Redox injectable gel protects osteoblastic function against oxidative stress and suppresses alveolar bone loss in a rat peri-implantitis model

Ozawa, Ryotaro; Saita, Makiko; Sakaue, Sho; Okada, Ryusaku; Sato, Takenori; Kawamata, Ryota; Sakurai, Takashi; Hamada, Naoki; Kimoto, Katsuhiko; Nagasaki, Yukio

doi:10.1016/j.actbio.2020.04.003

Cited by 25 publications

(20 citation statements)

References 42 publications

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“…There is, however, surprisingly limited knowledge on the influence of the biomechanical environment in the bone and bone-implant interface on the redox balance, with some of the information available based on maxillofacial implantology focusing on the effects of the implant itself. It is recognized that ROS boost the inflammatory response and cause both RANKL-induced osteoclastogenesis and osteoblast apoptosis, leading to periprosthetic osteolysis aseptic loosening, the most frequent cause of implant failure ( Borys et al, 2018 ; Ozawa et al, 2020 ; Galliera et al, 2021 ). Bone unloading such as observed in disuse and microgravity conditions leads to decreased bone mass and quality, through redox-mediated pathways.…”

Section: Discussionmentioning

confidence: 99%

In Sickness and in Health: The Oxygen Reactive Species and the Bone

Reis

Ramos

2021

Front. Bioeng. Biotechnol.

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Oxidative stress plays a central role in physiological and pathological bone conditions. Its role in signalment and control of bone cell population differentiation, activity, and fate is increasingly recognized. The possibilities of its use and manipulation with therapeutic goals are virtually unending. However, how redox balance interplays with the response to mechanical stimuli is yet to be fully understood. The present work summarizes current knowledge on these aspects, in an integrative and broad introductory perspective.

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Section: Discussionmentioning

confidence: 99%

In Sickness and in Health: The Oxygen Reactive Species and the Bone

Reis

Ramos

2021

Front. Bioeng. Biotechnol.

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“…The most important components of the oxidation system are ROS (Newsholme et al., 2016). The excessive accumulation of ROS can lead to cell apoptosis, lipid peroxidation and mitochondrial dysfunction (Badgley et al., 2020; Ozawa et al., 2020; Yang & Kim, 2018). Studies have shown that HCB can increase the content of ROS and induce oxidative stress (Addae et al., 2013; Ezendam et al., 2004).…”

Section: Discussionmentioning

confidence: 99%

The endocrine disruptor hexachlorobenzene can cause oxidative damage in the testis of mice

Dou

Mou

et al. 2021

Andrologia

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Hexachlorobenzene (HCB) was originally used as a common pesticide but was subsequently identified as an endocrine-disrupting chemical (Chiappini et al., 2019). Consequently, the use of HCB as a pesticide was terminated in the mid-1970s and is only used in laboratory scenarios at present (Iatrou et al., 2019;Yu et al., 2019). However, since HCB degrades slowly in natural environments and can accumulate in organisms, HCB residues have been detected in soil, water, humans, animals and plants in many regions and countries across the world. As a consequence, HCB remains one of the largest environmental pol-

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“…H 2 O 2 could inhibit osteoblast differentiation by triggering oxidative stress, thus inducing cellular senescence. 29 Here we further evaluated the effects of BM on H 2 O 2 -induced weakness of osteoblast differentiation due to cellular senescence. Compared to the control group, the expression of cellular senescence-related genes p16 and p21 was dramatically upregulated in the H 2 O 2 treatment group (ESI Fig.…”

Section: Bm Recovered Hydrogen Peroxide (H 2 O 2 )-Induced Inhibition...mentioning

confidence: 99%

“…23 Much research showed H 2 O 2 induced the production of reactive oxygen species (ROS), which caused the oxidative stress and accelerated senescence in the body. 29,46,47 In order to evaluate the function of BM on the cellular senescence-related inhibition of osteoblast differentiation, H 2 O 2 was used to induce senescence in osteo-blasts. 24 We detected the expression of p16 and p21, reported as marker genes in cellular senescence.…”

Section: Papermentioning

confidence: 99%