Clinical Presentation and Evaluation of Glenohumeral Arthritis.

Last updated Thursday, January 27, 2005

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Figure 11

Cuff tear arthropathy

About cuff tear arthropathy

Cuff tear arthropathy occurs when a chronic, massive rotator cuff defect subjects the uncovered humeral articular cartilage to abrasion by the undersurface of the coracoacromial arch (see figure 7). The humeral head becomes femoralized and the coracoacromial arch acetabularized (see figure 8). The erosion of the humeral articular cartilage begins superiorly rather than centrally as is the case in degenerative joint disease and capsulorrhaphy arthropathy.

In 1981, McCarty and co-workers described a shoulder condition: the "Milwaukee shoulder." This included significant rotator cuff disease and shoulder arthritis in older patients, often women. (Garancis, Cheung, Halverson, et al., 1981; Halverson, Cheung, McCarty, et al., 1981; McCarty, Halverson, Carrera, et al., 1981) The synovial fluid contained aggregates of hydroxyapatite crystals, active collagenase, and neutral protease. At that time, these authors hypothesized that the crystals within the synovial fluid were phagocytized by the macrophage-like synovial cells, and the cells in turn released enzymes, resulting in damage of the joint and joint-related structures. The inciting process could not be identified.

In 1983, the hypothesis was further refined. The crystals were identified as basic calcium phosphate (BCP). (McCarty, 1983) It was thought these crystals would form in the synovial fluid by unknown mechanisms. They would then be phagocytosed by the synovial lining cells. These cells would then secrete the collagenase and neutral protease. This would damage the tissues and, in addition, cause the release of additional crystals. The importance of this concept may be a more universal understanding of crystal-related arthropathies and a better understanding of how multiple joint structures can be affected by an underlying problem. (Halverson, Cheung, McCarty, 1982; Halverson, Garancis, McCarty, 1984; Halverson, McCarty, Cheung, et al., 1984; Klimaitis, Carroll and Owen, 1988)

Nguyen and Nguyen (Nguyen and Nguyen, 1990) and Campion (Campion, McCrae, Alwan, et al., 1988) have described an "idiopathic destructive arthritis" of the shoulder, which may be another form of the same condition.

In 1983, Neer and co-workers published an article on cuff tear arthropathy describing pathological changes in 26 patients. (Neer, Craig and Fukuda, 1983) These changes included massive rotator cuff tearing, glenohumeral instability, loss of articular cartilage of the glenohumeral joint, humeral head collapse, and related bone loss. This entity was distinctly different from osteoarthritis, which he had defined earlier. Neer felt that mechanical factors associated with extensive rotator cuff tearing played a prominent role in the creation of this problem and that secondary nutritional changes may augment the pathological changes that occur.

The relationship between &"Milwaukee shoulder" syndrome, crystal deposition arthritis and cuff tear arthropathy is unclear. They may be the same process or different process with similar end stages. For the surgeon, however, the challenge is an eroded joint lacking normal bone stock and lacking reconstructable rotator cuff tissue. In this condition the glenohumeral joint is deprived of several of its major stabilizing factors:

1. The normal cuff muscle force vector compressing the humeral head into the glenoid (see figure 9).
2. The superior lip of the glenoid concavity, which is typically worn away by chronic superior subluxation (see figure 10).
3. The cuff tendon interposed between the humeral head and the coracoacromial arch (see figure 11).

As a result of these deficits, the superior instability is of sufficient severity that it cannot be reversed in a dependable way at the time of reconstructive surgery.

Arntz et al (Arntz, Jackins and Matsen, 1993) reported their results from 21 shoulders with cuff tear arthropathy. These shoulders were not candidates for glenoid replacement because of the massive deficiency in the cuff and the fixed upward displacement of the humeral head. Thus they were treated with a special hemiarthroplasty, allowing the prosthesis to articulate with the coracoacromial arch. The prerequisites for successful hemiarthroplasty were an intact deltoid and a functionally intact coracoacromial arch to provide superior secondary stability for the prosthesis. One important aspect of the operative technique was the selection of a sufficiently small prosthesis so that excessive tightness of the posterior aspect of the capsule could be avoided. Eighteen shoulders in sixteen patients were available for follow-up, which ranged from twenty-five to 122 months. Pain decreased from marked or disabling in fourteen shoulders preoperatively to none or slight in ten and to pain only after unusual activity in four. Active forward elevation improved from an average of 66 degrees preoperatively to an average of 109 degrees postoperatively. One patient, who had an excellent result, fell and sustained an acromial fracture, so the functional result changed to poor. Three patients had persistent, substantial pain in the shoulder that led to a revision. Neither infection nor prosthetic loosening developed in any shoulder.

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