What it is
Researchers profiled the dorsal root ganglia neurons that innervate mouse bone using single-cell transcriptomics, before and after fracture, and find that CGRP+ and Aβ-Field LTMR neurons are the most represented classes of bone-innervating neurons. As repair proceeds through its phases, these sensory neurons shift their response and express morphogens including Tgfb1, Fgf9, and Shh. Removing the innervation produces poor bone repair, with defective mesenchymal cell proliferation and osteodifferentiation. The work identifies FGF9 as a major regulator of fracture repair that can be leveraged to promote bone healing.
Why it matters
Sensory neurons were known to carry fracture pain and to be required for regeneration, but the neuronal classes innervating bone and the signals they supply were uncharacterized. Profiling those neurons and naming FGF9 as a major regulator of fracture repair shows where the sensory contribution to healing acts.
How to read this
It points to FGF9 and the sensory-neuron signals around it as targets for promoting bone repair after fracture.
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