BackgroundAlthough the correlation between periodontal infection and atherosclerotic lesions has been well recognized, whether and how the nonsurgical periodontal treatment (NSPT) can improve the vascular inflammation has not been investigated clearly.MethodsThirty-two apolipoprotein E−/− (apoE−/−) mice were randomly divided into four groups: (1) Con group: no treatment, blank control group; (2) Lig group: ligature-induced-periodontitis group; (3) Lig-N group: ligatures were removed on the 7th day; (4) Lig-SRP group: ligatures were removed on the 7th day, and scaling and root planing (SRP) were performed on the 9th day. All the animals were euthanized on the 30th day. Alveolar bone loss (ABL) was assessed under microcomputed tomography. Systemic inflammatory status and lipid contents in the plasma were detected. Expression of several surrogate markers for vascular inflammation was evaluated by immunohistology and quantitative real time PCR.ResultsNSPT reduced ABL, improved lipid profile, and inhibited systemic inflammation with reduced plasma interleukin-6 (IL-6) level in apoE−/− mice; in addition, reduced inflammation in arterial wall was observed in NSPT treated mice, showing less vascular cell adhesion molecule-1 expression and less macrophage adhesion; furthermore, NSPT improved elastic fiber fragmentation disorder in the aortic wall, thus preserved elasticity of aortic artery.ConclusionLigature-induced periodontitis can lead to inflammatory response in the vascular wall and NSPT has beneficial effect on the early stage of atherosclerosis process in the articular wall by reducing systemic inflammation and improving lipid profile.
Hypoxia-inducible factors (HIFs) play an important role in angiogenesis, and they can activate the expression of several downstream angiogenic factors. HIF-1 is a major transcriptor of HIFs, composed of α and β subunits. Prolyl hydroxylase domain-containing protein 2 (PHD2) is the main catabolic enzyme for HIF-1α, and it can accelerate its degradation under normoxic conditions. PHD2 expression in bone marrow mesenchymal stem cells (BMMSCs) of SD rats was down-regulated under normoxic conditions in this study by utilizing lentiviral vector-mediated RNA interference to promote HIF-1α accumulation, thus enhancing the expression of angiogenic factors. A tissue-engineered compound was constructed using the composite collagen membrane of BMMSCs after PHD2 gene silencing to repair periodontal fenestration defects in SD rats. The results of this study indicated that, after PHD2 gene silencing, the osteogenic differentiation of BMMSCs was enhanced in vitro, the resistance of cells to oxidative stress was also validated in vitro, thereby illustrating the promotion of the repair of artificially constructed periodontal tissue defects in rats. The results of this study provide a reference and guidance for future applications of RNA interference in periodontal tissue engineering and serve as a basis for improving the survival of seed cells in recipient tissues.
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