Aggregatibacter actinomycetemcomitans Infection Enhances Apoptosis
            <i>In Vivo</i>
            through a Caspase-3-Dependent Mechanism in Experimental Periodontitis

Kang, Jun; Bezerra, Beatriz de Brito; Pacios, Sandra; Andriankaja, Oelisoa M.; Yu, Li; Tsiagbe, V. K.; Schreiner, Helen; Fine, Daniel H.; Graves, Dana T.

doi:10.1128/iai.06371-11

Cited by 56 publications

(57 citation statements)

References 43 publications

(53 reference statements)

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“…Moreover, normal Wistar rats exhibited no alveolar bone loss induced by oral A. actinomycetemcomitans infection (46). In short, bone loss does not occur or develops slowly in wild-type rodents infected with human periodontal pathogens.…”

Section: Discussionmentioning

confidence: 90%

Inflammatory Bone Loss in Experimental Periodontitis Induced by Aggregatibacter actinomycetemcomitans in Interleukin-1 Receptor Antagonist Knockout Mice

et al. 2014

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cThe interleukin-1 receptor antagonist (IL-1Ra) binds to IL-1 receptors and inhibits IL-1 activity. However, it is not clear whether IL-1Ra plays a protective role in periodontal disease. This study was undertaken to compare experimental periodontitis induced by Aggregatibacter actinomycetemcomitans in IL-1Ra knockout (KO) mice and wild-type (WT) mice. Computed tomography (CT) analysis and hematoxylin-and-eosin (H&E) and tartrate-resistant acid phosphatase (TRAP) staining were performed. In addition, osteoblasts were isolated; the mRNA expression of relevant genes was assessed by real-time quantitative PCR (qPCR); and calcification was detected by Alizarin Red staining. Infected IL-1Ra KO mice exhibited elevated (P, <0.05) levels of antibody against A. actinomycetemcomitans, bone loss in furcation areas, and alveolar fenestrations. Moreover, protein for tumor necrosis factor alpha (TNF-␣) and IL-6, mRNA for macrophage colony-stimulating factor (M-CSF), and receptor activator of NF-B ligand (RANKL) in IL-1Ra KO mouse osteoblasts stimulated with A. actinomycetemcomitans were increased (P, <0.05) compared to in WT mice. Alkaline phosphatase (ALP), bone sialoprotein (BSP), osteocalcin (OCN)/bone gla protein (BGP), and runt-related gene 2 (Runx2) mRNA levels were decreased (P, <0.05). IL-1␣ mRNA expression was increased, and calcification was not observed, in IL-1 Ra KO mouse osteoblasts. In brief, IL-1Ra deficiency promoted the expression of inflammatory cytokines beyond IL-1 and altered the expression of genes involved in bone resorption in A. actinomycetemcomitans-infected osteoblasts. Alterations consistent with rapid bone loss in infected IL-Ra KO mice were also observed for genes expressed in bone formation and calcification. In short, these data suggest that IL-1Ra may serve as a potential therapeutic drug for periodontal disease.

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Section: Discussionmentioning

confidence: 90%

Inflammatory Bone Loss in Experimental Periodontitis Induced by Aggregatibacter actinomycetemcomitans in Interleukin-1 Receptor Antagonist Knockout Mice

et al. 2014

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“…This explains the greater alveolar bone loss in diabetic NOD mice compared with prediabetic and non-diabetic NOD mice [41]. It has been reported that A. actinomycetemcomitans infection accelerates alveolar bone loss in diabetic GK rats by increased rates of cell apoptosis in gingival epithelial and connective tissues [42,43].…”

Section: Discussionmentioning

confidence: 86%

Diabetic Lactoferrin Deficient Mice Demonstrates Greater Susceptibility to Experimental Periodontal Disease

et al. 2015

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The objective of this study is to determine whether alloxaninduced diabetic Lactoferrin knockout (LFKO -/-) mice are more susceptible to periodontal disease caused by Aggregatibacter actinomycetemcomitans compared to the diabetic wild-type (WT) mice. Diabetes was induced in mice by a single dose of alloxan (60 mg/kg) injected intravenously. Mice were categorized as diabetic when blood glucose levels >250 mg/dL were measured on the 7 th day after the injection. Periodontal disease was experimentally induced by A. actinomycetemcomitans infection in alloxan induced diabetic WT and LFKO -/-mice. Fasting blood glucose levels and body weight were monitored throughout the study. At the end of the 12 th week of infection, mice were sacrificed and bone loss among the groups was estimated by measuring the distance between cemento-enamel junction (CEJ) to the alveolar bone crest (ABC) at 12 sites on the molars. A. actinomycetemcomitans infected mice groups developed more alveolar bone loss than sham-infected animals. Diabetic LFKO

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“…For example, the concentration of caspase 3 in gingival crevicular fluid and serum has been seen to proportionally increase with the progression of periodontal disease (Abuhussein et al, 2014;Pradeep et al, 2014). Moreover, Aggregatibacter actinomycetemcomitans infection enhances apoptosis of osteoblastic cells, reducing osseous coupling through a caspase 3-dependent mechanism (Kang et al, 2012;Pacios et al, 2013). Caspase 3 is also involved in the Porphyromonas gingivalis-derived lipopolysaccharide-mediated activation of the MAPK signaling pathway in human periodontal ligament fibroblasts (Seo et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

“…Many previous studies have elucidated the relationship between caspases and periodontitis. For instance, Aggregatibacter actinomycetemcomitans infection enhances apoptosis through a caspase 3-dependent mechanism (Kang et al, 2012). Furthermore, caspase 3 expression increases with progression of gingival inflammation, probing depth, and clinical attachment level in periodontitis (Pradeep et al, 2014), and tissue destruction by Porphyromonas gingivalis involves both caspase 1-dependent and -independent mechanisms (Taxman et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Assessment of CASP gene polymorphisms in periodontal disease

Sw¹,

Kim²,

Chung³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Caspases (CASP) are intracellular proteases that play roles as mediators of apoptosis. Activation of caspase 3 is enhanced in chronic periodontitis. Thus, we hypothesized that single nucleotide polymorphisms (SNPs) of CASP genes might be associated with this condition in the Korean population. To investigate whether such polymorphisms might be involved in the development of periodontal disease, 51 patients and 33 control subjects were assessed. A total of 201 CASP gene SNPs were analyzed with genotypes being determined using and Axiom™ genomewide human assay. SNPStats and SPSS 18.0 were used for the analysis of genetic data and logistic regression models were utilized to evaluate odds ratios, 95% confidence intervals, and P values. Of the 201 SNPs, only three (rs12108497, rs4647602, and rs113420705, all in the CASP3 gene) were significantly associated with chronic periodontitis (P < 0.05). The minor allele frequencies of these SNPs were higher in the patient group than in the control group. In addition, the TC and GT haplotypes 18070 S.W. Kang et al. ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 18069-18077 (2015) formed by rs4647602 and rs113420705 were found to be associated with chronic this disease (TC haplotype, P = 0.0039; GT haplotype, P = 0.002). These results suggest that CASP3 gene polymorphisms may be associated with susceptibility to periodontal disease in the Korean population.

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Aggregatibacter actinomycetemcomitans Infection Enhances Apoptosis In Vivo through a Caspase-3-Dependent Mechanism in Experimental Periodontitis

Abstract: ABSTRACTThe purpose of this study was to test the hypothesis that diabetes aggravates periodontal destruction induced byAggregatibacter actinomycetemcomitansinfection. Thirty-eight diabetic and 33 normal rats were inoculated withA. actin… Show more

Cited by 56 publications

References 43 publications

Inflammatory Bone Loss in Experimental Periodontitis Induced by Aggregatibacter actinomycetemcomitans in Interleukin-1 Receptor Antagonist Knockout Mice

Inflammatory Bone Loss in Experimental Periodontitis Induced by Aggregatibacter actinomycetemcomitans in Interleukin-1 Receptor Antagonist Knockout Mice

Diabetic Lactoferrin Deficient Mice Demonstrates Greater Susceptibility to Experimental Periodontal Disease

Assessment of CASP gene polymorphisms in periodontal disease

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