Purpose of review: In the process of bone fracture healing, inflammation is thought to be an essential process that precedes bone formation and remodeling. We review recent studies on bone fracture healing from an osteoimmunological point of view.
Recent findings: Based on previous observations that many types of immune cells infiltrate into the bone injury site and release a variety of molecules, recent studies have addressed the roles of specific immune cell subsets. Macrophages and interleukin (IL)-17-producing γδ T cells enhance bone healing, whereas CD8+ T cells impair bone repair. Additionally, IL-10-producing B cells may contribute to bone healing by suppressing excessive and/or prolonged inflammation. Although the involvement of other cells and molecules has been suggested, the precise underlying mechanisms remain elusive. Accumulating evidence has begun to reveal the deeper picture of bone fracture healing. Further studies are required for the development of novel therapeutic strategies for bone fracture.
Keywords: Bone formation; Bone repair; Cytokine; Inflammation; Osteoblast; γδ T cell.