Traumatic brain injury stimulates sympathetic tone-mediated bone marrow myelopoiesis to favor fracture healing.

Abstract in brief

• Traumatic brain injury (TBI) accelerates fracture healing by increasing sympathetic nervous system activity, which stimulates the bone marrow to produce anti-inflammatory immune cells, especially M2 macrophages, aiding the healing process.
• Blocking sympathetic signaling or deleting specific adrenergic receptors (Adrb2 and Adrb3) reduces this effect, impairing the proliferation of hematopoietic stem cells and the beneficial M2 macrophage response needed for faster fracture healing.
• The study suggests that targeting adrenergic signals could be a promising approach to improve fracture healing, highlighting the critical role of the nervous system in bone repair.]