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      Nonsurgical periodontal treatment reduced aortic inflammation in ApoE −/− mice with periodontitis

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          Abstract

          Background

          Although 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.

          Methods

          Thirty-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.

          Results

          NSPT 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.

          Conclusion

          Ligature-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.

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          Most cited references29

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          Patterns of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 expression in rabbit and mouse atherosclerotic lesions and at sites predisposed to lesion formation.

          The recruitment of mononuclear leukocytes and formation of intimal macrophage-rich lesions at specific sites of the arterial tree are key events in atherogenesis. Inducible endothelial cell adhesion molecules may participate in this process. In aortas of normal chow-fed wild-type mice and rabbits, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), but not E-selectin, were expressed by endothelial cells in regions predisposed to atherosclerotic lesion formation. En face confocal microscopy of the mouse ascending aorta and proximal arch demonstrated that VCAM-1 expression was increased on the endothelial cell surface in lesion-prone areas. ICAM-1 expression extended into areas protected from lesion formation. Hypercholesterolemia induced atherosclerotic lesion formation in rabbits, LDL receptor and apolipoprotein E knockout mice, and Northern blot analysis demonstrated increased steady-state mRNA levels of VCAM-1 and ICAM-1, but not of E-selectin. Immunohistochemical staining revealed that VCAM-1 and ICAM-1 were expressed predominantly by endothelium in early lesions and by intimal cells in more advanced lesions. In early and advanced lesions, staining was most intense in endothelial cells at and adjacent to lesion borders. ICAM-1 staining extended into the uninvolved aorta. These expression patterns were highly reproducible in both species. The only difference was that VCAM-1 expression in endothelium over the central portions of lesions was found frequently in rabbits and rarely in mice. The expression of VCAM-1 by arterial endothelium in normal animals may represent a pathogenic mechanism or a phenotypic marker of predisposition to atherogenesis.
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            Periodontal infections cause changes in traditional and novel cardiovascular risk factors: results from a randomized controlled clinical trial.

            Chronic infections, such as periodontitis, are associated with increased risk of systemic diseases driven by a persistent low-grade systemic inflammation and metabolic changes. Severity of periodontitis has also been associated with increased systolic blood pressure (BP). However, the issue remains poorly investigated. We aimed to estimate the effect of periodontal therapy on traditional and novel cardiovascular risk factors in systemically healthy individuals who have periodontitis. We enrolled 40 otherwise healthy patients with severe chronic generalized periodontitis in a 6-month pilot intervention trial. Individuals were randomized either to a standard course of periodontal therapy (subgingival scaling and root planing) or an intensive one (including the adjunctive use of a locally delivered antimicrobial, IPT). Compared to control, IPT produced significant reductions in a cluster of inflammatory markers at 1 (P = .0406) and 2 (P = .0060) months together with an improvement in lipid markers at 2 (P = .0320) and 6 (P = .0432) months after therapy. Intensive periodontal therapy produced greater reductions in IL-6 at 1 (0.4 +/- 0.2 ng/L difference, 95% CI 0.03-0.9, P = .0284) and 2 months (0.3 +/- 0.2 ng/L difference, 95% CI 0.1-0.8, P = .0284), together with decreases in C-reactive protein (0.4 +/- 0.2 mg/L difference, 95% CI 0.01-0.8, P = .0438) and total cholesterol (0.3 +/- 0.1 mmol/L difference, 95% CI 0.04-0.6, P = .0254). Moreover, a 7 +/- 3-mm Hg decrease in systolic BP was observed at 2 months in the IPT group (95% CI 1-12, P = .0211), and this difference was greater in current smokers (14 +/- 5 mm Hg 95% CI 3-25, P = 0.0124). Intensive periodontal therapy subjects exhibited a 1.53% +/- 1.20% (95% CI 1.05-2.24, P = .0290) and 2.00% +/- 1.42% (95% CI 0.98-4.09, P = .0568) decreases in cardiovascular risk scores (Framingham) at 2 and 6 months, respectively, when compared to those in the standard group. Our findings suggest that intensive periodontal treatment reduces systemic inflammatory markers and systolic BP, and improves lipid profiles with subsequent changes in cardiovascular risk when compared to standard therapy.
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              Applications of myeloid-specific promoters in transgenic mice support in vivo imaging and functional genomics but do not support the concept of distinct macrophage and dendritic cell lineages or roles in immunity.

              Ian D Hume (2011)
              Myeloid lineage cells contribute to innate and acquired immunity, homeostasis, wound repair, and inflammation. There is considerable interest in manipulation of their function in transgenic mice using myeloid-specific promoters. This review considers the applications and specificity of some of the most widely studied transgenes, driven by promoter elements of the lysM, csf1r, CD11c, CD68, macrophage SRA, and CD11b genes, as well as several others. Transgenes have been used in mice to generate myeloid lineage-specific cell ablation, expression of genes of interest, including fluorescent reporters, or deletion via recombination. In general, the specificity of such transgenes has been overinterpreted, and none of them provide well-documented, reliable, differential expression in any specific myeloid cell subset, macrophages, granulocytes, or myeloid DCs. Nevertheless, they have proved valuable in cell isolation, functional genomics, and live imaging of myeloid cell behavior in many different pathologies.
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                Author and article information

                Contributors
                cd_nju@163.com
                lihouxuan3435_0@163.com
                leilangdental@163.com
                ccx88202365@126.com
                + 86-025-83620253 , yanfh@nju.edu.cn
                Journal
                Springerplus
                Springerplus
                SpringerPlus
                Springer International Publishing (Cham )
                2193-1801
                30 June 2016
                30 June 2016
                2016
                : 5
                : 1
                : 940
                Affiliations
                Nanjing Stomatological Hospital, Medical School of Nanjing University, 30 Zhong Yang Road, Nanjing, 210008 Jiangsu People’s Republic of China
                Article
                2637
                10.1186/s40064-016-2637-z
                4929118
                27386384
                4c547476-1517-4bdd-a0ab-a103769ab2b5
                © The Author(s) 2016

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 25 January 2016
                : 21 June 2016
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 81371152
                Award Recipient :
                Funded by: Provincial Nature Science Foundation of Jiangsu Province
                Award ID: BK20131079
                Award Recipient :
                Funded by: the Key Project of Science and Technology Bureau of Jiangsu Province
                Award ID: BL2013002
                Award Recipient :
                Categories
                Research
                Custom metadata
                © The Author(s) 2016

                Uncategorized
                atherosclerosis,lipid,periodontitis,srp
                Uncategorized
                atherosclerosis, lipid, periodontitis, srp

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