Hence Miller advocated an essential role of 3 factors in the caries process: the oral
microorganisms, the carbohydrate substrate, and the acid.
 Even though, at that time, this theory couldn’t explain 1) predilection of specific
sites on a tooth 2) initiation of smooth surface caries 3) why some populations are
caries free 4) the phenomenon of arrested caries. This theory is still considered as
the backbone of current knowledge and understanding of the etiology of dental
caries.

 Stephan curve:
2-4 minutes of rinsing with a solution of glucose or sucrose
pH drops about 6.5-5 and returns to origal within 40minutes.

 The Proteolytic theory:
 By Gottlieb and Gottlieb. According to this theory, the organic or protein elements
of tooth (not the inorganic constituents of enamel ) are the initial pathways of
invasion by microorganisms; And, caries is essentially a proteolytic process , in
which the microorganisms invade the organic pathways and destroy them while
advancing through them by forming acids.

 Drawbacks of this theory 1)It couldn’t provide sufficient evidences to support the
claim that the initial attack on enamel is proteolytic; 2)also experimental studies
have shown the occurrence of caries even in the absence of proteolytic
microorganisms However , this theory is still helpful in explaining the
progression of a more advanced carious lesion.

 Proteolysis Chelation theory:
 This theory proposed by Schatz et al. implies a simultaneous microbial
degradation of the organic components (hence, proteolysis), and the dissolution of
the minerals of the tooth by the process of chelation.
 According to the proteolytic-chelation theory, dental caries results from an
initial bacterial and enzymatic proteolytic action on the organic matter of enamel
without acid production.

Epidemiological factors of Dental Caries

TOOTH
 Presence of deep, narrow, occlusal fissures or
buccal and lingual pits.
 Alteration of tooth structure by disturbance
in formation or in calcification
 Teeth which are malaligned, rotated or out of
position may be difficult to clean and tends to
favor the accumulation of food and debris .

OTHER HOST FACTORS
 1) Saliva Composition pH Quantity Viscosity Antibacterial
factors.
 2) Race and ethnic groups
 3) Age
 4) Gender
 5) Hereditary
 6) Socio-economic Status

SALIVA
 The fact that teeth are in constant contact with and bathed in saliva would suggest
that this factor 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

SALIVA..
 SALIVARY pH
Determined mainly by the Bicarbonate concentration Salivary
pH increases with flow rate

SALIVA..
Quantity of saliva
 Normal: 700-800 ml/day salivary gland Aplasia and Xerostomia where
salivary flow is reduced results in rampant dental caries.
Viscosity
 High Caries Incidence Is Associated With Thick Mucinous Saliva.

SALIVA..
 ANTI-MICROBIAL PROPERTIES
• Lactoperoxidase
• Lysozyme
• Lactoferrin
• IgA
Proline rich proteins- mucin and glycoprotein

AGE
 Maximum caries activity is noticed among children and later
root caries prevalence will be more in elderly people.

GENDER
 Many studies have shown higher caries experience in girls than boys during
childhood period & also later at adolescence period. Increased susceptibility
may be due to: 1. Early eruption of teeth in females 2. Morphological
difference in teeth 3. Increased fondness towards sweets among girls 4. Due to
hormonal changes Root caries is more prevalent in males

RACE
 Non-European races such as African and Asian enjoyed freedom from caries
than Europeans. Moreover, certain groups, once thought to be resistant to caries
became susceptible when they moved area with different cultural and dietary
pattern.

SOCIO-ECONOMIC STATUS
 It is noticed that low SES groups have more number of decayed & missing teeth
but less number of filled teeth and vice versa in high SES group.
 Good economic status and social pressure in the direction of good appearances
are both strong factors in creating demand for dental treatment.

FAMILIAL HEREDITY
 “ GOOD OR BAD TEETH RUN IN THE FAMILY”
 Family studies have shown that offspring have the same score as parents and
this happens due to transmission of dietary and oral hygiene habits through
family.
 Mansbridge found a greater resemblance between identical twins or fraternal
twins than unrelated pair of children

MICROFLORA WITH A CARIOGENIC
POTENTIAL
 Mutans Streptococcus – initiation of smooth surface caries
 Lactobacillus - Initiation of pit and fissure caries, progression of smooth
surface caries
 Actinomyces - Root caries

 Role of dental plaque:
Dental plaque is a complex, metabolically interconnected, highly organized,
bacterial ecosystem. It is a structure of vital significance of the carious lesion. An
important component of dental plaque is acquired pellicle, which forms just prior
to or with bacterial colonization and may facilitate plaque formation.

SUITABLE LOCAL SUBTRATE-DIET
 The role of diet and nutritional factors deserves special consideration. The
physical properties of food may be significant by affecting food retention, food
clearance, solubility and oral hygiene

Environment
 All that which is external to the individual human host living or non-living and
with which he is in constant interaction.
 Ultraviolet light from the sun is known for its ability to promote synthesis of
vitamin D in skin tissue and thus reduce caries incidence
 lower the temperature, higher the caries prevalence.
 Rainfall which leaches minerals from the soil increasing the caries incidence.

Classic Dietary Studies
 VIPEHOLM STUDY Gustaffson et al 1954
 5year investigation
 436 adult inmates in a mental institution at the Vipeholm
hospital near Sweden.
 The institutional diet was nutritious but contained little sugar
with no provision for between meal snacks.

VIPEHOLM STUDY…
 An increase in carbohydrate mainly sugar definitely increase
caries activity. Risk of caries is greater if the sugar is sticky in
nature. The caries activity is greatest, if the sugar is
consumed between meals A high concentration of sugar in
solution and its prolonged retention on tooth surfaces leads to
increase caries activity

HOPEWOOD HOUSE STUDY (SULLIVAN-
1958, HARRIS –1963)
 3 -14 years age children
 Hope wood house, Bowral , New south WalesAustralia, 10 years. 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 carbohydrate
The meals were supplemented by vitamin concentrates and an occasional
serving of nuts and honey. The fluoride content of water and food was
insignificant and no tea was consumed.

 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 effe
HOPEWOOD HOUSE STUDY…

TURKU SUGAR STUDIES (Scheinin,
Makinen et al 1975)
 Finland studies
 Aim : To Study the effects of the chronic consumption of sucrose, fructose and
xylitol on dental caries. 2 year study of 125 young adults 125 young adults
Sucrose group – 35 people Fructose group – 38 people Xylitol group – 52
people

TURKU SUGAR STUDIES
 After 2 years Sucrose group increased Cariogenicity Fructose group
fructose as cariogenic as sucrose for first 1 year, less cariogenic at the end of 24
months. Xylitol group dramatic reduction in the incidence of dental caries
after 2 years Frequent chewing of xylitol gum in between meals produced anti-
cariogenic effect.

z
CARIES RISK ASSESSMENT
 Risk is defined as “the probability that some harmful event will occur”.
 To predict if new carious lesions will develop, or if early lesions will continue to
grow, is to assess the caries risk.

z
CARIES RISK ASSESSMENT..
 1. INDICATIONS FOR CARIES RISK ASSESSMENT –
 In populations where large portion is caries free but some individuals are still
highly caries active.
 Where resources are available to take care of these targeted persons.

z
 2. HOW TO SELECT RISK GROUP OR RISK INDIVIDUALS?
 Evaluation of risk indicators (Indirect relation) - Socially deprived, no work,
bad economy - Low knowledge, low education of parents - No regular dental
checkup - General health :diseases & handicapped - Epidemiological factors :
high past caries experience, intake of cariogenic food - Clinical findings which
indicate increased caries risk

z
 Evaluation of biochemical factors (direct relation) Attack or Defense
mechanisms - Salivary protective system and fluoride exposure - Dose and
duration of microbial plaque High risk – Large amount of plaque on teeth Low
risk – Few bacteria (good oral hygiene)

z
CARIOGRAM
 It is a model proposed by Bratthall D(1996) to illustrate the
interactions between bacteria, diet and host response.
 The process of making the evaluation is termed “cariography”
 Mainly to know the “chance to avoid new caries” in the near
future.

z
CARIOGRAM..
 Illstrates the interaction of caries related factors
 Illustrates the chance to avoid caries
 Expresses caries risk graphically’recommends targeted
preventive actions.
 Can be used in the clinic.
 Also can be used as an educational program.

z
CARIOGRAM..
 FIVE SECTORS OF CARIOGRAM - GREEN SECTOR: actual
chance to avoid new caries. - DARK BLUE SECTOR: diet
content + diet frequency - RED SECTOR: bacteria, amount of
plaque and mutans streptococci. - LIGHT BLUE SECTOR:
susceptibility, fluoride program + saliva secretion + saliva buffer
capacity - YELLOW SECTOR: combination of past caries
experience and related diseases.

z
CARIOGRAM..
 1.Bigger the green sector, better it
is from a dental health point of
view. 2. Smaller green sector
means high risk caries 3. For
smaller other sectors it is better
from dental health point of view
WHEN CHANCE IS HIGH, THE
RISK IS SMALL AND VICE
VERSA.

z
DENTAL CARIES VACCINES
 Vaccine means a suspension of attenuated/killed microorganism
administered for the prevention or treatment of infectious
disease. WHY VACCINATION AGAINST DENTAL CARIES? 1.
Transmissible and infectious nature of dental caries. 2.
Discovery and understanding of immune system.

z
DENTAL CARIES VACCINES
 IMMUNITY
 Resistance offered by the host against any pathogenic microorganisms. Natural
resistance by the body can be increased by immunization.
IMMUNITY
NATURAL
ACQUIRED
ACTIVE
PASSIVE

z
DENTAL CARIES VACCINES..
 1. Natural Immunity - Inherited resistance to infection. - E.g. Phagocytosis of bacteria
by WBC, destruction of acid secretions of stomach.
 2. Acquired immunity - Acquired during lifetime of an individual 2a. Active Immunity:
Acquired by an individual in response to the introduction of microorganisms or their
toxins into the body. They may be natural and artificial

z
 Natural active immunity: Acquired after an infection or recovery from disease or
subclinical infection. Artificial active immunity: Acquired artificially by inoculation of
bacteria, virus or their products.
 2b. Passive immunity - Acquired by immunization of antibodies - Body cells of the
subject do not take any active part in the production of immunity

z
 Immunization
 Immunization is the process by which an individual immune system becomes
resistant against an agent (immunogen). Immunization can be achieved in A. Active
immunization B. Passive immunization
 Vaccination is an active form of immunization

z
 A. Active immunization - Subjects immune system actively take part in antibody
formation.
 Introduction of foreign molecules into the body
 Activation of T cells and B cells
 Body itself generate immunit

z
 A1. Natural active immunization: When a person comes in contact with
a microbe immune system will create antibodies against microbe. Next
time the immune response against this microbe will be efficient.
 A2. Artificial active immunization: Injection of microbes or its parts.
Subject develop antibodies and become immune. It uses dead
microbes, parts of microbes or pretreated toxins from microbes
depending on severity of disease.

z
 . Passive immunization - Subjects immune system do not take part in
the formation of immunity. - Antibodies are transferred to a person -
Faster in action - Short lasting
 B1. Natural passive immunization: Antibodies transfer from mother to
fetus during pregnancy.

z
 B2. Artificial passive immunization: Antibodies are given by injection. It
is used during any outbreak of a particular disease or emergency
treatment to poison.(tetanus)

z
 TYPES OF CARIES VACCINES Vaccines may be prepared from :
Live modified organism Inactivated or killed organism Extracted
cellular fraction ,toxoid or combination Most commonly used vaccine
was prepared from heat killed or formalin treated S. mutans .But it
induced Heart Cross Reactive Antigens [HCRA] that could damage the
heart .

z
 TYPES OF IMMUNIZATION 1.PERIGLANDULAR SALIVARY
IMMUNIZATION Repeated s.c injection of formalin killed S.
mutans in freunds adjuvant were administered adjacent to
salivary glands along with installation of S. mutans into parotid
duct . Resulted in formation of both salivary Ig A and serum Ig
G antibodies Inoculation with similar antigen in site remote
from salivary gland were less successful

z
 2. PARENTRAL IMMUNIZATION Killed S. mutans were
administered to germ free rats in drinking water for 45 days.
Result : Significant reduction in caries Inference : a)increased
level of salivary Ig A antibodies to S.mutans [acquired by passive
transfer through milk of lactating rats to their litter] b)Ig G
antibodies were absorbed by GIT tract of offspring to enter blood
Passive transfer of Ig A: direct protection by preventing
adherence of S.mutans to tooth Absorbed IgG : indirect
protection affecting tooth via crevicular fluid or saliva.

z
 3 . ORAL SUB MUCOUS IMMUNIZATION Cells or cell wall +
adjuvant injected under mucosa of bucal sulci of 4 quadrants of
mouth Result: significant reduction in caries {similar to s.c
immunization} Untried route which might lead to some
discomfort and complications

z
 4. INGESTION OF WHOLE S.MUTANS People who
moderately effected by S.mutans may swallow several millions
these micro organism per day without any effect This
technique involves swallowing encapsulated S. mutans to
stimulate antibody response when it reaches Payer's patches
Reactive with homologous micro organism

z
 5. MURINE MONO CLONAL ANTIBODY Applying murine
monoclonal Ig G Ab resulted in decreased colonization in of S.
mutans and reduced caries Do not show tissue reactive
properties Passive immunization 6. IMMUNE BOVINE MILK
Ingestion of food supplemented with immune bovine milk
resulted in decreased S.mutans less plaque and reduced caries
Passive immunization

z
 7. EGG YOLK ANTIBODY Passive immunization
 Immunization of hens with GTF
 Purification of Ab enriched Ig G from egg
yolk
 Experimental use of this Ab as dietary
additive
 Dental caries reduced by 50%

z
 8. REPLACEMENT THERAPY Replacing the native flora with
genetically modified strains of S. mutans [BCS3-L1] Proposed
by Dr. Jeffrey. D. Hillman BCS3-L1were incapable of
producing lactic acid and aggressively replaces native flora
They produce Lantiboitics called MU1140 that out compete S.
mutans Adv : life time protection with occasional reapplication
Disadv : BCS3-L1 might be more harmful than S. mutans as
causative agents of inflammatory heart disease

z
NEED & TIMING OF IMMUNIZATION
 The period of 2 years after primary teeth begin to erupt is
called “window of infectivity”. Salivary Ig A is very low at birth
that increases during first year of life Colonization of teeth with
streptococci require presence of teeth S.sanguis can be found
in oral cavity by end of first year S.mutans only found in oral
cavity after 3 years.

z
 Dental caries vaccine can be advantageous to : a)Patients undergoing head & neck
radiation b)Xerostomia patients c)Mentally or physically handicapped patients
d)Chronically sick children on continuous medication presented with high sucrose
syrup.

z
CARIES ACTIVITY/SUSCEPTIBILITY
 CARIES ACTIVITY-Caries activity refers to the increment of active lesions over a
stated period of time. caries activity is a measure of the speed of progression of a
carious lesion. CARIES SUSCEPTIBILITY- Caries susceptibility refers to the inherent
tendency of the host and target tissue, the tooth, to be afflicted by the caries process .
This is the susceptibility of a tooth to a caries producing environment.

z
CARIES ACTIVITY/SUSCEPTIBILITY..
 PURPOSE OF CARIES ACTIVITY TEST... 1.Identify high risk groups and individuals
2.Need for personalized preventive measure and motivate the individual 3.Monitor the
effectiveness of oral health 4.Ensure a low level of caries activity before starting any
extensive restorative procedure. 5.Index help to reduce S.mutans n lactobacilli.

z
 IDEAL REQUISITES OF A CARIES ACTIVITY TEST Should have a sound theoretical
basis Show maximum correlation with clinical status. Should be accurate with respect
to duplication of results. Should be simple Inexpensive & less time consuming

z
 LACTOBACILLUS COLONY COUNT TEST:- Introduced by HODLEY IN 1933
PRINCIPLE: This test estimates the number of acidogenic and aciduric bacteria in the
patients’ saliva by counting the number of colonies appearing on tomato peptone agar
plates after inoculation with a sample of saliva. Selective media favoring the growth of
aciduric lactobacilli is the basis for the test.

z
CARIES ACTIVITY/SUSCEPTIBILITY TESTS..
 EQUIPMENTS: saliva collecting bottles, paraffin, 29ml tubes of saline, 2 agar plates, 2
bent rods, incubator, Quebec counter and pipettes PROCEDURE: patients chews a
piece of paraffin before breakfast. Then saliva get accumulated and collected and then
mix it. Saliva sample is diluted to 1:10 by pipetting 1 ml of the saliva.
LACTOBACILLUS COLONY COUNT TEST

z
 DISADVANTAGES : 1. Inaccurate for predicting the onset of caries 2. It does not
completely exclude the growth of other relatively aciduric organisms 3. Requires
relatively complex equipment. 4. Its only takes few minutes to do the test result are not
several days
LACTOBACILLUS COLONY COUNT TEST

z
 PRINCIPAL INVOVLED: It measures the ability of salivary microorganism to form
organic acids from a carbohydrate medium. The medium contains an indicator
dye,bromocresol green this dye changes of ph 5.4 to 3.8. PROCEDURE • Saliva is
collected by chewing paraffin. • A tube of synder glucose agar is melted n then cooled
to 50’C. • 0.2 ml of saliva is pitted into the tube n mix it. • The agar is solidified &
incubated. • Amount of acid produced by acidogenic organism is detected by changes
in the ph indicator n then compared to the uninoculated control tube against a white
background after 24,48 and 72 hours. • The rate of color change from green to yellow
is indicative of degree of caries activity
COLORIMETRIC SYNDER TEST

z
 ADVANTAGES: 1. Relative simple to carry out 2. Cost is moderate.
DISADVANTAGES: 1. Time consuming 2. Color changes are not very clear
COLORIMETRIC SYNDER TEST

z
 Grainger et al in 1965 PRINCIPLE: It measures the ability of salivary microorganism to
form organic acids from a carbohydrate medium. The medium contains an indicator
dye,bromocresol green this dye changes of ph 5.4 to 3.8. PROCEDURE: Swab the
buccal surface of the teeth with cotton applicator. And it is subsequently incubated in
the medium
 ADVANTAGES: 1. No collection of saliva is required 2. Predicts caries increment
THE SWAB TEST

z
 PRINCIPLE: It measures no. of S.mutans colony forming units for detecting and
quantitating S.mutans colonized on teeth . PROCEDURE: Sample is obtained by the
use of tongue blades(wooden spatulas). They are pressed against S.mutans selective
Mitus Salivarius Bacitracin(MSB) The agar plates are incubated at 37degree C for 48
hours in 95%at 5% CO2 gas mixture.
S.MUTANS LEVEL IN SALIVA

z
 ADVANTAGES: Frequency of isolation of S.mutans is high so this test is utilized as an
adjunct in caries management. DISADVANTAGES: • S.mutans are located at specific
site • Difficulty to differentiate between carrier state and cariogenic bacteria • S.Mutans
may constitute less than 1%of total flora of plaque.
S.MUTANS LEVEL IN SALIVA

z
 Estimates S.mutans levels in saliva PROCEDURE:- Undiluted paraffin stimulated
saliva is poured on special plastic slide that is coated with MSA(mitis salivarius agar)
containg 20%sucrose. The agar surface is thoroughly moistened and excess saliva is
allowed to drain off. Two discs containing 5ug of bacitracin are placed on the agar
20mm apart. The slide is tightly screwed into cover tube after inserting a CO2 tablet
Incubated at 37degree C for 48 hours .
DIP SLIDE METHOD FOR S.MUTANS COUNT

z
DIP SLIDE METHOD FOR S.MUTANS COUNT

z
SALIVARY BUFFER CAPACITY TEST
 PRINCIPLE: Buffer quantitated using either a Ph meter or color
indicator. This test measures the Number of milliliters of acid
requires to lower the Ph of Saliva through an arbitrary Ph
interval,such as from Ph 7.0 to 6.0,or the amount of acid or base
necessary to bring color indicators to their end point.

z
 PROCEDURE: • Ten ml of stimulated saliva is collected under oil at least 1 hour after
eating. • 5ml of this is measured into a beaker. After correcting the pH meter to room
temperature, the pH of saliva is adjusted to 7.0 by addition of lactic acid or base. •
Lactic acid is then added to the sample until a pH of 6.0 is reached. • The amount of
lactic acid needed to reduce the pH from 7.0 to 6.0 is a measure of buffer capacity
.This number can be converted to milli equivalents per litre

z
 EVALUATION: There is an inverse relationship between buffering capacity of saliva
and caries activity. The saliva of individuals whose mouths contain a considerable
number of carious lesions frequently have a lower acid buffering capacity than the
saliva of those who are relatively caries free. ADVANTAGES: Simple to carry out
DISADVANTAGES: Does not correlate adequately with caries activity

z
SALIVARY REDUCTASE TEST
 This test measures the activity of the reductase enzyme present in salivary bacteria.
PROCEDURE: • Saliva is collected by chewing paraffin and expectorated directly into
the collection tube. • The sample is then mixed with the dye diazo-resorcinol. • The
“Caries Conduciveness” reading or color change is done after 15 minutes. No
incubation procedures are required.
 ADVANTAGES: • No incubation required. • Quick results. DISADVANTAGES: • Test
results vary with time after food intake and after brushing.

z
ALBAN TEST
 It is a simplified substitute for the snyder test. Main features:  Use of a somewhat
softer medium that permits the diffusion of saliva and acids without the necessity of
melting the medium.  Use of a simpler sampling procedure in which the patient
expectorates directly into tubes that contain the medium.

z
ALBAN TEST
 60grams of Snyder test agar is placed in 1liter of water and the suspension is brought
to a boil over a low flame. When thoroughly melted , the agar is distributed using
about 5ml per tube. These tubes should be autoclaved for 15 minutes, allowed to cool
and stored in a refrigerator. 2 tubes of Alban medium are taken from the refrigerator
and the patient is asked to expectorate a small amount of saliva directly into the tubes.
The tubes are labeled and incubated at 98.6 degree Fahrenheit for up to 4 days.
 The tubes are daily observed for:  Change of color from bluish green (pH 5) to definite
yellow(pH 4 or below). 

z
ALBAN TEST
 Advantages:  Simple.  Low cost.  Diagnostic value when negative results are
obtained.  Its motivational value (ideal for education). DISADVANTAGES:  More
armamentaria required.  Based on subjective evaluation of color change that may not
be clear cut.

z
ORATEST
 This test was developed by Rosenberg et al in 1989 for estimating oral microbial
levels. PRINCIPLE: • It is based on the rate of oxygen depletion by microorganisms in
expectorated milk samples. In normal conditions the bacterial enzyme, the aerobic
dehydrogenase transfers electrons or proton to oxygen . • Once oxygen gets utilized
by the aerobic organisms, ethylene blue acts as an electron acceptor and gets reduced
to leucomeyhylene blue. This reflects the metabolic activity of the aerobic organisms.

z
ORATEST
 PROCEDURE: • Mouth is rinsed vigorously with 10ml of sterile milk for 30 seconds
and the expectorate is collected. • 3ml of this is transferred to the screw cap tube with
the help of a disposable syringe. • To this ,0.12ml of 0.1# methylene blue is added,
thoroughly mixed and placed on a stand in a well illuminated area.

z
ORATEST
 The tubes are observed every 10 minutes for any color change at the bottom using a
mirror. o The time taken for the initiation of color change within 6mm ring is recorded. o
The higher the infection ,lesser was the time taken for the change in color of the
expectorate reflecting higher oral microbial levels. Advantage:  Less time consuming. 
Economic.  Non-toxic vehicle.  Can be easily learnt by auxiliary personnel.
DISADVANTAGES:  Lack of specificity

z
CONCLUSION
 For developing country like India the focus should be on
assessing the caries risk and identifying those individuals at high
risk to develop caries.
 Preventive measures can then be targeted at this group.

EPIDEMIOLOGY OF Dental Caries.pptx

Recommended

Recommended

More Related Content

Similar to EPIDEMIOLOGY OF Dental Caries.pptx

Similar to EPIDEMIOLOGY OF Dental Caries.pptx (20)

More from Aswini sekar

More from Aswini sekar (8)

Recently uploaded

Recently uploaded (20)

EPIDEMIOLOGY OF Dental Caries.pptx