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Mechanisms Linking Periodontal Disease and Cardiovascular Disease: a Review and Update

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Mechanisms Linking Periodontal Disease and Cardiovascular Disease: a Review and Update Galore International Journal of Health Sciences and Research DOI: https://doi.org/10.52403/gijhsr.20210403 Vol.6; Issue: 2; April-June 2021 Website: www.gijhsr.com Review Article P-ISSN: 2456-9321 Mechanisms Linking Periodontal Disease and Cardiovascular Disease: A Review and Update Kamalkishor Mankar1, Pranjali Bawankar2, 1Associate Professor, 2Lecturer, VSPM Dental College & Research Centre, Department of Periodontology, Digdoh Hills, Hingna Road, Nagpur-440019 Corresponding Author: Pranjali Bawankar ABSTRACT Keywords: Coronary Artery Disease, Chronic Periodontitis, Interrelationship, Periodontal Aim: To present review of current literature disease, Systemic conditions. regarding association between periodontal and cardiovascular diseases and the mechanisms INTRODUCTION involved in the association. Concept of periodontal medicine Materials and Methods: Thorough search was which explores relationship between carried out on PUBMED, MEDLINE databases periodontal disease and systemic diseases and Google on the association between has been introduced in 1996, by periodontal disease and cardiovascular diseases .[1] and the mechanisms involved selected literature Offenbacher Periodontitis is a chronic inflammatory disease caused by bacterial included review articles, observational studies, [2] case control studies, randomized control trials infection of tooth supporting tissues, and and meta-analysis. Priority was placed on papers is the most common oral condition affecting published within last 10 years. Brief description human population.[3] According to a survey of periodontal disease and atherosclerosis in united states about 50% of adults above underlying pathophysiology has also been 30 years have some periodontitis, and nearly included. 10% have severe disease.[4] Annually CVD Results and Conclusion: Preponderance of data accounts for 40% of all deaths worldwide, appears to support the concept that a potential with atherosclerosis as underlying etiology link does exist between periodontal disease and in majority of cases.[5,6] Atherosclerosis is a CVD independent of confounding factors. Interventional trials have shown that periodontal disease process in which fatty deposits, therapy is associated with reduction in surrogate inflammation, cells and scar tissue buildup markers of atherosclerotic cardiovascular within the walls of arteries. Inflammation disease. Prospective interventional studies are plays a central role in the pathogenesis of required to determine the exact link between PD atherosclerosis, from its initial stage to and CVD as well as to evaluate whether development of clinical signs and periodontal treatment may reduce the risk of symptoms.[7] Several factors are defined as developing CVD. risk factors for cardiovascular diseases; Clinical Significance Pre assessment of however incidence of atherosclerosis cannot developing cardiovascular disease using be explained by traditional factors alone.[8] biomarkers can help in diagnosis of developing American Heart Association (AHA) or worsening periodontal diseases at earlier stages and can aid in providing screening working group concluded that periodontal services and advice to seek immediate dental disease is associated with atherosclerotic care. vascular disease (ASVD) independent of [9] known confounders. This relationship was demonstrated with level A evidence. The focal infection theory proposed by William Galore International Journal of Health Sciences and Research (www.gijhsr.com) 13 Vol.6; Issue: 2; April-June 2021 Kamalkishor Mankar et.al. Association of periodontitis and cardiovascular disease Hunter in 1909 was revisited in 1951 by the bacteria disrupt host mechanisms involved American Dental Association and a in bacterial clearance by activating many confirmation of the link of periodontal host immunoinflammatory processes. Host diseases and systemic diseases was inflammatory processes are dependent on established. [10’11] European society of environmental, genetic and acquired risk cardiology concluded that “oral health has factors. Although periodontitis is initiated an influence on systemic health in general by microbes, host modifying factors play an and on cardiovascular disease (CVD) in important role in determining severity and particular. Therefore we should promote extent of disease. oral health in general and periodontal health Periodontal disease occurs due to a in particular as part of a healthy life style complex interplay of bacterial infection and and hence as an important component in the host response. [18] Bacteria interacts with prevention of CVD.[12] Several systematic host through there virulence factors and reviews have shown a significant induce an innate and humoral immune association between periodontal disease and response.[19,20] Immune response to bacterial atherosclerotic cardiovascular disease, challenge shows interindividual variations independent of known confounders. [13,14,15] [21] and leads to release of proinflammatory Patients with periodontal disease share factors, PGE2, IL-1β.[22] Inflammatory many of the same risk factors as patients processes at periodontium results in increase with CVD including age, gender level of CRP and other mediators such as (predominantly male), lower socioeconomic fibrinogen leading to systemic response. status, stress, and smoking.[16] Several direct Cytokine and MMP levels also increase in and indirect mechanisms have been periodontitis. Increase in levels of MMPs proposed as pathophysiological links along with proliferation of bacteria lead to between chronic periodontitis and activation of different cells, such as atherosclerotic cardiovascular disease.[9] In fibroblasts, keratinocytes, macrophages and order to ensure optimal treatment it is endothelial cells. Macrophages secrete large important for cardiologists to be aware of all amount of TNF and IL-1 β leading to bone of the potential risk factors for CVD. This resorption. review provides an overview of research on the relationship between periodontal disease Atherosclerosis and CVD in the light of current literature. Atherosclerosis is a chronic inflammatory disease; inflammatory Pathophysiology of periodontitis processes are the vital part of If biofilms on the teeth are not pathophysiology of atherosclerosis and are disrupted on regular basis, it leads to supposed to be involved from initiation to emergence of gram negative bacteria. Low final stages of infarction. Normally redox potential, supply of nutrients in endothelial cells does not allow for the crevicular fluid and limited amount of attachment of leukocytes to vessel wall. oxygen in periodontal pocket provides Dysfunctional lipid homeostasis plays a favorable environment for survival and vital role in initiation and progression of multiplication of gram negative bacteria. endothelial alterations. When initial damage Periodontal disease is caused by bacteria in of epithelium occurs, either by infection or dental plaque, pathogens frequently by an atherogenic diet, endothelial cells associated with periodontal disease include express adhesion molecules that allow Aggregatibacter actinomycetemcomitans, leukocytes to bind vessel wall. Adhesion Capnocytophaga, Campylobacter rectus, molecules are called vascular cell adhesion Fusobacterium nucleatum, Porphyromonas- molecule (VCAM), intercellular adhesion gingivalis, Prevotella intermedia, Tannerella molecule (ICAM). Selectins and integrins forsythia and Treponema denticola.[17] These also support leukocyte attachment. Galore International Journal of Health Sciences and Research (www.gijhsr.com) 14 Vol.6; Issue: 2; April-June 2021 Kamalkishor Mankar et.al. Association of periodontitis and cardiovascular disease Endothelial dysfunction is considered as initiate coagulation, when in contact with primary step in pathogenesis of platelets and cause thromboembolism. atherosclerosis, and may act as risk marker Following are the potential for future cardiovascular events. [23, 24, 25, 26] mechanisms linking periodontitis to After adhesion to arterial wall, cardiovascular disease: monocyte penetrates the vessel wall by diapedesis or migration between endothelial a) Direct bacterial effects on platelets and cells. This accumulation of monocytes in host cells. vessel intima leads to development of fatty b) Systemically or locally induced streak, an early atherosclerotic lesion. Fatty inflammatory mediators. streak develops at 11-12 years and fibrous c) Autoimmune responses. plaque at 15-30 years.[27] LDLs (low density lipoproteins) play a key role in development a. Bacteremias and endotoxemias of atherosclerotic lesions.[28,29,30] LDLs Inflamed periodontal tissue give accumulated under intima layer are access to periodontal bacteria and its subsequently phagocytosed by macrophages products, into bloodstream through inflamed and transform them into foam cells. periodontal tissues, especially after dentaltreatment,[31,32,33] gentle mastication or Accumulation of foam cells in [32,34] subendothelial space is the hallmark of fatty tooth brushing. Bacteria may access the streak. Foam cells along with altered circulation during daily routine, oral endothelium release various growth factors hygiene procedures and during periodontal and cytokines, which stimulates migration therapy. Virulent Gram-negative organisms of smooth muscle cells from tunica media in the blood stream causes recurrent and [23] transient bacteremia, as well as low-grade into tunica intima. Smooth muscle cells [32,33,35] synthesize majority of extracellular matrix
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