Abstract
Although the complex mechanism by which skeletal tissue heals has been well described, the role of reactive oxygen species (ROS) in skeletal tissue regeneration is less understood. It has been widely recognized that a high level of ROS is cytotoxic and inhibits normal cellular processes. However, with more recent discoveries, it is evident that ROS also play an important, positive role in skeletal tissue repair, specifically fracture healing. Thus, dampening ROS levels can potentially inhibit normal healing. On the same note, pathologically high levels of ROS cause a sharp decline in osteogenesis and promote nonunion in fracture repair. This delicate balance complicates the efforts of therapeutic and engineering approaches that aim to modulate ROS for improved tissue healing. The physiologic role of ROS is dependent on a multitude of factors, and it is important for future efforts to consider these complexities. This review first discusses how ROS influences vital signaling pathways involved in the fracture healing response, including how they affect angiogenesis and osteogenic differentiation. The latter half glances at the current approaches to control ROS for improved skeletal tissue healing, including medicinal approaches, cellular engineering, and enhanced tissue scaffolds. This review aims to provide a nuanced view of the effects of ROS on bone fracture healing which will inspire novel techniques to optimize the redox environment for skeletal tissue regeneration.
Highlights
The influx of skeletal biology research over the past 20 years has improved our understanding of how bones develop, remodel, and repair via very complex mechanisms that requires the interaction of cells from different lineages (General 2004; Hadjidakis and Androulakis 2006)
Reactive oxygen species (ROS) are increasingly being recognized as a key component of the bone repair paradigm. Are they “good”, or are they “bad”? There is much debate over the role reactive oxygen species (ROS) play in the entire bone repair process, as some studies show they are necessary for bone repair and others say they are ROS in Bone Regeneration detrimental to the process
Redox signaling has an important role in bone remodeling and bone repair (Garrett et al, 1990; Lean et al, 2003; X.; Sun et al, 2020, 2; Deng et al, 2019), and research has shown that oxidative stress, which leads to aging and estrogen deficiency, may be one of the most critical factors contributing to bone loss (Almeida et al, 2007b; Manolagas and Almeida 2007)
Summary
The influx of skeletal biology research over the past 20 years has improved our understanding of how bones develop, remodel, and repair via very complex mechanisms that requires the interaction of cells from different lineages (General 2004; Hadjidakis and Androulakis 2006). Reactive oxygen species (ROS) are increasingly being recognized as a key component of the bone repair paradigm. Are they “good”, or are they “bad”? This review provides a general understanding of how ROS interact and influence key regulators in the bone healing process. For better therapeutics and bioengineering approaches to be developed, we need to understand how they influence the oxidative balance during skeletal tissue healing
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