ReviewNutrition journal2026
The role and therapeutic potential of vitamins in fracture healing.
Review in Nutrition journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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7 authors.
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Abstract
Fracture healing is an energetically demanding, highly orchestrated process in which inflammation, angiogenesis, callus formation and remodelling must be tightly coordinated, yet up to 10% of fractures progress to delayed union or non-union. Emerging evidence positions vitamins as key modulators of osteoimmunology, cellular metabolism and matrix mineralisation across distinct phases of repair. In this Review, we first outline the cellular and metabolic landscape of fracture healing, highlighting the roles of osteoblasts, osteoclasts, osteocytes, bone-lining cells and mesenchymal progenitors, and the coupling of bone and immune cells. We then synthesise data on vitamins A, C, E, K and B in bone health and fracture repair. Physiological retinoid signalling supports early osteoblast differentiation, whereas both deficiency and chronic excess of vitamin A drive osteoclastogenesis, disturb FGF23-vitamin D-Wnt axes and impair mineralisation in a dose-, time- and site-dependent manner. Vitamin C, as a cofactor for collagen crosslinking and a potent antioxidant, promotes osteoblast and mesenchymal stem-cell differentiation, modulates osteoclast survival and may mitigate oxidative blockade of callus formation. Vitamin E, particularly tocotrienols, limits oxidative stress, suppresses RANKL-driven osteoclastogenesis and activates Wnt/β-catenin and BMP pathways to favour bone formation. Vitamin K integrates γ-carboxylation of bone vitamin K-dependent proteins with PXR/SXR- and mitochondria-mediated signalling to support proper calcification and restrain excessive resorption. B vitamins regulate fracture healing through the one-carbon metabolism-homocysteine and NAD⁺-sirtuin axes, influencing epigenetic control of osteogenic genes, collagen crosslinking and skeletal stem-cell function. Finally, we discuss synergistic and antagonistic interactions among vitamins (for example, vitamins D-K and C-E versus excess vitamin A or α-tocopherol), and propose a stage-specific, biomarker-guided, minimal-effective-dose strategy for personalised vitamin-based adjuncts to fracture care.
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