Avascular Necrosis

Updated: Oct 10, 2017
  • Author: Sunny B Patel, MD; Chief Editor: Herbert S Diamond, MD  more...
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Overview

Practice Essentials

Avascular necrosis (AVN) is defined as cellular death of bone components due to interruption of the blood supply; the bone structures then collapse, resulting in pain, loss of joint function and long-term joint damage.

AVN usually involves the epiphysis (end part of a long bone), such as the femoral and humeral heads and the femoral condyles, but small bones can also be affected. In clinical practice, AVN is most commonly encountered in the hip. [1, 2] Most available data regarding the natural history, pathology, pathogenesis, and treatment of AVN pertains to femoral head necrosis.

AVN is associated with numerous conditions. Patients taking corticosteroids and organ transplant recipients are particularly at risk of developing AVN. AVN of the jaw has been described in patients taking bisphosphonates and, more recently, denosumab. [3, 4] For full discussion of this entity, see Bisphosphonate-Related Osteonecrosis of the Jaw.

Early diagnosis and appropriate intervention can delay the need for joint replacement. However, most patients present late in the disease course. Without treatment, the process is almost always progressive, leading to joint destruction within 5 years.

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Pathophysiology

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 [5] .

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 [5] . 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. [6] Lipid-level–lowering drugs in animals reverse this process. Corticosteroid administration was associated with fat emboli in the femoral heads of rabbits. [7]
  • 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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Epidemiology

Frequency

United States

The frequency of AVN depends on the site involved. The most common site is the hip; other locations include the carpals, talus, femur, metatarsal, mandible, and humerus. In the United States, approximately 15,000 new cases of AVN are reported each year. AVN accounts for more than 10% of total hip replacement surgeries performed in the United States. Osteonecrosis of the jaw associated with bisphosphonate has also been well studied and reported. Most patients with osteonecrosis of the jaw also had an ongoing malignancy and/or had undergone a recent dental procedure. [8, 3, 9]

International

In most countries, the incidence and prevalence of AVN are not well reported. A Japanese survey estimated that 2500-3300 cases of AVN of the hip occur each year; of these, 34.7% were due to corticosteroid use, 21.8% to alcohol abuse, and 37.1% to idiopathic mechanisms. [10]

Mortality/morbidity

Data on mortality rates associated with AVN are not available. Most data involve AVN of the hip. Mortality rates are low and vary based on the operative procedure used to treat AVN.

Morbidity rates are high and depend on the underlying cause. Morbidity rates associated with AVN of the hip are high; the prevalence of long-term disability is significant. Despite advances in orthopedic procedures, most patients with advanced AVN require more than one hemiarthroplasty or total hip replacement during their lifetime.

In a study that included 1706 patients who underwent total hip replacement for AVN of the femoral head, Lovecchio et al concluded that AVN is an independent risk factor for transfusion up to 72 hours postoperatively and for readmission up to 30 days postoperatively. Bleeding requiring transfusion was the most common medical complication, occurring in 19.6% of patients with AVN compared with 13.9% of those without AVN (P<0.001). [11]

Race-, sex-, and age-related demographics

AVN has no racial predilection except for cases associated with sickle cell disease and hemoglobin S and SC disease, which predominantly occur in people of African and Mediterranean descent.

With the exception of AVN associated with systemic lupus erythematosus, AVN is more common in men, with an overall male-to-female ratio of 8:1.

AVN is a disease of middle age that most often occurs during the fourth or fifth decade of life and is bilateral in more than half of cases.

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