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OSTEOCHONDROSIS/OSTEOCHONDRITIS
No inflammation/ No cartilage involvement
Disease of epiphyses
Begins as necrosis followed by full regeneration of
healthy bone tissue
Epiphyseal necrotic areas heal and convert into
normal bone
Prominent metaphyseal changes may also be present
(e.g. femoral head)
>40 sites---mechanism of pathological changes is diff.
at all sites
e.g. vascular occlusion , bone avulsion, eosinophilic
granuloma , discal herniation etc
FEMORAL HEAD 10
Aseptic necrosis Legg-Calve-Perthe-
TARSAL NAVICULAR 10
Aseptic necrosis
Necrosis following #
Kohler
METATARSAL HEAD 10
Aseptic necrosis
Necrosis following #
Freibergs
LUNATE 10
Aseptic necrosis
Necrosis following #
Keinbocks
TIBIAL TUBERCLE Necrosis following partial
avulsion of patellar
tendon
Osgood-Schlatter
LOWER POLE OF
PATELLA
Necrosis following partial
avulsion of patellar
tendon
Sinding-Larsen
CALCANEAL
APOPHYSIS
Necrosis following partial
avulsion of tendoachillis
Severs
VERTBRAL BODY
EPIPHYSIS
Eosinophilic granuloma Calves
RING LIKE EPIPHYSIS
OF VERTEBRA
Disc herniation thru
defective end plate
Scheuermanns
OSTEOCHONDRITIS OF TIBIAL TUBERCLE
Osgood-Schlatters disease
Adolescent males
 typically lasts 12-24 months
Epiphysial aseptic necrosis of the tibial tubercle---due
to avulsion injury
Soft tissue lateral film(May be normal )
Local soft tissue swelling over a
fragmented and dense tuberosity
Compare with other knee(for soft tissues)
Osgood-Schlatter disease.
Fragmentation of the tibial tuberosity with
thickening of the ligamentum patellae.
Note the prominence, irregularity and
fragmentation of the tibial tuberosity
(arrowed).
OSTEOCHONDRITIS OF TARSAL NAVICULAR
Kohlers disease l
M>F Age----3-10 years
Peak 5 and 6 years
Appears earlier in girls
Earlier---irregularity of navicular and fissure
formation
Later---bone may appear as dense disc
No cartilagenous loss
OSTEOCHONDRITIS OF TARSAL NAVICULAR
This comparison view was performed after
the right foot image was reviewed.
This 3 year old girl presented with a
spontaneous right sided limp. The
navicular appears small and abnormally
dense.
OSTEOCHONDRITIS OF METATARSAL HEAD
Friebergs infarction , Kohlers disease ll
F>M between 10 – 15 yrs
Chronic trauma e.g. girls wearing high heals
2nd
MT head is commonly involved
Epiphysis shows
condensation
increased density
irregularity
Joint space may increase with splaying of opposing
bone surfaces
Gradual thickening of MT neck and shaft
Osteochondritis of the second metatarsal head.
(A) Minimal change of increased density of the epiphysis. (B) Later
stage of flattening of the epiphysis, increased joint space and loose
body separation.
Note that central bone has undergone re-
absorption.
Typical osteonecrosis of the head of the
second metatarsal seen in Freiberg's
infraction
OSTEOCHONDRITIS OF THE VERTEBRAL BODY
Vertebra plana/ Calves disease
Manifestation
collapse and increase density of vertebral
body
adjacent disc spaces are normal or
increased in width
Mostly caused by histiocytosis
May be associated with paraplegia
Regeneration is also expected
DDs-----Leukemia
Ewing's Sa
Mets
Tuberculosis
ADOLESCENT KYPHOSIS
Vertebral epiphysitis , Osteochondritis of vertebral
epiphyseal plates ,Scheurmanns disease
M=F
Begins at puberty , peak incidence 15 to 16 yrs
Region ---mid and lower thoracic spine
usually several adjacent vertebra
RADIOGRAPHIC APPEARANCES
Irregularity of superior and inferior parts of the
vertebral bodies
Wedging of vertebral bodies and kyphosis
later
Some scoliosis may be present
Schmorls nodes present with narrowing of disc spaces
Paraspinal bulge at the level of lesion
Improvement is slow and consolidation may take
several years
Radiographic recovery is often incomplete
Old kyphosis is most frequent abnormality
Vertebral defects are bounded by sclerotic rims(Not
seen in Tb. Lesions )
Residual wedging in late cases may be
indistinguishable from that caused by a previous
compression fracture.
Discography shows a disc filled with contrast medium
which extends between the vertebral body and the
detached fragment of bone.
protrusions of disc material into the surface of the vertebral body,
Discogram showing discal herniation into defects
MRI
Affected disc is narrowed
Loss of signal indicative of dehydration
Disc herniation into end plate defect and beneath the
non fused ring apophysis
T1 sag. of lumbar spine.
Rounded central end plate defects with herniation of discal material
OSTEOCHONDRITIS AT OTHER SITES
Hip and spine mostly involved
Capitellum
Patella---10
center Kohlers
Patella---20
center Sinding-Larsen
or Osgood-Schlatter
Sinding-Larsen disease. A good plain film will demonstrate thickening of the
ligamentum patellae origin, together with irregularity of the bone from which it
originates. The lower pole seems irregular and lengthened.
Medial tibial condyle(Blounts disease)/ tibia sara
From 1 to 12 yrs
Irregular defect at medial aspect of proximal
metaphysis
Spur at Rt< to and just below the defect
Adjacent tibial epiphysis may also be defective with
femoral spur
Lateral aspect is normal
Overall it is a varus deformity
Blount's disease. There is a large medial spur at the upper tibial metaphysis
with irregularity of the bone adjacent to the growth plate
OSTEOCHONDRITIS IN ADULT BONES
Usually associated with trauma
Scaphoid
Carpal lunate(Keinbocks)
Tarsal navicular
Medial seasamoid bone of great toe
Os trigonum
PLAIN FILMS
Fragmentation
Collapse
Sclerosis
Cyst formation
CT----Also shows same features
MRI
Mixture of
Low signals indicating collapse , condensation and
sclerosis
High signals of fluid ,cyst or vascularity (Healing)
The patient's injury was followed up 2
weeks later. The lunate showed little
sclerosis
Further imaging after a month suggested a
possible increase in the previously noted
lunate sclerosis
Thank you

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Osteochondrosis

  • 1.
  • 2. OSTEOCHONDROSIS/OSTEOCHONDRITIS No inflammation/ No cartilage involvement Disease of epiphyses Begins as necrosis followed by full regeneration of healthy bone tissue
  • 3.
  • 4. Epiphyseal necrotic areas heal and convert into normal bone Prominent metaphyseal changes may also be present (e.g. femoral head) >40 sites---mechanism of pathological changes is diff. at all sites e.g. vascular occlusion , bone avulsion, eosinophilic granuloma , discal herniation etc
  • 5. FEMORAL HEAD 10 Aseptic necrosis Legg-Calve-Perthe- TARSAL NAVICULAR 10 Aseptic necrosis Necrosis following # Kohler METATARSAL HEAD 10 Aseptic necrosis Necrosis following # Freibergs LUNATE 10 Aseptic necrosis Necrosis following # Keinbocks TIBIAL TUBERCLE Necrosis following partial avulsion of patellar tendon Osgood-Schlatter LOWER POLE OF PATELLA Necrosis following partial avulsion of patellar tendon Sinding-Larsen CALCANEAL APOPHYSIS Necrosis following partial avulsion of tendoachillis Severs VERTBRAL BODY EPIPHYSIS Eosinophilic granuloma Calves RING LIKE EPIPHYSIS OF VERTEBRA Disc herniation thru defective end plate Scheuermanns
  • 6. OSTEOCHONDRITIS OF TIBIAL TUBERCLE Osgood-Schlatters disease Adolescent males  typically lasts 12-24 months Epiphysial aseptic necrosis of the tibial tubercle---due to avulsion injury Soft tissue lateral film(May be normal ) Local soft tissue swelling over a fragmented and dense tuberosity Compare with other knee(for soft tissues)
  • 7. Osgood-Schlatter disease. Fragmentation of the tibial tuberosity with thickening of the ligamentum patellae.
  • 8. Note the prominence, irregularity and fragmentation of the tibial tuberosity (arrowed).
  • 9. OSTEOCHONDRITIS OF TARSAL NAVICULAR Kohlers disease l M>F Age----3-10 years Peak 5 and 6 years Appears earlier in girls
  • 10. Earlier---irregularity of navicular and fissure formation Later---bone may appear as dense disc No cartilagenous loss
  • 12. This comparison view was performed after the right foot image was reviewed. This 3 year old girl presented with a spontaneous right sided limp. The navicular appears small and abnormally dense.
  • 13. OSTEOCHONDRITIS OF METATARSAL HEAD Friebergs infarction , Kohlers disease ll F>M between 10 – 15 yrs Chronic trauma e.g. girls wearing high heals 2nd MT head is commonly involved
  • 14. Epiphysis shows condensation increased density irregularity Joint space may increase with splaying of opposing bone surfaces Gradual thickening of MT neck and shaft
  • 15. Osteochondritis of the second metatarsal head. (A) Minimal change of increased density of the epiphysis. (B) Later stage of flattening of the epiphysis, increased joint space and loose body separation.
  • 16. Note that central bone has undergone re- absorption. Typical osteonecrosis of the head of the second metatarsal seen in Freiberg's infraction
  • 17. OSTEOCHONDRITIS OF THE VERTEBRAL BODY Vertebra plana/ Calves disease Manifestation collapse and increase density of vertebral body adjacent disc spaces are normal or increased in width
  • 18. Mostly caused by histiocytosis May be associated with paraplegia Regeneration is also expected DDs-----Leukemia Ewing's Sa Mets Tuberculosis
  • 19. ADOLESCENT KYPHOSIS Vertebral epiphysitis , Osteochondritis of vertebral epiphyseal plates ,Scheurmanns disease M=F Begins at puberty , peak incidence 15 to 16 yrs Region ---mid and lower thoracic spine usually several adjacent vertebra
  • 20. RADIOGRAPHIC APPEARANCES Irregularity of superior and inferior parts of the vertebral bodies Wedging of vertebral bodies and kyphosis later Some scoliosis may be present Schmorls nodes present with narrowing of disc spaces Paraspinal bulge at the level of lesion
  • 21. Improvement is slow and consolidation may take several years Radiographic recovery is often incomplete Old kyphosis is most frequent abnormality Vertebral defects are bounded by sclerotic rims(Not seen in Tb. Lesions )
  • 22. Residual wedging in late cases may be indistinguishable from that caused by a previous compression fracture. Discography shows a disc filled with contrast medium which extends between the vertebral body and the detached fragment of bone.
  • 23. protrusions of disc material into the surface of the vertebral body,
  • 24. Discogram showing discal herniation into defects
  • 25. MRI Affected disc is narrowed Loss of signal indicative of dehydration Disc herniation into end plate defect and beneath the non fused ring apophysis
  • 26. T1 sag. of lumbar spine. Rounded central end plate defects with herniation of discal material
  • 27. OSTEOCHONDRITIS AT OTHER SITES Hip and spine mostly involved Capitellum Patella---10 center Kohlers Patella---20 center Sinding-Larsen or Osgood-Schlatter
  • 28. Sinding-Larsen disease. A good plain film will demonstrate thickening of the ligamentum patellae origin, together with irregularity of the bone from which it originates. The lower pole seems irregular and lengthened.
  • 29. Medial tibial condyle(Blounts disease)/ tibia sara From 1 to 12 yrs Irregular defect at medial aspect of proximal metaphysis Spur at Rt< to and just below the defect
  • 30. Adjacent tibial epiphysis may also be defective with femoral spur Lateral aspect is normal Overall it is a varus deformity
  • 31. Blount's disease. There is a large medial spur at the upper tibial metaphysis with irregularity of the bone adjacent to the growth plate
  • 32. OSTEOCHONDRITIS IN ADULT BONES Usually associated with trauma Scaphoid Carpal lunate(Keinbocks) Tarsal navicular Medial seasamoid bone of great toe Os trigonum
  • 34. MRI Mixture of Low signals indicating collapse , condensation and sclerosis High signals of fluid ,cyst or vascularity (Healing)
  • 35. The patient's injury was followed up 2 weeks later. The lunate showed little sclerosis Further imaging after a month suggested a possible increase in the previously noted lunate sclerosis