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Extremity and Joint Conditions/Section Articles

Myositis Ossificans in Sport: A Review

Devilbiss, Zachary DO1; Hess, Matthew MD1; Ho, Garry W.K. MD, FACSM, FAAFP, RMSK, CIC2

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Current Sports Medicine Reports: September 2018 - Volume 17 - Issue 9 - p 290-295
doi: 10.1249/JSR.0000000000000515
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Participation in both competitive and recreational sporting activity and exercise is an excellent means for many people, both young and old, to fulfill daily exercise recommendations and engage in an active and healthy lifestyle. With all sporting activity comes the risk of injuries, including soft tissue and muscle injuries. In skeletal muscle traumatology, two lesion-producing mechanisms have been described. Internal lesions — commonly referred to as “strains,” “pulls,” or “tears” — occur indirectly when the muscle alone is “responsible for its lesion.” External lesions occur from direct trauma or impact resulting in a muscle contusion or hematoma (1). Inadequate healing of muscle lesions can result in various complications, such as delayed healing time, encysted hematoma or fibrosis, and arguably the most difficult to manage, myositis ossificans (MO).

Some authors consider the term myositis ossificans a misnomer — implying that the primary pathologic process is inflammation, a notion that has been challenged for some time (2). In 1905, Jones and Morgan first questioned whether MO is purely an inflammatory entity (3). Throughout the remainder of the early 1900s, other researchers recognized an absence of inflammation with more mature lesions and that they were extremely challenging to differentiate from more worrisome etiologies at the time (4,5).

Accordingly, MO is widely described as a benign, solitary, self-limiting, ossifying soft tissue mass typically occurring within skeletal muscle (6). In the 1920s, Lewis classified MO into three categories: traumatica, nontraumatica, and neurotic (7) only to be supplanted 1 year later into myositis (fibrous) ossificans progressive, traumatic MO circumscripta, and MO circumscripta without history of trauma (8). More recently, the World Health Organization recognizes four subtypes of MO: 1) MO traumatica/posttraumatica/circumscripta; 2) MO associated with paraplegia; 3) nontraumatic/pseudomalignant MO; and 4) progressive MO (also known as fibrodyspolasia ossificans progressive) (6). For this review, we will focus on the most common form of MO encountered in the athletic and exercising populations: MO traumatica/posttraumatica/circumscripta.


MO traumatica can occur in any person and comprises 60% to 75% of all MO cases (9), but is most common in athletes as a result of frequent exposure to sport-related trauma to skeletal muscle. Simon et al. reported on 19 cases of posttraumatic MO in sport from 2006 to 2012 and found that, in general, muscle traumatology represented 10% to 55% of all athletic lesions, but not all cases led to the formation of MO. While as much as 40% of MO traumatica cases developed insidiously without a clear history of trauma, most lesion usually result from contusions, hematoma, strains, or repeated microinjuries due to overuse (9,10). MO traumatica occurs more often in male than female athletes, and most often in the second and third decades of life (6). MO most commonly occurs along the diaphysis of long bones and in the larger muscle groups of the upper and lower extremities — most notably the brachialis, quadriceps, and adductor muscle groups. Ngai et al. (11) estimated that 9% to 20% of quadriceps injury or contusion resulted in MO, and risk factors for MO included quadriceps contusion with knee flexion <120°, prior history of quadriceps contusion, a sympathetic knee effusion, and muscle injury with a delay of treatment of more than 3 d. However, since MO may occur with or without a traumatic history, it is difficult to definitively report on its incidence and risk factors. Hence, further study on MO in athletes is warranted.


The precise pathophysiology of MO is poorly understood and several hypotheses have been proposed. The lesion is thought to develop through inappropriate differentiation of fibroblasts into osteogenic cells. In the most widely accepted hypothesis, the lesion begins with an acute traumatic injury of skeletal muscle, followed by a local inflammatory cascade including the release of a myriad of cytokines, most notably bone morphogenic protein-2 (BMP-2), BMP-4, and transforming growth factor (TGF). In response to these cytokines, perivascular mesenchymal cells to BMP induce the mesenchymal cells to differentiate into osteoblasts and chondroblasts. Some of the resulting osteoblasts and chondrocytes will then undergo endochondral bone formation in extraskeletal osteoid tissue. Additionally, proinflammatory prostaglandin synthesis occurs as a result of muscle damage, further promoting the formation of heterotopic bone. In cases resulting from hematoma formation, it is thought that tissue necrosis and hemorrhage, followed by reparative fibroblastic and vascular proliferation, contributes to heterotopic ossification (6,12).

The natural history of MO traumatica typically progresses through three well-described stages — the early, intermediate, and mature stages — each stage with its own unique radiographical and histological findings, further discussed below. While reported timeframes vary, it is commonly accepted that the early stage occurs within the first 4 wk of injury, the intermediate stage occurs between weeks 4 and 8, and the mature stage occurs from 8 wk onward, possibly lasting for several months. Calcifications are usually visible on radiographs during the early stage. As the lesion progresses, calcifications become more radiographically apparent in the intermediate stage. In the mature stage, marked calcification can be demonstrated on radiographs. These peripheral calcifications typically consolidate over several months and may, but not always, regress or resolve over many years (13) (see Table).


In the very early stage of MO, the lesion histologically features fibroblasts and myofibroblasts, with only a very minor component of osteoid formation (13). The high mitotic activity in this stage results in spindle cell and hyperchromatic nuclei, which may make it difficult to distinguish this lesion microscopically from other more malignant lesions — such as sarcoma. For this reason, this is often referred to as the “pseudosarcomatous stage.” As the lesion matures and progresses through the early stage, a centrifugal zonal pattern develops called the “zonation phenomenon” (14). This pattern helps differentiate MO from a more malignant lesion. The centrifugal zonal pattern arises from immature osteoid formation gradually becoming more organized and mature in the periphery of the lesion; varying thickness of the lesion is often seen at this time creating different “zones.” In a typical MO lesion, three distinct zones are described (2). The center of the lesion consists of proliferating fibroblasts with varying amounts of hemorrhagic and necrotic foci. The intermediate or middle zone consists more of osteoblasts with immature osteoid formation. The peripheral or outer zone now consists more of mature bone. Once the lesion reaches the intermediate-stage, the proliferative fibroblastic core involutes and is replaced by osteoid with a peripheral shell of mature lamellar bone. During the mature-stage, the lesion consists purely of lamellar bone. Complete maturation of the lesion will typically occur by 6 to 12 months (14). It is important to note that osteosarcomas calcify from the center to the periphery, as opposed to MO, which calcifies from the periphery to the center (15). This can be reassuring to the clinician that, in the right historical setting, a lesion with peripheral calcification after 4 wk is most likely representative of an MO lesion.

Clinical Presentation

Just as MO may occur with or without trauma, the clinical presentation also may vary. In sports, athletes may recall a specific injury or traumatic event from when their symptoms originated. Collision sports give the highest risk of traumatic injury that may give rise to lesions responsible for MO development, with football and soccer incurring the highest number of case reports. However, as described by Anderson et al. in 2001, any sport that subjects an athlete to muscle injury can lead to development of MO, depending on the severity of the initial injury (16).

Typically, patient-athletes present with localized pain and joint stiffness, following blunt soft-tissue trauma, as seen in football or soccer players sustaining injury to the thigh either from a tackle or a direct kick. However, the literature also contains case reports describing MO resulting from repetitive micro-trauma, including MO in equestrian sports involving the adductor muscle group, known as “rider’s bone;” shooters developing MO in the deltoid muscle group, known as “shooter’s bone;” and ballet dancers developing MO in the soleus muscle (12).

Characteristic of myositis ossificans during each stage.

Initially, patient-athletes are often diagnosed with a muscle strain or contusion and are treated conservatively. Suspicion for the development of MO should arise when pain persists longer than would be expected for an otherwise, apparently uncomplicated muscle strain or contusion. Primarily located in the area of the trauma, the pain also may be associated with stiffness in the adjacent joints. In cases involving the proximal thigh, difficulty with weight-bearing and knee flexion also may be present. Tenderness, ecchymosis, and swelling also can occur in the anterior thigh (17). Persistent pain from MO is likely a result of mechanical irritation of myotendinous or bursal structures surrounding the lesion. Furthermore, since MO lesions can develop anywhere in skeletal muscles, nearby neurovascular structures can be compromised and compressed, causing more worrisome physical symptoms, such as muscle weakness, parasthesia, lymphedema, and even venous thromboembolic disease (12). The lesions will typically undergo a period of active growth until — after approximately 10 wk — it has progressed to a painless resting state, before undergoing spontaneous regression (18).

Laboratory Testing

Studies on laboratory tests such as serology have yet to prove any to be diagnostic. As would be expected, nonspecific acute-phase reactants — such as C-reactive protein, erythrocyte sedimentation rate, and prostaglandin-E2 serum levels — may be elevated during the initial stages of MO. As a laboratory marker of MO, serum alkaline phosphatase (SAP) is often normal during the first 3 wk following acute muscle injury, but as the lesion forms, SAP levels may rise in parallel to MO maturation. SAP levels will typically peak around 10 wk and return to baseline by 18 wk. However, peak SAP levels can vary anywhere from 1.3 to 13.4 times above baseline levels. Additionally, SAP do directly correlate with the maturity or other activity of the bone lesion, and are of limited utility in staging MO. SAP levels also are diagnostically limited, as these can be elevated in other differential diagnoses of MO, such as in osteosarcoma. Trending SAP levels in the setting of MO at 10- to 18-wk intervals may be appropriate to ensure that the levels return to baseline if they are initially elevated. Additionally, serum calcium levels may slightly decrease after initial injury, but typically return to baseline within 3 wk, prior to SAP levels rising. No scientific evidence exists correlating creatinine phosphokinase (CPK) levels to the probability of developing MO. Certain principles may be extrapolated from Singh et al. who concluded that CPK levels are typically elevated in muscle injury, and unlike SAP, may be predictive for the subsequent development and severity of MO. At 3 wk post-spinal cord injury, mean CPK values in patients who developed heterotopic ossification (HO) was 359, compared to those patients who did not develop HO, which was 118 (19). While this was a statistically significant difference, clearly further studies utilizing these lab values in the development of MO is warranted.

It seems that there may be a very limited role for following any of the above lab values when suspicious for the development of MO. During the acute injury period, the nonspecific acute phase reactants would not be able to differentiate MO from other musculoskeletal etiologies. The most valuable laboratory test to trend, if any, appears to be SAP levels from week 4 through week 18 postinjury. Checking any serology values seems to be more beneficial to help confirm suspicious cases of MO rather than serving any purpose in changing management if an MO lesion begins to or has developed.


Plain Film Radiography

Plain film radiographs are an appropriate initial imaging modality for MO, but are infrequently ordered early in most muscle injuries. Plain radiographs are useful to rule out underlying fracture in the context of acute blunt trauma. In early-stage MO, plain radiographs are typically negative, until faint radiopacities develop 2 to 6 wk after the initial injury (20). Periosteal reactions may be noticeable as early as 2 wk, but more typically between weeks 3 and 4 are when a soft tissue mass may be evident on radiographs. During this time, calcifications of MO may appear similar to other extraskeletal lesions such as an osteosarcoma, but may appear more coarse and peripherally oriented (12). As the lesion progresses to the intermediate phase between weeks 6 and 8, a sharply well-circumscribed mass with a peripheral radiopaque rim and a radiolucent center may be apparent. With the continued maturation of the lesion by 5 to 6 months postinjury, the radiolucent center becomes more radiopaque. Between months 6 and 12, the lesion may spontaneously regress slightly or completely and appear smaller on repeat radiographs (20).

While most radiographs with MO will show a radiolucent space between the lesion and the adjacent long bone, this is not always the case. Li et al. described three separate radiographic appearances of MO traumatica: 1) periosteal, where flat MO formation occurs adjacent to the long-bone shaft, damaging the periosteum; 2) stalk, where MO formation is attached to the long-bone shaft; and 3) intramuscular or disseminated, where intramuscular MO formation occurs without periosteal disruption (6). If mature lesions occur or are suspicious for adherence to the adjacent bone, advanced imaging in the form of computed tomography (CT) or magnetic resonance imaging (MRI) is recommended to help differentiate these lesions from periosteal osteosarcoma.

CT Scanning

CT scanning may be an early diagnostic in MO before the characteristic calcification pattern is undetectable radiographically. Initially, soft tissue edema or mass may be evident on CT scan with or without associated calcifications. Computed tomography can show a rim of mineralization around the lesion better than MRI by 4 to 6 wk. The center of the lesion will typically be less mineralized and will be more isodense than the surrounding or adjacent muscle tissue. As the lesion matures and the peripheral rim becomes more calcified, CT will show a more diffuse ossification pattern (20). Therefore, CT scanning has its greatest utility in the late-to-early-stage to intermediate-stages, where demarcation of the classic zonal arrangement may be detected before the lesions become apparent on plain radiographs. However, if the zonal patterns are not evident on CT, and suspicion for MO is still high, further imaging with MRI is recommended.

Magnetic Resonance Imaging

MRI is often considered the gold standard imaging modality of choice for soft tissue masses and can be used to definitively diagnose MO lesions. However, it is important to remember that the appearance of MO lesions on MRI can vary depending on the stage of the lesion and not all calcifications are well demonstrated. As such, MRI studies should be interpreted in conjunction with all other available imaging modalities.

In early MO, often when a hematoma is present, T1-weighted images will demonstrate either isodense or slightly hyperintense signal, and T2-weighted images will demonstrate hyperintensity at the site of the lesion. MRI without contrast is often sufficient to demonstrate these lesions; however, if contrast is ordered, the lesions will often demonstrate diffuse and markedly enhanced signal hyperintensity.

In intermediate-stage, MRI will depict isointense to hypointense signal at both the peripheral and central zones on all sequences when compared with adjacent or surrounding skeletal muscle. Diffuse surrounding edema can remain quite prominent in lesions imaged within 8 wk of the onset of symptoms or injury, and may persist for several months. MRI during this stage may show the characteristic zonal pattern which is considered diagnostic for MO.

Once the lesion matures, well-defined inhomogeneous masses are more evident with signal intensity approximately that of fat on both T1- and T2-weighted images consistent with a pattern of characteristic mature, lamellar bone. A lesion is considered fully mature once surrounding edema has completely resolved and is not evident on MRI (13,20).


Diagnostic ultrasound (US) can help differentiate between solid or fluid-filled cystic lesions. In 2011, Abate et al. (9) suggested US as the most suitable imaging modality for MO due to its ease of performance, low cost, and favorable safety profile. The group described a grading scale from 0 to 4 based on neovascularity of the lesion and confirmed the diagnosis of posttraumatic MO via core needle biopsy. In 2016, Simon et al. examined the utility of US screening in suspected MO lesions by using the presence of an echogenic lesion — with or without central hypoechogenicity — within muscle tissue and surrounding hyperactivity on power Doppler imaging. They concluded that postinjury US findings of MO can be seen between weeks 3 and 5 and recommended US as the preferred method of screening for MO in muscle injuries (1). In later more-mature MO, the peripheral power Doppler positivity decreases, eventually becoming absent, and the peripheral calcification layer becomes increasingly distinct and hyperechoic (Fig.).

(A) Lateral plain film radiograph demonstrating radio-opacity in anterior thigh. (B) Axial T1-weighted MRI image with isodense signal of anterior thigh lesion. (C) Axial T2-weighted fat saturation MRI image with hyperintense signal of anterior thigh lesion. (D) Coronal T2-weight fat saturation MRI image with hyperintense signal of anterior thigh lesion. (E) Longitudinal view of markedly hyperechogenic mass in anterior thigh using ultrasonography. (F) Transverse view of markedly hyperechogenic mass in anterior thigh using ultrasonography. All images courtesy of Dr. Chris O’Donnell,, rID: 35714.


Since most MO lesions are self-limiting and self-resolving, conservative treatment is a reasonable first-line approach. The guiding principal for MO treatment is to minimize symptoms (particularly pain) and to restore function and range of motion.

Initial management of muscle injuries typically begins with the classic RICE (rest, ice, compression, and elevation) treatment, with the goal of preventing or controlling hematoma formation (16). Non-steroidal anti-inflammatory drug use for pain control is controversial, especially in the early stages, as they may increase risk of further bleeding. Acetaminophen may be a better option for pain control during the early stages. Cryotherapy in the form of icing every 15 to 20 minutes every 30 to 60 minutes may decrease blood flow to the injured site by as much as 50%. A brief period of immobilization for 3 to 7 d in addition to crutch use may further minimize hematoma formation (12). Aggressive rehabilitation exercises can exacerbate symptoms in the very early stages of disease progression and therefore should be avoided; however, gentle, assisted range-of-motion exercise can begin as early as 48 to 72 h. Some discomfort is acceptable; significant pain is not. While it is known that aggressive static stretching can help improve early flexibility for some muscular contusions, there does not seem to be a substantial role with the use of static stretching in the prevention or the development of an MO lesion. In fact, if aggressive static stretching is performed too soon, within 48 h of injury, it may exacerbate any symptoms. Specific guidelines for when to start a structured rehabilitation program do not exist. However, as a general rule, a patient should be allowed to initiate a gradual progressive exercise or therapy program beginning with isometric training once they achieve pain-free range of motion.

Other nonoperative treatment options include extracorporeal shockwave therapy (ECSWT), aspiration of hematomas, and pharmacologic prophylaxis of MO formation after muscle injury. In a 2017 case report, a 15-year-old male soccer player with vastus intermedius MO lesion underwent five weekly sessions of ECSWT, starting at week 8 postinjury. He reported decreased pain with improved range of motion after two sessions, and at week 12, his examination exhibited full range-of-motion in the knee. The athlete was able to begin jogging at that time, with return to full sport at week 16 (11). An older case series of 42 Vanderbilt football players demonstrated some benefit of aspiration of large, fluctuant, and symptomatic hematomas and their early recovery and return to sport (21). However, evidence to support hematoma aspiration in preventing MO is otherwise lacking. Due to the resulting controversy regarding benefit of needle aspiration and the invasive nature of the procedure, it is recommended that decisions to proceed with needle aspiration be made on a case-by-case basis, weighing its potential risks and benefits with the patient. There remains a paucity of evidence supporting pharmacologic prevention of MO development after muscle injury; support is mostly extrapolated from data in patients with significant pelvic trauma and hip surgery. One case report of traumatic MO in an athlete given two doses of pamidronate was associated with improvement in clinical and radiographic findings (22). Despite the increasing popularity of injection therapies for musculoskeletal injuries, there remains no current evidence to support the use of corticosteroid injections, proliferative therapy or platelet-rich plasma injections to treat MO lesions.

Mature lesions typically cause little to no pain since inflammation is typically resolving with partial or complete spontaneous regression in this stage. Should mature MO lesions remain symptomatic despite conservative measures, surgical excision may be considered. Indications for and optimal timing of surgical excision of MO lesions are not well established (23). Most authors will agree delaying surgical excision to at least 6 months postinjury is the most appropriate time course. The rationale for waiting is that excising a mature lesion — as opposed to one more metabolically active — may minimize chances of recurrence. Orava et al. in 2017 were the first to report characteristics and outcomes of surgical excision of MO in a series of adult athletes. They concluded that surgical excision of symptomatic mature posttraumatic MO resulted in effective clinical improvement and that 30 of their 32 patients returned to preinjury level. However, the current paradigm of only considering excision for well-matured MO lesions is being challenged, as it has been suggested that early excision has minimal risk of recurrence. Nevertheless, surgical excision seems to have a more definitive role in resolution of persistent pain and improvement in range of motion; however, it should still be discussed in a multidisciplinary setting and considered after failed conservative treatment (23).

While there are no specific return-to-play guidelines for athletes with MO, it is important to set expectations for the athlete hoping to resume their chosen activities. Generally, symptoms will gradually subside between 6 and 8 wk after injury with relative rest and return to sport competitively occurs between 4 and 6 months (2). Simon et al. in 2016 found that, in their 19 cases reviewed, 90% of their patients had returned to light physical activity at 3 months, which corresponded to power Doppler negativity under US. Furthermore, 90% of their patients returned to sport at preinjury activity levels without pain by 6 months, and all patients had returned to sport at preinjury levels by 1 year. While deeper ossifications are more likely to persist than more superficial lesions, there do not seem to be any consequences on return to sport at 1 year after initial injury, even if lesions remain visible radiographically (1).


MO is a benign, solitary, typically self-limiting, ossifying soft tissue mass occurring within skeletal muscle that occurs with or without a history of blunt trauma. During the early stages, MO may be difficult to diagnose and often can mimic a more malignant lesion, such as osteosarcoma. The characteristic zonal pattern of MO can help a clinician differentiate MO from an osteosarcoma. Plain film radiographs are often the initial imaging modality of choice; however, the role of ultrasonography is seeing increasing use for both the initial diagnosis, as well as for follow-up management of these lesions. MRI remains the gold standard for soft tissue mass imaging, albeit with limitations. Conservative treatment is the mainstay for management of these lesions and most patients do very well. However, in the setting of a persistent pain or decreased range of motion, surgical excision remains an option, with most experts delaying surgery until the lesion is well matured. Athletes tend to return to sport at a preinjury level with slow and progressive implementation of a therapy program. It may take 6 to 12 months for an athlete to return to this preinjury level of competition.

The authors declare no conflict of interest and do not have any financial disclosures.


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