Bone Drug Already on Pharmacy Shelves May Treat Chronic Back Pain

Millions of Americans know the grinding reality of chronic low back pain: the morning stiffness, the careful maneuvering to tie shoes, the cancelled plans because standing or sitting too long becomes unbearable. Current treatments offer little beyond anti-inflammatories, muscle relaxants, and advice to keep moving through the discomfort.

Now researchers at Johns Hopkins University have discovered that a medication already sitting in pharmacy aisles might tackle this pain in an entirely new way. Parathyroid hormone (PTH), approved since 2002 for strengthening bones in osteoporosis patients, reduced pain in three different mouse models of spinal degeneration by altering bone signals in a way that keeps pain-sensing nerves from growing into damaged tissue.

The findings, published in Bone Research, could shorten the path to clinical testing since PTH-based drugs like teriparatide and abaloparatide already have two decades of safety data. Between 28% and 42% of Americans ages 40 to 69 experience chronic low back pain, costing the U.S. healthcare system over $100 billion annually, yet few treatments address the underlying biology driving those pain signals.

Dr. Janet Crane’s team tested PTH injections on aged mice, young mice with surgically damaged spines, and a genetically modified strain prone to premature disc problems. Across all three groups, daily PTH treatment for one to two months reduced bone porosity in vertebral endplates, thin layers of bone separating spinal discs from vertebrae. More importantly, treated mice tolerated more pressure on their lower backs, ran greater distances voluntarily, and showed increased tolerance to heat applied to their paws.

How Aging Spines Become Pain Generators

As spines age or sustain repeated stress, vertebral endplates undergo damaging changes. Cartilage calcifies, bone becomes porous, and cells that break down bone, called osteoclasts, create openings in the endplate structure. Some of these osteoclasts become senescent, or aged and dysfunctional, and secrete factors including a protein called Netrin-1 that works like a homing beacon for sensory nerve fibers.

The nerves follow that signal and grow into porous bone regions where they don’t belong, detecting acidic byproducts and stress signals from damaged tissue. The brain interprets this as constant pain, even without acute injury. More osteoclast activity creates more pores, more Netrin-1, and more wayward nerves in a vicious cycle.

Dr. Crane’s earlier work showed that eliminating senescent cells in degenerating mouse spines decreased sensory innervation and reduced pain. But the new study reveals PTH works through a different route entirely.

A Molecular “Keep Out” Sign

When exposed to PTH, bone-building cells called osteoblasts ramp up production of a protein named Slit3. This protein acts as a repellent signal, essentially posting “keep out” signs around damaged bone regions that tell growing nerve fibers to turn back.

Laboratory experiments confirmed the mechanism. When researchers added PTH to cultured osteoblast cells, Slit3 production increased in a dose-dependent manner. They then added this PTH-treated cell medium to dishes containing sensory neurons from dorsal root ganglia, clusters of nerve cell bodies near the spinal cord where pain signals originate. The nerve fibers grew shorter. When scientists blocked Slit3 with antibodies, the nerve fibers grew longer again.

The team engineered mice lacking either the PTH receptor or the Slit3 gene specifically in osteoblasts. When these modified mice underwent spine instability surgery and received PTH injections, the treatment showed no significant improvement in most measures. Their endplates remained porous, pain behaviors didn’t meaningfully change, and nerve fiber density stayed elevated. PTH required functional osteoblasts producing Slit3 to work.

The research offers a biological explanation for observations from earlier osteoporosis trials. Some patients taking teriparatide or abaloparatide reported back pain improvements, though the drugs were prescribed solely to prevent fractures. Those trials weren’t designed to measure pain, and results varied between studies. This research suggests those patient reports may have reflected genuine biological changes, not just placebo effects.

From Lab Mice to Human Patients

Repurposing an approved drug offers major advantages. The FDA approval process for new compounds takes 10 to 15 years and costs billions. Repurposed drugs bypass early safety studies since their risks, drug interactions, and dosing ranges are established.

Both teriparatide (Forteo) and abaloparatide (Tymlos) require daily self-injections and typically cost several thousand dollars monthly, though insurance often covers them for osteoporosis patients meeting specific criteria.

Several questions remain before doctors could prescribe PTH specifically for chronic back pain. The mouse studies didn’t determine minimum effective doses or whether less frequent injections work. Researchers also didn’t examine whether stopping treatment allows nerve fibers to regrow and pain to return.

Future clinical trials will need to carefully screen participants. Previous osteoporosis studies enrolled patients based on bone density without screening for spinal degeneration patterns. Trials testing PTH for pain relief might use advanced imaging to identify patients with porous endplates, the specific pathology PTH improved in mice.

Chronic low back pain has multiple causes: muscle strain, herniated discs, arthritis, spinal stenosis, nerve compression. PTH would likely help only patients whose pain stems from endplate degeneration and aberrant nerve growth in porous bone. Dr. Crane noted that trials specifically designed to measure pain as a primary outcome, with standardized assessments and imaging before and after treatment, would determine which patients benefit most.

The mixed results from earlier trials suggest patient selection matters. Not everyone with back pain will respond, but for the subset whose pain comes from degenerating endplates attracting wayward nerves, PTH might address the biological source rather than masking symptoms.

What Comes Next

The research reframes chronic skeletal pain as a communication problem between bone cells and nerves. Treatments that modify those chemical conversations by adjusting osteoclast activity or boosting osteoblast Slit3 production might work better than current approaches focused solely on symptom management.

For patients, the practical takeaway is straightforward: a medication already available could potentially treat chronic back pain by targeting its source. It would still require prescription and monitoring, but doctors could eventually consider prescribing it once trials establish efficacy and clear protocols.

Whether that happens depends entirely on future clinical studies specifically testing PTH’s pain-relieving effects in people with documented spinal degeneration. If those trials succeed, millions of Americans might find relief from a medication that’s been available for over twenty years, just prescribed for a different purpose.

Repurposing an existing medication offers a faster, cheaper path than developing entirely new drugs. For researchers, patients, and healthcare systems managing one of America’s costliest medical complaints, PTH’s unexpected potential as a pain reliever could provide relief hiding in plain sight.

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DISCLAIMER: This article reports on preclinical research conducted in mouse models. The findings have not been tested or confirmed in human clinical trials. This information is intended for educational purposes only and should not be used as a basis for medical decisions. Anyone experiencing chronic low back pain should consult with a qualified healthcare provider for diagnosis and treatment options. Do not start, stop, or change any medication without consulting your physician.

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