Myositis ossificans (MO), in its literal translation, implies an inflammatory ossification of muscle. As early as 1905, Jones and Morgan1 questioned whether a benign ossifying tumor following trauma was a true inflammatory neoplastic entity. In 1913, Coley2 reported on three cases of traumatic MO and recognized the difficulty but importance of differentiating it from sarcoma. Ackerman3 in 1953 clearly argued that MO was a poor designation, “established by custom,” for a group of lesions appearing in soft tissue that may or may not be associated with the periosteum. He sometimes found no associated inflammation and occasionally found no bone or muscle in the pathophysiologic process. Ackerman3 not only challenged the literal definition of the term MO but also, like Coley,2 clearly recognized the challenges of distinguishing it from more sinister etiologies.3
Historically, the term MO has been used to describe a broad spectrum of processes ranging from benign solitary lesions to progressive congenital syndromes (eg, MO progressiva). In 1923, Lewis4 classified MO into three forms: traumatic, nontraumatic, and neurotic. A year later, Noble5 classified MO into myositis (fibrous) ossificans progressiva, traumatic MO circumscripta, and MO circumscripta without history of trauma. The latter includes the more descriptive pseudomalignant as well as idiopathic forms associated with burns, polio, paraplegia, or infections.
More recently, Kransdorf et al6 defined MO as a benign, solitary, self-limiting, ossifying soft-tissue mass typically occurring within skeletal muscle; this is likely the most current accepted understanding of the term. Moreover, the actual pathophysiologic process is not dependent on the associated etiology.7 The variability in terminology, clinical presentation, imaging characteristics, and histopathology at times continues to make the diagnosis of MO challenging. However, accurate diagnosis is paramount to the formation of an optimal treatment plan. Similarly, a multidisciplinary team approach is helpful because MO may share similarities with malignancy, and the imaging characteristics, histopathology, and subsequent treatment vary depending on its stage of evolution.
The pathophysiology of MO formation is incompletely understood.8,9 It is believed to occur through inappropriate differentiation of fibroblasts into osteogenic cells.10 Kan et al11 demonstrated that the cellular mechanism of heterotopic bone formation is the result of the dysregulation of local stem cells in response to tissue injury and subsequent inflammation. Recent studies have demonstrated that extraskeletal bone formation may be dependent on a process known as endothelial-mesenchymal transition (Figure 1). Skeletal muscle injury induces a local inflammatory cascade, which leads to release of cytokines (bone morphogenetic protein-2 and -4 and transforming growth factor). These cytokines act on vascular endothelial cells of skeletal muscle and cause them to undergo endothelial-mesenchymal transition. These endothelial-derived mesenchymal stem cells may differentiate into chondrocytes or osteoblasts when exposed to an inflammatory-rich environment. Chondrocytes will then undergo endochondral bone formation in extraskeletal tissue.12
Clinically, MO progresses through parallel radiographic, clinical, and histopathologic stages7,9,10 (Table 1). Description of these stages varies slightly between authors; however, three overlapping stages of evolution are commonly described: early, intermediate, and mature.7,9 The early stage occurs during the first 4 weeks following injury and is characterized by an inflammatory cascade that precedes ossification; therefore, calcifications are often not apparent radiographically during this period. As the lesion matures through the intermediate stage (4 to 8 weeks), calcification becomes apparent radiographically.7,9 The mature stage follows, characterized by pronounced peripheral bone formation. Lesion maturation continues during the following months, culminating in consolidation and, finally, regression.9
The presentation of MO is variable. Most often, patients recall a specific injury or repetitive minor trauma. The classic scenario is pain and joint stiffness following blunt soft-tissue trauma (eg, a football player who suffers blunt trauma to the thigh); young active males are the most commonly affected.7,13 Similarly, repetitive minor trauma is commonly associated with the development of MO. For example, horseback riders may develop MO in the adductor muscle groups, a condition commonly known as rider’s bone, and shooters may develop MO in the deltoid, commonly referred to as shooter’s bone.10 Thus, the flexor muscles of the arm and extensor muscles of the thigh are the most commonly affected locations.7,10 However, an inciting event may not be initially disclosed.
Subjectively, patients report muscle pain that persists longer than would be expected for a simple muscle strain or contusion. Pain is commonly the result of the lesion causing mechanical irritation of a surrounding bursa, tendon, or joint. However, associated paresthesia, weakness, lymphedema, and venous thromboembolic disease have been reported when MO compresses nearby neurovascular structures.10 Symptoms often abate as the lesion matures.14 Consequently, patients who present late may not have significant symptomatology.9,10,14
Garland15 reported that the most common initial sign is limited range of motion of an adjacent joint, with up to 20% of patients developing clinically significant functional limitations. Similarly, <10% of patients develop frank ankylosis. Edema is often present acutely; however, it may be difficult to identify when muscle injury occurs in large muscle groups.15 Decreased range of motion to the knee after injury has been correlated with the development of MO in the thigh.16 Ryan et al16 reported that patients with <120° of knee flexion had a greater risk of developing MO.
Patients may present atypically, especially when the history is not clear. It is possible that many of these patients suffered unnoticed minor muscle injury. Moreover, MO has been reported to occur in all ages, including the very young (as young as 1 year of age) and in atypical locations, including hands, feet, ribs, head, and neck.17 Although the pathophysiologic process is the same, the clinical diagnosis may be more challenging in this setting. This atypical clinical presentation, combined with nonspecific imaging findings, often raises concern for malignancy. Some authors therefore have suggested use of the more descriptive term pseudomalignant MO.18
Several authors have examined the utility of serum laboratory tests.13 Although no test is currently diagnostic, several associations have been identified. The serum alkaline phosphatase (SAP) level initially remains normal but after 3 weeks, in parallel with bone formation, becomes acutely elevated, especially in patients with clinically significant MO.15 Levels peak (1.3 to 13.4 times normal) at approximately 10 weeks and return to normal by 18 weeks.19 The SAP level cannot be used to determine the maturity or activity of a lesion and can remain normal even in active lesions.19 Acute phase reactants, including the C-reactive protein level, erythrocyte sedimentation rate, and prostagandin-E2 serum level, are elevated during the initial stages of MO.10 The serum calcium level typically decreases for a short period and then returns to normal before the rise in SAP.19 The creatine phosphokinase level is generally elevated if there is involvement of muscle and, unlike SAP, may be predictive for the subsequent development and severity of MO20 (Figure 2).
MRI is the preferred modality in the evaluation of a soft-tissue mass, but some patients may undergo ultrasonography as an initial diagnostic test. The principle value of ultrasonography is in differentiating between cystic and solid lesions. Interestingly, ultrasonography reportedly is able to detect the zonal pattern of MO, especially in the early stages, even before calcification is detected on CT.21 Thomas et al22 demonstrated the role of ultrasonography in the early diagnosis of heterotopic bone formation. They described three concentric zones: an outer hypoechoic zone that surrounds the lesion, a middle hyperechoic zone that corresponds to the calcifying rim, and a central hypoechoic zone that corresponds to the central fibroblastic stroma (Figure 3). The advantages of ultrasonography include the lack of radiation exposure, low cost, and potential usefulness in the early stages of MO development. However, its utility is dependent on the experience and skill of the operator, and ultrasonography is not recommended as the initial study for suspected MO. If MO is encountered incidentally on ultrasonography, confirmation is recommended with CT or correlation with serial radiographs to confirm the classic zone of peripheral mature calcification.
MO can often be diagnosed with radiographs alone, especially in its mature phase when the patient’s clinical presentation correlates. In its early stages, however, determining the diagnosis may be difficult because of the lack of bone formation. Initial plain radiographs of MO in the first 2 weeks are typically normal but occasionally demonstrate periosteal reaction, possibly because of associated subperiosteal hematoma, and can be associated with adherence to the periosteum.17 A soft-tissue mass may be noticed in the radiographs of acute MO. Soft-tissue calcifications begin to become apparent radiographically at approximately 3 to 4 weeks.9,14 The calcifications may first appear as amorphous and flocculent. It is during this phase that the calcifications may simulate osteoid matrix and can have an appearance similar to that of extraskeletal osteosarcoma, which also may be juxtacortical in location. MO may also mimic soft-tissue sarcomas associated with calcifications, such as synovial sarcoma (Figure 4). The calcifications typically become more peripherally oriented and coarse in appearance. These calcifications mature during the next several weeks to produce a densely calcified peripheral rim with a lucent center, typically around 6 to 8 weeks (Figure 3). Mature lesions may have a lightly calcified center; this process can take up to 6 months or more. Mature lesions typically run in parallel with the long axis of the muscle (Figure 5). Once the lesion has matured, there is often a radiolucent cleft between the mass and adjacent bone, which might help to differentiate it from parosteal osteosarcoma.22,23 Mature lesions are sometimes adherent to the adjacent bone, and differentiation from parosteal osteosarcoma may thus require CT or MRI (Figure 4).
Bone scintigraphy is of little diagnostic value in the imaging workup of trauma-induced MO, especially when presenting as an isolated soft-tissue mass. However, a bone scan may be ordered when other inflammatory conditions, such as cellulitis, osteomyelitis, or thrombophlebitis, are considered.24 A bone scan will demonstrate increased uptake in injured muscle because of the presence of calcium salts and is the most sensitive imaging modality for detecting heterotopic bone formation in the very early stages.22,24 Several authors have found that three-phase bone scintigraphy is more useful in differentiating MO from other inflammatory conditions compared with a standard bone scan, which generally includes only delayed images.22,24 Although serial bone scans have been suggested to aid in the timing of surgical intervention, the practical application of relying on bone scintigraphy to determine successful treatment is largely unfounded in this setting.22,24 Because increased uptake on a bone scan can be seen chronically in trauma-induced MO, the authors have not found bone scans to be a reliable test for determining either the timing of surgical excision or for predicting the theoretic risk of recurrence (Figure 5).
CT is the best modality for delineating the zonal pattern of calcification and can be diagnostic before the characteristic calcification pattern becomes radiographically detectable.25,26 In the initial stages, CT demonstrates soft-tissue swelling or a low-attenuation soft-tissue mass without associated calcifications. Typically the peripheral rim becomes increasingly calcified as it matures (Figure 3). The central lucent zone is typically isodense to adjacent muscle.25 However, if the peripheral zonal pattern is not evident, it may be difficult to diagnose MO reliably by CT alone, necessitating additional imaging evaluation or follow-up.
MRI is the best single modality for imaging soft-tissue masses. An MRI for the evaluation of a soft-tissue mass should be interpreted in conjunction with recent radiographs because calcifications may not be well demonstrated on MRI.27 Recently, Papp et al28 discussed the utility of MRI for diagnosing soft-tissue masses. They classified lesions as determinate or indeterminate based on imaging characteristics and clinical presentation. A determinate lesion can be definitively diagnosed by means of history and physical examination combined with appropriate imaging modalities such as MRI. A lesion in a characteristic location (eg, anterior femoral cortex) supports the diagnosis of MO and is, therefore, also an important consideration. By comparison, indeterminate lesions (eg, type of sarcoma) require biopsy for an accurate diagnosis. Because each physician’s experience guides him or her in classifying lesions as determinate or indeterminate, a thorough history and physical examination cannot be understated, and a multidisciplinary team approach is useful for optimizing diagnostic accuracy and minimizing risks associated with further evaluation, including biopsy.29
Although MO can often be diagnosed definitively by MRI, its appearance can vary depending on the histologic stage;30 therefore, other diagnostic considerations must be excluded (eg, soft-tissue sarcoma, abscess). In the acute phase, when hematoma is often present, MO typically demonstrates a heterogeneous signal intensity on T1-weighted areas of high signal intensity that are representative of blood products. Fluid-weighted sequences may also be heterogeneous in appearance. T2-weighted hyperintensity suggests regions of granulation tissue, blood products, and edema. T2-weighted hypointensity may correspond to hemosiderin deposition or calcifications. Lack of lesion enhancement is characteristic when hematoma is present. Although intralesional enhancement has been reported in MO, heterogeneous or solid enhancement should raise the suspicion of sarcoma.31 Furthermore, a rim of bright T1-weighted signal is often suggestive of peripheral methemoglobin; surrounding inflammatory edema may also be present (Figure 6). Gradient-echo sequences can be used to investigate areas of hemosiderin deposition during this stage.31
The MRI appearance that follows the acute phase classically demonstrates a lesion that is isointense to slightly hypointense to skeletal muscle on T1-weighted sequences. Fluid-weighted sequences will appear hyperintense to surrounding muscle. At this stage, surrounding edema may or may not be present. If the zonal pattern of growth, characterized by peripheral low signal intensity, can be identified, this supports the diagnosis of MO and corresponds to a determinant lesion. However, in some instances, the lesion may be subtle and identified only by an alteration in fascial planes, thus stressing the importance of careful examination of the area in question (Figure 3).
As lesions progress, a pattern of mature, lamellar bone becomes better defined and demonstrates low signal intensity on all sequences, and the surrounding edema has resolved. Mature lesions may have areas of internal fat, which correspond to marrow production in the heterotopic bone. If MO is suspected on the basis of MRI, then CT and/or radiographs are recommended to confirm the characteristic peripheral mature calcification.31,32
When MO presents with a characteristic history and a clear zonal pattern on imaging, diagnosis is relatively straightforward. However, it is not uncommon for the appearance of MO to be suggestive of other considerations, thereby making the diagnosis challenging3,7,9,10,18,33 (Table 2). Nuovo et al17 reviewed 23 patients with MO that had “atypical” presentation. Of these 23 patients, 3 presented before the age of 10 years. Fifteen lesions were in unusual locations, including fingers and the chest wall. Only eight of their patients had a history of trauma. Two patients had constitutional symptoms that led to a presumptive diagnosis of infection. In eight of their patients, histology suggested a malignant diagnosis.17 Thus, a malignancy may be suspected despite advanced cross-sectional imaging and biopsy.
In the acute phase of MO, the MRI appearance can simulate a soft-tissue abscess. However, a soft-tissue abscess classically demonstrates a uniform appearance with high signal intensity on T2-weighted sequences, low signal intensity on T1-weighted sequences, and peripheral enhancement on post-contrast images.34 CT with intravenous contrast demonstrates a bright, rim-enhancing fluid collection, often confirming the suspicion of abscess.34
It is also important to distinguish MO from soft-tissue sarcoma, which can have very similar imaging and pathologic characteristics (Figure 4, A). A high level of suspicion is often salient to accurate diagnosis. Atypical presentation (eg, apparent hematoma lacking ecchymosis), intralesional post-contrast enhancement, and calcifications that lack the characteristic zonal pattern of peripheral ossifications may lead the clinician to favor sarcoma.31,32 For example, up to 58% of patients with synovial sarcoma have calcifications evident on diagnostic imaging and generally lack the peripheral rim of ossification that is seen with MO.35 A more mature calcification pattern might also be confused with parosteal osteosarcoma on radiographs alone (Figure 4), highlighting the importance of advanced cross-sectional imaging.35
Less commonly encountered considerations that may have soft-tissue calcifications include reactive periostitis and, when associated with the surface of the bone, bizarre parosteal osteochondromatous proliferation (ie, Nora lesion). Occasionally, a chronic abscess will develop calcification and thickening of its outer wall, which may appear similar to MO.34
Melorheostosis is a rare benign sclerotic bone dysplasia that follows a sclerotomal distribution and is known to have a “myositis-like” variant. The key to differentiate melorheostosis from MO is identification of the sclerotomal pattern, which is not characteristic of MO. One rare but notable mimicker of MO is a soft-tissue recurrence of giant cell tumor of bone. Recurrent giant cell tumor of bone in the soft tissues will often have peripheral eggshell calcifications, which may appear identical to MO.
MO can be classified as a determinate lesion when it presents with a clear history of an inciting event and peripheral calcification on radiographs. However, in early lesions, radiographs may be nondiagnostic, and subsequent MRI findings are often nonspecific. For patients with an indeterminate lesion, a tissue sample is necessary before forming a treatment plan. A biopsy can be performed using a variety of techniques depending on the surgeon’s preference. A fine-needle aspiration, core biopsy, incisional biopsy, and excisional biopsy are all methods that have been used to sample tissue. Regardless of the technique used, it is important for the treating surgeon to be familiar with the limitations of each method and the principles involved with biopsy should malignancy be identified. Fine-needle aspiration for cytology has been reported to be nondiagnostic and was unable to rule out sarcoma in some patients with MO; it is generally not recommended when core tissue samples can be obtained for pathologic analysis.29 Therefore, image-guided core biopsy is the authors’ preferred technique. Moreover, CT guidance is ideal for sampling representative tissue from both the central and peripheral aspects of the lesion.
Incisional biopsy allows direct visualization of the lesion and offers the greatest amount of tissue for analysis, but it is also the more invasive compared to closed needle biopsies. Incisional biopsies may be used when image-guided biopsy is unavailable, after a core-needle biopsy when the diagnosis is uncertain, or when additional tissue is needed. Excisional biopsies are reserved for small, easily accessible lesions when imaging is consistent with a benign etiology. The authors’ recommend a multidisciplinary team approach when considering histological analysis.
The histologic course of MO progresses from an immature, highly cellular fibroblastic lesion to a mature mass with peripheral lamellar bone.7 The timing of this process varies but generally occurs over several weeks and correlates with the development of calcifications on imaging.7,30 Early lesions demonstrate mesenchymal metaplasia, intermediate lesions display mixed chondro-osseous differentiation, and mature lesions demonstrate mature bone.9 In the early stages, it may be difficult microscopically to distinguish MO from sarcoma (eg, extraskeletal osteosarcoma).7,10 Grossly, a mature lesion will present as a thin shell of bone covering a soft red-gray central area7 and is typically 3 to 6 cm in size. Microscopically, MO is characterized by a distinct zonal pattern that correlates to its stage of maturity.7,9 Centrally, proliferating fibroblastic tissue and interstitial microhemorrhages are seen. Mild cellular pleomorphism and mitotic activity may be present.7 An intermediate zone has areas of immature woven bone mixed with fibroblastic tissue. At the periphery of the lesion, mature lamellar bone is seen (Figure 7). Although the development of sarcoma in the setting of previous MO has been reported, the ability of MO to transform into sarcoma has been questioned and has not been universally accepted.7
The goal of nonsurgical treatment is to minimize symptoms and maximize function. Nonsurgical treatment is often successful because MO is self-limiting and often is a self-resolving process.14,36 Although well-designed studies are lacking, the observation that MO is more common in patients with bleeding disorders37 supports the hypothesis that MO is associated with hematoma formation, with or without concomitant periosteal injury. Therefore, initial treatment of muscle injury with the purpose of controlling the development of hematoma and maintaining function is a reasonable approach.
For the initial treatment of muscle injury, Järvinen et al37 recommend a brief period of relative immobilization for 3 to 7 days combined with rest, ice, compression, and elevation. Crutches may assist with resting the affected area and minimizing hematoma formation.36,37 Cryotherapy—15 to 20 minutes of ice every 30 to 60 minutes—can decrease intramuscular blood flow by 50%. Aggressive physical therapy should be avoided in the very early stages to prevent exacerbation of symptoms.36,38
Assisted range-of-motion exercises, within a pain-free arc of motion, may begin as early as 48 to 72 hours.39 A gradual progressive exercise program begins with isometric training, followed by isotonic training, and finally isokinetic and dynamic exercises. Large fluctuant and symptomatic hematomas may benefit from aspiration.36 In one series, 42 of 42 football players at Vanderbilt University returned to full participation without loss of function after moderate to severe quadriceps contusion. The authors stressed the importance of early and persistent nonsurgical treatment.36 In more mature lesions, active range-of-motion and resistive strengthening exercises are important to maintain and improve joint range of motion and function.10,36,38
The use of drugs in the prophylaxis of MO after injury is limited and has largely been extrapolated from studies examining the development of heterotopic bone formation after pelvic trauma and hip surgery. However, in a case report of traumatic MO developing in an athlete, two doses of pamidronate were associated with improvement in both the clinical and radiographic findings.40
Surgical excision is generally reserved for symptomatic lesions that have failed nonsurgical treatment. The goal of surgery is to improve function and limit pain. Surgical indications include intractable pain resulting from mechanical irritation of nearby tendons, bursa, or joints; lesions that are causing compression of important neurovascular structures; and decreased range of motion that compromises activities of daily living.38 Marginal excision is adequate, but recurrence has been reported.10
Historically, surgical intervention has been delayed 6 to 18 months following injury because it was thought that surgery does not alter the maturation process and, therefore, premature surgery may predispose to recurrence.15 However, conclusive evidence supporting this approach is lacking.7,10,13-15,38,39 In fact, more recent research has challenged the risk of recurrence with early intervention. Ogilvie-Harris and Fornasier33 reported on 26 patients with nontraumatic MO and suggested that early excision has minimal risk of recurrence. Similarly, Garland15 suggested that the decision when to excise should include the etiology of MO rather than be based solely on chronology. He suggested delaying surgery for 6 months following traumatic MO, 1 year after spinal cord injury, and 18 months following head injury.15
It is possible that the risk of recurrence and severity of MO is dependent on the initial degree of local soft-tissue trauma. Those who present without disclosing a history of trauma may have suffered a mild injury that went unnoticed and may do well with early excision if symptomatic, as opposed to patients who developed heterotopic bone secondary to severe soft-tissue injury (eg, elbow dislocation), who may do better with delayed excision, once the lesion has reached maturity. Therefore, the decision to proceed with surgery is optimized in a multidisciplinary setting, accounting for the etiology, radiographic findings, laboratory values, and patient symptoms.
MO is a self-limiting, reactive, bone-forming process of soft tissues that occurs following injury. It may mimic malignancy early in its development, especially when it is not associated with a characteristic presentation and imaging findings. The pathophysiology is incompletely understood; however, it likely involves the inappropriate differentiation of mesenchymal stems cells into chondrocytes and osteoblasts in an inflammatory-rich environment. Diagnosis is often made with a thorough history, physical examination, and orthogonal radiographs. However, a variety of advanced imaging modalities may be useful depending on the stage of evolution. A biopsy is necessary to confirm the diagnosis for indeterminate lesions. Nonsurgical treatment focuses on reducing symptoms and maximizing function. Surgical excision is reserved for lesions that have failed nonsurgical treatment. The optimal timing of surgical excision is undetermined but has traditionally been felt to be best performed once a lesion has reached maturity. A multidisciplinary approach is helpful to accurately diagnose and optimize treatment.
Evidence-based Medicine: Levels of evidence are described in the table of contents. In this article, references 20 and 32 are level II studies. References 1-3, 6, 14, 17, 19, 21, 22, 26, 27, 29, 33, 35, and 40 are level IV studies.
References printed in bold type are those published within the past 5 years.
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