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Patients with bone fractures have a 10 to 15 percent risk that the fracture will not heal adequately after undergoing state-of-the-art surgery. Paradoxically, bones heal much more readily in such patients with concomitant traumatic brain injury. Up until now, the reason for this has been largely unclear. Understanding this phenomenon opens up the possibility of therapeutically using the underlying mechanisms to improve bone healing in pseudarthrosis patients. Over the past eight years, trauma surgery researchers from the Center for Musculoskeletal Surgery of Charité – Universitätsmedizin Berlin, from University Medical Center Hamburg-Eppendorf (UKE) and from the Berlin Institute of Health at Charité (BIH), have intensively studied the phenomenon together, concluding that it is caused by an increased activation of receptors in the sympathetic nervous system, specifically the beta-adrenergic receptors in the periosteum. This improves vascularization, leading to better flood flow to the bone fracture during the healing process, while also accelerating the formation and remodeling of bone tissue in the fracture gap.

Several BIH research groups were involved in the research, which was made possible in part by funding from the Clinician Scientist Program and the Junior Clinician Scientist Program as well as through collaboration with the Julius Wolff Institute for Biomechanics and Musculoskeletal Regeneration, the BIH Center for Regenerative Therapies (BCRT) and the BIH Core Unit Bioinformatics. The trauma surgery researchers have now published their findings in the journal Science Translational Medicine. The experimental and clinical data collected not only indicate that patients receiving beta-blocker therapy may exhibit impaired fracture healing, but also show that the use of beta-adrenergic stimulants, which have long been used to treat asthma or COPD, could be an effective local therapy for impaired bone healing.

Literature: Jahn, Knapstein, Otto, Köhli et al. “Increased β2-adrenergic signaling promotes fracture healing through callus neovascularization in mice.” Science Translational Medicine, 2024. DOI: 10.1126/scitranslmed.adk912