The relationship between periodontitis and systemic diseases have been a debatable topic since over a century, yet the debate is still ongoing. Various epidemiological and interventional studies have been carried out to prove its biologic plausibility. This ppt compiles the main systemic diseases that have consistently shown to have an impact because of periodontal infection.

3.  PATHOBIOLOGY OF PERIODONTITIS
 FOCAL INFECTION THEORY REVISITED
 SUBGINGIVAL ENVIRONMENT AS A
RESERVOIR OF BACTERIA
 PERIODONTAL DISEASE AND SYSTEMIC
DISEASES

4.  Pathogenesis of Periodontitis

6.  Can the inflammatory response to
bacterial infection of the periodontium
have an effect remote from the oral
cavity???
 Is periodontal infection a risk factor for
systemic diseases or conditions that
affect the human health???

7.  William Hunter (1909)- A British physician : Oral
micro-organisms were responsible for a wide
range of systemic diseases which were not
easily recognised as infectious in nature.
 Extract rather than restore.
 Widely accepted and widespread extraction
of teeth.
 Frank Billings- Father of theory of focal
infection; Coined the term ‘Focal Sepsis’

8.  In 1940s and 1950s
 Widespread extraction often of the
entire dentition failed to reduce or
eliminate the systemic conditions to
which the supposedly infected dentition
had been linked.
 No scientific evidence

9.  Mechanism of Focal Infection. J Am
Dent Assoc, Vol 42, June 1951
 Article states clearly that ‘The concept of
focal infection in relation to systemic
diseases is firmly established.’

10.  Focus of Infection: ‘A circumscribed area
infected with micro-organisms which
may or may not give rise to clinical
manifestations.’
 Focal infection: ‘Sepsis arising from a
focus of infection that initiates a
secondary infection in a nearby or
distant tissue or organs’.

11.  2 major mechanisms of focal infection:
a) An actual metastasis of organisms from
the focus
b) The spread of toxins or toxic products
from a remote focus to other tissues by
the blood stream

13.  Once the infection passes about the
tooth:
a) They may multiply in the blood setting
up an acute or chronic septicaemia.
b) They may be carried live to a suitable
nidus where they infect the surrounding
tissues.
c) They may produce a slow but
progressive atrophy with replacement
fibrosis in various organs of the body.

14.  CVS
› Atherosclerosis
› CHD
› Angina
› MI
 Cerebrovascular system
› Stroke
 Endocrine System
› DM
 Reproductive System
› Pre-term LBW infants
› Preeclampsia
 Respiratory System
› COPD
› Acute Bacterial Pneumonia

17. Endothelial injury
Surface adhesion molecules (Endothelial cells)
Monocyte adhesion by MCP-1
Macrophage in intima layer of vessel wall
Secrete GF, Cytokines
Smooth muscle proliferation in vessel wall
Stimulate endothelial cells
Accumulate LDL
Progressive oxidation
Lipid peroxidases
FOAM CELLS, FATTY STREAK

18. Fatty Streak
Complex fibrous plaque
with lipid core (Along with
extra cellular proteins)
Attached to vessel wall

20. Fibrotic
Plaque (thin)
Ruptures
Activation of
clotting system
Thrombus
formation
MI

24.  Inbred mice when challenged orally or
IV with invasive strains of P.g, increased
aortic athrosclerosis.
Li et al (2002), Lalla et al (2003), Chi et al
(2004), Gibson et al (2004)

30. 1. Direct bacterial effects on platelets
2. Auto-immune responses
3. Invasion and/or uptake of bacteria in
endothelial cells and macrophages
4. Endocrine like effects of pro-
inflammatory mediators

31.  2 oral bacteria P.g. and S. Sanguis
express virulence factors called
‘Collagen- like platelet aggregation
associated proteins” (PAAP) that induce
platelet aggregation in vitro and in vivo.
(Hertzberg 1996 & Meyer 1998)

32.  Antibodies that cross react with
periodontal bacteria and human heat
shock proteins have been identified.
(Hinode et al 1998 and Sims et al 2002)

33.  Deshpande et al (1998) have demonstrated
that P.g. can invade aortic and heart
endothelial cells via fimbriae.
 Chui et al (1999) and Haraszthy et al (2000)
have idntified specific oral pathogens in
atheromatous tissues.
 Giacona et al (2004) demonstrated that
macrophages incubated in vivo with P.g.
and LDL uptake the bacteria intracellularly
and transform into foam cells.

34.  Systemic pro-inflammatory mediators are
up-regulated for effects in vascular
tissues
 Elevation in CRP and fibrinogen
consistently seen among periodontally
diseased subjects.
(Slade et al 2000, Wu et al 2000)

47. Persistent bacterial challenge
to the arterial endothelium
Monocyte macrophage
driven inflammatory process
Atheromatosis
Narrowing of vessel lumen

48.  Elevated production of fibrinogen and
CRP
Atheroma formation

49.  Platelets selectively bind with some
strains of S. Sanguis and P.g.
 Aggregation of platelets is induced by
Platelet aggregation associated protein
(PAAP) expressed on some strains of
these bacteria
 Thrombus formation
 Thromboembolism
 Stroke

50.  Retinopathy
 Nephropathy
 Neuropathy
 Macrovascula
r disease
 Altered
wound
healing
 Periodontal
disease

56. Gram negative
periodontal
infection
Increased
insulin
resistance
Worsened
glycaemic
control
Periodontal
treatment
Decreased
inflammation
Improved insulin
sensitivity
Improved
glycaemic control

58.  <2500g at birth
 Vaginal colonisation with group B
streptococci or Bacteroides species
increases the risk of premature rupture of
membrane, preterm delivery and LBW
infants.
 Prostaglandins, proinflammatory
cytokines (IL-1, IL-6, TNF-α) have been
found in the amniotic fluid of women
with pre-term labor.

59.  Culture positive amniotic fluid, isolated F.
nucleatum in preterm labor
 Hill GB (1993) found F. Nucleatum to be
closely matched to those found in
subgingival plaque than in the lower
genital tract.
 Occasional isolation of
Capnocytophaga in amniotic fluid in
preterm labor

60.  Haematogenous spread
 Oral-genital contact