Dental Health: Current ResearchISSN: 2470-0886

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Review Article, Dent Health Curr Res Vol: 7 Issue: 3

Association between Periodontal Disease and Cardiovascular Disease

Gurman Mallhi*

Doctor of Dental Medicine (DMD) McGill University, Montreal Canada

*Corresponding Author:
Gurman Mallhi
Doctor of Dental Medicine (DMD), McGill University, Montreal Canada
E-mail: [email protected]

Received Date: April 27, 2020; Accepted Date: March 09, 2021; Published Date: March 16, 2021

Citation: Mallhi G (2021) Association between Periodontal Disease and Cardiovascular Disease. Dent Health Curr Res 7:3.

Copyright: © All articles published in Dental Health: Current Research are the property of SciTechnol, and is protected by copyright laws. “Copyright © 2021, SciTechnol, All Rights Reserved.

Abstract

There has been recent surge of information in various studies thathave demonstrated that there may be correlations between heartdisease and periodontitis. We must anticipate at this point in timethat there do appear some connections between periodontitis andcardiovascular disease. There seems an apparent possibility thatthe patients who are at risk for one disease may be genetically atrisk for another.

Keywords: Cardiovascular, Periodontitis, Coronary diseases

Epidemiology

In developed countries cardiovascular (CV) diseases are thereason of death in 50 percent of the patients and certainly CV diseasesis the number one reason of deaths in the U.S.

In the most recent National Health and Nutrition ExaminationSurvey (NHANES) 45 percent of U.S. adults (30 years +) hadperiodontitis.

A cohort study conducted by De Stefano et al. [1] showed thatpatients with periodontitis have 25 percent more risk of coronaryartery disease as compared to those without it.

A case control study by Grau et a l. [2] was conducted on nearly300 patients after ischemic stroke. It was determined that periodontitisis an independent risk factor for stroke following his research.

An observational study conducted on patients admitted to hospitalemergency for acute coronary diseases had very poor periodontalstatus as compared to healthy controls.

Risk Factors

Periodontitis and CV diseases have common risk factorssuch as- Smoking, Obesity, Diabetes Mellitus and Hypertension.Large observational studies conducted over time have shown thatinflammation, auto-immune mechanism and host response play acommon role in both initiation and progress of these diseases [3].

Role of Inflammatory Mediators

The important mediators of inflammation include

• Nuclear factor-β(NF-β)

• Interleukin-1 (IL-1)

• Tumor Necrosis Factor (TNF-

• Matrix Metalloproteinases (MMPs)

• C-reactive protein (C-RP)

• Interleukin-6 (IL-6)

• Interferon-γ

These markers are actively involved with connective tissuebreakdown in both myocardial and periodontal tissues [4]. Theyfurther limit the repair activity inside tissues through expression ofapoptosis matrix producing cells. MMPs play an important role incollagen breakdown hence leading to connective tissue degeneration.

Biological Plausibility

Meta-analysis study conducted by Danesh et al [5] demonstrateda weak connection between heart conditions and H. Pylori(Helicobacter Pylori).

Pathogens that have been studied include Herpes SimplexVirus (HSV), Hepatitis a virus, Chlamydia Pneumoniae andCytomegalovirus (CMV). There is a stronger link between Chlamydiaand CMV with CV disease as compared to H. Pylori. However noproved conclusion has been reached.

Zhu et al [6-12] conducted a study and concluded that there wasan increase in association between presence of Serum IgG antibodiesto Hepatitis A virus and coronary artery disease. This study alsohighlighted the increased levels of CRP (C-reactive protein) incoronary artery disease subjects [13].

Research from most recent times emphasise on assessing thetotal pathogenic burden and its effects on heart diseases rather thanstudying the role of an individual pathogen in CV diseases [7].

However, the increased level of CRP and its correlation with CVdiseases is one of the very consistent finding from almost all majorstudies done so far [12].

There are conflicting results on whether by products of DNAof putative pathogens like Toxins; Lipopolysaccharides (LPS)[11] travelling through the system contribute to formation ofatherosclerotic plaques, which could possibly contribute to an acutemyocardial infarction (MI).

Many questions seem unanswered at this point in time to linkdirect dots between periodontal and cardiovascular diseases. Thedirect role of periodontal pathogens in CV diseases is not convincinglyproved yet.

Effects of Periodontal Treatment on Cardio VascularDiseases

A retrospective cohort study on nearly 800000 patients with/without periodontal disease reported that risk of acute MI/ MyocardialInfarction [8] was higher in patients with untreated periodontal disease as compared to ones that received periodontal treatment.

The data from another Study depicted that poor respondersto advanced periodontal treatment have been reported to have ahigher incidence rate ratio for heart diseases (95% CI=1.07-1.54; pvalue=0.007). Thus progression of heart diseases and recurrenceof acute MI episodes can be thought to be linked to the success ofperiodontal treatment in the affected subjects.

Another prospective cohort pilot study conducted by Beck J.Garcia [9] in 25 patients who had Generalised Chronic Periodontics(GCP) and Refractory Hypertension showed a huge reduction inmany cardiovascular risk markers after periodontal treatment.

However, prospective cohort study by NHANES [10] (NationalHealth and Nutritional Health Examination Survey) has shown nochanges in the level of inflammatory mediators after periodontaltreatment.

Conclusion

Based on the research conducted so far it is indicated that moreRandomized Controlled Trials (RCTs)and longitudinal studies arerequired with prolonged follow-up periods to establish a definitiveconclusion regarding the possible links between Periodontitis and CVdiseases.

There seems a fair responsibility that the apparent associationbetween these two diseases can be attributed to the common riskfactors and underlying common pathophysiologic events.

Until then it’s premature to counsel our patients ‘To floss or die’.

References

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