TY - JOUR
T1 - Osteogenesis Activity and Porosity Effect of Biodegradable Mg-Ga Alloys Barrier Membrane for Guided Bone Regeneration
T2 - An in Vitro and in Vivo Study in Rabbits
AU - Luo, Qiyue
AU - Gao, Kang
AU - Li, Yan
AU - Zhang, Ziyue
AU - Chen, Su
AU - Zhou, Jian
N1 - Publisher Copyright:
© 2025 by the authors.
PY - 2025/8
Y1 - 2025/8
N2 - Background/Objectives: Guided bone regeneration (GBR) requires barrier membrane materials that balance biodegradation with mechanical stability. Magnesium (Mg)-based metals have good prospects for use as biodegradable barrier materials due to their elastic modulus, good biocompatibility, and osteogenic properties. In this study, gallium (Ga) was introduced into Mg to enhance the mechanical strength and optimize the degradation behavior of the alloy, addressing the limitations of conventional magnesium alloys in corrosion control and strength retention. Methods: Mg-xGa alloys (x = 1.0–3.0%, wt.%) were evaluated for biocompatibility, degradation, and osteogenic potential. Corrosion rates were calculated via weight loss, Mg2+ release, and pH changes. Osteogenic effects were assessed using rat bone marrow mesenchymal stem cells (rBMSCs) for alkaline phosphatase (ALP) activity, extracellular matrix (ECM) mineralization, and osteogenic-related gene expression. Optimal alloy was fabricated into barrier membranes with different pore sizes (0.85–1.70 mm) for the rabbit mandibular defect to evaluate the porosity effect on new bone formation. Results: Cytocompatibility tests established a biosafety threshold for Ga content below 3 wt.%. Mg-1Ga demonstrated uniform corrosion with a rate of 1.02 mm/year over 28 days. In vitro, Mg-1Ga enhanced ALP activity, ECM mineralization, and osteogenic gene expression. The 1.70 mm pore size group exhibited superior new bone formation and bone mineral density at 4 and 8 weeks. Conclusions: These results highlight Mg-1Ga’s biocompatibility, controlled degradation, and osteogenic properties. Its optimized pore design bridges the gap between collagen membranes’ poor strength and titanium meshes’ non-degradability, offering a promising solution for GBR applications.
AB - Background/Objectives: Guided bone regeneration (GBR) requires barrier membrane materials that balance biodegradation with mechanical stability. Magnesium (Mg)-based metals have good prospects for use as biodegradable barrier materials due to their elastic modulus, good biocompatibility, and osteogenic properties. In this study, gallium (Ga) was introduced into Mg to enhance the mechanical strength and optimize the degradation behavior of the alloy, addressing the limitations of conventional magnesium alloys in corrosion control and strength retention. Methods: Mg-xGa alloys (x = 1.0–3.0%, wt.%) were evaluated for biocompatibility, degradation, and osteogenic potential. Corrosion rates were calculated via weight loss, Mg2+ release, and pH changes. Osteogenic effects were assessed using rat bone marrow mesenchymal stem cells (rBMSCs) for alkaline phosphatase (ALP) activity, extracellular matrix (ECM) mineralization, and osteogenic-related gene expression. Optimal alloy was fabricated into barrier membranes with different pore sizes (0.85–1.70 mm) for the rabbit mandibular defect to evaluate the porosity effect on new bone formation. Results: Cytocompatibility tests established a biosafety threshold for Ga content below 3 wt.%. Mg-1Ga demonstrated uniform corrosion with a rate of 1.02 mm/year over 28 days. In vitro, Mg-1Ga enhanced ALP activity, ECM mineralization, and osteogenic gene expression. The 1.70 mm pore size group exhibited superior new bone formation and bone mineral density at 4 and 8 weeks. Conclusions: These results highlight Mg-1Ga’s biocompatibility, controlled degradation, and osteogenic properties. Its optimized pore design bridges the gap between collagen membranes’ poor strength and titanium meshes’ non-degradability, offering a promising solution for GBR applications.
KW - biodegradable Mg-Ga alloy
KW - biomaterials
KW - guided bone regeneration
KW - osteogenesis
KW - porosity effect
UR - https://www.scopus.com/pages/publications/105014506726
U2 - 10.3390/biomedicines13081940
DO - 10.3390/biomedicines13081940
M3 - Article
AN - SCOPUS:105014506726
SN - 2227-9059
VL - 13
JO - Biomedicines
JF - Biomedicines
IS - 8
M1 - 1940
ER -