Osteonecrosis is a disease process characterized by the ischemic death of subchondral bone, that is, bone under the cartilage near the joint surface, culminating in the possible collapse of the bone and damage to the joint. Osteonecrosis is distinguished from “bone infarction,” which is also characterized by ischemic death of bone – but in the diaphyseal shaft, and thus not associated with a risk of arthritis. Osteonecrosis is also known as “avascular necrosis” or “aseptic necrosis,” older terms that are no longer preferred. Osteonecrosis has many causes, including trauma, sickle cell disease, corticosteroid use, and excessive alcohol intake, though in many instances a cause is not identified. In those cases, the osteonecrosis is labeled “idiopathic.” Osteonecrosis is frequently encountered in the femoral head, proximal humerus, medial femoral condyle, talus, scaphoid, and lunate.

Structure and Function

Interruption of the supply of oxygen-rich blood is the key step to the development of osteonecrosis, as this causes ischemia of the bone, though the interruption may be subtle. For example, sickled red blood cells may clog flow in small spaces without any frank arterial occlusion. An overt interruption of blood flow via trauma, especially in bone regions with a tenuous blood supply, can lead to osteonecrosis. Osteonecrosis can be painful, but its main clinical significance is that death of sub-chondral bone can lead to collapse of the joint surface and end stage arthritis.

Bone remodeling – namely, the biologic processes of osteoclasts removing older, worn out pieces of bone, with osteoblasts synthesizing new bone to replace them – requires oxygen and nutrients. When the blood supply to the bone is interrupted, these necessary supplies are not provided, and the bone can die. However, dead bone, at the instant of death, is structurally indistinguishable from living bone. Thus, it is the later consequences, namely the loss of bone remodeling, that causes the joint to fail via the following cascade:

  • Ischemia → cell death,
  • Cell death → decreased bone remodeling,
  • Less bone remodeling → poorer structural properties of bone (notably loss of compliance),
  • Decreased bone compliance → increased chance to collapse with load (see Figure 1),
  • Collapse of subchondral bone → irregularities of the joint surface above that bone,
  • Irregularities of the joint surface on one side of the joint plus motion → damage to the other side of the joint.
Figure 1: Osteonecrosis of the femoral head with subchondral collapse. The region of dead bone and the area of collapse are shown [black and red arrows, respectively]. Notably, the surface in this specimen removed at surgery looks remarkably smooth [yellow arc] yet with any loading, this sphericity can be lost.

Patient Presentation

Most patients with osteonecrosis present because of pain, either from the infarction itself or from the resulting arthritis. Rest pain occurs in about two-thirds of patients, while night pain occurs in about one-third of patients. Osteonecrosis can also be asymptomatic and found incidentally on imaging. In some cases, known risk factors of osteonecrosis are present, but not always.

The initial physical exam findings are often non-specific. As osteonecrosis progresses and joint function deteriorates, the patient will present with the usual findings of arthrosis: swelling, tenderness, restricted motion, and deformity.

Osteonecrosis of the hip can be caused by a femoral neck fracture or dislocation. Branches of the femoral circumflex arteries are prone to disruption with a femoral neck fracture (see Figure 2). With a dislocation, the blood vessels might remain in continuity but can be stretched. This stretching might damage to the inner lining (endothelium) of the vessel, causing thrombosis and occlusion.

Osteonecrosis of the hip may be seen in patients with sickle cell disease, steroid use, and alcoholism as well. When the etiology is not traumatic, both hips are usually involved.

Figure 2: The medial and lateral femoral circumflex arteries branch off the profunda femoris (blue arrow). The green arrow points to a branch from the lateral femoral circumflex ascending the femoral neck to supply the femoral head. Disruption of this artery in the region shown by the orange box can cause osteonecrosis in the area of the head (pink circle). (Image modified from https://www.cureus.com/articles/13561-osteonecrosis-of-the-femoral-head-etiology-investigations-and-management)

Osteonecrosis of the proximal humerus may be found after fracture, but dislocation usually is not the cause. That is because normal glenohumeral mechanics are not as tightly constrained as the hip and the nearby neurovascular structures are more accommodating of displacement.

Patients may present with spontaneous osteonecrosis of the knee (known as “SONK”). SONK is most commonly seen in middle-aged females, and almost always is found in the epiphysis of the medial femoral condyle. The typical presentation is a sudden onset of severe knee pain without trauma (Figure 3).

Figure 3: MRI imaging of spontaneous osteonecrosis of the knee (SONK) showing bone marrow edema and flattening of the medial femoral condyle. (Case courtesy of Dr Fazel Rahman Faizi, Radiopaedia.org, rID: 66265)

In the wrist, osteonecrosis of the scaphoid usually follows fracture. The lunate may also be affected without a fracture, called Kienbock's Disease.

Like the scaphoid, the talus does not have any muscles/tendons inserting on it, so it too has a more tenuous blood supply and is accordingly prone to osteonecrosis when there is a fracture.

Objective Evidence

No laboratory test findings specifically confirm the presence of osteonecrosis, though testing may identify conditions that increase its likelihood.

Because dead bone does not have active osteoclasts, old and worn bone is not removed. This is seen on plain x-rays as increased density and sclerosis.

Osteonecrosis of the hip can be staged according to its appearance on imaging. There are several popular classification systems, but all unite around a similar theme of evaluation of the lesion based on plain radiographs and other modalities, especially MRI.

In its initial stage, osteonecrosis is not detectable. As osteonecrosis progresses, a subchondral radiolucency can be seen. This so-called crescent sign is produced by subchondral trabecular fracture and is a sign of impending collapse (see Figure 4).

Figure 4: Imaging of osteonecrosis of the femoral head, including MRI (left), CT (center) and plain x-ray (right) demonstrating “crescent sign,” outlined in red. (Reproduced from https://eor.bioscientifica.com/view/journals/eor/4/3/2058-5241.4.180036.xml)

In late stages of AVN, loss of sphericity and collapse of the femoral head, joint space narrowing, and degenerative changes in the acetabulum can be seen.

Bone scanning can show increased bone turnover at the junction of dead and reactive bone, but it is significantly less sensitive than MRI in diagnosing osteonecrosis.

MRI has very high sensitivity, and changes can often be seen on MRI early in the course of disease.


There is no single demographic for osteonecrosis, but the following observations apply to the various “bones at risk”:

  • Hip. The femoral head is the most commonly affected area. The US incidence is ~20,000 cases annually. Osteonecrosis is thought to account for 10% of all total hip arthroplasties. The average age of patients with osteonecrosis of the hip is about 50, and males are more commonly affected. Fracture or dislocation is implicated in about 10 to 25% of cases.
  • The shoulder is the second most commonly affected area. Osteonecrosis of the shoulder is often bilateral, because systemic factors, not trauma, are the cause (Figure 5).
  • Osteonecrosis of the knee commonly seen a middle-aged female without identifiable risk factors. The prevalence is unknown, as cases of arthritis may have been caused by undetected spontaneous osteonecrosis.
  • Osteonecrosis of the lunate (Kienböck’s disease) most commonly affects males aged 20 to 40 years old. There is a higher incidence of Kienböck’s disease in patients with negative ulnar variance (Figure 6).
Figure 5: Osteonecrosis of the proximal humerus. (Case courtesy of Dr Jeremy Jones, Radiopaedia.org, rID: 7404)
Figure 6: Radiograph of the wrist showing negative ulnar variance, namely, a “short” ulna that does not reach as far distally as the radius. The blue lines show the area where the ulna does not make contact with the lunate. This loss of contact creates greater pressure from the radius, which is thought to be the cause of the disease. (The articulation between the radius and the scaphoid and lunate is shown in red.)

Differential Diagnosis

The differential diagnosis can be thought of in a few separate ways. That is, the clinician may wonder "why does this person (with normal x-rays) have pain?" or "why does this fairly young person have arthritis?" or "what could be the cause of this lesion I see on x-rays?".

To be sure, osteonecrosis is a possible cause of pain in the setting of normal x-rays, but is likely only in patients with known risk factors (see below). Without risk factors present, hip pain is the setting of normal x-rays is more reasonably attributed to common causes of joint symptoms, such as sprains/strains or mild arthritis.

Labral tears of the hip may be a source of pain, but can be missed on MRI if contrast is not used [see https://orthopaedia.com/page/Labral-Tears-of-the-Hip-and-FAI ])

Similarly, osteonecrosis is a possible reason that a person may have premature osteoarthritis. Again, the likelihood of this without a risk factor is low.

The differential diagnosis for an isolated lesion within the bone includes osteonecrosis but osteomyelitis and bone tumors must be excluded.

Red Flags

Severe bone pain, especially in patients with known risk factors for osteonecrosis, as listed below, should prompt consideration of a diagnosis of osteonecrosis. It is theoretically helpful to detect osteonecrosis before there is joint collapse, as protecting the joint while the infarcted area might heal may be able to prevent end-state arthrosis.

Reperfusion and healing of the infarcted area, if there is no collapse, should lead to resolution of the condition. On the other hand, there is little evidence that interventions such as limiting weight bearing are actually effective to promote healing and prevent collapse when the osteonecrosis is related to systemic factors. What is clear is that preventing displacement of a fracture can protect the blood supply. Thus, for example, if patient falls on an outstretched hand and has tenderness in the “anatomic snuff box” (Figure 6), such a patient should be temporarily immobilized in a splint or cast – even if x-rays are normal. Snuff box tenderness suggests a scaphoid fracture, an injury that can be difficult to detect on routine radiographs if there is no displacement. Immobilization of the wrist can prevent displacement, which thus decreases the risk of osteonecrosis by protecting the scaphoid’s tenuous blood supply.

Figure 7: The white arrow points to the center of “anatomic snuff box.” The lateral (radial/thumb sided) border of this box is formed by the extensor pollicis brevis and abductor pollicis longus tendons. The medial (ulnar) border is the extensor pollicis longus tendon. The scaphoid lies directly below the skin here.

Treatment Options and Outcomes

Treatments of hip osteonecrosis in the pre-collapse stage include physical therapy and restricted weight-bearing, though robust evidence of efficacy is absent. (That is, these treatments are offered empirically. Some lesions apparently resolve spontaneously, and it cannot be known with certainty if an empirically employed intervention actually affected the natural history of the disease.)

Various medications, such as vasodilators to promote increased blood flow, anticoagulants to prevent thrombosis, and bisphosphonates to decrease bone resorption, have been tried.

Joint preservation surgical interventions include core decompression, bone grafts, and osteotomy. Core decompression is a completed by drilling a channel in the femoral head, to decrease pressure and increase perfusion (Figure 8). Some surgeons advocate using a vascularized bone graft to increase the blood supply.

Treatment of avascular necrosis of the femoral head after collapse of the articular surface is dictated by the extent of arthritis. Osteotomies can move a collapsed region of the femoral head away from points of maximal weight-bearing regions to less central locations. In patients with sufficiently severe signs and symptoms, total hip arthroplasty is indicated.

Figure 8: Core decompression of an area of osteonecrosis in the femoral head (shown in red). (Reproduced from DOI: https://doi.org/10.1016/j.eats.2021.08.015)

In the initial stage of disease, spontaneous osteonecrosis of the knee can be treated with analgesics and protected weight-bearing. If there is no subchondral collapse, arthroscopy, core decompression, and osteochondral autologous transplantation have been recommended. Advanced disease is treated with either unicompartmental knee arthroplasty or total knee arthroplasty.

For osteonecrosis of the lunate in patients with negative ulnar variance and no extensive degenerative changes, a radial shortening osteotomy to balance the radio-lunate joint can be tried. When more extensive degenerative changes are present, proximal row carpectomy or fusion may be needed.

Risk Factors and Prevention

The following is a list of some of the more common causes of osteonecrosis:

  • trauma
  • corticosteroid use or Cushing's disease
  • alcohol abuse
  • Sickle cell disease/Hemoglobinopathies
  • Systemic lupus erythematosus
  • Antiphospholipid antibody syndrome
  • metabolic diseases such as hyperlipidemia
  • renal failure (in renal transplantation, medication may be responsible)
  • HIV
  • prior radiation therapy
  • chemotherapy
  • decompression sickness (diving)
  • bisphosphonate use

There are no proven steps to prevent osteonecrosis, but some advice can be offered on that basis of rationale. For instance, if corticosteroids are medically indicated, the minimum effective dose should be used, for the shortest possible duration.

Trauma should be avoided, but if a bone at risk is injured, maximal care should be taken to help preserve the blood supply. As noted, possible non-displaced fractures of the scaphoid should be protected. In the case of a femoral neck fracture, open (as opposed to percutaneous) surgery for fixation may be preferable, to ensure anatomic reduction and to decompress the fracture hematoma (which might otherwise impede blood flow via a tamponade effect).

Also, patients at high risk of osteonecrosis should be educated about osteonecrosis to facilitate early (and perhaps less extensive) intervention.


Specific sites of osteonecrosis are known by eponyms, including the following: Freiberg infraction, denoting osteonecrosis of the second metatarsal head; Legg-Calvé-Perthes disease, denoting osteonecrosis of the femoral head in the pediatric population; Panner disease, which is osteonecrosis of the humeral capitellum; and Sever disease, for osteonecrosis of the calcaneal epiphysis.

Acute decompression syndrome (Caisson’s disease) is a neurological condition seen in divers when nitrogen gas emerges from the blood as bubbles after ascending from underwater too rapidly, leading to decreased blood flow to the brain and other tissues. Nitrogen bubbles can also impede blood flow to the bone, causing dysbaric osteonecrosis.

Hyperbaric oxygen treatment may be useful for patients with osteonecrosis without collapse. Patients receiving hyperbaric oxygen are placed in a special chamber and breathe pure oxygen at approximately double normal atmospheric pressure. This treatment may increase oxygenation of the bone but also may modulate inflammation.

Key Terms

Osteonecrosis, Subchondral collapse, Bone remodeling


Recognize patients at risk for osteonecrosis. Describe imaging findings.

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