🟢Under physiological conditions, sympathetic neurons release DBH (dopamine β‑hydroxylase), which catalyzes the conversion of dopamine to norepinephrine. Part of DBH is released into the bloodstream and can reflect systemic sympathetic tone. Norepinephrine binds to β2‑adrenergic receptors on osteoblasts/osteocytes, maintaining the balanced expression of RANKL/OPG, ensuring normal osteoclast differentiation, preserving jaw‑bone remodeling, and resisting osteonecrosis.

🔴Under the pathological condition of MRONJ, patients exhibit markedly reduced circulating DBH levels, indicating impaired sympathetic regulation. Downstream signaling of β2‑receptors is attenuated, the RANKL/OPG ratio declines, and osteoclast differentiation is excessively suppressed. Combined with the anti‑resorptive drug zoledronic acid, a superimposed inhibitory effect occurs, greatly elevating the risk of jaw osteonecrosis; propranolol‑mediated β‑receptor blockade further aggravates osteonecrotic injury.

This study establishes a complete evidence chain of “clinical proteomics → independent cohort plus UK Biobank population validation → animal models → cell co‑culture”. As a candidate circulating biomarker, DBH builds a bridge linking sympathetic nerves and bone pathology.

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