The Role of Inflammatory and Immunological Mediators in Periodontitis and Cardiovascular Disease

Abstract

Epidemiological studies have implicated periodontitis (PD) as a risk factor for development of cardiovascular disease (CVD). Persistent infections such as periodontitis induce inflammatory and immune responses which may contribute to coronary atherogenesis, and, in conjunction with other risk factors, may lead to coronary heart disease (CHD). In this review, mechanisms are described that may help explain the association between periodontal infections and CHD. Periodontal diseases are bacterial infections associated with bacteremia, inflammation, and a strong immune response, all of which may represent significant risk factors for the development of atherogenesis, CHD, and myocardial infarction (MI). Several mechanisms may participate in this association, including those induced by oral organisms, and those associated with host response factors. This review will focus on host factors. Oral pathogens and inflammatory mediators (such as interleukin [IL]-1 and tumor necrosis factor [TNF]-alpha) from periodontal lesions intermittently reach the bloodstream inducing systemic inflammatory reactants such as acute-phase proteins, and immune effectors including systemic antibodies to periodontal bacteria. This review will describe the potential role of various inflammatory as well as immunologic factors that may play a role in periodontitis as a possible risk factor for CHD.

El neutrófilo y su importancia en la enfermedad periodontal

“…Existen diferentes causas, entre las que encontramos: disminución de IL-8 (11); disminución de C5a (11,12); disminución de fMLP (péptidos de N-formilmetionil) (12,13,14); y disminución de la glicoproteina superficial GP110 (15), aunque todavía existen dudas sobre su influencia.…”

Anti-inflammatory effect of polyphenol-rich extract from the red alga Callophyllis japonica in lipopolysaccharide-induced RAW 264.7 macrophages

“…According to previous reports, the expression of iNOS is stimulated by pro-inflammatory cytokines, including TNF-α and IL-1β, which play key roles in the induction of inflammation in macrophages (De Nardin 2001, Marcus et al 2003. TNF-α exhibits its pro-inflammatory activity by regulating several intracellular pathways and can stimulate the production or expression of IL-6 and IL-1β.…”

Diagnostic Value of Acute Phase Proteins in Periodontal, Psychosomatic and Cardiometabolic Diseases: Response to Treatment

“…Based on the biological properties of these pro-inflammatory cytokines, high plasma levels of TNF- and IL-6 have been associated with an increased risk for developing cardiovascular events, morbidity and mortality (Abeywardena et al 2009;Ryan et al 2009). Periodontal diseases seem to act as a source of pathogenic species, virulence factors and inflammatory mediators that are conveyed systemically, creating and sustaining a chronic systemic inflammatory burden (Haraszthy et al 2000;De Nardin 2001;. The magnitude of this inflammatory burden would depend on the degree of inflammation present at the time of examination.…”