Periodontitis as a risk factor for systemic diseases

IMPACT OF PERIODONTAL INFECTION

ON SYSTEMIC HEALTH

DR. KRITIKA JANGID(MDS- PERIO)

CONTENTS

PATHOBIOLOGY OF PERIODONTITIS

FOCAL INFECTION THEORY REVISITED

SUBGINGIVAL ENVIRONMENT AS A RESERVOIR OF BACTERIA

PERIODONTAL DISEASE AND SYSTEMIC DISEASES

INTRODUCTION Pathogenesis of Periodontitis

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???

FOCAL INFECTION THORY

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’

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

FOCAL INFECTION THORY REVISITED

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.’

Def. By ADA

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’.

Mechanism of Focal Infection. J Am Dent Assoc, Vol 42, June 1951

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

Mechanism of Focal Infection. J Am Dent Assoc, Vol 42, June 1951

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.

Organ Systems or Conditions possibly influenced by Periodontal Infection

CVS› Atherosclerosis› CHD› Angina› MI

Cerebrovascular system› Stroke

Endocrine System› DM

Reproductive System› Pre-term LBW infants› Preeclampsia

Respiratory System› COPD› Acute Bacterial Pneumonia

CVS

Pathophysiology of CHDEndothelial 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 wallStimulate endothelial cells

Accumulate LDL

Progressive oxidation

Lipid peroxidases

FOAM CELLS, FATTY STREAK

Fatty Streak

Complex fibrous plaque with lipid core (Along

with extra cellular proteins)

Attached to vessel wall

MI

Fibrotic Plaque (thin)

Ruptures

Activation of clotting system

Thrombus formation

MI

CHD

Periodontitis as a risk factor for CVS diseases

Animal model

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)

Biological Rationale

Role of Sub-gingival plaque

4 Pathways

1. Direct bacterial effects on platelets2. Auto-immune responses3. Invasion and/or uptake of bacteria in

endothelial cells and macrophages4. Endocrine like effects of pro-

inflammatory mediators

Direct bacterial effects on platelets

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)

Auto-immune responses

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

Invasion and/or uptake of bacteria in endothelial cells and macrophages

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.

Endocrine like effects of pro-inflammatory mediators

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)

Role of Obesity

Stroke/ Ischaemic Cerebral Infarction

Periodontitis as a risk factor for Stroke

Biological Rationale

Direct bacterial challenge

Persistent bacterial challenge to the arterial

endothelium

Monocyte macrophage driven inflammatory process

Atheromatosis

Narrowing of vessel lumen

Indirect Systemic effects

Elevated production of fibrinogen and CRP

Atheroma formation

Platelet aggregation

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

Diabetes

Retinopathy Nephropathy Neuropathy Macrovascula

r disease Altered

wound healing

Periodontal disease

Periodontitis as a risk factor for Diabetes

Conclusion

Biological Rationale

Gram negative periodontal

infection

Increased insulin

resistance

Worsened glycaemic

control

Periodontal treatment

Decreased inflammation

Improved insulin sensitivity

Improved glycaemic control

ADVERSE PREGNANCY OUTCOMES

LBW babies

<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.

Detection of Oral microbes

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

2 Possible route of spread

Haematogenous spread

Oral-genital contact

Pre-eclampsia

Periodontitis as a risk factor for Adverse Pregnancy Outcomes

Biological Rationale

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Periodontitis as a risk factor for COPD

Biological Rationale