This review discusses how reactive oxygen species drive bone repair in osteo-inflammation, suggesting biomaterials may improve outcomes.
This review elucidates the complex interplay among oxidative stress (OS), macrophage polarization, and stem cell-driven osteogenesis, emphasizing the regulatory influence of reactive oxygen species (ROS) on bone repair and regeneration. It demonstrates that an imbalance in ROS can impede bone healing by disrupting the equilibrium between pro-inflammatory (M1) and pro-repair (M2) macrophage phenotypes. Furthermore, the review delineates the mechanisms through which ROS can influence mesenchymal stem cell differentiation and osteoclast activity, while also highlighting the body's antioxidant defenses that counteract OS. Innovative strategies are explored, particularly the use of biomaterials and nanomedicine, which aim to modulate ROS levels and macrophage polarization, thereby fostering a conducive microenvironment for bone regeneration. The integration of nanotechnology, biomaterials, and cellular biology emerges as a promising frontier for advancing bone regeneration therapies, with the necessity for clinical validation underscored throughout.
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Min et al. (2025) studied this question.
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