How Periodontitis and Cardiovascular Disease Are Intricately Linked

A causal link between periodontitis and cardiovascular disease has long been difficult to establish. They share common risk factors, such as male gender, age, cigarette smoking, type 2 diabetes mellitus, and low socioeconomic status. And, after adjusting for confounders, most studies report a positive association between these disease processes. This is due to the direct and indirect pathways that connect the pathogenesis of periodontitis to cardiovascular disease, and vice versa.¹

Oral bacteria and their byproducts can enter the bloodstream, damaging the vascular endothelium and increasing oxidative stress. In fact, periopathogens were found in 30% of resected human carotid plaques, with 44% containing at least one or more oral pathogens.² Local oxidation attracts macrophages to the site of injury. As these cells ingest various lipoproteins and lipids that accumulate along the vascular wall, they become pathogenic foam cells. A release in platelet-derived growth factor then causes collagen deposition and fibrous encapsulation. This fatty plaque or atheroma increases tunica intima-media wall thickness, which is a preclinical measure of atherosclerosis associated with coronary heart disease and stroke.¹

Indirectly, periodontitis increases systemic inflammation and alters macrophage activity to promote atheroma formation.³ Nonsurgical and surgical periodontal treatment, however, can reduce proinflammatory markers over time. A clinical trial of 65 healthy subjects showed a significant decrease in C-reactive protein and interleukin-6 (IL-6) two months after prophylaxis and scaling and root planing.⁴ In another interventional study, three months after full-mouth tooth extractions, inflammatory and thrombotic markers decreased when severe periodontitis was eliminated.⁵

Periodontal patients should be informed of the comorbidities associated with cardiovascular disease. In the nationwide Atherosclerosis Risk in Communities Study, the odds of carotid artery intima-media wall thickness ≥ 1 mm were 1.4 to 2.09 times higher for patients with moderate to severe periodontitis compared to healthy controls.⁶ A meta-analysis later revealed the prevalence and incidence of coronary heart disease were significantly increased in periodontitis, especially for subjects with less than 10 teeth.⁷ Periodontal treatment will not guarantee reduced risk for cardiovascular disease, but instead should be seen as a means to offset the body’s inflammatory burden, thereby improving overall health.

References

1. Demmer RT, Desvarieux M. Periodontal infections and cardiovascular disease: the heart of the matter. J Am Dent Assoc. 2006;137(Suppl):14S–20S.
2. Haraszthy VI, Zambon JJ, Trevisan M, Zeid M, Genco RJ. Identification of periodontal pathogens in atheromatous plaques. J Periodontol. 2000;71:1554–1560.
3. Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men.N Engl J Med. 1997;336:973–979.
4. D’Aiuto F, Nibali L, Parkar M, Suvan J, Tonetti MS. Short-term effects of intensive periodontal therapy on serum inflammatory markers and cholesterol. J Dent Res.2005;84:269–273.
5. Taylor BA, Tofler GH, Carey HM, et al. Full-mouth tooth extraction lowers systemic inflammatory and thrombotic markers of cardiovascular risk. J Dent Res. 2006;85:74–78.
6. Beck JD, Elter JR, Heiss G, Couper D, Mauriello SM, Offenbacher S. Relationship of periodontal disease to carotid artery intima-media wall thickness: the atherosclerosis risk in communities (ARIC) study. Arterioscler Thromb Vasc Biol. 2001;21:1816–1822.
7. Bahekar AA, Singh S, Saha S, Molnar J, Arora R. The prevalence and incidence of coronary heart disease is significantly increased in periodontitis: a meta-analysis. Am Heart J.2007;154:830–837.

This information originally appeared in Saltz A. Periodontal medicine: from teeth to total body health. Decisions in Dentistry. 2021;7(3):25–31.