Periodontitis increases vascular cyclooxygenase‐2: potential effect on vascular tone

Mendes, Reila Tainá; Olchanheski, Luiz Ricardo; Machado, Willian Moreira; Stanczyk, C. P.; Assreuy, Jamil; Santos, Fábio André dos; Fernandes, Daniel

doi:10.1111/jre.12083

Cited by 9 publications

(13 citation statements)

References 36 publications

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“…We have previously shown that COX-2-derived prostanoids have an important role in periodontal disease, as treatment of rats with etoricoxib, a specific COX-2 inhibitor, results in decreased alveolar bone loss secondary to ligature-induced periodontitis (Holzhausen, Spolidorio, Muscará, Hebling, & Spolidorio, 2005). Using the same model, although placing four ligatures instead of one, Brito et al (2013) have shown that on the 28th day after the induction of periodontitis, thee is a transient systemic and vascular inflammation that leads to impaired endothelium-dependent vasodilatation, and that on the 21st day, increased COX-2 expression ocurs in mesenteric vessels, which endothelial function is worsened by treatment with etoricoxib (Mendes et al, 2014). In this way, the present study not only confirms previous observations but also strengthens the important relationship that exists between PD and endothelial dysfunction, as differently from the long-lasting, more aggressive and generalized periodontal inflammation studied by the above mentioned authors, in our model, data were collected just 7 days after placement of a single ligature.…”

Section: Discussionmentioning

confidence: 99%

“…Prostaglandins, thromboxanes and prostacyclin from both type-1 and -2 cyclooxygenase (COX) isoforms are the major vasoactive eicosanoids (Katusi c & Shepherd, 1991), and the balance between platelet-derived thromboxane A 2 and endothelial prostacyclin is an important factor for the maintenance of vascular homeostasis (Sellers & Stallone, 2008). Previous studies have shown an increased COX-2 expression in mesenteric vessels and a transient systemic and vascular inflammation in animals with a 28 days of bilateral mandibular and maxillary ligatureinduced periodontitis (Brito et al, 2013;Mendes et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Endothelial dysfunction in rats with ligature-induced periodontitis: Participation of nitric oxide and cycloxygenase-2-derived products

Campi

Herrera

Jesus

et al. 2016

Archives of Oral Biology

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Endothelial dysfunction in rats with ligature-induced periodontitis: Participation of nitric oxide and cycloxygenase-2-derived products

Campi

Herrera

Jesus

et al. 2016

Archives of Oral Biology

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“…Indeed, the levels of MMP-9 in gingival crevicular fluid have been used to diagnose the progression of periodontitis (Sorsa et al 2006). COX-2 is also known to contribute to the development of periodontitis as it is a key mediator maintaining vascular homeostasis (Mendes et al 2014). SHI has been previously reported to down-regulate IL-1 and TNF-a expression in the joints of arthritic mice Figure 4.…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effects of shikonin in human periodontal ligament cells

Fan

Zhang

Upton

2018

Pharmaceutical Biology

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Context: Shikonin (SHI), an active component extracted from Radix Arnebiae, has been reported to possess anti-inflammatory properties in various cells. However, its effect on lipopolysaccharide (LPS)-stimulated human periodontal ligament cells (hPDLCs) is unknown. Objective: To investigate the effects of SHI on the expression of inflammatory related cytokines in LPSstimulated hPDLCs. Materials and methods: The effects of SHI (0.125, 0.25, 0.5, 1, and 2 lg/mL) on hPDLCs proliferation for 1, 3 and 7 days were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression of interleukin-1 (IL-1), IL-6, tumor necrosis factor-a (TNF-a), matrix metalloproteinase-2 (MMP-2), MMP-9 and cyclooxygenase-2 (COX-2) were detected in hPDLCs following SHI treatment (0.25 and 0.5 lg/mL) using Quantitative Reverse Transcriptase Polymerase Chain Reaction (qRT-PCR). The signaling pathways triggered by SHI in hPDLC were evaluated using western blotting. Results: LD50 of SHI is 1.7 lg/mL (day 1) and 1.1 lg/mL (day 3 and 7) in hPDLCs. No morphological changes were observed when hPDLCs were treated with LPS only (1 lg/mL) or LPS with SHI (0.25 and 0.5 lg/mL). Data from qRT-PCR suggests that SHI attenuates LPS-induced increases of IL-1, IL-6, TNF-a, MMP-2, MMP-9 and COX-2 in hPDLCs. Down-regulation of phosphorylated extracellular signal-regulated kinase (ERK) and nuclear factor-jB (NF-jB), and up-regulation of I-jB, were observed in LPS-stimulated hPDLCs after exposed to SHI at 0.25 or 0.5 lg/mL. Discussion and conclusions: SHI possesses anti-inflammatory effects in LPS-stimulated hPDLCs via phospho-ERK and NF-jB/I-jB signaling pathways; this suggests that SHI may hold potential as an anti-inflammatory agent against periodontitis.

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“… 2 However, despite lasting systemic and vascular inflammation, impairment in the acetylcholine response is restored 21 days onwards after the procedure. 2 , 24 Since endothelium-dependent relaxation is the main mechanism for assessing endothelial dysfunction, 5 the compensatory effect could mask a lack of NO and an increased risk of cardiovascular disease.…”

Section: Introductionmentioning

confidence: 99%

The role of potassium channels in the endothelial dysfunction induced by periodontitis

et al. 2018

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Objective:Periodontitis is associated with endothelial dysfunction, which is clinically characterized by a reduction in endothelium-dependent relaxation. However, we have previously shown that impairment in endothelium-dependent relaxation is transient. Therefore, we evaluated which mediators are involved in endothelium-dependent relaxation recovery.Material and methods:Rats were subjected to ligature-induced experimental periodontitis. Twenty-one days after the procedure, the animals were prepared for blood pressure recording, and the responses to acetylcholine or sodium nitroprusside were obtained before and 30 minutes after injection of a nitric oxide synthase inhibitor (L-NAME), cyclooxygenase inhibitor (Indomethacin, SC-550 and NS- 398), or calcium-dependent potassium channel blockers (apamin plus TRAM- 34). The maxilla and mandible were removed for bone loss analysis. Blood and gingivae were obtained for C-reactive protein (CRP) and myeloperoxidase (MPO) measurement, respectively.Results:Experimental periodontitis induces bone loss and an increase in the gingival MPO and plasmatic CRP. Periodontitis also reduced endothelium-dependent vasodilation, a hallmark of endothelial dysfunction, 14 days after the procedure. However, the response was restored at day 21. We found that endothelium-dependent vasodilation at day 21 in ligature animals was mediated, at least in part, by the activation of endothelial calcium-activated potassium channels.Conclusions:Periodontitis induces impairment in endothelial-dependent relaxation; this impairment recovers, even in the presence of periodontitis. The recovery is mediated by the activation of endothelial calcium-activated potassium channels in ligature animals. Although important for maintenance of vascular homeostasis, this effect could mask the lack of NO, which has other beneficial properties.

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Periodontitis increases vascular cyclooxygenase‐2: potential effect on vascular tone

Cited by 9 publications

References 36 publications

Endothelial dysfunction in rats with ligature-induced periodontitis: Participation of nitric oxide and cycloxygenase-2-derived products

Endothelial dysfunction in rats with ligature-induced periodontitis: Participation of nitric oxide and cycloxygenase-2-derived products

Anti-inflammatory effects of shikonin in human periodontal ligament cells

The role of potassium channels in the endothelial dysfunction induced by periodontitis

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