Disinfection of Infected Root Canals: Nanosilver Has Good Potential

Yin, Wei; Zheng, Zhong; Liu, Yaoli; Wang, Lina; Shi, Chun; Zhang, Lianlian; Liu, Shuo; Niu, Weidong; Ting, Kang; Bian, Zhuan

doi:10.1002/smtd.201900378

Cited by 7 publications

(6 citation statements)

References 15 publications

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“…Noncanonical inflammasomes may also participate in the pathogenesis of periapical bone loss. The increased expression of caspase-1 and caspase-11 in RAW264.7 cells treated with LPS was found to be significantly reduced by nanosilver, and this decreased inflammasome activity may contribute to the alleviation of canine periapical periodontitis progression ( 185 ). In addition, estrogen deficiency can induce activation of the NLRP3/caspase-1/IL-1β axis and aggravate periapical bone loss in postmenopausal patients and ovariectomized rats with periapical periodontitis ( 267 ).…”

Section: Inflammasomes In Inflammatory Osteolysis Of the Alveolar Bone And Jawsmentioning

confidence: 99%

Inflammasomes in Alveolar Bone Loss

2021

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Bone remodeling is tightly controlled by osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Fine tuning of the osteoclast–osteoblast balance results in strict synchronization of bone resorption and formation, which maintains structural integrity and bone tissue homeostasis; in contrast, dysregulated bone remodeling may cause pathological osteolysis, in which inflammation plays a vital role in promoting bone destruction. The alveolar bone presents high turnover rate, complex associations with the tooth and periodontium, and susceptibility to oral pathogenic insults and mechanical stress, which enhance its complexity in host defense and bone remodeling. Alveolar bone loss is also involved in systemic bone destruction and is affected by medication or systemic pathological factors. Therefore, it is essential to investigate the osteoimmunological mechanisms involved in the dysregulation of alveolar bone remodeling. The inflammasome is a supramolecular protein complex assembled in response to pattern recognition receptors and damage-associated molecular patterns, leading to the maturation and secretion of pro-inflammatory cytokines and activation of inflammatory responses. Pyroptosis downstream of inflammasome activation also facilitates the clearance of intracellular pathogens and irritants. However, inadequate or excessive activity of the inflammasome may allow for persistent infection and infection spreading or uncontrolled destruction of the alveolar bone, as commonly observed in periodontitis, periapical periodontitis, peri-implantitis, orthodontic tooth movement, medication-related osteonecrosis of the jaw, nonsterile or sterile osteomyelitis of the jaw, and osteoporosis. In this review, we present a framework for understanding the role and mechanism of canonical and noncanonical inflammasomes in the pathogenesis and development of etiologically diverse diseases associated with alveolar bone loss. Inappropriate inflammasome activation may drive alveolar osteolysis by regulating cellular players, including osteoclasts, osteoblasts, osteocytes, periodontal ligament cells, macrophages, monocytes, neutrophils, and adaptive immune cells, such as T helper 17 cells, causing increased osteoclast activity, decreased osteoblast activity, and enhanced periodontium inflammation by creating a pro-inflammatory milieu in a context- and cell type-dependent manner. We also discuss promising therapeutic strategies targeting inappropriate inflammasome activity in the treatment of alveolar bone loss. Novel strategies for inhibiting inflammasome signaling may facilitate the development of versatile drugs that carefully balance the beneficial contributions of inflammasomes to host defense.

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Section: Inflammasomes In Inflammatory Osteolysis Of the Alveolar Bone And Jawsmentioning

confidence: 99%

Inflammasomes in Alveolar Bone Loss

2021

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“…Caspase inhibition can be classified into direct and indirect approaches. Direct inhibitors of caspase include caspase pan inhibitor (Z‐VAD‐FMK), 104 caspase‐1 inhibitors (Ac‐YVAD‐CHO, Ac‐YVAD‐CMK, VX765), 67,68,81,93 caspase‐3 inhibitor (Ac‐DEVD‐FMK), 21 caspase‐4 inhibitor (Z‐LEVD‐FMK), 104 and caspase‐1 and caspase‐11 common inhibitor (nanosilver) 125 . Indirect inhibitors of caspase‐1 consist of peroxisome proliferator‐activated receptor γ (PPARγ) activator (Arhalofenate), 126 and Hedgehog inhibitor (GANT‐61) plus indomethacin 127 …”

Section: Targeting Strategies Of Pyroptosis In Inflammatory Bone Dise...mentioning

confidence: 99%

“…One study demonstrated that adding nanosilver to the particle-poly(lactic-co-glycolic acid) (PLGA) carrier showed not only great bactericidal activity but also excellent biocompatibility. 125 What is more, recent studies revealed that combining EVs with miRNAs could effectively block the pyroptosis-related signaling pathway and alleviate inflammatory conditions. 142,149 Thus, extracellular vesicles (including exosomes and microvesicles), which might be a potential strategy for treating inflammatory diseases, should be extensively explored further.…”

Section: Caspase Direct Inhibitorsmentioning

confidence: 99%

“…Second, the application of nanomaterials in clinics is also a promising strategy for pyroptosis (Figure 5). One study demonstrated that adding nanosilver to the particle‐poly(lactic‐co‐glycolic acid) (PLGA) carrier showed not only great bactericidal activity but also excellent biocompatibility 125 . What is more, recent studies revealed that combining EVs with miRNAs could effectively block the pyroptosis‐related signaling pathway and alleviate inflammatory conditions 142,149 .…”

Section: Perspective and Conclusionmentioning

confidence: 99%

“…Direct inhibitors of caspase include caspase pan inhibitor (Z-VAD-FMK), 104 caspase-1 inhibitors (Ac-YVAD-CHO, Ac-YVAD-CMK, VX765), 67,68,81,93 caspase-3 inhibitor (Ac-DEVD-FMK), 21 caspase-4 inhibitor (Z-LEVD-FMK), 104 and caspase-1 and caspase-11 common inhibitor (nanosilver). 125 Indirect inhibitors of caspase-1 consist of peroxisome proliferator-activated receptor γ (PPARγ) activator (Arhalofenate), 126 and Hedgehog inhibitor (GANT-61) plus indomethacin. 127 Second, NLRP3 plays a significant part in the assembly of inflammasomes during pyroptosis, indicating that it has the potential to be a target for the therapy of inflammatory bone diseases.…”

Section: Drugs Targeting Strategiesmentioning

confidence: 99%

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Pyroptosis in inflammatory bone diseases: Molecular insights and targeting strategies

2022

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Inflammatory bone diseases include osteoarthritis (OA) and rheumatoid arthritis (RA), which can cause severe bone damage in a chronic inflammation state, putting tremendous pressure on the patients' families and government agencies regarding medical costs. In addition, the complexity of osteoimmunology makes research on these diseases difficult. Hence, it is urgent to determine the potential mechanisms and find effective drugs to target inflammatory bone diseases to reduce the negative effects of these diseases. Recently, pyroptosis, a gasdermininduced necrotic cell death featuring secretion of pro-inflammatory cytokines and lysis, has become widely known. Based on the effect of pyroptosis on immunity, this process has gradually emerged as a vital component in the etiopathogenesis of inflammatory bone diseases. Herein, we review the characteristics and mechanisms of pyroptosis and then focus on its clinical significance in inflammatory How to cite this article: Zhang R-N, Sun Z-J, Zhang L. Pyroptosis in inflammatory bone diseases: Molecular insights and targeting strategies. The

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Persistent and Enhanced Elimination of Bacteria‐Induced Periodontitis Using a Local Drug Delivery Nanoreactor

Chen

Feng

et al. 2022

Advanced Therapeutics

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Periodontitis, one of the most common dental diseases, is the main cause of tooth loss. Bacterial infection and the host immune response are the dominant factors that determine periodontal disease. Therefore, the key factors in the treatment of periodontitis are to remove pathogenic factors and repair periodontal supporting tissues. In this work, a facile and versatile strategy to prepare pH-sensitive biomineralized nanoparticles constructed with antibiotic to simultaneously deliver antibacterial, anti-inflammatory, and bone repair capabilities is presented. The experiments in vitro show that the nanoreactor achieves good inhibitory effects on three common periodontal pathogens and has activity against damaging inflammatory mediators, reducing lipopolysaccharide-induced inflammatory responses. In vivo CT images of the maxillary molar area and histomorphological and immunohistochemical analyses demonstrate that the nanoparticles repair function for periodontal supporting tissues, reverse the loosened alveolar bone tissue, and remodel the periodontal inflammatory microenvironment. Therefore, the present research provides a feasible approach to both prevent the loss of alveolar bone and repair periodontal tissue.

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Disinfection of Infected Root Canals: Nanosilver Has Good Potential

Cited by 7 publications

References 15 publications

Inflammasomes in Alveolar Bone Loss

Inflammasomes in Alveolar Bone Loss

Pyroptosis in inflammatory bone diseases: Molecular insights and targeting strategies

Persistent and Enhanced Elimination of Bacteria‐Induced Periodontitis Using a Local Drug Delivery Nanoreactor

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