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.
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.
Pathophysiology
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.
Etiology
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]
Epidemiology
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.
Prognosis
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.
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Shoulder osteonecrosis stage II disease.
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Shoulder osteonecrosis stage IV disease.
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Shoulder hemiarthroplasty in a patient with shoulder osteonecrosis.
