Abstract
Background:
The usefulness of arthroscopic Bankart repair for collision/contact athletes has varied in previous reports.
Purpose:
To investigate the influence of glenoid rim morphologic characteristics on the clinical outcome after arthroscopic Bankart repair without additional reinforcement procedures in male collision/contact athletes, including athletes with a large glenoid defect.
Study Design:
Case-control study; Level of evidence, 3.
Methods:
Eighty-six athletes (93 shoulders) followed for a minimum of 2 years were retrospectively investigated. The sports were rugby (36 shoulders), American football (29 shoulders), and other collision/contact sports (28 shoulders). Preoperative glenoid defect size, bone fragment size, and bone union after bony Bankart repair were investigated regarding factors influencing postoperative recurrence. Postoperative changes in glenoid defect size and bone fragment size were investigated as well as their influence on the clinical outcome.
Results:
Postoperative recurrence of instability was noted in 22 shoulders (23.7%). The recurrence rate was 33.3% in rugby, 17.2% in American football, and 17.9% in other collision/contact sports. The recurrence rate was only 7.1% in 28 shoulders without a preoperative glenoid defect, but it increased to 43.8% in 16 shoulders that did not have a bone fragment even though there was a preoperative glenoid defect. Additionally, the recurrence rate was 7.7% in 26 shoulders with bone union after arthroscopic bony Bankart repair but rose to 45% in 20 shoulders without bone union. In the shoulders with bone union, the mean bone fragment size increased from 8.2% preoperatively to 15.2% postoperatively, while the mean glenoid defect size decreased from 18.0% to 2.8%, respectively. The recurrence rate was 8.3% in shoulders with a final glenoid defect 5% or less versus 38.1% in shoulders with a defect greater than 5%. While the recurrence rate was low among athletes other than rugby players with a final defect of 10% or less, it was low in only the rugby players with a defect of 0%.
Conclusion:
In male collision/contact athletes, while the overall clinical outcome was unsatisfactory, a favorable outcome was achieved in athletes without a preoperative glenoid defect and athletes with bone union. The glenoid defect decreased in size postoperatively due to remodeling of the united bone fragment, and the recurrence rate was low when the final glenoid defect size was 5% or less.
Keywords
In the treatment of traumatic anterior shoulder instability in collision/contact athletes, although some authors have reported good results with arthroscopic Bankart repair in athletes without significant glenoid defects,4,7,8 other studies have shown high recurrence rates in this population.1,2,11 This has led some authors to advocate for a return to open surgery for collision/contact athletes.
Since Sugaya et al 15 investigated anterior glenoid rim morphologic characteristics in shoulders with recurrent anterior instability by using 3-dimensional reconstruction of computed tomography scans (3D-CT), assessment of the glenoid defect has come to be considered essential when planning surgery for traumatic anterior shoulder instability. However, few reports are available regarding the relationship between preoperative glenoid rim morphologic characteristics and clinical outcomes after arthroscopic Bankart repair in athletes. Regarding the management of large glenoid defects, Sugaya et al 16 stated that arthroscopic repair of bony Bankart lesions using suture anchors was successful because most of the bone fragments were preserved, even in patients with a chronic glenoid defect. However, few investigations have been conducted regarding postoperative glenoid rim morphologic characteristics in athletes. We hypothesized that both the preoperative glenoid defect size and the bone fragment size could influence the clinical outcome of Bankart repair in male collision/contact athletes. We also hypothesized that bone union after arthroscopic bony Bankart repair and the postoperative glenoid defect size could influence the recurrence of instability. Accordingly, we investigated male collision/contact athletes with or without a large glenoid defect undergoing arthroscopic Bankart repair without additional reinforcement procedures. The purpose of this study was to determine the influence of the following factors on the clinical outcome: the preoperative and postoperative glenoid defect size, the size of the bone fragment from the bony Bankart lesion, and bone union after arthroscopic bony Bankart repair.
Methods
Between January 2010 and December 2013, primary arthroscopic Bankart repair for traumatic anterior shoulder instability was performed in 162 patients (173 shoulders) at our hospital, excluding patients with recurrent instability after previous anterior stabilization surgery (12 shoulders). Among 96 male collision/contact athletes (104 shoulders), 86 athletes (93 shoulders) followed for a minimum of 2 years were enrolled in this study. This was a retrospective investigation of prospectively collected clinical data, and institutional review board approval was obtained. The sports played by the athletes were rugby (36 shoulders), American football (29 shoulders), and other collision/contact sports (28 shoulders) (martial arts, 7; basketball, 6; judo, 4; handball, 3; wrestling, 2; soccer, 2; boxing, 1; ice hockey, 1; water polo, 1; and naginata [similar to kendo], 1). The athletes were attending junior high school (4 shoulders), high school (41 shoulders), or college (36 shoulders), and there were 6 semiprofessional and 6 recreational athletes. The mean age at primary injury was 17.3 years (range, 14-27 years), and the mean age at operation was 18.8 years (range, 14-30 years). The mean number of dislocations and subluxations was 10.9 (range, 1-100) (1-10, 70 shoulders; 11-20, 13 shoulders; 21-50, 6 shoulders; 51-100, 4 shoulders).
Preoperative evaluation of glenoid rim morphologic characteristics was conducted in all patients. Computed tomography (CT) was usually performed at the first hospital visit. Patients who underwent surgery more than approximately 3 months after the first CT scan were evaluated by CT again just before the operation. CT scanning and reconstruction of images were performed with a whole-body scanner (spiral scan, 0.5-mm slice thickness, 0.3-mm reconstruction, and 3D edit mode). CT data were analyzed in Digital Imaging and Communications in Medicine (DICOM) mode with DICOM software to perform multiplanar reconstruction (MPR). To quantify the glenoid defect, the inferior portion of the glenoid rim was approximated to a true circle on en face 3D-CT scans that were reconstructed with elimination of the head of the humerus. The extent of the glenoid defect was calculated as a percentage of the glenoid rim length (B/A × 100%, where A is the diameter of the fitted circle and B is the width of the defect) (Figure 1). The width of the bone fragment (C) was measured on the image that gave the clearest view of the articular surface of the fragment. The size of the bone fragment was defined relative to the glenoid rim and was calculated as a percentage (C/A × 100%). 10 The mean preoperative glenoid defect size was 11.3% (0%-33.6%). A glenoid defect was not detected in 28 shoulders, while a large glenoid defect (>20%) was seen in 19 shoulders. Among the 65 shoulders with a glenoid defect, the mean glenoid defect size was 16.2% (3.5%-33.6%) and the mean size of the bone fragment was 5.4% (0%-18.9%). A bone fragment was not found in 17 shoulders, and the mean size of the bone fragments associated with bony Bankart lesions was 7.3% (1.1%-18.9%).

Quantification method for glenoid defect size, and measurement of bone fragment size. (A) The inferior portion of the glenoid rim was approximated to a true circle on en face 3D-CT scans that were reconstructed with elimination of the head of the humerus. The extent of the glenoid defect was calculated as a percentage of the glenoid rim length (B/A × 100%), where A is the diameter of the fitted circle and B is the width of the glenoid defect. (B) The width of the bone fragment was measured on the image that gave the clearest view of the articular surface of the fragment. The size of the bone fragment was defined relative to the glenoid rim and was calculated as a percentage (C/A × 100%), where C is the width of the bone fragment.
Arthroscopic Bankart repair was performed by the single-row suture anchor fixation technique. The anteroinferior glenohumeral ligament (AIGHL)–labral complex was detached and mobilized from the glenoid neck to the 6-o’clock position. Because the aim of our Bankart repair is to avoid residual capsular redundancy by elevating the AIGHL-labral complex, capsuloligamentous tissue was separated up to 7-o’clock in the right shoulder if mobilization was inadequate or capsular laxity was severe, which was diagnosed by preoperative positive sulcus sign and by redundancy of anteroinferior capsule at arthroscopy. To accelerate union of the anterior labrum with the glenoid, the anterior 3 to 4 mm of the articular cartilage on the glenoid was resected. Then, 4 to 7 suture anchors were placed at the anterior bone trough created in the glenoid. Screw-in metallic suture anchors (Fastak anchor, Arthrex) were used until June 2011, and soft anchors (JuggerKnot anchor, Zimmer Biomet) have been used since July 2011. For the treatment of bony Bankart lesions, arthroscopic bony Bankart repair was performed without resection of the fragment. 10 Even in shoulders with a large glenoid defect, no bone grafting or rotator interval closure was performed during the study period. No patients had isolated capsular tears or isolated humeral avulsion of the glenohumeral ligament (HAGL). However, 20 capsular tears and 2 HAGL lesions were repaired simultaneously with the arthroscopic Bankart procedure in patients with Bankart lesions. A Hill-Sachs lesion was recognized in 58 shoulders, but remplissage or bone grafting was not performed even for a large Hill-Sachs lesion.
Patients wore a brace (allowing 90° of internal rotation and 0° of abduction) for 4 weeks postoperatively and started passive range of motion exercises after 2 weeks. Until 4 weeks after surgery, flexion and external rotation with the arm at the side were restricted to 150° and 30°, respectively, but no restriction was required after 4 weeks. Return to contact training and competition was not permitted for at least 6 months and 8 months after surgery, respectively.
Postoperative evaluation of glenoid rim morphologic characteristics by CT was done at least once in all patients who were available for follow-up. Especially in patients who underwent arthroscopic bony Bankart repair, postoperative CT was performed at 4 to 5 months and at 8 months to 1 year after surgery (if possible) to evaluate bone union. However, this was retrospective study, so the timing of CT was highly variable. Arthroscopic bony Bankart repair was performed in 48 shoulders, and 46 shoulders underwent postoperative evaluation for longer than 6 months, with the mean final evaluation time being 14.3 months (range, 6-54 months) after surgery. To assess bone union, both 3D-CT and MPR images were used.
Postoperative recurrence was defined as a report of dislocation or subluxation; the postoperative recurrence rate in each sport and the characteristic findings on CT at recurrence were investigated. Return to sporting activity was investigated in the athletes without postoperative recurrence of dislocation or subluxation. As well, we investigated the relationship between postoperative recurrence and preoperative glenoid defect size, preoperative bone fragment size, or bone union after bony Bankart repair. Postoperative changes of glenoid defect size and bone fragment size were also investigated, as well as the influence of the planned and final glenoid defect sizes on postoperative recurrence. Finally, the relationship between postoperative recurrence and the preoperative or postoperative glenoid defect size was investigated for each sport.
The planned glenoid defect size was defined as the size of the postoperative glenoid defect assuming successful union of the bone fragment to the defect without remodeling (ie, the size of the bone fragment subtracted from the size of the preoperative glenoid defect). For example, for a preoperative glenoid defect size of 20% and a bone fragment size of 5%, the planned glenoid defect size would be 15%. The actual postoperative glenoid defect size on final CT was defined as the final glenoid defect size. To quantify the final glenoid defect size, the inferior portion of the glenoid rim was approximated to a true circle, as was done for preoperative evaluation, and the defect was measured at the 4-o’clock position (right shoulder).
For statistical analysis, comparison of mean values between 2 groups was performed with Student t test, while comparison of mean values among 3 groups was done with 1-factor analysis of variance and the Kruskal-Wallis test, and a post-hoc Tukey’s test was performed after analysis of variance. Comparison of the postoperative recurrence rate was conducted with Fisher’s exact probability test. Statistical significance was set at P < .05, but differences were not considered significant if the statistical power was too low because of a small number of subjects.
Results
Clinical Outcome
Among 93 shoulders, postoperative instability occurred in 22 shoulders for a recurrence rate of 23.7%. The recurrence rate was 33.3% (12/36) in rugby players, 17.2% (5/29) in American football players, and 17.9% (5/28) in athletes playing other collision/contact sports: 66.7% (2/3) for handball, 50% (1/2) for wrestling, 16.7% (1/6) for basketball, and 14.3% (1/7) for martial arts. There was no recurrence among the athletes playing other sports, including 4 judo athletes.
Fracture of the anterior glenoid rim is a characteristic CT finding at recurrence, and it was recognized in 6 shoulders (4 rugby players and 2 American football players). Refracture occurred at the original fracture site in 1 rugby player, whose bony Bankart lesion had partially united, but a new fracture occurred at a different site in the other 5 shoulders, including 1 American football player in whom a preoperative glenoid defect was not present (Figure 2).

Postoperative recurrence of instability due to a new glenoid rim fracture in a 20-year-old, male American football player without a preoperative glenoid defect. (A) CT after primary Bankart repair. (B) CT after recurrence (arrow: new fragment).
Among the 71 athletes without postoperative recurrence, 55 (77.5%) returned to their previous sport at the preinjury level and 2 (2.8%) returned to sport at a lower level because of postoperative pain. Although physically able to play, the other 14 athletes retired from sport because of graduation or work.
Postoperative Recurrence of Instability
Among 22 athletes (22 shoulders) with postoperative recurrence of instability, we were able to assess 20 by examination and CT. One rugby player and 1 wrestler underwent reoperation at other hospitals after recurrence of instability and wecould not obtain detailed information regarding these patients, so they were excluded from this analysis. One basketball player without postoperative recurrence was also excluded from this analysis because he refused postoperative CT scanning. Accordingly, 90 shoulders were investigated by examination and CT, and postoperative recurrence was identified in 20 shoulders (22.2%).
To begin, we investigated the influence of preoperative glenoid defect size, bone fragment size, and bone union after arthroscopic bony Bankart repair on postoperative recurrence of instability. Among 28 shoulders without a preoperative glenoid defect, postoperative recurrence occurred in only 2 shoulders (7.1%) and both athletes were American football players. In contrast, postoperative recurrence occurred in 7 of 16 shoulders (43.8%) that did not have a bone fragment even though a preoperative glenoid defect was present. Bone union after arthroscopic bony Bankart repair was evaluated in 46 shoulders by postoperative CT and was confirmed in 26 shoulders (56.5%). Among the 26 shoulders with bone union, postoperative recurrence was recognized in only 2 shoulders (7.7%), including one rugby player with refracture at the original site and another rugby player with a new glenoid rim fracture at a different site. Postoperative recurrence was recognized in 9 of 20 shoulders without bone union (45%). The overall recurrence rate for shoulders without a preoperative glenoid defect and shoulders with bone union was only 7.4%, while the overall recurrence rate for shoulders without a preoperative bone fragment and shoulders without bone union was 44.4% and was significantly higher (P < .0001).
The relation between recurrence and preoperative glenoid defect size was investigated by comparing 4 glenoid defect categories: 0%, >0% to ≤10%, >10% to ≤20%, and >20% (Table 1). As a result, compared with the recurrence rate in shoulders without a glenoid defect, the rate was higher in shoulders with a glenoid defect regardless of its size. The relation between recurrence of instability and preoperative bone fragment size was also investigated by comparing 4 categories: no fragment (0%), small fragment (>0% to ≤5%), medium fragment (>5% to ≤10%), and large fragment (>10%) (Table 2). This analysis showed that the recurrence rate was higher in shoulders with a small fragment than in the other categories and it was similar to the rate in shoulders without a bone fragment.
Association Between Recurrence Rate and Preoperative Glenoid Defect Size a
Values are numbers of shoulders with recurrence out of the total number of shoulders in each group, with percentages in parentheses. ABBR, arthroscopic bony Bankart repair.
Association Between Recurrence Rate and Preoperative Bone Fragment Size a
Values are numbers of shoulders with recurrence out of the total number of shoulders in each group, with percentages in parentheses. ABBR, arthroscopic bony Bankart repair.
The bone fragment size and the glenoid defect size were compared between 26 shoulders with bone union and 20 shoulders with nonunion. In the shoulders with bone union, the mean bone fragment size was 8.2% ± 4.7%. In addition, the mean preoperative glenoid defect size was 18.0% ± 7.1%, the planned defect size was 9.8% ± 7.0%, and the final size was 2.8% ± 4.6%. In the shoulders with nonunion, the mean bone fragment size was 6.3% ± 3.9%, the mean preoperative glenoid defect size was 14.6% ± 8.4%, and the mean planned defect size was 8.3% ± 7.0%. There were no differences of the bone fragment size, preoperative glenoid defect size, and planned glenoid defect size between the 2 groups. In contrast, the final glenoid defect size was significantly smaller than the preoperative defect size (P < .0001) and also the planned size (P < .0001) in the shoulders with bone union. Also, when the difference between the preoperative and final glenoid defect sizes was defined as the final bone fragment size in shoulders with bone union, it was calculated to be 15.2% on average. Accordingly, the final bone fragment size was significantly larger than the mean preoperative size of 8.2% (P = .0007).
In the shoulders undergoing arthroscopic bony Bankart repair, the relation between the recurrence rate and the planned glenoid defect size was investigated by comparing 4 categories, as was done for the preoperative glenoid defect size (Table 3). Among the shoulders with bone union, postoperative recurrence occurred in only 2 shoulders with a planned defect of 0% to 10%. In contrast, postoperative recurrence was consistently high in shoulders with nonunion regardless of the planned glenoid defect size.
Association Between Recurrence Rate and Planned Glenoid Defect Size a
Values are numbers of shoulders with recurrence out of the total number of shoulders in each group, with percentages in parentheses. ABBR, arthroscopic bony Bankart repair.
To investigate the relationship between final glenoid defect size and postoperative recurrence, the glenoid defect size was compared between 20 shoulders with postoperative recurrence and 70 shoulders without recurrence. Final glenoid defect size was defined as the glenoid defect size on final CT in shoulders with bone union and as the glenoid defect size measured by assuming that there was no bone fragment in the other shoulders. In shoulders with postoperative recurrence, the mean final glenoid defect size was 13.1% ± 9.4%, while the mean defect size was only 5.2% ± 7.9% in shoulders without recurrence, and there was a significant difference between these groups (P = .0003). We investigated recurrence of instability by setting the cutoff value of the final glenoid defect size at 0%, 5%, 10%, 15%, or 20% and comparing shoulders with larger or smaller defects divided by each cutoff value (Table 4). When the cutoff value was set at 0% or 5%, both recurrence rates in shoulders with smaller defects were below 10% and were significantly lower than the rates in shoulders with larger defects. When the cutoff value was set at 10%, 15%, or 20%, the recurrence rates also differed between the groups with smaller and larger defects, but the differences were not significant because of insufficient statistical power.
Comparison of Recurrence Rates Between Shoulders With Larger and Smaller Final Glenoid Defects Divided by Each Cutoff Value a
Recurrence rates are expressed as numbers of shoulders with recurrence out of the total number of shoulders in each group, with percentages in parentheses.
Words in parentheses describe statistical power.
Influence of the Type of Sport
Rugby players had a higher recurrence rate compared with the other collision/contact athletes, including American football players, so factors influencing postoperative recurrence were analyzed by comparing rugby players with the other athletes. Regarding the age at operation, 91.7% of rugby players were teenagers versus 54.4% for the other sports, and there was a significant difference between the 2 groups (P = .0002). However, other patient factors were not different between the 2 groups, including the preoperative glenoid defect size and bone fragment size.
Analysis was performed of the shoulders that showed a higher postoperative recurrence rate, which were shoulders without a preoperative bone fragment and shoulders with nonunion. The relation between postoperative recurrence and the preoperative glenoid defect size was compared between rugby and the other sports after the shoulders were classified into 3 glenoid defect categories: ≤10%, >10% to ≤20%, or >20% (Table 5). Rugby players had a high recurrence rate even among shoulders with small defects (≤10%), while postoperative recurrence occurred in only 1 shoulder among other athletes with small defects. For shoulders with larger defects (>10%), the recurrence rates were high in both groups.
Association Between Recurrence Rate and Preoperative Glenoid Defect Size Between Rugby and Other Sports in Shoulders Without a Preoperative Bone Fragment and Shoulders With Nonunion a
Values are numbers of shoulders with recurrence out of the total number of shoulders in each group, with percentages in parentheses.
Postoperative recurrence rates were compared between rugby and other sports by dividing all of the subjects into 3 categories according to the final glenoid defect size: 0%, >0% to ≤10%, and >10% (Table 6). For shoulders with a defect of 0% and shoulders with a defect greater than 10%, there were no differences between the 2 groups in these glenoid defect categories. For shoulders with a defect of 10% or less, the recurrence rate was much higher in rugby players. Accordingly, when the recurrence rate was compared between 2 groups of rugby players stratified by a final glenoid defect size of 0%, it was only 6.7% for shoulders with a defect of 0% and increased to 50% for shoulders with a defect greater than 0%. When recurrence was compared among the other athletes by setting a glenoid defect size of 10% as the cutoff value, the rate was 7.3% for shoulders with a defect of 10% or less and increased to 42.9% for shoulders with a defect greater than 10%.
Association Between Recurrence Rate and Final Glenoid Defect Size Between Rugby and Other Sports in All Patients a
Values are numbers of shoulders with recurrence out of the total number of shoulders in each group, with percentages in parentheses.
Four rugby players with a final glenoid defect size of 10% or less (0% [bone union after bony Bankart repair], 3.0% [bone union], 6.4%, and 7.3%) and 1 American football player with a final defect of 0% (no preoperative glenoid defect) had recurrence, and they all showed a new glenoid rim fracture on CT after recurrence.
Discussion
The present study investigated the clinical outcome of arthroscopic Bankart repair without additional reinforcement procedures in male collision/contact athletes with traumatic anterior shoulder instability, including athletes with a large glenoid defect. We found that the overall outcome was unsatisfactory due to a high postoperative rate of recurrent instability (almost 20%). While recurrence rates were significantly higher in athletes who did not have a bone fragment preoperatively even though a glenoid defect was present and in athletes with nonunion after bony Bankart repair, a favorable outcome was achieved in athletes without a preoperative glenoid defect and athletes with bone union after bony Bankart repair. In shoulders with bone union, the united bone fragment became significantly larger over time, and the final glenoid defect size decreased significantly compared with the preoperative glenoid defect size and planned glenoid defect size. The mean final glenoid defect size was 13.1% in shoulders with recurrent instability and 5.2% in shoulders without recurrence, being significantly larger in recurrent shoulders. Accordingly, the recurrence rate was significantly lower in shoulders with a final glenoid defect size of 5% or less than in shoulders with a final defect size greater than 5%. Regarding the influence of the type of sport, among the athletes other than rugby players, postoperative recurrence seldom occurred when the preoperative glenoid defect size was 10% or less, even in shoulders without a preoperative bone fragment and shoulders with nonunion. In contrast, rugby players frequently developed recurrence, even if their shoulders had small defects. One of the reasons for postoperative recurrence in shoulders with a small glenoid defect was shown to be a new glenoid rim fracture on CT, especially in rugby players. Therefore, while the recurrence rate was low for shoulders with a final glenoid defect of 10% or less among other athletes, it was only low for shoulders with a defect size of 0% among rugby players, suggesting that the cutoff value of the final glenoid defect for avoiding postoperative recurrence was different between rugby and other sports.
The present study showed that no preoperative glenoid defect was preferable for achieving a favorable clinical outcome after arthroscopic Bankart repair. However, if a residual bone fragment was present in a shoulder with a preoperative glenoid defect and bone union was achieved after arthroscopic bony Bankart repair, the clinical outcome was still favorable and similar to that of athletes without a preoperative glenoid defect. In fact, there was no postoperative recurrence in 10 shoulders with bone union, despite a large preoperative glenoid defect (>20%). Nakagawa et al 10 reported that when postoperative union of the bone fragment was achieved in patients with bony Bankart lesions, the postoperative recurrence rate was significantly lower and glenoid rim morphologic characteristics became closer to normal because the united bone fragment was frequently enlarged by remodeling. Kitayama et al 6 also studied the glenoid rim morphologic characteristics after bony Bankart repair and reported that it was normalized in all patients at 5 to 8 years of follow-up. Accordingly, we believe that a large preoperative glenoid defect is not a definite contraindication to arthroscopic bony Bankart repair, which should be performed if a residual bone fragment is detected.
However, the processes of bone union and remodeling after arthroscopic bony Bankart repair are still controversial. Nakagawa et al 9 reported that the bone fragment displays a marked decrease in size relative to the glenoid defect within 1 year of the initial event, suggesting that most bone fragments undergo extensive absorption within 1 year after primary trauma. Nakagawa et al 10 also reported that the postoperative bone union rate was lower and union was delayed after arthroscopic bony Bankart repair when the residual bone fragment was small (<5%) or medium (5%-10%), while the postoperative recurrence rate was significantly higher when the bone fragment was small (<5%). However, those investigators found a significantly lower postoperative recurrence rate in shoulders with complete bone union, even if the bone fragment was small, and reported that remodeling was frequently detected around the fragment after bone union and that the fragment became larger over time. Accordingly, they emphasized the importance of achieving bone union. In contrast, Jiang et al 5 found no remodeling in shoulders with bone union and reported that the size of the reconstructed glenoid defect was less than 80% of its preoperative size (final glenoid defect >20%) in 3 of the 4 patients with failure. The investigators suggested that preoperative simulation of the postoperative glenoid defect size could be useful for predicting the risk of recurrence.
In the present study, we focused on the planned glenoid defect size and the final glenoid defect size, and we investigated their relation with postoperative recurrence of instability. In shoulders with nonunion, we found that postoperative recurrence was frequent regardless of the planned defect size and even occurred in shoulders with a planned defect size of 0%. Accordingly, postoperative recurrence could not be prevented after fibrous union, even if the planned defect size was small. In contrast, the final glenoid defect size decreased significantly when bone union was achieved, both compared with the preoperative glenoid defect size and also relative to the planned glenoid defect size. The major reason for the reduction of glenoid defect size appeared to be remodeling of the united bone fragment, since the average final bone fragment size was almost double the preoperative size. Therefore, even if the residual bone fragment is smaller than the glenoid defect preoperatively, it can be expected to show enlargement by remodeling after successful bone union, so operative indications might reasonably be decided by assuming that the glenoid defect will decrease in size over time. While postoperative bone union was essential to achieve better outcomes, the preoperative glenoid defect size, planned glenoid defect size, and bone fragment size were not different between shoulders with and without bone union, making it impossible to predict bone union preoperatively. However, Nakagawa et al 10 reported that the postoperative bone union rate was lower when the residual bone fragment was small or medium, suggesting that earlier bony Bankart repair should be performed to improve bone union. Furthermore, to improve the bone union rate, Nakagawa et al 10 reported that it is important to remove scar tissue, refresh the glenoid and fragment sufficiently, and expose the subchondral bone. In addition, to stimulate the healing potential of the bone fragment, multiple piercing to the bone fragment using a suture hook should be done to stimulate the blood supply. Moreover, to achieve sufficient apposition of the bone fragment to the glenoid, other operative procedures, such as double-row repair technique, should be attempted. In future research, we would like to pursue biological augmentation, such as injection of osteoinductive agents at the site of repaired bony defects.
In the present study, detailed investigation of the relationship between glenoid defect size and recurrence of instability showed that a preoperative glenoid defect of 20% to 25% was generally the critical size at which arthroscopic repair was definitely unsafe for male collision/contact athletes. Shaha et al 13 investigated clinical outcomes in active duty military personnel, a high-risk group who were not athletes, and reported that a preoperative glenoid defect of 13.5% was an appropriate threshold for “subcritical” bone loss, which led to a clinically significant worsening in the Western Ontario Shoulder Instability Index (WOSI) scores consistent with an unacceptable outcome. We also found that postoperative recurrence was more strongly influenced by the final glenoid defect size than by the preoperative glenoid defect size. Jiang et al 5 reported that arthroscopic bony Bankart repair was successful when the final glenoid defect size was less than 20%, but those investigators provided no description of the sports played by the subjects. Findings based on all male collision/contact athletes including rugby players indicated that the final glenoid defect size should be no more than 5% to prevent postoperative recurrence, but the critical bone loss threshold is stricter for rugby players because postoperative recurrence was frequent even in shoulders with a small final glenoid defect (≤10%). So, for young rugby players who have small or no bone fragment even though there is a large glenoid defect, arthroscopic Bankart repair may be contraindicated, and open repair or arthroscopic bony augmentation should be strongly recommended. In contrast, analysis excluding rugby players showed that the recurrence rate was low when the final glenoid defect size was 10% or less. Accordingly, decision making regarding arthroscopic surgery should consider the characteristics of the subjects and the planned final glenoid defect size.
A detailed analysis of patients with postoperative recurrence showed that a new fracture of the anterior glenoid rim was a characteristic finding. Sporadic reports have discussed new glenoid rim fracture after Bankart repair, but few previous reports have summarized data from a large group of patients. It was interesting that recurrence was due to the glenoid rim fracture even in a player with no glenoid defect at the primary operation. Regarding the mechanism of this type of postoperative glenoid rim fracture, we previously considered that fracture occurred at the sites of insertion of large metallic anchors. However, glenoid rim fracture still occurred after the introduction of small suture-based soft anchors, so this matter needs to be investigated in consideration of the influence of number of suture anchors, enlargement of the anchor holes, and other factors. Moreover, 2 rugby players had recurrence due to refracture after bone union, and new glenoid rim fracture on CT was shown to be one of the reasons for postoperative recurrence in shoulders with a small glenoid defect. While such recurrences could represent unrelated injuries, bone grafting might be required to prevent this type of reinjury.
A limitation of the present study was its retrospective design. While preoperative CT data that had been collected prospectively were used to evaluate preoperative glenoid rim morphologic characteristics, the timing of postoperative CT was highly variable, so it inevitably had an influence on the assessment of bone union and remodeling and the final glenoid defect size. Another limitation was the method of quantifying lesions on CT scans. Several investigators have reported the difficulty of quantifying preoperative glenoid defects,3,14 but we found that evaluation of postoperative glenoid defects was even more complicated. 10 After arthroscopic bony Bankart repair, the shape and position of the bone fragment varied, so the postoperative glenoid defect size would have differed slightly according to the CT slice used for measurement. The final glenoid defect size was measured at the 4-o’clock position (right shoulder), which was reported to be the direction of dislocation 12 ; future investigators should consider various quantification methods, including evaluation using the area of glenoid defect. The final glenoid defect size was measured in shoulders with nonunion by assuming that there was no bone fragment, because postoperative recurrence was found regardless of the planned defect size. However, some kind of bony support could be expected even in shoulders with fibrous union, so we hope to investigate better methods for definition and quantification of the final glenoid defect in the future.
Conclusion
In male collision/contact athletes, including athletes with a large glenoid defect, the clinical outcome of arthroscopic Bankart repair without additional reinforcement procedures was unsatisfactory due to a high postoperative rate of recurrent instability. However, if bone union was achieved after arthroscopic bony Bankart repair in shoulders with a preoperative glenoid defect, the clinical outcome was favorable and similar to that for shoulders without a preoperative glenoid defect. The united bone fragment showed significant enlargement, with the final glenoid defect size being significantly smaller than the preoperative glenoid defect size and the planned glenoid defect size. The final glenoid defect size had a stronger influence on postoperative recurrence than the preoperative glenoid defect size, and the postoperative recurrence rate was low in shoulders with a final defect size of 5% or less. However, the cutoff value of the final glenoid defect for avoiding postoperative recurrence might be different between rugby and other sports.
Footnotes
The authors declared that they have no conflicts of interest in the authorship and publication of this contribution.
