Abstract
The present study examined the hemodynamics [arterial pressure (AP), AP variability (APV), heart rate (HR), and heart rate variability (HRV)], cardiac function (echocardiographycally), and myocardial inflammation in Balb/c mice submitted to Periodontitis, through the ligation of the left first molar, or Sham surgical procedure. The first protocol indicated that the AP was similar (136 ± 2 vs. 132 ± 3 mmHg in Sham), while the HR was higher in mice with Periodontitis (475 ± 20 vs. 412 ± 18 bpm in Sham), compared to their Sham counterparts. The APV was higher in mice with Periodontitis when evaluated in the time domain (4.5 ± 0.3 vs. 3.4 ± 0.2 mmHg in Sham), frequency domain (power of the LF band of systolic AP), or through symbolic analysis (patterns 0V + 1V), indicating a sympathetic overactivity. The HRV was similar in the mice with Periodontitis, as compared to their Sham counterparts. In the second protocol, the mice with Periodontitis showed decreased cardiac output (10 ± 0.8 vs. 15 ± 1.4 mL/min in Sham) and ejection fraction (37 ± 3 vs. 47 ± 2% in Sham) associated with increased myocardial cytokines (Interleukin-17, Interleukin-6, and Interleukin-4). This study shows that experimental Periodontitis caused cardiac dysfunction, increased heart cytokines, and sympathetic overactivity, in line with epidemiological studies indicating an increased risk of cardiovascular events in clinical Periodontitis.
Highlights
Periodontitis is caused by a chronic inflammatory response to a periodontal biofilm that deranges the supporting tissues around the teeth, causing dental loss[1]
The evaluation of the hemodynamics (HR and APV), cardiac function, and concentrations of myocardial cytokines revealed the impact of periodontitis in the cardiovascular system in this experimental model of periodontitis
Several pieces of evidence have shown an association between arterial pressure variability and cardiovascular diseases, independently of the basal arterial pressure levels[33,34,35]
Summary
Periodontitis is caused by a chronic inflammatory response to a periodontal biofilm that deranges the supporting tissues around the teeth (alveolar bone, periodontal ligament, and cementum), causing dental loss[1]. This inflammatory disease represents a major public health problem, with an estimated prevalence of over 790 million people worldwide[2,3]. Biofilms can release biologically active products, including bacterial lipopolysaccharides, chemotactic mediators, protein toxins, and organic acids These active products elicit different components of innate and adaptive immunity[6] followed by the production of inflammatory mediators, mainly cytokines produced by immune cells[7].
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