Abstract: Bone aging represents the core manifestation of systemic aging within the skeletal system. Its fundamental feature lies in the irreversible disruption of the dynamic balance between bone formation and bone resorption, leading to progressive bone loss and degenerative changes in bone microstructure. This review systematically elucidates that the process of bone aging is driven by a multi-layered cellular and molecular regulatory network. At the cellular level, it is primarily characterized by the functional decline of osteoblasts and osteocytes, along with an enhanced tendency of bone marrow mesenchymal stem cells to differentiate into adipocytes, ultimately resulting in decreased bone formation capacity and abnormal accumulation of bone marrow fat. At the molecular level, mitochondrial dysfunction plays a central role: energy metabolism disturbances, reactive oxygen species accumulation, and impaired quality control triggered by mitochondrial damage not only directly impair cellular function but also exacerbate the local chronic inflammatory microenvironment in the bone marrow through pathways such as cGAS-STING. Meanwhile, imbalances and functional attenuation of multiple key signaling pathways collectively determine the metabolic reprogramming and senescent phenotype of cells. These alterations are interconnected and mutually amplified, forming a vicious cycle that progresses from intracellular energy metabolism disorders to dysregulation of the local immune microenvironment, ultimately culminating in structural and functional failure at the organ level.