Study Finds Bone‑Loss Hormone May Block Source of Chronic Back Pain

Researchers at Johns Hopkins University report that parathyroid hormone (PTH) — already FDA‑approved for osteoporosis — prevented and even reversed the abnormal growth of pain‑sensing nerves into damaged spinal tissue in animal models, a process thought to underlie much chronic low‑back pain. Led by Dr. Janet L. Crane, the team found that one to two months of PTH treatment made vertebral endplates denser and more stable and prompted bone‑building osteoblast cells to release a protein called Slit3, which repels invading nerve fibers. When Slit3 was removed in mice, PTH’s pain‑relieving effect disappeared, indicating the protein is critical to how the hormone acts on spinal nerves. Because some osteoporosis patients on PTH have reported unexpected relief from back pain, the findings offer a plausible biological explanation and suggest the drug could be repurposed as a disease‑modifying therapy rather than just a symptom reliever. The scientists stress that the work is preclinical and carries limitations, including possible central‑nervous‑system effects not yet studied, but say it lays the groundwork for human trials that could eventually change how chronic back pain is treated in the U.S.