Continuous mechanical compression-induced intervertebral disc degeneration and pain in the caudal spine in rats.
5 affiliations
- 1Department of Orthopedics, The First People's Hospital of Yunnan Province, Kunming, 651000, China.
- 2Department of Anesthesiology, 920th Hospital of Joint Logistic Support Force, Kunming, 650032, China.
- 3Kunming Medical University, Kunming, Yunnan, 650500, China.
- 4Department of Neurology, Affiliated Hospital of Yunnan University, Kunming, Yunnan, 650021, China. [email protected].
- 5Department of Orthopedics, The First People's Hospital of Yunnan Province, Kunming, 651000, China. [email protected].
Abstract
Background
Chronic low back pain imposes substantial social and economic burdens due to its rising prevalence and associated disability. Intervertebral disc degeneration is the primary driver of discogenic back pain, though the mechanistic links between degenerative changes and persistent pain remain incompletely defined. Aberrant mechanical loading is recognised as a key trigger of disc degeneration. This work built a caudal spine compression rat model to explore how the P2Y2 receptor mediates load-induced disc degeneration and associated pain.Methods
Fifty-six eight-week-old male laboratory rats were randomised into four cohorts: 2-week sham surgery, 2-week axial compression, 3-week sham surgery, and 3-week axial compression. An external fixator delivered 8 N continuous caudal spine compression to experimental animals, while sham rats received identical implantation without compressive force. Degenerative severity was evaluated via magnetic resonance imaging and two histological staining protocols. Von Frey filament testing measured mechanical pain sensitivity at baseline and multiple time points after device removal. Immunofluorescence and Western blotting detected target protein levels within degenerative disc tissue collected from both human surgical patients and experimental rats.Results
Intervertebral disc degeneration was markedly aggravated after two weeks of compression and worsened further with three weeks of sustained loading. Sham-operated rats only had transient mechanical hypersensitivity at day 3 and fully recovered by days 9-15. By contrast, compressed rats maintained persistently lowered pain thresholds over the whole observation window. The P2Y2 receptor was elevated in degenerative disc tissue and co-localised with YAP and TAZ in human and rat disc core cells. In human samples, receptor levels rose alongside advancing degeneration; YAP and TAZ were elevated in moderately degenerated tissue and decreased in severely degenerated specimens.Conclusions
Prolonged mechanical compression of the rat caudal spine produces disc degeneration and pain. The findings suggest that the P2Y2 receptor and downstream Hippo pathway mediators YAP and TAZ are involved in the degenerative process, offering a basis for future mechanistic studies.
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BibTeX
@article{chen2026continuous,
title = {{Continuous mechanical compression-induced intervertebral disc degeneration and pain in the caudal spine in rats.}},
author = {Fei Chen and Na Li and Junjie Pu and Yiling Deng and Junhui Qi and Fanyi Kong and Jiayu Chen},
journal = {BMC musculoskeletal disorders},
year = {2026},
month = jul,
doi = {10.1186/s12891-026-10252-x},
url = {https://europepmc.org/article/MED/42902307},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Continuous mechanical compression-induced intervertebral disc degeneration and pain in the caudal spine in rats.
AU - Fei Chen
AU - Na Li
AU - Junjie Pu
AU - Yiling Deng
AU - Junhui Qi
AU - Fanyi Kong
AU - Jiayu Chen
PY - 2026
DA - 2026/07/01
JO - BMC musculoskeletal disorders
DO - 10.1186/s12891-026-10252-x
UR - https://europepmc.org/article/MED/42902307
AB - Background Chronic low back pain imposes substantial social and economic burdens due to its rising prevalence and associated disability. Intervertebral disc degeneration is the primary driver of discogenic back pain, though the mechanistic links between degenerative changes and persistent pain remain incompletely defined. Aberrant mechanical loading is recognised as a key trigger of disc degeneration. This work built a caudal spine compression rat model to explore how the P2Y2 receptor mediates load-induced disc degeneration and associated pain.Methods Fifty-six eight-week-old male laboratory rats were randomised into four cohorts: 2-week sham surgery, 2-week axial compression, 3-week sham surgery, and 3-week axial compression. An external fixator delivered 8 N continuous caudal spine compression to experimental animals, while sham rats received identical implantation without compressive force. Degenerative severity was evaluated via magnetic resonance imaging and two histological staining protocols. Von Frey filament testing measured mechanical pain sensitivity at baseline and multiple time points after device removal. Immunofluorescence and Western blotting detected target protein levels within degenerative disc tissue collected from both human surgical patients and experimental rats.Results Intervertebral disc degeneration was markedly aggravated after two weeks of compression and worsened further with three weeks of sustained loading. Sham-operated rats only had transient mechanical hypersensitivity at day 3 and fully recovered by days 9-15. By contrast, compressed rats maintained persistently lowered pain thresholds over the whole observation window. The P2Y2 receptor was elevated in degenerative disc tissue and co-localised with YAP and TAZ in human and rat disc core cells. In human samples, receptor levels rose alongside advancing degeneration; YAP and TAZ were elevated in moderately degenerated tissue and decreased in severely degenerated specimens.Conclusions Prolonged mechanical compression of the rat caudal spine produces disc degeneration and pain. The findings suggest that the P2Y2 receptor and downstream Hippo pathway mediators YAP and TAZ are involved in the degenerative process, offering a basis for future mechanistic studies.
SN - 1471-2474
ER -