Experimental periodontitis promotes transient vascular inflammation and endothelial dysfunction
Autor: | Silvia DalBó, Tatiane Michelle Striechen, Lorena C.W. Brito, Giovani Marino Favero, Daniel Fernandes, Reila Tainá Mendes, Luiz Ricardo Olchanheski, Jamil Assreuy, José Carlos Rebuglio Vellosa, Fábio André dos Santos, Regina Sordi, Jéssica M. Farias |
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Rok vydání: | 2013 |
Předmět: |
Male
Nitroprusside Pathology medicine.medical_specialty medicine.medical_treatment Alveolar Bone Loss Inflammation Vasodilation Phenylephrine Superoxides medicine Animals Endothelial dysfunction Endothelium Rats Wistar Ligature Periodontitis General Dentistry Analysis of Variance medicine.diagnostic_test biology business.industry Interleukin-6 Dentistry(all) Superoxide Nitric oxide General Medicine Cell Biology medicine.disease Acetylcholine Mesenteric Arteries Rats Nitric oxide synthase Cholesterol C-Reactive Protein Microscopy Fluorescence Otorhinolaryngology biology.protein Sodium nitroprusside medicine.symptom Nitric Oxide Synthase Lipid profile business Biomarkers medicine.drug |
Zdroj: | Archives of Oral Biology. 58(9):1187-1198 |
ISSN: | 0003-9969 |
DOI: | 10.1016/j.archoralbio.2013.03.009 |
Popis: | Objectives This study aimed to evaluate the systemic inflammatory response and cardiovascular changes induced by experimental periodontitis in rats. Design Experimental periodontitis was induced by placing a cotton ligature around the cervix of both sides of mandibular first molars and maxillary second molars in each male rat. Sham-operated rats had the ligature removed immediately after the procedure. Seven, 14 or 28 days after procedure, the effects of acetylcholine, sodium nitroprusside and phenylephrine were evaluated on blood pressure, aortic rings and isolated and perfused mesenteric bed. The blood was obtained for plasma Interleukin-6 (IL-6), C-reactive protein (CRP) and lipid evaluation. The mesenteric vessels were obtained to evaluate superoxide production and nitric oxide synthase 3 (NOS-3) expression. Results Ligature induced periodontitis reduced endothelium-dependent vasodilatation, a hallmark of endothelial dysfunction. This effect was associated with an increase in systemic inflammatory markers (IL-6 and CRP), worsens on lipid profile, increased vascular superoxide production and reduced NOS-3 expression. It is interesting to note that many of these effects were transitory. Conclusion Periodontitis induced a transient systemic and vascular inflammation which leads to endothelial dysfunction, an initial step for cardiovascular diseases. Moreover, the animal model of periodontitis used here may represent a valuable tool for studying the relationship between periodontitis and endothelial dysfunction. |
Databáze: | OpenAIRE |
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