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Updated: May 6, 2026
Longitudinal Evaluation of Mouse Hind Limb Bone Loss After Spinal Cord Injury using Novel, in vivo, Methodology
Published on: December 7, 2011
Bone biomarkers in patients with chronic traumatic spinal cord injury
Hadis Sabour1, Abbas Norouzi Javidan1, Sahar Latifi1
1Brain and Spinal Injury (BASIR) Research Center, Imam Khomeini Hospital, Tehran University of Medical Sciences, Keshavarz Avenu, Tehran, Iran.
Background Context:
Bone loss after spinal cord injury (SCI) occurs because of pathologic changes in osteoblastic and osteoclastic activities due to mechanical unloading. Some biochemical changes in bone metabolism after SCI are described before that were related to bone mineral loss.
Purpose:
Our purpose was to determine bone markers' changes and related effective factors in patients with chronic traumatic SCI.
Study Design:
This investigation was designed as an observational cross-sectional study.
Patient Sample:
All patients with chronic SCI who were referred to Brain and Spinal Injury Research Center and did not meet our exclusion criteria entered the study.
Outcome Measures:
Self-reporting measures including patient's demographic features and date of accident were obtained using a questionnaire and physiologic measures including spinal magnetic resonance imaging to determine the level of injury accompanied with physical examination along with dual-energy X-ray absorptiometry were performed. Blood samples were analyzed in the laboratory.
Methods:
Dual-energy X-ray was used to determine bone mineral density in femoral and spinal vertebrae bone sites. Serum level of C-telopeptide cross-linked Type 1 collagen (CTX), parathyroid hormone, calcitonin, osteocalcin, and bone alkaline phosphatase (BALP) were measured.
Results:
We detected a negative association between CTX level and bone mineral density in femoral and spinal bone sites that confirms that CTX is a bone resorption marker. C-telopeptide cross-linked Type 1 collagen and BALP levels did not show any significant correlation with postduration injury. Patients with spinal injury at lumbar level had the highest calcitonin level (p<.04). C-telopeptide cross-linked Type 1 collagen was positively related with osteocalcin and BALP (p<.0001, r=0.51), and osteocalcin was positively related with BALP (p<.0001, r=0.44). Osteocalcin was related negatively only to femoral intertrochanteric zone bone mineral density.
Conclusions:
Some bone biomarkers undergo noticeable changes after SCI. C-telopeptide cross-linked Type 1 collagen was positively correlated with BALP and osteocalcin that shows the coincidental occurrence of osteoblastic and osteoclastic activities. Our data also support this fact that although bone reduction after 2 years is slower than acute phase after SCI, bone resorption rate is higher than bone formation. These bone markers also revealed different site of action as osteocalcin level only affected femoral intertrochanteric bone mineral density. Generally, it seems that the coincidental consideration of these factors that influence bone mineral density can lead to a better understanding of bone changes after SCI.
