Periodontal Disease: A Hidden Risk Factor for Cardiovascular Health
Source: Aleksijević et al., 2022; Pathogens
Periodontal disease (PD) is a chronic infectious and inflammatory condition of the supporting tissues of the teeth, driven largely by pathogenic bacteria such as Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), Treponema denticola (Td), Aggregatibacter actinomycetemcomitans (Aa), and Fusobacterium nucleatum (Fn). Increasing evidence supports a bidirectional link between PD and systemic conditions, particularly cardiovascular disease (CVD), including atherosclerosis, coronary heart disease, and stroke.
Mechanistic Insights
Several pathways explain how PD may contribute to cardiovascular pathology:
Systemic Inflammation: Periodontal pathogens stimulate host immune responses, producing elevated systemic inflammatory mediators such as C-reactive protein (CRP), IL-6, and TNF-α. These markers are also implicated in vascular endothelial dysfunction, plaque formation, and progression of atherosclerosis (Olsen, 2015; Lee et al., 2012).
Bacterial Translocation: Oral bacteria and their virulence factors can disseminate into the bloodstream during daily activities such as chewing or brushing, leading to direct colonization of vascular tissues. P. gingivalis DNA and antigens have been detected in atherosclerotic plaques, suggesting a role in plaque instability and thrombogenesis (Groeger & Meyle, 2019).
Molecular Mimicry: Certain periodontal pathogens express heat shock proteins and other antigens that resemble host proteins, potentially inducing autoimmune responses that exacerbate vascular injury (Tlaskalová-Hogenová et al., 2004).
Platelet Activation and Coagulation: P. gingivalis and A. actinomycetemcomitans produce enzymes (gingipains, leukotoxin) that can activate platelets and enhance thrombus formation, increasing the risk of myocardial infarction and stroke (Kapila, 2021).
Clinical and Epidemiological Evidence
Epidemiological studies consistently show that individuals with moderate-to-severe PD have a higher incidence of CVD events. Periodontal treatment has been associated with reductions in systemic inflammatory markers and improvements in endothelial function, although causal relationships remain under investigation (Somma et al., 2010; Passariello et al., 2021). The American Heart Association acknowledges an independent association between PD and atherosclerotic vascular disease, though definitive proof of causality requires further longitudinal and interventional studies.
Conclusion
PD contributes to systemic inflammation, immune dysregulation, and microbial dissemination that may promote the onset and progression of CVD. While the exact causal mechanisms remain to be fully clarified, maintaining periodontal health may be an important strategy in reducing cardiovascular risk. Integrated medical-dental approaches are therefore essential in managing systemic inflammatory burden.
References (For extensive reference list- click here)
Olsen I. From the Acta Prize Lecture 2014: the periodontal-systemic connection seen from a microbiological standpoint. Acta Odontol Scand 73, 585–591 (2015).
Lee J, Taneja V, Vassallo R. Cigarette smoking and inflammation: cellular and molecular mechanisms. J Dent Res 91, 142–149 (2012). doi:10.1177/0022034511421200.
Groeger S, Meyle J. Oral mucosal epithelial cells. Front Immunol 10, 208 (2019). doi:10.3389/fimmu.2019.00208.
Tlaskalová-Hogenová H, et al. Commensal bacteria, mucosal immunity and chronic inflammatory and autoimmune diseases. Immunol Lett 93, 97–108 (2004). doi:10.1016/j.imlet.2004.02.005.
Kapila YL. Oral health’s inextricable connection to systemic health. Periodontol 2000 87, 39–78 (2021). doi:10.1111/prd.12398.
Somma F, Castagnola R, Bollino D, Marigo L. Oral inflammatory process and general health. Eur Rev Med Pharmacol Sci 14, 1065–1074 (2010).
Passariello C, Di Nardo D, Seracchiani M, et al. Harnessing the power of biologic agents on the oral microbiota. J Contemp Dent Pract 21, 1125–1133 (2021). doi:10.5005/JP-JOURNALS-10024-2949.