scholarly journals Correlations of inflammatory cytokines, oxidative stress markers, and matrix metalloproteinases in gingival crevicular fluid with peri-implantitis

2019 ◽  
Vol 17 ◽  
pp. 205873921984554
Author(s):  
Zhiming Song ◽  
Paul Weigl ◽  
Bi Wang
Keyword(s):  
Oxidative Stress ◽  
Matrix Metalloproteinases ◽  
Inflammatory Cytokines ◽  
Gingival Crevicular Fluid ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Probing Depth ◽  
Tnf Α ◽  
Hs Crp ◽  
Crevicular Fluid

This study aimed to analyze the correlations of inflammatory cytokines, oxidative stress markers, and matrix metalloproteinases (MMPs) in gingival crevicular fluid (GCF) with peri-implantitis (PI). Forty patients receiving dental implantation were enrolled. There were 52 implants, which were divided into PI group (42 implants) and health implant (HI) group (10 implants). Fifty-two healthy teeth (HT) with the same names with affected teeth in the patients were selected as the control group. The periodontal status was recorded. The GCF was collected and quantified. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), hypersensitive C-reactive protein (hs-CRP), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), MMP-13, and MMP-8 were detected using enzyme-linked immunosorbent assay (ELISA). Results showed that the probing depth, sulcus bleeding index, GCF volume, and TNF-α, IL-6, hs-CRP, MMP-8, and MMP-13 levels in GCF in PI group were significantly higher than HI and HT groups, respectively ( P < 0.01 or P < 0.05). The SOD and GSH-Px levels in PI group were significantly lower than HI and HT groups, respectively ( P < 0.05). Excepting hs-CRP, there was no significant difference of each index between HI and HT groups ( P > 0.05). In conclusion, TNF-α, IL-6, hs-CRP, SOD, GSH-Px, MMP-8, and MMP-13 are involved in the occurrence of PI, and they may be used as auxiliary indicators to evaluate the degree of PI. In addition, the clinical periodontal index probing depth and sulcus bleeding index are positively correlated with GCF volume, hs-CRP, MMP-8, and MMP-13.

Gingival crevicular fluid and plasma oxidative stress markers and TGM-2 levels in chronic periodontitis

2017 ◽  
Vol 83 ◽  
pp. 47-54 ◽  
Author(s):  
Sema Becerik ◽  
Veli Özgen Öztürk ◽  
Peter Celec ◽  
Natalia Kamodyova ◽  
Gül Atilla ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Periodontitis ◽  
Gingival Crevicular Fluid ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Crevicular Fluid

scholarly journals Physiological Responses and Gene Expression in Ultrasound-Guided Supraclavicular Brachial Plexus Block: a Comparative Study

2018 ◽  
Vol 46 (6) ◽  
pp. 2412-2420 ◽  
Author(s):  
Hayam G Sayyed ◽  
Naglaa K. Idriss ◽  
Marwa A. Gaber ◽  
Sherif Sayed ◽  
Rasha Ahmed
Keyword(s):  
Oxidative Stress ◽  
Brachial Plexus Block ◽  
Mrna Levels ◽  
Oxidative Stress Markers ◽  
Ultrasound Guided ◽  
Stress Markers ◽  
Pain Scores ◽  
Tnf Α ◽  
Supraclavicular Brachial Plexus Block ◽  
Plexus Block

Background/Aims: Ultrasound-guided supraclavicular brachial plexus block (BPB) has come into wider use as a regional anesthetic during upper limb operations. This study assessed the neurological and hemodynamic changes and gene expression after co-administration of midazolam or neostigmine with bupivacaine during supraclavicular BPB. Methods: The study involved 90 adults divided into three groups: control (bupivacaine), midazolam (bupivacaine plus midazolam), and neostigmine (bupivacaine plus neostigmine). Blood samples were taken and interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) mRNA levels were measured by real-time PCR, and oxidative stress markers were identified. In addition to the hemodynamic variables, the onset and duration of sensory and motor blockades, duration of analgesia, pain scores, time of first request for an analgesic, and amounts of analgesics ingested were evaluated. Results: Compared with the control and neostigmine groups, the midazolam group experienced longer sensory and motor blockades, prolonged analgesia, lower pain scores at 12 h and 24 h, and lower need for postoperative analgesics. Moreover, the midazolam group exhibited lower oxidative stress markers with a higher fold change in IL-6 and TNF-α mRNA levels. Conclusion: Midazolam co-administered with bupivacaine provided better analgesic quality than did neostigmine with bupivacaine. This might be due to its superior antioxidant and anti-inflammatory effects.

scholarly journals Hyperoxalemia Leads to Oxidative Stress in Endothelial Cells and Mice with Chronic Kidney Disease

2021 ◽  
pp. 1-10
Author(s):  
Ke Sun ◽  
Xiaojing Tang ◽  
Shuwei Song ◽  
Yuan Gao ◽  
Hongjing Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vascular Calcification ◽  
Systemic Inflammation ◽  
Inflammatory Factors ◽  
Uremic Toxin ◽  
Inflammatory Factor ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Tnf Α

<b><i>Introduction:</i></b> Cardiovascular disease is the most common cause of morbidity and mortality in patients with ESRD. In addition to phosphate overload, oxalate, a common uremic toxin, is also involved in vascular calcification in patients with ESRD. The present study investigated the role and mechanism of hyperoxalemia in vascular calcification in mice with uremia. <b><i>Methods:</i></b> A uremic atherosclerosis (UA) model was established by left renal excision and right renal electrocoagulation in apoE<sup>−/−</sup> mice to investigate the relationship between oxalate loading and vascular calcification. After 12 weeks, serum and vascular levels of oxalate, vascular calcification, inflammatory factors (TNF-α and IL-6), oxidative stress markers (malondialdehyde [MDA], and advanced oxidation protein products [AOPP]) were assessed in UA mice. The oral oxalate-degrading microbe <i>Oxalobacter formigenes</i> (<i>O. formigenes</i>) was used to evaluate the effect of a reduction in oxalate levels on vascular calcification. The mechanism underlying the effect of oxalate loading on vascular calcification was assessed in cultured human aortic endothelial cells (HAECs) and human aortic smooth muscle cells (HASMCs). <b><i>Results:</i></b> Serum oxalate levels were significantly increased in UA mice. Compared to the control mice, UA mice developed more areas of aortic calcification and showed significant increases in aortic oxalate levels and serum levels of oxidative stress markers and inflammatory factors. The correlation analysis showed that serum oxalate levels were positively correlated with the vascular oxalate levels and serum MDA, AOPP, and TNF-α levels, and negatively correlated with superoxide dismutase activity. The <i>O. formigenes</i> intervention decreased serum and vascular oxalate levels, while did not improve vascular calcification significantly. In addition, systemic inflammation and oxidative stress were also improved in the <i>O. formigenes</i> group. In vitro, high concentrations of oxalate dose-dependently increased oxidative stress and inflammatory factor expression in HAECs, but not in HASMCs. <b><i>Conclusions:</i></b> Our results indicated that hyperoxalemia led to the systemic inflammation and the activation of oxidative stress. The reduction in oxalate levels by <i>O. formigenes</i> might be a promising treatment for the prevention of oxalate deposition in calcified areas of patients with ESRD.

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