Oxidative Stress and Bone Remodeling: An Updated Review

Oxidative stress has emerged as a pivotal factor in bone remodelling, significantly influencing the balance between osteoclastmediated resorption and osteoblast-driven formation.Reactive oxygen species (ROS), generated through various mechanisms, disrupt osteoblastic differentiation and function while enhancing osteoclastic activity, thereby promoting bone loss.This review consolidates recent findings on oxidative stress's molecular impact on bone remodelling, focusing on key signalling pathways, such as MAPKs, NF-B, and Wnt/-catenin.We explore the roles of glucocorticoids and inflammatory cytokines in exacerbating ROS production, leading to decreased bone mass, increased apoptosis, and altered osteoblast-osteoclast interactions.Insights into the regulatory mechanisms of osteocytes and the RANKL/OPG axis further elucidate the connection between redox imbalance and skeletal fragility.Understanding these processes underscores the therapeutic potential of antioxidants and targeted signaling pathway modulation in mitigating oxidative stress-related bone diseases.Further research into these mechanisms is crucial for developing precise interventions to improve bone health and reduce fracture risk in aging and chronic inflammation contexts. Oxidative stress influences osteoblastic differentiationFrom embryo to adulthood, bones form and dissolve.

Publication Details

Journal
Annals of Case Reports
Published
2025-02-03
DOI
https://doi.org/10.29011/2574-7754.102174
Citations
5
Primary Topic
Bone health and osteoporosis research
Type
article
Field-Weighted Citation Impact
8.61
Controls
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article

Oxidative Stress and Bone Remodeling: An Updated Review

5 citations
Annals of Case Reports
Bone health and osteoporosis research
8.61
article

Oxidative Stress and Bone Remodeling: An Updated Review

article en
5 citations

Abstract

Oxidative stress has emerged as a pivotal factor in bone remodelling, significantly influencing the balance between osteoclastmediated resorption and osteoblast-driven formation.Reactive oxygen species (ROS), generated through various mechanisms, disrupt osteoblastic differentiation and function while enhancing osteoclastic activity, thereby promoting bone loss.This review consolidates recent findings on oxidative stress's molecular impact on bone remodelling, focusing on key signalling pathways, such as MAPKs, NF-B, and Wnt/-catenin.We explore the roles of glucocorticoids and inflammatory cytokines in exacerbating ROS production, leading to decreased bone mass, increased apoptosis, and altered osteoblast-osteoclast interactions.Insights into the regulatory mechanisms of osteocytes and the RANKL/OPG axis further elucidate the connection between redox imbalance and skeletal fragility.Understanding these processes underscores the therapeutic potential of antioxidants and targeted signaling pathway modulation in mitigating oxidative stress-related bone diseases.Further research into these mechanisms is crucial for developing precise interventions to improve bone health and reduce fracture risk in aging and chronic inflammation contexts. Oxidative stress influences osteoblastic differentiationFrom embryo to adulthood, bones form and dissolve.

Annals of Case ReportsVol. 10(1)
Zero hunger
Openalex Percentile: Top 2%
Bone health and osteoporosis research
8.61
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