25 research outputs found

    Periodontitis and vascular inflammatory biomarkers: an experimental in vivo study in rats

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    The objective of this preclinical in vivo study was to determine changes in vascular inflammatory biomarkers in systemic circulation after injection of lipopolysaccharide (LPS) from Porphyromonas gingivalis (Pg) in rats. Experimental periodontitis was induced by injections of Pg-LPS. Gingival soft and hard tissues changes were analysed by means of magnetic resonance imaging and micro computed tomography. Serum levels of interleukin (IL)-6, IL-10, pentraxin (PTX) 3, and soluble fragment of tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) were determined at baseline and 24 h, 7, 14, and 21 days after periodontal induction. Significant periodontal inflammation and alveolar bone loss were evident at the end of periodontal induction. Experimental periodontitis posed an acute systemic inflammatory response with increased serum levels of IL-6 and PTX3 at 24 h post-induction, followed by a significant overexpression of sTWEAK at 7 days. This inflammatory state was maintained until the end of the experiment (21 days). As expected, IL-10 serum levels were significantly lower during the follow-up compared to baseline concentrations. In the present animal model, experimental periodontitis is associated with increased systemic inflammation. Further studies are needed to confirm whether PTX3 and sTWEAK could be useful biomarkers to investigate potential mechanisms underlying the relationship between periodontitis and atherosclerotic vascular diseases

    Non-equilibrium supramolecular polymerization

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    Supramolecular polymerization has been traditionally focused on the thermodynamic equilibrium state, where one-dimensional assemblies reside at the global minimum of the Gibbs free energy. The pathway and rate to reach the equilibrium state are irrelevant, and the resulting assemblies remain unchanged over time. In the past decade, the focus has shifted to kinetically trapped (non-dissipative non-equilibrium) structures that heavily depend on the method of preparation (i.e., pathway complexity), and where the assembly rates are of key importance. Kinetic models have greatly improved our understanding of competing pathways, and shown how to steer supramolecular polymerization in the desired direction (i.e., pathway selection). The most recent innovation in the field relies on energy or mass input that is dissipated to keep the system away from the thermodynamic equilibrium (or from other non-dissipative states). This tutorial review aims to provide the reader with a set of tools to identify different types of self-assembled states that have been explored so far. In particular, we aim to clarify the often unclear use of the term “non-equilibrium self-assembly” by subdividing systems into dissipative, and non-dissipative non-equilibrium states. Examples are given for each of the states, with a focus on non-dissipative non-equilibrium states found in one-dimensional supramolecular polymerization

    Complexity from small molecules

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    Porphyromonas gingivalis lipopolysaccharide-induced periodontitis and serum amyloid-beta peptides

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    Objective The aim of this investigation was to determine the circulating levels of amyloid beta (Aβ) peptides using the Porphyromonas gingivalis (Pg) lipopolysaccharide (LPS) model to induce periodontitis. Methods Experimental periodontitis was induced in 6 male Sprague-Dawley rats. Alveolar bone loss was measure by micro computed tomography. Serum concentrations of Aβ1–40 and Aβ1–42 prior to periodontal induction, at 24 h, 7, 14, and 21 days the last injection of Pg-LPS. Results The distance between the cemento-enamel junction and the bone crest (i.e., alveolar bone loss) was significantly higher at the end of periodontal induction compared to baseline (2.92 ± 0.29 mm vs. 3.8 ± 0.28 mm, P < 0.001). Periodontitis evoked a slight acute elevation of Aβ1–40 serum levels that were maintained during the whole experiment. Aβ1–42 peptide levels peak at the end of the study. A positive strong correlation was observed between alveolar bone loss and Aβ1–40 serum levels at 7 days (r = 0.695, P = 0.012) and as well as with serum Aβ1–42 concentrations at 21 days (r = 0.968, P = 0.002). Conclusions Periodontitis induced Pg-LPS produced increased serum levels of Aβ peptides. Further studies are needed to confirm our results and to investigate the mechanisms by which periodontitis could be associated with an overexpression of Aβ
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