Article

Prevention: Reducing the risk of CVD in patients with periodontitis

Department of Oral Biology, State University of New York at Buffalo, Baird Research Park, 1576 Sweet Home Road, Amherst, NY 14228, USA.
Nature Reviews Cardiology (Impact Factor: 10.15). 09/2010; 7(9):479-80. DOI: 10.1038/nrcardio.2010.120
Source: PubMed

ABSTRACT The association between periodontitis and other chronic diseases, such as cardiovascular disease (CVD) and type 2 diabetes mellitus, could be related to systemic inflammation initiated by a local inflammatory challenge. Oliveira et al. have added lack of oral hygiene, and its link with systemic inflammation, to the spectrum of risk factors for CVD.

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    • "These findings suggested that Del-1 could act homeostatically to regulate local inflammation. This concept was demonstrated by studies in animal models of periodontitis (Eskan et al., 2012), a chronic inflammatory disease that leads to inflammatory destruction of tooth-supporting tissues (Pihlstrom et al., 2005) and, in its severe form, adversely affects systemic health, thereby increasing the risk for atherosclerosis and diabetes (Genco and Van Dyke, 2010; Kebschull et al., 2010; Lalla and Papapanou, 2011). Specifically, Del-1- deficient mice were shown to spontaneously develop excessive neutrophil infiltration in the periodontium, leading to severe inflammation and alveolar bone loss (Eskan et al., 2012). "
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    ABSTRACT: New insights into the biological mechanisms involved in modulating periodontal inflammation and alveolar bone loss are paving the way for novel therapeutic strategies for periodontitis. The neutrophil adhesion cascade for transmigration in response to infection or inflammation is a key paradigm in immunity. Developmental endothelial locus-1 (Del-1) is one of several newly identified endogenous inhibitors of the leukocyte adhesion cascade. Del-1 competes with intercellular adhesion molecule-1 (ICAM-1) on endothelial cells for binding to the LFA-1 integrin on neutrophils, thereby regulating neutrophil recruitment and local inflammation. In animal periodontitis models, Del-1 deficiency resulted in severe inflammation and alveolar bone loss, but local treatment with recombinant Del-1 prevented neutrophil infiltration and bone loss. The expression of Del-1 is inhibited by the pro-inflammatory cytokine IL-17. Nucleic-acid-receptor-mediated inflammatory responses may be important in periodontal disease pathogenesis. Bacterial nucleic acids released during inflammation are detected by host microbial DNA sensors, e.g., Toll-like receptor-9 (TLR-9), leading to the activation of pro- and/or anti-inflammatory signaling pathways. DNA from periodontitis-associated bacteria induced pro-inflammatory cytokine production in human macrophage-like cells through the TLR-9 and NF-κB signaling pathways, but had less effect on human osteoblasts. Inhibition of TLR-9 signaling in human macrophages reduced cytokine production in response to P. gingivalis DNA. Differential expression of a polymorphic site in the TLR-9 gene promoter region and increased TLR-9 gene and protein expression were reported in chronic periodontitis. Further research to confirm that periodontal bacterial DNA contributes to destructive inflammation in vivo could provide alternative therapeutic targets to control periodontitis.
    Advances in dental research 05/2014; 26(1):23-9. DOI:10.1177/0022034514526240
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    • "An attractive model to address this issue is periodontitis, an oral inflammatory disease induced by a multispecies biofilm that is readily accessible for investigation (Pihlstrom et al., 2005). Porphyromonas gingivalis, a low-abundance oral anaerobic bacterium, is implicated in periodontitis and associated systemic conditions (Desvarieux et al., 2005; Genco and Van Dyke, 2010; Lundberg et al., 2010; Pihlstrom et al., 2005; Tonetti et al., 2007). However, the fundamental mechanism by which P. gingivalis contributes to this polymicrobial disease has remained elusive. "
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    ABSTRACT: Porphyromonas gingivalis is a low-abundance oral anaerobic bacterium implicated in periodontitis, a polymicrobial inflammatory disease, and the associated systemic conditions. However, the mechanism by which P. gingivalis contributes to inflammation and disease has remained elusive. Here we show that P. gingivalis, at very low colonization levels, triggers changes to the amount and composition of the oral commensal microbiota leading to inflammatory periodontal bone loss. The commensal microbiota and complement were both required for P. gingivalis-induced bone loss, as germ-free mice or conventionally raised C3a and C5a receptor-deficient mice did not develop bone loss after inoculation with P. gingivalis. These findings demonstrate that a single, low-abundance species can disrupt host-microbial homeostasis to cause inflammatory disease. The identification and targeting of similar low-abundance pathogens with community-wide impact may be important for treating inflammatory diseases of polymicrobial etiology.
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