-incidence of positive family hx ranges from 1.6% to 20%, but no hard evidence of predisposition -is more common in certain geographic areas (urban>rural)=nutritional?, later born children, strong association with ADHD (33%)
-Phemister- thought it was infectious but cx neg -Axhausen- thought bacillary embolism with weak infection which healed quickly -1975 Matsoukas showed association with prenatal rubella -1973 Sanches, infarcted animal femoral heads, unable to produce typical histologic picture of LCPdz with one infarction, could do it with a second. Supported by Inoue using human histologic material
-few human specimens have been studied, each showing only a stage of the dz and usually from sample of just one part of the involved head. Histologically not well illucidated
-changes in zone 2 are abnormal, have different histochemical and US properties vs normal, also see small 2ndary ossification centers directly on the abnormal cartilage matrix -synovial fluid nourishes 2 superficial layers, continue to proliferate -deep layer affected by ischemic process
-physeal plate: thinner than normal, irregular cell columns and cartilage masses -metaphysis: cartilage does not ossify, proliferates with bone, causes tongues of cartilage extending into metaphysis -skeletal surveys shows contour irregularities in 48% of normal contralateral capital epiphysis, suggesting it is a generalized disorder, more appropriately named a syndrome
-growth failure due to lack of blood supply -affected femoral ossific nucleus appears radiodense (relative osteopenia of surrounding bone vs. increased mass in that area?) -affected femoral head appears smaller vs. other side -wide med joint space due to: synovitis? Decreased head volume from necrosis and collapse? Due to increased blood flow to soft tissues (eg. Lig teres) causing lateral displacement? Most likely due to epiphyseal cartilage hypertrophy (x-ray phenomenon) -crescent sign= subchondral radiolucent zone, likely results from a subchondral stress fracture and the extent of this zone determines the extent of the necrotic fragment
-increased radiodensity due to new bone forming on old bone
-AVN process after fx/dislocation does not undergo fragmentation
-25% of anterocentral head involved -no sequestrum, no subchondral fx’s, normal metaphysis
-50% of anterolateral region involved -evidence of sequestrum/ subchondral (anterior) fx, med/lat pillars intact
-75% of head involved -large sequestrum, lat pillar (column) involved, sclerotic junction btwn normal/abnormal -subchondral fx line extends into post ½ of epiphysis
-whole head involved, widespread epiphyseal collapse -diffuse or central metaphyseal lesion -Posterior remodeling of ephiphysis -poor prognosis
![History ,[object Object],[object Object],[object Object]](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)