IADR Abstract Archives
Plausible Mechanistic Link between Periodontitis and Cardiovascular Disease
Objectives: Periodontitis is a risk factor for cardiovascular disease (CVD). However, the mechanistic link between both diseases is unknown. We aimed to explore the role of systemic inflammation, innate immune cell activation and vascular wall inflammation in patients with severe periodontitis and control subjects.
Methods: Patients with severe periodontitis (“patients”, n=14) and subjects with no to mild periodontitis (“controls”, n=14) were recruited and underwent venepuncture and 18F - fluorodeoxyglucose (FDG) positron-emission tomography (PET/CT) scanning. Study protocol was approved by the Review Board and all individuals signed an informed consent. Cytokine production capacity was assessed after 24 hours of ex vivo stimulation in PBMCs. Vascular wall inflammation and hematopoietic tissue activity were determined on 18F-FDG PET/CT scans. All analyses were done independently by specialists blinded for the status of the participants. Differences were considered significant when p< 0.05.
Results: Characteristics of the study groups are presented in Table 1. Circulating interleukin 6 (IL-6) was higher in “patients” compared to “controls” 1.54 pg/ml versus 2.47 pg/ml (p<0.05). Cytokine production capacity of PBMCs revealed no differences. Vascular wall 18F-FDG uptake was higher in “patients” compared to “controls” only for the femoral arteries (p=0.07) after correction for blood pool. For the rest of the big arteries (i.e. aorta, carotic arteries) the standard uptake values (SUVmean) were comparable between “patients” and “controls”. Hematopoietic tissue activity appeared higher in “patients” compared to “controls” prior to target- to background validation (mild SUVmean,p <0.01).
Conclusions: Patients with severe periodontitis have pro-inflammatory monocyte phenotype and significantly increased systemic inflammation. Vascular wall inflammation and hematopoietic tissue activation appear higher, but not significantly. Within its limitations, this study provides for the first time a plausible mechanistic link responsible for the association periodontitis and CVD. The results justify an intervention study on the effect of periodontal treatment on systemic inflammation as prevention of CVD.
Methods: Patients with severe periodontitis (“patients”, n=14) and subjects with no to mild periodontitis (“controls”, n=14) were recruited and underwent venepuncture and 18F - fluorodeoxyglucose (FDG) positron-emission tomography (PET/CT) scanning. Study protocol was approved by the Review Board and all individuals signed an informed consent. Cytokine production capacity was assessed after 24 hours of ex vivo stimulation in PBMCs. Vascular wall inflammation and hematopoietic tissue activity were determined on 18F-FDG PET/CT scans. All analyses were done independently by specialists blinded for the status of the participants. Differences were considered significant when p< 0.05.
Results: Characteristics of the study groups are presented in Table 1. Circulating interleukin 6 (IL-6) was higher in “patients” compared to “controls” 1.54 pg/ml versus 2.47 pg/ml (p<0.05). Cytokine production capacity of PBMCs revealed no differences. Vascular wall 18F-FDG uptake was higher in “patients” compared to “controls” only for the femoral arteries (p=0.07) after correction for blood pool. For the rest of the big arteries (i.e. aorta, carotic arteries) the standard uptake values (SUVmean) were comparable between “patients” and “controls”. Hematopoietic tissue activity appeared higher in “patients” compared to “controls” prior to target- to background validation (mild SUVmean,p <0.01).
Conclusions: Patients with severe periodontitis have pro-inflammatory monocyte phenotype and significantly increased systemic inflammation. Vascular wall inflammation and hematopoietic tissue activation appear higher, but not significantly. Within its limitations, this study provides for the first time a plausible mechanistic link responsible for the association periodontitis and CVD. The results justify an intervention study on the effect of periodontal treatment on systemic inflammation as prevention of CVD.