The etiology of avascular necrosis (AVN) is multifactorial. Independen
t of its etiology and localization it shows typical pathologies and ra
diological images. In the early stages localized subchondral edema is
characteristic. In 50 % of all cases accompanying joint effusion may b
e found. Due to necrosis of the cells of bone marrow and bone fibrovas
cular, reactions with hyperemia can be delineated. These reactions all
ow us to visualize necrosis indirectly. The best imaging methods are M
RI and, to a lesser extent, bone scintigraphy. In later stages calcifi
cation as well as new bone formation and microfractures are typically
demonstrated and visualized best with plain X-rays and CT. Why reparat
ions in many cases, particularly in the hip, are incomplete and may st
op in any stage is unknown. Over years clinically complete silent AVNs
are not an uncommon finding. Prognosis depends on the localization an
d size of the AVN. The number of repair mechanisms is best outlined wi
th contrast-enhanced MRI and return of fatty marrow.