Histological aspects of bone fracture healing

Bone fracture healing is a multistep phenomenon leading to full restoration of the damaged tissue. It replicates the events that happen during endochondral bone formation in prenatal life. The mechanisms which control bone fracture healing are basically the same as those regulating bone formation in the embryo. For bone fracture healing the first phase is the most important, i.e. blood clot formation, followed by the inflammatory reaction. During this phase the platelet-derived growth factors (PDGF), released from the blood clot and from the inflammatory cells, recruit and activate mesenchymal cells to differentiate into cartilage-forming cells. The hyaline cartilage thus formed is the scaffolding for endochondral osteogenesis. Periosteal cells also participate in hyaline cartilage formation. Endochondrally-formed bone (primary bone) is woven bone and has poor mechanical properties. It is replaced by lamellar bone by the process of 'bone modelling'. Primary bone trabeculae are resorbed by osteoclasts whilst mesenchymal-derived osteoblasts synthetise osteoid for bone lamellae (secondary bone). The stromal cells of bone marrow are an additional source of bone forming cells capable of differentiating into osteoblasts. The application of non steroid anti- inflammatory drugs (NSAID) impairs the early inflammatory phase and delayes bone fracture healing, by inhibiting the formation of prostaglandins - one of many factors which activate both osteoblasts and osteoclasts.