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  4. Peripheral denervation participates in heterotopic ossification in a spinal cord injury model

Peripheral denervation participates in heterotopic ossification in a spinal cord injury model

PLoS ONE, 2017 · DOI: https://doi.org/10.1371/journal.pone.0182454 · Published: August 30, 2017

Spinal Cord InjuryNeurologyMusculoskeletal Medicine

Simple Explanation

This study investigates how nerve damage outside the spinal cord (peripheral denervation) affects the formation of new bone in soft tissues (heterotopic ossification, HO) after a spinal cord injury (SCI). The study uses a mouse model to mimic these conditions. The researchers surgically cut nerves in the hind limbs of mice with SCI and then injected a toxin to cause muscle injury. They then compared bone formation in the denervated limbs to the non-denervated limbs. The study found that peripheral denervation increased the amount of heterotopic bone formation after SCI and muscle injury, suggesting that nerve damage outside the spinal cord plays a role in this process.

Study Duration
28 days
Participants
21 C57Bl6 mice
Evidence Level
Not specified

Key Findings

  • 1
    Peripheral denervation increases heterotopic bone volume in mice with spinal cord injury and muscle damage.
  • 2
    Peripheral nerve section reinforces pathological propensity for intra muscular progenitors to differentiate into bone cells.
  • 3
    SCI alone does not significantly alter intramuscular BMP2 expression at the measured time point (18 hours post-injury).

Research Summary

This study explored the role of the peripheral nervous system in heterotopic ossification (HO) following spinal cord injury (SCI) using a mouse model. The researchers found that peripheral denervation, combined with SCI and muscle injury, significantly increased heterotopic bone volume compared to the contralateral side. The study suggests that injury-induced neuroinflammation contributes to increased HO volume and highlights the complex multicellular processes involved in ectopic osteogenesis.

Practical Implications

Therapeutic targets

The findings suggest potential therapeutic targets for preventing or treating HO by modulating neuroinflammation and related signaling pathways.

Improved understanding

Improved understanding of the complex interplay between the nervous and immune systems in HO pathogenesis, potentially leading to more effective treatment strategies.

Clinical relevance

The mouse model developed in this study provides a valuable tool for further investigating the pathophysiology of NHO and testing preventive therapies.

Study Limitations

  • 1
    Global nerve transection
  • 2
    Preliminary molecular analyses
  • 3
    Time point for BMP expression

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