Bone loss already is a key danger of oral conditions such as chronic periodontitis. But patients who take the antidepressant fluoxetine are at additional risk, since the drug instructs the brain to send out signals that increase bone breakdown. A beta-blocker can intercept these signals, according to the Columbia University Medical Center.
Selective serotonin-reuptake inhibitors (SSRIs), which are broadly prescribed for mood disorders and nonpsychiatric conditions, have been associated with an increased risk of bone fracture. Fluoxetine, one of the most prescribed SSRIs, affects bone physiology through 2 mechanisms.
Initially, fluoxetine protects bone by inhibiting the cells in the skeleton that constantly break down and resorb bone. But after a few weeks of treatment, fluoxetine triggers a brain-mediated signal that not only counteracts this effect but also impairs bone formation, leading to bone loss.
The brain signals cause bone loss by increasing the amount of epinephrine in the bloodstream. Working with mice, the researchers found they could neutralize these signals by co-treating the mice with a low dose of the beta-blocker propranolol.
Bone loss, then, was no longer observed with long-term fluoxetine treatment. The mice’s behavior did not change with co-treatment either, suggesting that fluoxetine’s effect on the brain and mood was not impaired. Adding low-dose propranolol to depression treatment could potentially block the SSRI’s effect on bone mass, the researchers said.
The study, “Serotonin-Reuptake Inhibitors Act Centrally to Cause Bone Loss in Mice by Counteracting a Local Anti-Resorptive Effect,” was published by Nature Medicine.
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