Osteonecrosis (see images below) of the humeral head 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 researched more thoroughly and is therefore better understood than osteonecrosis of the shoulder. The major difference between osteonecrosis of the hip and osteonecrosis of the humeral head is that the shoulder bears less weight than the hip.
History of the Procedure
The earliest literature on osteonecrosis involves that of the hip. The first significant data on shoulder osteonecrosis came from Cruess in 1976 and then in 1978. The information Cruess published in 1978 provided data from which the current classification system originated. [1, 2]
Osteonecrosis of the humeral head ultimately can result in collapse of the humeral head articular surface and joint destruction. 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.  Atraumatic osteonecrosis also is believed to involve abnormalities of humeral head blood flow from multiple etiologies. Atraumatic osteonecrosis often involves the hip as well as other bones.
The incidence of both forms of osteonecrosis of the shoulder, particularly the atraumatic form, is difficult to determine. However, it definitely 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 occurs secondary to disruption of the vascular supply, which is secondary to fracture or dislocation of the humeral head. Atraumatic necrosis has multiple associated risk factors. Steroid use and alcohol abuse predominate, but dysbarism, hemoglobinopathies, coagulopathies, Gaucher disease, connective tissue disorders, and idiopathic disorders have been identified as risk factors. [1, 4]
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.  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. Sickle cell disease causes infarcts in the subchondral bone via infarcts of diseased red blood cells.
Following the initial insult, the pathogenesis of the disease is the same, despite 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. Therefore, 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.
The traumatic form of shoulder osteonecrosis can occur at any age in the face of three-part, four-part, or anatomic neck humeral fractures and/or dislocations. The atraumatic form usually occurs in patients aged 20-60 years with appropriate risk factors.
Presentation depends on etiology. Typically, pain is poorly localized and severe. Night and rest pain are present and are escalated 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.
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 is 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.
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.
No specific contraindications to treatment exist, other than those pertaining to high surgical risk situations. Infection or severe systemic disease may preclude surgical intervention.
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