Expression of Interleukin-1β and Matrix Metalloproteinase-8 in Cytolytic and Noncytolytic Enterococcus faecalis–induced Persistent Apical Periodontitis: A Comparative Study in the Rat

Lu, Bingling; Zhang, Jinxiu; Huang, Xiaojing; Xiao, Suli; Zhang, Ming; Cai, Zhiyu

doi:10.1016/j.joen.2015.04.019

Cited by 10 publications

(7 citation statements)

References 35 publications

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“…This study validated the effects of CAP by different bacterial infections on periapical tissues of different teeth. By establishing different types of Ef-CAP models, a previous study (Lu et al 2015) confirmed that E. faecalis of several haemolytic types also exhibits differences in the destruction of periapical tissues. Thus, considering the crucial role of the type and composition of bacteria in CAP, standards for how to induce CAP should be harmonized, which is an important baseline for the study of the destructive nature of CAP on periapical tissues.…”

Section: Discussionmentioning

confidence: 76%

Micro‐CT analysis of chronic apical periodontitis induced by several specific pathogens

et al. 2019

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Aim To conduct three‐dimensional micro‐CT analysis of bone destruction, periapical sclerotic changes and inflammatory root resorption (IRR) to compare the differences between Enterococcus faecalis (Ef)‐ and Porphyromonas gingivalis (Pg)‐induced chronic apical periodontitis (CAP). Methodology Mono‐species bacteria‐induced CAP was established in the first and second molars of the right maxilla and mandible of male Sprague–Dawley rats. Fifteen animals were divided into three groups with five rats in each group: control group, Ef‐CAP group and Pg‐CAP group. The maxilla and mandible were harvested and then scanned by micro‐CT. Alveolar bone destruction was evaluated by measuring the volume of alveolar bone resorption, bone volume fraction (BV/TV), trabecular thickness (Tb. Th), trabecular number (Tb. N) and trabecular spacing (Tb. Sp). The results were analysed using one‐way analysis of variance and Fisher's least significant difference methods (LSD). The sclerotic changes in the periapical bone were graded and the IRR indexes were scored. The data were analysed using the chi‐square test. Results The alveolar bone resorption volume of the Pg‐CAP group was significantly larger than that of the Ef‐CAP group (P < 0.01). In the maxilla, both Pg‐CAP and Ef‐CAP groups had a significant decrease in BV/TV and increase in Tb. Sp (P < 0.01) with the more significant changes of trabecular bone in the Pg‐CAP group. A significant reduction of Tb. N was only found in the Pg‐CAP group (P < 0.05). There was no significant change in Tb. Th in either group (P > 0.05). In the mandible, except for an increase in Tb. Sp in the Pg‐CAP group (P < 0.05), there was no significant change in BV/TV, Tb. Th or Tb. N (P > 0.05). No obvious sclerotic change was observed. IRR was detected in significantly more root surfaces in the Pg‐CAP group (240 surfaces, 60%) than those in the Ef‐CAP group (178 surfaces, 44.5%) (P < 0.001). The IRR extension was also significantly more advanced in the Pg‐CAP group (P < 0.05). Conclusions Pg‐CAP caused more substantial alveolar bone destruction and IRR than Ef‐CAP. The maxilla was more susceptible to CAP in terms of microstructural changes of trabecular bone than the mandible. Tb. Sp was the most sensitive index for evaluating the residual alveolar bone of CAP.

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Section: Discussionmentioning

confidence: 76%

Micro‐CT analysis of chronic apical periodontitis induced by several specific pathogens

et al. 2019

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“…A study by Wu Qing et al (Wu, Zhou, Huang, Ji, & Kang, 2017) showed that IL-6 enhanced osteocyte-mediated osteoclastogenesis, and the JAK2 inhibitor AG490 inhibited RANKL expression in osteocyte-like cells pretreated with IL-6/IL-6R. Enterococcus faecalis LTA can induce the expression of IL-6, IL-1β, TNF-α, and other inflammatory factors (Baik et al, 2008;Lu et al, 2015;Park, Han, et al, 2013) and can inhibit the proliferation and induce apoptosis of human osteoblast-like MG63 cells (Tian et al, 2013). Staphylococcus aureus LTA promoted NO activation by JAK2 (Han et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

JAK2‐STAT3 signaling pathway is involved in rat periapical lesions induced by Enterococcus faecalis

Wang

Jin

et al. 2019

Oral Diseases

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Objectives This study aimed to investigate the role of JAK2‐STAT3 (Janus kinase 2/signal transducer and activator of transcription 3) in periapical disease caused by Enterococcus faecalis, as well as the correlation between lipoteichoic acid (LTA) in E. faecalis and the activity of the JAK2‐STAT3 signaling pathway and osteoclast formation. Materials and Methods A rat model of periapical periodontitis induced by E. faecalis was established. Periapical bone resorption was confirmed by HE staining. The expression of JAK2, p‐JAK2, STAT3, and p‐STAT3 was assessed with immunohistochemical staining. Osteoclasts were observed through enzyme histochemical staining. LTA acted on mouse osteoclast precursor cells (RAW264.7 cells); a JAK2 inhibitor (AG490) was used to inhibit the JAK2‐STAT3 pathway in RAW264.7 cells. The expression of proteins in the JAK2‐STAT3 pathway and TRAP (tartrate resistant acid phosphatase) in RAW264.7 cells was also detected. Results Rat periapical periodontitis was successfully established and bone resorption peaked at day 21. The expression of critical components in the JAK2‐STAT3 pathway increased with the progression of inflammation. LTA promoted the differentiation of RAW264.7 cells into osteoclasts. NFATc1 was highly expressed and was inhibited by AG490. Conclusions JAK2‐STAT3 signaling pathway plays an important role in the process of periapical bone resorption and osteoclastogenesis.

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“…At present, little research has been done on the animal study of persistent AP. In 2015, Lu et al successfully established persistent AP models of rats with E. faecalis to mimic the clinical situation, which was accomplished by a two-step infection procedure [ 14 ]. However, because of the narrow pulp chamber and tiny root canal in the teeth of rats, it is subject to greater endodontic treatment failure by missing the root canal, teeth fracture or incomplete disinfection, making it a less-than-ideal model for the evaluation of dental materials in persistent AP.…”

Section: Introductionmentioning

confidence: 99%

Effect of Antibacterial Root Canal Sealer on Persistent Apical Periodontitis

et al. 2021

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The infection of Enterococcus faecalis and its interacting microorganisms in the root canal could cause persistent apical periodontitis (AP). Antibacterial root canal sealer has favorable prospects to inhibit biofilms. The purpose of this study was to investigated the antibacterial effect of root canal sealer containing dimethylaminododecyl methacrylate (DMADDM) on persistent AP in beagle dogs for the first time. Persistent AP was established by a two-step infection with Enterococcus faecalis and multi-bacteria (Enterococcus faecalis, Lactobacillus acidophilus, Actinomycesnaeslundii, Streptococcus gordonii). Root canal sealer containing DMADDM (0%, 1.25%, 2.5%) was used to complete root canal filling. The volume of lesions and inflammatory grade in the apical area were evaluated by cone beam computer tomography (CBCT) and hematoxylin-eosin staining. Both Enterococcus-faecalis- and multi-bacteria-induced persistent AP caused severe apical destruction, and there were no significant differences in pathogenicity between them. DMADDM-modified sealer significantly reduced the volume of periapical lesion and inflammatory grade compared with the control group, among them, the therapeutic effect of the 2.5% group was better than the 1.25% group. In addition, E.faecalis-induced reinfection was more sensitive to the 2.5% group than multi-bacteria reinfection. This study shows that root canal sealer containing DMADDM had a remarkable therapeutic effect on persistent AP, especially on E. faecalis-induced reinfection.

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Expression of Interleukin-1β and Matrix Metalloproteinase-8 in Cytolytic and Noncytolytic Enterococcus faecalis–induced Persistent Apical Periodontitis: A Comparative Study in the Rat

Cited by 10 publications

References 35 publications

Micro‐CT analysis of chronic apical periodontitis induced by several specific pathogens

Micro‐CT analysis of chronic apical periodontitis induced by several specific pathogens

JAK2‐STAT3 signaling pathway is involved in rat periapical lesions induced by Enterococcus faecalis

Effect of Antibacterial Root Canal Sealer on Persistent Apical Periodontitis

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