Pathophysiology and risk factors for osteonecrosis

Abstract

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.

Fig. 1

Histopathological hallmarks of osteonecrosis. a Necrotic marrow with interstitial edema and empty lacunae indicating necrotic osteocytes. b Subchondral fracture through partially resorbed trabeculae. c Lamination of loving on dead bone. Osteocytes are present in lacunae of living but not dead bone (reprinted with permission from Wolters Kluwer/LWW)

Fig. 2

Specimen radiograph exhibiting both sclerotic and lucent areas. Sclerotic areas represent both dead and repair bone; lucent areas reflect bone resorption. A subchondral fracture is also present (reprinted with permission from Wolters Kluwer/LWW)

Fig. 3

Unified concept of circulatory pathophysiology. Diverse etiologies contribute to ischemia and necrosis (reprinted with permission from Wolters Kluwer/LWW)

Fig. 4

Concept of the Starling resistor as applied to bone microcirculation. a Raising the pressure in a rigid-walled chamber can decrease fluid flow in a flexible-walled tube passing through the chamber, b In the case of bone, the intraosseous extravascular compartment may function like a rigid-walled chamber. Intraosseous hypertension or space-occupying tissue may sufficiently restrict microcirculatory blood flow to produce ischemia (reprinted with permission from Elsevier)