Bone regeneration declines with age in part because osteoblasts lose mitochondrial metabolic fitness, a defect that conventional osteoconductive scaffolds do not address. The metabolic dysfunction that connects osteoblast senescence to failed repair, however, remains poorly defined. Here, we identify mitochondrial phosphoenolpyruvate carboxykinase 2 (PCK2) as a regulator of aged bone regeneration and use this insight to design a local poly(lactic acid)/nano-hydroxyapatite (PLA/nHA) scaffold plus systemic metformin strategy. In senescent hBMSCs and osteoblast-specific Pck2 conditional knockout mice, PCK2 loss reduced oxidative phosphorylation and ATP production, increased mitochondrial superoxide, activated p53/p21-associated senescence, and impaired osteogenic differentiation. PLA/nHA provided a degradable osteoconductive matrix and sustained calcium/phosphate release, whereas metformin supported mitochondrial metabolic recovery. In combination, the treatment restored mitochondrial respiration and ultrastructure, reduced ROS accumulation, normalized senescence markers, and recovered osteogenesis without altering cell viability. In aged femoral defects, PLA/nHA/metformin reduced local senescence and accelerated new bone formation, with the clearest effect in Pck2-deficient mice. These findings place the PCK2-mitochondria axis upstream of osteoblast senescence in aged bone repair and show that scaffold-based regeneration can be strengthened by correcting the metabolic state of the repair niche.