The most common areas for the development of fibrosis in frozen shoulder include the coracohumeral ligament, the interval between the base of the coracoid and the top of the subscapularis, known as the rotator interval, between the conjoined tendon and the subscapularis, between the rotator cuff and the overlying acromion, and the deltoid bursae and musculature in the scapulothoracic region [31]. Higher rates of contracture are seen with procedures that tighten the anterior glenohumeral capsule or expose the deltopectoral interval (i.e., open procedures). Loss of motion following both arthroscopic and open Bankart repair has also been associated with excessive imbrication of the anteroinferior capsule including the anterior band of the inferior glenohumeral ligament [16, 17].

Mengiardi et al. conducted a quantitative analysis of MR arthrogram in patients with severe frozen shoulder and those without clinical or arthroscopic indications of frozen shoulder [15]. The blinded quantitative analysis showed a significantly thicker coracohumeral ligament and thicker capsule in the open rotator interval. The authors also found that patients with severe frozen shoulder had a significantly smaller capsular volume in the area of the axillary recess; however, there was no difference in capsular thickness in the axillary recess. We have previously shown that the rotator interval is dynamic with glenohumeral motion [18]. The rotator interval closes with internal rotation and opens with external rotation. Therefore, if the arm is positioned in internal rotation during imbrication, overtightening will occur and subsequent loss of external rotation [18]. A case-controlled study by Lee et al. demonstrated a thicker coracohumeral ligament and unlike the by Mengiardi et al, study they found the capsule in the axillary recess was thicker in patients with frozen shoulder. Loss of internal and external rotation range of motion was only correlated with a thickened coracohumeral ligament [11].

Rotator interval closure is often indicated for patients with inferior or multidirectional instability. The rotator interval acts to control posterior (in vitro only) and inferior (in vivo) glenohumeral translatory motion [7]. While imbrication of the rotator interval minimizes translation posteriorly and inferiorly, it may also restrict motion in flexion and external rotation [2, 7]. Computer-simulated models have demonstrated that when imbrication of the anterior band of the inferior glenohumeral ligament was increased by 3, 6, and 9 mm, a loss of external rotation range of motion of 10°, 22°, and 36° was seen, respectively [26].

Precise surgical placement of the anterior band of the inferior glenohumeral ligament is a key component in ensuring an excellent instability repair. Similar computer models, previously mentioned, have shown that when the anatomic insertion deviates superiorly by 3, 6, and 9 mm, a loss of external rotation of 5°, 11°, and 13°, can be seen respectively. When the anatomic insertion deviates inferiorly by the same amount, there is increased anteroinferior humeral head displacement [26].

Postoperative immobilization or restrictions in range of motion can contribute to frozen shoulder following surgery [3]. A key element to consider in the immediate postoperative period to minimize the incidence of secondary loss of motion following surgical intervention for repair of shoulder instability is immobilization time. Immediate postoperative external rotation with limits placed on the exercises in a controlled environment may help to overcome shoulder stiffness following instability repair.

When faced with postsurgical shoulder stiffness following instability surgery, physical therapy is always the first line of management. An individualized approach to rehabilitation is important when treating shoulder stiffness in patients following instability repair [20]. The duration of each phase of the rehabilitation program may need to be lengthened depending on the patient’s progress. The focus must be on early restoration of shoulder range of motion without stretching the repaired capsule. Aggressive stretching should be avoided for fear of exacerbating pain and stiffness. Restrictions at both the glenohumeral and scapulothoracic joints must both be addressed in order to restore ranges of motion. Furthermore, return to functional activities should be dictated by the patient’s tolerance rather than on the phase of the rehabilitation program in order to maintain gains in range of motion. Oral steroids and nonsteroidal anti-inflammatories or intra-articular steroid injections should be administered for pain control, to help decrease inflammation, to calm the tissues, and to aid in maximizing gains in physical therapy.