Gene expression signatures in chronic and aggressive periodontitis: a pilot study

Papapanou, Panos N.; Abron, Armin; Verbitsky, Miguel; Picolos, Doros; Yang, Jun; Qin, Jie; Fine, James Burke; Pavlidis, Paul

doi:10.1111/j.1600-0722.2004.00124.x

Cited by 30 publications

(30 citation statements)

References 28 publications

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“…In contrast, culture-based identification methods require viable cells (22). The application of methods targeting gene expression (23) in oral samples might better target VBNC E. faecalis. Despite the greater overall sensitivity of PCR, there were two culturepositive samples from one patient (#26) that did not show a corresponding PCR product ( Table 1).…”

Section: Discussionmentioning

confidence: 93%

Prevalence of Enterococcus faecalis at Multiple Oral Sites in Endodontic Patients Using Culture and PCR

Sedgley¹,

Buck²,

Appelbe³

2006

Journal of Endodontics

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Section: Discussionmentioning

confidence: 93%

Prevalence of Enterococcus faecalis at Multiple Oral Sites in Endodontic Patients Using Culture and PCR

Sedgley¹,

Buck²,

Appelbe³

2006

Journal of Endodontics

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“…Many studies have used microarray to investigate differences in the transcriptome of periodontal tissue cells (gingival biopsies) or circulating neutrophils from CP patients [17], [18], [20]. However, the present study is the first to focus on transcriptome changes in neutrophils as they migrate from circulation into the periodontal tissues.…”

Section: Discussionmentioning

confidence: 96%

“…This approach has been used to identify target genes associated with type I diabetes [14], arthritis [15] and lupus [16]. In addition, a number of studies have attempted to identify inflammatory markers associated with periodontal diseases [17]–[21]. However, a specific marker for active periodontitis has yet to be identified [22], [23].…”

Section: Introductionmentioning

confidence: 99%

Oral Neutrophil Transcriptome Changes Result in a Pro-Survival Phenotype in Periodontal Diseases

2013

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BackgroundPeriodontal diseases are inflammatory processes that occur following the influx of neutrophils into the periodontal tissues in response to the subgingival bacterial biofilm. Current literature suggests that while neutrophils are protective and prevent bacterial infections, they also appear to contribute to damage of the periodontal tissues. In the present study we compare the gene expression profile changes in neutrophils as they migrate from the circulation into the oral tissues in patients with chronic periodontits and matched healthy subjects. We hypothesized that oral neutrophils in periodontal disease patients will display a disease specific transcriptome that differs from the oral neutrophil of healthy subjects.MethodsVenous blood and oral rinse samples were obtained from healthy subjects and chronic periodontitis patients for neutrophil isolation. mRNA was isolated from the neutrophils, and gene expression microarray analysis was completed. Results were confirmed for specific genes of interest by qRT-PCR and Western Blot analysis.Results and DiscussionChronic periodontitis patients presented with increased recruitment of neutrophils to the oral cavity. Gene expression analysis revealed differences in the expression levels of genes from several biological pathways. Using hierarchical clustering analysis, we found that the apoptosis network was significantly altered in patients with chronic inflammation in the oral cavity, with up-regulation of pro-survival members of the Bcl-2 family and down-regulation of pro-apoptosis members in the same compartment. Additional functional analysis confirmed that the percentages of viable neutrophils are significantly increased in the oral cavity of chronic periodontitis patients.ConclusionsOral neutrophils from patients with periodontal disease displayed an altered transcriptome following migration into the oral tissues. This resulted in a pro-survival neutrophil phenotype in chronic periodontitis patients when compared with healthy subjects, resulting in a longer-lived neutrophil. This is likely to impact the severity and length of the inflammatory response in this oral disease.

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“…The effect of TNFα on global gene expression profiles has previously been investigated in synovial fibroblasts, preosteoblasts and HeLa cells, but not in gingival cells [52-56]. With regard to periodontal disease, microarray analysis of gingival tissue has been used in an attempt to define subclasses of periodontitis and to evaluate the effect of periodontal therapy [57,58]. In addition, blood cell gene expression profiling has been performed in subjects with aggressive periodontitis [59].…”

Section: Discussionmentioning

confidence: 99%

Signal pathways JNK and NF-κB, identified by global gene expression profiling, are involved in regulation of TNFα-induced mPGES-1 and COX-2 expression in gingival fibroblasts

et al. 2010

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BackgroundProstaglandin E2 (PGE2) is involved in several chronic inflammatory diseases including periodontitis, which causes loss of the gingival tissue and alveolar bone supporting the teeth. We have previously shown that tumor necrosis factor α (TNFα) induces PGE2 synthesis in gingival fibroblasts. In this study we aimed to investigate the global gene expression profile of TNFα-stimulated primary human gingival fibroblasts, focusing on signal pathways related to the PGE2-synthesizing enzymes prostaglandin E synthases (PGES), as well as the upstream enzyme cyclooxygenase-2 (COX-2) and PGE2 production.ResultsMicroarray and western blot analyses showed that the mRNA and protein expression of the inflammatory induced microsomal prostaglandin E synthase-1 (mPGES-1) was up-regulated by the cytokine TNFα, accompanied by enhanced expression of COX-2 and increased production of PGE2. In contrast, the expression of the isoenzymes microsomal prostaglandin E synthase-2 (mPGES-2) and cytosolic prostaglandin E synthase (cPGES) was unaffected by TNFα treatment. Using oligonucleotide microarray analysis in a time-course factorial design including time points 1, 3 and 6 h, differentially expressed genes in response to TNFα treatment were identified. Enrichment analysis of microarray data indicated two positively regulated signal transduction pathways: c-Jun N-terminal kinase (JNK) and Nuclear Factor-κB (NF-κB). To evaluate their involvement in the regulation of mPGES-1 and COX-2 expression, we used specific inhibitors as well as phosphorylation analysis. Phosphorylation analysis of JNK (T183/Y185) and NF-κB p65 (S536) showed increased phosphorylation in response to TNFα treatment, which was decreased by specific inhibitors of JNK (SP600125) and NF-κB (Bay 11-7082, Ro 106-9920). Inhibitors of JNK and NF-κB also decreased the TNFα-stimulated up-regulation of mPGES-1 and COX-2 as well as PGE2 production.ConclusionIn the global gene expression profile, the enrichment analysis of microarray data identified the two signal transduction pathways JNK and NF-κB as positively regulated by the cytokine TNFα. Inhibition of these TNFα-activated signal pathways reduced the expression of mPGES-1 and COX-2 as well as their end product PGE2 in gingival fibroblasts. The involvement of the signal pathways JNK and NF-κB in the regulation of PGE2 induced by TNFα may suggest these two pathways as possible attractive targets in the chronic inflammatory disease periodontitis.

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Gene expression signatures in chronic and aggressive periodontitis: a pilot study

Cited by 30 publications

References 28 publications

Prevalence of Enterococcus faecalis at Multiple Oral Sites in Endodontic Patients Using Culture and PCR

Prevalence of Enterococcus faecalis at Multiple Oral Sites in Endodontic Patients Using Culture and PCR

Oral Neutrophil Transcriptome Changes Result in a Pro-Survival Phenotype in Periodontal Diseases

Signal pathways JNK and NF-κB, identified by global gene expression profiling, are involved in regulation of TNFα-induced mPGES-1 and COX-2 expression in gingival fibroblasts

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