Category: Education

Presentation Description

No description available.


Presentation Transcript




Segment of bone loses its blood supply so that cellular elements within it die


Pathology Occlusion of artery or vein →ischemia→death of hematopoitic tissue within 6 to 12 hrs→of osteoclasts,osteocytes and osteoblasts within12 to 48 hrs→and of marrow fat in 2 to 5 days. Dead bone at this stage is normal radiologically bcz trabecular framework remains intact.


Diagram shows how the vascular supply to the femoral head is maintained by the retinacular blood vessels in the pertrochanteric fracture of the femur.


Diagram shows how a subcapital fracture of the femoral neck cuts off of the blood supply to the femoral head, resulting in osteonecrosis.


blood supply to the humeral head.


blood supply to the talus via the artery of the tarsal canal.


blood supply to the scaphoid bone.


REVASCULARIZATION Revascularization is seen at live marrow-dead marrow interface. →necrotic zone is invaded by capillaries,fibroblasts and macrophages.→Fibrous tissue replaces dead marrow and in turn may calcify. OSSIFICATION New osteoblasts lay down fresh woven bone on the devitalized trabeculae.


This advancing front of neovascularization and ossification has been termed creeping substitution(phemister).


At bone ends cartilage receives nutrition from synovial fluid. Cartilage and subcartilaginous bone are therefore not necessarily affected.


Causes of osteonecrosis Interruption to flow of blood t o bone most commonly follows trauma with tearing of blood vessels Emboli or sludging, this occurs in sickle cell disease where abnormal red cells aggregate,in pancreatitis where fat emboli obstruct vessels and in decompression disease wheere possibly gas bubbles occlude small vessels,Vasculitis in collagen disorders and following irradiation,also occludes small vessels. Intraosseous compression of vessels occurs in Gaucher's disease;where masses of Gaucher cells pack marrow spaces.


Steroid and NSAIDS cause bone necrosis


Radiological changes Stege 1 No changes are visible Stage 2 osteporosis due to disuse in vascular bone abut avascular bone has normal or increase density Stage 3 At large joints subcortical necrotic zone and trabecular loss beneath a thin ans sclerotic cortex →structural failure in subcortical bone→cortical microfractures at areas of maximal stress →collapse and trabecular compression Stage 4 A flattened articular surface results with increased subarticular density as trabeculae are compressed. Stage 5 Osteoarthritis with joint space narrowing follows later.


Plain radiograph in a middle-aged man with shoulder discomfort demonstrates an irregularly calcified bone infarct in the diametaphysis of the right humerus.


Coronal T1-weighted MRI in a 12-year-old boy with early Legg-Calvé-Perthes disease demonstrates slight irregularity of the right femoral capital epiphysis with abnormal signal intensity. The left hip appears normal.


Coronal T1 weighted MR image of a 20-year-old woman with bilateral late-stage Legg-Calvé-Perthes disease demonstrates flattening of the right femoral head and acetabulum.


Coronal T1-weighted MRI of the left hip in the patient in the previous image, shows a short, broad femoral neck. This bone remodeling is associated with Legg-Calvé-Perthes disease.


Plain radiograph in a 68-year-old man with hip pain demonstrates patchy sclerosis of both femoral heads that is consistent with avascular necrosis.


Plain radiograph of the pelvis in a man demonstrates collapse of the left femoral head due to osteonecrosis.


Coronal T2-weighted MRI in a 35-year-old man with bilateral avascular necrosis of the hip demonstrates a central region of increased signal intensity and a peripheral region of decreased signal intensity. The double-line sign is characteristic of osteonecrosis.


Coronal T1-weighted MRI in a 42-year-old man with bilateral avascular necrosis shows an area of osteonecrosis in both femoral heads in which a serpentine area of low signal intensity surrounds a central area of intermediate signal intensity similar to that of fat.


Coronal T2-weighted MRI of the same patient as in the previous image.


Plain radiograph of the right knee joint in a 52-year-old woman with abrupt onset of right knee pain demonstrates subtle loss of bone density in the proximal aspect of the tibia (arrow).


Radionuclide bone scan of the right knee joint in a 52-year-old woman with abrupt onset of right knee pain shows increased accumulation of the isotope in the medial aspect of the tibia plateau consistent with spontaneous osteonecrosis.


Plain abdominal radiograph in a patient with sickle cell disease shows generalized coarsening of the bone trabeculae with characteristic H-shaped vertebrae due to a growth disturbance. Note the calcified and contracted spleen.


Lateral view of the knee in a deep-sea diver shows dysbaric osteonecrosis in the diaphysis of the femur and tibia. Note the irregular calcific deposits with a shell-like pattern, which is typical of a bone infarct.


Sagittal T1-weighted MRI of the cervical spine in a 37-year-old woman who underwent radiation therapy for a slow-growing cystic glioma of the cervical cord. The fatty marrow change in vertebral bodies C4 through T1 is a result of radiation-induced ischemia. Note the posterior vertebral scalloping of the C7 and T1 due to long-standing spinal cord expansion caused by the tumor.


Radiographs obtained in this patient, who has a history of scaphoid fracture, demonstrated increased opacity in the proximal pole. A computed tomography (CT) scan was obtained to evaluate healing and possible osteonecrosis. Increased density is demonstrated, but the previous fracture has completely healed. Without collapse or fragmentation, this should not be considered avascular necrosi


Avascular necrosis of the proximal pole in this chronic nonunion is evidenced by the collapse of the proximal pole. This patient does not have fragmentation at this time. Note the arthritis in the midcarpal joint consistent with a scaphoid nonunion advanced collapse (SNAC) wrist.


Vascular anatomy of the scaphoid. The number of perforators along the scaphoid waist is variable; therefore, among patients with a fracture in this same location, some have a better prognosis. (A) Dorsal view of the scaphoid. (B) Volar, or palmar, view of the scaphoid


Lateral view of the wrist at the time of impact during a fall on an outstretched hand shows the force (arrow) applied to the scaphoid bone (red).


Pictures show the locations of fracture within the scaphoid bone: (A) tubercle; (B) distal pole, or extra-articular (vs intra-articular to scaphotrapezium or trapezoid joint); (C) waist; and (D) proximal pole.


The hematopoietic cells are most sensitive to anoxia and are the first to die after reduction or removal of the blood supply, usually within 12 hours.[1] Experimental evidence suggests that bone cells (osteocytes, osteoclasts, osteoblasts etc.) die within 12–48 hours, and that bone marrow fat cells die within 5 days.[1] Upon reperfusion, repair of ischemic bone occurs in 2 phases; First, there is angiogenesis and movement of undifferentiated mesenchymal cells from adjacent living bone tissue grow into the dead marrow spaces, as well as entry of macrophages that degrade dead cellular and fat debris.[1] Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts.[1] Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue.[


In the diametaphysis and subarticular regions the infarcted area is surrounded by serpiginous lines of sclerosis,representing the advancing front of new bone laid down on the old trabecular framework.The central area within the infarct may look relatively lucent,or may actually be the site of osteoclastic resorption,but it may also contain foci of added density representing dystrophic calcification in debris.


In some diseases following infarction,a bone within a bone or split cortex is seen as a linear density lying within and parallel to the healthy cortex.This probably represents the old infarcted cortex left behind by process of growth and remodelling beneath the vital periosteum.This change is seen in Gauchers and sickle cell disease and following osteomyelitis.


Epiphyseal abnormalities Infarcts at growth plates for instance in the hands and at the vertebral endplates in sickle cell disease cause local arrest of growth or may result in cone epiphysis or premature fusion.The later also occurs after irreiation,infection or trauma. Infarcted bone,for example following irradiation,is susceptible to fractures.This is seen in the ribs following irradiation for breast cancer and in the femoral necks after pelvic irradiation,though it is less common nowadays.


Isotope scanning decrease uptake in early phase then increase in uptake when healing with vascular ingrowth takes place.


Radionuclide bone scan of the pelvis in a 68-year-old man with hip pain demonstrates a bilateral central area of diminished uptake surrounded by a zone of increased uptake in the femoral head consistent with avascular necrosis.


MRI MR scanning is the most accurate means of detecting changes in avascular necrosis. Sensitivity and specificity approach 100 %. Changes at MRI are usually seen at anterosuperior segment of femoral head. Initially,bright signal remains in the affected area but subsequently after a week,this decreases corresponding to progressive lymphocytic infiltration and fibrosis.Radiographs remain normal. Class T1 T2 Definition A Bright intermediate "fat" signal B Bright Bright "blood" signal C intermediate bright "fluid or edema" signal D dark dark "fibrosis" signal


A serpiginous zone of low signal on T1 and T2WI develops around avascular area,internal to which a zone of bright may be seen on T2W,this represents edema or vascularity.Hemorrhage,cyst formation,fibrosis and collapse alter shape and signal in the femoral head. Hemorrhage and cysts are of intermediate signal on T1W but bright on T2W and STIR sequences.Sclerotic bone radiologically is of low signal on all sequences. Anatomical changes of bone collapse and deformity may be seen on plain radiographs,CT and MR scans,but MRI is the most sensitive modality in the diagnosis of early disease.Sagittal,coronal and axial images allow optimal assessment of the extent of disease.The vascular response in healing can also be assessed.


OSTEOCHONDRITIS(osteochondrosis) It is a disease of epiphyses,beginning as necrosis and followed by healing.


Osteochondritis of femoral capital epiphyses. Legg -Calve-Perthes Disease M:F=4:1 Age 4-9 yrs The age of onset is earlier in girls and prognosis worse. Bilateral disease more common in boys M:F 7:1 But disease is rarely symmetrical If symmetry is present hypothyroidism or multiple epiphyseal dysplasia should be excluded. Increased incidence of other congenital anomalies Following ischemia,the ossific nucleus of epiphysis necroses causing growth arrest..The overlying cartilage which is supplied by synovial fluid survives and thickens especially in the non weightbearing regions medially and laterally .Dense necrotic bone resorbs and is slowly replaced by vital bone.The pre disease shape of necrotic nucleus doesnot return to normal and the nucleus ends up flat in whole or in part.


Arthur Legg of the United States


Jacques Calve of France


Georg Perthes of Germany


Pathogenesis Waldenstrom staged the pathological process of the disease as Initial or ischaemic stage Resorption or fragmentation stage Reparative stage Remodelling stage


Pathogenesis Ischaemic stage - Necrosis - Crushing of trabaculae. - degeneration of basal layer of articular cartilage - Thickening of peripheral cartilagenous cap. - Shape of head maintained.

Ischaemic stage:

Ischaemic stage

Pathogenesis cont…:

Pathogenesis cont… Resorption stage - Invasion of vascular connective tissue. - Resorption of dead bone by Osteoclasts. - loss of epiphyseal height due to 1) Collapse of bony trabaculae. 2) Resorption of dead bone

Resorption stage:

Resorption stage

Pathogenesis cont…:

Pathogenesis cont… Reparative stage - pathological fracture. - creeping substitution and apposition of viable bone in dead trabaculae.

Reparative stage:

Reparative stage


X-Ray Cresent Sign or Salters sign or Caffey’s sign


X-Ray Fragmentation of epiphysis


First Symptoms Unfortunately many patients with ON have had the disease for quite some time before symptoms are present. The initial symptoms are usually pain or aching in the affected joint with activity, which subsides after the activity has stopped. Symptoms usually begin slowly and initially may be intermittent. As the disease progresses, the pain increases and is associated with stiffness and loss of motion in the involved joint. Limping becomes common. The hip is the the most common joint affected, and the pain is usually felt in the groin.


Progression of the Disease In the earliest stage of the disease, x-rays appear normal and the diagnosis is made using MRI. Once it can be seen on x-ray, it is not actually the dead bone that can be seen but the healing response of the living bone to the area of necrosis. The advanced stages of ON begin when the dead bone starts to fail mechanically through a process of microfractures of the bone. Eventually, this will result in damage to the other side of the joint, requiring major joint reconstruction.


These x-rays of the hip show the different stages of the disease. At first (stage I), there are no detectable changes on x-ray (fig A). In stage II, there are some changes but the surface is still intact (fig B). As the disease progresses, the surace begins to collapse (fig C) until, finally, the integrity of the joint is destroyed (fig D).


In the more advanced stages of the disease and/or when more of the joint is damaged, it is less likely that the natural joint can be preserved. Fortunately, joint replacement procedures today are highly successful, even in the relatively young patients affected by ON. It is always the physician's desire to preserve the normal joint whenever possible. Unfortunately, many patients do not visit the doctor until their joint has an advanced stage of the disease.


Perthes’ disease is a self-limiting form of osteochondrosis of the capital femoral epiphysis of unknown aetiology that develops in children commonly between the ages of 5 – 12 years.


It is a condition of immature hip caused by necrosis of the femoral epiphysis; the femoral head subsequently deforms as necrotic bone is replaced by living bone. It is Hip disease occurring during early childhood and caused by impaired circulation in the femoral head.


21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 78 Classification of extent of lesion - (Acc to Catterall) Grade Characteristics I Only anterolateral quadrant affected II Anterior third or half of the femoral head III Up to 3/4 of the femoral head affected, only the most dorsal section is intact IV Whole femoral head affected

Grade – I:

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 79 Grade – I Only anterolateral quadrant affected

Grade - II:

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 80 Grade - II Anterior third or half of the femoral head

Grade – III :

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 81 Grade – III Up to 3/4 of the femoral head affected, only the most dorsal section is intact

Grade – IV :

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 82 Grade – IV Whole femoral head affected

Classification according to Salter & Thompson:

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 83 Classification according to Salter & Thompson Group Characteristics A Subchondral # involving <50% of the femoral dome B Subchondral # involving >50% of the femoral dome


21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 84 8-year old boy with subchondral fracture and incipient Legg-Calve- Perthes disease

Classification according to Herring:

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 85 Classification according to Herring Group Characteristics A Lateral pillar not affected B >50% of height of lateral pillar preserved C <50% of height of lateral pillar preserved

Classification according to Herring :

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 86 Classification according to Herring “A” Lateral pillar not affected

Classification according to Herring :

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 87 Classification according to Herring “B” >50% of height of lateral pillar preserved

Classification according to Herring :

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 88 Classification according to Herring “C” <50% of height of lateral pillar preserved

Stages of Perthe’s Disease (Waldenström Staging):

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 89 Stages of Perthe’s Disease (Waldenström Staging) Avascular stage Fragmentation stage Re-ossification stage Healed stage

Stage and Characteristics:

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 90 Stage and Characteristics Avascular stage. The femoral head appears slightly flattened & denser than normal on the x-ray. The joint space is widened (Waldenström sign). Lateralisation of the femoral head.

Stage and Characteristics cont…:

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 91 Stage and Characteristics cont… Stage of resorption (Fragmentation) Femoral head breaks up into fragments Lucent areas appear in the femoral head Increased density resolves Acetabular contour is more irregular

Stage and Characteristics cont…:

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 92 Stage and Characteristics cont… Stage of Re-ossification The femoral head is rebuilt New bone formation occurs in the femoral head

Stage and Characteristics cont…:

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 93 Stage and Characteristics cont… Healing stage End stage with or without defect healing (normal hip, coxa magna, flattened head etc.)

Stages of radiological changes in Perthe's disease::

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 94 Stages of radiological changes in Perthe's disease: Early Stage – Joint space widening (waldenstrom's sign) Increased density of femoral epiphysis Subchondral fracture, or “crescent sign,” seen on lateral radiograph Mid Stage – Fragmentation and flattening of head (Coxa magna) Widening of the physis (waldenstrom's sign) Femoral neck cysts Extrusion of the femoral head

Stages of radiological changes in Perthe's disease: cont…:

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 95 Stages of radiological changes in Perthe's disease: cont… Late Stage– Coxa magna High-riding trochanter Flattened femoral head Irregular articular surface

Caffey’s sign:

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 96 Caffey’s sign As the disease progresses, a subchondral # may occur in the anterolateral aspect of the femoral capital epiphysis. Is an early radiographic feature best seen on the frog-lateral projection. This produces a crescentic radiolucency known as the crescent, Salter’s or Caffey’s sign

Fragmentation of the femoral capital epiphysis:

21 June 2016 Dr.Ratan M.P.T.,(Ortho & Sports) 97 Fragmentation of the femoral capital epiphysis

Sclerosis of epiphysis & widening of joint space in the early stages:

Sclerosis of epiphysis & widening of joint space in the early stages

Metaphyseal cyst formation within the femoral neck:

Metaphyseal cyst formation within the femoral neck

Sagging Rope Sign’ :

Sagging Rope Sign’ This a curvilinear sclerotic line running horizontally across the femoral neck. It is confirmed by 3D CT studies. It is a finding in AP radiograph in a mature hip with Perthes’ disease.


Radiological features Lateral displacement of femoral head( waldenstroms sign) Subcortical fissue in the femoral ossific nucleus(best seen in frog lateral view) Reduction in the size of ossific nucleus of epiphysis Increase in density of femoral ossific nucleus due to trabecular compression,dystrophic calcification,creeping substitution Metaphyseal broadening and irregularity(the neck may end up shortened).


Arthrography it must be understood that ossific nucleus is not the entire femoral head and in perthes disease the cartilaginous outline of the femoral head is essentially normal and not flat,irregular or fragmented as the ossific nucleus may be.Arthrography doesnot diagnose Perthes disease but determines the size and shape of the articular cartliage and the presence or absence of congruity.


Ultrasound this can also be used to assess hip joint effusions in children.By scanning in the sagittal plane from the front of patient an image of the hip is obtained.If there is atleast 3mm of fluid depth,a differnence between the two sides of 2mm and convexity of capsule then decision can be made to aspirate fluid excluding infection and relieving pain.

Ultrasound features:

Ultrasound features Effusion, especially if persistent Synovial thickening Cartilaginous thickening Atrophy of the ipsilateral quadriceps muscle Flattening, fragmentation, irregularity of the femoral head New bone formation Revascularisation with contrast enhanced power Doppler


Radionuclide bone scanning


MRI MRI changes are seen in bone and cartliganous structures of the femoral head and acetabulum.


The double-line sign in a patient with multifocal avascular necrosis (AVN) secondary to steroid therapy. Coronal T2-weighted fast spin-echo MR image (3,000/75 [repetition time msec/effective echo time msec]) of the knee shows high signal intensity in the inner zone and a low-signal-intensity line (arrow) in the parallel outer zone.


Sagittal T1-weighted spin-echo MR image (600/20) of the knee in Figure 1 shows an abnormal low-signal-intensity band (arrow) in the proximal tibia.


Osteochondritis of tibial tubercle(osgood's schlatter disease) The diagnosis is essentially clinical and is confirmed radiologically by a soft tissue lateral film of the area.This demonstrates local soft tissue swellingover an often fragmented and dense tuberosity.The other knee should also be examined radiologically especially to confirm the soft tissues.The condition is self limiting and rest brings relief of symptoms. The tubercle fuses to the shaft at 15 yrs but occasionally remains unfused and fragmented.Examination of soft tissues will rule out ongoing disease.


Osteochondritis of tarsal navicular(kohler's disease) The combination of pain and radiological change is needed for the diagnosis to be made. More common in boys Age 3-10 and peak age 5-6 Disease appears earlier in girls,as does the ossific nucleus itself The process is thought to be ischemic in origin. between 15 and 20% are bilateral


Radiographic appearances Irregularity of the outline of the navicular bone and fissure fromation are early signs. The bone may later appear as a mere dense disc. No loss of cartilage on either side of bone occurs The onset of regeneration is shown by the production of new bone around the compressed disc


T1-weighted images with signal and volume loss of the navicular ossification centre (condensation phase).


Osteochondritis of metatarsal head (Frieberg's infacrtion,Kohler's disease II) The second metatarsal head is most frequently involved. The condition is commoner in girls Age 10-15 yrs There is history of chronic trauma,fro example girls wearing high heeled shoes for the first time.


Radiographic appearances Condensation,increased density and fragmentation of the piphysis are seen.The joint space may be increaed in size and opposing bone surfaces greatly splayed.Gradual thickening of the metatarsal neck and shaft occurs


Robert Kienböck (January 11, 1871 – September 8, 1953) was an Austrian radiologist who was a native of Vienna. In 1910 he described a disorder which consisted of breakdown of the lunate bone in the wrist. He called the disorder "lunatomalacia", which is now known as Kienböck's disease kienbock


Radiographic Features Plain film Sclerosis and flattening of the lunate. When flattening is marked there is rotation of the scaphoid which further adds to the stress on the lunate. Fragmentation of the lunate and secondary degenerative disease may develop later. A five stage radiographic classification system exists. See article Stahl classification of Kienbock disease. MRI Is the most sensitive and specific test and may detect very early disease. Pattern of lunate bone signal change allows the condition to be differentiated from ulnar impaction syndrome: the major differential diagnosis. Sclerosis (low T1 and T2) is usually seen centrally and within the radial aspect of the lunate. The sclerosis can be diffuse. Bone oedema (high T2, intermediate T1) may be seen in the acute phase, particularly on the radial side. Nuclear medicine A negative bone scan can be useful to exclude the disease however a positive scan is not specific enough for diagnosis.


There is diffuse sclerosis and some flattening of the lunate in association with slight negative ulnar variance. Findings are consistent with avascular necrosis of the lunate (Kienbock disease).


Stage one: The bone loses its blood supply, and a fracture of the lunate may occur. Stage two: The bone hardens (called sclerosis) because of the lack of blood supply. Stage three: The dead lunate bone collapses. It may break into several pieces and move out of its normal position. Stage four: The surfaces of the nearby wrist bones are damaged, resulting in arthritis of the wrist.


Osteochondritis of the vertebral body(vertebra plana,Calve's disease) Collapse and increased density of vertebral body ,the adjacent disc spaces are normal or increased in width.recovery to normal shape follows but it may be incomplete. Most cases may be shown to be a manifestation of histiocytosis. Regenration is expected but histiocytosis may be associated with paraplegia Leukemia,ewing's sarcoma,metastasis ,tuberculosis etc may cause similar appearances and should always be excluded before a diagnosis of Calves's disease is accepted.


AVN of a vertebral body with classical horizontal cleft of gas.


Adolescent kyphosis(vertebral epiphysitis,osteochondritis of vertebral epiphyseal plates,Scheuermann's disease) Usually begins at puberty Affect both males and females Peak age 15-16 yrs Most commonly in mid and lower thoracic spine Sometimes in lumbar region or upper thoracic Sometimes changes are confined to a single vertebra


Radiographic appearances Irregularity is seen affecting the superior and inferior parts of the vertebral bodies.later wedging of vertebral bodies and kyphosis appear. Some scoliosis may also be present Schmorl"s nodes are seen and disc spaces become narrowed Sometimes a small paraspinal bulge is observed at the level of the lesion


Preoperative lateral of a patient with an 85º thoracic deformity secondary to Scheuermann's disease.


Postoperative lateral demonstrating a 2-rod leverage technique after an anterior release allowing reduction of the deformity to 47º.


MRI Dorso Lumbar region spine sagittal T2w images show: Multiple and contiguous involvement of vertebral bodies, the anterior wedging, antero posterior elongation, associated Schmorl's nodes, end plate irregularity and disc space narrowing. The exaggerated kyphosis of Classical Scheuermann's is absent.


To apply the label of classical Scheuermann disease, one needs to meet a number of criteria (Sorensen classification): Kyphosis: thoracic spine : > 40 deg (normal 25-40 deg) or thoracolumbar spine : > 30 deg (normal 0 deg) and at least 3 adjacent vertebrae demonstrating wedging of > 5 degrees. The condition is associated with Schmorl nodes, scoliosis (~25%) and spondylolisthesis. Other signs include vertebral end plate irregularity intervertebral disc space narrowing


The radiographic picture tends to remain static for a while .improvement is slow radiographic recovery is often incomplete.various degrees of irregularity and wedging of thoracolumbar vertebrae may be permanent.Indeed evidence of old adolescent kyphosis is one of the most frequent abnormalities seen in spinal radiographs. No constitutional effects are found in adolescent kyphosis and the vertebral defects are bounded by sclerotic rims,which are not seen in tuberculous lesions.


Residual wedging in late cases may be indistinguishable from that caused by a previous compression fracture the ring apophysis may be displaced by discal herniation,never to unite.It is then seen as a triangular fragment of bone adjacent to the end plate.Discography shows a disc filled with contrast medium which extends between the vertebral body and the detached fragment of bone.


Changes at MRI reflect changes seen at plain film(and at discography).The affected disc is narrowed and usually shows loss of signal,indicating dehydration.The disc is seen to herniate into the endplate defect and beneath the non-fused ring apophysis.


Osteochondritis at other sites Most osteochondritis occur in hip or spine Other sites include Capitellum Patella (sinding larsen disease) This condition is almost always due to an avulsion strain by the patellar ligament.


Tibia vara(osteochondritis of the medial tibial condyle,Blount's disease) This change may be seen from 1st to 12th year of age. Abnormality is usually seen on the medial aspect of the knee joint.an irregular defect is often present on the medial aspect of the proximal tibial metaphysis beneath which a large and prominent spur sticks out,almost at right angles.The overall effect is varus deformity. the lateral aspect of tibial metaphysis is straight and not bowed as in physiological bow legs. The changes are possibly related to early onset of walking


Bilateral Blount Disease. Frontal and lateral radiographs of both the right and left lower legs show beaking of the medial tibial plateau (white arrows), downward angulation of both proximal tibias. The tibiofemoral angle (blue lines)shows a varus deformity and the metaphyseal-diaphyseal angle is greater then 11 degrees (yellow lines). - See more at: http://www.learningradiology.com/archives2013/COW%20547-Blount%20disease/blountcorrect.html#sthash.63FQw7CQ.dpuf


Osteochondritis dissecans Sub-articular, post-traumatic necrosis Occurs only on convex surfaces of bone Medial condyle of femur Capitellum Proximal surface of talus Head of 1st metatarsal Most patients are athletic


Direct blow is more common cause than a rotational injury Knee lesions are more common amongst high jumpers Most common cause of an intra-articular loose body In adults, loose body contains larger fragment of cartilage than bone


Possible outcomes Death of bony, but not cartilaginous, portion of loose body Loose body is invisible except to MRI Complete resorption of loose body Reincorporation or regrowth Usually not in adults In children, fragment is less likely to separate from bone and therefore more likely to reincorporate Cause of a “locking knee”


Osteochondritis dissecans. Blue arrow points to crescentric lucency in the convex surface of the medial condyle of the knee.


Osteochondritis dissecans. Red arrows point to osteochondral defect and bone edema on T1 and stir MRI images of the knee in same patient as above. .


Initial radiographic appearances of osteochondritis dissecans of the capitellum. These images were obtained in different patients. (a) Anteroposterior radiograph obtained with the elbow at 45° of flexion shows localized subchondral bone flattening without fragments (arrows)


Anteroposterior radiograph obtained with the elbow at 45° of flexion shows nondisplaced bone fragments (arrowheads).


Anteroposterior radiograph shows a displaced fragment (arrow)


Anteroposterior radiograph shows a loose fragment (arrowheads) and a bone defect (arrow).

authorStream Live Help