INTRODUCTION
Oral disease like periodontis and various other gum disease have placed a important role in various cardiovascular disease like atherosclerosis atrial fibrilation ect.,Photo credit: https://summitdentalhealth.net/gum-disease-and-heart-disease-whats-the-link/
PERIODONTITIS
There are evidences that dental infection, notably disease, is feasible a risk issue for hardening of the arteries coronary artery diseases.Photo credit: https://www.msdmanuals.com/home/mouth-and-dental-disorders/periodontal-diseases/introduction-to-periodontal-diseases
PATHOGENIC MECHANISM
Photo credit: https://intownsmilestudio.com/2017/04/12/cardiovascular-disease-part-1/
- There are several pathways which have been proposed as a potential link between CVS and PD.
- Indirect Mechanisms: Systemic Inflammation
- Atherosclerosis may begin during childhood with initial infiltration of the endothelium with fatty substances and progress over many decades.
- Plaques that contain a soft atheromatous core are unstable, and their rupture will expose highly thrombogenic contents to blood, with activation of thrombosis and ensuring ACS, MI or stroke.
- The link between ASVD and inflammatory mediators in blood is well-established, with consistent associations between levels of systemic inflammatory markers and increases in clinical events, such as MI and nonhemorrhagic stroke, and in surrogate markers such as increased cIMT.
- A well-studied inflammatory marker is CRP. Many studies of individuals with no prior history of ASVD have demonstrated that a single nonfasting measure of CRP is a predictor of future vascular events, including MI, stroke, peripheral arterial disease, and sudden cardiac death.
- Additional inflammatory markers associated with CVD include lipoprotein-associated phospholipase A221 and tissue inhibitor of matrix metalloproteinase,myeloperoxidase, and fibrinogen.Periodontal inflammation is associated with systemic markers such as CRP, tumor necrosis factor alpha, IL-1, IL-6, and IL-8.
- Systemic inflammation is similarly associated with cellular activation that involves cellular adhesion molecules, toll-like receptors, matrix metalloproteinase, and nuclear factor-k beta activation. The resulting interplay between endothelium, monocytes and platelets might be proatherogenic,contributing indirectly to atherogenesis or adverse cardiovascular outcome related to atheromatous plaque rupture in a subject with periodontitis.
Photo credit: https://jada.ada.org/article/S0002-8177(14)62727-6/fulltext
- Indirect Mechanism: Mimicry
- Molecular mimicry is thought to occur when sequence similarities between foreign and self-peptides produce cross-activation of autoreactive T or B cells that can lead to tissue pathology or autoimmunity.
- Expression of host protective heat shock proteins (HSPs) such as HSP60 on endothelial cells may be induced by a variety of factors, including cytokines and shear stress and antibodies to HSP60, which have been associated with higher morbidity and mortality from atherosclerotic ASVD.
- Proponents of molecular mimicry as a link between PD and ASVD suggest that endothelial damage may be aggravated by an immune response to bacterial HSP, such as molecular chaperone GroEL present in P. gingivalis and other periodontopathic bacteria.
Photo credit:Infection or inflammation: The link between periodontal and cardiovascular diseases - Scientific Figure on ResearchGate. Available from:
https://www.researchgate.net/figure/Molecular-mimicry-as-a-possible-link-between-periodontal-infection-and-atherosclerosis_fig1_24282175[accessed 30 May, 2020]
Photo credit: https://nutritionreview.org/2014/07/promising-new-approach-for-gum-disease-treatment-identified/
- Direct Mechanism:
- Bacteremia and Vascular Infection by Periodontal PathogensBacteremia that originates from the oral cavity is a common event that can occur during chewing and tooth brushing.
- It potentially occurs multiple times per day in individuals with some degree of gingivitis and periodontitis.
- A comprehensive search of literature provides a list of more than 275 bacterial species that have been identified in blood cultures after routine daily events or dental procedures.
- Viridans group streptococci represent a significant proportion of flora around teeth, particularly in the dental biofilm that grows about the gingival crest.
- From there periodontal organism circulates in the blood stream either within phagocytic cells or extracellularly and subsequently are deposited in an atheromatous plaque.
- Common PD pathogens including P. gingivalis adhere to and invade various human vascular cells in culture.
- Numerous studies have examined the effect of antichlamydial antibiotic therapy on outcomes in patients with coronary artery disease. Of note systemic antibiotics alone would not be expected to lead a long-term resolution of chronic
Photo credit https://www.cell.com/trends/endocrinology-metabolism/comments/S1043-2760%2815%2900045-4
Photo credit: www.periobasics.com
CONCLUSION
It is now clear from the epidemiologic studies that a possible link does exist between PD and CVD.It seems from the scientific evidence gathered to this point that interventional periodontal care remains invaluable not just for oral health except for general health similarly.
REFERENCE
- Pattnaik NK, Das SN, Biswal BN. Cardiovascular Diseases and Periodontal Diseases: Review and Update. Int J Sci Stud 2017;5(1):239-244.
- https://www.acc.org/latest-in-cardiology/articles/2016/08/15/13/38/periodontal-health-and-cardiovascular-disease-risk
- Prasad Dhadse, Deepti Gattani, and Rohit Mishra. The link between periodontal disease and cardiovascular disease: How far we have come in last two decades ?. doi: 10.4103/0972-124X.75908. PMCID: PMC3100856, PMID: 21760667https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3100856/#__ffn_sectitle
- Brinson CW, Lu Z, Li Y, Lopes-Virella MF, Huang Y. Lipopolysaccharide and IL-1ß coordinate a synergy on cytokine production by upregulating MyD88 expression in human gingival fibroblasts. Mol Immunol 2016;79:47-54.
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