Abstract
The widespread use of MRI in the diagnosis of articular pathology has allowed for an improved knowledge of a series of disturbances that occur with epiphyseal bone edema as a main radiological sign, featured as low signal intensity of the bone marrow on T1 and high signal on STIR and fat saturated T2 sequences. The new etiopathogenic theories postulate a clear differentiation between primary and secondary osteonecrosis. While secondary osteonecrosis is related to risk factors, primary osteonecrosis is a result of a subcondral insufficiency fracture. Both have different characteristic and MRI criteria. The pathogenesis of transient bone edema syndrome (BMES) is currently under discussion, divided between the biomechanic theory and the more classic one that relates to the complex and poorly understood mechanisms associated with complex regional pain syndrome type I (reflex sympathetic dystrophy). The BMES, classically considered a reversible form of osteonecrosis, has enough differentiated features to be considered as a distinct disease. Bone marrow edema can be as extensive in either insufficiency or fatigue stress fractures than in BMES. The diagnostic key is the display of a subcondral bone fracture. These can be resolved or occasionally evolve into a primary osteonecrosis.
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