Bone and muscle loss after spinal cord injury: Organ interactions

Weiping Qin, William A. Bauman, Christopher Cardozo

Research output: Contribution to journalArticlepeer-review

152 Scopus citations

Abstract

Spinal cord injury (SCI) results in paralysis and marked loss of skeletal muscle and bone below the level of injury. Modest muscle activity prevents atrophy, whereas much larger-and as yet poorly defined-bone loading seems necessary to prevent bone loss. Once established, bone loss may be irreversible. SCI is associated with reductions in growth hormone, IGF-1, and testosterone, deficiencies likely to exacerbate further loss of muscle and bone. Reduced muscle mass and inactivity are assumed to be contributors to the high prevalence of insulin resistance and diabetes in this population. Alterations in muscle gene expression after SCI share common features with other muscle loss states, but even so, show distinct profiles, possibly reflecting influences of neuromuscular activity due to spasticity. Changes in bone cells and markers after SCI have similarities with other conditions of unloading, although after SCI these changes are much more dramatic, perhaps reflecting the much greater magnitude of unloading. Adiposity and marrow fat are increased after SCI with intriguing, though poorly understood, implications for the function of skeletal muscle and bone cells.

Original languageEnglish
Pages (from-to)66-84
Number of pages19
JournalAnnals of the New York Academy of Sciences
Volume1211
DOIs
StatePublished - Nov 2010

Keywords

  • Body composition
  • Bone loss
  • Estrogen
  • Insulin-like growth factor 1
  • Methylprednisolone
  • Muscle atrophy
  • Spinal cord injury
  • Testosterone

Fingerprint

Dive into the research topics of 'Bone and muscle loss after spinal cord injury: Organ interactions'. Together they form a unique fingerprint.

Cite this