<i>Enterococcus faecalis</i>
            -Induced Macrophage Necroptosis Promotes Refractory Apical Periodontitis

Dai, Xingzhu; Ma, Rongyang; Jiang, Weiyi; Deng, Zhang; Chen, Lijuan; Liang, Yuqing; Shao, Longquan; Zhao, Wanghong

doi:10.1128/spectrum.01045-22

Cited by 29 publications

(19 citation statements)

References 40 publications

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“…It is well recognized that P. intermedia and P. gingivalis are closely related in dental biofilms and that their co-colonization is associated with chronic periodontitis [30]. Additionally, refractory periapical periodontitis or persistent root canal infections may be associated with E. faecalis [31,32]. According to the OD600 value and the agar diffusion experiments shown in Figure 5a,b, larger quantities of CHX were associated with a stronger inhibitory capability.…”

Section: Discussionmentioning

confidence: 91%

Polycaprolactone Electrospun Nanofiber Membrane with Sustained Chlorohexidine Release Capability against Oral Pathogens

Chen

Wang

et al. 2022

JFB

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Multiple-pathogen periodontal disease necessitates a local release and concentration of antibacterial medication to control inflammation in a particular location of the mouth cavity. Therefore, it is necessary to effectively load and deliver medicine/antibiotics to treat numerous complex bacterial infections. This study developed chlorhexidine (CHX)/polycaprolactone (PCL) nanofiber membranes with controlled release properties as periodontal dressings to prevent or treat oral disorders. Electrostatic spinning was adopted to endow the nanofiber membranes with a high porosity, hydrophilicity, and CHX loading capability. The release of CHX occurred in a concentration-dependent manner. The CHX/PCL nanofiber membranes exhibited good biocompatibility with human periodontal ligament stem cells, with cell viability over 85% in each group via CCK-8 assay and LIVE/DEAD staining; moreover, the good attachment of the membrane was illustrated by scanning electron microscopy imaging. Through the agar diffusion assay, the nanofiber membranes with only 0.075 wt% CHX exhibited high antibacterial activity against three typical oral infection-causing bacteria: Porphyromonas gingivalis, Enterococcus faecalis, and Prevotella intermedia. The results indicated that the CHX/PCL nanofiber holds great potential as a periodontal dressing for the prevention and treatment periodontal disorders associated with bacteria.

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Section: Discussionmentioning

confidence: 91%

Polycaprolactone Electrospun Nanofiber Membrane with Sustained Chlorohexidine Release Capability against Oral Pathogens

Chen

Wang

et al. 2022

JFB

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“…Interference with E. faecalis -modulated host cell responses may help to treat RAP. In vivo experiments demonstrated that inflammation and bone destruction were alleviated in RIPK3-deficient mice with E. faecalis -induced RAP [ 113 ]. Moreover, the CASP-1 inhibitor partly suppressed bone resorption in an experimental RAP rat model [ 114 ].…”

Section: E Faecalis -Modulated Host Cell Responsesmentioning

confidence: 99%

Role of Enterococcus faecalis in refractory apical periodontitis: from pathogenicity to host cell response

Deng

Lin

Liu

et al. 2023

Journal of Oral Microbiology

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Background: Refractory apical periodontitis (RAP) is an oral infectious disease characterised by persistent inflammation, progressive alveolar bone destruction, and delayed bone healing. RAP has received increasing attention, because it cannot be cured after repeated root canal therapies. The aetiology of RAP is related to the complex interplay between the pathogen and its host. However, the exact pathogenesis of RAP remains unclarified and includes several factors, such as microorganism immunogenicity, host immunity and inflammation, and tissue destruction and repair. Enterococcus faecalis is the dominant pathogen involved in RAP, and has evolved multiple strategies to ensure survival, which cause persistent intraradicular and extraradicular infections. Objective: To review the crucial role of E. faecalis in the pathogenesis of RAP, and open new avenues for prevention and treatment of RAP. Methods: The PubMed and Web of Science databases were searched for pertinent publications, employing the search terms “Enterococcus faecalis”, “refractory apical periodontitis”, “persistent periapical periodontitis”, “pathogenicity”, “virulence”, “biofilm formation”, “dentine tubule”, “immune cell”, “macrophage”, and “osteoblast”. Results and Conclusion: Besides its high pathogenicity due to various virulence mechanisms, E. faecalis modulates the macrophage and osteoblast responses, including regulated cell death, cell polarisation, cell differentiation, and inflammatory response. An in-depth understanding of the multifaceted host cell responses modulated by E. faecalis will help to design potential future therapeutic strategies and overcome the challenges of sustained infection and delayed tissue healing in RAP.

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“…Yang et al, 2022). In E. faecalis-infected AP, the deletion of RIPK3 resulted in a significant reduction of inflammatory markers such as IL-6, IL-1β, and TNF, while periapical bone density was increased (Dai et al, 2022). Moreover, local knockdown of RIPK3 in F. nucleatuminfected AP was associated with decreased inflammatory cytokines and decreased bone loss (J.…”

Section: Necroptosis: a New Therapeutic Target For Apmentioning

confidence: 99%

Necroptosis in apical periodontitis: A programmed cell death with multiple roles

Liu

Fan

2023

Journal Cellular Physiology

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Programmed cell death (PCD) has been a research focus for decades and different mechanisms of cell death, such as necroptosis, pyroptosis, ferroptosis, and cuproptosis have been discovered. Necroptosis, a form of inflammatory PCD, has gained increasing attention in recent years due to its critical role in disease progression and development. Unlike apoptosis, which is mediated by caspases and characterized by cell shrinkage and membrane blebbing, necroptosis is mediated by mixed lineage kinase domain‐like protein (MLKL) and characterized by cell enlargement and plasma membrane rupture. Necroptosis can be triggered by bacterial infection, which on the one hand represents a host defense mechanism against the infection, but on the other hand can facilitate bacterial escape and worsen inflammation. Despite its importance in various diseases, a comprehensive review on the involvement and roles of necroptosis in apical periodontitis is still lacking. In this review, we tried to provide an overview of recent progresses in necroptosis research, summarized the pathways involved in apical periodontitis (AP) activation, and discussed how bacterial pathogens induce and regulated necroptosis and how necroptosis would inhibit bacteria. Furthermore, the interplay between various types of cell death in AP and the potential treatment strategy for AP by targeting necroptosis were also discussed.

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Enterococcus faecalis -Induced Macrophage Necroptosis Promotes Refractory Apical Periodontitis

Cited by 29 publications

References 40 publications

Polycaprolactone Electrospun Nanofiber Membrane with Sustained Chlorohexidine Release Capability against Oral Pathogens

Polycaprolactone Electrospun Nanofiber Membrane with Sustained Chlorohexidine Release Capability against Oral Pathogens

Role of Enterococcus faecalis in refractory apical periodontitis: from pathogenicity to host cell response

Necroptosis in apical periodontitis: A programmed cell death with multiple roles

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