2
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The role of the oral microbiome in smoking-related cardiovascular risk: a review of the literature exploring mechanisms and pathways

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Cardiovascular disease is a leading cause of morbidity and mortality. Oral health is associated with smoking and cardiovascular outcomes, but there are gaps in knowledge of many mechanisms connecting smoking to cardiovascular risk. Therefore, the aim of this review is to synthesize literature on smoking and the oral microbiome, and smoking and cardiovascular risk/disease, respectively. A secondary aim is to identify common associations between the oral microbiome and cardiovascular risk/disease to smoking, respectively, to identify potential shared oral microbiome-associated mechanisms. We identified several oral bacteria across varying studies that were associated with smoking. Atopobium, Gemella, Megasphaera, Mycoplasma, Porphyromonas, Prevotella, Rothia, Treponema, and Veillonella were increased, while Bergeyella, Haemophilus, Lautropia, and Neisseria were decreased in the oral microbiome of smokers versus non-smokers. Several bacteria that were increased in the oral microbiome of smokers were also positively associated with cardiovascular outcomes including Porphyromonas, Prevotella, Treponema, and Veillonella. We review possible mechanisms that may link the oral microbiome to smoking and cardiovascular risk including inflammation, modulation of amino acids and lipids, and nitric oxide modulation. Our hope is this review will inform future research targeting the microbiome and smoking-related cardiovascular disease so possible microbial targets for cardiovascular risk reduction can be identified.

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s12967-022-03785-x.

          Related collections

          Most cited references126

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Global, Regional, and National Burden of Cardiovascular Diseases for 10 Causes, 1990 to 2015

          Background The burden of cardiovascular diseases (CVDs) remains unclear in many regions of the world. Objectives The GBD (Global Burden of Disease) 2015 study integrated data on disease incidence, prevalence, and mortality to produce consistent, up-to-date estimates for cardiovascular burden. Methods CVD mortality was estimated from vital registration and verbal autopsy data. CVD prevalence was estimated using modeling software and data from health surveys, prospective cohorts, health system administrative data, and registries. Years lived with disability (YLD) were estimated by multiplying prevalence by disability weights. Years of life lost (YLL) were estimated by multiplying age-specific CVD deaths by a reference life expectancy. A sociodemographic index (SDI) was created for each location based on income per capita, educational attainment, and fertility. Results In 2015, there were an estimated 422.7 million cases of CVD (95% uncertainty interval: 415.53 to 427.87 million cases) and 17.92 million CVD deaths (95% uncertainty interval: 17.59 to 18.28 million CVD deaths). Declines in the age-standardized CVD death rate occurred between 1990 and 2015 in all high-income and some middle-income countries. Ischemic heart disease was the leading cause of CVD health lost globally, as well as in each world region, followed by stroke. As SDI increased beyond 0.25, the highest CVD mortality shifted from women to men. CVD mortality decreased sharply for both sexes in countries with an SDI >0.75. Conclusions CVDs remain a major cause of health loss for all regions of the world. Sociodemographic change over the past 25 years has been associated with dramatic declines in CVD in regions with very high SDI, but only a gradual decrease or no change in most regions. Future updates of the GBD study can be used to guide policymakers who are focused on reducing the overall burden of noncommunicable disease and achieving specific global health targets for CVD.
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            The Human Intestinal Microbiome in Health and Disease.

              Bookmark
              • Record: found
              • Abstract: found
              • Article: found
              Is Open Access

              Role of C-Reactive Protein at Sites of Inflammation and Infection

              C-reactive protein (CRP) is an acute inflammatory protein that increases up to 1,000-fold at sites of infection or inflammation. CRP is produced as a homopentameric protein, termed native CRP (nCRP), which can irreversibly dissociate at sites of inflammation and infection into five separate monomers, termed monomeric CRP (mCRP). CRP is synthesized primarily in liver hepatocytes but also by smooth muscle cells, macrophages, endothelial cells, lymphocytes, and adipocytes. Evidence suggests that estrogen in the form of hormone replacement therapy influences CRP levels in the elderly. Having been traditionally utilized as a marker of infection and cardiovascular events, there is now growing evidence that CRP plays important roles in inflammatory processes and host responses to infection including the complement pathway, apoptosis, phagocytosis, nitric oxide (NO) release, and the production of cytokines, particularly interleukin-6 and tumor necrosis factor-α. Unlike more recent publications, the findings of early work on CRP can seem somewhat unclear and at times conflicting since it was often not specified which particular CRP isoform was measured or utilized in experiments and whether responses attributed to nCRP were in fact possibly due to dissociation into mCRP or lipopolysaccharide contamination. In addition, since antibodies for mCRP are not commercially available, few laboratories are able to conduct studies investigating the mCRP isoform. Despite these issues and the fact that most CRP research to date has focused on vascular disorders, there is mounting evidence that CRP isoforms have distinct biological properties, with nCRP often exhibiting more anti-inflammatory activities compared to mCRP. The nCRP isoform activates the classical complement pathway, induces phagocytosis, and promotes apoptosis. On the other hand, mCRP promotes the chemotaxis and recruitment of circulating leukocytes to areas of inflammation and can delay apoptosis. The nCRP and mCRP isoforms work in opposing directions to inhibit and induce NO production, respectively. In terms of pro-inflammatory cytokine production, mCRP increases interleukin-8 and monocyte chemoattractant protein-1 production, whereas nCRP has no detectable effect on their levels. Further studies are needed to expand on these emerging findings and to fully characterize the differential roles that each CRP isoform plays at sites of local inflammation and infection.
                Bookmark

                Author and article information

                Contributors
                Katherine.Maki@nih.gov
                Sukirth-Ganesan@uiowa.edu
                Bkmeeks@gmail.com
                Nicole.Farmer@nih.gov
                Narjis.Kazmi@nih.gov
                BarbJ@mail.nih.gov
                Paule.Joseph@nih.gov
                Gwallen@cc.nih.gov
                Journal
                J Transl Med
                J Transl Med
                Journal of Translational Medicine
                BioMed Central (London )
                1479-5876
                12 December 2022
                12 December 2022
                2022
                : 20
                : 584
                Affiliations
                [1 ]GRID grid.410305.3, ISNI 0000 0001 2194 5650, Translational Biobehavioral and Health Disparities Branch, , National Institutes of Health, Clinical Center, ; 10 Center Drive, Building 10, Bethesda, MD 20814 USA
                [2 ]GRID grid.214572.7, ISNI 0000 0004 1936 8294, Department of Periodontics, , The University of Iowa College of Dentistry and Dental Clinics, ; 801 Newton Rd., Iowa City, IA 52242 USA
                [3 ]GRID grid.411024.2, ISNI 0000 0001 2175 4264, University of Maryland, School of Social Work, ; Baltimore, MD USA
                [4 ]GRID grid.420085.b, ISNI 0000 0004 0481 4802, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, ; Bethesda, MD USA
                [5 ]GRID grid.280738.6, ISNI 0000 0001 0035 9863, National Institute of Nursing Research, National Institutes of Health, ; Bethesda, MD USA
                Author information
                http://orcid.org/0000-0003-4578-960X
                http://orcid.org/0000-0001-7134-1636
                Article
                3785
                10.1186/s12967-022-03785-x
                9743777
                36503487
                1d21d508-6593-432a-82ec-a4e9b3b91de1
                © This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply 2022

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                : 11 October 2022
                : 21 November 2022
                Funding
                Funded by: National Institutes of Health, Clinical Center
                Award ID: intramural research funds
                Funded by: FundRef http://dx.doi.org/10.13039/100000027, National Institute on Alcohol Abuse and Alcoholism;
                Award ID: intramural research funds
                Award Recipient :
                Funded by: National Institutes of Health (NIH)
                Categories
                Review
                Custom metadata
                © The Author(s) 2022

                Medicine
                oral microbiome,microbiota,oral health,genetics,smoking,cardiovascular risk,cardiovascular disease

                Comments

                Comment on this article