Oral Infections and General Health: From Molecule to by Anne Marie Lynge Pedersen

By Anne Marie Lynge Pedersen

​This publication presents a wide-ranging replace at the institutions among oral infections and normal wellbeing and fitness. specified attention is given to the underlying mechanisms or pathways linking oral infections to basic overall healthiness, together with metastatic unfold of an infection from the oral hollow space because of temporary bacteremia, metastatic harm from the consequences of circulating oral microbial pollutants, and metastatic irritation because of immunological disorder precipitated via oral microorganisms. The e-book additionally reports the advanced constitution and improvement of oral biofilms in wellbeing and fitness and ailment, and the molecular instruments which are at present on hand for his or her research. the benefits and boundaries of such suggestions, in addition to their influence at the way forward for diagnostics, prevention and sufferer administration, are discussed.

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2000). Studies on the effects of periodontal therapy on fibrinogen levels (reviewed in (Teeuw et al. 2014; D’Aiuto et al. 2013)) yielded variable results; some studies reported a significant reduction in the fibrinogen levels in the patient groups that received active periodontal treatment; others measured no significant changes post-therapy. Other markers of coagulation or fibrinolysis (prothrombin fragments 1 + 2, D-dimer, von Willebrand factor, tissue plasminogen activator and plasminogen activator inhibitor-1) known to be modified in prothrombotic states, rendered inconclusive results when explored in periodontitis.

We hypothesize that an aberrant inflammatory reactivity, determined in part by genetic variants in ANRIL, CAMTA1 and VAMP3, could also explain the epidemiological link between periodontitis and atherosclerosis in coronary arteries (CAD). And recently, yet another CAD risk locus was also found to be associated with periodontitis; there is now evidence for PLASMINOGEN (PLG) as a shared genetic risk factor of CAD and periodontitis (Schaefer et al. 2015). When plasminogen is converted into plasmin, the latter enzyme can dissolve the fibrinogen fibers that entangle the blood cells in a blood clot; this is called fibrinolysis.

References Albandar J. Underestimation of periodontitis in NHANES surveys. J Periodontol. 2011;82:337–41. Andersen NN, Jess T. Risk of cardiovascular disease in inflammatory bowel disease. World J Gastrointest Pathophysiol. 2014;5(3):359–65. Armitage G. Development of a classification system for periodontal diseases and conditions. Ann Periodontol. 1999;4:1–6. Assinger A, et al. Periodontopathogens induce soluble P-selectin release by endothelial cells and platelets. Thromb Res. 2011;127(1):e20–6.

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