A dream came true!! Our paper: "Neutrophil-derived catecholamines mediate negative stress effects on bone" is now published in @NatureComms 🎉
This work is a joint project from my group at @OrthoLabUlm & @MolPsySoUlm! A fantastic cross-discipline collaboration!
A thread:
We found out earlier that chronic psychosocial stress during adulthood disturbs long bone growth and fracture healing in mice: doi.org/10.1073/pnas.1…
But the question was: what is the mechanism? We answered that in our latest study. Stress leads to catecholamine production ...
... in local immune cells in the bone marrow and the fracture callus. These catecholamines disturb endochondral ossification via the beta2-adrenoreceptor on chondrocyte-derived cells in mice. Most importantly, we could confirm this also in human samples:
Fracture patients...
...Fracture patients with high pre-existing mental trauma load display increased levels of tyrosine hydroxylase TH (=catecholamine production) in the fracture hematoma. AND TH levels correlated with pain and mobility impairment up to 12 months after ankle fracture! #orthotwitter
... This indicates that mental trauma/stress patients experienced before an orthopaedic injury interferes with regeneration!
We thank all collaborators: the clinics for psychosomatic medicine and for trauma surgery at @uni_ulm Ulm University Medical Center and all Ulm/international collaborators!