eMedicine Specialties > Radiology > Musculoskeletal

Heterotopic Ossification

Daniel S Moore, MD, Department of Radiology, Assistant Professor, University of Texas Southwestern Medical Center at Dallas
Gina Cho, MD, Assistant Professor, Department of Radiology, Parkland Hospital, University of Texas Southwestern Medical Center

Updated: Nov 6, 2007

Introduction

Background

Heterotopic ossification (HO) is the abnormal formation of true bone within extraskeletal soft tissues. Classically, many diseases sharing this common feature were lumped into the category myositis ossificans; however, the term has fallen into disfavor because primary muscle inflammation is not a necessary precursor for such ossification and the ossification does not always occur in muscle tissue (frequently showing a predilection instead for fascia, tendons, and other mesenchymal soft tissues). The term heterotopic ossification has largely replaced myositis ossificans in the literature.

Traditionally, various forms of HO have been classified according to the clinical setting and location of the lesions, as well as according to whether the lesions are progressive or isolated in occurrence. The varieties of HO are as follows:

• Myositis ossificans traumatica - HO occurring after recalled trauma, such as blunt injury, surgery, or burns
• Nontraumatic myositis ossificans - HO that occurs when no inciting trauma can be identified
• Panniculitis ossificans - HO confined to subcutaneous fat
• Rider's bones - HO found in the adductor muscles
• Shooter's bones - HO located in the deltoid muscle

A strong association exists between HO and spinal cord injury, with lesions occurring at multiple sites and showing a strong propensity to recur. Similarly, periarticular HO is seen in patients with traumatic brain injury, with the extent and functional severity of the HO directly related to the severity of the intracranial injury. (See also the eMedicine articles Heterotopic Ossification [in the Physical Medicine and Rehabilitation section], Traumatic Heterotopic Ossification, Posttraumatic Heterotopic Ossification, and Heterotopic Ossification in Spinal Cord Injury.)

Many other causes of neurologic compromise, including tetanus, poliomyelitis, Guillain-Barré syndrome, and prolonged pharmacologic paralysis during mechanical ventilation, also have been associated with HO formation.

Fibrodysplasia ossificans progressiva (FOP), or Münchmeyer disease, is an autosomal dominant, severely disabling condition that results in progressive ossification of fascial planes, muscles, tendons, and ligaments. (See also the eMedicine article Myositis Ossificans.) Congenital malformation of the great toes also is associated with FOP. HO is a feature of several other diseases as well, including Albright hereditary osteodystrophy, progressive osseous heteroplasia, and primary osteoma cutis, but these are beyond the scope of this article.

Pathophysiology

HO originates from osteoprogenitor stem cells lying dormant within the affected soft tissues.¹ With the proper stimulus, the stem cells differentiate into osteoblasts and begin the process of osteoid formation, eventually leading to mature heterotopic bone. A variety of bone morphogenetic proteins (BMPs) can stimulate HO when experimentally deposited into soft tissues, suggesting that BMPs play a role in the initiation of HO.² A degree of neurologic control is implied but is not well understood.

Potentially causative mutations for FOP have been mapped to 2 sites, adding to the evidence of the BMPs' role in HO formation. The first site lies on the long arm of chromosome 17, in the region of the noggin gene (NOG). The noggin protein inhibits BMPs. The second genetic location is on the long arm of chromosome 4, in the region of a known BMP-signaling pathway gene. Bone morphogenetic protein 4 is overproduced in patients with FOP.

The typical histologic evolution of HO following trauma begins with spindle cell proliferation within the first week of the traumatic event. Primitive osteoid develops at the periphery of the lesion within 7-10 days. Primitive cartilage and woven bone can be seen in the second week, with trabecular bone forming at 2-5 weeks after the inciting trauma. After approximately 6 weeks, a zonal phenomenon characterized by immature, undifferentiated, central tissues and mature, peripherally located lamellar bone can be observed.

Frequency

International

Risk factors for HO include the presence of other bone-forming disorders, such as diffuse idiopathic skeletal hyperostosis, ankylosing spondylitis, and Paget disease. A personal history of previous HO also increases the risk of future occurrences. HO complicates 8-71% of total hip arthroplasty procedures, with the risk approaching 100% if the patient has had HO in a previous total arthroplasty site. Of patients with neurologic deficits, 20-30% develop HO, with as many as 50% of patients with spinal cord injury affected in some studies.

Mortality/Morbidity

The clinical impact of HO depends on the clinical setting and extent of the disease. A single lesion caused by trauma usually stabilizes and may regress; resulting symptoms depend on the location and size of the lesion. HO related to spinal cord injury or traumatic brain injury tends not to regress and may cause pain and decreased range of motion in affected joints; in such cases, the condition occasionally results in complete ankylosis and severe disability.³  Among patients with neurologic deficits, 8-10% have severe functional limitations resulting directly from HO. The extent of involvement is correlated positively with poorer outcome in rehabilitation patients recovering from traumatic brain injury. In patients with spinal cord injuries, large foci of HO can lead to skin breakdown and the inability to sit upright. Malignant degeneration to osteosarcoma has been reported but is extremely rare.

In FOP, the number and extent of lesions progress inexorably, with a consequent loss of normal limb and spinal function. Death may occur from recurrent respiratory infections resulting from chest wall restriction.

Race

Race does not appear to be a strong predisposing factor for HO in the setting of injury of the spinal cord, a site for which data are available. FOP might be expected to have racial or ethnic predilections because of its heritable nature; however, most cases are sporadic in nature because frequently patients who are affected do not have children.

Sex

Male patients with spinal cord injury are twice as likely to develop HO as are female patients.⁴ No strong sex predilection exists in FOP.

Age

Isolated HO can occur at any age but is rare in very young children. Posttraumatic HO is, not surprisingly, most common in young, athletic persons. In some studies, HO has been found to more frequently affect young patients (20-30 y) with spinal cord injury. Other studies have found no correlation between age and HO formation. In contrast, FOP tends to manifest in patients by age 5 years, causing severe restriction of upper extremity movement in most patients by age 15 years.

Anatomy

Posttraumatic HO can be found at any site. The most common postsurgical site is the hip, following total hip arthroplasty. The hip is also the most common site of HO occurrence in patients with traumatic brain injury or spinal cord injury. The next most common sites of involvement in patients with traumatic brain injury are the shoulders and elbows, with the knees rarely being affected. In contrast, knees frequently are involved in patients with spinal cord injury.

In FOP, involvement typically progresses from the axial to the appendicular skeleton, from cranial to caudal, and from proximal to distal. The disease typically spares the tongue, extraocular muscles, and diaphragm, as well as the cardiac and smooth muscles.

Presentation

Following trauma, HO often begins as a painful, palpable mass that gradually becomes nontender and smaller, as well as firmer to palpation. In spinal cord injury, patients frequently complain of lower extremity pain and swelling without antecedent trauma.

Some FOP lesions follow a specific traumatic event that the patient clearly remembers, but more often they are spontaneous, with the patient being unable to recall the occurrence of any recent trauma. Swelling, warmth, erythema, and pain are initially present. Over a period of weeks, the pain and swelling improve and may resolve completely. Alternatively, a hard, nontender, ossified lesion may arise approximately 6-12 weeks after the onset of symptoms at the site.

Differentiating early HO from lower extremity deep venous thrombosis (DVT) presents a particularly difficult diagnostic dilemma. The 2 conditions can present with the same symptoms of lower extremity pain, swelling, and erythema. Both occur more frequently in similar patient populations, namely, patients with spinal cord and traumatic brain injuries. In addition, HO and DVT have been positively associated, perhaps because the mass effect and local inflammation of HO encourage adjacent thrombus formation by causing venous compression and phlebitis.

Preferred Examination

Radiography is the preferred method of initial assessment for virtually all musculoskeletal conditions, including HO. Given their relatively low expense, radiographs should be obtained first (even if other imaging modalities are planned) in order to assess the extent of known HO.

Bone scanning is the method of choice for earliest detection and, once the diagnosis is established, for assessing the maturity of a known lesion.

Ultrasonography may have a role as a screening tool in the hip region after spinal cord injury; ultrasonograms may be obtained during a DVT screening examination.

Limitations of Techniques

Radiographs cannot detect the mineralization of HO during the first 1-2 weeks after the inciting trauma or the onset of symptoms. However, radiographs are recommended in all patients with suggested HO to assess underlying bone pathology and exclude other pathology.

Neither radiography nor computed tomography (CT) scanning should be performed in the pelvic region during pregnancy because of radiation exposure to the fetus, unless the risks of radiation exposure are outweighed by the need for a timely diagnosis. Nuclear medicine bone scanning also involves exposure of the fetus to radiation, regardless of the anatomic site being imaged, and should, if possible, be postponed until after delivery.

Ultrasonography is an operator-dependent modality. Proper evaluation of soft-tissue masses, including HO, requires considerable training and experience, available at some centers in the United States and, more commonly, in Europe. Radiologists who are less familiar with musculoskeletal ultrasonographic images may be more comfortable using CT scanning or nuclear medicine modalities to make the diagnosis of early HO.

Differential Diagnoses

Deep Venous Thrombosis, Lower Extremity
Osteomyelitis, Chronic
Osteosarcoma, Variants

Other Problems to Be Considered

Cellulitis
Diabetic muscle infarct
Hematoma
Hydroxyapatite deposition disease
Pyomyositis
Tumoral calcinosis

Radiography

Findings

A soft-tissue mass is the earliest radiographic finding of HO, although a mass is often overlooked at sites such as the hip and thigh. Mineralization of the osteoid lesional content can be seen as early as 10-14 days after the inciting trauma. A peripheral zone of early mineralization is the most common pattern, although many lesions have a less organized appearance. Typically, HO associated with FOP first mineralizes centrally. If untreated, mature cortical bone ultimately results.

Degree of Confidence

Peripheral ossification of a soft-tissue mass at the site of recent trauma is consistent with HO. Performing a biopsy to exclude a neoplasm should be avoided. Instead, delayed radiographs should be performed in 4 weeks to confirm maturation of the lesion into typical HO.

False Positives/Negatives

False positives can be caused by avulsion fracture fragments, osteochondral bodies within a distended joint capsule, nonosseous soft-tissue calcification (which can resemble amorphous, early mineralization of woven bone), and osteosarcoma.

False negatives are common, most often occurring in lesions in which it is too early for mineralization to be seen radiographically or at sites that have been obscured by generous, overlying soft tissues or by normal bone. Sensitivity and specificity increase with time as lesions display more mature, dense ossification.

Computed Tomography

Findings

The earliest CT scan findings include a low-attenuation soft-tissue mass or an enlarged muscle belly, occasionally with indistinct, adjacent soft-tissue planes.⁵ Faint, immature bone mineralization becomes evident earlier than on radiographs, as lesions mature. With further maturation, lesions often demonstrate zonal mineralization with a mature peripheral cortex and may have central, fat-containing marrow elements. Abnormal, low-attenuation findings may persist in the soft tissues surrounding the mature cortex for months to years after the disease's onset.

Degree of Confidence

CT scans demonstrate high specificity for HO when the typical zonal pattern of peripheral mineralization is present.⁶ Earlier in the course of HO evolution, when the lesion appears as an enhancing mass with disorganized or absent mineralization, findings are nonspecific. A repeat CT scan after several weeks of further maturation may help resolve the diagnostic dilemma.

False Positives/Negatives

Many masslike conditions, including the presence of an inflammatory mass or a soft-tissue neoplasm, can mimic the early appearance of HO.

Magnetic Resonance Imaging

Findings

Magnetic resonance imaging (MRI) is not routinely employed for the evaluation of HO once the diagnosis is established. Cases are most often encountered when MRI is required to assess a mass that has been detected clinically. HO may be seen incidentally in patients at risk, such as paraplegics, in whom it may be found while they are undergoing assessment for pelvic osteomyelitis.

Early HO lesions demonstrate a heterogeneous, high T2 signal and a masslike enlargement of affected tissues.⁷ A low – signal-intensity rim may be seen. Frequently, an extensive, ill-defined, surrounding, high T2 signal is noted. Intravenous gadolinium administration results in early, intense, heterogeneous enhancement of lesions.

Delayed imaging that takes place weeks to months after onset demonstrates a low-signal rim corresponding to maturing cortical bone on radiographs, with persistence of the heterogeneous, high T2 signal lesional content and extensive surrounding edema.

Several months after HO's onset, imaging characteristics reveal decreasing edema within and surrounding the lesion. High T1 and T2 signals that are isointense to fat develop centrally, probably representing marrow fat. Late lesions typically do not enhance.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or magnetic resonance angiography (MRA) scans.

As of late December 2006, the Food and Drug Administration (FDA) had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

As on CT scans, early lesions have a very nonspecific appearance on magnetic resonance images.⁸ With time, the development of a zonal pattern of maturation may suggest HO, although the appearance is often misleading. Correlation with conventional radiographs is strongly recommended to confirm the diagnosis.

False Positives/Negatives

On magnetic resonance images, as on CT scans, many masslike conditions, including infectious, inflammatory, and neoplastic disorders, can have an appearance similar to that of HO.

Ultrasonography

Findings

Ultrasonography is not generally used to assess HO once the diagnosis is established. However, because of the overlap of clinical presentation with deep venous thrombosis, combined with the widespread use of ultrasonography to screen for DVT, ultrasonographers can expect to encounter HO in the lower extremities of patients at risk.⁹ Some authors have proposed the use of ultrasonography as a simultaneous screening tool for HO and DVT in patients with spinal cord injury.

Within a few hours of the onset of clinical symptoms, ultrasonograms demonstrate a chaotic disruption of the normal lamellar structure of skeletal muscle, which can be seen up to 10-14 days before radiographic evidence of HO appears. Later, still in the preradiographic phase, a zonal, masslike pattern develops that is peripherally echogenic and centrally hypoechoic. Once early mineralization becomes radiographically visible, ultrasonograms demonstrate sheets or irregular clumps of echogenic material with acoustic shadowing. Mature lesions have the echogenicity and dense shadowing of cortical bone.

Degree of Confidence

As with HO findings on magnetic resonance images, those on ultrasonograms should be confirmed with radiographs and followed for the typical maturation pattern of HO.

False Positives/Negatives

Early in the disorganized, preradiographic phase, HO can have an appearance similar to that of a variety of posttraumatic, inflammatory, and neoplastic conditions.

Nuclear Imaging

Findings

A 3-phase, radionuclide bone scan using technetium-99m (^99m Tc) methylene diphosphonate remains the criterion standard for detecting early HO.^10,11 The examination consists of a radionuclide angiogram followed by a blood pool image over the suggestive site. A delayed image is obtained 2-3 hours later.

Bone scans are typically positive more than 2 weeks before radiographic evidence of mineralization is seen, with some authors reporting positive findings on bone scan 4-6 weeks earlier than on radiographs. In very early lesions, only the first-pass or blood pool image findings may be abnormal, reflecting the hypervascularity of early HO. Soft-tissue uptake in the third phase subsequently develops within 1 week of the appearance of first-pass and second-pass abnormalities. Soft-tissue uptake is considered diagnostic of HO in the appropriate clinical setting.

Gallium-67 uptake is commonly demonstrated and may potentially be confused with infection in patients with spinal cord injuries.

Angiography

Findings

Early on, HO lesions are hypervascular, with numerous fine vessels that lack the disordered characteristics of tumor neovascularity (eg, arteriovenous shunting or puddling). Mature HO is usually avascular but may cause the extrinsic compression of adjacent vessels.

Intervention

Successful prophylaxis of patients at high risk for HO has included the use of external beam radiation and the administration of nonsteroidal anti-inflammatory agents such as indomethacin and naproxen. Long-term oral therapy using etidronate (typically for several months) is an effective treatment for early HO that has been detected by bone scan or ultrasonography. (See also the article Pharmacological Interventions for Treating Acute Heterotopic Ossification, on Medscape.)

Resection of HO has variable results but usually produces an improvement of function in all clinical settings except FOP (in which recurrence is a virtual certainty). Prophylaxis using indomethacin decreases the risk of recurrence after resection, except in FOP.

Medicolegal Pitfalls

• Failure to distinguish HO from an osteoblastic neoplasm, such as osteosarcoma. Aggressive imaging findings may lead to a percutaneous biopsy, which can yield a sample with high cellular activity and new bone formation; these characteristics can potentially be confusing to the pathologist. An open biopsy may fare no better; it can exacerbate the severity of HO or, if the biopsy follows an early resection, cause a recurrence of the condition. Biopsy is contraindicated in patients with an established diagnosis of FOP.
• Failure to use a conservative approach to follow-up radiologic imaging if developing HO is in the differential for a soft-tissue mass. Films can be obtained over a period of a few months at 2- to 4-week intervals to assess for the maturation of the osseous elements and increasing circumscription of the lesion (as opposed to the characteristics of an aggressive neoplasm's progression).

Multimedia

Media file 1: Anteroposterior radiograph of the right shoulder in a young man with a painful mass following recent blunt trauma. Soft-tissue swelling is present. A linear band of early mineralization (arrows) is faintly visible.

Media file 2: Delayed image from a technetium-99m (^99mTc) methylene diphosphonate bone scan (performed at the time of the first radiograph) demonstrates marked soft-tissue uptake of tracer.

Media file 3: Coronal, oblique, T2-weighted, fast spin-echo magnetic resonance image of the right shoulder obtained on the same day as the initial radiograph. A mass in the soft tissues lateral to the proximal right humerus has a central, heterogeneous, high T2 signal with a surrounding zone of lower signal intensity (arrows).

Media file 4: Anteroposterior radiograph obtained 5 weeks after the initial film demonstrates that maturing peripheral bone (black arrows) has replaced the initial mineralization. The mineralization pattern roughly corresponds with the peripheral low signal seen on magnetic resonance images. A solid periosteal reaction extends distally from the lesion (white arrow).

Media file 5: Noncontrast, axial computed tomography (CT) scan through the proximal thighs in a paraplegic patient with long-standing spinal cord injury. Mature heterotopic ossification surrounds the femoral shafts bilaterally, nearly obscuring the right femur (black arrowhead). A large decubitus ulcer overlies the ossification posteriorly (white arrows).

Media file 6: Noncontrast, axial computed tomography (CT) scan through the hips of a young woman with long-standing spinal cord injury. Large masses of mature heterotopic ossification replace the iliopsoas muscles anterior to both femoral heads.

Media file 7: Anteroposterior radiograph of the left knee in a patient with traumatic brain injury. Mature heterotopic ossification surrounds the medial femoral condyle, with a solid peripheral cortex (arrows).

Media file 8: Anteroposterior radiograph of the right knee in a patient with traumatic brain injury (same patient as in Image 7) demonstrates mature heterotopic ossification in the same distribution as on the left knee. The hips, shoulders, and elbows are more common sites of involvement in the setting of traumatic brain injury.

Media file 9: Longitudinal ultrasonogram of the medial thigh in a 20-year-old patient with paraplegia who has a hard, palpable mass. The heterogeneous, central, hypoechogenic mass is surrounded peripherally by more echogenic material (arrows). A core biopsy under ultrasonographic guidance revealed immature heterotopic ossification (HO). A computed tomography (CT) scan at the time did not demonstrate mineralization, although later radiographs showed typical HO. Courtesy of Dr Robert Lopez, Department of Radiology, University of Alabama at Birmingham.

Media file 10: Attempted frog-leg, lateral radiograph of the left hip. Mature heterotopic ossification (HO) surrounds the greater and lesser trochanters of the femur in this patient, who had a bipolar hip prosthesis placed 2 months earlier. The large amount of HO resulted in a significantly reduced range of motion.

Media file 11: Magnified view of an anteroposterior radiograph of the right tibia in a patient with a palpable anterior mass of the lower leg and a remote history of trauma. Dystrophic-appearing calcifications project over the interosseous membrane and fibular shaft.

Media file 12: Noncontrast, axial computed tomography (CT) scan through a palpable mass demonstrates dystrophic-appearing calcifications scattered throughout a soft-tissue mass in the anterior compartment. An open biopsy revealed heterotopic ossification (HO). While mature HO typically has lamellar peripheral bone in a zonal distribution, bizarre patterns of mineralization also can occur.

Media file 13: Axial computed tomography (CT) scan in a male patient with lower extremity swelling 8 weeks after a spinal cord injury. Peripheral mineralization (arrows) is seen in immature heterotopic ossification within the quadratus femoris muscle.

Media file 14: Corresponding noncontrast, axial, T1-weighted image from a magnetic resonance imaging (MRI) scan performed on the same day as the axial computed tomography (CT) scan (same patient as in Image 13) demonstrates a masslike enlargement of the right quadratus femoris.

Media file 15: Axial, T2-weighted, fast spin-echo, fat-suppressed magnetic resonance image (same patient as in Images 13-14). Extensive edema is present bilaterally in several muscle groups. A high T2 signal alone is a nonspecific finding in patients with spinal cord injury, potentially heralding a site of heterotopic ossification development but often resolving spontaneously. A low signal seen peripherally in the right quadratus femoris (arrow) corresponds to the mineralization observed on the computed tomography (CT) scan seen in Image 13.

Media file 16: Axial, spin-echo, T1-weighted, fat-suppressed magnetic resonance image following intravenous gadolinium administration. In addition to extensive abnormal enhancement surrounding both hips, an unusual nonenhancing area (arrows) is noted anteromedial to heterotopic ossification (HO) demonstrated on computed tomography (CT) scan. The corresponding T2-weighted image does not show a discrete fluid collection in the region. A similar pattern has been seen in association with HO in other patients with spinal cord injuries.

Media file 17: Coronal, T1-weighted magnetic resonance image through the posterior pelvis in a patient with left-sided sciatica. An elongated mass of mature heterotopic ossification (arrowheads) with a peripheral low signal and a central fat signal replaces the proximal hamstrings parallel and adjacent to the sciatic nerve (arrow).

Media file 18: Axial, T2-weighted, fast spin-echo magnetic resonance image through the lower pelvis demonstrates the marrow fat (arrow) within the mature heterotopic ossification (HO) that replaces the semitendinosus and biceps femoris tendons. HO in this region results from a prior ischial tuberosity avulsion injury and can be symptomatic when it impinges on the adjacent sciatic nerve.

Media file 19: Anteroposterior radiograph of the right hip in a 16-year-old boy who had suffered trauma to the hip 2 years previously. The patient is currently experiencing hip pain. Mature heterotopic ossification (arrowheads) projects over and lateral to the femoral head.

Media file 20: Corresponding lateral view of the right hip (same patient as in Image 19). Distal to the mature heterotopic ossification (HO) seen on the anteroposterior view (arrowheads) is a subtle area of early mineralization (arrows) consistent with early HO.

Media file 21: First-pass, or angiogram phase, of a technetium-99m (^99mTc) methylene diphosphonate bone scan on a 16-year-old boy (same patient as in Images 19-20) demonstrates no significant abnormality.

Media file 22: Second-pass, blood pool image (same patient as in Images 19-21) demonstrates abnormal uptake in the right femoral head region (white arrow) corresponding to the mature heterotopic ossification (HO) seen radiographically. A second area of uptake over the proximal right femoral shaft (black arrow) correlates with the wispy mineralization of early HO, seen on the lateral view.

Media file 23: Third-phase, delayed image also shows abnormal tracer uptake over the femoral head (arrowhead) and proximal femoral shaft (arrow).

Media file 24: Axial, T1-weighted magnetic resonance image through the proximal, mature heterotopic ossification demonstrates a heterogeneous mass—replacing the rectus femoris and a portion of the iliopsoas—with a central fat signal anterior to the femoral head.

Media file 25: Axial, T2-weighted, short tau inversion recovery (STIR) image (same patient as in Image 24) demonstrates a low signal and shows no appreciable edema.

Media file 26: Axial, T2-weighted, short tau inversion recovery (STIR) image through the more distal area of early mineralization reveals prominent soft-tissue edema consistent with early, immature heterotopic ossification.

Media file 27: Anteroposterior radiograph performed in external rotation of the right shoulder in a 62-year-old female patient. Amorphous calcification is seen superolateral to the humeral head (arrows). The characteristics of this calcification are not indicative of heterotopic ossification (HO); the mature cortical or trabecular structures seen in mature HO are not found, nor are the well-defined margins that are consistent with the immature woven bone of early HO.

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Keywords

ectopic ossification, heterotopic bone formation, myositis ossificans, ossifying fibromyopathy, panniculitis ossificans, para-articular ossification, paraosteoarthropathy, periarticular new bone formation, HO

Contributor Information and Disclosures

Author

Daniel S Moore, MD, Department of Radiology, Assistant Professor, University of Texas Southwestern Medical Center at Dallas
Daniel S Moore, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Radiology, Association of University Radiologists, Radiological Society of North America, and Society of Skeletal Radiology
Disclosure: Nothing to disclose.

Coauthor(s)

Gina Cho, MD, Assistant Professor, Department of Radiology, Parkland Hospital, University of Texas Southwestern Medical Center
Gina Cho, MD is a member of the following medical societies: Alpha Omega Alpha, American Roentgen Ray Society, and Radiological Society of North America
Disclosure: Nothing to disclose.

Medical Editor

Giuseppe Guglielmi, MD, Associate Professor of Radiology, Department of Radiology, Scientific Institute Hospital
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

William R Reinus, MD, MBA, FACR, Professor of Radiology, Temple University; Chief of Musculoskeletal and Trauma Radiology, Vice Chair, Department of Radiology, Temple University Hospital
William R Reinus, MD, MBA, FACR is a member of the following medical societies: American College of Physician Executives, American College of Radiology, American Roentgen Ray Society, Missouri State Medical Association, and Radiological Society of North America
Disclosure: Nothing to disclose.

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Felix S Chew, MD, MBA, EdM, Professor, Department of Radiology, Vice Chairman for Radiology Informatics, Section Head of Musculoskeletal Radiology, University of Washington
Felix S Chew, MD, MBA, EdM is a member of the following medical societies: American Roentgen Ray Society, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

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