The subscapularis musculotendinous unit provides a stabilizing effect on the glenohumeral joint and thus, enables normal active range of motion. As pathologies of the subscapularis tendon (SSC) are diagnosed with increased regularity, treatment strategies and their long-term consequences are of relevant interest. Therefore, the primary objective of this retrospective case series was to evaluate clinical and radiological long-term results after open repair of large SSC tears.
Repair failure negatively influences clinical outcomes and the progression of secondary glenohumeral osteoarthritis (OA).
Between 1998 and 2007, 24 patients with traumatic large (Lafosse III and IV) SSC tears were treated with an open transosseous repair technique. Of those, 20 patients (83%) with a mean age of 55±8 years (range, from 31 to 68 years) at the time of surgery were subjected to a long-term follow-up after a mean of 14±3 years (range, from 10 to 18 years). The Subjective Shoulder Value (SSV), the Constant Score (CS), the University of California at Los Angeles (UCLA) Shoulder Score, and the American Society for Shoulder and Elbow Surgeons (ASES) Score were obtained. Magnetic resonance imaging (MRI) was performed to evaluate tendon integrity. The progression of secondary glenohumeral OA from pre- to postoperative was analyzed using the collective instability arthropathy (CIA) score.
One patient (5%) had to undergo revision surgery due to a symptomatic re-tear of the SSC tendon. Besides that, the mean SSV of the affected shoulder was 83%±12, the CS 78±10, the UCLA 32±2, and the ASES 89±14 points, respectively. MRI revealed a re-tear of the SSC tendon in 4 patients (29%). On the affected shoulder, glenohumeral OA progressed significantly from pre- (CIA, 0.3±0.5) to postoperative (CIA, 1.7±0.9; p=0.003) and was significantly associated with repair failure (p=0.040).
IV; retrospective case series.
Open repair of large SSC tears yielded good clinical long-term results. Nevertheless, repair failure was common and, in the further course, negatively affected clinical outcomes and the progression of secondary glenohumeral OA.