Periodontitis-activated monocytes/macrophages cause aortic inflammation

Abstract

A relationship between periodontal disease and atherosclerosis has been suggested by epidemiological studies. Ligature-induced experimental periodontitis is an adequate model for clinical periodontitis, which starts from plaque accumulation, followed by inflammation in the periodontal tissue. Here we have demonstrated using a ligature-induced periodontitis model that periodontitis activates monocytes/macrophages, which subsequently circulate in the blood and adhere to vascular endothelial cells without altering the serum TNF-α concentration. Adherent monocytes/macrophages induced NF-κB activation and VCAM-1 expression in the endothelium and increased the expression of the TNF-α signaling cascade in the aorta. Peripheral blood-derived mononuclear cells from rats with experimental periodontitis showed enhanced adhesion and increased NF-κB/VCAM-1 in cultured vascular endothelial cells. Our results suggest that periodontitis triggers the initial pathogenesis of atherosclerosis, inflammation of the vasculature, through activating monocytes/macrophages.

Biochemical and histopathologic analysis of the effects of periodontitis on left ventricular heart tissues of rats

“…However, our findings also indicate that EP caused a slight increase in serum TNF‐α levels. Although this finding is generally compatible with those of animal studies with similar designs , some studies detected a significant increase in TNF‐α level . Human studies have reported varying results .…”

“…In a recent study, Miyajima et al . found no significant changes in TNF‐α, CRP or IL‐6 serum levels in rats with EP. However, they found that TNF‐α and IL‐6 mRNA expression increased 2.7‐ and 2.6‐fold, respectively, in circulating mononuclear cells.…”

“…Our histopathological findings after 35 d of EP included inflammatory cell infiltration, degeneration of myocytes, collagen accumulation, capillary endothelial changes and perivascular fibrosis. Studies with similar designs reported that EP caused significant inflammatory cell infiltration in the aortic wall and the atrium . Miyajima et al .…”

Comparative analysis of immune cell subsets in peripheral blood from patients with periodontal disease and healthy controls

“…Previous studies have suggested a role for monocytes from patients with periodontitis in aortic inflammation [11,12]. These data suggested that monocytes during or after periodontal pathogen challenge could contribute to inflammation in periodontitis-associated systemic disease.…”

Porphyromonas gingivalis HSP60 peptides have distinct roles in the development of atherosclerosis

“…Periodontitis, an oral infectious disease predominantly by Porphyromonas gingivalis (P. gingivalis) (Darveau, 2010), has been one of the risk factors for cardiovascular diseases (Friedewald et al, 2009), by triggering the initial pathogenesis of atherosclerosis, inflammation of the vasculature, through activating monocytes/macrophages (Miyajima et al, 2014). P. gingivalis was detected in atheromatous plaques and reported to perpetuate systemic inflammation (Darveau, 2010;Kozarov et al, 2005).…”