Is prophylaxis for osteoporosis indicated after acute spinal cord injury?

Spinal cord injury (SCI)-related osteoporosis is a common complication, particularly in individuals with tetraplegia or paraplegia, leading to bone demineralization, fractures, and decreased quality of life. The primary cause is the loss of mechanical stimuli due to paralysis, not merely immobilization. After an acute SCI, bone loss occurs rapidly, with osteoclast activity significantly increasing. This can result in hypercalciuria and hypercalcemia, potentially leading to complications if not managed promptly through early mobilization and hydration. Supplementation with Vitamin D is necessary before starting antiresorptive drug therapy. Low vitamin D levels can lead to inadequate calcium absorption, and using antiresorptive agents without addressing this can cause severe hypocalcemia.

• 1
  Traumatic SCI results in various degrees of osteoporosis below the level of injury, primarily due to the loss of mechanical stimuli from paralysis.
• 2
  Early administration of bisphosphonates after injury, along with controlling calcium metabolism and engaging in rehabilitation programs that include walking, can limit bone loss and retain bone density, especially in individuals with incomplete lesions.
• 3
  Sclerostin levels increase after acute SCI, inhibiting bone formation, suggesting it as a potential target for preventing bone loss; however, anti-sclerostin antibody treatment may be ineffective in chronic SCI.