Synopsis
Atherosclerotic Cardiovascular Diseases (ACVD) encompasses a wide range of conditions including ischaemic cerebrovascular disease, coronary heart disease and peripheral arterial diseasei. Evidence has shown that periodontitis is associated with significant sub-clinical atherosclerosis. There is now also robust evidence linking periodontitis with ACVDii.
The mechanisms by which this occurs are:
- I. Bacteraemia
- II. Elevation of systemic inflammation
Information
Periodontitis is characterized by a chronic, destructive immune-inflammatory response. Periodontitis affects 45-50% of the global adult population. Both periodontal pathogenic bacteraemia and systemic elevation of inflammation have been attributed to the link between periodontitis and CVD. CVD led to 25% of all deaths in Australia in 2019iii.
Low grade chronic systemic inflammation has been linked to adverse cardiac outcomes iv. Artherosclerotic lesions are formed through chronic inflammatory reactions. Periodontitis contributes to systemic elevation of inflammatory markers including C-reactive protein, IL-6, IL-1 and TNF-α. Periodontal therapy has shown reductions in serum levels of CRP and IL-6v. Peripheral blood neutrophils from periodontitis also raises extracellular reactive oxygen species compared to control subjects. In comparing patients with periodontitis vs. those with CVD and periodontitis there is significant elevation in fibrinogen levels in those with both diseasesvi. These factors promote plaque formation and perpetuate inflammationi.
Individuals with periodontitis are subject to frequent episodes of bacteraemia through activities like toothbrushing or surgical interventions such as periodontal debridementvii. In susceptible patients, treatment is safe with antibiotic prophylaxis. Management of periodontal conditions is still a vital component of overall patient therapy. Periodontal pathogens have been shown to promote platelet aggregation, foam cell formation and the development of atheromasviiiix. Animal models have shown P. gingivalis and A. actinomycetemcomitans in atherothrombotic lesions utilising its fimbri to enter endothelial cellsx. Further in vitro testing has developed evidence of enhanced aortic endothelial oxidative stress after polymicrobial infection with P. gingivalis, treponema denticola and tannerella forsythiaxi
There is sufficient evidence to show that periodontal treatment reduces low grade inflammation as demonstrated by lowered levels of CRP, IL-6 and improvements in endothelial functioni. Dental professionals should inform patients with periodontitis that their risk for CVDs is higher and recommend treatment and/or referral for treatment of their periodontal disease [refer to i.].
i Tonetti MS, Van Dyke TE and on behalf of working group 1 of the joint EFP/ AAP workshop. Periodontitis and atherosclerotic cardiovascular disease: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. J Clin Periodontol 2013; 40 (Suppl. 14): S24–S29
ii Dietrich, T., Sharma, P., Walter, C., Weston, P. and Beck, J. (2013), The epidemiological evidence behind the association between periodontitis and incident atherosclerotic cardiovascular disease. Journal of Periodontology, 84: S70-S84.
iii Australian Institute of Health and Welfare. Heart, stroke and vascular disease: Australian facts. AIHW. 9 Feb 2023. Web Report
iv Tonetti M, D’Aiuto F, Nibali L, Donald A, Storry C, Parkar M, Suvan J, Hingorani A, Vallance P, Deanfield J. Treatment of Periodontitis and Endothelial Function. The New England Journal of Medicine. 2007: 356;9
v Gupta S, Suri P, Patil PB, Rajguru JP, Gupta P, Patel N. Comparative evaluation of role of hs C-reactive protein as a diagnostic marker in chronic periodontitis patients. J Family Med Prim Care. (2020) 9:1340. doi: 10.4103/jfmpc.jfmpc_1063_19
vi Sanz M, Marco Del Castillo A, Jepsen S, Gonzalez-Juanatey JR, D'Aiuto F, Bouchard P, Chapple I, Dietrich T, Gotsman I, Graziani F, Herrera D, Loos B, Madianos P, Michel JB, Perel P, Pieske B, Shapira L, Shechter M, Tonetti M, Vlachopoulos C, Wimmer G. Periodontitis and cardiovascular diseases: Consensus report. J Clin Periodontol. 2020 Mar;47(3):268-288
vii Reyes, L.; Herrera, D.; Kozarov, E.; Roldan, S.; Progulske-Fox, A. Periodontal bacterial invasion and infection: Contribution to atherosclerotic pathology. J. Clin. Periodontol. 2013, 40 (Suppl. 14), S30–S50. viii Lalla E, Lamster IB, Hofmann MA, et al. Oral infection with a periodontal pathogen accelerates early atherosclerosis in apolipoprotein E-null mice. Arterioscler Thromb Vasc Biol 2003;23:1405-11
ix Li L, Messas E, Batista EL Jr, Levine RA, Amar S. Porphyromonas gingivalis infection accelerates the progression of atherosclerosis in a heterozygous apolipoprotein E-deficient murine model. Circulation 2002;105:861-7 x Haraszthy VI, Zambon JJ, Trevisan M, Zeid M, Genco RJ. Identification of periodontal pathogens in atheromatous plaques. J Periodontol 2000;71:1554-60.
xi Velsko IM, Chukkapalli SS, Rivera-Kweh MF, Zheng D, Aukhil I, Lucas AR, Larjava H, Kesavalu L. Periodontal pathogens invade gingiva and aortic adventitia and elicit inflammasome activation in αvβ6 integrin-deficient mice. Infect Immun. 2015 Dec;83(12):4582-93.