https://www.sciencedaily.com/releases/2026/03/260323005542.htm Referred to by Max Pemberton in Daily Mail (one time advocate of CBT/GET, hope he's changed). Tales of "normal" scans and ongoing pain. Such patients are fair game for " forget what you have ever learned about pain" merchants, when in fact a bit of PTH might help and a plausible mechanism has been elucidated.
PTH induced osteoblast Slit3 to decrease aberrant sensory innervation in degenerated vertebral endplates to relieve low back pain in mice, 2026,Zhang+
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Chandelier
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PTH induced osteoblast Slit3 to decrease aberrant sensory innervation in degenerated vertebral endplates to relieve low back pain in mice, 2026, Zhang et al.
Abstract
During aging, the spine undergoes degenerative changes, particularly with vertebral endplate bone expansion and sclerosis, that are associated with nonspecific low back pain.
We report that parathyroid hormone (PTH) treatment reduced vertebral endplate sclerosis and improved pain behaviors in three mouse models of spinal degeneration (aged, SM/J, and young lumbar spine instability mice).
Aberrant innervation in the vertebral body and endplate during spinal degeneration was decreased with PTH treatment as quantified by PGP9.5 + and CGRP + nerve fibers, as well as CGRP expression in dorsal root ganglia.
The neuronal repulsion factor Slit3 significantly increased in response to PTH treatment mediated by transcriptional factor FoxA2.
PTH type 1 receptor and Slit3 deletion in osteocalcin-expressing cells prevented PTH-reduction of endplate porosity and improvement in behavior tests.
Altogether, PTH stimulated osteoblast production of Slit3, decreased aberrant sensory nerve innervation, and provided symptomatic relief of LBP associated with mouse spinal degeneration.
Web | DOI | PMC | PDF | Bone Research | Open Access
Zhang, Weixin; Otte, Arryn D.; Wang, Zhuolun; Barik, Sisir Kumar; Wan, Mei; Cao, Xu; Crane, Janet L.
Abstract
During aging, the spine undergoes degenerative changes, particularly with vertebral endplate bone expansion and sclerosis, that are associated with nonspecific low back pain.
We report that parathyroid hormone (PTH) treatment reduced vertebral endplate sclerosis and improved pain behaviors in three mouse models of spinal degeneration (aged, SM/J, and young lumbar spine instability mice).
Aberrant innervation in the vertebral body and endplate during spinal degeneration was decreased with PTH treatment as quantified by PGP9.5 + and CGRP + nerve fibers, as well as CGRP expression in dorsal root ganglia.
The neuronal repulsion factor Slit3 significantly increased in response to PTH treatment mediated by transcriptional factor FoxA2.
PTH type 1 receptor and Slit3 deletion in osteocalcin-expressing cells prevented PTH-reduction of endplate porosity and improvement in behavior tests.
Altogether, PTH stimulated osteoblast production of Slit3, decreased aberrant sensory nerve innervation, and provided symptomatic relief of LBP associated with mouse spinal degeneration.
Web | DOI | PMC | PDF | Bone Research | Open Access