Abstract

PRéCIS- A wound, or tissue defect can be defined as a disruption in the normal structure and function that occurs due to internal or external injury. In tissue bioengineering, natural hemostasis, and the inflammatory phase stand at the beginning of the wound and defect healing cascade. Briefly, the restorative, regenerative or reparative response to tissue injury is governed/driven by resident and circulating cells, homing to the injury site that release signals (soluble mediators) generated from the extracellular matrix. For bone defects, optimal healing can be simply classified as either primary (1o) or secondary (2o). It undergoes acascade of complex, orderly, and predictable events, that include four/five over-lapping phases: hemostasis/haematoma formation, inflammation, proliferation, callus formation (or not), and remodeling (Haversian/osteonal bone remodelling). Herein, the bone healing type is dependent on the removal of a fracture haematoma and the fixation (stabilization) strategy performed. For example, optimal stability results in 1o bone healing, with no callus formation, normal bone architecture and functional integrity restored within 3 months. On the other hand, in 2o healing, where fixation is not done, fracture haematoma, callus formation and healing via endochondral ossification ensues. Despite limitations, the main alternative for damaged or lost bone tissue replacement, restoration, regeneration, reconstruction, or repair is the autogenous bone graft, to date.

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