Novel antioxidative nanotherapeutics in a rat periodontitis model: Reactive oxygen species scavenging by redox injectable gel suppresses alveolar bone resorption

Periodontitis, an inflammatory disease of oxidative stress, occurs due to the excess reactive oxygen species (ROS) contributing to cell and tissue damage that in turn leads to alveolar bone resorption...

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Decoy Receptor 3 Promotes Preosteoclast Cell Death via Reactive Oxygen Species-Induced Fas Ligand Expression and the IL-1α/IL-1 Receptor Antagonist Pathway

Mediators of Inflammation ◽

10.1155/2020/1237281 ◽

2020 ◽

Vol 2020 ◽

pp. 1-11

Author(s):

Yi-Jen Peng ◽

Ching-Tsung Peng ◽

Yi-Hsuan Lin ◽

Gu-Jiun Lin ◽

Shing-Hwa Huang ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Bone Resorption ◽

Fas Ligand ◽

Interleukin 1 ◽

Reactive Oxygen ◽

Precursor Cells ◽

Osteoclast Precursor ◽

Oxygen Species ◽

Decoy Receptor ◽

Decoy Receptor 3

Purpose. Interleukin-1α (IL-1α) is a potent cytokine that plays a role in inflammatory arthritis and bone loss. Decoy receptor 3 (DCR3) is an immune modulator of monocytes and macrophages. The aim of this study was to investigate the mechanism of DCR3 in IL-1α-induced osteoclastogenesis. Methods. We treated murine macrophages with DCR3 during receptor activator of nuclear factor kappa Β ligand- (RANKL-) plus IL-1α-induced osteoclastogenesis to monitor osteoclast formation by tartrate-resistant acid phosphatase (TRAP) staining. Osteoclast activity was assessed using a pit formation assay. The mechanisms of inhibition were studied by biochemical analyses, including RT-PCR, immunofluorescent staining, flow cytometry, an apoptosis assay, immunoblotting, and ELISA. Results. DCR3 suppresses IL-1α-induced osteoclastogenesis in both primary murine bone marrow-derived macrophages (BMM) and RAW264.7 cells as it inhibits bone resorption. DCR3 induces RANKL-treated osteoclast precursor cells to express IL-1α, secretory IL-1ra (sIL-1ra), intracellular IL-1ra (icIL-1ra), reactive oxygen species (ROS), and Fas ligand and to activate IL-1α-induced interleukin-1 receptor-associated kinase 4 (IRAK4). The suppression of DCR3 during RANKL- or IL-1α-induced osteoclastogenesis may be due to the abundant secretion of IL-1ra, accumulation of ROS, and expression of Fas ligand in apoptotic osteoclast precursor cells. Conclusions. We concluded that there is an inhibitory effect of DCR3 on osteoclastogenesis via ROS accumulation and ROS-induced Fas ligand, IL-1α, and IL-1ra expression. Our results suggested that the upregulation of DCR3 in preosteoclasts might be a therapeutic target in inflammatory IL-1α-induced bone resorption.

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Sirtuin 6 suppresses hypoxia-induced inflammatory response in human osteoblasts via inhibition of reactive oxygen species production and glycolysis-A therapeutic implication in inflammatory bone resorption

BioFactors ◽

10.1002/biof.1320 ◽

2016 ◽

Vol 43 (2) ◽

pp. 170-180 ◽

Cited By ~ 11

Author(s):

Kuo-Liang Hou ◽

Sze-Kwan Lin ◽

Ling-Hsiu Chao ◽

Eddie Hsiang-Hua Lai ◽

Cheng-Chi Chang ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Bone Resorption ◽

Inflammatory Response ◽

Reactive Oxygen Species Production ◽

Reactive Oxygen ◽

Therapeutic Implication ◽

Oxygen Species ◽

Human Osteoblasts ◽

Species Production

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Ferric ion could facilitate osteoclast differentiation and bone resorption through the production of reactive oxygen species

Journal of Orthopaedic Research® ◽

10.1002/jor.22133 ◽

2012 ◽

Vol 30 (11) ◽

pp. 1843-1852 ◽

Cited By ~ 62

Author(s):

Peng Jia ◽

You Jia Xu ◽

Zeng Li Zhang ◽

Kai Li ◽

Bingyan Li ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Bone Resorption ◽

Osteoclast Differentiation ◽

Reactive Oxygen ◽

Ferric Ion ◽

Oxygen Species

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Cistanche deserticolapolysaccharide attenuates osteoclastogenesis and bone resorption via inhibiting RANKL signaling and reactive oxygen species production

Journal of Cellular Physiology ◽

10.1002/jcp.26882 ◽

2018 ◽

Vol 233 (12) ◽

pp. 9674-9684 ◽

Cited By ~ 10

Author(s):

Dezhi Song ◽

Zhen Cao ◽

Zaibing Liu ◽

Jennifer Tickner ◽

Heng Qiu ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Bone Resorption ◽

Reactive Oxygen Species Production ◽

Reactive Oxygen ◽

Oxygen Species ◽

Species Production

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Intracellular Fragmentation of Bone Resorption Products by Reactive Oxygen Species Generated by Osteoclastic Tartrate-resistant Acid Phosphatase

Journal of Biological Chemistry ◽

10.1074/jbc.274.33.22907 ◽

1999 ◽

Vol 274 (33) ◽

pp. 22907-22910 ◽

Cited By ~ 172

Author(s):

Jussi M. Halleen ◽

Seija Räisänen ◽

Jari J. Salo ◽

Sakamuri V. Reddy ◽

G. David Roodman ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Acid Phosphatase ◽

Bone Resorption ◽

Reactive Oxygen ◽

Tartrate Resistant Acid Phosphatase ◽

Oxygen Species

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The Dual Effects of Reactive Oxygen Species on the Mandibular Alveolar Bone Formation in SOD1 Knockout Mice: Promotion or Inhibition

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/8847140 ◽

2021 ◽

Vol 2021 ◽

pp. 1-15

Author(s):

Yunyan Zhang ◽

Yuzhi Yang ◽

Mingxue Xu ◽

Jingwen Zheng ◽

Yuchan Xu ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Bone Formation ◽

Alveolar Bone ◽

Bone Development ◽

Reactive Oxygen ◽

Enzyme Linked Immunosorbent Assay ◽

Oxygen Species ◽

Periodontal Tissues ◽

Ros Accumulation

The status of reactive oxygen species (ROS) correlates closely with the normal development of the oral and maxillofacial tissues. Oxidative stress caused by ROS accumulation not only affects the development of enamel and dentin but also causes pathological changes in periodontal tissues (periodontal ligament and alveolar bone) that surround the root of the tooth. Although previous studies have shown that ROS accumulation plays a pathologic role in some oral and maxillofacial tissues, the effects of ROS on alveolar bone development remain unclear. In this study, we focused on mandibular alveolar bone development of mice deficient in superoxide dismutase1 (SOD1). Analyses were performed using microcomputerized tomography (micro-CT), TRAP staining, immunohistochemical (IHC) staining, and enzyme-linked immunosorbent assay (ELISA). We found for the first time that slightly higher ROS in mandibular alveolar bone of SOD1(-/-) mice at early ages (2-4 months) caused a distinct enlargement in bone size and increased bone volume fraction (BV/TV), trabecular thickness (Tb.Th), and expression of alkaline phosphatase (ALP), Runt-related transcription factor 2 (Runx2), and osteopontin (OPN). With ROS accumulation to oxidative stress level, increased trabecular bone separation (Tb.Sp) and decreased expression of ALP, Runx2, and OPN were found in SOD1(-/-) mice at 6 months. Additionally, dosing with N-acetylcysteine (NAC) effectively mitigated bone loss and normalized expression of ALP, Runx2, and OPN. These results indicate that redox imbalance caused by SOD1 deficiency has dual effects (promotion or inhibition) on mandibular alveolar bone development, which is closely related to the concentration of ROS and the stage of growth. We present a valuable model here for investigating the effects of ROS on mandibular alveolar bone formation and highlight important roles of ROS in regulating tissue development and pathological states, illustrating the complexity of the redox signal.

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Mitochondria as a source of reactive oxygen species

Biochemical Journal ◽

10.1042/bj20090056 ◽

2009 ◽

pp. c3 ◽

Cited By ~ 1

Author(s):

Helena M. Cochemé ◽

Michael P. Murphy

Keyword(s):

Reactive Oxygen Species ◽

Reactive Oxygen ◽

Oxygen Species

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Clinical aspects of reactive oxygen and nitrogen species

Biochemical Society Symposium ◽

10.1042/bss0710121 ◽

2004 ◽

Vol 71 ◽

pp. 121-133 ◽

Cited By ~ 25

Author(s):

Ascan Warnholtz ◽

Maria Wendt ◽

Michael August ◽

Thomas Münzel

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Risk Factor ◽

Endothelial Dysfunction ◽

Vascular Tissue ◽

Rapid Development ◽

Reactive Oxygen ◽

Clinical Aspects ◽

No Production ◽

Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

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