Pathophysiological mechanism of acute bone loss after fracture.

BACKGROUND

Acute bone loss after fracture is associated with various effects on the complete recovery process and a risk of secondary fractures among patients. Studies have reported similarities in pathophysiological mechanisms involved in acute bone loss after fractures and osteoporosis. However, given the silence nature of bone loss and bone metabolism complexities, the actual underlying pathophysiological mechanisms have yet to be fully elucidated.

AIM OF REVIEW: To elaborate the latest findings in basic research with a focus on acute bone loss after fracture. To briefly highlight potential therapeutic targets and current representative drugs. To arouse researchers' attention and discussion on acute bone loss after fracture.

KEY SCIENTIFIC CONCEPTS OF REVIEW: Bone loss after fracture is associated with immobilization, mechanical unloading, blood supply damage, sympathetic nerve regulation, and crosstalk between musculoskeletals among other factors. Current treatment strategies rely on regulation of osteoblasts and osteoclasts, therefore, there is a need to elucidate on the underlying mechanisms of acute bone loss after fractures to inform the development of efficacious and safe drugs. In addition, attention should be paid towards ensuring long-term skeletal health.