eMedicine Specialties > Physical Medicine and Rehabilitation > Spinal Cord Injury

Heterotopic Ossification in Spinal Cord Injury

Author: 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
Contributor Information and Disclosures

Updated: Sep 5, 2008

Introduction

Background

Heterotopic ossification (HO) following spinal cord injury (SCI) was described first by Dejerine and Ceillier in 1918 as paraosteoarthropathy. The ossification process in this case involves the formation of mature lamellar bone, which is indistinguishable from normal bone, in soft tissues surrounding paralyzed joints. The bone is not connected to periosteum and becomes encapsulated as it matures.

The pathology is similar to that of fracture callus, except that bone forms in the connective tissue between the muscle planes. HO also is seen after other neurologic insults, such as traumatic brain injury (TBI) and stroke, as well as after thermal injuries and orthopedic procedures (eg, total hip replacement).

In experimental models of HO formation, ischemia and tissue expression of bone morphogenic proteins have been shown to play important roles. Bone morphogenic proteins likely act on mesenchymal stem cells present in tissue, activating the cells to differentiate into osteoblasts.1

Related eMedicine topics:
Heterotopic Ossification [Physical Medicine and Rehabilitation]
Heterotopic Ossification [Radiology]
Posttraumatic Heterotopic Ossification
Spinal Cord Injuries
Traumatic Heterotopic Ossification

Pathophysiology

The pathophysiology of heterotopic ossification (HO) involves an inflammatory process, with increased blood flow in soft tissue. Bone matrix is laid down and mineralized, and this sequence reaches completion in 6-18 months. Local, systemic, neural, and hormonal causes for the HO process have been hypothesized but have not been proven (see Causes). Debate continues over whether there is migration of distant mesenchymal cells or transformation of existing mesenchymal cells into osteoblasts.

Frequency

United States

The incidence of heterotopic ossification (HO) in spinal cord injury (SCI) is between 16% and 53%, depending on the incidence reports from various institutions. Once present, neurogenic HO is clinically significant in 18-27% of cases. Fortunately, only 3-5% of cases involve joint ankylosis.

Mortality/Morbidity

No direct mortality is associated with neurogenic heterotopic ossification. Morbidity is associated primarily with loss of range of motion (ROM) and the consequent loss of joint function.

Race

There is no known race predilection for neurogenic heterotopic ossification.

Sex

The male-to-female ratio for neurogenic heterotopic ossification is 1:1.

Age

The incidence of neurogenic heterotopic ossification (NHO) after spinal cord injury is lower in pediatric patients than in adults, ranging from 3-10%. In addition, spontaneous resorption of the NHO is frequently seen in pediatric patients.2

Clinical

History

The adult patient with neurogenic heterotopic ossification (NHO) gives a history of progressive loss of ROM accompanied by pain or swelling in the involved area. Most pediatric patients present with decreased ROM but are less likely to have physical symptoms. The average length of time reported between injury and diagnosis of NHO in the adult population is 6 months, in contrast to 14 months after injury in the pediatric population. The use of 3-phase bone scanning to detect HO may result in a shorter average reporting time between injury and diagnosis.

Physical

Limited ROM is seen at the involved joint, possibly accompanied by redness, warmth, or swelling.

Causes

  • Debate continues on whether there is migration of distant mesenchymal cells or transformation of existing mesenchymal cells into osteoblasts. Osteoinductive factors have been studied, including circulating biochemicals and local factors (eg, venous thrombosis, venous insufficiency, decubitus ulcers, edema, tissue hypoxia). None of these factors has been proven to play a pivotal role in NHO.
  • Genetic predisposition for NHO has not been confirmed.
  • Patients with limb spasticity have a greater risk of developing NHO, and patients with extensive amounts of NHO have severe spasticity.

More on Heterotopic Ossification in Spinal Cord Injury

Overview: Heterotopic Ossification in Spinal Cord Injury
Differential Diagnoses & Workup: Heterotopic Ossification in Spinal Cord Injury
Treatment & Medication: Heterotopic Ossification in Spinal Cord Injury
Follow-up: Heterotopic Ossification in Spinal Cord Injury
Multimedia: Heterotopic Ossification in Spinal Cord Injury
References

References

  1. Banovac K, Sherman AL, Estores IM. Prevention and treatment of heterotopic ossification after spinal cord injury. J Spinal Cord Med. 2004;27(4):376-82. [Medline].

  2. Hitzig SL, Tonack M, Campbell KA, et al. Secondary health complications in an aging Canadian spinal cord injury sample. Am J Phys Med Rehabil. Jul 2008;87(7):545-55. [Medline].

  3. Orzel JA, Rudd TG. Heterotopic bone formation: clinical, laboratory, and imaging correlation. J Nucl Med. Feb 1985;26(2):125-32. [Medline][Full Text].

  4. Rapuano BE, Boursiquot R, Tomin E, et al. The effects of COX-1 and COX-2 inhibitors on prostaglandin synthesis and the formation of heterotopic bone in a rat model. Arch Orthop Trauma Surg. Mar 2008;128(3):333-44. [Medline].

  5. Schurch B, Capaul M, Vallotton MB. Prostaglandin E2 measurements: their value in the early diagnosis of heterotopic ossification in spinal cord injury patients. Arch Phys Med Rehabil. Jul 1997;78(7):687-91. [Medline].

  6. Svircev JN, Wallbom AS. False-negative triple-phase bone scans in spinal cord injury to detect clinically suspect heterotopic ossification: a case series. J Spinal Cord Med. 2008;31(2):194-6. [Medline].

  7. Kim SW, Wu SY, Kim RC. Computerized quantitative radionuclide assessment of heterotopic ossification in spinal cord injury patients. Paraplegia. Nov 1992;30(11):803-7. [Medline].

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  11. Freebourn TM, Barber DB, Able AC. The treatment of immature heterotopic ossification in spinal cord injury with combination surgery, radiation therapy and NSAID. Spinal Cord. Jan 1999;37(1):50-3. [Medline].

  12. Finerman GA, Stover SL. Heterotopic ossification following hip replacement or spinal cord injury. Two clinical studies with EHDP. Metab Bone Dis Relat Res. 1981;3(4-5):337-42. [Medline].

  13. Banovac K, Gonzalez F, Wade N. Intravenous disodium etidronate therapy in spinal cord injury patients with heterotopic ossification. Paraplegia. Oct 1993;31(10):660-6. [Medline].

  14. Schuetz P, Mueller B, Christ-Crain M, et al. Amino-bisphosphonates in heterotopic ossification: first experience in five consecutive cases. Spinal Cord. Oct 2005;43(10):604-10. [Medline].

  15. Vanden Bossche LC, Van Maele G, Wojtowicz I, et al. Free radical scavengers are more effective than indomethacin in the prevention of experimentally induced heterotopic ossification. J Orthop Res. Feb 2007;25(2):267-72. [Medline].

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  18. Bravo-Payno P, Esclarin A, Arzoz T. Incidence and risk factors in the appearance of heterotopic ossification in spinal cord injury. Paraplegia. Oct 1992;30(10):740-5. [Medline].

  19. Colachis SC 3d, Clinchot DM, Venesy D. Neurovascular complications of heterotopic ossification following spinal cord injury. Paraplegia. Jan 1993;31(1):51-7. [Medline].

  20. Garland DE. A clinical perspective on common forms of acquired heterotopic ossification. Clin Orthop Relat Res. Feb 1991;13-29. [Medline].

  21. Garland DE, Shimoyama ST, Lugo C, et al. Spinal cord insults and heterotopic ossification in the pediatric population. Clin Orthop Relat Res. Aug 1989;303-10. [Medline].

  22. Jaovisidha S, Sartoris DJ, Martin EM. Influence of heterotopic ossification of the hip on bone densitometry: a study in spinal cord injured patients [see comments]. Spinal Cord. Sep 1998;36(9):647-53. [Medline].

  23. Nagaraj N, Elgazzar AH, Fernandez-Ulloa M. Heterotopic ossification mimicking infection. Scintigraphic evaluation. Clin Nucl Med. Sep 1995;20(9):763-6. [Medline].

  24. Renfree KJ, Banovac K, Hornicek FJ. Evaluation of serum osteoblast mitogenic activity in spinal cord and head injury patients with acute heterotopic ossification. Spine. Apr 1 1994;19(7):740-6. [Medline].

  25. Snoecx M, De Muynck M, Van Laere M. Association between muscle trauma and heterotopic ossification in spinal cord injured patients: reflections on their causal relationship and the diagnostic value of ultrasonography. Paraplegia. Aug 1995;33(8):464-8. [Medline].

  26. Stover SL, Hataway CJ, Zeiger HE. Heterotopic ossification in spinal cord-injured patients. Arch Phys Med Rehabil. May 1975;56(5):199-204. [Medline].

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Further Reading

Keywords

heterotopic ossification, HO, spinal cord injury, SCI, traumatic brain injury, TBI, ossification, ectopic calcification, heterotopic bone, heterotopic bone formation, ossified, neurogenic heterotopic ossification, paraosteoarthropathy of paraplegia

Contributor Information and Disclosures

Author

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: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching

Medical Editor

Robert L Sheridan, MD, Assistant Chief of Staff, Chief of Burn Surgery, Shriners Burns Hospital; Associate Professor of Surgery, Department of Surgery, Division of Trauma and Burns, Massachusetts General Hospital and Harvard Medical School
Robert L Sheridan, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Surgery of Trauma, American Burn Association, and American College of Surgeons
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Kat Kolaski, MD, Assistant Professor, Departments of Orthopedic Surgery and Pediatrics, Wake Forest University School of Medicine
Kat Kolaski, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation
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

Robert H Meier III, MD, Director, Amputee Services of America; Active Medical Staff, Presbyterian/St Luke's Hospital, Spalding Rehabilitation Hospital, Select Specialty Hospital; Consulting Staff, Kindred Hospital
Robert H Meier III, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists
Disclosure: Nothing to disclose.

 
 
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