Bone loss in shoulder instability: putting it all together

Introduction

The shoulder is the most frequently dislocated major joint, with an incidence in the United States of up to 24 per 100,000 person-years (1). While stability of the glenohumeral joint derives primarily from static and dynamic soft tissue restraints including the labrum, capsule, and rotator cuff, these structures are complemented by the osseous morphology of the shoulder. Traumatic dislocations may damage the bony architecture of the glenoid and humerus, while recurrent instability can be both a symptom and a cause of chronic bone loss. Notably, up to 90% of patients undergoing arthroscopic evaluation of recurrent shoulder instability demonstrate an osseous defect of the glenoid or humeral head (2).

Successful treatment of both primary and recurrent shoulder instability necessitates careful consideration of anterior and posterior glenoid bone loss, osseous (Hill-Sachs or reverse Hill-Sachs) lesions of the humeral head, and underlying ligamentous laxity that may predispose to multidirectional instability (MDI). Failure to address bone loss may lead to failure of surgical treatment, with rates of recurrent instability as high as 17.8% among contact athletes following arthroscopic soft tissue repair (3). Treatment algorithms in recent years have focused on defining “critical” versus “subcritical” glenoid bone loss (4), and in classifying bipolar glenoid and humeral lesions according to the glenoid track (GT) concept (5). While critical anterior bone loss has historically been defined as 20–25% of the glenoid diameter (6), studies have demonstrated increased failure rates with soft tissue stabilization in patients with as little as 13.5% glenoid bone loss (4). Furthermore, while bipolar lesions are typically characterized as “on-track” or “off-track” according to engagement of the Hill-Sachs lesion with the anterior glenoid rim, the recent concept of “distance to dislocation” (DTD) calls this binary framework into question (7). As the GT narrows and Hill-Sachs size increases, on-track lesions demonstrate a relatively small DTD, and become “near-track” lesions. Particularly in younger patients, “near-track” lesions may portend an increased risk of failure of soft-tissue procedures (7). Finally, the treatment of recurrent shoulder instability may be influenced by other osseous features, such as glenoid retroversion (8), and patient-specific factors, such as age, athletic status, and ligamentous laxity (9). It is important to note that in the setting of laxity and concomitant MDI, treatment algorithms differ, primarily favoring nonoperative over operative management (10).

The purpose of this paper is to provide a comprehensive review of the evaluation and management of bone loss in the context of shoulder instability. Both anterior and posterior glenoid bone loss, as well as humeral head and bipolar lesions will be discussed. Finally, the authors will describe an evidence-based treatment algorithm for both glenoid and humeral-sided lesions.

Pathophysiology

Anterior

Patients are at risk of anterior shoulder dislocations when the arm is in a position of 90 degrees of abduction with maximum external rotation of the shoulder. This position places stress on the anteroinferior capsule and the anterior band of the inferior glenohumeral ligament (IGHL), one of the principal static stabilizers of the shoulder (11). When the force applied exceeds the resistance force of the IGHL and/or anteroinferior capsule, the ligament is disrupted and the glenohumeral joint subluxates or dislocates. In younger patients, the energy involved is often substantial; common etiologies include motor vehicle accidents, sports collisions, and skiing accidents (12). In elderly patients, low energy etiologies, such as falls from standing, are often implicated (13).

Dislocation often requires manual closed reduction with the aid of muscle relaxation or sedation (14). After reduction, the amount of residual instability in the shoulder is dependent on many factors, including mechanism of injury, magnitude of force involved, and additional bony or soft tissue injury, among others. One common associated injury is an avulsion of the anterior inferior caspulolabral complex. This is defined as a Bankart lesion and is present in up to 85% of traumatic anterior dislocations (15,16). Capsulolabral complex injuries are not limited to the anteroinferior location and are often seen extending superiorly, inferiorly, and even circumferentially. Multiple anterior dislocations may lead to pathologic superior translation of the humeral head, producing superior extension of capsulolabral injuries that further contribute to the cycle of repetitive dislocation (17). Moreover, Bankart lesions are often found in conjunction with additional injuries, such as humeral avulsion of the IGHL, known as a humeral avulsion of the glenohumeral ligament (HAGL) lesion (18).

In addition to soft tissue injuries, shoulder dislocations can result in bony injuries. When the humeral head dislocates anteriorly, the posterior head can be impacted along the anterior glenoid rim, resulting in a Hill-Sachs lesion. The Hill-Sachs lesion is often analyzed in relationship to the GT, with “off-track” lesions engaging the anterior glenoid rim and resulting in subluxation. Repetitive subluxations or dislocations may also erode the anterior rim of the glenoid, causing glenoid bone loss and resulting in a cycle of recurrent dislocating events (13,19).

Instability may be present without history of a frank dislocation as well. Repetitive microtrauma, commonly seen in overhead athletes such as volleyball players and baseball pitchers, causes repetitive load of the glenohumeral joint in abduction and excessive external rotation, resulting in subluxation to pathologic limits while maintaining glenohumeral contact (19).

Posterior

While anterior shoulder instability is more commonly encountered, posterior shoulder instability remains a relevant and challenging clinical problem. Though seen as a sequalae of dislocation events stemming from seizures and electrocution, the pathology most commonly stems from repetitive microtrauma with the shoulder in a position of flexion and internal rotation. This position is often seen in exercise activities such as bench press and push-ups as well as in the blocking position of offensive linemen in American football and a variety of military exercises (20). Similar to anterior instability, adaptive changes within the shoulder of overhead athletes predisposes these patients to posterior labral injuries (21). The superior labrum undergoes permissive detachment to allow for the terminal external rotation required in overhead throwing motions, and when this detachment extends posterior to the biceps anchor, the posterior labrum loses its compressive capability and the posterior band of the IGHL becomes compromised, resulting in a symptomatic throwing shoulder (21-23).

Abnormal bony anatomy may also predispose patients to posterior instability. The morphology of the glenoid with respect to its articulation with the humeral head has been scrutinized, and retroversion and dysplasia have been shown to be risk factors. In fact, every degree of increased glenoid retroversion increases posterior instability risk by 17% (24). Another important risk factor is the amount of bone loss present in association with instability. Posterior glenoid bone loss has been characterized morphologically as a loss of posterior concavity with increased glenoid retroversion, both of which lower the threshold for posterior subluxation (25). One study assessing outcomes after posterior stabilization found inferior outcomes were more closely linked to bone loss than glenoid version (26), with a similar study finding a decreased return to full duty in military patients with posterior bone loss exceeding 13.5% (27).

Clinical evaluation

History

Assessment of shoulder instability and possible bone loss should begin with a detailed history. Important patient characteristics include age, gender, sport played, mechanism of injury, number of previous instability events, treatments received, and a personal or family history of hyperlaxity (28). Males aged 15 to 29 years account for 48.6% of shoulder dislocations presenting to the emergency room, with a male-to-female incidence ratio of 2.64. Patients under age 30 also account for the majority (64%) of recurrent dislocations (1). Age is therefore a critical risk factor for recurrent shoulder instability, with 72–100% of patients under 20 experiencing recurrent instability. For patients aged 20 to 30 years, the rate of recurrent instability is 70–82% (29). In college athletes, anterior and posterior subluxations represent the most common recurrent shoulder injuries (47.3% and 40.0%, respectively) (30).

Participation in contact sports or military service is associated with a high risk for shoulder instability. Collegiate athletes participating in ice hockey, lacrosse, football, and wrestling are more likely to sustain a shoulder injury than athletes engaging in other sports (31,32). A 5-year retrospective review of both male and female college athletes found an incidence rate of 31.3 per 100,000 for shoulder instability events, with wrestling and football having the highest incidence rates. A vast majority (86.5%) occurred from contact, and male athletes were two times as likely as female athletes to sustain an instability event (30). Quarterbacks have been found to experience shoulder instability events at a rate as high as 5.5 per 100,000 plays (20). The incidence of shoulder dislocations in the military was found to be 3.13 per 1,000 person-years in a retrospective 10-year review (33).

Scrutiny should be given to a history of shoulder instability events. Patients with recurrent instability may be at increased risk for glenohumeral bone loss, as each recurrent dislocation may contribute to cumulative bone defects (34). Although the number of instability events is not an accurate predictor for the magnitude of bone loss, any incident of instability has been correlated with the potential for bone loss as well as recurrent dislocation. Yoshida et al. found that recurrent anterior glenohumeral instability is associated with pathologic superior translation of the humeral head, leading to superior extension of capsulolabral injury, thereby increasing the likelihood of recurrent dislocation (17). Furthermore, Griffith et al. found some degree of bone loss in 41% of patients after an initial dislocation, and in 86% of patients with recurrent dislocation (35). A separate study found glenohumeral bone loss in 70% of patients after primary dislocation. In general, multiple instances of instability in a short timeframe, or previously failed capsulolabral repair suggest significant glenohumeral bone defects (19).

Physical examination

A thorough examination of the shoulder girdle should be performed in any case of instability, with or without suspected bone loss. A complete sensorimotor evaluation of the extremity is indicated to assess rotator cuff and periscapular muscle strength. Passive and active range of motion must also be evaluated and can provide insight into concomitant pathology. It is important to note that the specificity of individual physical exam maneuvers is poorly defined in the literature; thus, clinicians should combine several maneuvers for an accurate, pathology-based diagnosis (36,37).

The directionality of instability can be assessed through several maneuvers. The anterior apprehension and Jobe relocation tests have the highest positive predictive values (96%) for anterior shoulder instability, while the Jerk test, Kim test, and push-pull exams are most appropriate for posterior or MDI (21,37). Apprehension in lower degrees of abduction may indicate more significant bone loss (38). Any provocative maneuver should always be compared to the contralateral shoulder to assess baseline laxity. Generalized ligamentous laxity should also be assessed via the Beighton criteria, as underlying laxity may contribute to recurrent instability events (10,28).

Hill-Sachs defects are difficult to physically assess. Sensations of pain, crepitus, or catching when the arm is in a position of apprehension may be indicative of an engaging Hill-Sachs lesion, but the specificity of these findings is low (19). The Bony Apprehension Test was previously introduced as a method to assess for Hill-Sachs lesions but has since been shown to be inferior to the anterior apprehension test at identifying subcritical and critical bone loss (39,40). Glenoid bone loss may be assessed by the load and shift test, as decreased resistance may indicate a glenoid lesion in the direction of laxity (41).

While a combination of exam maneuvers maximizes sensitivity for glenohumeral instability, it does not always differentiate between soft tissue and bony pathology. Any abnormal or asymmetric finding during physical examination should be evaluated further by imaging (9).

Imaging

After a thorough history and physical examination, it is essential to obtain appropriate and complete imaging in the workup of patients with shoulder instability. Both capsulolabral and bony pathology, including the morphology and extent of bone loss, must be identified, as patients with bony defects are at risk of recurrent instability (42). The relationship between the glenoid and any Hill-Sachs or reverse Hill-Sachs lesion must also be identified. The “track” of the glenoid is the contact surface between the glenoid and the humeral head and consists of approximately 83–84% of the glenoid width (43,44). In the setting of anterior instability, if the Hill-Sachs lesion is “off-track”, it falls outside the GT and is at risk of engaging, levering on the rim of the glenoid, and dislocating the humeral head. If it is “on-track”, it will not engage with the glenoid during the arc of motion and is therefore less likely to contribute to dislocation. This can be assessed intra-operatively following repair of a Bankart lesion, as well as preoperatively with advanced imaging. Importantly, off-track lesions pose an increased risk of failure of Bankart repair, with subsequent instability if not addressed (4).

Radiographs

Imaging evaluation should begin with a dedicated shoulder radiograph series, including standard anteroposterior (AP), true AP or Grashey, scapular Y, and axillary lateral views. The AP views may demonstrate subluxation in the coronal plane, while the axillary lateral view may demonstrate subluxation in the axial plane and begin to characterize any anterior or posterior glenoid bone loss. Additional radiographs to consider include the Stryker notch view, in which the humerus is placed in internal rotation, for assessment of a Hill-Sachs lesion (13) as well as the West Point view, a modification of the axillary lateral that best assesses glenoid bone loss (45). Even with this view, glenoid bone loss is sometimes missed, and thus advanced imaging is recommended (46).

Advanced imaging

Computed tomography (CT) scans are useful for further evaluation of osseous anatomy, in situations of both acute injury and chronic bone loss. Characterization of anterior glenoid rim fractures, also known as “bony Bankart” lesions, is important as attrition of the fracture fragment may develop along with increased size of the glenoid defect if not addressed promptly (47) (Figure 1). In the setting of chronic bone loss, CT is indicated for assessment of the size and location of osseous deficiency. Multiple measurement techniques exist, including linear and area-based measurements. Controversy exists surrounding the superiority of such techniques, as well as the accuracy of two-dimensional (2D) versus three-dimensional (3D) modalities and CT versus magnetic resonance imaging (MRI) (48). In general, the literature suggests that area-based measurements are superior to linear-based measurements, which may overestimate bone loss (49,50). The “Pico” method described by Baudi et al. (51) is a popular area-based technique that has demonstrated high accuracy and reliability (48,50). In this method, a circle of best fit is placed according to the curvature of the posteroinferior glenoid and its area measured. The area of bone loss anteriorly is then measured and subtracted, giving a percentage area of deficiency (51).

Figure 1 3D-reconstructed CT scan with a red arrow pointing to a bony Bankart lesion. Adapted from Hughes et al. (13). 3D, three-dimensional; CT, computed tomography.

Similar best-fit circle techniques are also useful in examining bone loss in the setting of posterior instability. While glenoid bone loss is typically measured on a sagittal view, axial sequences should also be scrutinized for the presence of glenoid dysplasia or retroversion. Glenoid retroversion greater than 10° is considered abnormal in the setting of recurrent posterior instability and should prompt consideration of bony augmentation procedures (52).

When considering 2D versus 3D CT, the majority of studies indicate that 3D CT is preferred, as it provides the most reproducible measurements with the use of a standardized “en face” view (48-50). The superiority of CT over MRI is less well-defined. Although CT is generally considered to be the “gold standard” imaging modality in evaluation of glenoid bone loss due to bony resolution, high sensitivity and specificity, and easy availability (48), recent studies suggest that 3D MRI is equivalent to 3D CT in evaluating bone loss (53-55). Thus, when considering the optimal study, the risk of ionizing radiation inherent to CT must be weighed against the potential cost and limited availability of 3D MRI.

CT and MRI are also used to assess the interplay between the GT and any concomitant Hill-Sachs or reverse Hill-Sachs lesion. In the setting of anterior instability, a recent scoping review (56) found the most common assessment of the GT is that described by DiGiacomo and Burkhart via the Hill-Sachs Interval (HSI), which is the distance from the medial aspect of the Hill-Sachs lesion to the insertion of the rotator cuff on an axial image (5). Following calculation of the HSI, the GT is determined using the formula GT = (D × 0.83) − d, where D is the diameter of a best-fit circle on the glenoid and d is the diameter of bone loss (Figure 2). If the width of the HSI exceeds the size of the GT, then the lesion is considered “off-track” and will engage the glenoid rim. Conversely, if the HSI is smaller than the GT, the lesion is “on-track” and will not engage. The morphology of the Hill-Sachs lesion should also be considered, as lesions with more medial and inferior locations, greater width, and greater surface area loss have been associated with inferior clinical outcomes (57).

Figure 2 T2-weighted axial (A) and sagittal (B) images in the assessment of an off-track Hill-Sachs lesion using the HSI and the GT. The HSI is defined as the distance from the medial aspect of the Hill-Sachs lesion to the insertion of the rotator cuff (19 mm in this case). The GT is found using the formula GT = (D × 0.83) − d, where D is the diameter of the best fit circle on the glenoid (28.1 mm in this example) and d is the diameter of bone loss (5.4 mm). Thus, GT =17.9 mm, less than the HSI of 19 mm, making this an off-track lesion. Adapted from Hughes et al. (13). HSI, Hill-Sachs Index; GT, glenoid track.

Recent literature has also focused on the concept of “DTD” (7,58). The DTD is calculated according to the formula DTD = GT − HSI. While a DTD >0 mm indicates an on-track lesion, studies demonstrate that a DTD <8–10 mm may be predictive of failure following arthroscopic Bankart repair, particularly in patients younger than 20 (7,58). The GT and HSI must therefore be carefully evaluated preoperatively, as their relationship has significant implications for treatment.

It is important to quantify any reverse Hill-Sachs lesion present in the setting of posterior instability. Although less well-described than techniques for quantifying anteriorly engaging lesions, measurement of a reverse humeral defect may be performed via calculation of the “gamma angle” (59). On the axial cut in which the lesion appears widest, a best-fit circle is drawn around the humeral head. The gamma angle is measured between a line connecting the bicipital groove and the center of best-fit circle, and a line connecting the center of the circle and the medial border of the defect (Figure 3). Furthermore, if glenoid bone loss is present, 2.3° should be added to the gamma angle for each millimeter of posterior bone loss. A gamma angle >90° represents an engaging lesion that may necessitate treatment (52).

Figure 3 Axial CT image demonstrating a reverse Hill-Sachs lesion with the gamma angle depicted. This angle is less than 90°, indicating a nonengaging lesion. CT, computed tomography.

In conjunction with evaluation of bony anatomy, detailed evaluation of the soft tissue structures about the shoulder is necessary. MRI is therefore critical in assessing for associated injuries such as anteroinferior glenoid labrum defects (Bankart lesions), as well as HAGL lesions, anterior labral periosteal sleeve avulsions (ALPSAs), or glenoid articular cartilage defects (GLADs) (12) (Figure 4). This is true for assessing both suspected traumatic anterior instability as well as posterior instability, where the posterior inferior glenoid should be scrutinized for the presence of a reverse Bankart lesion (Figure 5). The integrity of the rotator cuff should also be evaluated, particularly in patients over the age of 40 years, as tearing of the rotator cuff frequently occurs concomitantly with shoulder instability events (60). The use of contrast should be considered, as magnetic resonance (MR) arthrography has been demonstrated more sensitive than nonenhanced MRI in assessing labral pathology, which remains important even in the setting of bone loss (61). Finally, in addition to conventionally obtained MRI images (including axial, coronal, and sagittal sequences), sequences that place the shoulder in abduction and external rotation should be performed as they increase the detection of labral lesions (62).

Figure 4 T2 axial image of an anteroinferior labral tear with medialization of the labrum and ALPSA lesion depicted by the blue arrow, as well as a small Hill-Sachs lesion about the posteroinferior humeral head depicted by the yellow arrow. ALPSA, anterior labroligamentous periosteal sleeve avulsion.

Figure 5 T1-weighted fat saturated axial (left) and T1 sagittal (right) MRI images demonstrating a reverse bony Bankart lesion with an associated posterior labral tear depicted by the yellow arrows. MRI, magnetic resonance imaging.

Treatment

When considering management options for glenohumeral instability, it is important to adequately assess both glenoid and humeral bone loss, as the presence of such defects is a known risk factor for recurrent instability (4,63). Nevertheless, many factors influence decision-making in addition to the presence of bone loss, such as patient age, activity level, and desire to return to sport.

Anterior instability

Nonoperative treatment

Nonoperative management plays a limited role in the care of a patient with anterior glenohumeral instability and associated bone loss. Although nonoperative treatment may be considered in the in-season athlete or first-time dislocator without bony injury (64), it is generally contraindicated in patients with osseous involvement due to the high risk of recurrent instability, as well as exacerbation of bone loss (65). Nonoperative treatment may, however, be considered in the non-athlete for whom the medical risks of surgery outweigh the benefits. Such treatment consists of physical therapy for range of motion and strengthening, as well as counseling regarding the increased risk of recurrent instability due to underlying bony deficiency.

Operative treatment

While operative intervention is generally indicated in patients with glenohumeral instability and associated bone loss, treatment is guided by the degree and pattern of bony deficiency. However, determining the amount of glenoid bone loss that is clinically significant is difficult due to a lack of consensus throughout the literature (4). “Critical” bone loss has been defined as glenoid bone loss >20–25%, as numerous studies have shown high rates of recurrent instability following isolated arthroscopic Bankart repair in such patients (63,66,67). Conversely, “subcritical” bone loss has been described as glenoid bone loss <20% (13). However, recent studies have shown that bone loss as low as 13.5% may be associated with inferior patient outcomes following arthroscopic soft tissue stabilization (4). Therefore, successful surgical decision-making can be challenging in these patients. The Instability Severity Index Score (ISIS) is a system designed to identify patients at risk for failure of isolated soft tissue stabilization, with a score greater than 6 corresponding with a 70% recurrence risk (68). Although the predictive value of the ISIS has been questioned (69), it remains a useful tool for identifying risk factors that correspond with failure of soft tissue procedures. Patient factors that increase the ISIS include age less than 20, the presence of visible glenoid bone loss or a Hill-Sachs lesion on X-ray, participation in competitive as well as contact or overhead sports, and the presence of hyperlaxity (68). All of these factors should be taken into account when considering surgical options.

Other useful predictors of recurrent instability include the Nonoperative Instability Severity Index Score (NISIS) (70) and the Glenoid Track Instability Management Score (GTIMS) (71). The GTIMS is particularly useful for surgical planning, as it has been demonstrated to delineate patients who would benefit from arthroscopic Bankart repair with more accuracy than the ISIS (71). A modification of the ISIS, the GTIMS replaces the radiographic parameters of the former and instead uses 3D CT as the sole radiographic criterion to assess whether an osseous lesion is on-track or off-track (71). With this scoring system, patients may be more conservatively recommended for soft tissue rather than bony stabilization.

In general, surgical treatment can be divided into soft-tissue procedures, including arthroscopic or open Bankart repair and remplissage (BRR), and bony procedures, including coracoid transfer (Latarjet, Bristow) and autograft or allograft reconstruction. In addition to assessing patient risk factors for recurrent instability, the primary step toward surgical decision-making for anterior instability is to identify which category of glenoid bone loss the patient falls into: <13.5% bone loss, 13.5–20% bone loss, 20–40% bone loss, or >40% bone loss. While patients with lesser degrees of bone loss may benefit from soft tissue procedures, increased severity of bone loss as well as the presence of bipolar lesions necessitates consideration of bony augmentation.

Arthroscopic Bankart repair, typically with capsular plication, is indicated in patients with minimal (<13.5%) bone loss and an on-track or absent Hill-Sachs lesion (72). In the setting of an acute bony Bankart fracture, arthroscopic repair may also be performed with a suture bridge technique, in which suture anchors are placed medially on the glenoid neck. The sutures are then passed around the fragment and loaded into a second row of anchors placed on the glenoid face (73). In both the acute and chronic settings, it is important to address any coexisting pathology, such as GLAD or ALPSA lesions, as failure to do so may increase the risk of recurrent instability (13). In appropriately selected patients, arthroscopic Bankart repair has demonstrated good clinical outcome scores and return to sport rates approaching 80% (74,75). Although open Bankart repair was historically considered superior to arthroscopic repair in patients with recurrent anterior instability (76), with the use of modern techniques the literature now supports arthroscopic Bankart repair as an equivalent or superior option (77,78). While open Bankart repair may be considered in patients requiring a large capsular shift, such as those with hyperlaxity or those undergoing revision surgery (76), arthroscopic repair still represents a viable treatment option in patients with minimal glenoid and humeral bone loss.

Patients with higher degrees of bone loss as well as engaging Hill-Sachs lesions may be indicated for bony augmentation procedures to increase the size of the GT. Hill-Sachs lesions at high risk of engagement, such as those that are medial or wide, can also be considered for such procedures (57). While the precise degree of bone loss that mandates the use of a bony procedure remains undefined, studies have demonstrated excellent clinical outcomes in patients undergoing bony augmentation for both critical and subcritical bone loss (42,79). The definition of subcritical bone loss varies in the literature, yet is generally accepted to be between 10–20% (75) or 13.5–20% (13). In the wake of studies demonstrating higher rates of failure with isolated Bankart repair (4,68), patients with subcritical bone loss have frequently been indicated for coracoid transfer procedures, particularly in the presence of concomitant Hill-Sachs lesions (80). Studies have demonstrated decreased rates of failure (81) as well as improved patient-reported outcomes (82) in patients with subcritical bone loss undergoing Latarjet versus arthroscopic Bankart repair. However, concerns exist regarding the complication rate as well as sequelae of the Latarjet procedure (83). While long-term studies demonstrate good functional outcomes following Latarjet (84,85), a recent systematic review reported a 38% rate of arthritic change as well as a 36% rate of residual shoulder pain at mean 16.6-year follow-up (84).

In recent years, attention has shifted from Latarjet towards the addition of remplissage to arthroscopic Bankart repair in patients with subcritical bone loss and Hill-Sachs lesions. In the remplissage procedure, the infraspinatus and posterior capsule are sutured into the Hill-Sachs defect, creating a mechanical block to bony engagement while also decreasing external rotation and translating the humeral head posteriorly (86). In patients with Hill-Sachs lesions and subcritical bone loss, arthroscopic BRR is associated with lower rates of recurrent instability when compared to Bankart repair alone (87). Furthermore, an early comparative study of BRR versus Latarjet for the treatment of off-track Hill-Sachs lesions with subcritical bone loss demonstrated a higher complication rate with Latarjet, yet improved outcomes following Latarjet in contact athletes, those undergoing revision surgery, and those with >10% glenoid bone loss (88). Subsequent systematic reviews and meta-analyses have reported overall similar outcomes between the two procedures, with a trend toward slightly increased complication rates with Latarjet and slightly increased failure rates with BRR in patients with increased glenoid bone loss (79,87,89). However, a recent study found similar patient-reported outcomes and failure rates at mean 2-year follow-up in patients undergoing BRR versus Latarjet for the treatment of anterior instability with >15% bone loss (90). Notably, the study cohort included patients with both on-track and off-track lesions. Thus, at this time the literature indicates similar outcomes in patients with subcritical bone loss following BRR and Latarjet, yet caution should be exercised when performing BRR in patients with combined off-track lesions and glenoid bone loss >10%.

In addition to remplissage, some authors have advocated for alternative humeral reconstructive techniques, including bone grafting (91) and disimpaction or balloon humeroplasty (92). While several technical descriptions exist in the literature, outcome studies are limited and demonstrate high rates of graft resorption and arthritic change, as well as complication and reoperation rates between 20% and 30% (93). Therefore, at this time, such procedures are not routinely recommended.

For patients with critical (>20–25%) bone loss, coracoid transfer procedures such as the Latarjet have traditionally been considered the standard of treatment due to excellent long-term outcomes with low rates of failure (80,94). However, alternative augmentation procedures have emerged to address limitations of the Latarjet, including the inability of the procedure to treat severe bone loss (>40%) and its lack of a true articular surface, as well as cases of failed Latarjet reconstruction (80). The most commonly performed bone-block procedures include distal tibia allograft (DTA), distal clavicle autograft, and allograft or autograft iliac crest bone graft (ICBG). The Eden-Hybinette (EH) procedure involves harvesting autograft from the inner table of the ilium, thereby allowing graft harvest of varying sizes to reconstruct the anterior glenoid (95). Although the EH has demonstrated good outcome scores and low recurrence rates similar to the Latarjet (96,97), donor site morbidity constitutes a significant drawback of the procedure. Benefits of the DTA and allograft ICBG procedures include the avoidance of donor-site morbidity while restoring articular cartilage as well as surface area to the anterior glenoid (13). While arthroscopic as well as open techniques have been described, similar outcomes have been reported between the two, comparable to those of the Latarjet (98-101). A recent systematic review comparing free bone block procedures versus Latarjet in the management of anterior shoulder instability with glenoid bone loss demonstrated no difference in rates of recurrence, complications, return to sport, or progression of arthritis (100). Similarly, a systematic review comparing free bone block autografts versus allografts in a comparable patient population demonstrated no significant difference in outcomes or complication rates (101). Comparison was limited, however, by the lack of high-quality studies with long-term follow-up. Future studies are needed to determine the long-term efficacy and sequalae of both open and arthroscopic free bone block procedures in the management of recurrent anterior shoulder instability with bone loss.

Posterior instability

Although treatment algorithms for posterior shoulder instability in the setting of bone loss are less well-defined than those for anterior instability, recurrent posterior instability represents a significant clinical concern. As with anterior bone loss, nonoperative treatment in patients with posterior bone loss demonstrates a high failure rate, particularly in high-risk populations such as the military or athletes performing repetitive posterior glenoid loading (102). While soft tissue repair alone yields good clinical outcomes in patients with minimal or no posterior bone loss (103), patients with erosive, traumatic, or dysplastic glenoid defects should be considered for bony augmentation procedures (104,105).

Although the threshold for critical bone loss in anterior instability has been highly scrutinized in the literature, the threshold for posterior instability remains unclear. Some authors have defined “critical” posterior bone loss requiring augmentation as 20% (106), while others recommend bone block augmentation according to a classification system that qualifies instability based on type (first-time, dynamic, static) and pathomechanism (107). A recent case-control study demonstrated a 10 times increased risk of failure of posterior capsulolabral repair with posterior bone loss of 11%, and a 24 times increased risk with bone loss of 15% (105). As a result, some authors recommend performing bone block augmentation, typically with DTA or ICBG allograft, in patients with recurrent posterior instability and glenoid bone loss greater than 10% (52,105). These recommendations are limited however by the lack of long-term as well as high-quality studies examining outcomes of posterior augmentation procedures for glenoid bone loss. While case series have shown improvements in patient-reported outcome scores (108), complication rates including graft lysis and progression of osteoarthritis are high (109,110). A recent systematic review found that the use of posterior bone block augmentation for recurrent posterior shoulder instability resulted in high rates of recurrent instability and revision surgery with inconsistent improvements in patient outcomes (110). Thus, further high-quality studies as well as possible modifications in indications and surgical technique are required to elucidate the appropriate treatment of posterior glenoid bone loss.

Other surgical considerations include the presence of glenoid retroversion and/or posterior dysplasia. Glenoid retroversion >10° and posteroinferior glenoid border deficiency have been identified as risk factors for failure of soft tissue repair in the treatment of recurrent posterior instability (111). While techniques of opening wedge osteotomy for the correction of retroversion have been described, both in isolation (112) and combined with bone block augmentation (113), these procedures are technically demanding and yield inconsistent clinical results (52,112,113). Larger studies with long-term follow-up are necessary to determine the utility of such techniques, which may still be considered experimental at this time.

Finally, it is also important to address any engaging reverse Hill-Sachs defect in the surgical treatment of posterior glenohumeral instability, as bipolar lesions are associated with failure of soft tissue repair (114). The previously described gamma angle (59) can be used to guide indications, although it has not been correlated with a specific treatment in the absence of a posterior glenoid defect. In patients with posterior glenoid bone loss and an engaging reverse Hill-Sachs lesion (defined as a gamma angle >90°), the preferred treatment is a reverse remplissage, in which the subscapularis tendon is sutured into the humeral defect (52,115). While numerous techniques have been published (115-118), outcome studies of the reverse remplissage or “modified McLaughlin” procedure in the setting of posterior bone loss and instability are lacking. Thus, as is common to the evidence-based management of posterior glenoid bone loss, further high-quality and comparative studies are indicated.

Authors’ preferred treatment algorithm

In all cases of recurrent shoulder instability, treatment should be individualized to the patient and his or her goals. While significant medical comorbidities may preclude operative management in certain patients, the high risk of recurrent instability inherent to glenohumeral bone loss mandates surgical treatment in most patients. The following sections will therefore describe operative treatment algorithms for glenohumeral bone loss in the settings of both anterior and posterior instability.

Anterior instability

All patients presenting with recurrent anterior shoulder instability are evaluated with a thorough history and physical examination to assess risk factors for recurrence as well as baseline and pathologic laxity. In cases of suspected bone loss based on history, examination, and radiographs, advanced imaging is obtained. Both CT and MRI are typically performed to evaluate the magnitude and location of osseous deficiency, anchors from prior capsulolabral repair, and the integrity of surrounding soft tissue structures.

Once imaging has been obtained, bone loss is analyzed on both the humeral and glenoid sides. Patients are divided into four categories based on the degree of glenoid bone loss: <13.5%, 13.5–20%, 20–40%, and >40% (Figure 6). In patients with 20–40% glenoid bone loss, the senior author prefers Latarjet due to the combined bony reconstruction of the coracoid and the sling effect of the conjoint tendon (13,79). Conversely, patients with >40% glenoid bone loss typically require a larger graft and are indicated for free bone block augmentation using either DTA or ICBG allograft.

Figure 6 Treatment algorithm for the management of glenohumeral bone loss in the setting of anterior shoulder instability. DTD, distance to dislocation; DTA, distal tibia allograft.

Patients with <20% glenoid bone loss are managed differently according to age, status as a contact athlete, history of prior surgery, and the presence of a Hill-Sachs lesion. In noncontact athletes with minimal (<13.5%) bone loss, the preferred treatment is arthroscopic capsulolabral repair. However, if the patient has significant risk factors for recurrence according to the ISIS (68), further augmentation procedures are considered. In the presence of an off-track Hill-Sachs lesion, a remplissage is performed. For contact athletes, consideration is also given to performing an open Bankart repair or a Latarjet, as studies have demonstrated decreased rates of recurrence with the use of these procedures in athletes compared to arthroscopic repair (119,120). The authors have also recently incorporated the concept of DTD into their treatment algorithm (7,58). For on-track lesions, as the DTD approaches 0 mm, the risk of recurrent dislocation increases exponentially, particularly in contact athletes (58). Thus, in contact athletes demonstrating “near-track” lesions with subcritical bone loss and a DTD <10 mm, consideration is given to combined BRR, or Latarjet (7,58).

Posterior instability

Patients with suspected posterior bone loss in the setting of instability are similarly evaluated with a thorough history, physical examination, and advanced imaging. In patients with minimal (<10%) glenoid bone loss, posterior capsulolabral repair has demonstrated excellent outcomes, and is routinely performed (105). Those patients with an engaging reverse Hill-Sachs lesion, defined via preoperative measurement or intraoperative examination, may be indicated for reverse remplissage, although long-term outcomes of arthroscopic techniques are lacking. Due to the high rates of complication and recurrent instability associated with posterior bone block augmentation and opening wedge osteotomy for glenoid bone loss and retroversion (110), respectively, these procedures are not routinely performed by the senior author.

Conclusions

Glenohumeral bone loss commonly occurs with recurrent shoulder instability and is a risk factor for failure of both nonoperative treatment and soft tissue stabilization. Patients with suspected glenoid or humeral bone loss in the setting of recurrent instability should be evaluated with a thorough history and physical examination, as well as advanced imaging including CT and/or MRI. In cases of both anterior and posterior instability, the magnitude and location of bone loss should be determined, as well as the relationship between the GT and any humeral defects. While critical and subcritical thresholds guide treatment for the management of anterior instability, such thresholds are less defined in the setting of posterior instability. In either case, patient factors including age and level of sport should also be considered when determining treatment. Future studies should focus on the complex interplay between glenoid and humeral bone loss to establish evidence-based treatment algorithms in patients with both anterior and posterior glenohumeral instability.

Acknowledgments

Funding: None.

Footnote

Provenance and Peer Review: This article was commissioned by the editorial office, Annals of Joint for the series “Bone Loss in Shoulder Instability and Shoulder Arthroplasty”. The article has undergone external peer review.

Peer Review File: Available at https://aoj.amegroups.org/article/view/10.21037/aoj-23-6/prf

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://aoj.amegroups.org/article/view/10.21037/aoj-23-6/coif). The series “Bone Loss in Shoulder Instability and Shoulder Arthroplasty” was commissioned by the editorial office without any funding or sponsorship. JDH served as the unpaid Guest Editor for the series. The authors have no other conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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