Periodontal status, vascular reactivity, and platelet aggregation changes in rats submitted to hypercholesterolemic diet and periodontitis

Abstract

Background and objectives: Periodontitis can corroborate with development and progression of atherosclerosis and a possible bidirectional interaction between both pathologies has been hypothesized. The aim of this work was to study the interactions between diet-induced hypercholesterolemia and ligature-induced periodontitis in Wistar rats submitted to both conditions. Material and methods: Animals were divided into four experimental groups: C (control: standard diet without periodontitis), Perio (periodontitis plus standard diet), HC (high cholesterol diet without periodontitis), and HC + Perio (high cholesterol diet plus periodontitis). The diets were offered for 45 days and a silk ligature was applied in the lower first molars of Perio and HC-Perio animals on day 34 and maintained for 11 days until euthanasia. The mandibles were excised, and alveolar bone loss was determined by macroscopic and micro-tomographic (µ-CT) imaging. Blood samples were obtained, and platelet aggregation was induced in plasma rich in platelets by adenosine diphosphate (ADP) and collagen. Endothelium-dependent vascular reactivity and protein expression of endothelial (eNOS), phosphorylated endothelial (peNOS), and inducible (iNOS) nitric oxide synthases were evaluated in aorta samples. Results:The HC diet combined with periodontitis (HC + Perio group) was associated with an increased alveolar bone loss, when compared to the other groups. Both in Perio and HC groups, platelet aggregation induced by ADP or collagen was increased, while maximum aortic relaxation induced by acetylcholine was decreased.Periodontitis or HC diet alone decreased the expression of peNOS and HC diet increased the expression of iNOS. In contrast, no additive or synergistic effects were found in vascular reactivity or in platelet aggregation when the two conditions were associated (HC + Perio group). Conclusion:Hypercholesterolemia accelerated the process of bone loss induced by periodontitis while a high cholesterol diet or periodontitis individually increased

Effects of ω-3 PUFA-Rich Oil Supplementation on Cardiovascular Morphology and Aortic Vascular Reactivity of Adult Male Rats Submitted to an Hypercholesterolemic Diet

“…Besides, it is well known that diet-induced hypercholesterolemia can result in vascular damage, especially in the endothelium, leading to impaired vascular relaxant responses and an increased response to vasoconstrictor agonists such as phenylephrine (PEN) [ 50 , 51 , 52 ]. Regarding the contractile response to FEN, vasoconstriction was potentiated in CH56 but not in CN56, showing that the consumption of hypercholesterolemic food for 16 weeks was effective in inducing functional damage to the endothelium.…”

Osteoporosis and Alveolar Bone Health in Periodontitis Niche: A Predisposing Factors-Centered Review

“…This hyperlipidemia rat model demonstrates that a high-cholesterol diet induces spontaneous alveolar bone destruction but exhibits no addictive effect on periodontitis-induced bone loss [ 186 ]. On the opposite, some other studies found that obesity/hyperlipidemia induced by high fat and hypercaloric diet act as potentiating factors for ligature-induced periodontal destruction in rats [ 187 ]. Variations of diet composition, induction methods of periodontitis and timespan of experiment probably contribute to the inconsistency between results of animal studies.…”

Pharmacological effect of indolicidin-like peptides on vasoactive substances content in experimental periodontitis

“…The pathogenesis of endothelium injury in the inflammation is complicated. The direct damaging effect of periodontal microbes on the vascular endothelium is mainly developed due to their adhesion and invasion into endothelial cells [13]. Endothelial damage leads to intra-vascular changes: platelet aggregation and the activation of coagulation [13].…”

“…The direct damaging effect of periodontal microbes on the vascular endothelium is mainly developed due to their adhesion and invasion into endothelial cells [13]. Endothelial damage leads to intra-vascular changes: platelet aggregation and the activation of coagulation [13]. It has been also established that ET-1 was involved in the regulation of proinflammatory interleukins, especially interleukin-1b expression in gingival tissues [11].…”

“…Recently it was declared that periodontitis is characterized by a significant decrease in capillary perfusion in the periodontium [8]. A critical decrease in microcirculation and vasomotor activity of blood vessels in patients with periodontitis is followed by disturbances in the microcirculation adaptation to local metabolic needs [8,13].…”