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Fracture Repair: Its Pathomechanism and Disturbances

Healing of the bone fracture is a biological process that is based on various cell lineages recruited, activated and regulated by molecular mediators, namely chemokines, growth factors, and cytokines, cooperating in a cascade of events aimed to fill the fracture gap with callus. Remodeling of the callus rebuilds the microarchitecture to the mature bone— cancellous or compact, depending on the type of the bone that was primarily at the frac- ture gap. Restitution of the bone continuity requires activation of mesenchymal stem cells that transform into osteoblasts and mature into osteocytes. It is activated and regulated by molecules released from blood platelets from posttraumatic hematoma, traumatized tissues, nerve endings, and inflowing inflammatory cells. The significance of the inflam - matory cells in this process is inappreciable, as they eradicate pathogens, remove wound debris, and supply the fracture gap with molecules regulating forthcoming cellular events. They also provide immune regulation of the healing. To proceed uneventfully, healing requires an adequate bone contact and biomechanical environment, proper oxy- genation, and nutrition. Unfortunately, up to 15% of bone fractures show some kinds of disturbances that may result in cessation of reparative processes leading to non-union. Factors, responsible for that, are brought to date based on current literature and clinical observations.