EPIDEMIOLOGY OF

PERIODONTAL DISEASES

UNDER GUIDANCE OF : PRESENTED BY:

DR. ANOOJA LALL
DR. NAVKIRAN DR. RICHA SHARMA
(PROFESSOR AND HEAD) MDS STUDENT

DEPARTMENT OF PERIODONTOLOGY AND ORAL IMPLANTOLOGY,

SRI GURU RAM DAS INSTITUTE OF DENTAL SCIENCES & RESEARCH,
AMRITSAR.
 INTRODUCTION
• Derived from Greek word, EPIDEMIC.
• Epi= Upon
• Demos= people
• logos= study or science.

Epidemiology is the study of health and disease in

populations and how these studies are influenced
by heredity, biology, physical environment and
personal behaviour.
Epidemiology of Periodontal Disease. Position Paper. J Periodontol 2005
 DEFINITION
• Parkin (1873) defined epidemiology as “ the branch
of medical science which deals with the treatment
of epidemics”.

• MacMohan (1960) defined epidemiology as “the

study of 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 stated or events in a specified
population, and the application of this study to
the control health problems.

Textbook of Preventive and Community Dentistry; Soben peter, 4th Edition

 HISTORY
• Hippocrates (460-375 BC) : “ No disease is sent by
devils or demons, but is the result of natural causes.
He concieved the realtionship between habit,
physique, weather and disease.

• Claudius Galen (130-200 AD) : “reason alone

discovers some things; experience a;one discovers
some things; but to find others require both
experience and reason.

• Sydenham (1624-1689) stressed the importance of

careful clinical observation. Was called “ Father of
English medicine” or “English Hippocrates”.
• John Snow (1813-1858) : Father of
Epidemiology. Investigated many instances of
occurrence of cholera and outbreaks in period
between 1848 and 1854.

• The statistical analysis of the affected cases

showed that the drinking water was the vessel
for transmission of disease ;( centre of outbreak
being Broad street Pump)

• William Budd (1811-1890) similar reasoning

was employed; carried a study on typhoid
fever.
• Dental Field Studies reported in Britain in Naval
Chronicle of 1803.
• Sir John Lincour collected details of all health
habits and dental state of 96 year old men (all aged
over 80 years)

• Edwin Saunders : conducted the first systematic

dental epidemiology in Britain, studying eruption
of teeth between 9-37 years of age.

• Towards the end of 19th century, public health

aspects of dentistry were investigated by William
Fischer; publication “ compulsory attention to
the teeth of school children.”
Epidemiologists are constantly in the field observing
diseases and conditions in the populations, seeking
unexpected differences between groups that may
provide another public health advance.
 AIMS OF EPIDEMIOLOGY

To describe the size and distribution of disease

problems in human populations.

To provide the data essential for the planning, implementation and

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

To identify etiological factors in the pathogenesis of

disease.
EPIDEMIOLOGIC MEASURES OF A
DISEASE
Medical needs, health care Presence , absence or
facilities, utilization of health distribution of the
services and other health- characteristic or attributes of
related events. the disease.

Mortality , morbidity, MEASUREMENT

OF Demographicvariables
disability, natality

Presence , absence or distribution of the

environmental and other factors suspected of
causing the disease
 EXACT OBSERVATION CORRECT INTERPRETATION
(Strict, vigorous, accurate, (Free from error)
precise)

PRINCIPLES OF
EPIDEMIOLOGY

RATIONAL EXPLANATION SCIENTIFIC CONSTRUCTION

(Intelligent, Sensible, (by Expert knowledge and

Reasonable) technical skill)
 TOOLS OF MEASUREMENT IN EPIDEMIOLOGY

• RATE
• RATIO
• PROPORTION
 RATE
• It is the frequency of a disease or characteristic
expressed per unit size of the population or group in
which it is observed.
• A rate measures the occurrence of some particular
event (development of disease or occurrence of
death) in a population during a given time period.

Number of events (deaths or disease)

in a specified period X 10n

Population at risk of experiencing the

event or disease
 CRUDE RATES:
These are actual observed rates such as the birth and
death rates.

SPECIFIC RATES:
These are the actual rates of disease due to specific
causes or diseases occuring in specific groups or
diseases during specific time periods.

STANDARDIZED RATES:
These are obtained by direct or indirect method of
standardization or adjustment like the age and sex
standardized rates.

The common examples of rates are : birth rate, death rate, fertility rate, reproduction rate,
growth rate, marriage rate etc.
 RATIO

• Denotes the relation in size between two random

quantities.
• In ratio, the numerator is not the part of a
denominator.
• Can be expressed as the result of one quantity
divided by the other and is usually represented by
the formula:
A:B or A/B.
PROPORTION
• It is a ratio which expresses the relation in magnitude
of a part of the whole.
• Numerator is always a part of denominator.
• Usually expressed in percentage.

Number of school children with caries

at a certain time period X 100

Total number of children in the school

at the same time
INCIDENCE
• Can be defined as “ the number of new cases of a specific
disease occuring in a defined poupulation during a
specified period of time.”
• Expressed as rate; cases per population per time.
• Range from 0 to infintiy.

Number of new cases of a specific disease

during a given time period X 100

Population at risk
 ATTACK RATE SECONDARY ATTACK RATE

• Used only when population • it is the “number of persons

is exposed to the risk for a exposed to the risk factor for
limited period of time as in developing the disease within
case of epidemic. the range of incubation period
following exposure to the
primary case.
• Usually used in the studies of
infectious diseases
Number of new cases of a specific
disease during a given time period
X 100

Population at risk during same time

interval
Uses of INCIDENCE RATES

• Gives clues to the research into etiology and

pathogenesis of disease.

• Helps with the study of distribution of disease.

• Helps in taking action to control the disease.

• Useful in evaluating the efficacy of preventive and

therapeutic measures.
PREVALENCE
• Used to indicate all current cases (both old and new)
existing in a given population at a given point of
time or over a period of time.
• Usually expressed as a percentage.
• Range from 0 to 100%.

Two types:
• Point prevalence
• Period prevalence
 POINT PREVALENCE PERIOD PREVALENCE
“ The number of all current “the total number of existing
cases of a specific disease at cases (old and new) of a
one point in time in relation specific disease during a
to a defined population.” defined period of time (eg.
Annual prevalence)
expressed in relation to a
defined population.”

Number of all cases of a specific Number existing cases of a specific

disease at a given point in time disease during a given period of time
X 100 X 100
Estimated total population Estimated mid-interval
at the same point in time population at risk
Uses of Prevalence Rate

• Useful in estimating the magnitude of a disease or

health problems in a community.
• In identifying the potential high-risk populations.
• Useful in administrative and planning purposes like,
assessing manpower needs in health services,
delivery of health services.

RELATIONSHIP BETWEEN PREVALENCE AND INCIDENCE:

PREVALENCE = INCIDENCE X MEAN DURATION

(P=I X D)
 DESCRIPTIVE EPIDEMIOLOGY
Concerned with the observation of distribution
of disease or any health related events in human
populations and identification of characteristics
with which the diseases or conditions under
study seems to be associated.

EPIDEMIOLOGICAL METHODS

EXPERIMENTAL EPIDEMIOLOGY
ANALYTICAL EPIDEMIOLOGY Designed to provide a method of
Designed primarily to establish the cause of measuring the effectiveness and efficiency
disease by investigating association between of health services for the prevention,
exposure to the risk factor and occurrence of control and treatment of the disease and
the disease; objective is to test the hypothesis. improve the health of community.
USES OF EPIDEMIOLOGY
Community diagnosis

Rise and fall of disease

Planning and evaluation

Evaluation of individuals risk and chances

Syndrome identification

Search for causes / risk factors

Completing the natural history of disease.

 DIAGNOSIS

Ability to identify individuals with

Important for epidemiologists to study
disease i.e. distinction b/w normal
disease in populations or for clinicians
and abnormal and health and
to care for individual patients.
disease.

In epidemiologic studies, the misdiagnosis

Misdiagnosing could mean that of subjects would result in the
persons without disease would underestimation or overestimation of the
face the costs and risks of prevalence of disease.
unnecessary treatment while It also could lead to invalid conclusions
persons with disease go untreated. about the association between a disease
and some exposure or characteristic.
 The diagnosis of periodontal disease is made by:

Immunologic and biochemical tests to measure the individual's

response to periodontal pathogens are being developed.

Because periodontal disease is a chronic, infectious disease,

microbiologic tests have been developed to detect the presence of
specific periodontal pathogens in the gingival sulcus or pockets.

The assimilation of clinical and radiographic information, such as

bleeding on probing, pocket depth, attachment loss, and bone loss.

These tests are useful for planning treatment for new patients, selecting
appropriate recall intervals, monitoring periodontal therapy, determining
appropriate antibiotic therapy for patients who do not respond to conventional
therapy, and screening patients before extensive restorative or implant therapy.
 (a) SENSITIVITY AND SPECIFICITY

The ability of a diagnostic test to give a correct answer is indicated by its sensitivity and
specificity.

-The specificity of a test is the proportion of

-The sensitivity of a test is the proportion of
subjects without the disease who test
subjects with the disease who test positive.
negative.
--Sensitive tests also are useful when a clinician
Specific tests are especially indicated when the
wants to rule out possible diseases during the
misdiagnosis of disease in the absence of
early stages of diagnostic work-ups or screen
disease could harm a person either emotionally,
for diseases during routine physical
physically, or financially.
examinations.
-Because highly specific tests rarely give false-
-Because sensitive tests rarely give false-
positive results, sensitive tests are most
negative results, sensitive tests are most
informative to clinicians when the results are
informative when the results are negative.
positive.
 Ideally, a diagnostic test
should be highly sensitive Most diagnostic test results
and specific but diagnostic take on values distributed
tests are rarely both sensitive over a range of values.
and specific.

In such cases, a threshold, or As the threshold is moved

cut-off point, has to be higher or lower, the
established to distinguish sensitivity and the specificity
between positive and change in opposite
negative results. directions.

The decision of where to

place a threshold for a test
depends on the penalty for
making the wrong decision.
(b) PREDICTIVE VALUE

The probability that a diagnostic test result is right is the

predictive value of the test.

The probability that a person with a positive test has the

disease is called the positive predictive value of the test.

The probability that a person with a negative test; does not

have the disease is referred to as the negative predictive value.

As the prevalence of disease in a population approaches zero,

the positive predictive value of a test also approaches zero.

As prevalence approaches 100%, negative predictive value

approaches zero.
 RISK VERSUS PROGNOSIS

The likelihood The

that a person characteristics Exposure to a
The process
will get a of individuals risk factor Rarely does a
of predicting
disease in a that place may have single risk
an individual's
specified time them at been at a factor explain
probability of
period is increased risk single point in a person's
disease is
called risk for getting a time, entire risk for
called risk
(differs disease are episodic, or a disease.
assessment.
among called risk continuous.
individuals). factors.
 RISK MARKERS/PREDICTORS:
These are associated with increased risk for disease, but do not cause the
disease. These factors are identified in cross-sectional and longitudinal studies.
A risk factor that can be used to predict the future course of disease, is known
as a risk marker.

RISK INDICATORS:
Are probable or putative risk factors that have been
identified in cross-sectional studies but have not been
confirmed through longitudinal studies.

RISK DETERMINANTS:
These are defined as those risk factors that cannot be modified.
Prognosis is the prediction of the course or outcome of the disease based on a general
knowledge of the pathogenesis of the disease and the presence of risk factors for the
disease.

Eg : For periodontal disease, important outcomes include tooth

loss, recurrent disease, and loss of function.

The characteristics or factors that predict the outcome of a

disease once disease is present are known as prognostic
factors,
and the process of using prognostic factors to predict the
course of a disease is called prognosis assessment.
• Advances in research over recent years have led to a fundamental change in
our understanding of the periodontal diseases.
• As recently as the mid-1960s, the prevailing model for the epidemiology of
periodontal diseases included these precepts:

1) All individuals were considered more or less equally susceptible

to severe periodontitis;
2) Gingivitis usually progressed to periodontitis with consequent
loss of bony support and eventually loss of teeth;
3) Susceptibility to periodontitis increased with age and was the
main cause of tooth loss after age 35.

Advances in our understanding of periodontal diseases since that

time have led to this old disease model being reevaluated.
WHAT ARE THE LEVELS OF DISEASE IN THE The answers are important:
POPULATION??
1. There are essential in order
to determine the health
care resources needed to
PERIODONTAL DISEASE alleviate the burden
EPIDEMIOLOGY POSES TWO conferred by the disease to
QUESTIONS the population.

2. Identification of risk factors

is prerequisite for the
WHAT ARE THE MAJOR DETERMINANTS OF ITS development of a successful
EXTENT AND SEVERITY???
intervention strategy that
may be used to control the
disease on the population
level.
INDICES USED FOR ASSESSING GINGIVAL DISEASE

1) PAPILLARY-MARGINAL-ATTACHMENT INDEX(PMA
INDEX)
It was developed by Maury Massler and Schour I. in 1944.

METHOD:
A gingival unit is divided into 3 components:
1.Papillary gingiva
2. Marginal gingiva
3. Attached gingiva
The presence or absence of inflammation on each gingival unit
is recorded.
The number of gingival units affected were counted rather than the
severity of the inflammation.

Although all the teeth could be assessed in this manner, usually only the
maxillary and mandibular incisors, canines and premolars are examined.

Papillary Component (P):

0 : Normal; no inflammation;
1+ : Mild papillary engorgement; slight increase in size.
2+ :Obvious increase in size of gingival papilla; bleeding on pressure.
3+ :Excessive increase in size with spontaneous bleeding.
4+ :Necrotic papilla.
5+ :Atrophy and loss of papilla (through inflammation)
ATTACHED COMPONENT
0 – normal , pale rose , stippled
1 - slight engorgement with loss of
stippling, changes in color may not
be present.
2 - obvious engorgement of attached
gingiva with
marked increase in redness.
3 - advanced periodontitis. Deep Marginal Component (M)
pockets evident. 0 Normal; no inflammation visible.
1+ Engorgement; slight increase in
size, no bleeding.
2+ Obvious engorgement; bleeding
upon pressure.
3+ Swollen collar; spontaneous
bleeding; beginning infiltration into
attached gingiva.
4+ Necrotic gingivitis .
5+ Recession of the free marginal
gingiva below the CEJ due to
inflammatory changes
CALCULATION OF THE INDEX
The number of affected units are counted and are totaled separately and
then added together and expressed numerically as PMA index score
per person.

PMA score = P+M+A

USES
1) In clinical trails.
2) On individual patients.
3) For epidemiologic surveys.
2) Modified PMA-PM INDEX
Measured gingivitis by concentrating on P and M units and discarding the A units. In
addition, the severity of gingivitis was evaluated.

Modified PMA- Muhlemann H.R. and Mazor Z.S.

0- No inflammation
I: Bleeding from the gingival sulcus on gentle probing,
the P-M showing no change of color and no swelling.
The papillary and marginal gingiva have a "normal
appearance."
II. Bleeding from the gingival sulcus on probing plus
change of color due to inflammatory disturbances of
P-M Units. No swelling or microscopic edema.
III. Bleeding plus change of color plus edematous swelling
of P-M Units. For example: P(I) means healthy
papilla. PM(II): papilla and marginal gingiva,
bleeding and hyperemic. A(II) Attached gingiva with
inflammatory color change.

Average PM index= Sum of all scores/ No. of areas scored

3) GINGIVAL INDEX (GI)

It was developed by Loe H. and Silness P in 1963 for assessing the

severity of gingivitis and its location in 4 possible areas by examining
the qualitative changes of the gingival soft tissues.
Most widely accepted because of its reliability, validity and ease of use.

The four areas of the tooth distofacial papilla, facial margin, mesio-facial
papilla and the entire lingual gingival margin 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
instruments used are mouth mirror and periodontal probe.
The four areas of the tooth RECORDING FORMAT
distofacial papilla, facial margin,
mesio-facial papilla and the entire
lingual gingival margin is assessed
for inflammation and given a
score from 0 to 3.

SCORING CRITERIA

The index teeth are:

16 - Maxillary Right First Molar
12 - Maxillary Right Lateral Incisor
24 - Maxillary Left First Premolar
36 - Mandibular Left First Molar
32 - Mandibular Left Lateral Incisor
44 - Mandibular Right First Premolar.
SCORING CRITERIA

Score Criteria
0 Absence of gingival inflammation
1 Mild inflammation , slight change in color
no bleeding on probing
2 Moderate inflammation , redness ,edema
hypertrophy, bleeding on probing
3 Severe inflammation , marked redness
spontaneous bleeding , ulceration.
GI score for the area: GI score for the individual:
CALCULATION
Each area is assigned a The indices for each of the teeth are added and
score from 0 to 3. then divided by the total number of teeth
examined. The scores range from 0 to 3.
GI score for a tooth : GI score for a group:
The scores from the four The indices for each member of a group or
areas of the tooth are population is added up and then divided by the
added and then divided total number of individuals in the group or
by four. population
INTERPRETATION

A GI score of :
0.1 to 1.0 indicates mild inflammation.
1.1 to 2.0 indicates moderate inflammation.
2.1 to 3.0 indicates severe inflammation

USES

1. To determine the prevalence and severity of gingivitis in

epidemiologic surveys.

2. For assessment of severity of gingivitis in individual

dentition.

3. In controlled clinical trials of preventive or therapeutic

agent.
 MODIFIED GINGIVAL INDEX(MGI):

The modified gingival index (MGI) introduced two

important changes to the GI:
Probing was eliminated as it could disturb
Elimination of gingival probing to assess the plaque and irritate the gingiva.
presence or absence of bleeding and
Redefinition of the scoring system for mild and
moderate inflammation.
By R.R. Lobene et al (1986)

With the GI, four gingival units per tooth (two A noninvasive index would allow for repeated
marginal, two papillary) are assessed. Either a full evaluations and permit intra calibration and
or partial mouth assessment can be performed. inter calibration of examiners.

A mean score for an individual can be

calculated by :
Summing the gingival unit scores and
dividing by the number of gingival units
examined.

More sensitive to earlier index, perhaps the

most widely used index in clinical trials of
therapeutic agents.
CALCULATION
The labial/facial and lingual surfaces of the gingival margins and the interdental papilla of all
erupted teeth are examined.

MGI index = Total score (papillary + marginal)

total number of sites
INDICES FOR ASSESSMENT OF GINGIVAL BLEEDING
1) SULCUS BLEEDING INDEX (SBI)
The SBI is an index for assessment of gingival bleeding ,
developed by MUHLEMANN H.R. and SON S. in 1971.
This index system is a modification of PMI of Muhlemann and
Mazor (1958).
The purpose of this index is to locate areas of gingival sulcus
bleeding upon gentle probing and thus recognize and record
the presence of early inflammatory gingival disease.
Four gingival units
are scored
systematically for
each tooth: the labial Scores for these
Adding the scores of
and lingual marginal units are added and
the individual teeth and
gingival (M units) divided by four dividing them by the
and the mesial and
number of teeth can
distal papillary
determine the sulcus
gingival (P units).
bleeding index
Muhlemann and Son suggested the use of a "sulcus bleeding
index" (SBI) because they believed that bleeding from the
sulcus is the earliest clinical symptom of gingivitis and that it
even precedes discoloration and swelling.
This index evaluated the labial and lingual marginal gingiva i.e.
the M unit and mesial and distal papillary gingiva i.e. the P
unit.
SCORING CRITERIA
The assessment of the gingival bleeding is done on a scale from 0-5 , according to
the following criteria:

SCORE CRITERIA
0 Healthy appearance of P and M unit
No bleeding on probing
1 Apparently healthy P and M unit showing no color and
showing no contour changes , bleeding on probing
2 Bleeding on probing with color changes. No
swelling or edema.
3 Bleeding on probing , change in color , slight
edematous swelling.
4 1) bleeding on probing , color changes and
obvious swelling.
2) bleeding on probing & obvious swelling
5 Spontaneous bleeding on probing , color change
marked swelling with or without ulceration.

CALCULATION
Total SBI of all tooth surfaces
No. of teeth examined
2) PAPILLARY BLEEDING INDEX (PBI)
This index was given by Muhlemann H.R. in 1977 and is a
modification of SBI Index.
It is based on bleeding following gentle probing of the
interdental papilla.

METHOD
The PBI is performed by sweeping the papillary sulcus on the
mesial and distal aspects with a periodontal probe.
The probe is inserted into the gingival sulcus at the base of
papilla on the mesial aspect and then moved coronally to the
tip of papilla . This is repeated on the distal aspect of the
same papilla.
SCORING CRITERIA
SCORE CRITERIA
0 No bleeding after probing.
1 A single discrete bleeding point appears after probing
2 Several isolated bleeding points appear.
3 The interdental triangle fills with blood shortly after
probing.
4 Profuse bleeding occurs after probing , blood flows
immediately into marginal sulcus.

CALCULATION
PBI Index= Total score
no. of papilla examined
3) GINGIVAL BLEEDING INDEX (GBI)
This index was given by CARTER H.G. and BARNES G.P. in 1974 to record
the presence or absence of gingival inflammation determined by gingival
bleeding from interproximal sulcus.

Bleeding is generally
It is readily available, immediately evident in the
disposable, and can area or on the floss; however,
be used by the thirty seconds is allowed for
instructed patient for reinspection of each segment.
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.
If copious For each patient a
hemorrhage occurs Gingival Bleeding Score
the patient may be is obtained by noting the
allowed to rinse in total units of bleeding
between segments. and the total susceptible
areas at risk
4) GINGIVAL BLEEDING INDEX (GBI- Ainamo & Bay):
 By Ainamo & Bay (1975).
 Is performed through gentle probing of the orifice of the
gingival crevice.
 If bleeding occurs within 10 seconds a positive finding is
recorded and the number of positive sites is recorded and
then expressed as a percentage of the number of sites
examined.
 Bleeding can also function as a motivating factor in activating
the patient to better oral home care. Has been used in profile
studies and short-term clinical trials.
 5) PAPILLARY BLEEDING INDEX

Immediate evaluation of the

Introduced by Saxer patient’s gingival condition
and Muhlemann and his motivation, based
(1975), as cited by upon the actual bleeding
Muhlemann (1977). tendency of the gingival
papillae

The intensity of any bleeding is recorded as:

Score 0 – no bleeding;
A periodontal probe is inserted Score 1 – A single discrete bleeding point;
into the gingival sulcus at the base Score 2 – Several isolated bleeding points or
of the papilla on the mesial aspect, a single line of blood appears;
and then moved coronally to the Score 3 – The interdental triangle fills with
papilla tip. This is repeated on the
blood shortly after probing;
distal aspect of the papilla
Score 4 – Profuse bleeding occurs after
probing; blood flows immediately into the
marginal sulcus
 6) PAPILLARY BLEEDING SCORE
 This is performed using 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 PBS is determined on all papillae anterior to the second
molars.
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.
 7) MODIFIED PAPILLARY BLEEDING INDEX
• Barnett et al. (1980) 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.
The appearance of bleeding graded 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

Indices were derived for the maxillary left
from the second molar to the lateral
and mandibular right buccal segments, and
incisor assessed
the maxillary right and mandibular left
lingual segments, and from these a full-
More sensitive than the visual aspects of
mouth index was calculated
the GI.
 8) BLEEDING TIME INDEX (BTI)
 By Nowicki et al. (1981)
 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.
9) EASTMAN INTERDENTAL BLEEDING INDEX
(EIBI):
 Caton & Polson (1985) developed the Eastman Interdental
Bleeding Index (EIB).
 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).
10) QUANTITATIVE GINGIVAL BLEEDING INDEX
(QGBI)
Bleeding is generally
immediately evident on
In 1985, Garg & Kapoor the bristles of the
formulated a brush; however, 30
quantitative gingival seconds were allowed
bleeding index. for reinspection of each
segment

The criteria scores are: This index takes into

0 –No bleeding on brushing; bristles free from consideration the magnitude of
blood stains; blood stains covering tooth brush
1 - Slight bleeding on brushing; bristle tips stained bristles on brushing and
with blood; squeezing gingival tissue units in
2 - Moderate bleeding on brushing; about half of a segment, with one score for
bristle length from tip downwards stained with entire one segment (canine to
blood; canine, or left or right pre-molars
3– Severe bleeding on brushing; entire bristle and molars in maxillary or
length of all bristles including brush head covered mandibular arches – six segments
with blood. in all).
10.BLEEDING ON INTERDENTAL BRUSHING INDEX (BOIB):
 Developed by Hofer et al. (2010)
 Indices that use wooden spatulas, according to its shape and
rigidity, may represent a potential for trauma.
 A light interdental brush placed buccally, just under the
contact point is 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.

Measures of gingival inflammation Advantages :

through indices of bleeding can be Atraumatic manipulation of the
influenced by : papillae,
Angulation of the probe, Ease of application,
The probe insertion depth, Integration into existing oral hygiene
Direction, and motion of the probe instruction and
and Motivating patients to monitor their
Probing force. own progress at home.
11) NIDCR PROTOCOL FOR THE ASSESSMENT OF
GINGIVAL BLEEDING
The National Institute of Dental and Craniofacial Research
(NIDCR) has used the presence or absence of gingival
bleeding as an indication of gingival health
The NIDR probe which is color coded and is graduated at 2, 4,
6, 8,10, and 12 mm is used
The facial and mesiofacial sites of teeth in two randomly
selected quadrants, one maxillary and one mandibular, are
assessed for bleeding.
• To begin with the teeth of the quadrant are dried with air.
• Then, starting with the most posterior tooth in the quadrant
(excluding the third molar), a periodontal probe is placed 2
mm into the sulcus at the facial site and carefully sweeps the
probe into the mesial inter proximal area.
• After probing the sites in the quadrant, the examiner assesses
the presence or absence of bleeding at each probed site
• For an individual, the number or percent of teeth or sites
with bleeding can be calculated.
• For population groups, the prevalence of gingival bleeding,
usually defined as bleeding at one or more sites, can be
determined.
• Adolescents have a higher prevalence of gingivitis than pre
pubertal children or adults because of rise of sex hormones
affecting the composition of the subgingival microflora..
• Increased serum levels of testosterone in boys and Estradiol
and progesterone in girls was associated with increased levels
of the periodontal pathogens Prevotella intermedia and
Prevotella nigrescens.
(Bergstrom J et al,1990).
• Hormonal effects also may be responsible for the
increased prevalence during pregnancy and among
women using oral contraceptives.
• Males in all age groups are more likely to have
gingivitis than females especially those aged 13 to 17
years because of poorer plaque control among males
12)MODIFIED SULCULAR BLEEDING INDEX (mSBI)
This index was given by A.mombelli , M.A.Van Oosten , E.Schurch
, Jr. and N.P. Land in 1987 to determine the severity of
gingival bleeding.

PROCEDURE
A periodontal probe is passed along the gingival margin to
provoke bleeding and clinical findings are recorded according
to the following criteria.
SCORE CRITERIA
0 No bleeding on probing
1 Isolated bleeding spots present
2 Blood forms a red line on gingival margin
3 Heavy profuse bleeding.
 GINGIVITIS: PREVALENCE AND DISTRIBUTION

• National survey data show that gingivitis is found in early

childhood, is more prevalent and severe in adolescence, and
then tends to level off in older age groups. (Stamm 1986)
• In the national survey of employed adults in 1985-86, 47% of
males and 39% of females aged 18 to 64 exhibited at least one
site which bled on probing.

• In the first U.S. national survey of adults in 1960-62, which

scored gingivitis visually, 85% of men and 79% of women were
found to have some degree of gingivitis.
• In the third National Health and Nutrition Examination
Survey (NHANES III, 1988-94), 50% of adults were found to
have gingivitis on at least three or four teeth.
U.S. Public Health Service, National Centre for Health Statistics. Periodontal disease in adults
• Plaque deposits are closely correlated with gingivitis, a
relationship long considered one of cause-and-effect.
• Longitudinal studies among Norwegian professionals
and students, among whom oral hygiene was excellent,
found no increase in prevalence and severity of gingivitis
between the late teen years and age 40.
Anerud A, Loe H, Boysen, Smith M. The natural history of periodontal disease in man. J Per Res 1979

• In related study among Sri Lankan tea workers, both

oral hygiene and the gingival condition were poorer at all
ages.

Loe H, Anerud A, Boysen, Morrison E. The natural history of periodontal disease in man. Rapid,
Moderate and no loss of attachment in Sri Lankan laborers. J Clin Periodontol 1986.
• This EXPERIMENTAL GINGIVITIS study by Loe and colleagues,
helped to establish the infectious etiology of gingival
inflammation by demonstrating that plaque accumulation is
paralleled by the development of gingivitis.

Loe et al. Experimental gingivitis in man. JP 1965.

• In addition, the observation that gingivitis is a fully reversible

condition provided a foundation for the development of
population based preventive and therapeutic strategies.
Axelsson P et al. Effect of controlled oral hygiene
procedures on caries and periodontal disease in
adults. J Clin Periodontal 1978.
• Research dating back to the 1980s has shown that
relatively few sites with gingivitis go on to develop
periodontitis. (Listgarten 1985; Haffajee 1988; Lindhe
1989; Macheti 1999; Kornman 2001)

• Even so, prevention of gingivitis, in the individual patient

or in populations, is still the first step toward preventing
periodontitis.

Why some gingival sites make the transition from being

periodontally healthy to those which bleed on probing,
there are indications that more than just plaque
accumulations are involved!!!!
• Lindhe et al.’s experimental animal studies in the beagle dog
indicated that the induction of destructive periodontitis is a
much more complex process, as plaque accumulation at the
ligated tooth surfaces did not invariably result in loss of
periodontal attachment or alveolar bone, a puzzle that
translates directly to humans and remains unresolved to this
day. Lindhe J, Hamp SE, Loe H. Experimental periodontitis in beagle dogs. Int Dent J 1973.

• Individuals with abundant plaque may sometimes show few

signs of periodontitis progression beyond gingival
inflammation while, conversely, persons with relatively clean
mouths may have severe disease resulting in tooth loss.
 In a study carried out in Africa, Baelum and coworkers
described cross-sectional findings on dental plaque, calculus,
gingivitis, loss of attachment, periodontal pockets, and tooth
loss in a sample of 30- to 69-year-old Tanzanians.
Baelum V. Fejerskov O, Karring T. Oral hygiene, gingivitis and periodontal breakdown in adult
Tanzanians. J Periodontal Res 1986.

Despite highly prevalent plaque and calculus, pockets deeper than 3 mm and
attachment loss exceeding 6 mm occurred at less than 10% of the tooth
surfaces.

75% of the tooth sites with attachment loss >6 mm were found in 31% of the
subjects; indicating that advanced periodontal disease was not readily
correated to supragingival plaque levels.
At approximately the same time, Loe and coworkers published data from a
longitudinal study which showed that the progression of untreated periodontitis
shared similar features
Loe H, Anerud A, Boysen, Morrison E. The natural history of periodontal disease in man. Rapid,
Moderate and no loss of attachment in Sri Lankan laborers. J Clin Periodontol 1986.

Drawn from a population never exposed to any preventive or therapeutic

intervention related to oral diseases in Sri Lanka, a cohort of 480 14- to 31-year-old
male tea-plantation laborers was initially recruited in 1970 and underwent
subsequent follow-up examinations.
DESPITE POOR PLAQUE CONTROL AND VIRTUALLY UBIQUITOUS GINGIVAL
INFLAMMATION IN THE ENTIRE SAMPLE, THREE DISTINCT PATTERNS OF
PROGRESSION OF PERIODONTITIS WERE OBSERVED OVER THE FOLLOW-UP
PERIOD:
ONE GROUP, comprising approximately 8% of the total,
with rapid progression of periodontal disease (RP);
ANOTHER GROUP (approximately 11%) who exhibited no
progression (NP) of periodontal disease beyond gingivitis;
THIRD GROUP between the two extremes (approximately
81%) with moderate progression (MP).
A clear message emerged from the above studies: despite
the infectious etiology of the gingival lesion, plaque and
gingivitis do not account for the majority of the destructive
periodontitis encountered in the population which, in turn,
indicates that other exposures, either environmental or host
related, must have a decisive impact on the development of
the ‘‘severe periodontitis’’ phenotype.
There may be an AGE RELATIONSHIP; a more pronounced
inflammatory response to the same plaque challenge has been
reported in older than in younger people.

A GENETICALLY DETERMINED RESPONSE has also been suggested,

with non-smoking or former smoking interleukin (IL)-1 genotype-
positive individuals having greater risk of bleeding on probing
(BOP)than non-smoking and former-smoking IL-1 negatives.

SMOKERS also appear to be at higher risk than nonsmokers of making

the transition from gingiva that do not bleed on probing to those that
do “The OverRiding Effects of Smoking”.

Epidemiology of Periodontal Diseases AAP Position Paper 2005

STRESS has also been associated with increasing IL-1β levels.

ORAL CONTRACEPTIVES have long been considered a risk factor for

gingival bleeding and some still are.

Modern oral contraceptives may not affect the inflammatory response

of the gingiva to dental plaque.

Epidemiology of Periodontal Diseases AAP Position Paper 2005

 PERIODONTITIS

MEASUREMENT AND DIAGNOSIS

 INDICES USED FOR ASSESSING PERIODONTAL
DISEASE

1) RUSSELL’S PERIODONTAL INDEX (PI)

It was developed by Russell A.L. in 1956.
This index estimates deeper periodontal disease by measuring
the presence or absence of gingival inflammation and its
severity , pocket formation, and masticatory function.
PI is a composite index because it records both the reversible
changes due to gingivitis and the irreversible changes for
gingival inflammation and deeper periodontal disease.

INSTRUMENTS USED
Mouth mirror
Plain probe
SCORE CRITERIA ADDITIONAL RADIGRAPHIC
FEATURES

0 NEGATIVE: there is neither inflammation R/G features normal

in the investing tissues nor loss of
function
1 MILD GINGIVITIS: There is area of
inflammation in free gingiva,which does
not circumscribe the tooth
2 GINGIVITIS: Inflammation completely
circumscribing the tooth

4 Used only when radiographs are There is notch like resorption

available in alveolar crest.

6 GINGIVITIS WITH POCKET FORMATION There is horizontal bone loss

:pocket formation , tooth is firm in involving entire alveolar crest
socket and not drifted and half the root length

8 ADVANCED DESTRUCTION WITH LOSS OF Advanced bone loss involving

MASTICATORY FUNCTION half the tooth root or definite
infrabony pocket
RUSSELL’s RULE
‘WHEN IN DOUBT ASSIGN THE LESSER SCORE’

CALCULATION
PI score per person=sum of individual score/number of
teeth present

No calibrated probe is used, so there might be an

underestimation of the true level of periodontal disease
INTERPRETATION
0-0.2-clinically normal supportive tissues
0.3-0.9-simple gingivitis
1.0-1.9-beginning destructive periodontal disease
2.0-4.9-established periodontal disease
5.0-8.0-terminal disease

DRAWBACK
1)Since no calibrated probe is used there can be underestimation
especially early bone loss.
2)The no. of periodontal pockets without obvious supragingival
calculus is also underestimated.
 2) PERIODONTAL DISEASE INDEX (PDI)

 It was developed by Sigurd P. Ram fjord in 1959.

 It is a modification of Russell's periodontal index.
 The most important feature of PDI is measurement of the level of
periodontal attachment related to CEJ of the teeth.

OBJECTIVES
1) To assess severity and prevalence of gingivitis and periodontitis.
2) To provide meaningful basis for estimation of need for periodontal
therapy.
3) To provide accurate recordings for clinical trials of preventive and
therapeutic procedures
4) To provide measureable reference data for assessment of correlations
with factors of potential significance in etiology of periodontal
disease.
SCORING METHOD:
Only six selected teeth are scored which are-16,21,24,36,41,44.

INSTRUMENT USED
Mouth mirror , dental explorer

COMPONENTS:
1) PLAQUE COMPONENT
2) CALCULUS COMPONENT
3) GINGIVAL AND PERIODONTAL COMPONENT
1) Scoring criteria for plaque component

Scoring of plaque is
done after staining
with Bismarck
Brown solution.

After the disclosing solution

flows over all the surfaces of
the teeth, the patient is
instructed to spit and rinse
thoroughly twice.

The scoring is
then done, by
noticing the
stained surfaces.

Instruments used:
Mouth mirror and a
dental explorer
Score Criteria
0 no plaque present
1 Plaque present on some but not on all
interproximal , buccal & lingual surfaces
2 Plaque present on all surfaces but
covering less than half of these.
3 Plaque extending on all surfaces
covering more than half of these.

CALCULATION
PLAQUE SCORE= Total score
no of teeth examined
 SHICK & ASH MODIFICATION OF PLAQUE COMPONENT:

It consists of examining the six

selected teeth by excluding
The original criteria of the
consideration of the
Plaque component of The teeth selected are the
interproximal areas of the
Ramfjord's Periodontal same as in the plaque
teeth and restricting the
Disease Index (PDI) was component of Ramjford's
scoring of plaque to the
modified by Shick R.A. and periodontal disease index.
gingival half, of the facial and
Ash M.M. in 1961.
lingual surfaces of the index
teeth.

The Plaque Score per

person is obtained by
SCORING CRITERIA: totaling all of the individual
tooth scores and dividing by
the number of teeth
examined.
2) Scoring criteria for calculus index
The calculus component of the periodontal Disease
Index (PDI) assesses the presence and extent of
calculus on the facial (buccal/labial) and lingual
surfaces of the 6 index teeth.

Mouth mirror and a dental explorer are used.

The calculus score per tooth are totaled and

then divided by the number of teeth
examined to yield the calculus score per
person.
Score Criteria
0 Absence of calculus
1 Supragingival calculus extending only
slightly below the free gingival margin
2 Moderate amount of supra and sub-
gingival calculus
3 Abundance of supra and sub-gingival
calculus
3) Gingival and periodontal component-University of
Michigan Number o probe is used

The gingivae around

The gingival status the teeth to be
is scored first. scored are first
dried.

Examined for
changes in color, Then the crevice
form, consistency depth is recorded in
and for any evidence relation to the
of ulceration with Cemento-Enamel
bleeding. Junction

If any of the six

Mouth mirror and preselected teeth are
University of missing, another tooth is
Michigan O probe not substituted in its
are used. place.
 Score Criteria
0 Absence of signs of inflammation
1 Mild to moderate inflammatory changes
2 Mild to moderately severe gingivitis
extending all around the tooth
3 Severe gingivitis , redness, swelling
ulceration
4 Gingival crevice in any of the 4 measured areas
extending apically to CEJ not more
than 3 mm
5 Gingival crevice in any of the 4 measured areas
extending apically b/w 3-6 mm
6 Gingival crevice in any of the 4 measured areas
extending apically more than 6 mm from CEJ

CALCULATION
PDI score= total of individual tooth score
number of teeth examined
 In addition to the PDI score for periodontal disease,
the PDI provides a method for calculating tooth
scores for calculus, occlusal attrition, mobility, and
proximal contacts.
 Although the PDI is rarely used today, two aspects of
the index are commonly used: Selection of the six
Ramjford teeth .The method for measuring pocket
depth and loss of periodontal attachment.
 Ramjford's technique for measuring pocket depth and
periodontal attachment loss has been used in national
surveys such as the National Health and Nutritional
Examination Surveys.
 3)Navy Periodontal Disease Index (NPDI)
As for the Ramfjord PDI, this index consists of two components, a gingival
score and a pocket score of six selected teeth, namely tooth numbers 16,
21, 24, 36, 41,44.

Criteria for the Navy Periodontal Disease Index.

0- Gingival tissue is normal in color and tightly adapted to the tooth and
tissue is firm and no exudate is present.
1- Inflammatory changes are present, but do not completely encircle the
tooth.
Changes may include one or a combination of the following:
Any change from normal gingival color , loss of normal density and
consistency , Slight enlargement or blunting of the
papilla or gingiva , tendency to bleed upon palpation
or probing.
2- Inflammatory changes listed above completely encircle the tooth.
 4) COMMUNITY PERIODONTAL INDEX OF TREATMENT NEEDS (CPITN)

1)This index was given by Jukka Ainamo , David Barmes , George Beagrie , Terry
Cutress , Jean Martin and Jennifer Sardo-Infirri in 1982.
2)This index was developed to survey and evaluate treatment needs rather than
determining past and present periodontal status , i.e. the recession of the gingival
margin and alveolar bone.
3)The CPITN records the common treatable conditions namely periodontal pockets ,
gingival inflammation and other plaque retentive factors.
4)It does not record the irreversible changes such as recession or other deviation
from periodontal health such as tooth mobility or loss of periodontal attachment.
5) It is a screening procedure to identify the actual and potential problems passed by
periodontal disease to community or individuals.

ADVANTAGES
Simplicity
Speed
International uniformity
 RULES TO BE FOLLOWED:

2. If in a posterior sextant, one

The index (and substitute)
1. Two or more functioning of the two index teeth is not
teeth are excluded from the
teeth must be present in a present or has to be excluded,
CPITN scoring when the
sextant for it to quality for then the recording is based on
decision has been made to
scoring. the examination of the
extract for any cause.
remaining index tooth.

3. If both index teeth in a 4. In the anterior maxillary

posterior sextant are absent or sextant if tooth 11 is excluded, 5. In subjects under 20 years of
excluded from the substitute 21, if 21 is also age, if the first molar is not
examination, all the remaining excluded then identify the present or has to be excluded,
teeth in that sextant are worst score for the remaining the nearest adjacent premolar
examined and the highest score teeth. Similarly, substitute is examined.
is recorded. tooth 41 if tooth 31 is missing.

7. A single tooth in a sextant is

considered as a tooth in the 8. The third molars are not
6. If all teeth in a sextant are
adjacent sextant and subject to included, except where they
missing or only one functional
the rules for that sextant. If the are functioning in place of
tooth remains the sextant is
single tooth is an index tooth, second molars.
coded as missing.
then the worst index tooth
score is recorded.
 For adults, 20 years The probe has a 'ball
or more, only ten tip' of 0.5 mm
teeth, known as the diameter that allows
'Index Teeth' are easy detection of
examined. subgingival calculus

The probing may be done by

A tooth should be probed in withdrawing the probe between each
at least six points, the mesio- probing or alternatively, with the
buccal, midbuccal, disto- probe tip remaining in the sulcus or
buccal, and the corresponding pocket, the probe may be 'walked'
sites on the lingual surface. around the tooth.

Mouth mirror and CPITN probe are

used.
Two types:
For people up to 19 'CPITN-E' for the epidemiological
years, only six 'Index probe with 3.5 and 5.5 mm
Teeth' are examined. markings.
'CPITN – C' for the clinical probe
with additional 8.5 and 11.5 mm
markings.
CODES AND CRITERIA

CODE CRITERIA

CODE X When only one tooth or no teeth are present in a sextant

CODE 4 Pathological pocket of 6 mm or more present i.e. the black area of CPITN
probe is not visible.
CODE 3 Pathological; pocket of 4 mm-5 mm present , i.e., when the gingival
margin is on the black area of the probe.
CODE 2 Presence of supra or sub-gingival calculus
CODE 1 Gingival bleeding after gentle probing

CODE 0 No signs of disease

 CLASSIFICATION OF TREATMENT NEEDS

TN 0 A recording of code 0 for all six sextants that there is no need for
periodontal treatment.

TN 1 A recording of code 1
Indicates a need for improving personal oral hygiene.

TN 2a A recording of code 2
Indicates need for scaling
Indicates a need for improving personal oral hygiene
TN 2b A recording of code 3
Indicates a need for scaling and root planing
Indicates need for improving the personal oral hygiene
Scaling and root planning will usually reduce inflammation and bring 4mm
or 5mm pockets to 3mm or below

TN 3 A recording of code 4
Complex treatment which could involve deep scaling , root planning and
more complex surgical procedures.
• As our understanding of periodontitis etiology has
deepened, some markers have emerged as likely
candidates.
• The most promising are the inflammatory cytokines
that are expressed in gingival crevicular fluid (GCF) as
part of the host response to inflammation, a number of
which have been associated with active disease.
(Offenbacher 1994, Page 1992).
• These cytokines include prostaglandin E2 (PGE2), tumor
necrosis factor-alpha (TNF-α), IL-1 alpha (IL-1α), IL-1
beta (IL-1β), and others.
• One cross-sectional study found greater quantities of PGE2
expressed by persons with gingivitis only than by those with
gingivitis plus untreated periodontitis. (Heasman 1998)
• The enzyme aspartate aminotransferase (AST), which has
been identified as present in the GCF of periodontitis
patients, also has been studied. (Magnusson 1996)
• Initial tests have been promising, and AST can be identified
by a simple chairside test. To date, however, these
approaches to measure periodontitis by means of
inflammatory cytokines in GCF are still being tested.
• It will be a distinct help to both clinicians and researchers if
one or more of them can become established as valid and
reliable measures of active periodontitis.
 PREVALENCE OF PERIODONTAL DISEASES

• The old model of periodontal diseases, described earlier, held

that susceptibility to periodontal diseases was virtually
universal.
• Today, however, it is well documented that only some 5% to
15% of any population suffers from severe generalized
periodontitis, even though moderate disease affects a
majority of adults.
• What epidemiology has demonstrated is that the majority of
just about any adult population has chronic periodontitis to
some degree, but that mild attachment loss, as measured by
CAL of 2 mm or so, is compatible with good health and
function for many years.
• The host response is now seen as a key factor in the
clinical expression of periodontitis, with only some
20% of periodontal diseases now attributed to
bacterial variance.

• Some 50% of periodontal diseases have been

attributed to genetic variance and more than 20%
to tobacco use, although the role of tobacco has also
been estimated as higher.
 Determining the prevalence of periodontitis in the U.S. population,
sAeemingly a straightforward issue, in fact is complicated by the various
case definitions used.

If periodontitis is defined as the identification of at least one site

with CAL of ≥2 mm, around 80% of all adults are affected, and
around 90% of those aged 55 to 64.

When the case definition is at least one site with CAL of ≥4 mm,
the prevalence in those aged 55 to 64 drops to around 50%.

When it is CAL of ≥6 mm, prevalence is less than 20%.

Using pockets of ≥4 mm as a case definition, 30% of adults had

met that criterion on at least three to four teeth.

U.S Public health Service, National Institute of Dental Research. Oral health of United States Adults; National Findings; 1987.
Third National Health and Nutrition Examination Survey , 1988-94. Hyattsville, 1997)
Prevalence is found to be greater in African- Americans
and in Native Americans.

• These national data make it clear that the milder

forms of periodontitis are close to universal.
• The more severe manifestations of the disease,
meaning those that lead to tooth loss or at least
threaten it, are less prevalent.
• Even just these few data demonstrate that any
prevalence data need the reference markers of the
relevant case definition and the age group to which
they apply.
 INCIDENCE OF PERIODONTITIS

• In periodontitis, “incidence” is often taken to mean

new sites that meet a definition of periodontitis,
even if these occur in people who already have
other diseased sites.
• The term is also applied to an increase in CAL or
bone loss in a site that has already been recorded as
diseased.
• As with prevalence, measures of periodontitis
incidence will vary according to the case definition
of the disease.
• Some longitudinal studies have confirmed the results of cross-
sectional studies in identifying age as a risk factor for
progression of CAL, although others concluded that
progression of CAL is more closely related to the extent of
baseline CAL than to age.
In the Piedmont study in North Carolina,
Healthy older people in the which followed a population sample
Baltimore Longitudinal Study of aged 65 to over 80 for 3 years, baseline
Aging did not show much findings were that CAL was much more
attachment loss even over a 10-year extensive in study participants than it
period. (Ship JA 1996) was in younger groups.(Beck 1990,
Brown 1994, Beck 1994,1997)

In Loe et al study, the rapid- and moderate-progression

groups, periodontitis progressed with age (much more
rapidly in the first group), whereas in the non-progressing
group age was not a factor. This Sri Lanka study, like the
Piedmont study, demonstrated that loss of CAL became
severe over time only for a small group of susceptible
individuals. (Loe et al 1986)
 DETERMINANTS IN PERIODONTITIS
AGE

• The prevalence and severity of CAL is invariably related

directly to age in cross-sectional surveys.
• Taking the 1985-86 NIDR NATIONAL SURVEY of
employed adults, the proportion of adults with at least
one CAL site of ≥2 mm exceeded 70% even in adults
aged 35 to 44 years, and was more than 90% in those
aged 55 to 64.8
• For ≥4 mm loss of attachment, prevalence was 13.8% of
25- to 34-year-olds and 53.6% of 55- to 64-year-olds.
• The 1985-86 national survey found that pockets of 4 to 6
mm were present in 13.4% of all adults and were more
frequent in older age groups.
Brown L, Oliver R, Loe H. Evaluating periodontal status of US employed adults. J Am Dent Assoc 1990;121:226-31.

• Pockets of ≥7 mm were found in only 0.6% of those

examined and were not related to age.

• The current view sees the greater periodontal

destruction in the elderly as reflecting lifetime disease
accumulation rather than an age-specific condition.
 Surveys of older people in the United States, Canada, and Australia have found
that CAL or PD of 6 mm or more was prevalent in 15% to 30% of persons
examined.44,77-79 In all of these studies, CAL of 4 to 6 mm was common.
(Hunt 1990, Gilbert 1992, Slade 1993)

The New England study was of persons aged 70 to 96, older than those in the
1985-86 national survey, and the results could reflect cohort effects (i.e., results
specific to the generation studied and which may not be seen in subsequent
generations).

All of these reports agree that CAL increases with age, but most did not find
extensive loss of function in the affected teeth.
It is uncommon for elderly people with reasonably intact dentition to exhibit
sudden bursts of periodontitis.
Tooth retention, good oral hygiene, and periodontal health (exhibited by little
gingival inflammation and few deep pockets) are closely associated, regardless of
age. (Abdellatif 1987, Burt 1985)
 GENDER

• CAL of all levels of severity is generally more prevalent in

males than in females. (Abdellatif 1987)
• This has been a consistent finding in all national surveys
in the United States since the first such survey in 1960-
62.
• Males usually exhibit poorer oral hygiene than females,
whether measured as calculus or soft plaque deposits.
• Is also more related to poorer oral hygiene, less positive
attitudes toward oral health, and dental-visit behavior
among males than to any genetic factor.

U.S. Public Health Service, national Centre for Health Statistics. Basic data on dental
Examination findings of persons 1-74 years; 1971-74..
• There are certain gender related temporary
syndromes such as hormonal conditions, such as
pregnancy-associated gingivitis, as well as puberty-
associated gingivitis which can affect children of
both sexes.
 SOCIO-ECONOMIC STATUS (SES)

• A multitude of disease conditions are associated with

socioeconomic status, and cause/effect (e.g., social stress
as a contributory cause of heart disease) is plausible.
• Generally, those who are better educated, wealthier, and
live in more desirable circumstances enjoy better health
status than the less educated and poorer segments of
society.
• Gingivitis and poor oral hygiene are clearly related to
lower SES, but the relationship between periodontitis
and SES is less direct.
The 1985-86 National Survey found that the prevalence of CAL at all levels
of severity was not closely related to household income. (Bethesda 1987)

On the other hand, CAL of ≥4 mm and ≥7 mm in at least one site were both
closely correlated with educational levels.

It is likely that the widely observed relation between SES levels and
gingival health is a function of better oral hygiene among the
better educated, more positive attitudes toward oral hygiene,
and a greater frequency of dental visits among the more dentally
aware and those with dental insurance (who are more likely to
be white-collar employees; i.e., those with more education).
 GENETICS
• First report identifying a genetic component in periodontitis
appeared as recently as 1997. (Kornman 1997)
• The original 1997 report,using data from patients in private
practices, found that a specific genotype of the polymorphic
IL-1 gene cluster was associated with more severe
periodontitis.
• This relationship could be demonstrated only in non-smokers,
which suggested right away that the genetic factor was not as
strong a risk factor as smoking.
• IL-1 has been identified as a contributory cause of
periodontitis among some patient groups (Laine 2001, Lang
2000) and in one epidemiological study (Thomson 2001)
• At one end, a study among 169 twin pairs concluded that
about half of the variance in periodontitis was attributable to
heritability. (Mikalowicz 2000)
• At the other end, there were no differences in tooth loss
attributable to IL-1 variation over 10 years in a non-smoking,
well-maintained population.
• Further research, especially epidemiological studies of people
with and without disease, will be necessary before the genetic
contribution to the initiation and progression of periodontitis
can be specified.
• With current knowledge, inducing periodontal patients to
stop smoking would be a higher priority than genetic testing.
 RISK FACTORS FOR PERIODONTITIS
PLAQUE, MICROBIOTA, ORAL HYGIENE

• Oral hygiene can favourably influence the ecology of the

microbial flora in shallow-to-moderate pockets, but it does
not affect host response.
• Oral hygiene alone has little effect on subgingival microflora
in deep pockets and personal oral hygiene practices among
health professionals have been shown to be unrelated to
periodontitis in these individuals.
• The conclusion from older studies, mostly cross-sectional, in
populations with poor oral hygiene is that plaque and
supragingival calculus accumulations correlate poorly with
severe periodontitis.
(Loe 1986, Baelum 1986, 1988, Okamoto 1988, Cutress 1982,
Ismail 1987, Lembariti 1988, Loe 1992)
• Clinical findings from the Karlstad studies in Sweden
(Axelsson 1981, 1991), however, concluded that CAL
in susceptible adults can be halted almost
completely when meticulous self-performed plaque
control is combined with professional prophylaxis
three to six times per year.
• It has long been thought that Gram-negative anaerobes
were the primary pathogens in periodontal pockets, but
for many years efforts to identify specific causative
microorganisms have been unsuccessful.

• More recently it has become clearer that in the broad

Gram-negative profile found at diseased sites there are
several putative pathogens that are consistently found.

• The predominant group includes Actinomyces

actinomycetemcomitans (Aa), Bacteroides forsythus (Bf)
(now Tannerella forsythensis), Porphyromonas gingivalis
(Pg), Prevotella intermedia (Pi), Fusobacterium nucleatum,
Campylobacter rectus, and Treponema denticola.
• Some of these putative pathogens can become
established in young children.
• When the bacterial insult is strong enough to
overwhelm host defense, bacteria in supragingival
plaque migrate subgingivally to form a subgingival
biofilm.
• Frequent professional supragingival cleaning, added to
good personal oral hygiene, has been shown to have a
beneficial effect on subgingival microbiota in
moderately deep pockets.
 TOBACCO

• Smoking was first identified as a risk factor from an

analysis of data from the 1971-75 National Health and
Nutrition Examination Survey in the United States
(NHANES I), which showed an association between
smoking and periodontal diseases, independent of oral
hygiene, age, or other factors.
• The evidence to identify smoking as a risk factor for
periodontitis has continued to mount since then and
assessments of randomly chosen patient groupings
invariably show a higher prevalence of periodontitis
among smokers.
• It has been stated that 90% of persons with refractory chronic
periodontitis are smokers, and healing following mechanical
treatment is slower in smokers. (Grossi 1997, Kinane 1997)

• Slower healing could come from the inhibition of growth and

attachment of fibroblasts in the periodontal ligament of
smokers and in their slower post-therapy reduction of white
blood cells and neutrophils. (James 1999, Christan 2002)
• Evidence on whether smoking promotes the growth of
periodontal pathogens is mixed. Earlier studies showed no
difference in prevalence of these bacteria subgingivally
(Presber 1992, Stolenberg 1993); but more recent evidence
suggests that smokers may have higher prevalence, rather
than counts or proportions, of pathogenic species
subgingivally. (Haffajee 2001, Zambon 1996)

• Smoking appears to promote a favorable habitat for these

species in shallow pockets.(Haffajee 2001, Eggert 2001)
• In experimental plaque-induced gingivitis, despite the
rate of plaque accumulation being equal in smokers and
non-smokers, the increase in gingival vascularity in
smokers was only half of that seen in the non-smokers.
(Bergstrom 1988, 1994)

• In effect, this is a masking effect on the signs of

inflammation and may be related to one reported
finding of no difference in the risk of gingival recession
between smokers and non-smokers with minimal
disease.
In other aspects of host response, smoking inhibits granulocyte function
and interactions between smoking and the IL-1 gene cluster have also been
identified. (Meisel 2002)

In that interesting study, no difference in mean CAL could be detected

between smokers and non-smokers in those who were genotype-negative
but for those who were genotype-positive, the smokers had considerably
greater CAL than non-smokers.

Smoking aggravates all tissue-destructive diseases, periodontitis included,

by priming the production of TNF-α, and it also causes the release of
cytokines. (Gustaffson 2000, Fredriksson 2002)

Smoking has been shown to be a stronger risk factor for periodontitis than
insulin-dependent diabetes mellitus. (Moore 1999)

The evidence is clear that smoking is a major risk factor for periodontitis.
 PREDICTING THE RISK OF PERIODONTITIS

• The research design has to be longitudinal, where

participants have measures of suspected predictors
measured at baseline (e.g., plaque, subgingival calculus,
tobacco use, diabetes, SES, specific cytokines in GCF,
psychic stress), and development of new periodontal
lesions or progression in existing lesions is noted over a
period of time.
• Cross sectional assessments are limited in their
usefulness.
• In a longitudinal design, the disease outcome can then be
related to the baseline measures.
• The presence of visible plaque and calculus, as one
example of a hypothesized marker, was long assumed to
predict future CAL or bone loss, but studies have shown
that clinical measures of plaque and calculus by
themselves do not predict future disease to any useful
extent.
• Models that have included the subgingival presence of
specific pathogens such as Aa,Pi, Pg, and Tf with other
indicators have shown a moderate degree of
predictability.
• Host response needs to be worked into the equation, and
it is now recognized that smoking and genetic
predisposition are major players in this regard.
• The baseline clinical indicators performed much better in
a model that included IL-1 genotype status in non-
smokers.

• What this body of research has demonstrated is that

multiple predictors work better than any one single
predictor by itself, although the nearest we come to a
universal predictor is tobacco use.
• Stress does seem to be associated with progressive
periodontitis, whether assessed in a case-control study,
cross-sectionally, or in a longitudinal design.

• Since psychosocial distress is a well-documented risk

factor for a number of different diseases,the
identification of its predictive role in periodontitis
strengthens the hypothesis that periodontitis is related
to systemic diseases.
 SUMMARY
1. Data on the prevalence of periodontitis are dependent
on how the disease is defined and the age group from
which they were taken.
• Some 5% to 20% of any population suffers from severe,
generalized periodontitis, although mild to moderate
periodontitis affects a majority of adults.
• For those who are most susceptible, periodontitis
becomes evident in teenage and early adult years rather
than the later years.
2. Risk factors for periodontitis include smoking, genetic
predisposition, probably psychosocial stress, diabetes,
and several uncommon systemic diseases.
3. Improved molecular biology techniques for measuring
bacteria and inflammatory cytokines haveaided recent
research in both epidemiology and clinical studies, and in
the future are likely to permit more precise diagnosis in
the clinic.
THANK YOU!!!   