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07:17
Establishing a Mouse Contusion Spinal Cord Injury Model Based on a Minimally Invasive Technique
Published on: September 7, 2022
Severe Spinal Cord Injury Causes Immediate Multi-cellular Dysfunction at the Chondro-Osseous Junction
Leslie R Morse1, Yan Xu, Bethlehem Solomon
1Spaulding-Harvard Spinal Cord Injury Model System, Spaulding Rehabilitation Hospital, Boston, MA, USA. Department of Cytokine Biology, Forsyth Institute, Boston, MA, USA. Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, MA, USA. Department of PMR, Harvard Medical School, The Forsyth Institute, 140 The Fenway, Boston, MA 02118, USA.
Translational Stroke Research
|February 28, 2012
Summary
Severe spinal cord injury in adolescent rats causes rapid bone loss by increasing bone resorption and decreasing bone formation. This leads to growth plate arrest and altered gene expression in sublesional bone.
Area of Science:
- Orthopedics
- Neuroscience
- Cell Biology
Background:
- Spinal cord injury (SCI) is linked to significant bone loss and impaired long bone growth.
- The underlying mechanisms driving these skeletal changes post-SCI remain largely unknown.
Purpose of the Study:
- To investigate the impact of severe T10 contusion spinal cord injury on the sublesional bone microenvironment in adolescent rats.
- To elucidate the cellular and molecular changes contributing to bone abnormalities after SCI.
Main Methods:
- Induction of severe T10 spinal cord injury in adolescent male Sprague-Dawley rats using a weight-drop model.
- Histological analysis, TUNEL assay, immunohistochemistry, real-time PCR, and Western blot analysis at 3 and 5 days post-injury.
- Assessment of hindlimb function and bone microenvironment in injured versus uninjured control rats.
Main Results:
- SCI induced severe hindlimb functional deficits.
- Observed uncoupled bone remodeling characterized by increased osteoclast activity and absent osteoblast activity.
- Detected apoptosis in osteoblasts, osteocytes, and chondrocytes, alongside suppressed proliferation and growth plate arrest.
- Identified altered gene expression in bone tissue and bone marrow monocytes post-SCI.
Conclusions:
- Spinal cord injury disrupts the sublesional bone microenvironment, leading to premature cellular apoptosis and suppressed proliferation.
- SCI causes growth plate arrest and uncoupled bone remodeling with dominant osteoclastic resorption.
- Altered gene expression of key regulators contributes to impaired osteoblast and chondrocyte function following spinal cord injury.
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