Understanding residual inflammatory risk sheds new light on the clinical importance of periodontitis in cardiovascular disease

Extract

The role of inflammation in mediating risk in atherosclerotic cardiovascular disease (CVD) has been highlighted by the CANTOS trial.¹ This showed for the first time, that in patients with established CVD, targeting chronic residual systemic inflammation after myocardial infarction, with Canakinumab, a monoclonal antibody against the interleukin (IL)-1 beta innate immunity pathway, reduced cardiovascular (CV) events in patients with high residual inflammatory risk identified by elevated high-sensitivity C-reactive protein (CRP) and IL-6 levels. Whilst the study established a causal role for inflammation in the pathophysiology of complications of atherosclerosis, discussion continues on the best approaches to target inflammation in a safe and sustainable way.²

Identifying and treating previously unrecognized but common sources of systemic inflammation causally associated with CVD could create a unique, safe, and cheap opportunity to reduce cardiovascular risk. Periodontitis (PD) represents one the most prevalent forms of chronic inflammatory diseases (both local and systemic) worldwide.³ Recent surveillance surveys estimate that at least 40% of dentate adults, aged ≥30 years, have some form of PD and this rises to >60% in people >65 years.⁴