2009
DOI: 10.1016/s1349-0079(09)80018-2
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Profiling of Differentially Expressed Genes in Peri-implantitis and Periodontitis in vivo by Microarray Analysis

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Cited by 5 publications
(3 citation statements)
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“…Importantly, the leading-edge analyses revealed important differentially activated genes that are involved in multiple inflammations and immune responses related to biological processes or molecular pathways, including IL-1β, CDK3, IL-27 and CD86 in the FI vs. NI comparison, in addition to CXCL6, CXCL1, CCL7, CCL13 and IL18 in the SI vs. NI comparison. Previous transcriptomics studies profiling the differentially expressed genes in peri-implantitis have pointed out that the significantly altered pathways were related to extracellular matrix molecules [26], matrix-degrading enzymes [27] and inflammatory pathways including the RANKL/OPG pathway and the cyclooxygenase2 pathway [28].…”
Section: Discussionmentioning
confidence: 99%
“…Importantly, the leading-edge analyses revealed important differentially activated genes that are involved in multiple inflammations and immune responses related to biological processes or molecular pathways, including IL-1β, CDK3, IL-27 and CD86 in the FI vs. NI comparison, in addition to CXCL6, CXCL1, CCL7, CCL13 and IL18 in the SI vs. NI comparison. Previous transcriptomics studies profiling the differentially expressed genes in peri-implantitis have pointed out that the significantly altered pathways were related to extracellular matrix molecules [26], matrix-degrading enzymes [27] and inflammatory pathways including the RANKL/OPG pathway and the cyclooxygenase2 pathway [28].…”
Section: Discussionmentioning
confidence: 99%
“…Because bacteria and i-TiPs require similar membrane internalization events, it is not possible to disaggregate differences due to endocytosis and intracellular processing of i-TiPs in peri-implant disease. One study comparing transcriptome expression patterns between peri-implantitis and periodontitis showed that certain genes involved in actin regulation, endosomal processing, and antigen presentation are expressed differently between the groups, furthering the idea that upregulation of these processes may be unique to peri-implantitis (Roediger et al 2009). These findings are crucial because some compounds (CK-666, CK-869) have been shown to inhibit Arp2/3 actin nucleation activity in vitro and thus potentially function to reduce inflammation and other pathology instigated by i-TiPs in peri-implantitis (Hetrick et al 2013).…”
Section: Discussionmentioning
confidence: 99%
“…We identified gene expression differences between groups that pinpoint molecules and processes that may be responsible for the inflammation and bone degradation related to the endosomal-lysosomal pathway. Existing transcriptomics studies have pointed to altered gene expression pathways related to extracellular matrix molecules (Roediger et al 2009), matrixdegrading enzymes (Roediger et al 2009;Cho et al 2020), and inflammatory pathways such as the cyclooxygenase 2 pathway (Liu et al 2020) and the RANKL/OPG pathway (Becker et al 2014;Liu et al 2020). Importantly, when Becker et al ( 2014) compared genome-wide transcriptome profiles of 7 patients with peri-implantitis versus 7 with periodontitis, they observed drastic The top of the chart signifies relatedness of individual samples, with bottom groups showing the highest degree of similarity and top groups showing less similarity.…”
Section: Discussionmentioning
confidence: 99%