Despite advancements in the detection and treatment of cardiovascular events, heart disease remains the number one killer of humans worldwide, claiming over 17 million lives each year. Inflammation is a main component of the most common form of heart disease, coronary heart disease, and a potential causal relationship between oral inflammation and the disease has been hotly debated in recent years.
The inflammatory nature of both conditions has been explored at length. But a new study published in the June 2014 issue of Scientific Reports suggests that periodontitis may, in fact, be an initial trigger for the development of atherosclerosis.
The study, which used ligature-induced periodontitis in a mouse model, involved several phases in which researchers tested the genetic, inflammatory, and immune responses to periodontitis in the aorta in particular.
Their findings show the detailed and linear mechanisms by which periodontitis might indeed trigger atherosclerosis:
- Periodontitis increases inflammatory gene expression.
- Periodontitis appears to activate circulating monocytes/marcophages (immune cells).
- Periodontitis increases the attachment of these immune cells to the aortic artery wall.
- The attachment of these cells to the artery wall plays an important role in the inflammatory response.
They concluded:
“Our results suggest that periodontitis triggers the initial pathogenesis of atherosclerosis, inflammation of the vasculature, through activating monocytes/macrophages.” [emphasis added]
The study’s authors go on to recommend that periodontal disease be treated not only for improved oral health but also to prevent aortic inflammation.
Will this study tip the scales in the “cause vs. link” debate? Only time—and likely further studies—will tell. It is encouraging, however, to see such intricate research being done on the connection between oral health and heart disease.
Periodontitis-activated monocytes/macrophages cause aortic inflammation
