eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury

Osteoporosis and Spinal Cord Injury

Author: David Weiss, MD, Medical Director of Physical Medicine and Rehabilitation, Assistant Professor, Internal Medicine, Marianjoy Medical Group
Contributor Information and Disclosures

Updated: Apr 1, 2008

Introduction

Background

One of the inevitable complications of spinal cord injury (SCI) is the associated osteoporosis that occurs predominantly in the pelvis and the lower extremities. The acute treatment of patients with SCI has always focused on the injury itself and on the immediate complications that subsequently arise. Bone loss as a consequence of SCI has been of secondary concern historically. Osteoporosis in persons with SCI was first studied in relation to calcium metabolism and the associated hypercalcemia and renal calculi that followed.

The differences between SCI-induced osteoporosis and other causes of bone loss (disuse), such as prolonged bed rest, space travel, and lower motor neuron disorders, have since become clearer. New technologies allow monitoring of osteoblastic and osteoclastic activity at the microscopic level, while modern radiographic techniques have allowed more refined studies to be undertaken at the macroscopic level.1,2

See also the following related Medscape topic:
 Resource Center Fracture
Resource Center Osteoporosis

Pathophysiology

The mechanism behind SCI-induced osteoporosis is accepted as being multifactorial in the acute and chronic stages.3 These mechanisms differ from those observed in subjects without SCI after prolonged bed rest and in subjects with other neurologic deficits. SCI causes immediate and, in some regions, permanent gravitational unloading. The result is a disuse structural change with associated metabolic consequences. Hypercalciuria is seen by 10 days following the SCI and reaches a peak 1-6 months postinjury. This level of hypercalciuria is 2-4 times that of persons without SCI who undergo prolonged bed rest. This marked increase in urine calcium is the direct result of an imbalance between bone formation and bone resorption.4,5

The activity of osteoblasts and osteoclasts is triggered by the SCI; however, markers of osteoblastic activity rise only slightly, while osteoclasts have a significant increase in their activity, peaking at 10 weeks following the SCI with values 10 times the upper limits of normal. In addition, the increased bone resorption precedes the increase in osteoblastic activity. This model at the skeletal level following SCI resembles the high bone turnover rate seen in postmenopausal osteoporosis.

The loss of bone also may be enhanced by lack of muscle traction on bone or by other neural factors associated with SCI. These other factors further separate SCI-induced osteoporosis from other causes of disuse demineralization. Absorption of calcium from the gastrointestinal tract has been found to decrease in the acute period following SCI. Even so, in the past, dietary calcium reduction commonly was recommended as a way to decrease calcium excretion and prevent the complications of hypercalciuria.

The body that has sustained SCI has been considered the model of premature aging, and the role of parathyroid hormone in osteoporosis following SCI illustrates this point. Acutely, the parathyroid gland is relatively inactive, with low parathyroid hormone levels observed up to the 1-year point following injury. Hypercalcemia seen immediately postinjury leads to this low level. A reversal in activity during years 1-9 is noted.6,7,8

The parathyroid gland is stimulated to the point that parathyroid hormone levels are above the reference range. The result is an increase in bone re-absorption or osteoporosis related to parathyroid dysfunction in the chronic stages of SCI. This chronic-stage mechanism of osteoporosis is balanced by an increase in bone mineral in regions of the body in which weight bearing is resumed (eg, in the upper extremities, spine) and adds to the demineralization observed in regions that are chronically non – weight-bearing (eg, the pelvis, lower extremities).

Frequency

United States

Bone loss following SCI occurs throughout the skeletal system, with the exception of the skull. These losses are regional; areas rich in trabecular bone are demineralized to the greatest degree. The distal femur and proximal tibia are the bones most affected, followed by the pelvis and arms.9,10 The amount of demineralization in the skull, pelvis, and lower limbs is independent of the neurologic level.

A positive correlation exists between the time following the injury and the degree of bone loss. Rapid loss of bone mineral occurs during the first 4 months following SCI. In patients with SCI, less than 1 year following the injury, reduction in bone mineral densities has been noted in the femoral neck (27%), midshaft (25%), and distal femur (43%), as compared with controls.

Bone mineral loss continues, but to a lesser degree, in the pelvis and lower extremities over the next 10 years.11 By 10 years postinjury, over 50% of bone content in these regions has been demineralized. The arms and trunk demonstrate an increase in bone content after the 4-month point. This gain in mineral content over the next 10-year period helps to offset some of the initial losses in the arms. The net effect is an approximate 10-21% loss of bone at the 10-year point. Interestingly, the trunk has a net gain in mineral content by 12 years postinjury.

Significant differences in upper extremity bone density are observed between paraplegic patients and tetraplegic patients. The bone mineral density of the arms of paraplegic patients returns to near normal by the 10-year postinjury point, which is approximately 16% more bone mineral than is found in the arms of tetraplegic patients.

Individuals with complete injuries tend to have less bone mineral density than those with incomplete lesions. With complete lesions, significantly lower lumbar spine bone mineral densities have been noted (z value -1.47) in patients 1-26 years post injury. In addition, individuals with incomplete motor SCI demonstrate greater bone mineral density at the areas of greater lower extremity muscle strength.

Some controversy exists surrounding the protective effect of spasticity on bone mineral content. Studies have found a decrease in losses of bone density in patients exhibiting spasticity, compared with the flaccid group.

Mortality/Morbidity

The most measurable complication of osteoporosis following SCI is pathologic fracture. The historical incidence of fractures in the SCI population has been 1.45-6%; however, this historically low incidence may be deceptive, because most patients with SCI who sustain subsequent traumas and fractures are not treated in SCI centers. In addition, these studies on fractures have come from inpatient charts. The Model Spinal Cord Injury System has produced figures on fracture rates based on time following SCI, with incidences of 14% at 5 years, 28% at 10 years, and 39% at 15 years postinjury. These incidence rates are based on outpatient studies and have been confirmed.

The sites of fractures correspond to the sites of greatest osteoporosis, with fractures most commonly occurring in the supracondylar region and the tibia.12 A bone mineral density fracture threshold of 50% appears to exist for the knee, and this most likely is the bone mineral density fracture threshold for most regions in the body.

Fracture rates in the lower extremities are 10 times greater in patients with complete SCI than in patients with incomplete injuries. Paraplegic patients are at higher risk than are tetraplegic patients, due to the higher level of function that paraplegic individuals have with regard to mobility and participation in physical activities.

The inciting events that lead to fractures frequently are unknown or are associated with relatively minimal traumas. The reason is that less torque is needed to produce failures in bone in persons with SCI than in individuals who have not sustained SCI.

See also the following related eMedicine topic:
Functional Outcomes per Level of Spinal Cord Injury

Race

No studies have examined whether a correlation exists between race and osteoporosis following SCI.

Sex

Limited studies exist on the connection between sex and osteoporosis following SCI. However, it does appear that, as in the population without SCI, women have more bone loss than do males.

Age

In the last few decades, only one study has included age as a risk factor for osteoporosis. For every 1-year increase in age, the rate at which osteoporosis of the knees developed was shown to increase by 3.54%. In another study, rates for femoral (including hip) fractures in patients following SCI were found to be greater than those in the general population by factors of 104 and 24 at age 50 years and 70 years, respectively.

Clinical

History

Osteoporosis by itself is a subclinical condition. Thus, no associated clinical signs or symptoms exist for this entity. The most common way osteoporosis is discovered in SCI patients is when radiographs are taken following fractures; the radiographs reveal the fracture and significant bone loss.

Physical

No overt physical examination findings exist that lead to the diagnosis of osteoporosis. However, patients with SCI may be predisposed to knee effusions due to osteoporosis, heterotopic ossification, trauma, and benign hydrarthrosis.

Causes

Osteoporosis following an SCI is a primary complication of the SCI itself. For more discussion on risk factors, please see Pathophysiology.

More on Osteoporosis and Spinal Cord Injury

Overview: Osteoporosis and Spinal Cord Injury
Differential Diagnoses & Workup: Osteoporosis and Spinal Cord Injury
Treatment & Medication: Osteoporosis and Spinal Cord Injury
Follow-up: Osteoporosis and Spinal Cord Injury
Multimedia: Osteoporosis and Spinal Cord Injury
References
[ CLOSE WINDOW ]

References

  1. Garland DE, Stewart CA, Adkins RH, et al. Osteoporosis after spinal cord injury. J Orthop Res. May 1992;10(3):371-8. [Medline].

  2. Jiang SD, Jiang LS, Dai LY. Effects of spinal cord injury on osteoblastogenesis, osteoclastogenesis and gene expression profiling in osteoblasts in young rats. Osteoporos Int. Mar 2007;18(3):339-49. [Medline].

  3. Yilmaz B, Yasar E, Goktepe AS, et al. The relationship between basal metabolic rate and femur bone mineral density in men with traumatic spinal cord injury. Arch Phys Med Rehabil. Jun 2007;88(6):758-61. [Medline].

  4. Kaplan PE, Roden W, Gilbert E, et al. Reduction of hypercalciuria in tetraplegia after weight-bearing and strengthening exercises. Paraplegia. 1981;19(5):289-93. [Medline].

  5. Stewart AF, Adler M, Byers CM, et al. Calcium homeostasis in immobilization: an example of resorptive hypercalciuria. N Engl J Med. May 13 1982;306(19):1136-40. [Medline].

  6. Chantraine A, Heynen G, Franchimont P. Bone metabolism, parathyroid hormone, and calcitonin in paraplegia. Calcif Tissue Int. Jul 3 1979;27(3):199-204. [Medline].

  7. Claus-Walker J, Carter RE, Compos RJ, et al. Hypercalcemia in early traumatic quadriplegia. J Chronic Dis. Feb 1975;28(2):81-90. [Medline].

  8. Merli GJ, McElwain GE, Adler AG, et al. Immobilization hypercalcemia in acute spinal cord injury treated with etidronate. Arch Intern Med. Jun 1984;144(6):1286-8. [Medline].

  9. Garland DE, Maric Z. Bone mineral density about the knee in spinal cord injured patients with pathologic fractures. Contemp Orthop. 1993;26:375-9.

  10. Garland DE, Adkins RH, Kushwaha V, et al. Risk factors for osteoporosis at the knee in the spinal cord injury population. J Spinal Cord Med. 2004;27(3):202-6. [Medline].

  11. Reiter AL, Volk A, Vollmar J, et al. Changes of basic bone turnover parameters in short-term and long-term patients with spinal cord injury. Eur Spine J. Jun 2007;16(6):771-6. [Medline].

  12. Szollar SM, Martin EM, Sartoris DJ, et al. Bone mineral density and indexes of bone metabolism in spinal cord injury. Am J Phys Med Rehabil. Jan-Feb 1998;77(1):28-35. [Medline].

  13. Maïmoun L, Couret I, Mariano-Goulart D, et al. Changes in osteoprotegerin/RANKL system, bone mineral density, and bone biochemicals markers in patients with recent spinal cord injury. Calcif Tissue Int. Jun 2005;76(6):404-11. [Medline].

  14. Maïmoun L, Couret I, Micallef JP, et al. Use of bone biochemical markers with dual-energy X-ray absorptiometry for early determination of bone loss in persons with spinal cord injury. Metabolism. Aug 2002;51(8):958-63. [Medline].

  15. Liu CC, Theodorou DJ, Theodorou SJ, et al. Quantitative computed tomography in the evaluation of spinal osteoporosis following spinal cord injury. Osteoporos Int. 2000;11(10):889-96. [Medline].

  16. Sabo D, Blaich S, Wenz W, et al. Osteoporosis in patients with paralysis after spinal cord injury. A cross sectional study in 46 male patients with dual-energy X-ray absorptiometry. Arch Orthop Trauma Surg. 2001;121(1-2):75-8. [Medline].

  17. BeDell KK, Scremin AM, Perell KL, et al. Effects of functional electrical stimulation-induced lower extremity cycling on bone density of spinal cord-injured patients. Am J Phys Med Rehabil. Jan-Feb 1996;75(1):29-34. [Medline].

  18. Chen SC, Lai CH, Chan WP, et al. Increases in bone mineral density after functional electrical stimulation cycling exercises in spinal cord injured patients. Disabil Rehabil. Nov 30 2005;27(22):1337-41. [Medline].

  19. Eser P, de Bruin ED, Telley I, et al. Effect of electrical stimulation-induced cycling on bone mineral density in spinal cord-injured patients. Eur J Clin Invest. May 2003;33(5):412-9. [Medline].

  20. de Bruin ED, Frey-Rindova P, Herzog RE, et al. Changes of tibia bone properties after spinal cord injury: effects of early intervention. Arch Phys Med Rehabil. Feb 1999;80(2):214-20. [Medline].

  21. Needham-Shropshire BM, Broton JG, Klose KJ. Evaluation of a training program for persons with SCI paraplegia using the Parastep 1 ambulation system: part 3. Lack of effect on bone mineral density. Arch Phys Med Rehabil. Aug 1997;78(8):799-803. [Medline].

  22. Leeds EM, Klose KJ, Ganz W, et al. Bone mineral density after bicycle ergometry training. Arch Phys Med Rehabil. Mar 1990;71(3):207-9. [Medline].

  23. Moran de Brito CM, Battistella LR, Saito ET, et al. Effect of alendronate on bone mineral density in spinal cord injury patients: a pilot study. Spinal Cord. Jun 2005;43(6):341-8. [Medline].

  24. Pearson EG, Nance PW, Leslie WD, et al. Cyclical etidronate: its effect on bone density in patients with acute spinal cord injury. Arch Phys Med Rehabil. Mar 1997;78(3):269-72. [Medline].

  25. Sniger W, Garshick E. Alendronate increases bone density in chronic spinal cord injury: a case report. Arch Phys Med Rehabil. Jan 2002;83(1):139-40. [Medline].

  26. Gilchrist NL, Frampton CM, Acland RH, et al. Alendronate prevents bone loss in patients with acute spinal cord injury: a randomized, double-blind, placebo-controlled study. J Clin Endocrinol Metab. Apr 2007;92(4):1385-90. [Medline].

  27. Minaire P, Depassio J, Berard E, et al. Effects of clodronate on immobilization bone loss. Bone. 1987;8 Suppl 1:S63-8. [Medline].

  28. Nance PW, Schryvers O, Leslie W, et al. Intravenous pamidronate attenuates bone density loss after acute spinal cord injury. Arch Phys Med Rehabil. Mar 1999;80(3):243-51. [Medline].

  29. Albright F, Burnett CH, Cope O. Acute atrophy of bone (osteoporosis) simulating hyperparathyroidism. J Clin Endocrin Metab. 1941;1:711-6.

  30. Bauman WA, Spungen AM, Wang J, et al. Continuous loss of bone during chronic immobilization: a monozygotic twin study. Osteoporos Int. 1999;10(2):123-7. [Medline].

  31. Bauman WA, Wecht JM, Kirshblum S, et al. Effect of pamidronate administration on bone in patients with acute spinal cord injury. J Rehabil Res Dev. May-Jun 2005;42(3):305-13. [Medline].

  32. Bauman WA, Zhong YG, Schwartz E. Vitamin D deficiency in veterans with chronic spinal cord injury. Metabolism. Dec 1995;44(12):1612-6. [Medline].

  33. Bergmann P, Heilporn A, Schoutens A, et al. Longitudinal study of calcium and bone metabolism in paraplegic patients. Paraplegia. Aug 1977;15(2):147-59. [Medline].

  34. 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. Oct 1988;26(5):293-301. [Medline].

  35. Comarr AE, Hutchinson RH, Bors E. Extremity fractures of patients with spinal cord injuries. Am J Surg. Jun 1962;103:732-9. [Medline].

  36. Dauty M, Perrouin Verbe B, Maugars Y, et al. Supralesional and sublesional bone mineral density in spinal cord-injured patients. Bone. Aug 2000;27(2):305-9. [Medline].

  37. Demirel G, Yilmaz H, Paker N, et al. Osteoporosis after spinal cord injury. Spinal Cord. Dec 1998;36(12):822-5. [Medline].

  38. Dionyssiotis Y, Trovas G, Galanos A, et al. Bone loss and mechanical properties of tibia in spinal cord injured men. J Musculoskelet Neuronal Interact. Jan-Mar 2007;7(1):62-8. [Medline].

  39. Eichenholtz SN. Management of long bone fractures in paraplegic patients. J Bone Joint Surg. 1963;45(2):299-310.

  40. Freehafer AA, Hazel CM, Becker CL. Lower extremity fractures in patients with spinal cord injury. Paraplegia. 1981;19(6):367-72. [Medline].

  41. Freehafer AA, Mast WA. Lower extremity fractures in patients with spinal-cord injury. J Bone Joint Surg Am. Jun 1965;47:683-94. [Medline].

  42. Frisbie JH. Fractures after myelopathy: the risk quantified. J Spinal Cord Med. Jan 1997;20(1):66-9. [Medline].

  43. Garland DE, Adkins RH, Rah A. Bone loss with aging and the impact of spinal cord injury. Top Spinal Cord Inj Rehabil. 2001;6(3):47-60.

  44. Garland DE, Adkins RH, Stewart CA. Fracture threshold and risk for osteoporosis and pathologic fractures in individuals with spinal cord injury. Top Spinal Cord Inj Rehabil. 1995;11:61-9.

  45. Garland DE, Adkins RH, Stewart CA. Regional osteoporosis in women who have a complete spinal cord injury. J Bone Joint Surg Am. Aug 2001;83-A(8):1195-200. [Medline].

  46. Garland DE, Foulkes GD, Adkins RH. Regional osteoporosis following incomplete spinal cord injury. Contemp Orthop. 1994;28:134-9.

  47. Goktepe AS, Yilmaz B, Alaca R, et al. Bone density loss after spinal cord injury: elite paraplegic basketball players vs. paraplegic sedentary persons. Am J Phys Med Rehabil. Apr 2004;83(4):279-83. [Medline].

  48. Hangartner TN. Osteoporosis due to disuse. Phys Med Rehabil Clin North Am. 1995;6(3):579-93.

  49. Jiang SD, Dai LY, Jiang LS. Osteoporosis after spinal cord injury. Osteoporos Int. Feb 2006;17(2):180-92. [Medline].

  50. Jiang SD, Jiang LS, Dai LY. Spinal cord injury causes more damage to bone mass, bone structure, biomechanical properties and bone metabolism than sciatic neurectomy in young rats. Osteoporos Int. Oct 2006;17(10):1552-61. [Medline].

  51. Jones LM, Legge M, Goulding A. Intensive exercise may preserve bone mass of the upper limbs in spinal cord injured males but does not retard demineralisation of the lower body. Spinal Cord. May 2002;40(5):230-5. [Medline]. [Full Text].

  52. Kiratli BJ, Smith AE, Nauenberg T, et al. Bone mineral and geometric changes through the femur with immobilization due to spinal cord injury. J Rehabil Res Dev. Mar-Apr 2000;37(2):225-33. [Medline].

  53. Kirshblum S, Druin E, Phanteen K. Musculoskeletal conditions in chronic spinal cord injury. Top Spinal Cord Inj Rehab. 1997;2(4):23-35.

  54. Kunkel CF, Scremin AM, Eisenberg B, et al. Effect of "standing" on spasticity, contracture, and osteoporosis in paralyzed males. Arch Phys Med Rehabil. Jan 1993;74(1):73-8. [Medline].

  55. Leslie WD, Nance PW. Dissociated hip and spine demineralization: a specific finding in spinal cord injury. Arch Phys Med Rehabil. Sep 1993;74(9):960-4. [Medline].

  56. Pietschmann P, Pils P, Woloszczuk W, et al. Increased serum osteocalcin levels in patients with paraplegia. Paraplegia. Mar 1992;30(3):204-9. [Medline].

  57. Ragnarsson KT, Sell GH. Lower extremity fractures after spinal cord injury: a retrospective study. Arch Phys Med Rehabil. Sep 1981;62(9):418-23. [Medline].

  58. Roberts D, Lee W, Cuneo RC, et al. Longitudinal study of bone turnover after acute spinal cord injury. J Clin Endocrinol Metab. Feb 1998;83(2):415-22. [Medline]. [Full Text].

  59. Shields RK, Dudley-Javoroski S. Musculoskeletal plasticity after acute spinal cord injury: effects of long-term neuromuscular electrical stimulation training. J Neurophysiol. Apr 2006;95(4):2380-90. [Medline]. [Full Text].

  60. Shojaei H, Soroush MR, Modirian E. Spinal cord injury-induced osteoporosis in veterans. J Spinal Disord Tech. Apr 2006;19(2):114-7. [Medline].

  61. Staas WE, Formal CS, Freedman MK. Spinal cord injury and spinal cord injury medicine. In: DeLisa JA, Gans BM, eds. Rehabilitation Medicine: Principles and Practice. 3rd ed. Philadelphia, Pa: Lippincott-Raven; 1998:1259-91.

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

spinal cord injury, osteoporosis, osteoporosis and SCI, SCI-induced osteoporosis, functional electrical stimulation, FES, dual-energy radiographic absorptiometry scan, dual-energy X-ray absorptiometry scan, DRA, DXA

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

David Weiss, MD, Medical Director of Physical Medicine and Rehabilitation, Assistant Professor, Internal Medicine, Marianjoy Medical Group
David Weiss, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Sports Medicine, Association of Academic Physiatrists, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Medical Editor

Rajesh R Yadav, MD, Assistant Professor, Section of Physical Medicine and Rehabilitation, MD Anderson Cancer Center, University of Texas at Houston
Rajesh R Yadav, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain (Tailbone Pain, Coccydynia) Service, University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.

CME Editor

Kelly L Allen, MD, Consulting Staff, Department of Physical Medicine and Rehabilitation, Lourdes Regional Rehabilitation Center, Our Lady of Lourdes Medical Center
Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS, Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St. Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers, Phoenix
Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.