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Thread: Heterotopic ossification

  1. #1

    Heterotopic ossification

    How serious is heterotopic ossification ?

  2. #2
    Quote Originally Posted by Colin83 View Post
    How serious is heterotopic ossification ?
    This may be a topic for a new thread, but in the mean time, here is an article written by Dr. Young and posted on this thread in 2008. http://sci.rutgers.edu/forum/showthr...c+ossification

    A review of Heterotopic Ossification
    HETEROTOPIC OSSIFICATION
    Wise Young, Ph.D., M.D.
    25 August 2008


    Heterotopic ossification (HO) is a abnormal bone formation outside of the skeleton. It usually occurs in muscle but can also appear in tendon and tendon sheath and fat. It usually presents as a localized inflammatory mass in muscle, usually in the lower limbs. The limb may be warm and swollen. Fever may be present. If sensation is present, the area of swelling is tender and painful. Range of motion may be present. HO of the hip or knee may be associated with effusion at the knee. Blood tests may show elevated creatine kinase (indicative of muscle damage), inflammatory C-reactive protein, and occasionally elevated alkaline phosphatase; none of these, however, are specific to HO.

    HO syndromes. Myositis ossificans traumatica occurs after blunt injury, surgery, or burns. Nontraumatic myositis ossificans is when no trauma has occurred. Panniculitis ossificans is in subcutaneous fat. Rider’s bones are in leg adductor muscles and Shooter’s bones are in deltoid muscle. Münchmeyer disease or fibrodysplasia ossificans progressiva (FOP) is a very rare disease characterized by ossification of fascial planes, muscles, tendons, and ligaments. Albright hereditary osteodystrophy, progressive hteroplasia, and primary osteoma cutis are other genetic disease that manifest HO. In general HO can be classified into three types: FOP, traumatic, and neurogenic.

    Risk of HO. Many neurological diseases are associated with HO, including spinal cord injury, brain injury, tetanus, poliomyelitis, Guillain-Barre syndrome, and even prolonged pharmacological paralysis during mechanical ventilation. Other bone-forming disorders increase the risk for HO, including diffuse idiopathic skeletal hyperostosis, ankyosing spondylitis, and Paget disease. A prior history of HO increases the risk of further occurrences. HO is a common complication of arthroplasty procedures with a 20-30% risk, approaching 100% if the patient had a previous HO in a previous arthroplasty site or if the patient has spinal cord injury. Males are twice as likely to develop HO than females. It is rare in young children.

    Incidence. In spinal cord injury, the incidence ranges from a low of 3.4% to a high of 47% (e.g. 62 of 131 patients with SCI admitted to the Hot Spring Rehabilitation Center). Most reports indicate an incidence of 20-30% with severe functional limitations in 3-8%. Peak incidence is 4-12 weeks after spinal cord and can be develop as late as 5 months after trauma. Later onset have been reported but is very rare. Between 10-35% of patients with spinal cord injury have significantly reduced range of motion (ROM) of the affected joint; 3% of an ankylosed joint due to HO. In spinal cord injury, if HO occurs, it is always below the injury level The incidence of HO after severe head injury range from 11-76%. In one study by Garland, et al., HO affected 100 joints in 57 of 496 patients.

    Causes of HO. HO results from osteoprogenitor cells that are present in soft tissues. With proper stimulation, these cells produce osteoblasts, which begins osteoid formation, eventually forming heterotopic bone. Several bone growth factors, i.e. bone morphogenetic proteins (BMP), can cause HO when injected into soft tissues. The genetic disease FOP involves mutations of two sites, one in the region of the noggin gene (NOG) which inhibits BMP’s. The second site is on the long arm of chromosome 4, in the region of a known BMP-signalling pathway gene. People with FOP have an overproduction of BMP.

    Pathophysiology. HO starts with spindle cell formation within a week of a traumatic event. Primitive osteoid dvelops in the periphery of the lesion with 7-10 days. Primitive cartilage and woven bone can be seen at 2-5 weeks after trauma. At 6 weeks, mature lamellar bone can be observed. Thus, HO can form relatively quickly after a traumatic event. The most common site s the hip, following total hip arthroplasty, spinal cord injury, or brain injury. In head injury, the next most common sites are shoulder and elbows but not knees. In spinal cord injury, the next most common site is the knee.

    Diagnosis. HO usually manifests as a painful palpable mass that becomes non-tender and smaller and firmer to touch. In spinal cord injury, patients frequently have leg pain and swelling without any history of trauma to the leg. It may be difficult to differentiate HO from deep venous thrombosis (DVT), since both may present with leg pain, swelling, and erythema (redness). In fact, the two often occur together since the mass effect of HO may encourage DVT. The preferred imaging method is x-ray, either plain or CT but cannot detect HO during the first 2 weeks. Bone scanning may detect early formation. Ultrasound may be useful as a screening tool in the hip region and can be applied at the same time as a DVT exam. In inexperienced centers, a CT scan provides a definitive diagnosis of a calcified mass in soft tissue. A biopsy may be necessary if there is any reason to suspect neoplasm. A false negative is common because until mineralization is present. Therefore, followup CT or x-ray showing characteristic progression in 2-3 weeks will confirm the diagnosis. Magnetic resonance is not definitive, usually showing a heterogenous high T2 signal in soft tissue mass with gadolinium enhancement during the early phase and a low-intensity rim with high T1 and T2 intensification in the central portion, probably representing marrow fat. Percutaneous biopsy is contraindicated because it may yield a small sample that is potentially confusing to inexperienced pathologists. The presence of high cellular activity coupled with new bone formation may be mistakened for osteoblastic neoplasm, such a osteosarcoma. Open biopsy may exacerbate the HO, causing it to progress. If a biopsy is carried out after a resection, it may cause a recurrence of the condition. The recommended approach is:
    • Plain x-ray. One may see a faint band of calcification at early stages of swelling.
    • CT-scan. At later stages, both non-contrast CT scan and x-ray should ossified mass.
    • Technetium-99m methylene diphosphonate bone scan should show marked uptake.
    • MRI should show a central heterogeneous high T2 signal with low signal surrounding.
    • Ultrasound scan shows heterogeneous central hypo- and peripheral hyper-echogenic mass.

    Treatment. Four classes of therapies are used for HO.
    • Anti-inflammatory drugs such as indomethacin (75 mg/day) and the COX-2 inhibitor rofecoxib (25 mg/day) reduces the risk of HO by 2-3x.
    • Physical therapy. Controversy surrounds the benefits and extent of physical therapy to be used, once the HO has occurred. It is generally acknowledged that lack of range of motion and movement may lead to further loss of joint function. On the other hand, some people believe that physical therapy may aggravate the condition.
    • Surgical excision. Once the HO has developed to the extent of interfering with function, surgery is the only option. Most operations involve wedge resection.
    • Radiation therapy has been used but the dose, frequency, and timing has not yet been determined. The rationale is that mesenchymal stem cells that contribute osteoprogenitor cells are radiosensitive. Radiation is used more in Europe. The risk of local induction of malignancy have not been determined.
    • Bisphosphonates may reduce bone formation. Etidronate sodium (Didronel) is given 20 mg/kg PO p24h followed by 10 mg/kg q24h for 10 weeks.

    Pitfalls to avoid.
    • Surgical excision may aggravate HO. If surgery is done, the tissues must be minimally manipulated and care must be taken to achieve rigorous hemostasis. Be wary of lesions that cross tissue planes. Relief of pain is seldom achieved. For this reason, surgery should not be carried out until the lesion is matured and there is significant functional limitation. Traditionally, surgeons have delayed surgery by 18 months after brain injury. However, such case studies suggest that very early removal may be more effective.
    • Non-steroidal anti-inflammatory drugs may have significant side-effects. Long-term aspirin and indomethacin may not be well-tolerated and COX-2 inhibitors is likely to replace indomethacin use.
    • Do not be afraid of physical therapy. While animal studies suggest that excessive stretching and can aggravate HO, there is no evidence that this is the case in humans. Lack of physical therapy has much worse consequences including restricted range of motion, muscle atrophy, and other consequences of inactivity.

    References

    1. Moore DS (2007). Heterotopic Ossification. Emedicine. http://www.emedicine.com/radio/topic336.htm
    2. Campagnolo DI (2006). Heterotopic Ossification in Spinal Cord Injury. Emedicine. http://www.emedicine.com/pmr/TOPIC52.HTM
    3. Bruno-Petrina A (2008). Posttraumatic Heterotopic Ossification Emedicine. http://www.emedicine.com/pmr/TOPIC112.HTM
    4. McLean C, Hargrove R, Wood JB (2006). Traumatic Heterotopic Ossification. Emedicine http://www.emedicine.com/orthoped/TOPIC401.HTM
    5. Banovac K, Speed J (2008). Heterotopic Ossification. Emedicine. http://www.emedicine.com/pmr/TOPIC51.HTM
    Wise Young is offline Reply With Quote


    All the best,
    GJ

  3. #3
    The short answer (layman's terms) based upon the medical studies I've read (and the answer from gjnl) is that in most cases heterotopical ossification can be diagnosed and fixed, and it normally doesn't cause more than swelling and discomfort in most cases. Any of the pros want to corroborate that?
    Angelina Caradine is an ultrasound technician.

  4. #4
    Quote Originally Posted by ultrasoundtech View Post
    The short answer (layman's terms) based upon the medical studies I've read (and the answer from gjnl) is that in most cases heterotopical ossification can be diagnosed and fixed, and it normally doesn't cause more than swelling and discomfort in most cases. Any of the pros want to corroborate that?
    No, that is not the case in SCI. There is no easy "fix" for HO, and it causes major problems for most people with SCI who get it. Making the diagnosis is not difficult, but it can cause major problems with mobility, pain, and skin breakdown. Surgery to remove it is difficult, bloody, and commonly associated with fairly high infection risks, and should not be done until the bony growth matures, which may be several years. The medications used have many side effects. I have seen amputations and other serious complications as a result.

    (KLD)

  5. #5
    Senior Member
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    Quote Originally Posted by Colin83 View Post
    How serious is heterotopic ossification ?
    It is SERIOUS!

    My hips have been entirely fused for 45 years. This makes everything much more complicated than it would be without it. My HO is still growing bone, especially if there is any injury to the affected areas.

    I don't know why you are asking, but if you think you are getting HO you need competent medical advice, and you need it quickly.
    T4 complete, 150 ft fall, 1966. Completely fused hips, partially fused knees and spine, heterotopic ossification. Unsuccessful DREZ surgery about 1990. Successful bladder augmentation using small intestine about 1992. Normal SCI IC UTI problems culminating in a hospital stay in 2001. No antibiotics or doctor visits for UTI since 2001: d-mannose. Your mileage may vary.

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