Early bone health: exploring relationship between oxidative stress and skeletal development in newborn infants

Résumé fourni par la source

Bone health during childhood is critical for proper skeletal development and long-term quality of life. The process of bone formation relies on a balance of mineralization and cellular activity, which is regulated by oxidative stress (OS). While physiological levels of reactive oxygen species (ROS) are important for normal bone cell function and homeostasis, excessive OS can contribute to the development of bone diseases, such as osteoarthritis and osteoporosis. Enzymes like xanthine oxidoreductase are involved in amplifying ROS production, which can lead to cartilage degradation and disrupted bone remodeling. Despite increasing recognition of OS as a risk factor in adult skeletal health, its impact on fetal and neonatal bone development remains underexplored. In vitro and animal model studies, including those using free radicals exposure, have been performed to understand how OS impairs osteogenesis. This review examines the role of OS in perinatal bone development analyzing key environmental risk factors and the potential long-term consequences of early-life redox imbalance on skeletal health. The sensitivity of the fetal bone to OS suggests that oxidative damage during this critical period can result in impaired bone growth, low birth weight, and long-term skeletal disorders. Oxidative stress interferes with osteoblast differentiation, enhances adipocyte formation from mesenchymal stem cells, and stimulates osteoclast activity, leading to bone resorption. Clinical studies on the impact of OS on neonatal bone metabolism remain limited. Identifying key risk factors for early-life redox imbalance could be crucial in developing potential antioxidant therapies to support skeletal health during childhood

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