Longitudinal Examination of Bone Loss in Male Rats After Moderate–Severe Contusion Spinal Cord Injury

Calcif Tissue Int, 2019 · DOI: 10.1007/s00223-018-0471-8 · Published: January 1, 2019

Spinal Cord Injury Musculoskeletal Medicine

Simple Explanation

This study investigates bone loss after spinal cord injury (SCI) in rats. Researchers looked at changes in bone structure, bone turnover markers, and bone strength over time. The results showed that SCI caused rapid cancellous bone loss followed by gradual cortical bone loss. The study also found changes in bone turnover markers and bone strength. Low testosterone and leptin levels may also contribute to bone loss after SCI. This information could help develop new treatments to prevent bone loss in people with SCI.

Study Duration

3 Months

Participants

102 male Sprague–Dawley rats

Evidence Level

Level 2: Animal Study

Key Findings

1
SCI produced immediate sublesional paralysis and persistent hindlimb locomotor impairment in rats.
2
SCI animals exhibited rapid cancellous bone deterioration and more gradual cortical bone loss.
3
SCI animals also exhibited lower serum testosterone than SHAM, until 2-months post-surgery, and lower serum leptin throughout.

Research Summary

This study characterized the time courses of cancellous and cortical bone deficits in a clinically relevant rodent SCI model to assist in identifying the mechanism exacerbating skeletal deterioration after SCI. Severe cancellous bone loss at the distal femur and proximal tibia occurred within 2 weeks of SCI and temporally delayed cortical bone deficits thereafter. The study developed an experimental SCI model that mimics the predominant sex, age, and injury type occurring in the human SCI population.

Practical Implications

Understanding Bone Loss Mechanisms

The study helps elucidate mechanisms of bone loss after SCI by evaluating the time-course of bone microarchitectural deterioration, bone turnover indices, and whole bone mechanical deficits.

Relevance to Human SCI

The findings are relevant to the severe motor-incomplete and/or motor-complete SCI populations that are at risk of bone fracture, providing content validity to the preclinical model.

Potential Therapeutic Targets

The study suggests that low testosterone and leptin may contribute to bone deterioration after SCI, indicating potential therapeutic targets for preventing bone loss in this population.

Study Limitations

1
Comprehensive analysis of all hormones was beyond our scope
2
The reasons underlying the differences between these models and our 4-months-old male moderate–severe contusion SCI model remain unknown
3
It remains unknown whether an initial reduction in circulating leptin exists in persons with bodyweight loss after SCI or whether leptin influences bone homeostasis in this population.

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