Influence of experimental periodontitis on cardiac oxidative stress in rats: a biochemical and histomorphometric study

Köse, Oğuz; Arabacı, Taner; Yemenoğlu, Hatice; Özkanlar, Seçkin; Kurt, Nezahat; Gümüşsoy, İsmail; Gedikli, Semin; Kara, Adem

doi:10.1111/jre.12428

Cited by 13 publications

(27 citation statements)

References 48 publications

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“…They emphasized that increased oxidative stress in the presence of chronic periodontitis may cause endothelial dysfunction of the blood vasculature, predisposing to atherosclerotic plaque formation and increasing predisposition to ischemic heart disease [1]. Köse et al [52] examined the influences of periodontitis on levels of cardiac oxidative stress. Authors found that GSH-Px levels in the heart ventricular tissue of the rats with experimental periodontitis were higher than that of control group but statistically insignificant [52].…”

Section: Cardiovascular Diseasementioning

confidence: 99%

“…Köse et al [52] examined the influences of periodontitis on levels of cardiac oxidative stress. Authors found that GSH-Px levels in the heart ventricular tissue of the rats with experimental periodontitis were higher than that of control group but statistically insignificant [52]. They argued that this increase could be associated with adaptive response [52].…”

Section: Cardiovascular Diseasementioning

confidence: 99%

“…Authors found that GSH-Px levels in the heart ventricular tissue of the rats with experimental periodontitis were higher than that of control group but statistically insignificant [52]. They argued that this increase could be associated with adaptive response [52]. Moreover, they speculated that oxidative stress in the cardiac tissue may be the result of an increase in the amount of ROS rather than a decrease in antioxidant levels [52].…”

Section: Cardiovascular Diseasementioning

confidence: 99%

“…They argued that this increase could be associated with adaptive response [52]. Moreover, they speculated that oxidative stress in the cardiac tissue may be the result of an increase in the amount of ROS rather than a decrease in antioxidant levels [52].…”

Section: Cardiovascular Diseasementioning

confidence: 99%

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Periodontal Health and Disease in Glutathione Peroxidase

Dede¹

2020

Glutathione System and Oxidative Stress in Health and Disease

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Periodontal diseases are chronic, multifactorial inflammatory diseases that affect more than 10% of the world population. There are two general forms of periodontal diseases including gingivitis (reversible inflammation and confined with gingiva form) and periodontitis (irreversible, destruction form). Several studies have reported that periodontal disease was associated with a decreased antioxidant capacity and elevated oxidative damage within the oral cavity. Glutathione peroxidase (GSH-Px) is an important enzymatic antioxidant that protects periodontal tissues against oxidative stress. Hitherto, there is contradictory evidence concerning the relationship between the levels of GSH-Px and the periodontal status. Various studies have demonstrated that GSH-Px levels in different biological fluids increased, decreased, or are unaltered in individuals with periodontal disease. This discrepancy might be explained either by different determination protocols/assays applied among the studies or various dynamic processes of the periodontal disease progression. In this section, GSH-Px levels are summarized in the periodontal health and disease including the presence and absence of systemic disease, medication, wound healing, and smoking.

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Section: Cardiovascular Diseasementioning

confidence: 99%

Section: Cardiovascular Diseasementioning

confidence: 99%

Section: Cardiovascular Diseasementioning

confidence: 99%

Section: Cardiovascular Diseasementioning

confidence: 99%

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Periodontal Health and Disease in Glutathione Peroxidase

Dede¹

2020

Glutathione System and Oxidative Stress in Health and Disease

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“…18,19 Studies have proven MMPs, especially the MMP-9, to play a pivotal role in the pathogenesis of atherosclerosis, hypertension, myocardial infarction, and heart failure. 20 Experimental studies by our colleagues 3,21 and other researchers 12,22 showed that as a chronic low-level systemic inflammatory-oxidative disease, periodontitis causes significant inflammatory 3 and oxidative 12,21,22 changes in left ventricular tissue. Despite the well-known cardioprotective effect of melatonin, there is very limited information about its protective effects on periodontitis-related cardiac alterations.…”

Section: Introductionmentioning

confidence: 95%

Melatonin ameliorates periodontitis‐related inflammatory stress at cardiac left ventricular tissues in rats

Köse

Bayrakdar

Akyıldız

et al. 2020

Journal of Periodontology

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Background: The aim of this experimental rat study was to investigate the potential inflammatory effects of periodontitis on cardiac left ventricular tissue and the therapeutic activity of melatonin on these effects. Methods: Twenty-four male Sprague-Dawley rats were randomly divided into three groups: control, experimental periodontitis (Ep), and Ep-melatonin (Ep-Mel). Experimental periodontitis was induced by placing and maintaining 3.0 silk ligatures at a peri marginal position on the left and right mandibular first molars for 5 weeks. Afterward, following the removal of ligatures, melatonin (10 mg/body weight) to Ep-Mel group, and vehicle (saline) to Ep and control groups were administered intraperitoneally for 14 days. On the first day of the eighth week, mandibular and cardiac left ventricular tissue samples were obtained following the euthanasia of the rats in all groups. Alveolar bone loss measurements were made on histological and microcomputed tomographic slices. Cardiac tissue levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), matrix metalloproteinase-9 (MMP-9), and cardiac Troponin-T (cTnT) were evaluated by appropriate biochemical methods. Results: Measurements made on the histological and microcomputed tomographic slices showed that melatonin significantly limits the ligature-induced periodontal tissue destruction (P <0.01). In addition, melatonin was detected to cause a significant decrease of MDA, MMP-9, and cTnT levels which were found to be significantly higher on rats with Ep (P <0.05) while having no significant effect on antioxidant levels (GSH, SOD, and CAT) (P >0.05). Conclusion: Melatonin might be regarded as an important supportive therapeutic agent to reduce the early degenerative changes and possible hypertrophic remodeling at cardiac left ventricular tissues provoked by periodontitis-related bacteria and/or periodontal inflammation.

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Melatonin improves periodontitis‐induced kidney damage by decreasing inflammatory stress and apoptosis in rats

Köse

Bayrakdar²,

Unver

et al. 2020

Journal of Periodontology

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Background Two main aims of this animal study were to inspect the possible effects of periodontitis on the structure and functions of the kidneys and the therapeutic effectiveness of melatonin. Methods Twenty‐four male Sprague‐Dawley rats were randomly divided into three groups: control, experimental periodontitis (Ep), and Ep‐melatonin (Ep‐Mel). Periodontitis was induced by placing 3.0‐silk sutures sub‐paramarginally around the cervix of right‐left mandibular first molars and maintaining the sutures for 5 weeks. Then melatonin (10 mg/kg body weight/day, 14 days), and the vehicle was administered intraperitonally. Mandibular and kidney tissue samples were obtained following the euthanasia. Periodontal bone loss was measured via histological and microcomputed tomographic slices. On right kidney histopathological and immunohistochemical, and on the left kidney biochemical (malonyl‐aldehyde [MDA], glutathione, oxidative stress [OSI], tumor necrosis factor [TNF]‐α, interleukin [IL]‐1β, matrix metalloproteinase [MMP]‐8, MMP‐9, and cathepsin D levels) evaluations were performed. Renal functional status was analyzed by levels of serum creatinine, urea, cystatin‐C, and urea creatinine. Results Melatonin significantly restricted ligature‐induced periodontal bone loss (P <0 .01) and suppressed the levels of proinflammatory cytokines (TNF‐α and IL‐1β), oxidative stress (MDA and OSI), and proteases (MMP‐8, MMP‐9, and CtD) that was significantly higher in the kidneys of the rats with periodontitis (P <0.05). In addition, periodontitis‐related histological damages and apoptotic activity were also significantly lower in the Ep‐Mel group (P <0.05). However, the markers of renal function of the Ep group were detected slightly impaired in comparison with the control group (P >0.05); and the therapeutic activity of melatonin was limited (P >0.05). Conclusion Melatonin restricts the periodontitis‐induced inflammatory stress, apoptosis, and structural but not functional impairments.

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Influence of experimental periodontitis on cardiac oxidative stress in rats: a biochemical and histomorphometric study

Cited by 13 publications

References 48 publications

Periodontal Health and Disease in Glutathione Peroxidase

Periodontal Health and Disease in Glutathione Peroxidase

Melatonin ameliorates periodontitis‐related inflammatory stress at cardiac left ventricular tissues in rats

Melatonin improves periodontitis‐induced kidney damage by decreasing inflammatory stress and apoptosis in rats

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