Osteonecrosis, also known as avascular necrosis or AVN, is characterized by a stereotypical pattern of cell death and a complex repair process of bone resorption and formation. It is not the necrosis itself but rather the resorptive component of the repair process that results in loss of structural integrity and subchondral fracture. Most likely, a common pathophysiological pathway exists involving compromised subchondral microcirculation. Decreased femoral head blood flow can occur through three mechanisms: vascular interruption by fractures or dislocation, intravascular occlusion from thrombi or embolic fat, or intraosseous extravascular compression from lipocyte hypertrophy or Gaucher cells. In this review, we emphasize etiologic relationships derived mostly from longitudinal cohort studies or meta-analyses whose causal relationships to osteonecrosis can be estimated with confidence. Understanding risk factors and pathophysiology has therapeutic implications since several treatment regimens are available to optimize femoral head circulation, interrupt bone resorption, and preserve the subchondral bone.

Corticosteroids are the most common etiological factor in nontraumatic avascular necrosis (AVN) of bone, accounting for about 10% of arthroplasties performed annually in the United States. Evidence is conflicting on the relative importance of peak dose, daily dose, or cumulative dose, and most likely all three represent "high dose" corticosteroid administration and play a role in AVN. The etiology may be multifactorial with corticosteroids superimposed on genetic or pathological predispositions. Joint preservation depends upon early diagnosis and treatment before fracture of the subchondral trabeculae and joint incongruity. Early intervention depends upon identifying at-risk patients and quantifying their risk by understanding clinical and pathophysiological contributions to that risk. Our data and that of others suggest that a screening MRI of at-risk populations will permit detection of AVN at a prefracture stage when preservation of the joint is possible.

DCE-MRI can quantitatively assess subchondral bone perfusion kinetics in human OA and identify heterogeneous regions of perfusion deficits. The results are consistent with venous stasis in OA, reflecting venous outflow obstruction, and can affect intraosseous pressure, reduce arterial inflow, reduce oxygen content, and may contribute to altered cell signaling in, and the pathophysiology of, OA.