Positron Emission Tomography Measurement of Periodontal 18F-Fluorodeoxyglucose Uptake Is Associated With Histologically Determined Carotid Plaque Inflammation
Is metabolic activity within periodontal tissue (a possible surrogate for periodontal inflammation) predictive of inflammation in a remote atherosclerotic vessel?
A total of 112 patients underwent 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging 92 ± 5 minutes after FDG administration (13-25 mCi). Periodontal FDG uptake was measured by obtaining standardized uptake values from the periodontal tissue of each patient, and the ratio of periodontal to background (blood) activity was determined (target-to-background ratio [TBR]). Standardized uptake value measurements were obtained 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 computed tomography or magnetic resonance imaging. A subset of 16 patients underwent carotid endarterectomy within 1 month of PET imaging, during which atherosclerotic plaques were removed and subsequently stained with anti-CD68 antibodies to quantify macrophage infiltration. Periodontal FDG uptake was compared with carotid plaque macrophage infiltration.
Periodontal FDG uptake (TBR) is associated with carotid TBR (R = 0.64, p < 0.0001), as well as aortic TBR (R = 0.38; p = 0.029). This association remained significant after adjusting for age, sex, low-density lipoprotein cholesterol, history of hypertension, statin therapy, and diabetes (R = 0.56, p < 0.0001), as well as blood glucose concentration and tracer circulation time (R = 0.78, p < 0.0001). Moreover, a strong relationship was observed between periodontal TBR and histologically assessed inflammation within excised carotid artery plaques (R = 0.81, p < 0.001).
FDG-PET measurements of metabolic activity within periodontal tissue correlate with macrophage infiltration within carotid plaques. These findings provide direct evidence for an association between periodontal disease and atherosclerotic inflammation.
There is a considerable amount of evidence connecting abnormal gingival health and coronary and carotid disease as well as cardiovascular events. Whether there is a cause-effect or contribution of periodontal disease to plaque inflammation and effect of treatment has been difficult to establish. This technology provides an opportunity to test several hypotheses.
Clinical Topics: Dyslipidemia, Heart Failure and Cardiomyopathies, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Vascular Medicine, Lipid Metabolism, Heart Failure and Cardiac Biomarkers, Interventions and Imaging, Interventions and Vascular Medicine, Computed Tomography, Magnetic Resonance Imaging, Nuclear Imaging
Keywords: Lipoproteins, LDL, Inflammation, Fluorodeoxyglucose F18, Plaque, Atherosclerotic, Periodontal Diseases, Antigens, CD, Tomography, X-Ray Computed, Endarterectomy, Carotid, Carotid Stenosis, Magnetic Resonance Imaging, Positron-Emission Tomography
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