What is the pathophysiology of avascular necrosis (AVN)?

Updated: Dec 05, 2020
  • Author: Sunny B Patel, MD; Chief Editor: Herbert S Diamond, MD  more...
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Answer

Although the pathophysiology of AVN is not fully understood, the final common pathway is interruption of blood flow to the bone. AVN often affects bones with a single terminal blood supply, such as the femoral head, carpals, talus, and humerus. The earliest pathologic characteristics of osteonecrosis are necrosis of hematopoietic cells and adipocytes followed by interstitial marrow edema [6] .

Osteocyte necrosis occurs after approximately 3 hours of anoxia, but histological signs of osteocyte death do not appear until approximately 24 to 72 hours after oxygen deprivation [6] . Interruption of the vascular supply and resultant necrosis of marrow, medullary bone, and cortex are theorized to be caused by the mechanisms listed below. However, individual patients usually have more than one risk factor; this indicates that the pathogenesis of AVN is likely multifactorial.

  • Vascular occlusion: This is characterized by the interruption of the extraosseous blood supply via factors such as direct trauma (eg, fracture, dislocation), nontraumatic stress, and stress fracture.

  • Altered lipid metabolism: Animal studies have led to the hypothesis that increased levels of serum lipids leads to lipid deposition in the femoral head, causing femoral hypertension and ischemia. [7] Lipid-level–lowering drugs in animals reverse this process. Corticosteroid administration was associated with fat emboli in the femoral heads of rabbits. [8]

  • Intravascular coagulation: Disorders of the coagulation system have been implicated in the pathogenesis of AVN. Typically, it is a secondary event triggered by a familial thrombophilia, hypercholesterolemia, allograft organ rejection, other disorders (eg, infection, malignancy), or pregnancy.

  • Healing process: Necrotic bone triggers a process of repair that includes osteoclasts, osteoblasts, histiocytes, and vascular elements. Osteoblasts build new bone on top of the dead bone, leading to a thick scar that prevents revascularization of the necrotic bone, with resultant abnormal joint remodeling and joint dysfunction.

  • Primary cell death: Osteocyte death without other features of AVN has been seen in renal transplant patients, as well as in patients receiving steroids and those who consume significant amounts of alcohol.


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