Rotator Cuff Arthropathy

Issue: November 2016

ByAnn Ouyang, MD

The increasing aging population will present physicians with the challenges of addressing the functional limitations of shoulder arthritis. Our understanding of the pathogenesis and treatment options for rotator cuff tear arthropathy is continuing to evolve, especially with better surgical treatment options.

Several methods have been proposed to solve the bony and soft-tissue deficiencies in rotator cuff tear arthropathy (CTA), but most efforts have had difficulty balancing stability without limiting range of motion and therefore function. This excerpt will discuss the basic understanding of CTA.

Natural History and Etiology

The earliest reported cases of glenohumeral arthritis and cuff arthropathy were documented by Adams and Smith in the 1850s, with numerous subsequent case reports and descriptions following during the next 125 years. However, most recognize Neer and colleagues report in 1983 as the first to accurately define the disease process known as CTA. In the report, the distinct radiographic morphology of CTA were identified: superior migration and femoralization of the proximal humerus; collapse of the proximal aspect of the humeral articular surface; and acetabularization of the acromion.

There is a lack of data regarding the long-term outcomes of nonoperative care for massive rotator cuff tears. Without intervention, the shoulder in massive rotator cuff tears is thought to progress with a final picture that includes atrophy and fatty infiltration of the rotator cuff complex, degeneration of the glenohumeral cartilage and superior migration of the humeral head. Despite these distinct features, there is a lack of data correlating radiographic findings with the functional state of the patient. Overall, further study is necessary to elucidate the long-term natural history of massive rotator cuff tears and CTA.

Etiology

The evolution from massive rotator cuff tear to CTA continues to be an area of scientific interest. Not all patients who sustain small cuff tears progress to massive cuff tears, and not all patients with massive cuff tears develop CTA. Zingg and colleagues evaluated 19 patients with massive cuff tears treated nonoperatively. There was progression of glenohumeral osteoarthritis, superior migration of the humeral head, increasing tear size and progression of fatty infiltration during a 4-year period. Ironically, most patients maintained adequate shoulder function despite deteriorating radiographic studies.

Figure 2. Typical radiographic findings of a patient with advanced CTA. There is acetabularization of the acromion and distal clavicle, a high-riding humeral head and femoralization of the greater tuberosity as it has rubbed against the undersurface of the acromion. There is also loss of joint space between the humeral head and the glenoid (A). The same patient with a massive rotator cuff tear. A nonweight-bearing view is demonstrated with mild superior subluxation (B); but when a weight is added (C), there is significant superior subluxation of the humeral head relative to the glenoid.

The rheumatology literature has consistently advocated a biological pathway for the development of CTA. One of the etiologies proposed for CTA is based on a similar disease process described as the “Milwaukee shoulder.” The basis of this theory is that development of CTA is secondary to an inflammatory process that has developed within the shoulder that causes the destruction of cartilage and soft tissue around the glenohumeral joint. Their theory is based on several studies that observed an accumulation of calcium phosphate crystals within joints that developed CTA. The authors proposed calcium phosphate crystals initiate a cascade of events that trigger the release of collagenases and proteases, which cause degradation of cartilaginous tissue.

Figure 3. MRI of a shoulder with moderate CTA is shown. On the T2 coronal imaging, there is superior migration of the humeral head, and a significant rotator cuff tear is seen with medial retraction of the supraspinatus tendon (A). On the T1 sagittal imaging, there is a moderate amount of muscle atrophy and fatty infiltration throughout the entire rotator cuff muscles (B) (SS, supraspinatus; IS, infraspinatus; Sub, subscapularis; TM, teres minor).

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A second theory, termed the nutritional theory, suggests the underlying cause behind articular cartilage degradation is the lack of nutrition provided to the cartilage within the glenohumeral joint. In this theory, a torn rotator cuff allows the escape of nourishing synovial fluid and decreases the joint pressures required for the distribution of nutrients. These changes lead to a functional decline. With disuse of that joint, atrophy of the muscles and articular cartilage follow.

The mechanical theory behind the development of CTA focuses on the pathologic distributions of physical stresses placed on the humeral head after anterosuperior migration through the cuff tear. The deterioration of the articular cartilage is a result of repetitive trauma between the undersurface of the acromion and the superior aspect of the humeral head.

As with many diseases, a complex combination of these factors most likely contributes to the development of CTA. Neer and colleagues proposed a theory that included both nutritional and mechanical factors (Figure 1). Collins and Harryman proposed a logical pathway for the development of CTA using a combination of these previous theories. In their theory, CTA is initiated by the escape of the humeral head through a torn cuff. Repetitive mechanical wear between the humerus and acromion leads to inflammatory-inducing debris. This inflammation introduces an enzymatic milieu that exacerbates the damaged cartilage and leads to a clinical picture that consists of acute-on-chronic shoulder pain and immobility. Finally, the disuse of the joint only advances the deterioration of the articular surface and surrounding musculature, leading to atrophy and weakness of the rotator cuff muscles.

Demographics

Neer and colleagues original description of the CTA patient still holds today. The typical patient with CTA is a patient 60 years or older with a long history of pain in their dominant shoulder. It is more common in women than in men. It is rare for involvement of both extremities (10% to 25%) unless there is an underlying inflammatory disease, such as rheumatoid arthritis. In these situations, bilateral involvement of the shoulders is usually accompanied by polyarticular findings. Patients will consistently describe a long history (average 10 years) of progressive pain that is worse at night and weakness that leads to a major limitation of activities despite multiple corticosteroid injections. Often, a traumatic event can result in a more rapid progression of the disease process.

In CTA, the physical findings are directly related to the loss of the rotator cuff tendons. On inspection, a “fluid sign” along the anterosuperior aspect of the shoulder will hint at the presence of subacromial bursal swelling. However, the hallmark features of CTA include the loss of active and passive range of motion coupled with weakness. Isolated tears in the supraspinatus rarely lead to loss of active or passive motion, but tears in both the supraspinatus and infraspinatus result in a loss of the rotator cuff force couple with subsequent difficulties raising the shoulder above 70o. Patients will often have weakness in external rotation as demonstrated by a positive “hornblower’s sign.” Tears in the subscapularis have weakness in internal rotation but a more variable change in the range of motion. Impingement syndromes with rotator cuff tears alone do not show this combination of loss of active and passive range of motion.

Imaging

The plain radiographic findings in CTA are distinct and are thought to be secondary to the loss of the forces coupling the centers of the humeral head within the glenoid (Figure 2A). Overall, disuse of the shoulder leads to general osteopenia in the acromion and proximal humerus. On anteroposterior views, there is a characteristic superior migration of the humeral head in relation to the glenoid. The distance between the humeral head and underside of the acromion is often less than 7 mm but is not specific for CTA. It is often helpful to obtain weight-bearing views of the affected shoulder, as this will demonstrate superior migration in the setting of a massive cuff tear that may not always be present in non-weight-bearing or supine views. CTA often leads to gradual changes in the acromion that range from a sourcil sign (inferior sclerosis) to acetabularization. Occasionally, stress fractures of the acromion can be seen. Eventually, the greater tuberosity can be worn down in a process called femoralization of the humerus. This is a product of chronic superior migration of the humeral head and repetitive articulations with the acromion. In early CTA, there may only be mild superior migration of the humeral head on radiographs (Figure 2B), but if a weight-bearing view is obtained, there is significant superior migration of the humeral head and impingement on the acromion (Figure 2C).

On axillary views of the shoulder, glenohumeral joint space narrowing and peripheral osteophytes can be clearly demonstrated. Other features seen in this view include anterior or posterior migration of the humerus or wear of the coracoid process with chronic anterior subluxation of the humeral head. Humeral head erosion, flattening and subchondral cysts can all be seen on this view as well.

CT and MRI are not necessary for diagnosis of CTA, but may aid in surgical planning in specific situations, such as revision cases and cases where the amount of bone loss in the glenoid is concerning on standard radiographs (Figure 3). If abnormal glenoid wear patterns raise considerations for glenoid osteotomy or bone grafting, then CT may beneficial.

Patients who present with disabling pain that cannot be adequately examined may benefit from MRI to assess for the extent of rotator cuff tear, glenoid stock and orientation, and most importantly, tendon integrity. An MRI can be useful in specifically assessing teres minor and subscapularis integrity prior to planned surgical procedures in the setting of massive cuff tears without major glenohumeral arthritis.

Nonoperative Management

Many patients can function well despite a lack of rotator cuff as long as the deltoid and scapular stabilizing muscles are intact and strong. Tear size and pain do not always have a direct correlation. In these patients without distinct contraindications, pharmacologic management of symptoms includes ibuprofen, naproxen and cyclooxygenase inhibitors.

There has been little evidence that conclusively shows physical therapy can benefit functional outcomes in patients with massive rotator cuff tears. Trends in the literature suggest exercises that focus on strengthening the deltoid and scapular musculature in select patients can lead to improved function of the involved shoulder.

References:
Collins DN, et al. Orthop Clin North Am. 1997;28:225-239.
Frankle M, et al. J Bone Joint Surg Am. 2006;88(suppl 1 pt 2):178-190.
Garancis JC, et al. Arthritis Rheum. 1981;24:484-491.
Halverson PB, et al. Ann Rheum Dis. 1984;43:734-741.
Halverson PB, et al. Arthritis Rheum. 1981;24:474-483.
Klein SM, et al. J Bone Joint Surg Am. 2010;92:1144-1154.
McCarty DJ, et al. Arthritis Rheum. 1981;24:464-473.
Neer CS 2nd, et al. J Bone Joint Surg Am. 1983;65:1232-1244.
Tauber M, et al. J Bone Joint Surg Am. 2010;92 Suppl 1 Pt 2:226-239.
Zeman CA, et al. J Am Acad Orthop Surg. 1998;6:337-348.
Zingg PO, et al. J Bone Joint Surg Am. 2007;89:1928-1934.