Receptor activator of nuclear factor kappa B (RANK) as a determinant of peri-implantitis

Rakić, Mia; Nikolić-Jakoba, Nataša; Struillou, Xavier; Petković-Ćurčin, Aleksandra; Stamatovic, Novak; Matic, Smiljka; Janković, Saša; Aleksić, Zoran; Vasilic, Djurdja; Lekovic, Vojislav; Vojvodić, Danilo

doi:10.2298/vsp1304346r

Cited by 13 publications

(14 citation statements)

References 22 publications

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“…Additionally, one study showed that the TLR4 signaling pathway mediated the proinflammatory immune response to cobalt-alloy particles [35]. The level of the receptor activator of NF-κB was apparently increased in samples from patients with peri-implantitis compared with healthy implants [36]. The endotoxin LPS, a molecule found in the outer membrane of bacteria, can trigger stimulation of macrophages and microglial cells by activating various signal transduction pathways including NF-κB [37].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of NF-κB by Pyrrolidine Dithiocarbamate Prevents the Inflammatory Response in a Ligature-Induced Peri-Implantitis Model: A Canine Study

Jiang²,

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: The roles of toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) in peri-implantitis are unclear. Here, we used a canine model of peri-implantitis to explore the effects of inhibiting NF-κB with pyrrolidine dithiocarbamate (PDTC) on the inflammatory response in ligature-induced peri-implantitis. Methods: After successfully establishing the peri-implantitis model, beagles were randomly assigned to normal, model or PDTC groups. ELISA tests were used to determine the levels of interleukin (IL)-1, IL-6, IL-8 and tumor necrosis factor alpha (TNF-α). Immunohistochemistry was employed to assess the expression of NF-κB p65. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to determine the mRNA levels of TLR4 and NF-κB p65, and western blot analysis was used to measure the protein levels of TLR4 in periodontal tissues from each group. Periodontal ligament fibroblasts (PDLFs) were cultured and subsequently classified into PDLF normal, PDLF model, PDLF LPS, PDLF PDTC, and PDLF LPS + PDTC groups. An immunofluorescence assay was used to measure the expression level of NF-κB p65. The CCK-8 assay and flow cytometry were performed to evaluate cell proliferation and apoptosis. Results: The in vitro results indicated that NF-κB p65 and TLR4 were upregulated in canine periodontal tissues, and PDTC could suppress the expression levels of NF-κB p65 and TLR4. Inflammation could increase TLR4 protein expression in canine periodontal tissue, and PDTC could inhibit the inflammation-induced increase in TLR4 protein expression. These results revealed that PDTC could reverse the LPS-induced increases in the levels of IL-1, IL-6, IL-8 and TNF-α. In vivo, the results demonstrated that PDTC inhibited the LPS-induced NF-κB p65 upregulation, and PDTC could reverse the inhibitory effect of the PDLF model + LPS on the proliferation of periodontal fibroblasts. The results also showed that in the PDLF model, LPS promoted PDLF apoptosis by inducing implant periodontitis in canines, but PDTC inhibited the PDLF apoptosis and relieved implant periodontitis in canines. Conclusion: Based on our results, we concluded that PDTC can inhibit the expression of NF-κB and alleviate the inflammatory response induced by LPS, thereby preventing periodontal inflammation and reducing the development of peri-implantitis.

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Section: Discussionmentioning

confidence: 99%

Inhibition of NF-κB by Pyrrolidine Dithiocarbamate Prevents the Inflammatory Response in a Ligature-Induced Peri-Implantitis Model: A Canine Study

Jiang²,

Wang

et al. 2018

Cell Physiol Biochem

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“…The important structural differences and the different local factors related to peri‐implant tissues may also render differences in the reliability of these biomarkers when used in the diagnosis of peri‐implant diseases 3,23,46 . Recent studies showed that higher levels of sRANKL, RANK, and OPG were associated with peri‐implantitis compared with healthy peri‐implant tissues, although the pattern of these biomarkers was also different when peri‐implantitis and periodontitis sites were compared 19,20 . Monov et al 13 reported no significant correlation between the measured sRANKL and OPG levels and clinical parameters, whereas Arikan et al 15 investigating the same biomarkers reported a significant correlation between OPG and BOP.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies evaluating bone loss (BL) biomarkers comparing patients with peri-implantitis and chronic periodontitis demonstrated a good level of recovery and significant correlations between measured markers and corresponding clinical parameters. 19,20 In these studies, an optimized working protocol was reported that demonstrated 100% detectability rate, and significant correlations with clinical parameters were reached for almost all parameters. After optimization of the working protocol, the next step in promoting biomolecule as biomarker is usually a cross-sectional study to profile the marker concentration under different tissue conditions.…”

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confidence: 98%

“…This lack of consistency in the results reported in the literature complicates the interpretation of the diagnostic value of these biomarkers. Recent studies evaluating bone loss (BL) biomarkers comparing patients with peri‐implantitis and chronic periodontitis demonstrated a good level of recovery and significant correlations between measured markers and corresponding clinical parameters 19,20 . In these studies, an optimized working protocol was reported that demonstrated 100% detectability rate, and significant correlations with clinical parameters were reached for almost all parameters.…”

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confidence: 99%

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Estimation of Bone Loss Biomarkers as a Diagnostic Tool for Peri‐Implantitis

Rakić

Struillou

Petković-Ćurčin

et al. 2014

Journal of Periodontology

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“…A prior study indicated that the NF-B concentration increased 1.5–4-fold in patients with peri-implantitis compared to those with mucositis (6). Moreover, recent studies demonstrated that high levels of NF-B were associated with peri-implantitis (40,41). In addition, NF-B is upregulated in inflammatory bowel disease and is a transcription regulator of the immune response (42).…”

Section: Discussionmentioning

confidence: 99%

Identification of key genes and pathways for peri-implantitis through the analysis of gene expression data

Zhang

Huang

et al. 2017

Experimental and Therapeutic Medicine

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The present study attempted to identify potential key genes and pathways of peri-implantitis, and to investigate the possible mechanisms associated with it. An array data of GSE57631 was downloaded, including six samples of peri-implantitis tissue and two samples of normal tissue from the Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) in the peri-implantitis samples compared with normal ones were analyzed with the limma package. Moreover, Gene Ontology annotation and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses for DEGs were performed by DAVID. A protein-protein interaction (PPI) network was established using Cytoscape software, and significant modules were analyzed using Molecular Complex Detection. A total of 819 DEGs (759 upregulated and 60 downregulated) were identified in the peri-implantitis samples compared with normal ones. Moreover, the PPI network was constructed with 413 nodes and 1,114 protein pairs. Heat shock protein HSP90AA1 (90 kDa α, member 1), a hub node with higher node degrees in module 4, was significantly enriched in antigen processing, in the presentation pathway and nucleotide-binding oligomerization domain (NOD)-like receptor-signaling pathway. In addition, nuclear factor-κ-B1 (NFKB1) was enriched in the NOD-like receptor-signaling pathway in KEGG pathway enrichment analysis for upregulated genes. The proteasome is the most significant pathway in module 1 with the highest P-value. Therefore, the results of the present study suggested that HSP90AA1 and NFKB1 may be potential key genes, and the NOD-like receptor signaling pathway and proteasome may be potential pathways associated with peri-implantitis development.

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Receptor activator of nuclear factor kappa B (RANK) as a determinant of peri-implantitis

Cited by 13 publications

References 22 publications

Inhibition of NF-κB by Pyrrolidine Dithiocarbamate Prevents the Inflammatory Response in a Ligature-Induced Peri-Implantitis Model: A Canine Study

Inhibition of NF-κB by Pyrrolidine Dithiocarbamate Prevents the Inflammatory Response in a Ligature-Induced Peri-Implantitis Model: A Canine Study

Estimation of Bone Loss Biomarkers as a Diagnostic Tool for Peri‐Implantitis

Identification of key genes and pathways for peri-implantitis through the analysis of gene expression data

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