PERIODONTAL

MEDICINE
Dr Harshavardhan
Patwal
Historical backdrop –
evolution on the concept of “focal
infection”
Hippocrates (460-370BC) – noted a case of
rheumatism cured after infected tooth
extraction.

Benjamin Rush (1745-1813) – recognized

relation of oral infection to general health.

W.D.Miller (1853-1907) – proposed oral

infections as the cause of many diseases.
William Hunter (1861-1937) – indicted dentistry
as a cause of what he called “oral sepsis” –
that caused rheumatic & other chronic
diseases.

Major infectious oral focus was the

periodontium and not periapical disease.

G.V.Black – important part of dental profession

in preserving general health.

Frank Billings, Edward C. Rosenow, Charles H.

Mayo – interested in the same concept.
 Cecil.R (1938) – no improvement in
rheumatoid arthritis patients after teeth
extraction & tonsillectomy.

Williams & Burkett – found no good scientific

evidence to support “focal infection theory”.
 Many patients with diseases presumably caused by foci of
infection have not been relieved by removal of foci
 Patients with same diseases may not have detectable foci of
infection
 Foci of infection can occur in healthy persons with no ill
effects. Journal of the American Medical
Association (1952)
Concept of focal infection resurfaced
with the work by Mattila et al., 1989

Case-control study using a Dental Severity Index –

Dental health significantly worse in patients with MI
versus controls
CONCEPT OF “ FOCAL INFECTION”

 “Oral sepsis as a cause of disease” ( William

Hunter, 1900)

 Superseded by ‘focal infection’ – introduced

by Frank Billings (1911)

 “Circumscribed area infected with micro-

organisms which may or may not give rise to
clinical manifestations” (JADA, 1951)
Two major mechanisms of focal
infection

the spread of toxins or

an actual
metastasis their products from
of organisms a remote focus to
from a focus other tissues
by the blood stream
 Metastatic
Metastatic inflammation due to
infection from the Metastatic immunologic injury
oral cavity due to injury due to caused by oral
transient oral microbial micro-organisms
bacteremia toxins

Debelian et al., (1994) identified 3

pathways
 But why periodontal disease
is projected………..….
……..??
Is Periodontitis – a unique infection?

Unusual anatomic feature of the tooth – part of it

exposed to external environment while part is within
the connective tissues.

Non-shedding outer layers of the tooth – facilitates

diverse microbial colonization held in proximity to
soft tissues of periodontium.

Biofilm-induced disease – protective environment

for colonizing organisms.

Polymicrobial infection
It is a longstanding chronic infection that is
asymptomatic most of the times.

Normal daily activities like chewing, brushing

and flossing can cause a transient bacteremia ( in
the process, cytokines and mediators are also
pumped out into systemic circulation).

Complexity of treatment – physical,

antimicrobial, ecologic approach
 Periodontitis disturbs systemic homeostasis

Chronic damage of epithelial tissues

due to periodontitis

may induce the periodontal pocket to

ulcerate that allows access to
the bloodstream

Bacteria and their toxins,

cytokines,mediators of inflammation

disrupt homeostasis when toxins

gain entry to the systemic circulation
The proinflammatory cytokines TNF-α,
IL-1β, and gamma interferon as well as
PGE2 reach high tissue concentrations in
periodontitis
Periodontium –
as a cytokine
reservoir

renewing reservoir for spillover of these

mediators; enter the circulation induce
and perpetuate systemic effects
Comparison of surface areas in the human mouth
(J Dent Res 1991;70:1528-30)

AREA IN MALES FEMALES % TOTAL

MOUTH MEAN AGE MEAN AGE MOUTH AREA
20.7(SD 16.8(SD
13.4) 8.02)
Teeth 39.8cm2 35.9cm2 23.9

Palate, 127.0cm2 118.8cm2 76.1

buccal/lingua
l alveolar and
gingival
mucosa,
buccal
vestibular
mucosa,
tongue

Total mouth 166.8cm2 154.7cm2

area
Incidence of Bacteremia During Different Dental Procedures
(Heimdahl et al., 1990)
Surgical % of Patients %Viridans % Anaerobes
Procedure with group
Bacteremia streptococci

Dental Extraction
100 85 75
Scaling and Root
Planing 70 55 65

Third Molar
Surgery 55 40 45

Endodontic
Treatment 20 15 5
Bilateral
Tonsillectomy 55 40 40
Subgingival environment as a reservoir
of bacteria –
total surface area of pocket epithelium in contact
with subgingival bacteria & their products in a
patient with generalized moderate periodontitis –
estimated to be approximately the size of the palm
of an adult hand with larger areas of exposure in
cases of more advanced periodontal destruction
(Roy.C.Page,1998).
 What is Periodontal Medicine?

– a new insight into the old

problem envisioned!
 Periodontal Medicine

The term “Periodontal Medicine” - first

suggested by Steven Offenbacher
(1996)

Definition

“Rapidly emerging branch of periodontology

focussing on the wealth of new data establishing
a strong relationship between periodontal
ealth or disease and systemic health or disease”
 A paradigm shift

Inflammation
Infection
Commonality between Periodontitis and
systemic diseases

INFLAMMATION
Oral inflammation-systemic disease
association
Is periodontitis a risk factor for
systemic diseases?

Risk factor – distinctive characteristics/

exposures that increase the probability
of disease outcome (Albandar, 2002).

Bradford’s criteria (1971)

Temporal consistency Dose-response effect Strength of association

Specificity of association Consistency of

Biologic plausibility the findings
 IS PERIODONTITIS A RISK FACTOR
FOR………….??

Cardiovascular disease
Diabetes mellitus
Adverse pregnancy outcomes
Respiratory infections
Rheumatoid arthritis
Renal dysfunction
Alzheimer’s disease
 PERIODONTITIS & CVD
Cardiovascular disease
refers to the class of
diseases that involve the
heart and/or blood vessels. It
is usually used to refer to
those related to
atherosclerosis.

Atherosclerosis
variable combination of
changes of the intima of
arteries consisting of a focal
accumulation of lipids,
complex carbohydrates,
blood and blood products,
fibrous tissue and calcium
deposits and associated with
medial changes (WHO study
group).
Atherosclerosis

Stroke – Normative Aging study

(Jimenez,2010)
& (Joshipura et al.,2003) – positive
association between periodontal
disease and stroke.

Infective endocarditis
STAGES IN THE DEVELOPMENT OF
ATHEROSCLEROSIS
DEVELOPMENT OF FATTY STREAK

 Accumulation of monocytes in the vessel

intima – hallmark event in the development of
early atherosclerotic lesion – ‘fatty streak’.
 Adherence of monocytes to endothelium –
migration via diapedesis (chemoattractant
gradient – MCP-1).
 Maturation of monocytes to macrophages –
express scavenger receptors – engulf modified
lipoproteins.
 ‘Foam cells’ – lipid-laden macrophages in the
vessel intima.
Macrophages in the developing plaque

 Macrophages multiply, release GF and

cytokines – amplify and sustain the pro-
inflammatory signals.

 Macrophage colony-stimulating factor –

important mediator in the transformation and
proliferation steps; critical for the development
of atherosclerosis (Smith, Trogan, Ginsberg,
1995).

 Upregulation of scavenger and toll-like

receptors. (Peiser, Gordon, Mukhopadhyay,
Janeway, 2002).
PROGRESSION TO COMPLEX PLAQUE
 Accumulation of fibrous tissue in vessels –
complex plaque.

 GF and cytokines from endothelial cells or

monocytes stimulate migration of smooth
muscle cells into intima.

 PDGF, IL-1, TGF-Beta – stimulate smooth

muscle cells to produce interstitial collagen.

PLAQUE RUPTURE
 Clinical sequelae develops following rupture
and thrombosis.
 Physical disruption of the plaque – thrombus
formation, expansion of the lesion.
Potential mechanisms linking periodontal
infections and atherosclerosis

Role of bacteremias
 Entry of oral bacteria &/or their products into
bloodstream – key initiators of biological
events linking oral infections to AVD.

 Ulcerated surface amounting to up to 8-20cm2

(Hujoel et al.,2001) ; proximity of highly
vascularized tissue to subgingival biofilm
(Nanci & Bosshardt,2006).

 Disruption of the pocket epithelial integrity –

point of entry for pathogens.
 Vascular Endothelial Activation

 Streptococcus mutans (Abranches et al.,2009)&

Porphyromonas gingivalis – invades vascular
endothelial cells (Deshpande et al.,1998; Dorn
et al.,1999; Progulske-Fox et al.,1999)

 Invasion depends on fimbriae & hemagglutinin

(Takahashi et al.,2006).

 Arginine-specific gingipain – induces

exocytosis of Weibel-palade bodies through
activation of PARs(Protease activated
receptors).
 Endothelial dysfunction – more pronounced in
periodontitis patients (Amar et al., 2003;
Mercanoglu et al., 2004)

“Endothelial stunning” – transient reduction in

endothelium dependent dilatation when cells
are exposed to endotoxins (Bhagat et al.,
1996).

 Induction of apoptosis in endothelial cells

 Induction of vascular cell proliferation

smooth muscle cell proliferation

thickening of vessel media

Mechanistic pathway

Nuclear factor-kappa B – nuclear

transcription factor.

LPS,IL-1,TNF-alpha – nuclear
translocation & transcription

Macrophage activation (release of large

quantities of pro-inflammatory
cytokines) and regulation of smooth
muscle cell proliferation.
4 specific pathways proposed

Direct bacterial effects

on platelets

Autoimmune response

Invasion and/or uptake

of bacteria in endothelial cells
and macrophages

Endocrine-like effects of
pro-inflammatory mediators
 DIRECT BACTERIAL EFFECTS ON PLATELETS

Oral bacteria – P.gingivalis,

Streptococcus sanguis express
virulence factor, collagen-like
platelet aggregation
associated proteins –
induce platelet aggregation
in vitro and in vivo
(Hertzberg &Meyer
1996,1998)
AUTOIMMUNE RESPONSE

Antibodies cross-react with periodontal bacteria

and human HSP
(Hinode et al,1998, Sims et al., 2002)

‘Homotolerance’ – mechanism to fine-tune

immune system to ignore low-level
stimulation by PRR. Emerging as a
critical driver in periodontal disease and
atherosclerosis progression.
 INVASION OF BACTERIA INTO ENDOTHELIAL
CELLS AND MACROPHAGES

Deshpande et al demonstrated
that P.g can invade aortic and
heart endothelial cells via
fimbriae.

Macrophages incubated in vitro

with P.g and LDL take up
bacteria intracellularly and
transform into foam cells
(Giacona et al., 2004)
 ENDOCRINE-LIKE EFFECTS OF PRO-
INFLAMMATORY MEDIATORS

 Upregulation of mediators in
vascular tissues
 Elevation of CRP
and fibrinogen
(Slade et al.,2000,
Wu et al.,2000)
 Subgingival biofilm

Constitute an enormous and continuing bacterial load

Continually renewing reservoirs of LPS

ready access to the periodontal tissues and the circulation

Systemic challenge with gram-negative bacteria(LPS)

induces major vascular responses

inflammatory cell infiltrate in the vessel walls
vascular smooth muscle proliferation
vascular fatty degeneration-and intravascular coagulation

LPS upregulates
expression of ECAM,secretion of IL-1, TNF-α, and TXA2,
platelet aggregation and adhesion,
formation of lipid-laden foam cells,
deposits of cholesterol and cholesterol esters.
Microorganisms indicated in atherosclerosis

Viruses – Herpes virus

Cytomegalovirus
Bacteria – Chlamydia pneumoniae
Helicobacter pylori
Oral pathogens
Porphyromonas gingivalis
Streptococcus sanguis
Actinobacillus actinomycetemcomitans
Bacteroides forsythus
Campylobacter rectus
Fusobacterium nucleatum
Treponema species
Prevotella species
INTERVENTION STUDIES OF PERIODONTAL TREATMENT
TO IMPROVE PERIODONTAL STATUS AND REDUCE
SURROGATE MARKERS OF CVD RISK

CITATION RESULTS
Ide et al (2003) – SRP No significant change in any of
systemic markers
D’Aiuto et al., (2005) - Reduction of serum CRP
SRP compared with untreated controls

Tonetti et al., (2007) Significantly greater FMD in

treatment group compared to
control group. Plasma levels of E-
selectin were lower in treatment
than control group
Offenbacher et al., No reduction in GCF IL-1beta or
(2009) – SRP hs-CRP in treatment group
compared with control.
Paraskevas et al., (2008) Modest evidence for
treatment reduction of serum
CRP levels
Behle et al., (2009) Summary inflammatory
score – marked reduction in
systemic inflammation
Piconi et al., (2009) Mechanical treatment –
significant reduction of
carotid artery IMT
12months post-op
Metaanalysis - findings

Janket et al., (2003) Mustapha et al., (2007)

Humphrey et al., (2008)

Consistently conclude that the available evidence suggests a

moderate, positive association between periodontal diseases
and AVD.
Recent systematic review & meta-analysis – failed to
support that periodontal treatment can reduce
systemic high sensitivity CRP levels.
(Ioannidou et al.,2006)
 A consensus report has been drafted
jointly by the editors of The American
Journal of Cardiology and the Journal of
Periodontology and published
simultaneously in both these journals
(2009) –

“Although the inflammation hypothesis provides a

plausible and attractive explanation for the
periodontitis-atherosclerosis relationship, further
research is needed to define the mechanisms
linking the two diseases and how patients with
periodontitis should best be managed to reduce
their risk for CVD”.
A consensus document has been put
forward by the European workshop in
periodontal health and cardiovascular
disease (2010)
“Epidemiological studies have clearly shown a moderate but
significant association between periodontitis and CVD.
However no compelling evidence that preventive periodontal
care or therapeutic intervention will influence cardiac health.
As periodontitis continues to have a high prevalence within the
population and the fact that CVD remains cause of human
death in developed countries, in light of these associations we
can legitimately based on evidence state that oral health has
an influence on systemic health in general and in CVD in
particular and therefore we should promote oral health in
general periodontal health in particular as part of a healthy life
style and hence as an important component in the prevention
of CVD”.
Confounding variables

Confounding – which occurs when a

variable is associated with the exposure
and is an independent cause of outcome.

Directed Acyclic Graphs

provide quick visual method for selection

of potential confounders; minimizing bias.
PERIODONTITIS & ADVERSE
PREGNANCY OUTCOMES
Preterm birth – one of the most
complicated and challenging issues in
perinatal medicine

Spontaneous preterm birth – social

(maternal race/ethnicity, poverty) and
individual risk factors (underweight,
tobacco use, maternal infection).

Periodontal disease occurs in 40% of

pregnant women (Lieff et al.,2004)
PRE-TERM BIRTH birth <37wks gestational age
(Martin et al.,2007)
LATE PRE-TERM BIRTH
birth at 34-36wks gestational
(Martin et al.,2007)
age

VERY PRE-TERM Birth <32wks of gestational

(Martin et al.,2007) age
EXTREMELY PRE- Birth <28wks gestational age
TERM (Martin et
al.,2007)
LOW BIRTH WEIGHT <2500g
(WHO 2005)
VERY LOW BIRTH <1500g
WEIGHT (WHO 2005)
EXTREMELY LOW <1000g
BIRTH WEIGHT (WHO
2005)
PRE-TERM LABOUR Regular uterine contractions
(Goldenberg et al., accompanied by cervical
2008) change at <37wks gestation
PRE-TERM Spontaneous rupture of
PREMATURE RUPTURE membranes at <37wks
OF MEMBRANES gestation at least 1hr before
(Goldenberg et al., the onset of contractions
2008)
PRE-ECLAMPSIA
BP>140/90mmHg on 2
separate occasions & >/=1+
proteinuria on catheterized
urine specimen
PHYSIOLOGY OF NORMAL LABOUR
 Psychosocial factors
(Schneider et al., Socio-economical factors
2006) Demographic factors

Infections Disorganization of placentation

•Urinary passage •Preeclampsia
•Systemic •Placenta praevia
•Ascending •Abruptio placentae
Chrionammionitis

Preterm labour
Premature rupture of membranes
Medical induced interruption

Fetal pathology Uterus pathology

•Deformities •Deformities
•Chromosomal abnormalities •Myoma
Multiple •Cervix insufficiency
•Allo-immunopathies pregnancies
Landmark study
Greg Collins (1994) – series of experiments in
pregnant hamster animal model. Demonstrated
that chronic exposure to oral pathogens like
Porphyromonas gingivalis in a chamber model
enhances enhanced fetal-placental toxicity of
exposure during pregnancy.

Offenbacher et al., (1996) – human study

conducted a case-control study on 124 pregnant or
postpartum women. Significant association
between periodontal disease and low birth weight.
Proposed hypothetical model of the association between
periodontal disease and adverse pregnancy outcomes
(Ann Acad Med Singapore 2005)

Infection (bacterial vaginosis, Periodontitis)

Endotoxin/microbiological products

Inflammation

Pro-inflammatory mediator
activation

IL-1,TNF-alpha,MMPs

Fetal toxicity
Pre-term low birth weight
Fetal growth restriction
PERIODONTAL INFECTION MATERNAL
AGE,WEIGHT,
SMOKING, ETHNICITY,
STRESS, GENETICS
MATERNAL EXPOSURE
TO PERIODONTAL PATHOGENS
AND PRODUCTS INFLAMMATION

FETAL EXPOSURE
TO PERIODONTAL BACTERIAL
VAGINOSIS
FETAL RESPONSES
PRM,PTB,LBW,
PRE-ECLAMPSIA,
INTRAUTERINE
FETAL GROWTH RESTRICTION
CLINICAL TRIALS REPORTING SIGNIFICANT
EFFECT OF PERIODONTAL TREATMENT ON
ADVERSE PREGNANCY OUTCOMES
Lopez et al., (2002,2005)
Offenbacher et al., (2006)
Sadatmansouri et al., (2006)
Tarannum & Faizuddin (2007)

CLINICAL TRIALS NOT REPORTING SIGNIFICANT

EFFECT OF PERIODONTAL TREATMENT ON
ADVERSE PREGNANCY OUTCOMES

 Jeffcoat et al., (2003)

 Michalowicz et al., (2006)
Systematic reviews
AUTHOR CONCLUSION
Scannapieco et al., •Periodontal disease may be
(2003) a risk factor for PTB/LBW.
•Unclear if PD has a casual
role in APO.
•Additional studies needed.

Xiong et al., (2006) •Periodontal disease may be

associated with increased
risk of APO

Vettore et al., (2006) •Methodological limitations

of studies did not allow
conclusions concerning the
effects of PD on APO.
Systematic review on periodontal disease
& pre-eclampsia (Alina Kunnen et al.,2010)

A generalized inflammatory response plays an important

role in the pathogenesis of pre-eclampsia; periodontal
disease might contribute to its pathogenesis.

Questionable role of periodontal disease

None of RCTs till date reported reductions in pre-

eclamptic rate after periodontal therapy during
pregnancy.

Larger RCTs – required to explore causuality and

biologic mechanism.
Meta-analysis
AUTHOR CONCLUSION
Khader & Ta’ani (2005) Periodontal disease in pregnant
mother significantly increases
the risk of subsequent PTB/LBW

Vergnes & Sixou (2007) Likely association of periodontal

disease and APO
Xiong et al., (2007) Periodontal disease may be
associated with increased risk of
APO
Polyzos et al., (2009)
Metaanalysis of RCTs to
determine if periodontal
treatment during pregnancy
reduced preterm birth –
significantly lower PTB
 Macones et al., (2010)
PIPS study –
no significant difference
in PTB. Higher rate of
indicated PTB in
women with active
periodontal treatment
compared with placebo
PERIODONTITIS & DIABETES
Diabetes mellitus represents
a heterogeneous group of
metabolic disorders
characterized by elevated
blood glucose levels.

Type 1 – defect occurs at level of beta

cells

Type 2 – defect at level of insulin

receptor or molecule.
Pathophysiology
 Chronic
hyperglycemia

AGEs RAGE

AGE+RAGE

Alter intracellular signaling pathways

Upregulate pro-inflammatory cytokine
Production of oxygen free radicals
Bi-directional relationship – systemic
inflammation & excessive production of TNF-alpha

Diabetes mellitus Periodontitis

Microangiopathy
Alteration in GCF & collagen metabolism
Host inflammatory response
Quality of sub-gingival flora
Genetic predisposition
Periodontal disease – the sixth complication of
diabetes mellitus (Loe 1993)
Periodontitis & Diabetes -
association
Role of TNF-alpha
Antagonist to IRS-1. Inhibits
phosphorylation and translocation
of insulin receptor. Inhibits
intracellular glucose transport.

Hyper-responsive monocyte trait

in diabetes – 24 -32 times the level
of TNF-alpha compared to
non-diabetics

Dumping of TNF-alpha into

systemic circulation

insulin resistance
Studies
AUTHOR FINDING
Taylor et al., (1996) Longitudinal study on Pima
Indians – severe
periodontitis at baseline was
significantly associated with
the risk of worsening
glycemic control by 6-fold
over a 2yr period

Collin et al., (1998) People with advanced

periodontitis were more
likely to have higher HbA1c
levels than those who had
no or moderate periodontitis
at follow-up
Efficacy of periodontal therapy in subjects
with diabetes
Effects on periodontal
parameters
First RCT (Jones et 60% of deep sites
al.,2007) – to determine remained unchanged
efficacy of non-surgical after 4 months of healing
periodontal therapy on
improvement in
glycemic control
Effects on systemic
inflammatory markers
Iwamoto et al.,2001, Non-surgical therapy
Nishimura et al., 2003 +LDD minocycline –
reduced levels of TNF-
alpha
Pilot study (Lalla et Systemic levels of hs-
al.,2007) CRP, E-selectin –
significantly reduced
following non-surgical
periodontal
debridement
Effects on glycaemic
control
Meta-analysis (Janket et Following mechanical
al., 2005) debridement HbA1c
levels decreased on
average by 0.38% for all
studies. Not statistically
significant.
PERIODONTITIS & RESPIRATORY
DISEASE
Respiratory diseases – contribute considerably
to morbidity & mortality.
Bacterial pneumonia – community acquired or
hospital acquired (nosocomial).

COPD – chronic obstruction

to airflow resulting
from chronic bronchitis
or emphysema
Pneumonia – characterized by inflammation
of lungs resulting from microorganisms.

VAP – pneumonia developing in 48hrs or

more after initiation of mechanical
ventilation

HAP – pneumonia with an onset 48hrs or

more after admission to the hospital

Scannapieco’s report (1992) – oral and/or

periodontal infection may increase the risk
for bacterial pneumonia or COPD
Aspiration of bacteria from oral cavity

Entry into upper airway & lungs

Failure of host defense to clear bacteria

Lung infection

VAP

Bacteria adhere to endotracheal

tube surface

Growth of biofilm

Biofilm dislodged & embolize distally to set up foci of infection

Oral bacteria in respiratory infection (Genco)
Porphyromonas gingivalis (proteases)

Alters mucosal surface adhesion receptors

for respiratory pathogens (H. influenzae)

Aspirated into lung Infection

Enzymes

Degrade salivary molecules that Degrade salivary pellicle on mucosal

form a pellicle on the pathogens surface

Exposing adhesion receptors

for respiratory pathogens

Cytokines upregulate expression of adhesion receptors on mucosal surfaces

to promote repiratory pathogen colonization

A few published intervention studies of oral
disinfection to prevent VAP
REFERENCE ORAL RESULT
INTERVENTION
DeRiso et al., 0.12%CHX with 69% reduction in total
(1996) ventilator WP respiratory tract
infections
Houston et al., 0.12% CHX versus 52% reduction in overall
(2002) Listerine rate of pneumonia in
CHX group
Flanders et al., 0.12% CHX gel 3times Did not reduce
(2006) a day nosocomial infections

Scannapieco Oral topical 0.12% CHX reduced the

etal.,(2009) CHX or placebo number of S.aureus but
not enterics. Non-
significant reduction in
pneumonia rate noted in
CHX group
Systematic reviews

AUTHOR FINDING

Scannapieco et al., No sufficient evidence to

(2003) say there is an association
between periodontal disease
and COPD

Azarpazhooh & Leake No sufficient evidence to

(2006) say there is an association
between periodontal disease
and COPD
Emerging evidence for an association between
hospital-acquired pneumonia & periodontal
disease.

General conclusion on systematic reviews & meta-

analysis – (Pineda – 2006; Kollef – 2004;
Munro – 2004; Safdar – 2005; Gastmeier –
2007) topical chlorhexidine for oral care may lead
to delayed onset of VAP.
 Consensus report (6th European
Workshop on Periodontology, 2008)
Cardiovascular & Periodontitis (Persson &
Persson)

 Periodontitis contributes to the total infectious &

inflammation burden and may contribute to cardiovascular
events & stroke in susceptible subjects.

 Consistent positive but weak association between the two.

 Modest evidence to suggest that periodontal therapy lowers

levels of serum CRP.

 Evidence that periodontal therapy improves measures of

endothelial function.
 Adverse pregnancy outcome & Periodontal
disease (Wimmer & Pihlstom,2008)

 Findings indicate a likely association between

the two.

 No conclusive evidence that treating

periodontal disease improves the rate of positive
birth outcomes.

 Evidence that mechanical periodontal therapy

administered in the 2 nd trimester is safe and
does not have any adverse maternal or infant
effects.
 Diabetes mellitus & periodontal conditions
(Salvi et al.,2008)

 Represent a reciprocal influence.

 Periodontitis is associated with poor metabolic control &

diabetes-related complications.

 Inconclusive that periodontal treatment results in

improvement of metabolic control and markers of
inflammation.
Limitations
 Lack of well-defined criteria that reflect extent & severity
across entire range of periodontal conditions.

 Inconsistency in the definition of periodontitis in

epidemiologic research.

 Paucity & heterogeneity of available clinical research in

some areas.

 Role of confounders & effect modifiers in the association

between the diseases.
FUTURE OF PERIODONTAL MEDICINE

Interventional studies to reduce the risk

and to reverse the disease state

Knock out animals study

Controlled prospective study with large sample

Translation of animal work to human

Applying research evidence to
clinical patient management

Intervention trial

Longitudinal study

Cross-sectional study

Case series

Case report
CONCLUSION
Epidemiological data suggest that plenty of work remains to
be done in tackling biofilms and improving oral health – 72%
of adults have visible plaque biofilm, 73% have calculus and
40-45% have moderate periodontal disease (2006 report in
Dental Practice News)

Studies shown that people brush their teeth for 46secconds

on average, 2-10% floss regularly. People focus on the teeth
that make up just 23% of surface area of the mouth (Dent
Today 1998;17:76-8,80-2;, Am J Dent 2000;13:5A-14A, J
Dent Res 1991;70:1528-30)
The focal infection theory remains viable.

Strong epidemiologic evidence – suggests that oral infections

influence many systemic conditions and diseases by
mechanisms not yet fully clarified.

“We cant make a direct causal relationship but we can say very
safely with supporting evidence that there is a definite
connection between these biofilms and bacteria found in the
bloodstream” (Dr. Jim Grisdale, University of British Columbia,
Canada; Beyond brushing:changing paradigms in oral care –
industry update ;medical progress – CME journal for Asian
clinicians, sep 2010 vol 2, no.9)
Thank u!