By-Dr. Oinam Monica Devi

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BY- DR.

OINAM MONICA DEVI


CONTENTS
Introduction
Epidemiology
- Definition
- History
- Components of Epidemiology
- Aims of Epidemiology
- Principles of Epidemiology
Measurements of Epidemiology
A.Tools of Measurement
B. Incidence
C. Prevalence
D. Relationship Between Prevalence And Incidence
Types of Epidemiology
- Descriptive Epidemiology
- Analytical Epidemiology
- Experimental Epidemiology
Uses of Epidemiology
• Diagnosis
- Normal Versus Abnormal:Health Versus Disease
- Principles of Diagnostic Testing
• Risk Versus Prognosis
-Risk, Risk Factors & Risk Assessment
-Prognosis, Prognostic Factors & Prognosis Assessment
• Indices
• NIDCR Protocol for periodontal disease
assessment
• Periodontal Epidemiological Studies
INTRODUCTION
 The term epidemiology is of Hellenic origin; it consists of “epi”, which means “among” or
“against” and “demos”, which means “people”(Lindhe).

 The word epidemiology is derived from the Greek word(Epidemic). Epi = upon, demos =
people and logos = study or science(Soben Peter).

 Greenwood(1934) defines epidemiology as “the study of disease, any disease, as a mass


phenomenon.”

 MacMahon(1960) defines epidemiology as “the study of the distribution and determinants


of disease frequency in man”

 John M. Last(1988) defines epidemiology as "the study of the distribution and


determinants of health related states or events in specified populations, and the application
of this study to the control of health problems".
Epidemiology has three purposes:
1-To determine the amount and distribution of a disease in a
population.
2-To investigate causes for the disease.
3-To apply this knowledge to the control of the disease.

So, the purpose of epidemiology is to apply the


knowledge gained from studies to ”promote, protect
and restore health”.
1)HIPPOCRATES(460-375 B.C.)
-First known Epidemiologist

2) THOMAS SYDENHAM (17th Century)


- Father of English Medicine
- History Of Disease

3) JOHN SNOW (1813-1858)


-Father Of Epidemiology

4) WILLIAM BUDD (1811-1880)


-Physician & Epidemiologist
-Pioneer in The isolation of Infectious Diseases

5) W.H. FROST
- First Professor of Epidemiology (U.S.)
•Sir John Lincour had collected details of the health habits and dental state of
96 old men all aged over 80 years (ex-service pensioners) –first dental field
studies.

•Edwin Saunders, a young dentist carried out what was probably the first
systematic dental epidemiology in Britain, studying eruption of teeth between
ages of 9 and 13. In 1837 he addressed his findings to parliament in a report
entitled, "The teeth a test of age", considered with reference to the factory
children.

•Towards the end of the 19th century, the public health aspects of dentistry were
investigated by William Fisher
AIMS OF EPIDEMIOLOGY
The International Epidemiological Association has listed 3 main
aims of epidemiology( Lowe & Kostrzewski in 1973) as follows:

1- To describe the size and distribution of the disease problems in


human populations.

2- To provide the data essential for the planning, implementation &


evaluation of health services for the prevention, control and
treatment of diseases and for the setting up of priorities among those
services.

3- To identify etiological factors in the pathogenesis of disease.


PRINCIPLES OF EPIDEMIOLOGY
1. Exact Observation (Strict, vigorous, accurate, precise)

2. Correct Interpretation (Free from error)

3. Rational Explanation (Intelligent, sensible, reasonable)

4. Scientific Construction (By expert knowledge and technical skill).


1.RATE =
• Measures the occurrence of some particular event in
population during
a given time period.
• It indicates the change in some event that takes place in a
population over a period of time.

Number of events in a specified year


Rate = ------------------------------------------------ X 1000
Population at risk of experiencing the
Entiseas
2. RATIO
• It expresses a relation in size between two random quantities (x:y
or x/y)

3. PROPORTION
• A proportion is a ratio which indicates the relation in magnitude of
a part of the whole.
• A proportion is usually expressed as a percentage.
eg:
The number of children with scabies at a certain time
---------------------------------------------------------------- x 100
The total number of children in the village at the same
time.
Epidemiologic Measures Of Disease
 INCIDENCE :

Defined as- “The number of new cases of a specific disease occuring


in a defined population during a specific period of time”.

-It is the average percentage of unaffected persons who will develop the disease of
interest during a given period of time.

-Can be calculated as:


INCIDENCE = Number of new cases
Number of persons at risk

-It can be viewed as the risk or probability that a person will become a case.
 PREVALENCE: is the proportion of persons in a population who have
the disease of interest at a given point or over a period of time.
 Used to indicate all current cases(old &new)existing in a given time
period.
-Can be calculated as:
PREVALENCE: Number of person with disease
Number of person in the population

 Limitations-Not ideal measure for studying disease etiology /causation


of disease.

 Relation between prevalence and incidence:


Epidemiologic Study Designs
STUDY DESIGN

EXPERIMENTAL OBSERVATIONAL

A) COMMUNITY INTERVENTION ANALYTICAL DESCRIPTIVE


TRIALS
B) RANDOMIZED CLINICAL TRIALS
C) FIELD TRIALS
1.CASE CONTROL
2.COHORT
Descriptive Studies
 First phase of an epidemiological investigation.
 Concerned with observing the distribution of disease or health-related
events in human populations and identifying the characteristics with which
the disease in question seems to be associated.
USES OF DESCRIPTIVE
EPIDEMIOLOGY
 Provides data with regard to the types of disease problems and
their magnitude in the community.
 Provides information on the etiology of a disease and helps in
the formulation of an etiological hypothesis.
 Provides data required for the planning, organizing and
evaluating preventive and curative services.
 Leads the path for further research with regard to a particular
disease problem.
Analytical Studies
 Second major type of epidemiological studies.

 The focus - is the individual within a population unlike descriptive


epidemiology which focuses on the entire population.

 Designed primarily to establish the causes of disease by investigating


association between exposure to a risk factor and the occurrence of
disease.

 Objective - Test the hypothesis.

 2 types -a.Case control study


-b.Cohort study
CASE-CONTROL STUDY
 Retrospective or trohoc studies.
 First and common approach to test causal hypothesis.
Three distinct features are:
1. Exposure and Outcome have occurred before start of the
study.
2. The study proceeds backwards from effect to cause.
3. It uses a control or comparison group to support or refute an
inference.
 There are 4 basic steps in conducting a case control study:
1.Selection of cases and controls
2.Matching
3.Measurements of exposure
4.Analysis and interpretation(Odds Ratio)
 Odds Ratio (Cross-product ratio) is defined as a measure of
the strength of the association between risk factor and outcome.
-Odds ratio is closely related to relative risk.
-The derivation of odds ratio is based on three assumptions :
(a) The disease being investigated must be relatively rare.
(b) The cases must be representative of those with the
disease.
(c) The controls must be representative of those without the
disease.
Cohort Study
 Also k/a prospective study, longitudinal study, incidence study
& forward-looking study. This study follows subject over time.

 Purpose -To determine whether an exposure or characteristic is


associated with the development of a disease or condition.
Elements of Cohort studies

1.Selection of study subjects


2.Obtaining data on exposure
3.Selection of comparison groups
4.Follow-up
5.Analysis:
a.Incidence rates - Among exposed and non-exposed
b.Estimation of risk- Relative Risk.
- Attributable Risk.
Relative Risk (Risk ratio)
 Relative risk is the ratio of the incidence of disease among
exposed and incidence among non-exposed.
 RR =Incidence of disease among exposed/
Incidence of disease among non-exposed
 It is direct measure of strength of the association between
suspected cause and effect.

 It does not necessary implies the causal relationship.


Attributable Risk (AR)or Risk difference
 AR is the difference in incidence rates of disease among
exposed and nonexposed group.

 AR= I.R. among exposed - I.R. among non-exposed/Incidence


among exposed x 100

 Example - A.R.= 10-1/ 10 x 100 = 90 %


 AR is the proportion of disease due to particular risk factor
exposure.
Ex – 90% of lung cancers are due to smoking.

 That means- amount of disease eliminated if the suspected


risk factor is removed.
 Carried out under the direct control of the investigator.

 Involve intervention or manipulation in the experimental group while


making no change in the control group and observing and comparing the
outcome of the experiment in both the groups.

 This could mean the elimination of a dietary factor thought to cause allergy
or testing a new treatment on a selected group of patients.

 Effects of an intervention are measured by comparing the outcome in the


experimental group with that in a control group.

 2 types - Randomized Controlled Trials(RCT) & Non-randomized Trials


Objectives of Experimental Studies

1. To provide ‘scientific proof’ for etiology of disease and risk


factor which may allow modification of occurrence of disease.

2. To provide a method of measurement for effectiveness and


efficiency of therapeutic / preventive measure for disease.

3. To provide method to measurement for the efficiency health


services for prevention, control and treatment of disease.
 RCT is a planned experiment designed to asses the efficacy of
an intervention in human beings by comparing the effect of
intervention in a study group to a control group.

 The allocation of subjects to study or control is determined


purely by chance (randomization).

 For new programme or new therapy RCT is best method of


evaluation.
Basic steps involves in the RCT
1. Drawing up a protocol
2. Selecting reference and experimental populations
3. Randomization
4. Manipulation or intervention
5. Follow-up
6. Assessment of outcome
Blinding
 Blinding can be done in three ways:

(a) Single blind trial

(b) Double blind trial

(c) Triple blind trial


Non- Randomized Trials
 There is no randomization in non-experimental trials.

 Example:-Uncontrolled Trials
-Natural experiments
-Before and after comparison studies
USES OF EPIDEMIOLOGY
 Community diagnosis
 Rise and fall of diseae
 Planning and evaluation
 Evaluation of individual risk and chances
 Syndrome identification
 Search for causes
 Completing the natural history of disease
Diagnosis
 For epidemiologist to study a disease in population or for
clinician to care for an individual patients, they must be able to
identify individuals with or without disease.

 Various diagnostic tests are used for making correct diagnosis


of diseases.They are:
• Sensitivity & Specificity
• Predictive Value
Sensitivity
The clinician should choose a
highly sensitive test when the
Sensitivity of a Test A highly sensitive
consequences of not
is the Proportion of test is unlikely to be
identifying a person with a
subjects with the negative when
disease could be severe, such
disease who is test someone has the
as during testing for Human
positive. disease
Immunodeficiency Virus
(HIV).
Specificity
Specific tests are
especially indicated
The specificity of a test A highly specific test when the
is the proportion of is unlikely to be misdiagnosis of
subjects without the positive when a disease in the absence
disease who is person does not have of disease could harm
negative. the disease. a person emotionally,
physically or
financially.
PREDICTIVE VALUE
As the prevalence of disease
increases, a higher
proportion of negative tests
The probability that The probability that are false.
a person with a a person with a
positive test has the negative test does not
disease is Positive have the disease is As the prevalence of
predictive value of Negative predictive disease in the population
the test. value of the test. decreases, a higher
proportion of the positive
tests are false.
Risk Versus Prognosis
RISK :The likelihood
that a person will get a
disease in a specified
time
RISK FACTOR: The
characteristics of a
individuals that place
them at increased risk
for getting a disease
RISK ASSESSMENT:
The process of predicting
an individual probability
of a disease is risk
assessment
Prognosis
It is a prediction of the probable course,duration &outcome of a
Prognosis disease based on a general knowledge of the pathogenesis of the
disease & the presence of risk factors for the disease

Prognostic The characteristics or factors that predict the outcome of a


Factors disease once disease are present.

Prognostic The process of using prognostic factors, to


Assessments predict the course of disease.
INDEX

 “ A numerical value describing the relative status of a population on a


graduated scale with definite upper and lower limits, which is designed to
permit and facilitate comparsion with other populations classified by same
criteria and methods” (Russell A.L)

 Ideal requisites of an index:


1.Clarity,simplicity and objectivity
2.Validity
3.Reliability
4.Quantifiability
5.Sensitivity
6.Acceptability
GINGIVAL INDICES
(By Schour &
Massler, 1944)

• To count number of gingival units affected with gingivitis that is


correlated with severity of gingival inflammation.

• Revised in 1947 (Bleeding replaced by hemorrhage).

 The facial surface of gingiva around a tooth divided into three units:
 Papillary gingiva (P)
 Marginal gingiva (M)
 Attached gingiva (A)

• Usually central incisor to second premolars are examined.


Scoring Criteria of PMA Index:
Marginal Component (M)
Papillary Component (P) 0 -Normal; no inflammation visible.
0 -Normal; no inflammation 1+-Engorgement; slight increase in size, no
1+-Mild papillary engorgement; slight bleeding.
increase in size. 2+-Obvious engorgement; bleeding upon
2+-Obvious increase in size of gingival pressure.
papilla; hemorrhage on pressure. 3+-Swollen collar; spontaneous
3+-Excessive increase in size with hemorrhage.; beginning infiltration into
spontaneous hemorrhage. attached gingiva.
4+-Necrotic papilla. 4+ -Necrotic gingivitis.
5+-Atrophy and loss of papilla (through 5+-Recession of the free marginal gingiva
inflammation) below the CEJ due to inflammatory
changes.
Attached Component (A)
0 - Normal; pale rose; stippled
1+- Slight engorgement with loss of stippling; changes in color mayor may not be present.
2 +-Obvious engorgement of attached gingiva with marked increase in redness. Pocket
formation present.
3+- Advanced periodontitis. Deep pockets evident.
Calculation

Uses:-In clinical trials


-On individual patients
-For epidemiologic surveys.
•Proposed to assessing the severity of gingival inflammation.

•Only gingival tissues are assessed with the help of mouth mirror &
periodontal probe.

•According to this method, each of the four gingival areas of the tooth (facial,
mesial, distal,and lingual) is assessed for inflammation and given a score from
0 to 3.

•The severity of gingivitis is scored on all teeth or on selected index teeth.

The index teeth are: 16,12,24,36,32,44


Calculation
 GI score for a tooth:
The scores from the 4 areas of the tooth are added and then divided by 4.
 GI score for the individual:
The indices for each of the teeth are added and then divided by the total
numer of teeth examined.
(Lobene, Weatherford, Ross, Lamm and Menaker in
1986)

• Assess the prevalence and severity of gingivitis.

• Strictly based on non invasive approach i.e. visual examination only without
any probing.

• Allow for repeated evaluations.

• Labial and lingual surfaces of the gingival margins and the interdental papilla of
all erupted teeth except 3rd molars are examined & scored.
Calculation:
Summing the gingival unit scores/Number of gingival units examined

Most widely used for clinical trials of therapeutic agents because it does not assess
the presence of periodontal pockets or attachment loss.
GINGIVAL BLEEDING INDICES
SULCUS BLEEDING INDEX (SBI) , Muhlemann and Son (1971)
Score 0 – Healthy looking papillary and marginal gingiva , no bleeding on probing
Score 1 – Healthy looking gingiva, bleeding on probing
Score 2 –Bleeding on probing, change in color, no edema
Score 3 – Bleeding on probing, change in color, slight edema
Score 4 –Bleeding on probing, change in color, obvious edema
Score 5 -Spontaneous bleeding, change in color, marked edema

GINGIVAL BLEEDING INDEX (GBI) , Carter and Barnes (1974)


•Unwaxed dental floss into the proximal sulci. It is readily available, disposable, and
can be used by the instructed patient for self-evaluation.
•The mouth is divided into six segments and flossed in the following order; upper
right, upper anterior, upper left, lower left, lower anterior and lower right.
Bleeding is generally immediately evident in the area or on the floss; however, thirty
seconds is allowed for reinspection of each segment .
GINGIVAL BLEEDING INDEX (GBI )- Ainamo & Bay, 1975)

PAPILLARY
•Is BLEEDING
performed through gentle INDEX
probing of the orifice (PBI)crevice.
of the gingival ,SAXER AND
• If bleeding occurs within 10 seconds a positive finding is recorded and the number of positive
MUHLEMANN (1977)
sites is recorded and then expressed as a percentage of the number of sites examined.
•PAPILLARY BLEEDING
Bleeding can also function as a motivating INDEX (PBI)
factor in activating the ,SAXER AND
patient to better oral home
care. It has been show that the scores obtained with this index correlate significantly to GI (Löe
MUHLEMANN
and (1977)
Silness, 1963) and has been used in profile studies and short-term clinical trials.

PAPILLARY BLEEDING INDEX (PBI) ,Saxer and Muhlemann ,1977)


•A periodontal probe is inserted into the gingival sulcus at the base of the papilla on the mesial
aspect, and then moved coronally to the papilla tip.
•This is repeated on the distal aspect of the papilla. The intensity of any bleeding is recorded as:
Score 0 – no bleeding;
Score 1 – A single discreet bleeding point;
Score 2 – Several isolated bleeding points or a single line of blood appears;
Score 3 – The interdental triangle fills with blood shortly after probing;
Score 4 – Profuse bleeding occurs after probing; blood flows immediately into the marginal
sulcus.
PAPILLARY BLEEDING SCORE (PBS)
 A Stim-U-dent®, which is inserted interproximally (Loesche, 1979).

 Essentially, the PBS expands the score 2 of the Gingival Index (Löe and
Silness, 1963) into three recognized clinical conditions. The criteria are:
 0 = Healthy gingiva, no bleeding upon insertion of Stim-U-dent®
interproximally
 1 = Edematous, reddened gingiva, no bleeding upon insertion of Stim-U-
Dent® interproximally
 2 = Bleeding, without flow, upon insertion of Stim-U-dent ® interproximally
 3 = Bleeding, with flow, along gingival margin upon insertion of Stim-U-
dent® interproximally
 4 = Copious bleeding upon insertion of Stim-U-dent ® interproximally
 5 =Severe inflammation, marked redness and edema, tendency to
spontaneous bleeding.
 The PBS is determined on all papillae anterior to the second molars.
MODIFIED PAPILLARY BLEEDING INDEX
(MPBI)
•Barnett et al. (1980) modified the PBI index (Muhlemann, 1977) by stipulating that
the periodontal probe should be gently placed in the gingival sulcus at the mesial line
angle of the tooth surface to be examined and carefully swept forward into the mesial
papilla.
•They timed the appearance of bleeding and graded it as follows:
0 = No bleeding within 30 s of probing;
1 = Bleeding between 3 and 30 s of probing;
2 = Bleeding within 2 s of probing;
3 = Bleeding immediately upon probe placement.
•The mesial papillae of all teeth present from the second molar to the lateral incisor
assessed.
• Indices were derived for the maxillary left and mandibular right buccal segments,
and the maxillary right and mandibular left lingual segments, and from these a full-
mouth index was calculated.
BLEEDING TIME INDEX (BTI)
•Nowicki et al. (1981)- the first clinical evidence of gingival
inflammation. The method consisted of inserting a Michigan “0” probe
in the sulcus until slight resistance was felt and then the gingiva was
stroked back and forth once over an area of approximately 2 mm.
•The following scores are applied:

0= no bleeding within 15 seconds of second probing (i.e. 30 seconds


total time);
1= bleeding within 6 to 15 seconds of second probing;
2= bleeding within 11 to 15 of seconds of first probing or 5 seconds
after second probing;
3= bleeding within 10 seconds after initial probing
4= spontaneous bleeding.
EASTMAN INTERDENTAL
BLEEDING INDEX (EIBI) Caton & Polson
(1985)

•A wooden interdental cleaner is inserted between the teeth from the


facial aspect, depressing the interdental tissues 1 to 2 mm.

•This is repeated four times and the presence or absence of bleeding


within 15 s is recorded.

•Considering the over-all high levels of reliability between and within


examiners, this method would be suitable for use in clinical trials and
epidemiological studies (Blieden et al., 1992).
QUANTITATIVE GINGIVAL BLEEDING
INDEX (QGBI)
•In 1985, Garg & Kapoor - magnitude of blood stains covering tooth brush bristles on brushing
and squeezing gingival tissue units in a segment, with one score for entire one segment (canine
to canine, or left or right pre-molars and molars in maxillary or mandibular arches – six
segments in all).

•The criteria scores are:


0 – No bleeding on brushing; bristles free from blood stains
1 - Slight bleeding on brushing; bristle tips stained with blood
2 - Moderate bleeding on brushing; about half of bristle length from tip downwards stained
with blood
3 – Severe bleeding on brushing; entire bristle length of all bristles including brush head
covered with blood.

•Bleeding is generally immediately evident on the bristles of the brush; however, 30 seconds
were allowed for reinspection of each segment.
BLEEDING ON INTERDENTAL BRUSHING INDEX
(BOIB)
• Hofer et al. (2011) -This index is performed by inserting a light
interdental brush placed buccally just under the contact point and
guided between the teeth with a jiggling motion, without force.

• Bleeding is scored as either present or absent, for each interdental


site, after 30 s.

• Advantages: atraumatic manipulation of the papillae, ease of


application, integration into existing oral hygiene instruction and
motivating patients to monitor their own progress at home.
The National Institute of Dental and Craniofacial Research
(NIDCR) Protocol For The Assessment Of Gingival Bleeding

•NIDCR) has used the presence or absence of gingival bleeding as an indication of


gingival health.
•Gingival assessment is just one of several components of the NIDCR protocol for
the assessment of periodontal disease.

•For this approach, the facial and mesiofacial sites of teeth in two randomly selected
quadrants, one maxillary & one mandibular are assessed for bleeding.

• A special probe known as the NIDR probe is used (color coded & graduated at 2,
4, 6, 8, 10, and 12 mm )
• For the assessment, the examiner dries a quadrant of teeth with air.
• Starting with the most posterior tooth in the quadrant (excluding the third
molar), the examiner places a periodontal probe 2 mm into the sulcus at the
facial site and carefully sweeps the probe into the mesial interproximal area.

• After probing , the examiner assesses the presence or absence of bleeding at


each probed site. The same procedure is repeated for the remaining quadrant.

• For an individual, the number or percent of teeth or sites with bleeding can be
calculated.

 For population groups, the prevalence of gingival bleeding, is usually defined


as bleeding at one or more sites.
Does My Patient with Gingivitis Fit the Typical Profile?

 Gingivitis is so common that any patient presenting with gingivitis could be


considered typical; however, gingivitis is more prevalent among certain groups.

 Adolescents have a higher prevalence of gingivitis than pre pubertal children


or adults(Cause-rise of sex hormones during adolescence).

 Studies suggest that the increase in sex hormones during puberty affects the
composition of the subgingival microflora.
Why do Patients have Gingivitis & What
puts them at Risk?
•Clear from experimental and epidemiologic studies that microbial
plaque is the direct cause of gingivitis.
•Cause & effect relationship between plaque and gingival inflammation
was demonstrated in a study(Loe et al) include 12 individuals (9 dental
students, 1 instructor, and 2 laboratory technicians) ,were asked to
abstain from all measures of oral hygiene.
•Dental plaque began to form quickly & the amount increased with time.
All subjects developed gingivitis within 10 to 21 days.
•Mean GI score increased from 0.27 at baseline to 1.05 at the end of the
"no-brushing" period.
• Gingival inflammation resolved in all subjects within 1 week of
resuming hygiene measures.
• The authors concluded that bacterial plaque was essential in the
production of gingival inflammation.
• Studies of association between oral hygiene status and gingivitis :

• In NHANES I, information on toothbrushing frequency and oral


hygiene status were collected and investigated the associations
between these factors and the periodontal index (PI) reported that
increased toothbrushing frequency and better oral hygiene scores were
associated with lower PI scores and these associations remained
statistically significant .
• Prevalence of gingivitis is more in male because of poor oral hygiene.

• Although smoking is one of the most important risk factors for adult
periodontitis. In clinical practice, the smoking status of patients should
be considered when gingival bleeding is assessed.
PERIODONTAL INDICES
(Rusell AL ,1956)
• Estimate deeper periodontal disease by measuring the presence or absence of
gingival inflammation and its severity,pocket formation and masticatory function..

• Reported to be useful among large populations.

• All the teeth are examined.

• Instruments:Mouth mirror & Plain probe.

 The Russell’s rule states that “ when in doubt assign the lower score.”
Drawback: No calibrated probe is used,there might be an underestimation of the true
level of periodontal disease
Calculation
 PI score per person = Sum of individual scores
------------------------------------
Number of teeth present
PERIODONTAL DISEASE INDEX (Sigurd P.Ramfjord, 1959)
 Composed of 3 components:
1.Plaque Component
2.Calculus Component
3.Gingival & Periodontal Component.

• Important feature: Measurement of level of the Periodontal attachment related to the CEJ of
the teeth

• All The Three Components Will Be Scored Separately using 6 Ramfjord Selected
Teeth(16,21,24,36,41,44).

• Instruments used-Mouth mirror and dental explorer(for plaque and calculus component).

• Mouth mirror and university of Michigan Number 0 probe(for gingival and periodontal
component) .

• Plaque scoring: done after staining with Bismarck Brown solution.

• Surfaces(facial,lingual,mesial,distal)
 Calculation of PI component=Total score/number
of teeth examined.
SHICK & ASH MODIFICATION OF PLAQUE CRITERIA
•The original criteria of the Plaque component of Ramfjord's Periodontal Disease
Index (POI) was modified by Shick R.A. and Ash M.M. in 1961.
•The modified criteria consists of examining the six selected teeth by excluding
consideration of the interproximal areas of the teeth and restricting the scoring of
plaque to the gingival half, of the facial and lingual surfaces of the index teeth.
•The teeth selected are the same as in the plaque component of Ramfjord's
periodontal disease index.
 Calculus Component

Calculation=Total score of calculus/ No.of teeth examined


Gingival and periodontal
component

Calculation=Total of individual tooth scores/Number of teeth examined


•CPITN was developed for the "joint working
committee" of the "World Health Organization" and
"Federation Dentaire Internationale" (W.H.O./F.D.I.) by
Jukka Ainamo, David Barmes, George Beagrie, Terry
Cutress, Jean Martin, and Jennifer Sardo-Infirri in 1982.

•Developed primarily to survey and evaluate periodontal


treatment needs rather than determining past and present
periodontal status, i.e., the recession of the gingival
margin and alveolar bone.

•Primarily the CPITN is a screening procedure for


identifying actual and potential problems posed by
periodontal diseases both in the community and in the
individual.
INDICES USED FOR ASSESSING
ORAL HYGIENE AND PLAQUE
 Developed in 1960 by John C. Green and Jack R. Vermillion.
 Rapid, simple and sensitive.
 Composed of 2 components:
 -Debris index (DI)
 -Calculus index (CI)
DEBRIS SCORE CALCULUS SCORE

CALCULATION
•Debris Index (DI) =( Buccal Score+ Lingual Score) / NO. OF SEG
• Calculus Index (CI) =( Buccal Score+ Lingual Score) / NO. OF SEG
• Oral Hygiene Index= DI+CI
• DI and CI range from 0-6
• Maximum score for all segments can be 36 for debris or calculus
• OHI range from 0-12
• Higher the OHI, poorer is the oral hygiene of patient
 Developed by John C Greene and Jack R Vermillion in
1964

 Only fully erupted permanent teeth are scored

 Natural teeth with full crown restorations and surfaces


reduced in height by caries or trauma are not scored

 An alternate tooth is then examined if missing


PLAQUE INDEX(PlI)
Podshadley AG and Haley J.V in 1968)

 PROCEDURE
• Apply a disclosing agent before scoring.

 Patient is asked to swish for 30 sec and then expectorate but not rinse.

 Examination is made by using a mouth mirror.

 Each of the 5 subdivisions is scored for presence of stained debris:


 0= No debris(or questionable)
 1= Debris definitely present.

 Debris score for individual tooth:


 Add the scores for each of the 5 subdivisions.
 PHP index for an individual= (Total score for all the teeth /the number of teeth examined)
 developed by Grossman F.D & Fedi P.F in 1970.

 Plaque control status among naval personnels and to measure any subsequent change
METHOD :
 Scoring the amount of plaque found on six selected teeth (index teeth) by using a disclosing
solution.

 The teeth examined are. 16, 21,24,36,41,44 and surfaces are – facial and lingual of the
each six teeth, the facial surfaces are divided into three major areas as – Gingival Area
(G), Mesial Proximal Area (M) and Distal Proximal Area (D).
 The stained plaque in contact with the gingival is scored as follows-
 Area M = 3
 Area G = 2
 Area D = 3 -when plaque is found not in contact with gingival tissue but is found on
any tooth surface, one point is added to the facial or lingual score.

 Calculation – the highest for any of the six teeth scored is the patient’s NAVY plaque
index score.

 All teeth scores are added to give the total NPI score.
EXTENT AND SEVERITY INDEX

To provide separate estimates of the extent and


severity of periodontal disease in individuals and •When ESI scores from two sites per tooth
populations.‘ in the whole mouth were compared with
an assessment of one upper and one lower
Unlike the PI and PDI, the ESI does not assess quadrant, the developers of the ESI found
gingival inflammation. that little information was lost from the
half-mouth assessment.
It estimates the loss of periodontal attachment
at the mesiofacial and facial sites of 14 teeth in
one maxillary quadrant and 14 teeth in the •However, the ESI has been used for full
contralateral mandibular quadrant using the mouth examinations on as many as six
periodontal probing method developed by sites per tooth.
Ramfjord for the PDI .
NIDCR PROTOCOL FOR PERIODONTAL
DISEASE ASSESSMENT
•The NIDCR periodontal disease assessment, as used in NHANES 111,
contains three parts: a periodontal destruction assessment, gingival assessment,
and calculus assessment.

•The periodontal destruction examination involves an assessment of loss of


periodontal attachment and furcation involvement.

•Loss of attachment is the distance (in millimeters) from the cementoenamel


junction to the bottom of the gingival sulcus.

•This distance is measured at the facial and mesiofacial sites of teeth in two
randomly selected quadrants, one maxillary and one mandibular, using the
indirect measurement method developed by Ramfjord.
RADIOGRAPHIC ASSESSMENT OF
BONE LOSS
•It is an important part of the clinical diagnosis of periodontal disease.

•Radiographic assessments have been particularly common as screening


methods.

• Assessments of bone loss in intraoral radiographs :


(1) The presence of an intact lamina dura
(2) The width of the periodontal ligament space
(3) The morphology of the bone crest (“even” or “angular” appearance)
(4)The distance between the CEJ and the most coronal level at which
the periodontal ligament space is considered to exhibit normal width.

• Bone loss can be expressed as this distance in millimeters or as a


percentage of the root length.
Why Do Patients Have Chronic Periodontitis
& What Puts Them at Risk?
 The following lists are adapted from Page and Beck:
1. Nutrition: major nutritional deficiencies and imbalance has effect on
periodontal tissues.
2 . Low-socioeconomic and educational status.
3. Osteoporosis
4. HIV Infection and AIDS: elevate risk for periodontitis.
5. Infrequent Dental Visits
6. Bacteria
7. Bleeding on Probing: It is an indicator of active inflammation and likely to be
predictor of attachment loss rather than causal.
8. Previous periodontal disease
9. Genetic factors: Genetic factors are strongly associated with aggressive forms and,
to a lesser extent with chronic periodontitis.
10. Stress

 In addition Obesity has also been added as one factors for causing periodontal
disease.
AGGRESSIVE PERIODONTITIS
IN INDIAN POPULATION
( Joshipura et al. 2015)

 In a cross-sectional survey done to know the prevalence of aggressive


periodontitis in Moradabad population with their systemic manifestations, it
was concluded that the frequency of systemic manifestations such as fatigue,
weight loss, and loss of appetite was significantly greater in aggressive
periodontitis and a significant correlation between anxiety/ depression.

 In a study done by Rahul et al., neutrophil functions like chemotaxis,


phagocytosis, and microbicidal activity, are deficient in LAP patients.
 Viruses like herpes simplex virus (HSV)-1 and EBV were found to be
significantly associated with aggressive periodontitis.

 FcγRIIIa V/V genotype and/or V allele, as well as the FcγRIIIb NA2/NA2


and/or NA2 allele, along with the FcγRIIa-R allele, may be risk factors for
generalized aggressive periodontitits (GAgP) in the population of South India.

 In a study done by Shete et al., there was no gene polymorphism found in


patients with aggressive periodontitis.

 In Malayalam speaking Dravidian population, IL-4 + 33C/T loci appears to be


an important risk factor for periodontal disease with a leaning towards
aggressive periodontitis.
Classic” Periodontal Epidemiological Studies in
India

 The study by Greene J.C (1960) is one of the earliest studies. It used Russell index
for periodontitis.
 The periodontal index (Russell, 1956) includes both gingival inflammation and
periodontal destruction, with weight given to marked gingival inflammation, which
makes reversible marked inflammation equivalent to irreversible periodontal
destruction in the calculation of the index.
 Ramfjord et al.(1968) in their paper discuss a WHO survey done in India along
with 4 other countries. They observed that there was 100% prevalence of
periodontal disease (including gingivitis) in India. Periodontitis was found to start
after age 15; and at 17 years, 10% of Indian boys had periodontitis. This
periodontitis was due to accumulation of calculus, plaque and debris rather than due
to age, sex, geography, economic status or nutrition.
 Sanjana et al.[1956]did a study on Bombay residents in 1956 and found 83.2% had
signs of periodontal disease. As prevalence of pockets was not specified separately, the
true prevalence of periodontitis could not be ascertained. The population seemed to
belong to low socioeconomic strata, with age being a risk factor.

 Ranganathan et al.[2004] report the prevalence of periodontitis in 1,000 HIV-positive


patients; 22.6% females and 36.3% males had periodontitis, with an odds ratio of 1.96.
None of females examined were smokers, while 50% of males examined were
smokers. Smoking and increased age were important reasons for increased prevalence
of periodontitis among males.

 Parmar et al.[2008] compared chewers of areca nut with or without tobacco with non-
chewers in a hospital-based population and found 22.6% of chewers were smokers and
the chewers had a prevalence of periodontitis of 54.76%, while the controls had a
prevalence of 31%. The quid chewers were at higher risk for periodontitis and gingival
recession, irrespective of sex, age and smoking status.

 Rooban et al.[2008] compared drug abusers with controls from a dental hospital. They
found there was a higher prevalence of periodontitis among controls despite the
number of smokers being significantly high among drug abusers. This may be
probably as a result of selection bias; dental disease would obviously be more
prevalent among dental hospital patients.
LANDMARK STUDIES
(Akhilesh H Shewale et al., Prevalence of Periodontal Disease in India : Systematic Review..
2016 June)
EPIDEMIOLOGY OF PERIODONTAL DISEASES IN INDIAN
POPULATION
(Shaju JP, Zade RM, Das M. Prevalence of periodontitis in the Indian population: A literature
review,2011 )
Prevalence of Periodontal Diseases in
India (Agarwal V et al.,2010)

 Severity of periodontal disease increases with age.


 Periodontal health was shown to be better in females.
 Diet has been shown to have significant effect on periodontal
diseases.
 The better periodontal health in urban than rural areas.
•Periodontitis is one of the major reasons for tooth loss in
adults.
•India, with a population of over 1 billion, is bound to
become a developed nation soon.This transition will require
a population that is healthy, including in terms of
periodontal health.
•Early studies done in India gave an indication that the
population is highly susceptible to periodontitis.

There is a lack of data regarding prevalence of


Periodontitis among the Indian population.
REFERENCES
1.Carranza F. A, Newman M.G., Takei H.H. and Klokkevold P.R. Carranza’s Clinical Periodontology:
edth (2002) :74-94
2.Carranza F. A, Newman M.G., Takei H.H. and Klokkevold P.R. Carranza’s Clinical Periodontology:
edth (2006) :110-131
3.Park k.Park’s textbook of Preventive and Social Medicine :ed 20th (2009) :49-88
4.Peter S.Essentials of Preventive and Community Dentistry:ed 4th (2011) :42-82,312-359.
5.Podshadley AG and Haley J V. A Method for Evaluating Oral Hygiene Performance :Public health
reports 1968;83(3):259-264.
6.Maria Augusta Bessa Rebelo and Adriana Corrêa de Queiroz (2011). Gingival Indices: State of Art
,Gingival diseases- Their Aetiology, Prevention and Treatment Dr. Fotinos Panagakos (Ed.), ISBN
978-953-307-376- InTech.
7.Reddy S.Essentials of Clinical Periodontology and Periodontics:3rd (2011):42-54.
8 Clinical Periodontology And Implant Dentisitry (5TH Edition): Jan Lindhe, Niklaus P. Lang and
Thorkild Karring
9. Shaju JP, Zade RM, Das M. Prevalence of periodontitis in the Indian population: A literature review:J
Indian Soc Periodontol 2011;15(1):29-34
10.Yadav OP, Shavi GR, Panwar M, Rana S, Gupta R et al. (2017) Prevalence of Dental Caries and
Periodontal Disease in Deaf and Mute Children Attending Special Schools in Jaipur City, Rajasthan. J
Dent Health Oral Disord Ther 7(4): 00252.
11. Agarwal V, Khatri M, Singh G, Gupta G, Marya CM, Kumar V. Prevalence of periodontal diseases in
India. J Oral Health Community Dent 2010;4:7-16.
12.Shah N, Mathur VP, Kant S, Gupta A, Kathuria V, Haldar P, Pandey RM. Prevalence of dental caries and
periodontal disease in a rural area of Faridabad District, Haryana, India. Indian J Dent Res 2017;28:242-
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India : Systematic Review. Journal of Clinical and Diagnostic Research. 2016 Jun, Vol-10(6): ZE04-
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14.Chandra A, Yadav OP, Narula S, Dutta A. Epidemiology of periodontal diseases in Indian population
since last decade. J Int Soc Prevent Communit Dent 2016;6:91-6.

15. Macpherson LMD, Stephen KW, Joiner A, Schafer F, Huntington E: Comparison of a conventional and
modified tooth stain index. J Clin Periodontol 2000; 27: 854–859.

16. Lobene RR: Effect of dentifrices on tooth stain with controlled brushing.JADA 77:849–855, 1968..
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