Shoulder Osteonecrosis

Updated: Jan 29, 2022
Author: Michael Levine, MD; Chief Editor: Herbert S Diamond, MD 


Practice Essentials

Osteonecrosis of the humeral head (see images below) is a disorder that involves osteocytes and marrow and is characterized by bone death. Osteonecrosis of the humeral head may be traumatic or atraumatic. Most of the information regarding osteonecrosis of the humeral head is extrapolated from the research findings on osteonecrosis of the hip, which has been studied more thoroughly and is therefore better understood than osteonecrosis of the shoulder. 

Shoulder osteonecrosis stage II disease. Shoulder osteonecrosis stage II disease.
Shoulder osteonecrosis stage IV disease. Shoulder osteonecrosis stage IV disease.

Osteonecrosis of the humeral head ultimately can result in collapse of the humeral head articular surface and joint destruction. However, the shoulder is not subjected to the same weightbearing forces as the hip. The glenoid is less constrained and therefore accepts greater deformity of the humeral head. Also, the blood supply about the shoulder is abundant, and the scapula can compensate for some of the glenohumeral motion loss.

Traumatic osteonecrosis results from disruption of the blood supply caused by fracture or dislocation of the proximal humerus.[1]  Atraumatic osteonecrosis also is believed to involve abnormalities of humeral head blood flow; multiple etiologies exist (see Etiology), but corticosteroid therapy is the most common reported cause. Atraumatic osteonecrosis can be bilateral or multifocal. Osteonecrosis is considered multifocal when three or more joints are involved, with the femoral and humeral head most often affected.[2]

Disease prevention is key. Identifying those at risk and defining preventive measures is helpful. Many cases can be treated successfully without surgical intervention. Prosthetic fixation in patients with osteonecrosis of the shoulder often can be performed without cement because of good bone quality. Clinical identification of disease progression is critical to recognize and treat symptomatic disease in the early stages, thereby avoiding arthroplasty.

Relevant Anatomy

The major blood supply to the humeral head is from the ascending branch of the anterior humeral circumflex artery, which enters the humeral head through the bicipital groove. The posterior humeral circumflex artery pierces the rotator cuff attachments and provides a small amount of collateral flow. Collateral flow about the proximal humerus is minimal, putting the head at risk through trauma or other circulatory insults. Glenoid involvement is believed to occur secondarily to deformity of the humeral head. Intraosseous blood supply to the head arises from the arcuate artery.


The initiating insult appears to differ on the basis of causation. Traumatic disruption of the proximal humeral vasculature is a mechanical disruption. Several theories of steroid-induced disease exist.[3] One proposed theory is that increased intraosseous fat cell size results in increased intraosseous pressure and fat embolism. Alcohol abuse appears to work in a manner similar to that of steroids. Caisson disease or dysbarism causes cell death via air bubbles, with resultant congestion and ischemia. In sickle cell disease, the sickled red blood cells cause infarcts in the subchondral bone.

Following the initial insult, the pathogenesis of the disease is the same, regardless of etiology. Death of cells and marrow occurs. During the healing phase, bone resorption occurs to eliminate necrotic tissue. During this phase, the bone is weakened, and the forces across the subchondral plate of the weakened bone can result in microfractures and subsequent collapse. With progressive deformity of the humeral head, the glenoid becomes involved secondary to mechanical factors, with resultant arthritic changes.


Traumatic shoulder osteonecrosis results from disruption of the vascular supply of the humeral head due to fracture or dislocation. A growing number of case reports describe shoulder osteonecrosis following arthroscopic rotator cuff surgery.[6]   

Atraumatic osteonecrosis has multiple possible causes: steroid use and alcohol abuse predominate, but dysbarism, hemoglobinopathies, coagulopathies, Gaucher disease, connective tissue disorders, and idiopathic disorders have been identified as risk factors.[4, 5] Adults with sickle cell disease are at higher risk for shoulder osteonecrosis if hip osteonecrosis is present or if they have the S Beta or SC genotype.[7]  




The incidence of osteonecrosis of the shoulder, particularly the atraumatic form, is difficult to determine. However, it appears to occur less often than in the hip. The traumatic form has been reported in up to 34% of 3-part fractures and 90% of 4-part fractures, as well as nearly all fractures of the anatomic neck.

The traumatic form of shoulder osteonecrosis can occur at any age in the face of 3-part, 4-part, or anatomic neck humeral fractures and/or dislocations. The atraumatic form usually occurs in patients aged 20-60 years with appropriate risk factors.


The shoulder joint bears less weight than the joints of the lower extremity; therefore, symptoms can be mild, even in those with advanced disease. Many patients obtain good results when conservatively treated with analgesics and/or physical therapy for extended periods of time. Surgery can be reserved for those with severe pain, as early-stage disease often does not progress radiographically.




Presentation depends on etiology. Typically, pain is poorly localized and severe. Night and rest pain are present. Pain escalates with activity. Range of motion (ROM) is preserved in early disease; however, motion causes pain. Crepitation and locking are noted following subchondral collapse. With arthritic changes, ROM decreases mechanically.



Laboratory Studies

Laboratory studies are typically not indicated in the diagnosis of osteonecrosis. Tests can be utilized to identify inciting factors, such as the following:

Imaging Studies

Radiographs help establish the diagnosis in most cases. Essential radiographic views include anteroposterior (AP), true AP, and axillary. See the images below.

Shoulder osteonecrosis stage II disease. Shoulder osteonecrosis stage II disease.
Shoulder osteonecrosis stage IV disease. Shoulder osteonecrosis stage IV disease.

Magnetic resonance imaging (MRI) is the diagnostic modality of choice for cases in which there is clinical suspicion of shoulder osteonecrosis but radiographs are normal; MRI has sensitivity and specificity greater than 98% for shoulder osteonecrosis.[8]  The extent of humeral head necrosis on MRI is a good predictor of future collapse.[9]

Other imaging modalities include the following:

  • Bone scan [8]  – Can be helpful when disease is suggested clinically but is not apparent on radiographs; not commonly used because of the high success rates of MRI
  • Tomography – Helpful in stage II disease to further define the lesion

Other Tests

Additional studies may include the following:

  • Biopsy – Can be performed at the time of surgery (eg, core decompression), but the diagnosis usually is based on clinical and radiographic findings.
  • Venography
  • Intraosseous pressure measurements

Histologic Findings

The first phases involve cell and marrow necrosis. The reparative phase occurs as the dead bone is removed and replaced by healthy bone. During this period, the bone is weak and subject to subchondral collapse. Following collapse of the subchondral plate, damage to the articular cartilage occurs with resultant arthritic changes to the joint.


Osteonecrosis of the humeral head has been staged by Ficat and Arlet (modified for the shoulder)[10] :

  • Stage I - Normal

  • Stage II - Cystic and/or osteosclerotic lesions; humeral head contour is normal; see the image below

    Shoulder osteonecrosis stage II disease. Shoulder osteonecrosis stage II disease.
  • Stage III - Subchondral collapse or crescent sign

  • Stage IV - Narrowing of joint space; secondary osteoarthritic changes of the glenoid fossa and the glenohumeral head, such as cysts, marginal osteophytes, and destruction of cartilage, as seen in the image below

    Shoulder osteonecrosis stage IV disease. Shoulder osteonecrosis stage IV disease.


Approach Considerations

Treatment of humeral head osteonecrosis varies, depending on the stage and symptoms. Eliminating the inciting factor if and when it is recognized is an important initial step, but does not reverse the course of the disease process. Treatment often can be delayed or is not required because the shoulder is a non–weightbearing joint. However, in the face of severe pain and/or mechanical symptoms, conservative and surgical options are available. No specific contraindications to treatment exist, other than those pertaining to high surgical risk situations. Infection or severe systemic disease may preclude surgical intervention.

Medical Care

Removal of the offending agent, if possible, is the first line of treatment. Nonsurgical options often are more successful in cases of shoulder osteonecrosis than in hip osteonecrosis because the shoulder is a non–weight-bearing joint. Physical therapy that include modalities for pain control and range of motion (ROM) exercises with subsequent strengthening is helpful in all stages, but particularly in stage I and stage II.

Studies have shown that treatment with alendronate can possibly prevent a collapse of the femoral head caused by osteonecrosis; however, no research has been published regarding its effectiveness in treating osteonecrosis of the shoulder.

Surgical Care

In core decompression, a central core of bone is removed or drilled from the humeral head into the necrotic zone.[11]  Studies of core decompression have shown good and excellent results in up to 90% of cases of stage I and stage II disease.[12, 13] Core decompression also can be successful in stage III disease, with a 30% failure rate requiring subsequent arthroplasty. Failure occurs in all cases of stage IV or V disease; the procedure is palliative only.[11]  An alternative technique of decompression utilizing multiple passes of a small-diameter (3-mm) drill in a percutaneous fashion has been described.[14]

A prospective randomized clinical study of 50 patients with post-traumatic shoulder osteonecrosis compared the results of mesenchymal stem cell grafting of the humeral head versus simple core decompression alone. After more than a decade of follow-up, the rate of collapse was significantly lower in the group treated with stem cells (11.55 vs 87.5%, P < 0.0001).[15]

Limited experience with muscle pedicle grafting has shown no significant difference from core decompression alone, with increased morbidity. Further studies are required.[16]  Arthroscopic debridement of chondral lesions may be performed. Arthroscopy has no effect on the disease process, but it may be helpful in dealing with mechanical symptoms. 

Depending on the condition of the glenoid, hemiarthroplasty (HA) (see image below) or total shoulder arthroplasty (TSA) can be considered.[17, 18, 19] A 90% success rate has been reported for hemiarthroplasty and total shoulder arthroplasty in advanced-stage disease, with most patients regaining full ROM.[17, 19] Surface replacement arthroplasty is also an option.[20, 21]

Shoulder hemiarthroplasty in a patient with should Shoulder hemiarthroplasty in a patient with shoulder osteonecrosis.

The decision for a given surgical procedure is based on preoperative staging. Core decompression, muscle pedicle grafting, and arthroscopy are indicated in cases prior to collapse of the humeral head. These procedures can be helpful in stage I, stage II, and stage III disease.

Once irregularity of the joint surface occurs, arthroplasty is most beneficial. In patients with atraumatic osteonecrosis of the humeral head, both hemiarthroplasty and total shoulder arthroplasty can be expected to provide lasting pain relief and improved range of motion, but hemiarthroplasty has had longer follow-up. Schoch and colleagues recommend that hemiarthroplasty be strongly considered in patients with atraumatic osteonecrosis of the humeral head and preserved glenoid cartilage.[22]

In a comparision of 37 HAs and 46 TSAs performed for post-traumatic osteonecrosis of the humeral head after conservative treatments failed, HA provided improvements in range of motion but TSA provided superior pain relief with better patient-reported satisfaction.[23]  

 Intraoperative details vary according to the procedure chosen.

Core decompression is performed as follows:

  • Place the patient in the beach-chair position with the arm over the edge of the table
  • Use image intensification
  • Make a small incision in the lateral deltoid
  • Place a Kirschner wire (K-wire) into the necrotic lesion, and use a cannulated drill to take a core of bone.

If the drilling technique is utilized, the operative setup is identical, but instead of using a coring reamer, multiple passes are made into the lesion with a small-diameter drill (usually 3.2 mm) under image intensification.

Arthroscopy can be combined with decompression allowing for an intrarticular debridement. Articular cartilage flaps can be debrided back to a stable rim, loose bodies removed, and a selective capsular release can be performed as needed.

Hemiarthroplasty involves placement of a humeral head prosthesis, usually through a deltopectoral iapproach. For idiopathic osteonecrosis, the procedure is technically easier to perform than hemiarthroplasty for advanced arthritis, as the patient usually has minimal-to-no soft-tissue contracture and head deformity. By using the excised head as a sizer, near-perfect replacement of the articular surface can be achieved.

For total shoulder arthroplasty, multiple prostheses are available. The glenoid is resurfaced, usually with an all-polyethylene component. Total shoulder arthroplasty is indicated in individuals with stage IV disease.

In surface replacement arthroplasty, the humeral head only is resurfaced partially or completely with a metal component.

Postoperative Details

In patients who have undergone core decompression and muscle pedicle grafting, immediate ROM exercises can be initiated. Some limitations on ROM may be placed in cases of muscle pedicle grafting. Patients with core decompression are started on immediate passive ROM exercises, with active ROM as tolerated. Once full ROM is achieved, strengthening exercises can be initiated.

In patients who have undergone hemiarthroplasty and shoulder arthroplasty, immediate passive ROM is initiated, with limitation of external rotation to 45° for 6 weeks to allow for repair of the subscapularis from the surgical approach. Active ROM can be started as tolerated, with the same limitation in the absence of rotator cuff repair, which is rare. Strengthening usually is initiated at 6 weeks postsurgery.


Common surgical complications include infection and neurovascular injuries, which are particularly rare in these procedures.

When performing core decompression, care must be taken to avoid the axillary nerve anteriorly. Avoidance of penetration of the humeral head during core decompression is key.

Potential complications with arthroplasty include prosthetic loosening, dislocation, and intraoperative fracture. Fortunately, these problems are rare in avascular necrosis.