The main finding of this study was that the MGHL + group did not experience more reduced postoperative stiffness than the MGHL- group. Postoperative shoulder stiffness is a prevalent adverse event after ARCR that is associated with major limitations in daily activities and prolonged rehabilitaion (6, 19, 20).
The incidence of postoperative stiffness after ARCR has been reported to range from 4.91–32.7% and, if left untreated, may lead to substantial morbidity (19, 21, 22). The exact etiology of postoperative stiffness has not been established yet; capsular contractures and postsurgical adhesion to the surrounding soft tissues are considered responsible for causing postoperative stiffness (20). Preoperative risk factors for developing postoperative shoulder stiffness after ARCR have been reported to be preoperative shoulder stiffness, age less than 50 years, workers compensation, diabetes, hypothyroidism, and coexisting diagnosis of calcific tendonitis or adhesive capsulitis (6, 19, 23). Intraoperative risk factors reported include single-tendon tears, partial articular-sided tears, and concomitant labral repair (19). Several studies have reported that associated procedures, including long head of biceps tenotomy or tenodesis, acromioplasty, capsulotomy, and glenohumeral/acromioclavicular osteoarthritis, could also increase the rate of postoperative shoulder stiffness (24–26).
The CHL has been reported to originate from the base and horizontal limb of the coracoid process, enclosing the subscapularis, supraspinatus, and infraspinatus tendons (27). In this study, it enveloped vaster areas of the subscapularis than previously reported (28). A thickened CHL at the RI has been well known to be one of the most specific manifestations of a stiff shoulder and the primary restraint against ER (29). Neer et al. reported that ER could be increased up to an average of 32° when sectioning CHL (30). Harryman et al. reported that the sectioning of the RI increased the ROM of the shoulder (31). Tsai et al. reported that arthroscopic extended RI release for patients with refractory adhesive capsulitis improved the shoulder ROM (32). Furthermore, Jazrawi et al. examined the effects of arthroscopic RI closure and found that imbrication of the RI resulted in a loss of approximately 11° of ER (33). Mologne et al. also reported that arthroscopic RI closure significantly reduced ER in both neutral and abducted arm positions (34). These studies suggested that the RI is closely associated with the ROM of the shoulder.
If postoperative stiffness is not resolved, additional procedures such as manipulation under anesthesia or arthroscopic capsular release could be considered (5, 7, 35). Although many trials have been conducted on these clinical factors, only a few studies have investigated intraoperative procedures to prevent postoperative stiffness (8, 9). Kim et al. reported that preemptive RI release in ARCR presented significantly better ROM and functional scores at postoperative 3 months than in the RI non-release group (8). However, the functional scores and ROM were not significantly different between the two groups at postoperative 6 or 12 months or the final follow-up. Park et al. reported that concomitant CHL release in ARCR presented significantly better ER in the early postoperative period than in the CHL non-release group, which was effective in patients with a small-to-medium-sized rotator cuff tear (9). They concluded that CHL release in ARCR can be used as a selective procedure to prevent postoperative stiffness in patients that may benefit from this procedure with decreased preoperative ER compared to the normal side.
Capsulectomy is considered to be an effective procedure for patients with preoperative stiffness (32, 36, 37). Moreover, as previously mentioned, it has been reported that the capsule, including the glenohumeral ligaments, is one of the main causes of a restricted ROM (13). Therefore, we hypothesized that preemptive MGHL release could prevent postoperative stiffness after ARCR. However, there were no significant differences between the groups in all ROM and all functional scores at any of the assessed time points.
There is no consensus in the literature regarding the optimal extent of a glenohumeral ligament release. Bowen et al., in their cadaveric study, showed that releasing the superior glenohumeral ligament, the MGHL, the RI, and the CHL resulted in increased ER of the shoulder joint. Releasing the anteroinferior glenohumeral ligament and the anteroinferior capsule increased elevation, and releasing the posterior-superior capsule increased IR (38). Further comparative studies are needed according to the optimal extent of a glenohumeral ligament release, including with or without the CHL release.
Our study has several limitations. First, the study design was retrospective. Second, the number of enrolled patients was relatively small. Third, the mean follow-up period of 15.6 months was relatively short. Finally, the MGHL has the greatest variation in its shape and size among all the ligaments of the shoulder joint (39–41). The common variations of MGHL include a sublabral foramen, cord-like MGHL, and the Buford complex (40, 41). The incidence rate is reported to range from 8–12% for the sublabral foramen, 1.5–5% for the Buford complex, and 19–23% for the cord-like MGHL. We could not evaluate the variation of the MGHL in this study.