Abstract:
Introduction: Bone tissue regeneration following grafting is a complex biochemical and cellular
process that requires balanced osteoblast activity, controlled osteoclast resorption, and adequate
vascularization. In oncologic patients, chemotherapy and radiotherapy significantly disrupt systemic
redox homeostasis, leading to excessive production of reactive oxygen species (ROS). Elevated
oxidative stress may interfere with normal bone remodeling and compromise graft incorporation. The
objective of the study was to elucidate the biochemical mechanisms through which oxidative
imbalance affects bone graft integration after cancer treatment.
Material and methods: A narrative literature review was performed, using 10 articles from 2016-
2026, including data from ScienceDirect, PubMed Central, Biomed Central, MedScape, and others,
focusing on experimental and clinical studies evaluating oxidative stress biomarkers, mitochondrial
dysfunction, and alterations in bone cell metabolism in patients undergoing oncologic therapy.
Molecular pathways related to ROS generation, antioxidant defense systems, and intracellular
signaling involved in osteoblast and osteoclast regulation were examined.
Results: Increased ROS levels activate intracellular signaling cascades that promote osteoclast
differentiation and enhance bone resorption. At the same time, oxidative stress inhibits osteoblast
proliferation, reduces collagen type I synthesis, and decreases alkaline phosphatase activity, impairing
extracellular matrix formation and mineral deposition. Chemotherapeutic agents induce mitochondrial
dysfunction and reduce cellular energy availability, further compromising regenerative capacity.
Radiotherapy contributes to vascular damage, reduced osteocyte viability, and persistent inflammatory
signaling within bone tissue. Diminished antioxidant defenses, including superoxide dismutase and
glutathione-dependent pathways, exacerbate oxidative injury. This biochemical imbalance weakens
early graft stabilization and increases the risk of delayed healing or graft failure. Moreover, oxidative
stress alters angiogenic signaling pathways, reducing vascular endothelial growth factor (VEGF)
expression and impairing neovascularization essential for graft survival. Experimental findings suggest
that modulation of oxidative stress may partially restore osteoblastic activity and improve structural
graft incorporation.
Conclusion: Oxidative stress represents a significant biochemical determinant of impaired bone graft
integration in oncologic patients. Targeting redox imbalance may offer supportive therapeutic potential
in reconstructive protocols. Further clinical investigations are required to establish evidence-based
antioxidant strategies capable of improving transplantation outcomes.
