Abstract
Inflammation is a well-organized protective response to pathogens and consists of immune cell recruitment into areas of infection. Inflammation either clears pathogens and gets resolved leading to tissue healing or remains predominantly unresolved triggering pathological processes in organs. Periodontal disease (PD) that is initiated by specific bacteria also triggers production of inflammatory mediators. These processes lead to loss of tissue structure and function. Reactive oxygen species and oxidative stress play a role in susceptibility to periodontal pathogenic bacterial infections. Periodontal inflammation is a risk factor for systemic inflammation and eventually cardiovascular disease (CVD). This review discusses the role of inflammation in PD and its two way association with other health conditions such as diabetes and CVD. Some of the mechanisms underpinning the links between inflammation, diabetes, CVD and PD are also discussed. Finally, we review available epidemiological data and other reports to assess possible links between oral health and CVD.
Highlights
Periodontal disease (PD) is a chronic inflammatory disorder characterized by the destruction of the periodontium, or the supporting tissues of the teeth
Periodontal treatment resulted in significant reduction in markers of PD severity Periodontal treatment resulted in significant reduction of fibrinogen, C-reactive protein (CRP), and IL-6 Intensive periodontal treatment resulted in significantly improved measures of periodontal health at 3 months, but only PD remained significantly different at 6 months No significant difference between the groups inflammatory biomarkers at any time point Non−surgical periodontal treatment resulted in significant reduction of systemic levels of inflammatory markers (CRP, fibrinogen and WBCs) at 2-month follow-up
Oxidative stress arising from lifestyle diseases play a crucial role in progression of both PD and cardiovascular disease (CVD), indicating that host influence in terms of an imbalance between reactive oxygen species (ROS) production and endogenous antioxidant levels can increase susceptibility in individuals
Summary
Periodontal disease (PD) is a chronic inflammatory disorder characterized by the destruction of the periodontium, or the supporting tissues of the teeth (gingival tissue, periodontal ligament, and alveolar bone). All the major risk factors associated with PD either activate pathogen initiated inflammation signals (bacteria like P. gingivalis and A. actinomycetemcomitans B. forsythus, P. intermedia, P. micros, and F. nucleatum (Lovegrove, 2004; Saito et al, 2008) or a life style (diabetes mellitus, obesity, aging, smoking, vascular disease) driven inflammatory cascade (Jensen et al, 1991; Grossi and Genco, 1998; Cohen, 2000; Merchant et al, 2003; Humphrey et al, 2008; Hujoel, 2009; Kumar et al, 2011; Nakamura et al, 2011; Ozcaka et al, 2011). Epidemiologic data till date that suggest an association between PD and CVD (Humphrey et al, 2008; Blaizot et al, 2009; Tonetti, 2009) have monitored PD via indices of clinical
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