Testosterone Plus Finasteride Prevents Bone Loss without Prostate Growth in a Rodent Spinal Cord Injury Model

J Neurotrauma, 2017 · DOI: 10.1089/neu.2016.4814 · Published: November 1, 2017

Spinal Cord Injury Endocrinology Musculoskeletal Medicine

Simple Explanation

This study investigates the effects of testosterone and finasteride on bone loss and prostate growth in rats with spinal cord injuries. The goal was to find a treatment that prevents bone loss without causing prostate enlargement. Rats with spinal cord injuries were treated with testosterone alone or in combination with finasteride. The researchers then measured bone density, muscle mass, and prostate size. The results showed that testosterone, when combined with finasteride, prevented bone loss and muscle loss without increasing prostate size in rats with spinal cord injuries.

Study Duration

8 weeks

Participants

Forty-three 16-week-old male Sprague-Dawley rats

Evidence Level

Not specified

Key Findings

1
TE+FIN prevented the chronic cancellous bone deficits and LABC muscle loss in SCI animals without inducing prostate enlargement.
2
TE treatment normalized cancellous and cortical bone turnover and maintained cancellous bone mass at the level of SHAM animals, but produced prostate enlargement.
3
Neither drug regimen prevented SCI-induced cortical bone loss, although no differences in whole bone strength were present among groups.

Research Summary

This study aimed to determine if testosterone (TE) prevents bone deficits post-spinal cord injury (SCI) and if finasteride (FIN) is required for TE-induced skeletal preservation. The study found that TE, combined with FIN, prevented cancellous bone deficits and muscle loss without causing prostate enlargement in a rat SCI model. However, neither TE nor TE+FIN prevented cortical bone loss post-SCI, indicating divergent effects on cancellous and cortical bone.

Practical Implications

Therapeutic intervention

TE+FIN could be included in multimodal therapeutic interventions to alleviate musculoskeletal decline post-SCI.

Muscle maintenance

Type II 5α-reductase activity is not essential for TE-mediated preservation of androgen-sensitive muscle mass post-SCI, even without musculoskeletal loading.

Prostate enlargement

Actions of the type II 5α-reductase isozyme largely mediate TE-induced prostate enlargement.

Study Limitations

1
Rodents lack Haversian remodeling in cortical bone, which predominates intracortical remodeling in humans.
2
Only one small case series has evaluated the skeletal responses to TRT in humans with SCI and observed no changes in femur CSA or in the area of heterotopic ossification after 16 weeks of treatment.
3
These possibilities remain to be determined in our rodent SCI model.

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