Superoxide and bone resorption

Key, L. Lyndon; Wolf, W. Clark; Gundberg, Caren M.; Ries, William L.

doi:10.1016/8756-3282(94)90821-4

Cited by 110 publications

(18 citation statements)

References 11 publications

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“…Hydrogen peroxide stimulates phosphorylation of the Factor Nuclear kappa B-inhibitor of kappa B ( NF-κB–IκB) complex, activating NF-κB and facilitating nuclear translocation and downstream movement of proinflammatory cytokines, such as Tumour Necrosis Factor-α (TNF-α), which are very important in the pathogenesis of periodontal disease [ 24 ]. Superoxide generated at the osteoclast–bone interface is involved in bone matrix degradation [ 25 ]. Superoxide is removed from tissue by superoxide dismutase (SOD).…”

Section: Discussionmentioning

confidence: 99%

Effects of metformin on inflammation, oxidative stress, and bone loss in a rat model of periodontitis

et al. 2017

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AimTo evaluate the effects of metformin (Met) on inflammation, oxidative stress, and bone loss in a rat model of ligature-induced periodontitis.Materials & methodsMale albino Wistar rats were divided randomly into five groups of twenty-one rats each, and given the following treatments for 10 days: (1) no ligature + water, (2) ligature + water, (3) ligature + 50 mg/kg Met, (4) ligature + 100 mg/kg Met, and (5) ligature + 200 mg/kg Met. Water or Met was administered orally. Maxillae were fixed and scanned using Micro-computed Tomography (μCT) to quantitate linear and bone volume/tissue volume (BV/TV) volumetric bone loss. Histopathological characteristics were assessed through immunohistochemical staining for MMP-9, COX-2, the RANKL/RANK/OPG pathway, SOD-1, and GPx-1. Additionally, confocal microscopy was used to analyze osteocalcin fluorescence. UV-VIS analysis was used to examine the levels of malondialdehyde, glutathione, IL-1β and TNF-α from gingival tissues. Quantitative RT-PCR reaction was used to gene expression of AMPK, NF-κB (p65), and Hmgb1 from gingival tissues. Significance among groups were analysed using a one-way ANOVA. A p-value of p<0.05 indicated a significant difference.ResultsTreatment with 50 mg/kg Met significantly reduced concentrations of malondialdehyde, IL-1β, and TNF-α (p < 0.05). Additionally, weak staining was observed for COX-2, MMP-9, RANK, RANKL, SOD-1, and GPx-1 after 50 mg/kg Met. OPG and Osteocalcin showed strong staining in the same group. Radiographically, linear measurements showed a statistically significant reduction in bone loss after 50 mg/kg Met compared to the ligature and Met 200 mg/kg groups. The same pattern was observed volumetrically in BV/TV and decreased osteoclast number (p<0.05). RT-PCR showed increased AMPK expression and decreased expression of NF-κB (p65) and HMGB1 after 50 mg/kg Met.ConclusionsMetformin, at a concentration of 50 mg/kg, decreases the inflammatory response, oxidative stress and bone loss in ligature-induced periodontitis in rats.

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Section: Discussionmentioning

confidence: 99%

Effects of metformin on inflammation, oxidative stress, and bone loss in a rat model of periodontitis

et al. 2017

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“…16, 17 Mature osteoclasts at sites of active bone remodeling are also associated with an increase in ROS. 17–19 These findings suggest that hydrolytically stable biomaterials that degrade in response to cell-secreted ROS may be a useful new approach for the design of cell-degradable bone cements.…”

Section: Introductionmentioning

confidence: 98%

Oxidatively degradable poly(thioketal urethane)/ceramic composite bone cements with bone-like strength

McEnery

Gupta

et al. 2016

RSC Adv.

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Synthetic bone cements are commonly used in orthopaedic procedures to aid in bone regeneration following trauma or disease. Polymeric cements like PMMA provide the mechanical strength necessary for orthopaedic applications, but they are not resorbable and do not integrate with host bone. Ceramic cements have a chemical composition similar to that of bone, but their brittle mechanical properties limit their use in weight-bearing applications. In this study, we designed oxidatively degradable, polymeric bone cements with mechanical properties suitable for bone tissue engineering applications. We synthesized a novel thioketal (TK) diol, which was crosslinked with a lysine triisocyanate (LTI) prepolymer to create hydrolytically stable poly(thioketal urethane)s (PTKUR) that degrade in the oxidative environment associated with bone defects. PTKUR films were hydrolytically stable for up to 6 months, but degraded rapidly (<1 week) under simulated oxidative conditions in vitro. When combined with ceramic micro- or nanoparticles, PTKUR cements exhibited working times comparable to calcium phosphate cements and strengths exceeding those of trabecular bone. PTKUR/ceramic composite cements supported appositional bone growth and integrated with host bone near the bone-cement interface at 6 and 12 weeks post-implantation in rabbit femoral condyle plug defects. Histological evidence of osteoclast-mediated resorption of the cements was observed at 6 and 12 weeks. These findings demonstrate that a PTKUR bone cement with bone-like strength can be selectively resorbed by cells involved in bone remodeling, and thus represent an important initial step toward the development of resorbable bone cements for weight-bearing applications.

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“…In response to periodontal pathogens, polymorphonuclear cells (PMNs) release destructive reactive oxygen species (ROS), for example, superoxide, via the respiratory burst [7–9], proteinases, and other factors that can damage host tissues [10–12]. These molecules induce further oxidative damage to gingival tissue, periodontal ligaments, and elicit osteoclastic bone resorption [10, 13–15]. The secreted agents also enhance the production of numerous proinflammatory cytokines that contribute to the disease, including interleukin (IL)-1ß, IL-6, and tumor necrosis factor (TNF α ), among a broad array of biomolecules that have consistently been reported to be elevated in gingival crevicular fluid (GCF) and tissues of periodontitis patients [16–18], rhesus monkeys [19], and dogs [20].…”

Section: Introductionmentioning

confidence: 99%

Animal Models for Periodontal Disease

Puleo

2011

BioMed Research International

231

254

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Animal models and cell cultures have contributed new knowledge in biological sciences, including periodontology. Although cultured cells can be used to study physiological processes that occur during the pathogenesis of periodontitis, the complex host response fundamentally responsible for this disease cannot be reproduced in vitro. Among the animal kingdom, rodents, rabbits, pigs, dogs, and nonhuman primates have been used to model human periodontitis, each with advantages and disadvantages. Periodontitis commonly has been induced by placing a bacterial plaque retentive ligature in the gingival sulcus around the molar teeth. In addition, alveolar bone loss has been induced by inoculation or injection of human oral bacteria (e.g., Porphyromonas gingivalis) in different animal models. While animal models have provided a wide range of important data, it is sometimes difficult to determine whether the findings are applicable to humans. In addition, variability in host responses to bacterial infection among individuals contributes significantly to the expression of periodontal diseases. A practical and highly reproducible model that truly mimics the natural pathogenesis of human periodontal disease has yet to be developed.

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Superoxide and bone resorption

Cited by 110 publications

References 11 publications

Effects of metformin on inflammation, oxidative stress, and bone loss in a rat model of periodontitis

Effects of metformin on inflammation, oxidative stress, and bone loss in a rat model of periodontitis

Oxidatively degradable poly(thioketal urethane)/ceramic composite bone cements with bone-like strength

Animal Models for Periodontal Disease

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