Spinal hypermobility accelerates ossification in posterior longitudinal ligaments: insights from an in vivo mouse model

Frontiers in Physiology, 2025 · DOI: 10.3389/fphys.2025.1561199 · Published: March 19, 2025

Simple Explanation

This research investigates how excessive spinal movement affects the ossification of ligaments in the spine, a condition known as OPLL, using a mouse model. The study found that increased spinal movement accelerates ligament ossification. The researchers used a novel device to induce spinal hypermobility in mice and then observed the changes in their spines using micro-CT scans and other methods. They compared a control group with groups experiencing slow and fast hypermobility. The study also examined the molecular mechanisms involved in this process, focusing on proteins and signaling pathways that promote bone formation. They found that specific proteins like DLX5 and NOTCH signaling are more active in mice with hypermobility.

Study Duration

24 weeks

Participants

Seventy-two Enpp1-deficient male mice

Evidence Level

In vivo animal model study

Key Findings

1
Spinal hypermobility accelerates the progression of ossification in mice with heterotopic ossification of spinal ligaments.
2
Excessive spinal movement leads to reduced motor function and decreased range of motion in the cervicothoracic and thoracolumbar spine.
3
The DLX5 and NOTCH signaling pathways are involved in ossification progression induced by spinal hypermobility.

Research Summary

This study investigates the impact of spinal hypermobility on the development of ossification of the posterior longitudinal ligaments (OPLL) using an in vivo mouse model. The researchers induced hypermobility in Enpp1-deficient mice and assessed the resulting changes in spinal ligaments. The key findings indicate that spinal hypermobility accelerates the progression of ossification, reduces motor function, and decreases the range of motion in the spine. Molecular analysis revealed the involvement of DLX5 and NOTCH signaling pathways in this process. The conclusion of the study is that excessive spinal movement promotes ossification in mice with heterotopic ossification, providing new insights into the pathogenesis of OPLL and suggesting potential therapeutic targets.

Practical Implications

Understanding OPLL Pathogenesis

The study provides new insights into the mechanisms of OPLL development, highlighting the role of spinal hypermobility.

Potential Therapeutic Targets

Identifying the involvement of DLX5 and NOTCH signaling pathways suggests potential targets for therapeutic interventions.

Clinical Relevance

The findings emphasize the importance of managing spinal instability in patients with OPLL to prevent disease progression.

Study Limitations

1
The effect of water as an external factor on the progression of ligament ossification in mice could not be excluded.
2
It was difficult to detect subtle changes in the ligaments of Enpp1-deficient mice.
3
The genetically deficient mice employed in this work exhibit ossification of ligament tissue throughout the body rather than only in the PLL.

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