Periodontitis is a chronic inflammatory disease, initiated by the presence of a bacterial biofilm, called dental plaque, which affects both the periodontal ligaments and bone surrounding teeth. In the last decades, several lines of evidence have supported the existence of a relationship between periodontitis and systemic health. For instance, as periodontitis acts within the same chronic inflammatory model seen in cardiovascular disease (CVD), or other disorders, such as diabetes, several studies have suggested the existence of a bi-directional link between periodontal health and these pathologies. For instance, people with diabetes are more susceptible to infections and are more likely to suffer from periodontitis than people without this syndrome. Analogously, it is now evident that cardiac disorders are worsened by periodontitis, both experimentally and in humans. For all these reasons, it is very plausible that preventing periodontitis has an impact on the onset or progression of CVD and diabetes. On these grounds, in this review, we have provided an updated account on the current knowledge concerning periodontal disease and the adverse effects exerted on the cardiovascular system health and diabetes, informing readers on the most recent preclinical studies and epidemiological evidence.

https://www.mdpi.com/1422-0067/20/6/1414/pdf

Periodontal Disease: A Risk Factor for Diabetes and Cardiovascular Disease

Periodontal and cardiovascular disease are both major health issues. Poor oral health has long been associated with the development of systemic diseases, with the typical example being the risk of endocarditis posterior to dental procedures. Through the years, the association of periodontal disease with other non-infectious systemic diseases has been brought to attention. One of the most interesting associations is the one that exists with the development of cardiovascular disease. Many studies, including systematic reviews and meta-analyses, suggest an important association between periodontal disease and ischaemic heart disease, cerebrovascular disease, heart failure, atrial fibrillation and peripheral artery disease. Among the proposed mechanisms of this relationship, systemic inflammation appears to play a major role. Evidence suggests that periodontal inflammation triggers a systemic inflammatory state that, added to the damage mediated by antibodies that cross react between periodontal pathogens and components of the intimal wall, and the direct lesion of the intima by bacteria entering the circulation, promotes atheroma plaque development and progression. There are other studies that show a clear relationship between periodontal disease severity, elevations of inflammatory markers, and the presence of atherosclerosis. Here, we give a review of the available evidence supporting this association, and the possible mechanisms involved.

Periodontal Disease, Systemic Inflammation and the Risk of Cardiovascular Disease.

Periodontal disease is of established aetiology in which polymicrobial synergistic ecology has become dysbiotic under the influence of Porphyromonas gingivalis. Following breakdown of the host’s protective oral tissue barriers, P. gingivalis migrates to developing inflammatory pathologies that associate with Alzheimer’s disease (AD). Periodontal disease is a risk factor for cardiovascular disorders (CVD), type II diabetes mellitus (T2DM), AD and other chronic diseases, whilst T2DM exacerbates periodontitis. This study analysed the relationship between the P. gingivalis/host interactome and the genes identified in genome-wide association studies (GWAS) for the aforementioned conditions using data from GWASdb (P<1E-03) and, in some cases, from the NCBI/EBI GWAS database (P< 1E-05). Gene expression data from periodontitis or P. gingivalis microarray was compared to microarray datasets from the AD hippocampus and/or from carotid artery plaques. The results demonstrated that the host genes of the P. gingivalis interactome were significantly enriched in genes deposited in GWASdb genes related to cognitive disorders, AD and dementia, and its co-morbid conditions T2DM, obesity, and CVD. The P. gingivalis/host interactome was also enriched in GWAS genes from the more stringent NCBI-EBI database for AD, atherosclerosis and T2DM. The misregulated genes in periodontitis tissue or P. gingivalis infected macrophages also matched those in the AD hippocampus or atherosclerotic plaques. Together, these data suggest important gene/environment interactions between P. gingivalis and susceptibility genes or gene expression changes in conditions where periodontal disease is a contributory factor.

/pdf/the-porphyromonas-gingivalis-host-interactome-shows-ajbjkcyfew.pdf

The Porphyromonas gingivalis /Host Interactome Shows Enrichment in GWASdb Genes Related to Alzheimer's Disease, Diabetes and Cardiovascular Diseases.

Chronic inflammatory diseases, such as periodontal disease, associate with adverse wound healing in response to myocardial infarction (MI). The goal of this study was to elucidate the molecular basis for impaired cardiac wound healing in the setting of periodontal-induced chronic inflammation. Causal network analysis of 168 inflammatory and extracellular matrix genes revealed that chronic inflammation induced by a subseptic dose of Porphyromonas gingivalis lipopolysaccharide (LPS) exacerbated infarct expression of the proinflammatory cytokine Ccl12. Ccl12 prevented initiation of the reparative response by prolonging inflammation and inhibiting fibroblast conversion to myofibroblasts, resulting in diminished scar formation. Macrophage secretion of Ccl12 directly impaired fibronectin and collagen deposition and indirectly stimulated collagen degradation through upregulation of matrix metalloproteinase-2. In post-MI patients, circulating LPS levels strongly associated with the Ccl12 homologue monocyte chemotactic protein 1 (MCP-1). Patients with LPS levels ≥ 1 endotoxin units (EU)/ml (subseptic endotoxemia) at the time of hospitalization had increased end diastolic and systolic dimensions compared with post-MI patients with < 1 EU/ml, indicating that low yet pathological concentrations of circulating LPS adversely impact post-MI left ventricle (LV) remodeling by increasing MCP-1. Our study provides the first evidence to our knowledge that chronic inflammation inhibits reparative fibroblast activation and generates an unfavorable cardiac-healing environment through Ccl12-dependent mechanisms.

/pdf/periodontal-induced-chronic-inflammation-triggers-macrophage-26jht4g6j0.pdf

Periodontal-induced chronic inflammation triggers macrophage secretion of Ccl12 to inhibit fibroblast-mediated cardiac wound healing

Chupryna R. R. Prevention of menopausal disorders in women with unspecified benign uterine or ovarian tumors. – Manuscript. Thesis for academic degree of candidate of medical sciences in specialty 14.01.01 – Obstetrics and Gynecology. – P. L. Shupyk National Medical Academy of Post-Graduate Education, Kyiv, 2015. The paper deals with the peculiarities of preventive measures aimed at reducing menopausal disorders in women with unspecified benign uterine or ovarian tumors. Diagnostic criteria for early and late complications of natural and surgical menopause have been developed by studying the clinical course of the above conditions and the homeostasis system in the examined patients. Based on comprehensive clinical, lab and instrumental examination of women with unspecified benign uterine or ovarian tumors, the author provides a scientifically justified

/pdf/innovatsiini-zasobi-navchannia-na-tsikli-tematichnogo-4t6xucktiw.pdf

Інноваційні засоби навчання на циклі тематичного удосконалення по хірургії на кафедрі хірургії та трансплантології НМАПО імені П. Л. Шупика

Periodontal disease has been associated with an increased risk of cardiovascular events. The purpose of our study was to investigate whether a correlation between periodontitis and chronic heart failure exists, as well as the nature of the underlying cause. We enrolled 71 patients (mean age, 54 ± 13 yr; 56 men) who had stable chronic heart failure; all underwent complete cardiologic and dental evaluations. The periodontal screening index was used to quantify the degree of periodontal disease. We compared the findings to those in the general population with use of data from the 4th German Dental Health Survey. Gingivitis, moderate periodontitis, and severe periodontitis were present in 17 (24%), 17 (24%), and 37 (52%) patients, respectively. Severe periodontitis was more prevalent among chronic heart failure patients than in the general population. In contrast, moderate periodontitis was more prevalent in the general population (P <0.00001). The severity of periodontal disease was not associated with the c...

Periodontitis in Chronic Heart Failure.

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Periodontitis in Chronic Heart Failure.