ORAL - SYSTEMIC HEALTH:

INTERRELATIONSHIP

Dr P BANDYOPADHYAY
Prof & HOD
Dept of Periodontics
Dr R Ahmed Dental College and
Hospital
ORAL HEALTH FOR HEALTHY
LIFE

WHO - 1994
Koch’s Postulates are used to identify the aetiological for an
infectious disease.

Causal association between two diseases are defined as

Bradford Hill criteria. It includes

1.Epidemiological association
2.Biological plausibility
3.Impact of intervention of one on the second disease
Evidences exist in favour of association between
periodontal disease
AND

Diabetic Mellitus
CVD
CVD Stroke
OBESITY Obesity
PRETERM LOW
PTLB
Dental Focal Infection and So on…..
BIRTH WEIGHT
STROKE
Three mechanism seem to play a role in non-oral
manifestation of oral diseases.
1.Metastaticinfection
2.Dissemination of bacterial toxin
3.Immunological injuries

(Thoder Van Velzen et al 1984)

1984
• In the context of Periodontal Disease and its relationship to the systemic
disease the underlining assumption is that Periodontitis is an infection that
causes inflammatory disease that metastatize.

• Nesse et al in 2008 described a technique of calculating inflamed

periodontal site (PISA- Periodontally Inflamed Surface Area) to asses
inflammatory burden posed by Periodontitis.

They found a Dose-response relationship between

PISA and HbA1C in T2 DM
Bacteraemia following
1.Tooth brushing
2.Chewing coarse food
3.Periodontal examination
4.Endodontic examination
( Kinane et al 2005)
Tackled by Recticulo-Endothelial System ( Li et al 2000)

It is plausible that bacteria persist at distal sites

disseminating virulence factor that act as soluble antigen .
•Bacteria and Bacterial Antigen that are systematically dispersed
triggers a significant systemic inflammation.

•Leucocytes, Endothelial Cells and Hepatocytes responds to

Bacterial Virulence Factors with secretion of pro-inflammatory
immune mediators:
( Cytokines, Chemokines, CRP)

•With continues exposure soluble antigens react with specific anti-

bodies forming Immune Complexes that further amplify
inflammation at sites of deposition.
(Li et al 2000)
• Pro-inflammatory mediators like IL-1 β, IL-6, TNF α and
PGE2 produced locally in inflamed gingival tissue may
“spill” into circulation and have systemic impact such as
induction of endothelial dysfunction which is critical in the
initiation and development of CVS pathology –
Atherosclerosis

• Effect of Pro-inflammatory Cytokines in circulation to

induce Leucocytosis Acute Phase Protein (CRP).
Acute Phase Reactant includes

Serum amyloid A protein

Fibrinogen
Plasiminogen activated inhibitor 1
Complement protein
LBP
Soluble CD 14

All are implicated in systemic condition

FRAMINGHAM STUDY CRITERIA

High lipid
Hypertension
Diabetics
Smoking
CH. PERIODONTITIS

• Ridkar et al in 2000 implicated Chronic

Inflammation with CVD
 • In 1999 Chiu isolated microorganism which are exclusively
indigenous to oral cavity in Cholesterol Plaques extracted from
Carotid End Arterectomy
• Kweider et al 1993 reported significant ↑ in Fibrinogen +
WBC Count among individuals with Severe Gingivitis
 C Reactive
Protein

Fibrinogen

• Wu et al reported ↑ in C Reactive Protein +

Fibrinogen was associated with Periodontitis
 von Wilbrand Factor

• Matilla et al observed an significant ↑ in von Wilbrand

Factor in patients with Dental Disease than persons without
 Prevalence of Periodontitis(AL ≥ 3mm) in US
population is 40%

•CVD is the no. 1 cause of Death

•Population at risk is of Greater Importance

• Several Cohort Studies reported Periodontal
Disease was found to be a Significant Predictor for

FUTURE CARDIO-VASCULAR EVENT

Genco et al 1997,Beck et al 1996

Ford 2005,Eckel et al 2005
Heiden reich et al 2011,Eke et al 2012
Lockhart et al 2012,Tonetti and Vandyke 2013
• Relationship between periodontitis and CVD is

NOT SIGNIFICANT

Hujuel PP 2000, Joshipura 1996

Howell 2001,Holmlund et al 2010
And de Oliveira et al 2010
PREDICTOR OF INTEREST IS
WEAK

CONFOUNDING FACTORS ARE

STRONG
• Some Studies −−−−→ UNDERESTIMATED association between PD & CVD

• Some Studies −−−−→ OVERESTIMATED association between PD & CVD

• Meta-analysis Studies −−−−→ WEIGHTED AVERAGE

Janket et al 2003 claimed that Periodontal Disease associated with increased risk of

development of subsequent CVD by 19% (approx.)

 ZHU AND HOLLIS JH 2015
No. Of Natural Teeth is inversely
associated with presence of
METABOLIC SYNDROME

Metabolic Syndrome is the term referred

to a group of conditions that raise the
risk of CVD, Stroke, Diabetes and all
cause mortality (Eckel et al 2005, Ford
2005)
2005

CAUSAL RELATIONSHIP CANNOT

BE INFERRED
• Yu-Y-H et al 2015, reported that
incident Periodontal Disease also
associated with High Vascular
Events and put women at
significantly elevated risk
 BHARADAJ, PRABHUJI
AND KARTHIKHAYEN (2015)

• Reported ↑ed plasma Hcy in CP

and its subsequent decrease
after 12 weeks of Non-surgical
Periodontal Therapy

• They claimed that effective

adjunctive Hcy Lowering
Therapy (HLT) which continued
to Primary Prevention of CVD
 •In 2011,Joseph et al
demonstrated Elevated Plasma
Hcy Level in clinically healthy
Indian subjects with Chronic
Periodontitis
 D’ AIUTO EL AL
ORLANDI AND GUNSOLLEY(2013)
“Periodontal Therapy” triggers a short
term Inflammatory Response followed by

•Progressive and consistent reduction of

systemic inflammation

•Improvement of endothelial function

There is however a Limited evidence
that this Acute and Chronic changes
will either Increase or Reduce CVD
Burden of individuals suffering from
Periodontitis in the long run
 • However after critical appraisal of the
evidence reported to-date, we confirm that
there are still limited comparative evidence on
the effect of periodontal therapy on CVD
outcome and sub-clinical atherosclerosis.
(D’ Aiuto, Orlandi and Gunsolley - 2013)
 We found moderate evidence of a positive effective of periodontal therapy in
reducing CRP level and improving endothelial function in 6 months. (D’
Aiuto el al Orlandi and Gunsolley 2013)

 CRP has multiple pro- inflammatory and pro-atherogenic properties but no

causal role in atherogenesis. ( Casas et al 2006)

 CRP is primarily a non-specific marker of inflammation,auto-immune

disease & malignant process.In absence of inflammation 1mg/ml confers
lower risk of CVD. Level above 3mg/ml double the risk of CVD.(Majid et al
2004)
 DIABETES & PERIODONTAL DISEASE

A complex two-way relationship exits

between DM & periodontitis, creating a
viscious cycle that exacerbate both diseases
when present same individual.
Non-surgical periodontal therapy resulted in significant
improvement of glycemic control along with significant
reduction of serum TNF-α level in all the Indian subjects
of treatment group compared to there controlled
counter part.

The study result indicated that periodontal treatment

can be undertaken along with standard measures for
the diabetic patient care.Prevention & control of
periodontal disease might be considered intregal part
of glycemic control in T2 DM.
 Y O U
AN K
T H