Images from PET/CT demonstrate 18F-FDG activity localizing to periodontal tissues. Image source: J Am Coll Cardiol, 2011; 57:971-976

FDG-PET measurements of metabolic activity within periodontal tissue correlate with macrophage infiltration within carotid plaques, which researchers said provides “direct evidence for an association between periodontal disease and atherosclerotic inflammation.” The study was published in the Feb. 22 issue of the Journal of the American College of Cardiology.

Some evidence has established periodontal disease as an important risk factor for atherosclerosis, and FDG-PET is an established method for measuring metabolic activity in human tissues and blood vessels. Therefore, Kenneth M. Fifer, BA, and colleagues from the division of cardiology in the cardiac MR-PET-CT program at Massachusetts General Hospital in Boston, aimed to test the hypothesis that metabolic activity within periodontal tissue (a possible surrogate for periodontal inflammation) predicts inflammation in a remote atherosclerotic vessel, utilizing 18F-FDG-PET.

For the study, 112 patients underwent FDG-PET imaging 92 minutes after FDG administration (13 to 25 mCi). The researchers measured periodontal FDG uptake by obtaining standardized uptake values from the periodontal tissue of each patient and determined the ratio of periodontal to background blood activity. They also obtained standardized uptake value measurements in the carotid and aorta as well as in a venous structure. Localization of periodontal carotid and aortic activity was facilitated by PET co-registration with CT or MRI.

Also, a subset of 16 patients underwent carotid endarterectomywithin one month of PET imaging, during which atherosclerotic plaques were removed and subsequently stained with anti-CD68 antibodies to quantify macrophage infiltration. The investigators compared periodontal FDG uptake with carotid plaque macrophage infiltration.

Fifer and colleagues found that periodontal FDG uptake (using target-to-backgound ratios [TBR]) is associated with carotid TBR (R = 0.64), as well as aortic TBR (R = 0.38). “Moreover, a strong relationship was observed between periodontal TBR and histologically assessed inflammation within excised carotid artery plaques (R = 0.81),” they wrote.

The study authors wrote that their findings contribute to the growing literature linking periodontal disease and atherosclerosis by producing coincidental observations of carotid plaque inflammation with PET measures of periodontal disease.

“Althoughwe do not believe that PET measures of periodontal disease will provide valuableinformation for risk stratification, we do propose that the findings of this study may set the stage for future investigations regarding the effect of treatment of periodontal disease on carotid plaque inflammation,” they concluded.