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Myositis Ossificans
extra-osseous non neoplastic growth of new bone
Misnomer
Heterotopic ossification
not always inflammatory
within extra-skeletal soft tissues – mainly in
connective tissue than muscle
Ectopic Calcification ?!!
Deposition of radio dense
Calcium Phosphate
Difference in mineral phase
No true bone matrix is formed
Eg:- Hyper/Hypoparathyroidism,
Renal failure,
Following TB,
Calcific Supraspinatus Tendinopathy,
Scleroderma,
Dermatomyositis
Diffuse
cutaneous,
subcutaneous
and muscular
calcification:
Calcinosis
universalis in
Dermatomyositis
Types
 Myositis ossificans
circumscripta /traumatica
 fibrodysplasia ossificans progressiva (FOP)
Myositis ossificans
circumscripta /traumatica
In response to soft tissue injury:-
blunt trauma,
stab wound,
fracture/dislocation,
surgical incision (THR)
Systemic Conditions:-
Head injury,Spinal cord injury
Tetanus,
Burns
Without known injury:-
Nondocumented trauma,
Repeated small mechanical injuries(blunt trauma
in horse riders)
Nonmechanical injuries caused by ischemia or
inflammation.
Increased risk in patients with Diffuse Idiopathic
Skeletal Hyperostosis (DISH) and Paget’s
Disease
Pathophysiology
BMP stimulate primitive stem cells in soft tissues
to form osteoblasts
Organization of Haematoma
Fibroblastic hypoplasia
Osteoid formation
Radiographic evidence in 6-8 weeks
 The lesion begins to calcify at the periphery and
works toward the center (Reverse in
Osteosarcoma)
Histopath- 4 distinct zones:
the central undifferentiated zone- mitotically
active
the surrounding zone of immature osteoid
formation – less active
zone with new bone – osteoblast & fibrous
tissue with trabecular organization
Peripheral zone of fibrous tissue
At least 10 days are required following onset
of symptoms for these zones to become
apparent.



drug abusers
elbow ?!!
Paraspinal
most commonly in the second and third decade
Areas commonly affected - elbow, thigh, buttocks,
shoulder and calf ., erector spinae, pectoralis
muscles
(Quadriceps and brachialis - most affected.)
Majority –asymptomatic; may cause pain/ loss of
ROM
presents as a rapid enlargement and significant
pain one to two weeks after injury.
Swelling and warmth at the site
Hypercalcemia- contributing factor
Increased ESR and serum alkaline phosphatase.
Treatment
Watchful inactivity
Rest and gentle stretching.
Surgery if persistent pain – excised in toto in
mature cases
Risk of recurrence +
If left alone, the mass will shrink in size
Treatment
should not continue to play sports or use the
affected muscle.
Avoid Heat and massage.
Reinjury to the same area, returning to activity too
early, or initial passive forceful stretching can
lengthen recovery.
Prophylaxis: NSAIDS(Indomethacin), low dose
radiation
Heterotopic Ossification Osteosarcoma
Site: Diaphysis Metaphysis
Peripheral rimming Ossification center
(can mimic necrotic tr) to periphery
Improvement in pain over Pain worsens with time and
rest time
Biopsy:Zone phenomenon Undiff tissue- viable muscle
fibres similar to central intact cortex
zone
Myositis Ossificans Progressiva /
Fibrodysplasia Ossificans
Progressiva
rare autosomal dominant disorder
skeletal malformation and progressive, disabling
heterotopic osteogenesis.
fibrosing and ossification of muscle, tendon and
ligaments of multiple sites often in the upper
extremities and back that is disabling and
ultimately fatal
Nine-year-old Mexican girl with Fibrodysplasia
Ossificans Progressiva (FOP).

Chromosome 2q23-24
Heterozygous mutation (617G®R206H) in the
glycine-serine (GS) domain of the
Activin A receptor type I (ACVR1) gene, a bone
morphogenic protein (BMP) type I receptor
Incidence 1in 2 million
Age: Average 5 yrs (Fetus-25 yrs)
Their offspring have a 50% probability of
inheriting the condition.
painful lumps and stiffness in the adjoining joint.
 Lumps decrease in a few weeks, but joint
mobility reduction persists.
Exacerbating factors for ossifications at new sites
minor trauma, venipuncture,
biopsy of lumps, IM injections,
dental treatments, and excision of masses.
Most common sites:- sternocleidomastoid,
paraspinal muscles, the masticatory muscles,
shoulder and pelvic girdle muscles.
Spared are the abdominal muscles, extraocular
muscles,
muscles of facial expression, diaphragm,
larynx and tongue muscles.
Ossification progresses from proximal to distal
and cranial to caudal.
C/F
Digits: Short hallux in valgus with synostosis
short thumbs , Clinodactyly
Fibrous Tissues: Swelling in aponeuroses,
fasciae, and tendons- ossification in muscles
and fibrous tissues,
most prominent in the neck dorsal trunk and
proximal extremities (The sternocleidomastoid
muscle is commonly affected.)
Kyphoscoliosis: Restricted shoulder and
pelvic girdle movements

Lab
Hemogram, ESR, S.Ca, P:- WNL
ECG findings may be abnormal
spirometry :-restrictive pattern, reflective of chest
wall involvement.
Plain radiography of FOP
Short metacarpals and metatarsals
Phalangeal synostosis (eg, monophalangeal great
toe)
Vertebral fusions, vertebral anomalies (i.e., small
bodies), pedicle thickening
Thick, short femoral neck
Variations in bone maturation sequence
Increased incidence of enchondromas
Treatment
Once diagnosis is established, usually clinically,
any surgical biopsy is contraindicated in FOP.
No established medical therapy exists.
 Pain medications
 supportive measures -gentle occupational and/or
physical therapy.
Prevention is better!!
avoid falling or getting bruises
avoid IM injections since these can
cause bone to grow.
Never stretch their joints outside of
their normal ROM.
Flare-ups can occur spontaneously,
even perfect preventive care cannot
guarantee the absence of bone growths.
The mainstay of diagnosis is bilateral
great toe anomaly present from birth,
reported in 79 to 100% of patients
microdactyly of both halluces due to a
single phalanx in valgus position
The finding of congenital hallux valgus
must raise the possibility of FOP so that
management should be early and
adequate.


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Myositis ossificans

  • 2. extra-osseous non neoplastic growth of new bone Misnomer Heterotopic ossification not always inflammatory within extra-skeletal soft tissues – mainly in connective tissue than muscle
  • 3. Ectopic Calcification ?!! Deposition of radio dense Calcium Phosphate Difference in mineral phase No true bone matrix is formed Eg:- Hyper/Hypoparathyroidism, Renal failure, Following TB, Calcific Supraspinatus Tendinopathy, Scleroderma, Dermatomyositis
  • 5. Types  Myositis ossificans circumscripta /traumatica  fibrodysplasia ossificans progressiva (FOP)
  • 6. Myositis ossificans circumscripta /traumatica In response to soft tissue injury:- blunt trauma, stab wound, fracture/dislocation, surgical incision (THR) Systemic Conditions:- Head injury,Spinal cord injury Tetanus, Burns
  • 7. Without known injury:- Nondocumented trauma, Repeated small mechanical injuries(blunt trauma in horse riders) Nonmechanical injuries caused by ischemia or inflammation. Increased risk in patients with Diffuse Idiopathic Skeletal Hyperostosis (DISH) and Paget’s Disease
  • 8. Pathophysiology BMP stimulate primitive stem cells in soft tissues to form osteoblasts Organization of Haematoma Fibroblastic hypoplasia Osteoid formation
  • 9. Radiographic evidence in 6-8 weeks  The lesion begins to calcify at the periphery and works toward the center (Reverse in Osteosarcoma)
  • 10. Histopath- 4 distinct zones: the central undifferentiated zone- mitotically active the surrounding zone of immature osteoid formation – less active zone with new bone – osteoblast & fibrous tissue with trabecular organization Peripheral zone of fibrous tissue At least 10 days are required following onset of symptoms for these zones to become apparent.
  • 11.
  • 12.
  • 13.
  • 16.
  • 17. most commonly in the second and third decade Areas commonly affected - elbow, thigh, buttocks, shoulder and calf ., erector spinae, pectoralis muscles (Quadriceps and brachialis - most affected.) Majority –asymptomatic; may cause pain/ loss of ROM
  • 18. presents as a rapid enlargement and significant pain one to two weeks after injury. Swelling and warmth at the site Hypercalcemia- contributing factor Increased ESR and serum alkaline phosphatase.
  • 19. Treatment Watchful inactivity Rest and gentle stretching. Surgery if persistent pain – excised in toto in mature cases Risk of recurrence + If left alone, the mass will shrink in size
  • 20. Treatment should not continue to play sports or use the affected muscle. Avoid Heat and massage. Reinjury to the same area, returning to activity too early, or initial passive forceful stretching can lengthen recovery. Prophylaxis: NSAIDS(Indomethacin), low dose radiation
  • 21. Heterotopic Ossification Osteosarcoma Site: Diaphysis Metaphysis Peripheral rimming Ossification center (can mimic necrotic tr) to periphery Improvement in pain over Pain worsens with time and rest time Biopsy:Zone phenomenon Undiff tissue- viable muscle fibres similar to central intact cortex zone
  • 22. Myositis Ossificans Progressiva / Fibrodysplasia Ossificans Progressiva rare autosomal dominant disorder skeletal malformation and progressive, disabling heterotopic osteogenesis. fibrosing and ossification of muscle, tendon and ligaments of multiple sites often in the upper extremities and back that is disabling and ultimately fatal
  • 23. Nine-year-old Mexican girl with Fibrodysplasia Ossificans Progressiva (FOP). 
  • 24.
  • 25.
  • 26. Chromosome 2q23-24 Heterozygous mutation (617G®R206H) in the glycine-serine (GS) domain of the Activin A receptor type I (ACVR1) gene, a bone morphogenic protein (BMP) type I receptor Incidence 1in 2 million Age: Average 5 yrs (Fetus-25 yrs) Their offspring have a 50% probability of inheriting the condition.
  • 27. painful lumps and stiffness in the adjoining joint.  Lumps decrease in a few weeks, but joint mobility reduction persists. Exacerbating factors for ossifications at new sites minor trauma, venipuncture, biopsy of lumps, IM injections, dental treatments, and excision of masses.
  • 28. Most common sites:- sternocleidomastoid, paraspinal muscles, the masticatory muscles, shoulder and pelvic girdle muscles. Spared are the abdominal muscles, extraocular muscles, muscles of facial expression, diaphragm, larynx and tongue muscles. Ossification progresses from proximal to distal and cranial to caudal.
  • 29. C/F Digits: Short hallux in valgus with synostosis short thumbs , Clinodactyly Fibrous Tissues: Swelling in aponeuroses, fasciae, and tendons- ossification in muscles and fibrous tissues, most prominent in the neck dorsal trunk and proximal extremities (The sternocleidomastoid muscle is commonly affected.) Kyphoscoliosis: Restricted shoulder and pelvic girdle movements
  • 30.
  • 31.
  • 32. Lab Hemogram, ESR, S.Ca, P:- WNL ECG findings may be abnormal spirometry :-restrictive pattern, reflective of chest wall involvement.
  • 33. Plain radiography of FOP Short metacarpals and metatarsals Phalangeal synostosis (eg, monophalangeal great toe) Vertebral fusions, vertebral anomalies (i.e., small bodies), pedicle thickening Thick, short femoral neck Variations in bone maturation sequence Increased incidence of enchondromas
  • 34. Treatment Once diagnosis is established, usually clinically, any surgical biopsy is contraindicated in FOP. No established medical therapy exists.  Pain medications  supportive measures -gentle occupational and/or physical therapy.
  • 35. Prevention is better!! avoid falling or getting bruises avoid IM injections since these can cause bone to grow. Never stretch their joints outside of their normal ROM. Flare-ups can occur spontaneously, even perfect preventive care cannot guarantee the absence of bone growths.
  • 36. The mainstay of diagnosis is bilateral great toe anomaly present from birth, reported in 79 to 100% of patients microdactyly of both halluces due to a single phalanx in valgus position The finding of congenital hallux valgus must raise the possibility of FOP so that management should be early and adequate.
  • 37.