The treatment of periodontitis has numerous positive effects on established chronic health conditions, including cardiovascular disease and diabetes. However, ethical considerations do limit the establishment of human trials to investigate whether periodontitis promotes the early stages of chronic conditions. Therefore, the aim of this study was to investigate whether periodontitis induces endothelial dysfunction in hyperlipidemic apolipoprotein E gene-deficient (ApoE-/-) mice. Forty-five 8-week-old ApoE-/- mice were challenged by oral lavage with Porphyromonas gingivalis and Streptococcus gordonii for 4 weeks. A subgroup of animals (n = 15–17/group) was placed in a metabolic chamber immediately before euthanasia at 4 weeks to measure VO2/CO2 concentrations and voluntary locomotion. In infected and control animals alveolar bone levels were measured by x-ray imaging and endothelial function was determined by measuring endothelial-dependent vasorelaxation of aortic rings. The mRNA expression levels of serum amyloid A and tumor necrosis factor were determined in liver tissues by qRT PCR and protein concentrations in serum by ELISA. Caecal contents were analysed by sequencing to determine changes to the gut microbiota to investigate linkages between microbiome and systemic changes. The results showed that oral lavage of P. gingivalis and S. gordonii for 4 weeks, initiated periodontitis in ApoE-/- mice, similar to the human situation. The oral inflammation was accompanied by a significant increase in mRNA expression of pro-inflammatory mediators serum amyloid A1 and tumor necrosis factor in the liver. Mice with periodontitis also exhibited impaired endothelial-dependent vasorelaxation responses to acetylcholine. This systemic response was connected to increased energy expenditure, locomotion and respiratory quotient. No differences were detected in caecal microbiota between the infected and control animals. Overall, this is the first report that provide evidence that periodontitis induces endothelial dysfunction in mice. Other systemic responses observed in response to the local reaction need further investigation. The study suggests that early prevention of periodontitis may help limit the early stages of endothelial dysfunction that is linked to atherogenesis in humans.
Context Consumption of dietary macronutrients is associated with the progression of a wide range of inflammatory diseases, either by direct modulation of host immune response or via microbiome. This includes periodontitis, a disease affecting tooth-supporting tissues. Objective The aim of this work was to systematically review studies focusing on the effect of macronutrient (ie, carbohydrate, protein, fat) intake on periodontitis in rodents. Data Sources Electronic searches were performed in February 2021 using the PubMed and Web of Science databases. Out of 883 articles reviewed, 23 studies were selected for additional analysis. Data Extraction Investigators extracted relevant data, including author names; the year of publication; article title; macronutrient composition; number and species of animals and their age at the start of the experiment; intervention period; method of periodontitis induction; and primary and secondary periodontitis outcomes. Quality assessment was done using the risk-of-bias tool for animal studies. After completing the data extraction, descriptive statistical information was obtained. Data Analysis High intakes of dietary cholesterol, saturated fatty acids, and processed carbohydrates such as sucrose, and protein-deficient diets were positively associated with periodontitis in rodents. This included greater amounts of alveolar bone loss, more lesions on periodontal tissues, and dental plaque accumulation. In contrast, high doses of milk basic protein in diets and diets with a high ratio of ω-3 to ω-6 fatty acids were negatively associated with periodontitis in rodents. Conclusion This work highlights the fact that, despite the large body of evidence linking macronutrients with inflammation and ageing, overall there is little information on how dietary nutrients affect periodontitis in animal models. In addition, there is inconsistency in data due to differences in methodology, outcome measurement, and dietary formulation. More studies are needed to examine the effects of different dietary macronutrients on periodontitis and investigate the underlying biological mechanisms.
Background: Cardiovascular diseases (CVDs) encompass various conditions affecting the heart and its blood vessels. Some CVDs, such as ischemic heart disease, angina, stroke, and atherosclerosis, are often linked with oral microbes. The link between the oral cavity and CVDs is complex. Certain pathogenic oral microbes invade the systemic circulation via bacteraemia or other methods and can significantly increase pro-inflammatory cytokine production. Studies have linked oral microbes, systemic inflammation and immune cross-reactivity in the pathogenesis of atherogenesis. Our secondary data analysis aimed to identify oral bacteria from other non-oral sites (i.e. gut, arterial plaque and cultured blood) that could be linked with CVDs. Methods: Taxonomic profiling of the entire data set was performed using Kaiju software; bacteria were identified to the species level and compared with the Human Oral Microbiome Database (HOMD). The oral bacteria in the gut, cultured blood and arterial plaque samples were catalogued, with their average frequency calculated for each sample. Additionally, data were filtered by comparison with the Human Microbiome Project (HMP) database. Results: We identified 17,243 microbial species, of which 410 were present in the HOMD database and further denominated as “oral”. When considering identifications at the species level, all 410 different oral bacterial species were found in at least one gut sample, but only 221 and 169 species were identified in the cultured blood and plaque samples, respectively. Of the 410 species, 153 were present solely in oral-associated environments after comparison with the HMP database, irrespective of their presence in other body sites. The oral bacterial phyla Actinobacteria, Bacteroidetes, Firmicutes, Fusobacterium, Proteobacteria, Spirochetes, Synergistetes and Tenericutes were identified in all three sample types (faeces, arterial plaque and cultured blood) of patients with CVDs. Streptococcus salivarius species was identified as the highest-represented species in the faeces samples. Cutibacterium acnes and Lactobacillus crispatus were found at the highest frequency in cultured blood and plaque samples, respectively. Conclusion: Oral bacteria related to gingival and periodontal disease can be identified in the faeces, arterial plaque and blood samples of patients with CVDs. Identifying these oral bacterial species in nonoral sites of patients with CVDs would explore the link between oral health and general health, including diseases of the cardiovascular system via bacterial translocation.
Background: Cardiovascular diseases (CVDs) encompass various conditions affecting the heart and its blood vessels. Some CVDs, such as ischemic heart disease, angina, stroke, and atherosclerosis, are often linked with oral microbes. The link between the oral cavity and CVDs is complex. Certain pathogenic oral microbes invade the systemic circulation via bacteraemia or other methods and can significantly increase pro-inflammatory cytokine production. Studies have linked oral microbes, systemic inflammation and immune cross-reactivity in the pathogenesis of atherogenesis. Our secondary data analysis aimed to identify oral bacteria from other non-oral sites (i.e. gut, arterial plaque and cultured blood) that could be linked with CVDs. Methods: Taxonomic profiling of the entire data set was performed using Kaiju software; bacteria were identified to the species level and compared with the Human Oral Microbiome Database (HOMD). The oral bacteria in the gut, cultured blood and arterial plaque samples were catalogued, with their average frequency calculated for each sample. Additionally, data were filtered by comparison with the Human Microbiome Project (HMP) database. Results: We identified 17,243 microbial species, of which 410 were present in the HOMD database and further denominated as “oral”. When considering identifications at the species level, all 410 different oral bacterial species were found in at least one gut sample, but only 221 and 169 species were identified in the cultured blood and plaque samples, respectively. Of the 410 species, 153 were present solely in oral-associated environments after comparison with the HMP database, irrespective of their presence in other body sites. The oral bacterial phyla Actinobacteria, Bacteroidetes, Firmicutes, Fusobacterium, Proteobacteria, Spirochetes, Synergistetes and Tenericutes were identified in all three sample types (faeces, arterial plaque and cultured blood) of patients with CVDs. Streptococcus salivarius species was identified as the highest-represented species in the faeces samples. Cutibacterium acnes and Lactobacillus crispatus were found at the highest frequency in cultured blood and plaque samples, respectively. Conclusion: Oral bacteria related to gingival and periodontal disease can be identified in the faeces, arterial plaque and blood samples of patients with CVDs. Identifying these oral bacterial species in nonoral sites of patients with CVDs would explore the link between oral health and general health, including diseases of the cardiovascular system via bacterial translocation.
Background: Gum disease (periodontitis) is a risk factor for diabetes mellitus and treatment has been shown to improve markers of glucose management. The translocation of oral bacteria to the gut or other tissues (i.e., foot ulcer) may contribute to the development and progression of diabetes mellitus Aims: This secondary analysis of metagenomic and meta-transcriptomic studies within the last ten years (2011-2021) aims to identify bacteria of oral origin in the gut and foot ulcers of patients with diabetes mellitus and explore a potential pathway how gum disease and diabetes mellitus are connected.Method: An electronic search was conducted in Medline on the Ovid platform (updated in June 2022). Studies with whole-metagenomic or meta-transcriptomic data at the species level in populations of all ages and genders with type 1 or type 2 diabetes and diabetic complications such as diabetic foot ulcers were included. Patient demographics, diabetic status and bacteria detected in faecal or foot ulcer samples were extracted from a total of 7 included studies.Results: Out of 9612 (gut) and 9180 (foot ulcer) microbial species identified from the selected studies, 266 bacteria were identified as oral origin. These oral bacteria compromised 5.96% in foot ulcer and 1.51% in the gut. Eleven bacteria of oral origin were only found in patients with diabetes mellitus compared to healthy individuals of the Human Microbiome Project (HMP). These bacteria included key oral pathogens such as Tannerella forsythia, Prevotella nigrescens and Prevotella intermedia. Conclusion: The continuous swallowing of oral bacteria may be a reservoir for gut microbiota and its dysregulation, which has been linked to diabetes. Clinical trials aimed at simultaneously detecting and analysing gut and oral bacteria are required.
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