Abstract: Bone marrow adipocytes (BMAds) transition from metabolically quiescent cells to inflammatory active cells during aging, emerging as critical pathological drivers of skeletal aging. They disrupt the bone marrow microenvironment through multiple mechanisms, including the secretion of senescence-associated secretory phenotype factors, activation of the receptor activator of nuclear factor-κB ligand signaling, perturbation of the nicotinamide adenine dinucleotide-sirtuin1 metabolic axis, and induction of mesenchymal stem cell fate drift. These processes collectively suppress osteogenesis, promote osteoclastogenesis, and accelerate bone loss and deterioration.This review systematically analyzes the interactive network between BMAds senescence and mesenchymal stem cell dysfunction, as well as their causal relationship in bone degeneration. Furthermore, based on emerging intervention strategies such as senolytics/senomorphics and metabolic reprogramming, we propose that multi-mechanistic synergistic targeting of BMAds aging and SASP propagation may represent a novel approach to delaying skeletal aging. This work aims to provide theoretical foundations and intervention pathways for both fundamental research on bone aging and translational regenerative medicine.