Journals / Romatizma Dergisi / 2005 / Cilt: 20 - Sayı: 2

Osteoporosis in patients with spinal cord injury

Medulla spinalis yaralanmalı hastalarda osteoporoz

Pages
55–58
DOI
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

It is considered that the events appears with deafferantation of the sympathic nerve system causedby the neurologic lesion may take an important role at immobilization.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Calcium loss from bone in a short time after injury is one of the result of spinal cord injury (SCI).
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Key Findings & Data:The main findings in patients with spinal cord injury are; dramatic increase in bone degradation after a short time from the beginning and decrease in osteoblastic activity.
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Conclusion & Impact:It is considered that the events appears with deafferantation of the sympathic nerve system causedby the neurologic lesion may take an important role at immobilization.
🔬Design:Modeling & Simulation
📍Scope:Comprehensive Sample
⚙️Variables:Osteoporoz · Omurilik yaralanmaları · Osteoporosis

Abstract

Calcium loss from bone in a short time after injury is one of the result of spinal cord injury (SCI). Sequence of the events that results with bone loss is not known exactly. The main findings in patients with spinal cord injury are; dramatic increase in bone degradation after a short time from the beginning and decrease in osteoblastic activity. Bone mass loss occurs as a consequence of increase in remodelling and bone resorbtion that passes bone formation. Even though this problem is known approximately for 50 years, cause of osteoporosis in spinal cord injured patients is not completely understood. It is considered that the events appears with deafferantation of the sympathic nerve system causedby the neurologic lesion may take an important role at immobilization.

Özet

Yaralanmadan kısa bir süre sonra kemiklerden kalsiyum kaybının başlaması, medulla spinalis yaralanmasının (MSY) sonuçlarından biridir. Kemik kaybıyla sonuçlanan olayların sırası tam olarak bilinmemektedir. MSY'li hastalarda başlıca bulgular, başlangıçtan kısa bir süre sonra kemik degradasyonunda dramatik bir artma ve osteoblastik aktivitenin azalmasıdır. MSY'li hastalarda kemik formasyonunu aşan kemik rezorbsiyonuyla, remodelling artışından kaynaklanan kemik kitle kaybı meydana gelmektedir. Bu problem yaklaşık 50 yıldır bilinmesine rağmen MSY'li hastalardaki osteoporozun ana nedeni tam olarak anlaşılamamıştır. İmmobilizasyonun yanında nörolojik lezyondan kaynaklanan sempatik sinir sisteminin deafferantasyonuyla ortaya çıkan olayların da önemli bir rol oynadığı düşünülmektedir.

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Cite This Article

KAYA, K., ÜNSAL, S., ÖZEL, S. (2005). Osteoporosis in patients with spinal cord injury. Romatizma Dergisi, Cilt: 20 - Sayı: 2, 55–58. https://ajindex.com/articles/306000

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References (16)

  1. Dauty M, Perrouin VB, Maugars Y, et al. Supralesional and sublesional bone mineral density in spinal cordinjured patients. Bone 2000;27(2):305-309
  2. Leslie WD, Nance PW. Dissociated hip and spine demineralization: a specific finding in spinal cord injury. Arch Phys Med Rehabil 1993;74:960-964
  3. Szollar SM, Martin EME, Sartoris DJ, et al. Bone mineral density and indexes of bone metabolism in spinal cord injury. Am J Phys Med. 1998;77(1):28-35
  4. Biering-Sorensen F, Bohr H, Schaadt O, et al. Bone mineral content of the lumbar spine and lower extremities years after spinal cord lesion. Paraplegia 1988;26: 293-301
  5. Frost FS. Spinal Cord Injury Medicine In Physical Medicine & Rehabilitation by Randall L. Braddom Ed. Second Edition. USA: W.B. Saunders Company, 2000:1230-1282
  6. Jones LM, Legge M, Goulding A. Intensive exercise may preserve bone mass of upper limbs in spinal cord injured males, but does not retard demineralisation of the lower body. Spinal Cord 2002; 40(5):230-235
  7. Goemaere S, Von Laere M, De Neve P, Kaufman JM. Bone mineral status in paraplegic patients who do or do not perform standing. Osteoporosis Int 1994;4(3):138-143
  8. Sabo D, Blaich S, Hohmann M, Loew M. Osteoporosis in patient with paralysis after spinal cord injury. Arch Orthop Trauma Surg 2001;121:75-78
  9. Roberts D, Lee W, Cuneo RC, et al. Longitudinal study of bone turnover after acute spinal cord injury. J Clin Endocrinol Metab 1998;83(2):415-421
  10. Garland DE, Stewart CA. Osteoporosis after spinal cord injury. Orthop Res 1992; 10(3):371-378
  11. Wilmet E, Ismail AA, Heilporn A, et al. Longitudinal study of the bone mineral content and of soft tissue composition after spinal cord section. Paraplegia 1995;33:674-677
  12. Tsuzuku S, Ikegami Y, Yabe K. Bone mineral density differences between paraplegic and quadriplegic patients: a cross- sectional study. Spinal Cord 1999; 37:358-361
  13. Chantraine A, Nusgens B, Lapiere CM. Bone remodelling during the development of osteoporosis in paraplegia. Calcif Tissue Int 1986; 38:323-327
  14. Biering-Sorensen F, Bohr HH, Schaadt OP. Longitudinal study of bone mineral content in the lumbar spine, the forearm and the lower extremities after spinal cord injury. Eur J Clin Inues 1990;20:330-335
  15. Naftchi NE, Viau AT, Sell GH, Lowman EW. Mineral metabolism in spinal cord injury. Arch Phys Med Rehabil 1980;61:139-42
  16. Stewart A, Adler M. Calcium homeostasis in immobilization: an example of rezorptive hypercalciüria. The New