Osteoporosis after spinal cord injury.
Abstract
Osteoporosis is a known consequence of spinal cord injury (SCI) and occurs in almost every SCI patient. It manifests itself as an increase in the incidence of lower extremity fractures. The pattern of bone loss seen in SCI patients is different from that usually encountered with endocrine disorders and disuse osteoporosis. In general, there is no demineralization in supralesional areas following SCI. Several factors appear to have a major influence on bone mass in SCI individuals, such as the degree of the injury, muscle spasticity, age, sex and duration after injury. At the lumbar spine, bone demineralization remains relatively low compared to that of the long bones in the sublesional area. A new steady state level between bone resorption and formation is reestablished about 2 years after SCI. SCI may not only cause bone loss, but also alter bone structure and microstructure. Trabecular bone is more affected than cortical bone in the SCI population. Numerous clinical series have reported a high incidence ranging from 1 to 34% of lower extremity fractures in SCI patients. The pathogenesis of osteoporosis after SCI remains complex and perplexing. Disuse may play an important role in the pathogenesis of osteoporosis, but neural factors also appear to be important. SCI also leads to impaired calcium and phosphate metabolism and the parathyroid hormone (PTH)-vitamin D axis. Pharmacologic intervention for osteoporosis after SCI includes calcium, phosphate, vitamin D, calcitonin and biphosphonates. However, the concomitant prescription of bone-active drugs for the prevention and treatment of osteoporosis remains low, despite the availability of effective therapies. Functional stimulated exercises may contribute to the prevention of bone loss to some extent. In addition, many unanswered questions remain about the pathogenesis of osteoporosis and its clinical management.
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Spinal cord injury is associated with decreased BMD, increased fracture risk, and deterioration of cortical geometry.
“Spinal cord injury is associated with decreased BMD, increased fracture risk, and deterioration of cortical geometry (270, 271).”
From Receptor Activator of Nuclear Factor κB Ligand and Osteoprotegerin Regulation of Bone Remodeling in Health and Disease (2008) · cites this paper as [271]
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Kearns, A. E., Khosla, S., & Kostenuik, P. J. (2008) · Endocrine Reviews · doi:10.1210/er.2007-0014 · Cited by 824 · see citing works
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- Authors
- Jiang, S.-D., Dai, L.-Y., & Jiang, L.-S.
- Affiliations
- XinHua Hospital (CN)
- Corresponding author
- Dai, Li-Yang
- Venue
- Osteoporosis International
- Published
- 2005-10-11
- Volume
- 17
- Issue
- 2
- Pages
- 180-192
- ISSN
- 0937-941X (ISSN-L)
- 1433-2965
- OpenAlex
- W2097773954
- Cited by
- 282
- References
- 127
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 14 · 2023: 11 · 2022: 17 · 2021: 17 · 2020: 16 · 2019: 11 · 2018: 16 · 2017: 14 · 2016: 16 · 2015: 23 · 2014: 17 · 2013: 18 · 2012: 18
- FWCI
- 1.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Osteoporosis International (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Keywords
- spinal cord injury, osteoporosis, bone loss, lower limb fractures, bone demineralization, trabecular bone microarchitecture, disuse osteoporosis, spasticity, calcium and phosphate metabolism, bisphosphonates, calcitonin, vitamin D supplementation
- MeSH terms
- Aging, Bone Resorption, Calcium, Exercise Therapy, Female, Homeostasis, Humans, Male, Osteoporosis, Paraplegia, Parathyroid Hormone, Phosphates, Spinal Cord Injuries, Stress, Mechanical, Vitamin D, Signal Transduction, Bone Density, Fractures, Bone
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