The article reviews the role of inflammation in bone repair, focusing on the interactions between inflammatory cells (polymorphonuclear leukocytes and monocyte-macrophage-osteoclast lineage) and bone healing cells (mesenchymal stem cell-osteoblast lineage and vascular lineage). Acute inflammation, initiated by endogenous or exogenous stimuli, can become chronic if not resolved, leading to increased bone resorption and suppressed bone formation. The review highlights the importance of crosstalk between these cell types in bone formation, repair, and remodeling. It also discusses the clinical significance of bone loss and repair, emphasizing the need for a deeper understanding of the underlying mechanisms to improve treatment outcomes. The article further explores the stages of fracture healing, including primary and secondary fracture healing, and the factors that influence their success. Additionally, it examines the interactions between inflammatory cells and bone cells, such as macrophages and osteoblasts, and how these interactions can be modulated to enhance bone repair. Finally, the article outlines potential therapeutic strategies for improving bone repair by modulating inflammation, particularly in conditions like fragility fractures, fracture non-unions, osseointegration of implants, and bone defect reconstruction.The article reviews the role of inflammation in bone repair, focusing on the interactions between inflammatory cells (polymorphonuclear leukocytes and monocyte-macrophage-osteoclast lineage) and bone healing cells (mesenchymal stem cell-osteoblast lineage and vascular lineage). Acute inflammation, initiated by endogenous or exogenous stimuli, can become chronic if not resolved, leading to increased bone resorption and suppressed bone formation. The review highlights the importance of crosstalk between these cell types in bone formation, repair, and remodeling. It also discusses the clinical significance of bone loss and repair, emphasizing the need for a deeper understanding of the underlying mechanisms to improve treatment outcomes. The article further explores the stages of fracture healing, including primary and secondary fracture healing, and the factors that influence their success. Additionally, it examines the interactions between inflammatory cells and bone cells, such as macrophages and osteoblasts, and how these interactions can be modulated to enhance bone repair. Finally, the article outlines potential therapeutic strategies for improving bone repair by modulating inflammation, particularly in conditions like fragility fractures, fracture non-unions, osseointegration of implants, and bone defect reconstruction.