CardioExchange Archive

In addition to their well-known benefits in heart disease, high-dose statins appear to reduce gum inflammation caused by periodontal disease, a new report published in the Journal of the American College of Cardiology shows. The findings offer more evidence that heart disease and gum disease may be linked, and also help support the view that statins achieve at least some of their benefit not through their cholesterol-lowering effect but through separate inflammation-fighting mechanisms.

Researchers reported findings from 59 patients with cardiovascular disease or at high risk for cardiovascular disease who had evidence  of arterial inflammation on a PET scan. The patients were randomized to a low (10 mg/day) or high (80 mg/day) dose of atorvastatin. After 12 weeks, there was a significant reduction in periodontal inflammation as measured by PET in patients on high-dose therapy. The effect was greatest in those who had active periodontal disease. There was evidence of a significant effect as early as 4 weeks. Furthermore, there was a strong correlation between reductions in periodontal inflammation and atherosclerosis, though the authors acknowledge that the precise nature of the association remains undefined.

They write that their findings raise the possibility that statins may reduce not only LDL cholesterol and arterial inflammation but may also reduce non-arterial inflammation in “inflamed tissues such as the periodontium.” This effect, they write, “may exert secondary benefits on the systemic arterial milieu,” ultimately helping to reduce inflammation in atherosclerotic vessels.

The investigators call for larger randomized studies to examine the effect of statins in patients with periodontal disease, and speculate that statins might be a useful adjunctive therapy in periodontal disease. “Furthermore,” they write, “the possible interrelationship between periodontitis, atherosclerosis and statins might prove to be of substantial importance, due to the high prevalence of both periodontal and atherosclerotic diseases along with the wide-spread use of statins.”

In an accompanying editorial, Michael Blaha and Seth Martin write that “now that we have become a statin civilization,” with as many as 200 million people worldwide taking the drugs, “perhaps it is time to figure out exactly how these drugs work.” They propose three non-mutually exclusive paradigms to potentially explain the beneficial effects of statins:

• Paradigm #1: “Lipoprotein Load Hypothesis”
• Paradigm #2: “Systemic Inflammatory Hypothesis”
• Paradigm #3 “Plaque Modulation Hypothesis”