PERIODONTAL DISEASE AND SYSTEMIC HEALTH.pptx

PERIO

1. PERIODONTAL DISEASE AND SYSTEMIC HEALTH Dr. Jenish Manohar J 2 nd year postgraduate Dept of Periodontics

2. INTRODUCTION Periodontal diseases constitute one of the major global oral health burdens, and periodontitis remains a major cause of tooth loss in adults worldwide. Involves the inflammatory destruction of tooth supporting tissues in response to bacteria and subgingival plaque.

3. One of the salient features of biofilm is the complex communal physiology, allowing for the survival of the entire microbial community. Bacteria growing in biofilms are resistant to clearance mechanisms such as phagocytosis and killing by host immune system.

4. Most significant consequence of biofilms is constant shedding of bacterial products and byproducts . The ulcerated pocket epithelium becomes a significant portal of entry into the general circulation. In such manner, periodontal infection acts as nidus for systemic inflammation as well.

5. HISTORY Association of tooth extraction to arthritis cure (Hippocrates 400 B.C.) Oral sepsis: causal factor for systemic diseases (Miller 1890, Hunter 1900) Theory of “focal infections”: Extraction of teeth to prevent systemic diseases (Billings 1911) Rejection of “focal infection” theory ( Editorial, JAMA 1952) Association of heart attacks to oral infections ( Mattila et al, 1989, BMJ

6. Periodontitis and chronic inflammation Periodontal disease needs to be viewed more broadly in terms of systemic inflammation, either as a consequence of an underlying hyperinflammatory trait or as a factor contributing to systemic inflammation. ( Slade, Offenbacher , Beck et al. J. Dent Res 2000)

7. Conditions in which the influences of periodontal infections are noticed Coronary heart disease (CHD) and CHD-related events such as angina and infarction, atherosclerosis, stroke Diabetes mellitus, Preterm labor, low-birth-weight delivery(PLBW) Respiratory conditions such as chronic obstructive pulmonary disease (COPD)

8. Common pathophysiologic feature of most chronic diseases is; Chronic, sustained, exacerbated inflammatory response to a given stimulus. Increased production of proinflammatory cytokines, initially secreted to provide clearance of invading microrganisms . But exacerbated response may result in more tissue damage than repair.

9. Monocyte derived cytokines such as TNF- α , IL-1 β , IL-6,IL-8 may be released in response to periodontal infection. The endotoxin lipopolysacharide (LPS) from gram negative bacteria activate systemic inflammation. Two ways: Directly by action on the blood vessel walls Indirectly by inducing the liver to produce acute phase proteins

10. Porphyromonas gingivalis Can actively adhere to and invade bovine heart cells and aortic endothelial cells. P.gingivalis LPS and its outer membrane vesicles are able to induce macrophages to engorge LDL to form foam cells- characteristic of cardiovascular diseases.

11. Activate inflammatory cascade on the vascular endothelium and promote smooth muscle proliferation, platelet aggregation , fatty degeneration, and deposition on the vessel wall. Proteolytic enzymes from p.gingivalis activate factor x, prothrombin and protein c promoting thrombotic tendency.

12. ACUTE PHASE PROTEINS LPS and other cell products of periodontal bacteria indirectly stimulate the liver to produce the acute phase protein CRP(c reactive protein). CRP promotes deposits on injured blood vessels when secreted in excess. Increased levels of CRP is a marker of future myocardial infarction and stroke.

13. Periodontitis also increases the level of circulating fibrinogen. Fibrinogen associated with coagulation and increased blood viscosity. Net effect of increased CRP and fibrinogen levels is increased platelet aggregation and narrowing of the blood vessel lumen.

14. EPIDEMIOLOGY 55% of patients with severe periodontitis manifest positive arterial blood cultures after chewing paraffin.( M urray 1941) Immediately following dental scaling, bacteremia resulted in increased circulating serum TNF- α and IL-6. Perio treatment decreases systemic inflammation (serum CRP, TNF- α ).

15. ATHEROSCLEROSIS Atherosclerosis is a focal thickening of the arterial intima (the innermost layer lining the vessel lumen), and the media (the thick layer under the intima consisting of smooth muscle, collagen, and elastic fibers). The advanced lesion is the atheroma, which consists of elevated focal intimal plaques with a necrotic central core containing cholesterol ester crystals, lipid-laden foam cells and surface plasma proteins, including fibrin and fibrinogen (Boon et al., 1995).

16. Pathogenesis of atherosclerosis . 1, Monocytes/macrophages adhere to vascular endothelium. 2, Monocytes/macrophages penetrate into arterial media, producing pro-inflammatory cytokines and growth factors. 3, Ingestion of oxidized LDL enlarges monocytes to form foam cells. 4, Smooth muscle proliferation and plaque formation thicken vessel wall and narrow lumen

17. PATHOPHYSIOLOGY Enhanced smooth cell proliferation and extracellular matrix deposition. Enhanced thrombogenecity and vasoconstriction Decreased vessel lumen size and plaque rupture.

18. LPS and TNF- α from periodontal infection activate nuclear factor kappa- B. NFk -B is an inducible nuclear transcription factor that controls multiple aspects of inflammatory response. Activation of NFk -B up-regulates macrophages leading to secrete large quantities of pro inflammatory cytokines.

19. EPIDEMIOLOGY 70% atheromas removed from carotid arteries had bacteria in the atheroma . 44% were positive for atleast one type of perio pathogen .( G enco , j perio2000) 88.5% aorta samples during open heart surgery had bacterial DNA, many from perio pathogens .( S tetzel j perio 2002)

20. Increased intima medial thickness of the ICA is found in healthy patients with severe periodontitis compared to healthy patients with moderate perio and controls Perio infection with 4 periopathogens is associated with sub clinical atherosclerosis and the greater their presence in the mouth the higher the likelihood of disease.

21. Immune response Potential linking mechanism. Production of antibodies to periodontal bacteria, including antibodies to heat shock proteins that cross react with heat shock proteins of the heart. These auto reactive antibodies contribute to atheroma formation.

22. PERIODONTITIS AND CORONARY HEART DISEASE

23. Ischemic heart disease is associated with the processes of atherogenesis and thrombogenesis . Increased viscosity of blood may promote major ischemic heart disease and cerebrovascular accident (stroke) by increasing the risk of thrombus formation.

24. Elevated white blood cell (WBC) count is also a predictor of heart disease and stroke, and circulating leukocytes may promote occlusion of blood vessels. Von Willebrand factor ( vWF ) has also been associated with the risk of ischemic heart disease.

25. Fibrinogen levels and WBC counts are often increased in patients with periodontal disease.

26. Difficulty in drawing a cause and effect relationship between periodontitis and cardiovascular disease. The two groups of diseases share many risk factors. Smoking, genetics, stress and increasing age, sex, diabetes , poverty, hypertension, serum cholesterol.

27. Epidemiology Over 18 years, veterans with periodontitis were 1.9 times more likely to develop fatal heart disease and 3 times more likely to have a stroke.( adjusting for age, BP, smoking, BMI, serum cholesterol, and education) (cohort study, Beck 1996,1998) Periodontitis may be a stronger risk factor for heart disease than hypertension or high cholesterol.( Genco et al 1997)

28. PERIODONTITIS AND CEREBROVASCULAR DISEASES

29. Case control studies have shown that poor dental health to be associated with increased risk for cerebrovascular ischemia and stroke. In men <60 yrs subjects with periodontitis had 4.3 times more likely to have stroke than with mild or no periodontitis .( G rau 2004)

30. Severe loss of attachment was associated with a 4 time higher odds ratio than those without periodontitis . Severe radiographic bone loss associated with a 3 time higher odds ratio than minimal to no bone loss. Bleeding gums resulted in a 15 fold increase in risk compared with those with minimal or no bleeding.( D orfer JCP 2004)

31. DIABETES AND PERIODONTITIS Bi-directional Presence of one condition promotes the other. The management of either assists treatment of the other.

32. In a longitudinal study of patients with type 2 ( non insulin-dependent ) diabetes, severe periodontitis was associated with significant worsening of glycemic control over time. Diabetic adults with severe periodontitis at baseline had a significantly greater incidence of kidney and macrovascular complications

33. EFFECTS OF PERIODONTITIS Periodontitis triggers an infection mediated pathway of cytokine regulation, with regulation of TNF- α and IL-1 and a state of insulin resistance affecting glucose utlising pathways. All mediators like TNF-a, IL-6, and IL-l, are important in periodontal inflammation and have been shown to have effects on glucose and lipid metabolism. IL 6 and IL-l have also been reported to antagonize insulin action.

34. Contd.. Increase tissue resistance to insulin, Prevent glucose from entering target cells, Causing elevated blood glucose levels, and requiring increased pancreatic insulin production to maintain normoglycemia

35. Monocytes from patients with diabetes produce 24 to 32 times the level of TNF- α when stimulated by periodontal pathogens. TNF- α is an antagonist to cell surface insulin receptor substrate. Large quantities of TNF- α into the systemic circulation contributes to insulin resistance.

36. ADVERSE PREGNANCY OUTCOMES

37. “Adverse pregnancy outcomes” include conditions such as preterm low-birth weight (PLBW) infants, infants born small for gestational age, miscarriage, and preeclampsia( Bobetsis et al., 2006 ). According to the World Health Organization, low birth weight (LBW) is defined as a birth weight <2500g.

38. Infection of the chorioamnionic , or extraplacental membrane, may lead to chorioamnionitis , a condition strongly associated with a premature membrane rupture and preterm delivery(Mueller- Heubach et al., 1990).

39. Bacterial vaginosis a known risk factor for preterm labor , premature rupture, and low birth weights. Normal vaginal microflora replaced by more anaerobic organisms many of which produce LPS. P.gingivalis implanted subcutaneously resulted in increased TNF- α and PGE2 levels.

40. RESPIRATORY DISEASES

41. Microorganisms can contaminate the lower airways by four possible routes: Aspiration of oropharyngeal contents. Inhalation of infectious aerosols. Spread of infection from contiguous sites. Haematogenous spread from extra pulmonary sites.

42. Anaerobic organism from periodontal pockets may serve as the primary inoculum for suppurative respiratory diseases (e.g., pulmonary abscesses) that have significant morbidity and mortality. Oropharyngeal colonization with potential respiratory pathogens increase during hospitalization.

43. Subgingival plaque may also harbor PRPs, and putative periodontal pathogens have been associated with nosocomial pneumonia.

44. SUMMARY Although periodontal diseases have been traditionally considered as inflammatory diseases of the supporting tissues of the teeth, scientific evidence gathered during the last couple of decades have shown that the detrimental effects of these diseases can affect distant organs and adversely impact the systemic health of periodontitis patients.

45. CONCLUSION The role of dental professionals in the public healthcare system becomes more crucial, in prevention as well as treatment of periodontal diseases.

46. REFERRENCES Carranza text book of periodontology, 11 th edition Periodontics: medicine, surgery and implants. Rose, genco , cohen The Emerging Concepts on the Impact of Periodontitis on Systemic Health, Deshpande RG, Genco CA. 1998. Invasion of aortic and heart endothelial cells by Porphyromonas gingivalis . Infect Immun 66:5337-5343.

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