Bone fracture healing is a complex, dynamic process that involves a range of cellular interactions critical for successful tissue regeneration. Building on our previous single-cell RNA sequencing (scRNA-seq) studies, which mapped the cellular components of mouse fracture callus, this study employs spatial transcriptomics to elucidate the precise locations and interactions of these cells in a mouse model. We utilized an optimized decalcification method with Morse's solution to significantly improve RNA quality, thereby enhancing the sequencing output from mouse femur fractures. By applying the Visium CytAssist platform and integrating analyses with the CARD and SPATA2 frameworks, we have been able to derive detailed insights into the cellular composition and interactions within each spatial spot. Our approach identified distinct cellular clusters that delineate the transition from the inflammatory response to bone remodeling. Through this spatial mapping, we tracked the roles and differentiation trajectories of mesenchymal progenitor cells (MPCs), uncovering pivotal signaling pathways such as RANKL and Spp1. These pathways are crucial for cellular communication and play essential roles in bone regeneration. This study not only advances our understanding of the cellular and molecular mechanisms underpinning fracture healing but also demonstrates the potential of spatial transcriptomics as a powerful tool for identifying therapeutic targets. These insights pave the way for future research aimed at optimizing fracture management and developing targeted interventions to enhance bone repair in clinical settings.