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Epidemiology of Periodontal Diseases

and Risk factors

:Presented by
Mashael Foudah

Introduction
Types of epidemiologic researches
Epidemiologic Measures of Disease
Measures of association
Assessment of periodontal disease
Assessment of gingival inflammation
Assessment of Periodontitis
Assessment of Plaque
EPIDEMIOLOGY OF GINGIVITIS
EPIDEMIOLOGY OF AGGRESSIVE PERIODONTITIS
Epidemiology of Chronic Periodontitis
PATTERNS OF DISEASE AND TOOTH LOSS
PERIODONTITIS AS A RISK FACTOR FOR OTHER DISEASES
CAUSALITY OF PERIODONTAL DISEASES

Epidemiology is the science and practice concerned with


the distribution and determinants of states of health and
disease in populations
And
the application of this knowledge to control health problems.

goals of epidemiology are :


To understand the natural course of a disease and the
factors that influence its distribution.
To look for effective ways to reduce the occurrence or
sequelae of disease in the population.

Epidemiologists focus on groups of people rather


than on individuals.

Epidemiology is an interdisciplinary field that uses


methods from biostatistics, social and behavioral
sciences, immunology, genetics, microbiology,
clinical dentistry, and medicine.

Types of epidemiologic research

Observational

Experimental

Epidemiologic Measures of Disease


Incidence: Number of new cases that occur in a population over given
period of time.

Prevalence: Number or percentage of affected persons in population.

Extent: Number or proportion of teeth or examined site that are affected

with a given condition.

Severity: How advanced or serious a given condition.( slight,moderate


,severe)

Exposure: A factor that may possibly lead to disease or may be protective


against a disease ( cigarette smoker, ca intake, dental care ) Classified
according to the level of exposure or having been exposed or not.

Risk Factor: Characteristic (environmental-behavior-biologic

exposure) that is associated with a disease. The association may or


may not be causal and related to the disease through
longitudinal/cohort studies.

Risk Indicator: A probable risk factor that has been associated


with the disease through cross sectional studies. Not confirmed in
longitudinal study.

Risk Predictor / Marker: A factor that is associated with

increased probability of future disease, But where causality is usually


not implied.

Odds ratio:

Odds: represent the ratio of the probability of occurrence of an event to that


of nonoccurrence:
Odds ratio: is the ratio of two Odds.
Exposed

NON

disease

health

Odds of exposed among diseased :A\B ..... Odds of exposed among healthy: C\D
Odds ratio: ( A\B)/(C\D).
used as measures of association between exposure and disease in
cross-sectional ,case control studies.

Risk: it is the probability that a disease or event will occur.


Risk ratio: ratio of 2 risks
developed disease

non developed

non exposed C

exposed

Risk of disease development among exposed: A\(A+B).


Risk of disease development among non exposed: C\(C+D)
RR= A/(A+B) / C/(C+D)

It is frequently used as measure of association between exposure and disease in cohort studies.

Observational
studies

The researcher acts as a spectator who documents the


natural course of events and draws conclusions.

Disadvantage:
The effect of confounders can never be completely ruled
out.
A confounder : is an extraneous factor that distorts the
effect of the exposure or characteristic of interest.
(access to dental care and to education)

Observational

descriptive

analytic

casecontrol

Cross-*
sectional

case
reports

case
series

* Cross-sectional studies can be used as analytic as well

cohort
studies

ecologic
studies

Descriptive studies:

Used to provide basic knowledge about the characteristics,


frequency, and distribution of a health-related condition.

These studies characterize the occurrence of the disease with


respect to :
Personal (e.g., age, sex, race/ethnicity),
Geographic (i.e., geographic distribution),
Time.

Essential for the formulation of a hypothesis regarding :

the etiology of the disease.

the implementation of rational and cost-effective health care


programs.

establishing a baseline assessment for future evaluation of


preventive and therapeutic interventions.

Analytic studies:
To test a specific hypothesis regarding:

Etiologic or non-etiologic factors that may be


associated with the presence of the disease.
Factors predict the future occurrence of the
disease.

Cross- Sectional studies

The researcher examines a group of subjects with an unknown history of


exposure or disease and assesses
o their health status.
o the presence of factors that may be associated with disease.
The subjects are evaluated only at a single point in time.

Cross-sectional studies are valuable at studying chronic diseases that


affect a large proportion of the population (e.g., chronic periodontitis).
They are not efficient to study rare conditions or conditions that may
only last for short periods (e.g., periodontitis associated with PapillonLefvre syndrome).

Advantage:
1. examine changes in the prevalence of a disease or risk factors
that can vary over time.
2. demonstrate trends of the disease over time.
3. evaluate the effects of preventive or therapeutic programs.
. Disadvantage:
1. do not follow the population over time.
2. difficult to assess if a given factor preceded the onset of a disease.

Case- Control studies

CASE: group who


have the disease

Control subject: group


without the disease

- Assessed for the history of exposure or the presence of putative risk factors.
- Assessed the frequency, or levels, or both, of the exposure.

Compared statistically to assess if there are associations between


the exposure of interest and the presence of the disease.

Advantage:
Most efficient way to study conditions that are not
highly prevalent.
Used to study chronic and aggressive periodontitis.

Disadvantage:
Do not follow the subjects over time.
Difficult to assess if the exposure preceded the onset of
disease.
Difficult selecting a control group of individuals without
disease that is representative of the general population.

Cohort studies
The researcher
1. Will gather a group of individuals without disease
2. Will classify them according to the presence or levels of exposures of
interest .
3. The subjects are then followed over time.
. If the incidence of the disease is greater among the subjects who were
exposed to a given factor
This factor may be considered to predict the development of the disease.
Can establish if exposure to some environment or behavior
preceded the onset of disease.

For the study of periodontitis is difficult and expensive:


-To recruit a large group of young individuals without disease who are
representative of the overall population.
-Variations in the exposure over the follow-up period would complicate
interpretation of the results.
-To assess exclusively disease-free individuals.

Advantage:
Provides valuable information regarding predictors of disease progression
Disadvantage:
They cant ascertain if the exposure of interest preceded the onset BUT
they provided valuable information regarding progression.

Ecologic studies
-The unit of analysis is a group of persons rather than an individual.
-Not been frequently used in the study of periodontal diseases.
-Two types of ecologic studies:
ns
o
ris
a
mp
o
C

* the researcher gathers


information regarding the overall
prevalence or incidence of the
exposure and disease
in various populations
and categorizes them
according to their level of exposure

Tre
nd
s

* the researcher studies


possible relations between
changes of disease level
in a given population
over time

Experimental
studies
The researcher has control over
the exposure of interest
subjects assigned to exposed or non-exposed groups
the characteristics of the exposure and factors that may
influence the subject's response
Used to assess:
The role of potential determinants of a disease. OR
The effectiveness of therapeutic or preventive
interventions.

Study
group
Receive intervention

Control
group
Receiving another intervention
or no intervention

Experimental studies produce stronger evidence of the effects of


an exposure than observational studies.

Experimental

Clinical trials*

randomized
parallel-arm
design

crossover
design

Community trials

split-mouth
design

*to assess the safety and efficacy of new drugs, therapies, and procedures used for the
treatment of a disease.

Parallel arm design:

Studies in which subjects are randomly assigned to either


Control
group

Experimental
group
followed over time.

In parallel-arm studies, each subject will be part of one treatment


group and there may be two or more study groups.

The response to the intervention of each group will be compared with


the response of the other groups.

Cross over design:

Used to test the effects of interventions that are fully reversible


and do not have a lasting effect (e.g., antiplaque agents).

Crossover studies have three phases:


Experimental phase I.
Washout period.
Experimental phase II.

the responses of each subject during phase I of the study will be


compared with his/her response during phase II

Split mouth design:

Each subject will receive two or more types of therapy to treat


lesions of similar characteristics that are located in different
parts of the mouth.
conducted to compare the effects of surgical versus nonsurgical
therapy in the treatment of chronic periodontitis .

Community trials

Used to evaluate the effects of educational campaigns, behavior


change, or policy change on the health status of a population
Disadvantage:
It is impossible to control for the possible influence of
differences among populations.

MEASURES OF ASSOCIATION

Uses:
To assess the presence of a relation between an
exposure and the occurrence of the disease.
To describe the direction and magnitude of such
an association.

ssessment of periodontal disease

Periodontal tissue destruction is generally a gradual process.


Unevenly distributed within the mouth.
Often presents great variability of severity from site to site.

The prevalence of periodontal disease in a population have a limitation:


There is difficulty in establishing a valid threshold to distinguish health from
disease.
There is no consensus about the number of sites or teeth that should meet a
given threshold for an individual to be considered as having disease.
The lack of uniform criteria to define disease.

Differences among studies due to:


Examiner variability
The use of different partial-mouth recording systems
Differences in the parameters scored and indexes used
Variation in the instruments used
Differences in examination conditions.

-Numerous indexes and examination protocols were developed.


- The main purpose of such recording systems was to express the
gingival and/or periodontal condition in numerical values.
- Each of these index systems and examination protocols had
properties, assumptions, and limitations that influenced the study
results.
-The selection of the most appropriate approach is determined by
the research question and the study design.

sessment of gingival inflammation

Most of these methods categorize the extent and severity of gingival


inflammation based on the assessment of gingival color, contour, and
bleeding.
The first index described to assess the extent of gingival inflammation
was the PMA (papilla, margin, and attached gingiva) index.
Based on a count of the number of facial interdental papillae, marginal
gingival sites, and attached gingival units that were inflamed.
The sum of the affected units was used as the PMA score for a given
person
The most widely used systems to characterize gingival inflammation in
observational and experimental epidemiology are the 1 Gingival Index
(GI) of Le and Silness and 2 the bleeding on probing index.

Gingival Index (GI) of Le and Silness

Is sensitive enough to detect small differences in


gingival inflammation.
The gingival areas surrounding each selected tooth
are scored according to the criteria
The scores are averaged to determine a mean GI score for
each individual.

BOP Index

Induce bleeding by: periodontal probe, wooden wedges or floss.


Method of scoring :
Presence or absence of bleeding (most used).
Degree of bleeding.

Variation on BOP due to:


*Probing force.
*Probing type.
*Angulation.
*Time between probing & assessment.
It was reported that 14% sites bleed immediately and 55% sites delay.
(Stoltenberg JL et al.1993)

Histologic and clinical findings indicate that bleeding on probing is an


earlier and more sensitive sign of inflammation than redness and swelling.
Greenstein G et al. 1981 /Hirsch RS et al.1981./ Mhlemann HR and Son S,1971.

Assessment of Periodontitis

In contemporary epidemiology, the description of the periodontal


condition of populations is generally based on full- or partial-mouth
assessments of probing depths (PDs), CALs, and gingival recession.
In the description of periodontal disease in a population, three
features should be described: prevalence, extent, and severity of
periodontal destruction
It is difficult to compare results from the literature on
epidemiology of periodontal diseases due to:
Lack of a consensus definition for disease.
Different research methodologies.

Periodontal Index (PI) (described by Russell in 1956)


Combined assessments of:
Gingival inflammation, periodontal pockets, and tooth
mobility into a single score.
Limitation :
Does not distinguish between gingivitis and periodontitis.
Assessment of periodontal pockets is made visually
without the aid of a periodontal probe.

Periodontal Disease Index (PDI) (1959, Ramfjord)


The PDI includes both gingivitis and periodontitis in a
single index system .
It used a subset of teeth as representative of the overall
periodontal condition.
This tooth subset

(3, 9, 12, 19, 25, 28) *Universal


(16,21,24,36,41,44) *FDI

often referred to as the "Ramfjord teeth"

Computer-Assisted Subtraction Radiography

Advantages :
Very precise.
Detect bone level differences = 0.5 mm (between two radiographs).
Detects and quantifies differences in bone levels and bone density
between the two digitized radiographs.
Useful tool for clinical trials.

Assessment of progressive bone loss are currently not


practical for population-based studies, due to :
Technique-sensitive.
Expensive.
Time-consuming.
Radiographic bone levels are closely related to clinical attachment
levels BUT, they are more easily obtained with a probe.

Community Periodontal Index of Treatment Needs (CPITN)


(1978,WHO recommended)

Advantage :
Simple.
Practical.
Valid.
Disadvantage :
Unable to distinguish between pretreatment and posttreatment
conditions.
It overestimates certain treatment needs in the population.

Assessment of Plaque

Some plaque index system estimate :


Presence or absence of plaque(distribution).
Quantity of plaque.
Some index require plaque disclosing solution.

Systems :
Turesky modification of Quigley & Hein plaque index.
Plaque index.

Turesky modification of Quigley & Hein plaque index.


Used in clinical trial.
Used for evaluation of antiplaque measures such as tooth
brushing, flossing, and mouthrinses.
(need Disclosing solution)

Plaque Index
The most frequently used plaque indexes in
observational epidemiologic studies.

(no need for disclosing solution)

Disadvantage : need well trained examiner.

Full-Mouth Versus Partial-Mouth Examinations


A full-mouth examination, including individual recordings of
six sites (i.e., mesiofacial, facial, distofacial, mesiolingual,
lingual, and distolingual) on each of the teeth present in the
mouth, is the ideal method to characterize periodontal
conditions.
A variety of tooth subsets have been proposed for partial-mouth
examinations, but the most frequently used are the tooth
subsets originally proposed for the CPITN index, the Ramfjord
teeth, and the half-mouth examination protocol.

Accurate Extent & Severity

Half-mouth / Ramfjord

Overestimates Extent & Severity


Underestimate Prevalence

CPITN

ALL But CPITN is better than the other 2

PIDEMIOLOGY OF GINGIVITIS
Gingivitis is a gingival inflammation in the absence of clinical
attachment loss or in the presence of reduced but stable
attachment levels
(Mariotti A,1999)

In most epidemiologic studies, no distinction is made between


gingival inflammation with or without attachment loss (as a
clinical sign rather than a diagnosis).

All epidemiologic studies conducted have shown that


gingivitis are strongly associated with plaque levels.

"experimental gingivitis" study of Le and coworkers in 1965:


10-21 days are necessary to develop visible signs of gingivitis.
Gingivitis mostly affect the interdental area of posterior teeth.
Distribution reflects where patients are less effective at plaque control.
Changes in the composition of the bacterial flora
Aging, smoking, diabetes mellitus, HIV infection, and hormonal changes
may influence gingival inflammation by altering the host response to
bacterial plaque.
Gingivitis is also more prevalent, extensive, and severe in
groups
With low socioeconomic status.
Groups with limited access to dental care.
Groups with less education.
Mentally handicapped individuals.

Factors that influence gingivitis by altering host response:


Age

Gingivitis is a highly prevalent in early childhood.


Between 35% to 85% of 3- to 6-year-old.
Prevalence, extent, and severity of gingivitis gradually increase during
childhood, peaking in severity during puberty.
Increase may be influenced by:
- The effect of increasing levels of sex hormones.
- Change On tissue physiology
- The colonization of periodontal bacteria.

After puberty gingival inflammation decrease.


Throughout adulthood remain stable or slightly increase.
Absence of oral hygiene, younger develop gingivitis slightly faster
than older.

Tobacco use
- Delay in inflammatory response to plaque accumulation. Suppressed intensity of the vascular reaction to plaqueinduced gingivitis.
D.M.
Tend to present more gingival inflammation than healthy.

Pregnancy
Gingival inflammation and periodontal diseases gradually
increase during pregnancy, with resolution after parturition
which is unrelated to the amount of plaque.
An even more exaggerated inflammatory response is the
pregnancy-associated pyogenic granuloma0.5% to 5%
at first trimester.

EPIDEMIOLOGY OF
AGGRESSIVE
PERIODONTITIS
Aggressive periodontitis: which occurs in healthy patients, is
characterized by rapid clinical attachment loss and bone
destruction.
The true incidence or even prevalence of aggressive periodontitis is
difficult to determine from published reports because:

Most surveys were cross sectional in nature, making it impossible to


determine the rate of disease progression. Rates of disease progression
can only be determined through prospective or careful retrospective
evaluations of individuals.
Different tools (e.g., probes, radiographs) have been used to assess
participants.
A variety of diagnostic criteria have been used to define this disease.
In many surveys, especially the largest ones, cases were identified using
partial-mouth examination protocols.

WORLDWIDE DISTRIBUTION
More prevalent in black individuals including African, AfricanAmerican, or Afro-Caribbean than white individuals.
Scandinavians and whites individuals of northern European
descent are infrequently affected.
There is insufficient evidence to determine that differences.
AGE
Occur at any age.
Previously referred to as Juvenile or early-onset periodontitis
(young or adolescent-puberty to 25 )
In adolescents usually starts as localized condition (first molar and
incisors), it can remain localized or spread. In young adolescents,
localized form usually found more than generalized form.

About 35% of localized aggressive disease re- classified to G.A.P over


period of time.

SEX
Studies There is no sex predilection.
Some more common in female. ( Albandar JM et al 1991 /1993)
Other claim the opposite. (Le H and Brown LJ 1991 / Albandar JM et al 2002)
In U.S. adolescents male more likely to have generalized form.
RACE/ETHNICITY
Only two surveys, both conducted in the United States, have
been large enough to permit a robust comparison among
racial groups. Between 5,000 and 11,000 young adults :
- 2.1-2.9 % black
- 0.09 0.17% white
- 6.5 % Africa & 3.7 % South American youths

SOCIOECONOMIC STATUS
In the general population, the extent and severity of periodontitis is
inversely related to educational level attained and income.
Children from low socioeconomic strata (SES) also appear to be at
greater risk for attachment loss, but not necessarily aggressive
periodontitis.
Socioeconomic factors could be considered, at best, risk indicators and
not risk factors for disease.

DIABETES MELLITUS
The people with diabetes, especially those with long-standing poor
metabolic control, may be at increased risk for periodontitis in
general.
Diabetes mellitus has not been established as a risk factor for
aggressive periodontitis.
TOBACCO USE
Smoking is a strong risk factor for chronic periodontitis.
It is less clear in aggressive periodontitis.
Some evidence that smoking can alter the severity and extent of
generalized aggressive disease.

ORAL HYGIENE
Currently, no associations between aggressive periodontitis and
oral hygiene have been established.
Aggressive periodontitis can occur in healthy young individuals
with good oral hygiene.

Genetic Epidemiology of
Aggressive Periodontitis
The evidence that genetic factors affect the risk for AP
summarized as follows:
The prevalence rate of disease is greater in first-degree relatives
(parents, siblings, and offspring).
The disease is a consistent feature in several genetic or inherited
disorders. (Leukocyte adhesion deficiencies, Chediak-Higashi
syndrome)

Segregation analyses implicate the role of a major gene.


(Marazita ML et al 1994 / Beaty TH et al 1987)

At least one form of disease, which cosegregates with dentinogenesis


imperfecta, has been linked to a specific region on a chromosome.
(Boughman JA et al 1986)

Several genetic polymorphisms have been associated with the disease.

emiology of Chronic Periodontitis


Epidemiologic studies conducted between 1950 and 1970
used (PI) to characterize the periodontal conditions of
populations:.
Strongly associated with poor oral hygiene,
Calculus,
Low SES and
Lack of access to dental care and education.
groups with limited access to dental care and those from
developing nations were found to have more disease than
populations from industrialized countries.

The model of the pathogenesis of periodontitis in the


1950s to 1970s was based on these beliefs:
All individuals were equally susceptible to periodontitis.
Long-standing gingivitis invariably progresses to periodontitis
with subsequent tooth loss.
Susceptibility to periodontal disease increases with increasing age.
Risk for periodontal disease was determined by environmental
factors alone. Poor oral hygiene and age were believed to account
for 90% of the differences among individuals.

Recent concepts have been challenged by the following:


1. All individuals are not equally susceptible to periodontitis.
2. Small percentage of sites with untreated gingivitis will develop
periodontitis.
3. The susceptibility to future periodontal breakdown seems to be
independent of age.
4. Periodontal disease is a complex disease and can be attributed to
environmental exposures (e.g., Gram-negative bacteria, oral
hygiene, dental care, smoking, and others), whereas the remaining
variation is attributed to differences in host susceptibility.

In a longitudinal study of Sri Lankan tea laborers


with no access to dental care and poor oral
hygiene:
In this environmentally homogeneous population,
11% of the subjects had slow progression.
81% were categorized as having "moderate" progression.
8% experienced "rapid" progression.
(Le H et al 1986)

Sri Lankan
tea
laborers

Norwegian
scholars
and
students

Mean moderate CAL 5.4mm


at 41-45y.o

Mean moderate CAL 1.1 to 1.6mm


at 41-45y.o
They conclude two important feature :
1) Severe disease tends to cluster in a small fraction
of the population.
2) Differences in disease susceptibility within a
population that are independent of the environment.

Factors Associated with chronic Periodontitis


Age

Clinical attachment loss and alveolar bone loss become more


prevalent, extensive, and severe with advancing age.
Clinical attachment loss appears to be more commonly
associated with gingival recession than with pocket
deepening.
Reflects how long an individual has been exposed to etiologic
factors

Sex

In the United States and in most industrialized populations:


Male more than Female.(attachment loss, deep pocket,BOP).

Socioeconomic Status, Dental Care, and Race

SES is related to: Personal income, educational level, and


occupation.
Low SES has more severe Periodontitis.
Racial/ethnic differences are most likely the result of socioeconomic
differences, education, and access to health care rather than true
differences in disease susceptibility (e.g., genetic differences).
CAL (facial) + Recession (more in white).
CAL (Interproximal) + Pocket (in black).
When the periodontal conditions of white, black, and Mexican
American individuals are compared after standardizing for income,
frequency of dental visits, and calculus, most of the differences in
disease severity disappear

Oral Hygiene, Calculus, and Gingival Inflammation


Bacterial plaque is sufficient to cause gingivitis.
Undisturbed bacterial plaque alone is not sufficient to cause
periodontitis.
Plaque plays a central role in the initiation of gingival
inflammation and calculus.
Poor plaque control affect periodontal treatment success.

Tobacco Use

Cigarette smoking is the strongest modifiable risk factor for the


occurrence of periodontal disease. (two to six times )
This relation is independent of potential confounders including
oral hygiene.
With good O.H., smokers have more bone loss than nonsmokers.

The deleterious effects of tobacco on


periodontal health are:
*Impairment in the host immune response.
*Tobacco smoke may directly or indirectly influence
bacterial colonization in the oral cavity.
*The rate of recovery of periodontal pathogens from
relatively shallow pockets is greater in smokers.

Diabetes mellitus

Individuals with diabetes, especially those with poor metabolic control,


have more extensive and severe periodontal destruction than otherwise
healthy persons.
Patients with either type are at increased risk for periodontitis.
The deleterious effect of diabetes on the periodontium appears to be
cumulative, because patients with long-term diabetes tend to have
greater attachment or bone loss than those who have had diabetes for
shorter periods

The metabolic control of diabetes is also strongly related to the incidence


and severity of periodontal disease.

Well controlled D.M. = without D.M.(The same level of peridontitis)

Recent evidence suggests:

reciprocal relation between diabetes and


periodontitis.

each may influence the development of the other.


* Before, diabetes appears to increase the risk for
periodontitis.

* Recently hypothesized that periodontal


inflammation may increase insulin resistance, which
leads to increases in blood glucose.

HIV Infection
HIV,,,,,,CD4< 200 Cells L.
Increased risk for severe chronic periodontitis.
HIV-infected patients accompanied by gingival recession
and shallow pocket depths.
Intraoral lesions have been described in HIV-positive and
AIDS patients.

Osteoporosis
Individuals with osteoporosis (i.e., low skeletal bone density) are also
at increased risk for periodontitis.
Systemic up-regulation and increased production of IL-1 and IL-1,
TNF-, and IL-6 induce osteoclastic activity and increase bone
turnover rates that lead to loss of bone mass and osteoporosis.
Systemically up-regulated cytokine response may also be more
susceptible to periodontitis in the presence of local irritants.

Most observational studies conclude that patients with low skeletal


bone mineral density have slightly more periodontal disease than
healthy control subjects.

Nutrition

Severe nutritional deficiencies are at an increased risk for


development of acute periodontal lesions.
Severe vitamin C deficiency (i.e., scurvy) lead to severe inflammation
and spontaneous bleeding.
Most epidemiologic studies have failed to find significant relations
between nutritional status and chronic periodontal disease
A recent cross-sectional study indicated that adults in the United
States who reported low dietary intake of calcium and vitamin C
tended to have more clinical attachment loss than those with high
intakes.

Hormone Replacement Therapy

Women who use hormone replacement therapy have


slightly less gingival inflammation and clinical attachment
loss than age-matched women who do not.(Estrogen)

Psychological Factors

Recent epidemiologic studies suggest that periodontal


disease is more prevalent and severe among persons who
report being psychologically stressed or depressed.

Risk Factors
Risk Indicators
Possible Risk Factors

Tobacco
D.M
HIV
Age
Sex
SES
Osteo
porosi
s
Stress

Genetic Epidemiology of Chronic Periodontitis


Studies using family correlations (e.g., sibling, parent-offspring) to
estimate genetic and environmental variances.

Suggest that similarities within families are mainly because of


cultural inheritance and the common family environment, but not
shared genes

Twin studies have supported the theory that


genetic factors significantly influence the risk for
chronic periodontitis.
More specifically, these studies have found that a
significant portion of the variance in PD and clinical
attachment loss measures is attributable to genetic
variance.
It has been estimated that approximately 50% of the
variance in disease can be attributable to genetic
variance (i.e., heritability is about 50%).

Oral bacteria can be transmitted within families


This finding could explain, in part, why some forms of periodontitis are
familial.

-introduction of bacteria into the oral cavity is an environmental


event.
- long-term colonization may be determined by both host genetic
and environmental factors.
-although host genes may influence early bacterial colonization of
the oral cavity, the effect does not persist into adulthood.

In 1997, Kornman and colleagues :


First reported that a "composite" IL-1 genotype, was
associated with severe periodontitis in a small group of
nonsmoking Northern European adults.
Others have reported no association.
Inconsistencies in the specific alleles found to be associated
with periodontitis.
IL-1 composite genotype may be useful as a prognostic factor.
Gore and colleagues found the less common IL-1B allele, but
not the composite genotype, to be more prevalent in patients
with severe chronic periodontitis.

Chronic periodontitis is a complex and


multifactorial disease in which the host's
genetic makeup can modify the course of
disease rather than cause it.

Disease will not ensue in the absence of


pathogenic microorganisms.

PATTERNS OF
DISEASE AND
TOOTHAttachment
LOSSloss :
- Accompanied by pocket formation or associated with gingival recession.
- More commonly with ginigival recession.
- In a longitudinal study of elderly subjects, only 58% of sites that lost
attachment demonstrated an increase in PD. The remaining 42% of
progressing sites had gingival recession .
(Brown LF et 1994)

- Facial sites tend to have CAL accompanied by recession.


- Proximal sites are more prone to develop periodontal pockets.

The association between calculus and gingival recession because of:


-Calculus acts as a plaque-retentive factor.
- Recessed sites facilitate the formation of calculus.
-It is simply easier to detect calculus when the gingiva is recessed.

Tooth loss :
Severe periodontitis is most frequently found in the
posterior teeth, and the distribution appears to be
symmetric in both jaws.
Upper teeth are more frequently lost than lower teeth.
The lower canines were by far the teeth least frequently
lost.

In industrialized countries and many developing nations


Between 20% and 50% of the permanent teeth extracted
in industrialized nations are extracted for periodontal
reasons.
(Ong G,1998)

Various studies have indicated that periodontitis is the


leading cause of tooth loss in the United States among
adults 40 years and older
(Oliver RC and Brown LJ,1993)

Obviously , the percentage of


tooth loss associated with
periodontal disease is highly
dependent on the caries
rates of the population.

PERIODONTITIS AS A
RISK FACTOR FOR
OTHERHypothesized
DISEASES
that :
Persons with periodontitis are at increased risk for

development of cardiovascular diseases (e.g., myocardial


infarction and stroke) and respiratory diseases.

pregnant women with periodontal disease may be at


increased risk for having preterm delivery or LBW.

patients with diabetes, periodontal disease may lead to


increased glucose levels.

CAUSALITY OF
PERIODONTAL
DISEASES
No single environmental
factor(behavioral, microbial)or genetic
is both necessary and sufficient to cause periodontitis.

Diseases with etiologies that include various genetic and


environmental factors are referred to as
multifactorial Disease.
A sufficient cause a model to understand multifactorial diseases
represents a set group of minimal conditions or events that invariably
lead to disease occurrence.

Factor should be evaluated when considered as part of the


causality of the disease as following :
1) Strength of the association.
2) Presence of dose-response effects.
3) Temporal consistency (i.e., the exposure should consistently precede
the occurrence of disease).
4) Consistency of findings.
5) Specificity of the association.
6) Overall coherence of the evidence.

Future epidemiologic
research assessing
the interaction of
host susceptibility
factors (e.g., genetic
risk factors) and
environmental
factors are
necessary.

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