Introduction
Background
Osteonecrosis of the humeral head is a disorder that involves osteocytes and marrow and is characterized by bone death. Osteonecrosis of the humeral head consists of 2 forms: traumatic and atraumatic.
Osteonecrosis of the hip has been researched more thoroughly and is therefore better understood than osteonecrosis of the shoulder. Most of the information regarding osteonecrosis of the humeral head is extrapolated from the research findings of the disorder of the hip. 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 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
Problem
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.
Frequency
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.
Etiology
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.1,3
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.2 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.
Presentation
- The traumatic form of shoulder osteonecrosis can occur at any age in the face of 3-part, 4-part, or anatomic neck 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.
Indications
First, eliminate the inciting factor if it is recognized. Eliminating the inciting factor if and when it is recognized is important; however, it 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.
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.
Contraindications
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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References
Cruess RL. Steroid-induced avascular necrosis of the head of the humerus. Natural history and management. J Bone Joint Surg Br. Aug 1976;58(3):313-7. [Medline].
Cruess RL. Experience with steroid-induced avascular necrosis of the shoulder and etiologic considerations regarding osteonecrosis of the hip. Clin Orthop Relat Res. Jan-Feb 1978;86-93. [Medline].
Cushner MA, Friedman RJ. Osteonecrosis of the Humeral Head. J Am Acad Orthop Surg. Nov 1997;5(6):339-346. [Medline].
Mont MA, Ulrich SD, Seyler TM, Smith JM, Marker DR, McGrath MS, et al. Bone scanning of limited value for diagnosis of symptomatic oligofocal and multifocal osteonecrosis. J Rheumatol. Aug 2008;35(8):1629-34. [Medline].
Sakai T, Sugano N, Nishii T, Hananouchi T, Yoshikawa H. Extent of osteonecrosis on MRI predicts humeral head collapse. Clin Orthop Relat Res. May 2008;466(5):1074-80. [Medline].
Ficat RP, Arlet J. Necrosis of the femoral head. In: Hungerford DS. Ischemia and necrosis of bone. Baltimore, MD: Williams & Wilkins; 1980:171-82.
Soohoo NF, Vyas S, Manunga J, Sharifi H, Kominski G, Lieberman JR. Cost-effectiveness analysis of core decompression. J Arthroplasty. Aug 2006;21(5):670-81. [Medline].
Feeley BT, Fealy S, Dines DM, Warren RF, Craig EV. Hemiarthroplasty and total shoulder arthroplasty for avascular necrosis of the humeral head. J Shoulder Elbow Surg. Sep-Oct 2008;17(5):689-94. [Medline].
Smith RG, Sperling JW, Cofield RH, Hattrup SJ, Schleck CD. Shoulder hemiarthroplasty for steroid-associated osteonecrosis. J Shoulder Elbow Surg. Sep-Oct 2008;17(5):685-8. [Medline].
Tauber M, Karpik S, Matis N, Schwartz M, Resch H. Shoulder arthroplasty for traumatic avascular necrosis: predictors of outcome. Clin Orthop Relat Res. Dec 2007;465:208-14. [Medline].
LaPorte DM, Mont MA, Mohan V, Pierre-Jacques H, Jones LC, Hungerford DS. Osteonecrosis of the humeral head treated by core decompression. Clin Orthop Relat Res. Oct 1998;254-60. [Medline].
Mont MA, Maar DC, Urquhart MW, Lennox D, Hungerford DS. Avascular necrosis of the humeral head treated by core decompression. A retrospective review. J Bone Joint Surg Br. Sep 1993;75(5):785-8. [Medline].
Kawamura K, Kawate K, Yajima H, Kobata Y, Takakura Y. Vascularized scapular grafting for treatment of osteonecrosis of the humeral head. J Reconstr Microsurg. Nov 2008;24(8):559-64. [Medline].
Basmania CJ, Jaramillo JC, Wirth MA. Treatment of posttraumatic versus atraumatic avascular necrosis of the shoulder [abstract]. J Bone Joint Surg Orthop Trans. 1997;11:277.
Ficat RP. Idiopathic bone necrosis of the femoral head. Early diagnosis and treatment. J Bone Joint Surg Br. Jan 1985;67(1):3-9. [Medline].
Iannotti JP, Williams GR. Osteonecrosis: Pathophysiology, classification and pathoanatomy. In: Disorders of the Shoulder: Diagnosis and Management. Lippincott Williams and Wilkins;1999:439-46.
Loebenberg MI, Plate AM, Zuckerman JD. Osteonecrosis of the humeral head. In: Zuckerman JD. Instructional course lectures. Rosemont: American Academy of Orthopaedic Surgeons;1999: 349-58.
Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am. Mar 1995;77(3):459-74. [Medline].
Neer CS. Avascular necrosis of the humeral head. In: Shoulder Reconstruction. WB Saunders;1990:194-9.
Petri M, Baker J, Goldman D. Risk factors for osteonecrosis in SLE [abstract]. Arthritis Rheum. 1992;35 Suppl:S110.
Further Reading
Related eMedicine topics
Osteonecrosis, Hip
Osteonecrosis, Knee
Bisphosphonate-Related Osteonecrosis of the Jaw
Arthrocentesis, Shoulder
Anterior Glenohumeral Instability
Multidirectional Glenohumeral Instability
Posterior Glenohumeral Instability
Clinical guidelines
ACR Appropriateness Criteria® shoulder trauma. American College of Radiology - Medical Specialty Society. 1995 (revised 2005). 6 pages. NGC:004632
Shoulder complaints. American College of Occupational and Environmental Medicine - Medical Specialty Society. 1997 (revised 2004). 31 pages. NGC:004752
Clinical trials
Bone Repair Cell (BRC) Treatment of Patients With Osteonecrosis of the Femoral Head
Mesenchymal Stem Cell for Osteonecrosis of the Femoral Head
MBCP Safety and Performance in the Osteonecrosis of Femur Head
Proposal For The Development Of A Well Defined Database For Patients With Oral Bisphosphonate-Related Osteonecrosis
Molecular Genetic Study of Avascular Necrosis of the Femoral Head
Keywords
shoulder osteonecrosis, aseptic necrosis, avascular necrosis, osteonecrosis of the humeral head






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