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Myositis Ossificans

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Other Names

  • Myositis Ossificans Traumatica
  • Myositis Ossificans (MO)
  • Myositis (fibrous) ossificans progressive
  • Traumatic circumscripta
  • MO circumscripta
  • Fibrodyspolasia ossificans progressive
  • Rider’s bone
  • Shooter’s bone


  • This page refers to Myositis Ossificans (MO)
    • This can be defined as a benign, solitary, frequently self-limiting, ossifying soft-tissue mass found in skeletal muscle often encountered in the active sporting population
    • Although there are multiple types, this review will primarily focus the traumatic form seen in Athletes


  • WHO subtypes
    • Traumatic
    • Atraumatic, sometimes termed pseudomalignant
    • MO associated with paraplegia
    • Progressive MO


  • In 1905, Jones and Morgan questioned whether MO is a pure inflammatory condition[1]
  • In 1913, Coley described the challenges in distinguishing it from malignancy[2]


  • Incidence is somewhat challenging because it may occur with or without trauma
  • Traumatic MO represents 60-75% of all cases[3]
  • Simon et al estimated that muscle trauma represents 10% - 55% of athletic lesions, but not all muscle trauma leads to MO[4]
  • Up to 40% of cases can be insidious without clear history of trauma
  • Demographics[5]
    • More common in males than females
    • Most often in 20s, 30s
  • Location


  • General
    • Internal lesions: Strains, pulls and tears
    • External lesions: direct trauma or impact
  • Inadequate healing of muscle lesions can result in various complications including
    • Delayed healing time
    • Encysted hematoma
    • Fibrosis
    • Leads can all lead to myositis ossificans (MO)
  • Precise pathophysiology is poorly understood, several proposed etiologies include
    • Inappropriate differentiation of fibroblasts into osteoblasts, chondroblasts following trauma
    • This is primarily due to bone morphogenic protein (BMP-2, BMP-4) and transforming growth factor (TGF)
    • Proinflammatory prostaglandin synthesis occurs following muscle damage can contribute
    • In the case of hematoma formation, subsequent necrosis and hemorrhage, followed by reparative fibroblastic and vascular proliferation
  • Description
    • Liquefaction, formation of nonspecific sheets of cells in damaged muscle following injury
    • Cytokines recruit further inflammatory cells, macrophages into necrotic tissue
    • Mediators encourage the formation of heterotopic bone
    • Bone is laid down from outside to inside pattern (distinguishing it from neoplastic process)
  • Natural history
    • Early stage: occurs within first 4 weeks of injury, calcifications can be seen on xray
    • Intermediate stage: between weeks 4 and 8
    • Mature stage: 8 weeks onward, potentially for months, marked calcifications visible on xray
  • Location
  • Can be challenging to distinguish from other lesions, namely myosarcomas

Other Locations

  • "Rider's Bone"
    • Occurs in the adductor muscle group among equestrian sports
  • "Shooter's Bone"
    • Occurs in the deltoid muscle
  • Occurs in the soleus muscle among ballet dancers

Associated Conditions

Risk Factors

  • For Quad MO
    • Quadriceps Contusion with knee flexion < 120°
    • Prior history of quadriceps contusion
    • Sympathetic knee effusion
    • Muscle injury with a delay of treatment of more than 3 days
  • Sports
    • Football
    • Soccer

Differential Diagnosis

Differential Diagnosis Thigh Pain

Clinical Features

  • History
    • Athletes will typically recall a specific injury or traumatic event
    • Often treated for muscle strain or contusion and treated conservatively
    • If pain or symptoms persist longer than anticipated, should suspect MO
    • Will report localized pain, joint stiffness
    • Will have difficult using muscle group, e.g. weight bearing if quad affected
  • Physical Exam
    • Pain and tenderness at site of injury
    • Careful evaluation for any evidence of neurovascular compromise
  • Special Tests



  • Standard initial imaging modality
    • Not ordered in the case of most suspected uncomplicated muscle injuries
    • Can rule out fracture
  • Findings
    • 2-4 weeks: can see faint radiopacities or periosteal reactions
    • 4-8 weeks: sharply well-circumscribed mass with a peripheral radiopaque rim, radiolucent center
    • 8 weeks and on: becomes more radiopaque, well defined with radiolucent center
    • 6-12 months: lesion may spontaneously regress slightly, appear smaller
  • Li et al describes 3 separate radiographic appearances[7]
    • A) Periosteal, flat MO formation occurs adjacent to the long-bone shaft, damaging the periosteum
    • B) Stalk, where MO formation is attached to the long-bone shaft
    • C) Intramuscular disseminated, where intramuscular MO formation occurs without periosteal disruption


  • May be useful early on
    • Can detect calcifications that may not be detectable on radiographs initially
    • Greatest utility late-to-early-stage to intermediate-stages
    • Where classic zonal arrangement may be detected before the lesions become apparent on plain radiographs
  • Findings[8]
    • 2-4 weeks: soft tissue edema, mass, with or without calficiations
    • 4-8 weeks: mineralization with low attenuation center
    • 8 weeks and on: more diffuse ossification pattern


  • General
    • Often considered gold standard for soft tissue masses
    • May not demonstrate early calcifications well
    • Contrast is not typically required
  • Findings
    • 2-4 weeks: Hematoma which is isodense (T1), hyperintense (T2)
    • 4-8 weeks: Isointense/hypointense signal peripherally and centrally compared to surrounding skeletal muscle
    • 8 weeks and on: well defined mass, isodense to all fat sequences, resolution of surrounding edema


  • General
    • Helpful to distinguish between solid and fluid filled cystic structures
    • Abate et al suggests US is most suitable modality for MO due to low cost, ease of performance and favorable safety profile[3]
  • Findings
    • 2-4 weeks: Increased power Doppler signal with hyperechoic outer layer
    • 4-8 weeks: Increased power Doppler signal with increased peripheral hyperechogenicity
    • 8 weeks and on: Little to no power Doppler signal with more evident peripheral layer, hyperechogenicity


  • No clear diagnostic test
  • Acute phase
    • CRP, ESR elevated
  • Alkaline Phosphatase
    • Begins to elevate around 3 weeks following acute injury
    • Peak around week 10, return to baseline at week 18
    • Can vary from 1.3x to 13.4x normal
    • Nonspecific to MO, however trending to ensure they return to baseline may help exclude neuplastic process
  • Creatinine Phosphokinase
    • Role is not clearly defined in MO


Radiographic Stages of Myositis Ossificans

  • Early (0-4 weeks)
    • X-ray: Normal or faint calcification
    • CT: Soft tissue edema
    • MRI: Isodense on T1; hyperintense on T2
    • US: Increased power Doppler signal with hyperechoic outer layer
  • Intermediate (4-8 weeks)
    • X-ray: Peripheral calcified rim, central lucency
    • CT: Peripheral mineralization with low attenuated center
    • MRI: Iso/hypodense to adjacent skeletal muscle on all images
    • US: Increased power Doppler signal with increased peripheral hyperechogenicity
  • Mature (>8 weeks)
    • X-ray: Diffuse soft tissue calcification
    • CT: Diffuse ossification pattern
    • MRI: Well-defined mass, isodense to fat on all images
    • US: Little to no power Doppler signal with more evident peripheral layer, hyperechogenicity



  • General
    • Self limited with most athletes able to return to sport
  • Surgical management
    • Orava (2017) found 30/32 patients were able to return to preinjury level of competition[9]


  • General
    • First line approach in virtually all cases
    • Goal is to minimize symptoms, restore function and range of motion
  • Initial management
    • Relative rest
    • Ice Therapy or Cryotherapy can reduce blood flow to injury by up to 50% (need citation)
    • Brief period of immobilization, compression may reduce risk or size of hematoma formation
    • Consider avoiding in first 1-3 days due to antiplatelet effects
    • Then use of NSAIDs for 1-2 weeks is recommended
  • Acetaminophen
    • Recommended by some experts for pain control
  • Physical Therapy
    • Avoid aggressive rehab early on to prevent exacerbation of symptoms
    • Can begin gentle range of motion early
    • Role of static stretching in prevention or development of MO is not well defined
  • Extracorporeal Shockwave Therapy (ECSWT)
    • One case report demonstrated full return to sport at 16 weeks[10]
  • Aspiration of hematoma
    • Case series among Vanderbilt football players demonstrated benefit of aspiration for recovery, return to sport (need citation)
    • No clear guidelines on when to utilize this procedure
  • Bisphosphonates
    • Suppress bone turnover, slow down minieralize process
    • One case report describing an athlete receiving two doses of IV Pamidronate was associated with improvement in radiograph and clinical findings[11]
    • Note should not be used in premenopausal women


  • Indications
    • Not clearly established
    • Most lesions will regress when mature and become asymptomatic
    • Failure of conservative therapy by at least 6 months

Rehab and Return to Play


  • No clear guidelines for rehabilitation
    • Should not begin gradual progressive exercise or physical therapy until pain free range of motion

Return to Play

  • No clear guidelines for RTP
  • General
    • Symptoms start to subside between weeks 6-8
    • Competitive return to sport typically occurs between 4 and 6 months
  • Simon et al[4]
    • Found 90% of patients returned to light physical activity at 3 months
    • 90% of athletes returned to pre-injury level of sport at 6 months
    • 100% returned to sport by 1 year


  • Chronic pain
  • Inability to return to sport

See Also


  1. Jones R, Morgan D. On osseous formations in muscle due to injury (traumatic myositis ossificans). Archive of the Roentgen. 1905; 9:245.
  2. Coley WB. I.Myositis ossificans traumatica: a report of three cases illustrating the difficulties of diagnosis from sarcoma. Ann. Surg. 1913; 57:305Y37.
  3. 3.0 3.1 Abate M, Salini V, Rimondi E, et al. Post traumatic myositis ossificans: sonographic findings. J. Clin. Ultrasound. 2011; 39:135Y40.
  4. 4.0 4.1 Simon T, Guillodo Y, Madouas G, Saraux A. Myositis ossificans traumatica (circumscripta) and return to sport: a retrospective series of 19 cases. Joint Bone Spine. 2016; 83:416Y20.
  5. Ackerman LV. Extra-osseous localized non-neoplastic bone and cartilage formation (so-called myositis ossificans): clinical and pathological confusion with malignant neoplasms. J. Bone Joint Surg. Am. 1958; 40:279Y98.
  6. Ngai A. Post-traumatic myositis ossificans. In: Roger B, Guermazi A, Skaf A, editors. Muscle Injuries in Sport Athletes. Sports and Traumatology. Springer. New York (NY): 2017.
  7. Li W-T, Horng S-Y, Chien H-F. Abdominis rectus intramuscular myositis ossificans. Formosan Journal of Surgery. 2016; 49:20Y6.
  8. Kransdorf MJ, Meis JM, Jelinek JS. Myositis ossificans: MR appearance with radiologic-pathologic correlation. AJR Am. J. Roentgenol. 1991; 157:1243Y8.
  9. Orava S, Sinikumpu JJ, Sarimo J, et al. Surgical excision of symptomatic mature posttraumatic myositis ossificans: characteristics and outcomes in 32 athletes. Knee Surg. Sports Traumatol. Arthrosc. 2017; 25:3961Y8.
  10. Ngai A. Post-traumatic myositis ossificans. In: Roger B, Guermazi A, Skaf A, editors. Muscle Injuries in Sport Athletes. Sports and Traumatology. Springer. New York (NY): 2017
  11. Mani-Babu S, Wolman R, Keen R. Quadriceps traumatic myositis ossificans in a football player: management with intravenous pamidronate. Clin. J. Sport Med. 2014; 24:e56Y8.
Created by:
John Kiel on 14 June 2019 10:20:35
Last edited:
15 August 2021 22:09:19