Role of Oxidative Stress in Bone Ageing

Portal‐Núñez, Sergio; Esbrit, Pedro

doi:10.1007/978-1-4614-6166-1_6

Cited by 12 publications

(13 citation statements)

References 122 publications

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“…VEGF is known to play a key role in neovascularization (Byrne et al, 2005), as the correlation between VEGF concentrations and vascular density has been demonstrated in many experimental models (Faviana et al, 2002;Shohara et al, 2012). As pointed out above, vascularization plays an important role in bone development and fracture healing (Portal-Nunez et al, 2012). The mediator VEGF exerts its effect on bone healing, presumably indirectly, by early chemotactic attraction of endothelial cells and endothelial progenitor cells (EPCs), resulting in neovascularization (Asahara et al, 1997;Henrich et al, 2009;Peng et al, 2002;Seebach et al, 2012).…”

Section: Vegf Expression In Induced Membranessupporting

confidence: 70%

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Establishment and characterization of the Masquelet induced membrane technique in a rat femur critical-sized defect model

Henrich

Seebach

Nau

et al. 2013

J Tissue Eng Regen Med

112

149

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The Masquelet induced membrane technique for reconstructing large diaphyseal defects has been shown to be a promising clinical treatment, yet relatively little is known about the cellular, histological and biochemical make-up of these membranes and how they produce this positive clinical outcome. We compared cellular make-up, histological changes and growth factor expression in membranes induced around femur bone defects and in subcutaneous pockets at 2, 4 and 6 weeks after induction, and to the periosteum. We found that membranes formed around bone defects were similar to those formed in subcutaneous pockets; however, both were significantly different from periosteum with regard to structural characteristics, location of blood vessels and overall thickness. Membranes induced at the femur defect (at 2 weeks) and in periosteum contain mesenchymal stem cells (MSCs; STRO-1 ) which were not found in membranes induced subcutaneously. BMP-2, TGFβ and VEGF were significantly elevated in membranes induced around femur defects in comparison to subcutaneously induced membranes, whereas SDF-1 was not detectable in membranes induced at either site. We found that osteogenic and neovascular activity had mostly subsided by 6 weeks in membranes formed at both sites. It was conclude that cellular composition and growth factor content in induced membranes depends on the location where the membrane is induced and differs from periosteum. Osteogenic and neovascular activity in the membranes is maximal between 2 and 4 weeks and subsides after 6. Based on this, better and quicker bone healing might be achieved if the PMMA cement were replaced with a bone graft earlier in the Masquelet technique. Copyright © 2013 John Wiley & Sons, Ltd.

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Section: Vegf Expression In Induced Membranessupporting

confidence: 70%

“…Vascularization plays an important role in bone development and fracture healing (Portal-Nunez et al, 2012). In our rat model we found that early on (2 weeks) the membranes were highly vascularized.…”

Section: Vascularizationmentioning

confidence: 99%

Establishment and characterization of the Masquelet induced membrane technique in a rat femur critical-sized defect model

Henrich

Seebach

Nau

et al. 2013

J Tissue Eng Regen Med

112

149

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“…(205,206) Cells, fortunately, have means to eliminate ROS, mainly through the activity of enzymatic catalases (glutathione reductase; superoxide dismutase [SOD]) and the Forkhead box O (FoxO) family of transcription factors. (207) ROS metabolites have been shown to increase, while protective mechanisms decrease, with age in bone. For example, Almedia and colleagues (126) showed glutathione reductase shows an approximate 50%-75% reduction in activity from skeletal maturity to advanced age (25 months) in the bone marrow of female and male C57BL/6J mice.…”

Section: Oxidative Stressmentioning

confidence: 99%

Similarities Between Disuse and Age-Induced Bone Loss

Buettmann

Goldscheitter

Hoppock

et al. 2020

Journal of Bone and Mineral Research

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Disuse and aging are known risk factors associated with low bone mass and quality deterioration, resulting in increased fracture risk. Indeed, current and emerging evidence implicate a large number of shared skeletal manifestations between disuse and aging scenarios. This review provides a detailed overview of current preclinical models of musculoskeletal disuse and the clinical scenarios they seek to recapitulate. We also explore and summarize the major similarities between bone loss after extreme disuse and advanced aging at multiple length scales, including at the organ/tissue, cellular, and molecular level. Specifically, shared structural and material alterations of bone loss are presented between disuse and aging, including preferential loss of bone at cancellous sites, cortical thinning, and loss of bone strength due to enhanced fragility. At the cellular level bone loss is accompanied, during disuse and aging, by increased bone resorption, decreased formation, and enhanced adipogenesis due to altered gap junction intercellular communication, WNT/β‐catenin and RANKL/OPG signaling. Major differences between extreme short‐term disuse and aging are discussed, including anatomical specificity, differences in bone turnover rates, periosteal modeling, and the influence of subject sex and genetic variability. The examination also identifies potential shared mechanisms underlying bone loss in aging and disuse that warrant further study such as collagen cross‐linking, advanced glycation end products/receptor for advanced glycation end products (AGE‐RAGE) signaling, reactive oxygen species (ROS) and nuclear factor κB (NF‐κB) signaling, cellular senescence, and altered lacunar‐canalicular connectivity (mechanosensation). Understanding the shared structural alterations, changes in bone cell function, and molecular mechanisms common to both extreme disuse and aging are paramount to discovering therapies to combat both age‐related and disuse‐induced osteoporosis. © 2022 American Society for Bone and Mineral Research (ASBMR).

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“…[21][22][23] Neovascularization of injured tissue is key to successful bone repair, providing oxygen, facilitating metabolic waste removal, and delivering progenitor cells of haematopoietic origin. 8,24 Whereas mechanical stability preserves vascular integrity and promotes osteogenesis, instability disrupts microvessels producing hypoxic conditions that favor chondrogenesis, as occurs in the central avascular region of the callus. 25 This determines that stabilized fractures have less cartilage and a reduced callus volume.…”

Section: Cell and Molecular Mechanisms Underlying The Process Of Bone...mentioning

confidence: 99%