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
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
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.
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
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
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.