Positron Emission Tomography Measurement of Periodontal 18F-Fluorodeoxyglucose Uptake Is Associated With Histologically Determined Carotid Plaque Inflammation

This study 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-fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging. Several lines of...

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Published inJournal of the American College of Cardiology Vol. 57; no. 8; pp. 971 - 976
Main Authors Fifer, Kenneth M., Qadir, Sadia, Subramanian, Sharath, Vijayakumar, Jayanthi, Figueroa, Amparo L., Truong, Quynh A., Hoffman, Udo, Brady, Thomas J., Tawakol, Ahmed
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 22.02.2011
Elsevier
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Online AccessGet full text
ISSN0735-1097
1558-3597
1558-3597
DOI10.1016/j.jacc.2010.09.056

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Abstract This study 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-fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging. Several lines of evidence establish periodontal disease as an important risk factor for atherosclerosis. FDG-PET imaging is an established method for measuring metabolic activity in human tissues and blood vessels. One hundred twelve patients underwent FDG-PET imaging 92 ± 5 min after FDG administration (13 to 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 (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 coregistration 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). 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.
AbstractList This study 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-fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging. Several lines of evidence establish periodontal disease as an important risk factor for atherosclerosis. FDG-PET imaging is an established method for measuring metabolic activity in human tissues and blood vessels. One hundred twelve patients underwent FDG-PET imaging 92 ± 5 min after FDG administration (13 to 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 (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 coregistration 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). 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.
This study 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 (18)F-fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging. Several lines of evidence establish periodontal disease as an important risk factor for atherosclerosis. FDG-PET imaging is an established method for measuring metabolic activity in human tissues and blood vessels. One hundred twelve patients underwent FDG-PET imaging 92 ± 5 min after FDG administration (13 to 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 (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 coregistration 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). 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.
This study 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 (18)F-fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging.OBJECTIVESThis study 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 (18)F-fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging.Several lines of evidence establish periodontal disease as an important risk factor for atherosclerosis. FDG-PET imaging is an established method for measuring metabolic activity in human tissues and blood vessels.BACKGROUNDSeveral lines of evidence establish periodontal disease as an important risk factor for atherosclerosis. FDG-PET imaging is an established method for measuring metabolic activity in human tissues and blood vessels.One hundred twelve patients underwent FDG-PET imaging 92 ± 5 min after FDG administration (13 to 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 (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 coregistration 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.METHODSOne hundred twelve patients underwent FDG-PET imaging 92 ± 5 min after FDG administration (13 to 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 (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 coregistration 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). Moreover, a strong relationship was observed between periodontal TBR and histologically assessed inflammation within excised carotid artery plaques (R = 0.81, p < 0.001).RESULTSPeriodontal 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). 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.CONCLUSIONSFDG-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.
Author Subramanian, Sharath
Vijayakumar, Jayanthi
Truong, Quynh A.
Tawakol, Ahmed
Qadir, Sadia
Brady, Thomas J.
Figueroa, Amparo L.
Hoffman, Udo
Fifer, Kenneth M.
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Issue 8
Keywords atherosclerosis
CT
PD
inflammation
MRI
SUV
TBR
FDG
periodontal
carotid
PET
CEA
Radionuclide study
Measurement
Carotid
Inflammation
Circulatory system
Cardiology
Positron emission tomography
Uptake
Emission tomography
Language English
License http://www.elsevier.com/open-access/userlicense/1.0
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Snippet This study aimed to test the hypothesis that metabolic activity within periodontal tissue (a possible surrogate for periodontal inflammation) predicts...
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SubjectTerms Age Distribution
Aged
atherosclerosis
Biological and medical sciences
Cardiology. Vascular system
carotid
Carotid Stenosis - diagnostic imaging
Carotid Stenosis - epidemiology
Carotid Stenosis - physiopathology
Cohort Studies
Comorbidity
Female
Fluorodeoxyglucose F18 - pharmacokinetics
Humans
Incidence
inflammation
Male
Medical sciences
Middle Aged
periodontal
Periodontal Diseases - diagnostic imaging
Periodontal Diseases - epidemiology
Periodontal Diseases - physiopathology
PET
Plaque, Atherosclerotic - diagnostic imaging
Plaque, Atherosclerotic - epidemiology
Plaque, Atherosclerotic - pathology
Positron-Emission Tomography - methods
Predictive Value of Tests
Risk Assessment
Severity of Illness Index
Sex Distribution
Survival Rate
Title Positron Emission Tomography Measurement of Periodontal 18F-Fluorodeoxyglucose Uptake Is Associated With Histologically Determined Carotid Plaque Inflammation
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0735109710048059
https://dx.doi.org/10.1016/j.jacc.2010.09.056
https://www.ncbi.nlm.nih.gov/pubmed/21329844
https://www.proquest.com/docview/852912437
Volume 57
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