A common cause of bone loss is an overactive parathyroid gland, which doctors usually treat with surgery. New research on how excess parathyroid hormone affects immune cells suggests that doctors could repurpose existing drugs to treat hyperparathyroidism without surgery.
The results were publishedÂ October 8 inÂ Cell Metabolism. [My apologies for not posting thisÂ in October.]
“Surgery is sometimes not an appropriate remedy for hyperparathyroidism because of the condition of the patient, and it is also expensive,” says lead author Roberto Pacifici, MD. “Also, the one pharmacological treatment that is available, cinacalcet, is not always the ideal solution. This work could potentially lead to alternatives.”
Roberto Pacifici, MD
Researchers at Emory University School of Medicine led by Pacifici teamed up with doctors from the University of Turin in Italy, combining observations of human patients with an overactive parathyroid with experiments on mice.
The drugs identified as potential treatments are: calcium channel blockers, now used to treat high blood pressure, and antibodies that block the inflammatory molecule IL-17A, under development for the skin disease psoriasis. Clinical trials would be necessary to show that these drugs are effective against parathyroid hormone-induced bone loss in humans. Read more
Neale Weitzmann and George Beck have been publishing a series of papers describingÂ how silica nanoparticles can increase bone mineral density in animals. Their findings could someday form the basis for a treatment for osteoporosis.
In 2012, we posted an article and video on this topic. We wanted to call attention to a few of theÂ team’sÂ recent papers, one of which probes the mechanism for aÂ remarkable phenomenon: how can very fine silica particles stimulate bone formation?
The particlesâ€™ properties seem to depend on their size: 50 nanometers wide â€“ smaller than a HIV or influenza vision.Â In a 2014 ACS Nano paper, Beck, Weitzmann and postdoc Shin-Woo Ha show that the particles interact with particular proteins involved in the process of autophagy, a process of â€œself digestionâ€ induced by stress.
â€œThese studies suggest that it is not the material per se that stimulates autophagy but rather size or shape,â€ they write. Read more
Iâ€™d like to highlight a paper in PLOS One from anesthesiologists Shan Ping Yu and Ling Weiâ€™s group that was published earlier this year. [Sorry for missing it then!] They are investigating potential therapies for stroke, long a frustrating area of clinical research. The â€œclot-bustingâ€ drug tPA remains the only FDA-approved therapy, despite decades of work on potential neuroprotective agents.
Yuâ€™s team takes a different tactic. They seek to bolster the brainâ€™s recovery powers after stroke by mobilizing endogenous progenitor cells. I will call this approach â€œstem cells lite.â€
PTH appears to encourage new neurons in recovery in a mouse model of ischemicÂ stroke. Green = recent cell division, red = neuronal marker
It is similar to that taken by cardiologistÂ Arshed Quyyumi and colleagues with peripheral artery disease: use a growthÂ factorÂ (GM-CSF), which is usually employed for another purpose, to get the bodyâ€™s own regenerative agents to emerge from the bone marrow.
In this case, Yuâ€™s team wasÂ using parathyroid hormone (PTH), which is an FDA-approved treatment for osteoporosis. They administered it, beginning one hour after loss of blood flow, in a mouse model of ischemic stroke. They foundÂ that daily treatment with PTH spurs production of endogenousÂ regenerative factors in the stroke-affected area of the brain. They observed both increased new neuron formation and sensorimotor functional recovery. However, PTH does not pass through the blood-brain barrier and does not change the size of the stroke-affected area, the researchers found.
The conclusion of the paper hints at their next steps:
As this is the first report on this PTH therapy for ischemic stroke for the demonstration of the efficacy and feasibility, PTH treatment was initiated at 1 hr after stroke followed by repeated administrations for 6 days. We expect that even more delayed treatment of PTH, e.g. several hrs after stroke, can be beneficial in promoting chronic angiogenesis and other tissue repair processes. This possibility, however, remains to be further evaluated in a more translational investigation.