Infection with Porphyromonas gingivalis Exacerbates Endothelial Injury in Obese Mice

Abstract

BackgroundA number of studies have revealed a link between chronic periodontitis and cardiovascular disease in obese patients. However, there is little information about the influence of periodontitis-associated bacteria, Porphyromonas gingivalis (Pg), on pathogenesis of atherosclerosis in obesity.Methods In vivo experiment: C57BL/6J mice were fed with a high-fat diet (HFD) or normal chow diet (CD), as a control. Pg was infected from the pulp chamber. At 6 weeks post-infection, histological and immunohistochemical analysis of aortal tissues was performed. In vitro experiment: hTERT-immortalized human umbilical vein endothelial cells (HuhT1) were used to assess the effect of Pg/Pg-LPS on free fatty acid (FFA) induced endothelial cells apoptosis and regulation of cytokine gene expression.ResultsWeaker staining of CD31 and increased numbers of TUNEL positive cells in aortal tissue of HFD mice indicated endothelial injury. Pg infection exacerbated the endothelial injury. Immunohistochemically, Pg was detected deep in the smooth muscle of the aorta, and the number of Pg cells in the aortal wall was higher in HFD mice than in CD mice. Moreover, in vitro, FFA treatment induced apoptosis in HuhT1 cells and exposure to Pg-LPS increased this effect. In addition, Pg and Pg-LPS both attenuated cytokine production in HuhT1 cells stimulated by palmitate.ConclusionsDental infection of Pg may contribute to pathogenesis of atherosclerosis by accelerating FFA-induced endothelial injury.

Glutathione levels in plasma, saliva and gingival crevicular fluid after periodontal therapy in obese and normal weight individuals

“… stated a significant association between the increase in some bacterial groups and obesity. Another study reported that dental infection of Porphyromonas gingivalis could contribute to endothelial injury in obese mice . Saito and Shimazaki suggested that the bacterial flora in dental plaque might differ in obese subjects.…”

“…They emphasized that obesity did not have a negative impact on the periodontal clinical response after nonsurgical periodontal treatment. Furthermore, Ao et al (42) suggested that periodontal therapy may prevent or minimize the side effects of bacterial infection in obese patients. Our study demonstrated the percentage increase in gingival crevicular fluid and plasma GSH levels of the OCP group compared to the chronic periodontitis group from baseline to post-periodontal treatment, but BMI values did not change.…”

Interaction between periodontal disease and atherosclerotic vascular disease – Fact or fiction?

“…In other experiments, C57BL/6J mice were made obese by feeding them with a high-fat diet followed by infection with P. gingivalis. It could be demonstrated that the obese mice reacted to infection with more pronounced endothelial injury compared with lean controls and more P. gingivalis bacteria were detected deep in the smooth muscle of the aorta from obese mice [66].…”

Porphyromonas gingivalis Lipopolysaccharide Stimulation of Vascular Smooth Muscle Cells Activates Proliferation and Calcification

“…Therefore, as a common inflammatory disease, periodontitis may contribute to the development of vascular diseases, resulting in cardiovascular disease (CVD). Although the mechanisms of this relationship have not been fully elucidated, it has been proposed that Pg and LPS can access systemic circulation to cause the breakdown of vascular cells and increase the inflammatory response, which is verified to be the source of CVD risk in patients with periodontal diseases 10 , 11 …”

“…Although the mechanisms of this relationship have not been fully elucidated, it has been proposed that Pg and LPS can access systemic circulation to cause the breakdown of vascular cells and increase the inflammatory response, which is verified to be the source of CVD risk in patients with periodontal diseases. 10,11 In general, vascular ectopic calcification as a wellknown major risk factor for the adverse CVDs is a highly prevalent vascular pathophenotype that is closely associated with atherothrombotic CVDs, aging, renal failure, and diabetes mellitus. 12 It predicts a worse clinical outcome and major disadvantageous cardiovascular events.…”