Influence of systemic disorders on periodontal diseases is well established. However, of growing interest is the effect of periodontal diseases on numerous systemic diseases or conditions like cardiovascular disease, cerebrovascular disease, diabetes, pre-term low birth weight babies, preeclampsia, respiratory infections and others including osteoporosis, cancer, rheumatoid arthritis, erectile dysfunction, Alzheimer's disease, gastrointestinal disease, prostatitis, renal diseases, which has also been scientifically validated. This side of the oral-systemic link has been termed Periodontal Medicine and is potentially of great public health significance, as periodontal disease is largely preventable and in many instances readily treatable, hence, providing many new opportunities for preventing and improving prognosis of several systemic pathologic conditions. in this power point Dr Harshavardhan Patwal , highlights the importance of prevention and treatment of periodontal diseases as an essential part of preventive medicine to circumvent its deleterious effects on general health.

1. PERIODONTAL
MEDICINE
Dr HarshavardhanDr Harshavardhan
PatwalPatwal

3. 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.

4. 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.

5. 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)

6. 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

7. 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)

8. Two major mechanisms of focal
infection
an actual
metastasis
of organisms
from a focus
the spread of toxins or
their products from
a remote focus to
other tissues
by the blood stream

9. Debelian et al., (1994) identified 3
pathways
Metastatic
infection from the
oral cavity due to
transient
bacteremia
Metastatic
injury due to
oral microbial
toxins
Metastatic
inflammation due to
immunologic injury
caused by oral
micro-organisms

10. But why periodontal disease
is projected………..….
……..??

11. 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

12. 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

13. 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

14. The proinflammatory cytokines TNF-α,
IL-1β, and gamma interferon as well as
PGE2
reach high tissue concentrations in
periodontitis
renewing reservoir for spillover of these
mediators; enter the circulation induce
and perpetuate systemic effects
Periodontium –
as a cytokine
reservoir

15. Comparison of surface areas in the human mouth
(J Dent Res 1991;70:1528-30)
AREA IN
MOUTH
MALES
MEAN AGE
20.7(SD
13.4)
FEMALES
MEAN AGE
16.8(SD
8.02)
% TOTAL
MOUTH AREA
Teeth 39.8cm2
35.9cm2
23.9
Palate,
buccal/lingua
l alveolar and
gingival
mucosa,
buccal
vestibular
mucosa,
tongue
127.0cm2
118.8cm2
76.1
Total mouth
area
166.8cm2
154.7cm2

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

17. 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).

18. What is Periodontal Medicine?
– a new insight into the old
problem envisioned!

19. 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”

20. A paradigm shift
Infection
Inflammation

21. Commonality between Periodontitis and
systemic diseases
INFLAMMATION

22. Oral inflammation-systemic disease
association

23. 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)
Strength of associationDose-response effectTemporal consistency
Biologic plausibility
Specificity of association Consistency of
the findings

24. IS PERIODONTITIS A RISK FACTOR
FOR………….??
Cardiovascular disease
Diabetes mellitus
Adverse pregnancy outcomes
Respiratory infections
Rheumatoid arthritis
Renal dysfunction
Alzheimer’s disease

25. 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).

26. Atherosclerosis
Stroke – Normative Aging study
(Jimenez,2010)
& (Joshipura et al.,2003) – positive
association between periodontal
disease and stroke.
Infective endocarditis

27. 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.

28. 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).

30. 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.

33. 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.

34. 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).

35. 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

37. 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.

38. 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

39. 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)

40. 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.

41. 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)

42. 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)

43. 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- , and TXA2,α
platelet aggregation and adhesion,
formation of lipid-laden foam cells,
deposits of cholesterol and cholesterol esters.

44. 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

45. 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) -
SRP
Reduction of serum CRP
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.,
(2009) – SRP
No reduction in GCF IL-1beta or
hs-CRP in treatment group
compared with control.

46. 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

47. Metaanalysis - findings
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.
Janket et al., (2003) Mustapha et al., (2007)
Humphrey et al., (2008)
(Ioannidou et al.,2006)

48. 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”.

49. 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”.

50. Confounding variables
Confounding – which occurs when a
variable is associated with the exposure
and is an independent cause of outcome.
provide quick visual method for selection
of potential confounders; minimizing bias.
Directed Acyclic Graphs

51. 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)

52. PRE-TERM BIRTH
(Martin et al.,2007)
LATE PRE-TERM BIRTH
(Martin et al.,2007)
birth <37wks gestational age
birth at 34-36wks gestational
age
VERY PRE-TERM
(Martin et al.,2007)
Birth <32wks of gestational
age
EXTREMELY PRE-
TERM (Martin et
al.,2007)
Birth <28wks gestational age
LOW BIRTH WEIGHT
(WHO 2005)
<2500g
VERY LOW BIRTH
WEIGHT (WHO 2005)
<1500g

53. EXTREMELY LOW
BIRTH WEIGHT (WHO
2005)
<1000g
PRE-TERM LABOUR
(Goldenberg et al.,
2008)
Regular uterine contractions
accompanied by cervical
change at <37wks gestation
PRE-TERM
PREMATURE RUPTURE
OF MEMBRANES
(Goldenberg et al.,
2008)
PRE-ECLAMPSIA
Spontaneous rupture of
membranes at <37wks
gestation at least 1hr before
the onset of contractions
BP>140/90mmHg on 2
separate occasions & >/=1+
proteinuria on catheterized
urine specimen

54. PHYSIOLOGY OF NORMAL LABOUR

56. (Schneider et al.,
2006)
Psychosocial factors
Socio-economical factors
Demographic factors
Preterm labour
Premature rupture of membranes
Medical induced interruption
Disorganization of placentation
•Preeclampsia
•Placenta praevia
•Abruptio placentae
Infections
•Urinary passage
•Systemic
•Ascending
Chrionammionitis
Fetal pathology
•Deformities
•Chromosomal abnormalities
•Allo-immunopathies
Uterus pathology
•Deformities
•Myoma
•Cervix insufficiencyMultiple
pregnancies

57. 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.

58. 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

59. MATERNAL
AGE,WEIGHT,
SMOKING, ETHNICITY,
STRESS, GENETICS
MATERNAL EXPOSURE
TO PERIODONTAL PATHOGENS
AND PRODUCTS
FETAL EXPOSURE
TO PERIODONTAL BACTERIAL
VAGINOSIS
FETAL RESPONSES
INFLAMMATION
PERIODONTAL INFECTION
PRM,PTB,LBW,
PRE-ECLAMPSIA,
INTRAUTERINE
FETAL GROWTH RESTRICTION

60. 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)

61. Systematic reviews
AUTHOR CONCLUSION
Scannapieco et al.,
(2003)
•Periodontal disease may be
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.

62. 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.

63. 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)
Polyzos et al., (2009)
Periodontal disease may be
associated with increased risk of
APO
Metaanalysis of RCTs to
determine if periodontal
treatment during pregnancy
reduced preterm birth –
significantly lower PTB

64. 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

65. 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.

66. Pathophysiology

67. AGEs RAGE
Chronic
hyperglycemia
AGE+RAGE
Alter intracellular signaling pathways
Upregulate pro-inflammatory cytokine
Production of oxygen free radicals

68. 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)

69. Periodontitis & Diabetes -
association

71. 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

72. 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

73. Efficacy of periodontal therapy in subjects
with diabetes
Effects on periodontal
parameters
First RCT (Jones et
al.,2007) – to determine
efficacy of non-surgical
periodontal therapy on
improvement in
glycemic control
60% of deep sites
remained unchanged
after 4 months of healing
Effects on systemic
inflammatory markers
Iwamoto et al.,2001,
Nishimura et al., 2003
Non-surgical therapy
+LDD minocycline –
reduced levels of TNF-
alpha

74. Pilot study (Lalla et
al.,2007)
Systemic levels of hs-
CRP, E-selectin –
significantly reduced
following non-surgical
periodontal
debridement
Effects on glycaemic
control
Meta-analysis (Janket et
al., 2005)
Following mechanical
debridement HbA1c
levels decreased on
average by 0.38% for all
studies. Not statistically
significant.

75. 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

76. 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

77. 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

78. 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

79. A few published intervention studies of oral
disinfection to prevent VAP
REFERENCE ORAL
INTERVENTION
RESULT
DeRiso et al.,
(1996)
0.12%CHX with
ventilator WP
69% reduction in total
respiratory tract
infections
Houston et al.,
(2002)
0.12% CHX versus
Listerine
52% reduction in overall
rate of pneumonia in
CHX group
Flanders et al.,
(2006)
0.12% CHX gel 3times
a day
Did not reduce
nosocomial infections
Scannapieco
etal.,(2009)
Oral topical 0.12%
CHX or placebo
CHX reduced the
number of S.aureus but
not enterics. Non-
significant reduction in
pneumonia rate noted in
CHX group

80. Systematic reviews
AUTHOR FINDING
Scannapieco et al.,
(2003)
No sufficient evidence to
say there is an association
between periodontal disease
and COPD
Azarpazhooh & Leake
(2006)
No sufficient evidence to
say there is an association
between periodontal disease
and COPD

81. 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.

82. 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.

83. 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 2nd
trimester is safe and
does not have any adverse maternal or infant
effects.

84. 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.

85. 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.

86. 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

87. Applying research evidence to
clinical patient management
Intervention trial
Longitudinal study
Cross-sectional study
Case series
Case report

88. 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)

89. 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)

90. Thank u!