Fracture healing is a complex physiological process involving a coordinated interaction of hematopoietic and immune cells within the bone marrow, in conjunction with vascular and skeletal cell precursors. Multiple factors regulate this cascade of molecular events, which affects different stages in the osteoblast and chondroblast lineage during processes such as migration, proliferation, chemotaxis, differentiation, inhibition, and extracellular protein synthesis. A clear understanding of the cellular and molecular pathways in fracture healing is not only critical for advancing fracture treatment, but it may also enhance further our knowledge of the mechanisms involved within skeletal growth and repair, as well as the mechanisms of aging. An overview of the important molecules involved in fracture healing, including osteogenic autocoids and inhibitory molecules, and their interactions and possible mechanisms of synergy during the healing process is presented in this article.