Epigenetic Regulation of Bone Healing: Implications for Fracture Repair and Clinical Treatment Strategies

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Bone healing and fracture repair are complex processes involving multiple phases that rely on coordination and differentiation of multiple cell types, such as mesenchymal stem cells (MSCs), osteoblasts, osteoclasts, chondrocytes, and endothelial cells. The functions of growth factor and mechanical force in bone regeneration are well established, but recent research has revealed epigenetic mechanisms to play a major role in regulating cellular differentiation and tissue repair. Various studies have indicated epigenetic mechanisms like DNA methylation, histone modifications, and regulation by non-coding RNAs (ncRNA) are responsible for major gene expression regulation during bone regeneration. Moreover, systemic factors such as inflammation, aging, and metabolic disturbances regulate epigenetic regulation of bone cells to result in defective fracture healing. Emerging concepts in epigenetic therapy reveal new approaches to optimize bone regeneration and improve clinical results. This review focuses on the role of epigenetic regulation in the process of bone healing, highlighting its clinical implications.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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