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Periodontal diseases & cardiovascular system By Dr Sachin Rathod
Periodontal disease is an infectious disease that can affect and be affected by systemic health conditions. Studies have found an association between periodontal disease and coronary heart disease/atherosclerosis. Periodontal pathogens have been found in atherosclerotic plaques, and periodontal disease may increase systemic inflammation and coagulation factors like CRP and fibrinogen that promote atherosclerosis and thrombosis. This systemic inflammation and increased coagulability from chronic periodontal infection could lead to acute events like myocardial infarction.
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Discusses the infectious nature of periodontal disease and its link to systemic health.
Explores the relationship between periodontal disease and coronary heart disease with significant findings on dental health in MI patients.
Explores the relationship between periodontal disease and coronary heart disease with significant findings on dental health in MI patients.
Covers thrombogenesis, blood viscosity, and factors related to ischemic heart disease and its relationship to periodontal infections.
Highlights how specific oral organisms contribute to thrombogenesis, affecting cardiac health.
Describes the pathogenesis of atherosclerosis including the formation of foam cells and arterial thrombosis.
Details how periodontal infections can trigger systemic inflammation and increase the risk of cardiovascular events.
Provides the contact email of Dr. Sachin Rathod.
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Periodontal diseases & cardiovascular system By Dr Sachin Rathod
- 3. INTRODUCTION • Periodontal diseaseis an infectious disease but environmental, physical, social & host stresses may affect & modify disease expression. • Evidences also show the converse sides of relationship between systemic health & oral health i.e., the potential effect of periodontal disease on a wide range of organ system.
- 6. Periodontal Disease &Coronary Heart disease/Atherosclerosis • To further explore the periodontal disease & CHD/atherosclerosis association, investigators have studied specific disorders & medical outcomes to determine their relationship to periodontal status. • In cross sectional studies of patients with acute myocardial infection compared with age & gender matched control patients, MI patients had significantly worse dental health than did controls.
- 8. • This associationbetween poor dental health and myocardial infarction was independent of known risk factors for heart diseases such as age, cholesterol level, hypertension, diabetes & smoking. • There may be a greater risk for CHD related events such as MI when periodontitis affects a greater number of teeth in mouth as compared to subjects having periodontitis of fewer teeth.
- 10. THROBOEMBOLISMATHEROSCLEROSIS NARROWING OF CORONARRY ARTERIS CORONARYHEART DISEASES RISK FACTOR OCCLUSION OF CORONARRY ARTERIES MYOCARDIAL ISCHEMIA ANGINA MYOCARDIAL INFARCTION AcuteChronic
- 11. ISCHEMIC HEART DISEASE •IHD is associated with the process of atherogenesis and thrombogenesis. • Increased viscosity of blood may promote major ischemic heart disease and cerebrovascular accident by increasing risk of thrombus formation.
- 12. Systemic/ periodontal infection Plasmafibrinogen Plasma lipoproteins White blood cell count Fibrinogen Von willebrand factor
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- 14. THROMBOGENESIS • Platelet aggregationplays a major role in thrombogenesis,& most cases of acute MI are precipitated by thromboembolism. • Oral organisms may be involved in coronary thrombogenesis. • Platelet selectively bind some strains of Streptococci sanguis, a common component of supragingival plaque & Porphyromonas gingivalis, a pathogen closely related with periodontitis.
- 15. • Aggregation ofplatelets is induced by the platelet aggregation associated protein (PAAP) expressed on some strains of these bacteria. • It results in formation of thromboemboli and resultant cardiac and pulmonary changes.
- 16. ATHEROSCLEROSIS • Atherosclerosis isa local thickening of arterial intima,the innermost layer lining the vessel lumen, and the media, the thick layer under the intima consisting of smooth muscle, collagen & elastic fibres.
- 17. Pathogenesis • First, circulatingmonocytes adhere to the vascular endothelium, mediated by various adhesion molecules including intercellular adhesion molecule-1(ICAM- 1), endothelial leukocyte adhesion molecule-1 (ELAM-1) & vascular adhesion molecule-1(VCAM-1). • After binding of the monocots, they penetrate the endothelium & migrate under the arterial intimae.
- 18.
- 19. • Monocytes nowinjest the circulating low density lipoprotein (LDL), & form foam cells which are characterstics of atheromatous plaques. • Proinflammatory cytokines, such as interleukin-1, tumor necrosis factor & prostaglandin E-2 are produced, which propogate the atheromatous lesion.
- 20. • Further thereis smooth muscle and collagen proliferation within the media, thickening the arterial wall. Atheromatous plaque formation & thickening of vessel wall narrow the lumen & decrease the blood flow. • Arterial thrombosis occurs after an atheromatous plaque ruptures.
- 21. Role of periodontalinfection in myocardial infarction • In several studies of atheromas obtained during endarterectomy, more than half of the lesions contained periodontal pathogens. • Periodontal diseases result in chronic system exposure to products of these bacteria. • Low level bacterimia may initiate host responses that alter the coagulability, endothelial & vessel wall integrity, platelet function, resultin in thromboembolic events.
- 22. • There iswide variation in host response to bacterial challenge. • Patients with exuberant inflammatory response have a hyper inflammatory monocyte/ macrophage phenotype. • Here monocytes secrete increased levels of proinflammatory mediators in response to bacterial LPS compared to normal monocyte phenotype.
- 23. • The monocytecell line is intimately involved in pathogenesis of both periodontal disease and atherosclerosis. • Diet induced increased LDL level may increase secretion of destructive & inflammatory cytokines by monocytes. • The presence of an Mф phenotype may place patient at risk of both CHD & periodontitis.
- 24. • Also, detectionof systemic inflammatory markers play an important role in risk assesment for vascular events such as MI & cerebral infarction. • Acute phase protein such as C- reactive protein (CRP) & fibrinogen are produced in liver in response to inflammatory or infectious stimuli & act as inflammatory markers. • CRP induces monocytes to stimulate coagulation pathway & increases blood coagulability.
- 25. • Recent effortshave focused on periodontitis as a potential trigger for systemic inflammation. • Serum CRP & fibrinogen levels are often elevated in subjects with periodontitis compared with non periodontitis subjects & may act as intermediary steps in the path way from periodontal infection to cardiovascular disease.
- 26.