Back to A-Z

Milwaukee shoulder syndrome

Milwaukee shoulder syndrome is characterized by severe degenerative arthritis of the glenohumeral joint with loss of the rotator cuff associated with the presence of BCP crystals. Often, large joint effusions are present on physical examination. Patients with Milwaukee shoulder syndrome are usually women in their 70s. Bilateral shoulder involvement is common, with the dominant side more severely affected. Many of these patients have had shoulder impingement with calcific tendonitis in the past. It is postulated that BCP crystals shed from the tendon/bursa deposit calcium into the joint. These BCP crystals localize to the synovium, where they act as mitogens, causing cytokine and matrix metalloproteinase production by synovial macrophages and fibroblasts. In turn, the collagenase and other MMPs contribute to the rotator cuff disruption and accelerated degenerative changes in the shoulder.

Symptoms vary from minimally symptomatic with shoulder motion to severe pain at rest. Physical examination reveals reduced active and passive ranges of motion with glenohumeral crepitus. Effusions can be large. Synovial fluid, which often has streaks of blood, is noninflammatory with few white blood cells that are predominantly mononuclear. Roentgenograms show severe OA of the glenohumeral joint associated with upward migration of the head of the humerus, indicating a defect in the rotator cuff. Notably, there is a relative paucity of osteophytes (atrophic degenerative arthritis) compared to CPPD disease and primary OA. Soft tissue calcifications may also be present.