Abstract
Fracture healing is the most common regeneration form in clinical practice. Bone as a tissue has the unique ability to heal itself without forming a scar. After the fracture, a chain of healing reactions is activated, both at the cellular and tissue level, that lead to full bridging of the gap between the two bony ends of the fracture. There are many immune cells that take part in this healing process and they play a significant role. There are three sequential phases to the process of fracture healing that remain independent. It has been revealed that the immune cells take part not only in the inflammation phase but also in the repair phase, where some of these cells act as intermediates to the transformation of soft callus to hard callus. In conclusion, immune cells serve as initial responders at the site of injury, restore vasculature, and initiate cascades of signals to recruit cells to carry out the repair processes. Thus the immune system can be considered a promising therapeutic target for bone fracture healing.
Highlights
BackgroundBone is a tissue that has a unique ability to heal itself without forming a scar [1]
This interaction between bone cells and constituents of the immune system involved in bone repair remains of great scientific interest to researchers and clinicians [6], as it is known that bone fracture healing is under the control of the immune system [4]
Bone fracture healing consists of three phases: inflammation, repair and remodeling
Summary
Bone is a tissue that has a unique ability to heal itself without forming a scar [1]. Various immune cells, including neutrophils, macrophages and lymphocytes, infiltrate this hematoma [8] These cells are believed to be activated by molecules derived by the injured tissues, and after activation these cells release pro-inflammatory cytokines at the injury site to elicit acute inflammation [4]. While the inflammation response lasts for a short time, the effects of the immune cells extend beyond the early stages of fracture [1] These immune cells are believed to be activated by molecules derived from the damaged tissues and these cells release pro-inflammatory cytokines at the injury site to elicit acute inflammation [4]. A 2015 study suggests that M1 macrophages preferentially infiltrate into the bone fracture site in the acute phase, while M2 macrophages increase in number in the subacute phase [30] Both M1 and M2 macrophages play significant roles in the healing process by regulating the early and later phases. Despite the fact that CD8+ T cells can produce TNF-α and interferon (IFN)-γ, which suppress the mineralization of bone marrow mesenchymal stem cells (MSCs), the precise mechanisms remain unclear [4]
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