Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases

Schenkein, Harvey A.; Loos, Bruno G.

doi:10.1902/jop.2013.134006

Cited by 174 publications

(139 citation statements)

References 152 publications

Supporting

Mentioning

120

Contrasting

Unclassified

Order By: Relevance

“…However, based on the crosssectional analysis, no firm conclusions in terms of causality and pathological pathways can be drawn for the relationship between periodontitis and atherosclerosis/CVD. 5 Besides periodontitis, also age, gender and MAP were significantly associated with PWV in the full-adjusted model. These results are in agreement with previous studies.…”

Section: Discussionmentioning

confidence: 91%

“…How periodontitis might contribute to ACVD is not clear. 5 Interestingly, periodontal treatment improves the atherosclerotic profile, suggesting that periodontitis negatively affects the process of atheroinflammation. 6 Recently, arterial stiffness (AS), measured with pulse-wave velocity (PWV), has been identified as a novel biomarker for atherosclerosis and ACVD.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Arterial stiffness in periodontitis patients and controls

et al. 2015

View full text Add to dashboard Cite

Increased arterial stiffness (AS) is an important indicator for atherosclerotic cardiovascular disease (ACVD). Epidemiologically, periodontitis and ACVD are associated. Therefore, we aimed to investigate AS in periodontitis patients and controls. In addition, we explored the effect of periodontal therapy on AS in a sub-group of cases. Pulse-wave velocity (PWV), a non-invasive chair-side function test for AS, was measured in periodontitis patients (n=57; mean age 46.6 years) and compared with a reference group (n=48; mean age 45.5 years). In addition, 45 cases (mean age 46.9 years) were 6 months followed after periodontal treatment, to explore a possible effect on arterial function. Periodontitis patients showed a significantly increased PWV compared with the reference group (8.01±0.20 vs. 7.36±0.22 m s(-1) respectively; P=0.029) and this remained significant after adjustments for ACVD risk factors (P=0.019). After periodontal therapy, no significant reduction in PWV was seen (8.00±1.8 to 7.82±1.6 m s(-1); P=0.13), but systolic blood pressure (SBP) was significantly reduced (119.8±14.6 to 116.9±15.1 mm Hg; P=0.040). It can be concluded that periodontitis is associated with increased AS. This confirms with a new parameter the association of periodontitis with ACVD. Although periodontal treatment did not lower AS significantly, a modest reduction of SBP after 6 months was observed.

show abstract

Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Arterial stiffness in periodontitis patients and controls

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Both diseases may share vascular risk factors, such as age, sex, diabetes mellitus, hypertension or hypercholesterolemia. However, pathogenic factors such as an increase in the proinflammatory state caused by a rise in systemic pro-inflammatory mediators, stimulation of innate and adaptive immune system, a pro-thrombotic state caused by an increase in thrombotic and haemostatic markers from systemic and liver production, and a rise in the biosynthesis of cholesterol in liver could also play a key role in these associations by increasing the potential for atherogenesis or exacerbating atherosclerotic lesions [19].…”

Section: Introductionmentioning

confidence: 99%

Association between periodontitis and ischemic stroke: a systematic review and meta-analysis

et al. 2016

View full text Add to dashboard Cite

Several observational studies have suggested an association between periodontitis and cerebral ischemia. This meta-analysis aimed to investigate whether this link exists, and if so, the degree to which it is significant. The Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) guideline for systematic review was used. The search strategy included using electronic databases and hand searching works published up to March 2015. MEDLINE via PubMed, EMBASE, Proceedings Web of Science and Current Contents Connect were searched by two independent reviewers. Case-control, cross-sectional or cohort studies including patients with measures of periodontitis and ischemic stroke were eligible to be included in the analysis. Quality assessments of selected studies were performed. From a total of 414 titles and abstracts, 57 potentially relevant full text papers were identified. After inclusion criteria were applied, 8 studies were included in the present systematic review (5 case-control and 3 cohort studies). Although it was not the intention, cross-sectional studies were excluded due to eligibility criteria were not accomplished. Therefore, meta-analyses were conducted with data retrieved from the 8 studies included. These meta-analyses showed statistically significant association between periodontitis and ischemic stroke in both cohort pooled relative risks at 2.52 (1.77-3.58), and case-control studies pooled relative risks at 3.04 (1.10-8.43). In conclusion, the present meta-analysis demonstrated an association between periodontitis and ischemic stroke. However, well-designed prospective studies should be carried out to provide robust evidence of the link between both diseases. In regards to ischemic stroke subtypes, further case-control studies should be carried out to investigate whether there is any association between the different subtypes of cerebral infarcts and periodontitis.

show abstract

“…Although a dysbiotic biofilm structure initiates the disease, the periodontal tissue destruction occurs as a result of a dysregulated immune response to the microbial insult (2). Chronic, persistent immune responses to this complex microbiome not only can lead to tooth loss but also are associated with increased risk for several systemic complications, including atherosclerosis, diabetes, adverse pregnancy outcomes, pulmonary diseases, rheumatoid arthritis, and cancer (3)(4)(5)(6)(7)(8). Periodontal research currently focuses primarily on identifying disease biomarkers, understanding mechanisms of pathogenesis, and identifying therapeutic targets to prevent the deleterious effects of periodontal inflammation on both local and systemic tissues.…”

mentioning

confidence: 99%

Toll-Like Receptor 9-Mediated Inflammation Triggers Alveolar Bone Loss in Experimental Murine Periodontitis

et al. 2015

View full text Add to dashboard Cite

Chronic periodontitis is a local inflammatory disease induced by a dysbiotic microbiota and leading to destruction of the toothsupporting structures. Microbial nucleic acids are abundantly present in the periodontium, derived through release after phagocytic uptake of microbes and/or from biofilm-associated extracellular DNA. Binding of microbial DNA to its cognate receptors, such as Toll-like receptor 9 (TLR9), can trigger inflammation. In this study, we utilized TLR9 knockout (TLR9 ؊/؊ ) mice and wild-type (WT) controls in a murine model of Porphyromonas gingivalis-induced periodontitis and report the first in vivo evidence that TLR9 signaling mediates the induction of periodontal bone loss. P. gingivalis-infected WT mice exhibited significantly increased bone loss compared to that in sham-infected WT mice or P. gingivalis-infected TLR9 ؊/؊ mice, which were resistant to bone loss. Consistent with this, the expression levels of interleukin 6 (IL-6), tumor necrosis factor (TNF), and receptoractivator of nuclear factor kappa B ligand (RANKL) were significantly elevated in the gingival tissues of the infected WT mice but not in infected TLR9؊/؊ mice compared to their levels in controls. Ex vivo studies using splenocytes and bone marrow-derived macrophages revealed significantly diminished cytokine production in TLR9؊/؊ cells relative to the cytokine production in WT cells in response to P. gingivalis, thereby implicating TLR9 in inflammatory responses to this organism. Intriguingly, compared to the cytokine production in WT cells, TLR9؊/؊ cells exhibited significantly decreased proinflammatory cytokine production upon challenge with lipopolysaccharide (LPS) (TLR4 agonist) or Pam3Cys (TLR2 agonist), suggesting possible cross talk between TLR9, TLR4, and TLR2. Collectively, our results provide the first proof-of-concept evidence implicating TLR9-triggered inflammation in periodontal disease pathogenesis, thereby identifying a new potential therapeutic target to control periodontal inflammation.

show abstract

Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases

Cited by 174 publications

References 152 publications

Arterial stiffness in periodontitis patients and controls

Arterial stiffness in periodontitis patients and controls

Association between periodontitis and ischemic stroke: a systematic review and meta-analysis

Toll-Like Receptor 9-Mediated Inflammation Triggers Alveolar Bone Loss in Experimental Murine Periodontitis

Contact Info

Product

Resources

About