Senescent cells release a coordinated arsenal of inflammatory cytokines, growth factors, and matrix enzymes—collectively called SASP—that systematically guides fracture repair through four distinct phases. During inflammation, CCL2 and pro-inflammatory signals recruit immune cells. In soft-callus formation, PDGF and VEGF position stem cells and build blood vessels. Hard-callus development relies on TGF-β and matrix proteases MMP-9/13 to convert cartilage to bone. Finally, remodeling couples bone breakdown with formation through regulated SASP signaling. This represents a paradigm shift from viewing cellular senescence as purely detrimental to recognizing it as an essential coordinator of tissue repair. The critical insight is timing: transient SASP activation facilitates healing, while sustained overproduction blocks proper bone remodeling. This framework explains why fracture healing deteriorates with age—accumulated senescent cells likely shift from beneficial acute SASP to harmful chronic secretion. The stage-specific nature suggests therapeutic windows where selectively eliminating senescent cells might enhance healing, while preserving them during early repair phases could be beneficial.