Bony Augmentation for Anterior and Posterior Glenohumeral Instability in the Contact Athlete

Author’s Accepted Manuscript Bony Augmentation For Anterior and Posterior Glenohumeral Instability in the Contact Athlete Kyle P. Lavery, Kevin J. McHale, William H. Rossy, George Sanchez, Matthew T Provencher www.elsevier.com/locate/enganabound

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To appear in: Operative Techniques in Sports Medicine Cite this article as: Kyle P. Lavery, Kevin J. McHale, William H. Rossy, George Sanchez and Matthew T Provencher, Bony Augmentation For Anterior and Posterior Glenohumeral Instability in the Contact Athlete, Operative Techniques in Sports Medicine, http://dx.doi.org/10.1053/j.otsm.2016.09.009 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Bony Augmentation For Anterior and Posterior Glenohumeral Instability in the Contact Athlete Kyle P. Lavery, MD* Kevin J. McHale, MD* William H. Rossy, MD* George Sanchez, BS^ Matthew T Provencher, MD^ *Department of Orthopaedic Surgery, Division of Sports Medicine Massachusetts General Hospital 175 Cambridge Street, Suite 400, Boston, MA 02114 [email protected] No Conflicts of Interests to Disclose ^ The Steadman Clinic 181 W. Meadow Drive, Suite 200 Vail, CO 81657 Abstract Glenoid and humeral bone loss is an increasingly recognized cause of recurrent instability and failure of soft tissue stabilization in both anterior and posterior glenohumeral instability. Given that participation in contact and collision sports is associated with a greater risk of recurrent glenohumeral instability, a thorough understanding of the pathoanatomy, clinical evaluation and treatment of this condition is paramount. This review provides an overview of the pathoanatomy and clinical evaluation of shoulder instability with bone loss as well as bony augmentation procedures for treatment of the condition.

Keywords glenohumeral instability, glenoid bone loss, Hill-Sachs lesion, reverse Hill-Sachs lesion, Bristow-Latarjet, Eden-Hybinette

Introduction Glenohumeral instability is an extremely common shoulder injury in a young athletic population. Athletes are often able to return to competition following an instability event after a brief period of rest and rehabilitation. However, their effectiveness is often unpredictable, with recurrent dislocations and subluxations often compromising performance and resulting in significant lost time from sport. Dickens, et

al. followed 45 collegiate athletes after an in-season anterior instability event. [1] While 73% were able to return to play after a mean 5 days lost from competition, 64% of the athletes who returned to sport experienced at least one recurrent instability event during the season. Buss, et. al demonstrated a similarly high rate of recurrence of anterior instability in athletes who were able to return to play. [2] Although 26 of 30 of the athletes studied were able to complete their season, 37% experienced an in-season recurrence, and over 50% underwent stabilization in the offseason. Shoulder instability has consistently been shown to be complicated by a high rate of recurrence by numerous authors. [3] [4] [5] [2] [6] [7] [8] In a systematic review and meta-analysis, Longo, et al. analyzed 2,811 patients (mean age 28.1 years ) who sustained an initial anterior dislocation. [8] Of those that underwent initial non-operative management, 37.5% had a recurrence. A similar systematic review, including 10 studies and 1324 individuals, demonstrated a 39% risk of recurrence. [9] In a prospective study by Cameron et al., 714 physically active students were followed during their tenure at the United States Military Academy. [5] Subjects with a self-reported history of instability were 4.3 times more likely to experience an acute anterior or posterior instability event than those with no prior instability. Hovelius et al. followed 255 patients (aged 40 years and younger) initially treated non-operatively for an anterior shoulder dislocation longitudinally over a 25-year period [6]. Fifty-seven percent sustained a recurrent dislocation with 27% eventually undergoing surgical stabilization. While younger age and male gender have long been known to be risk factors for recurrent instability, participation in contact and collision sports is an increasingly recognized risk. [10] [11] [3] [12] Athletes who participate in contact sports such as American football, rugby, hockey, and wrestling have been shown to be more prone to developing recurrent dislocation or subluxation events. [13] [14] Owens et al. studied the epidemiology of glenohumeral instability in collegiate athletes over a 15-year period using the National Collegiate Athletic Association injury database. Sixty-eight percent of occurrences involved contact with another athlete, with football by far the most common sport involved. [13] Contact athletes are also more prone to failing soft tissue stabilization. [11] [15, 16] [17] Yamamoto et al. recently demonstrated a recurrence rate 2 and 3 times higher in contact athletes than non-contact athletes undergoing open and arthroscopic Bankart repair, respectively. [18]

While recurrent instability can result in significant lost time for athletes, it also leads to repeated trauma to the static stabilizers of the glenohumeral joint. Each instability event has the potential to cause greater soft tissue injury and greater glenoid and humeral-sided osseous deficiency. The limits of soft tissue stabilization in treating bone loss are increasingly recognized, as glenohumeral osseous defects have been associated with inferior functional outcomes and recurrence following soft tissue repair. [19] [20] [21] [22] [23] [24] This review highlights the pathoanatomy of instability-related bone loss, the clinical evaluation of athletes with osseous deficiencies, and the treatment of anterior and posterior instability in contact athletes using bony augmentation procedures.

Pathoanatomy Anterior Instability Traumatic anterior instability occurs when a force is applied to the arm in a position of abduction and external rotation. The initial event and subsequent recurrences can result in a spectrum of soft tissue and bony injuries to the glenohumeral joint. Soft tissue injuries to the anterior capsulolabral structures are well described and include anteroinferior capsulolabral avulsions (Bankart lesions),[25] anterior labral periosteal sleeve avulsion variants (ALPSA lesions), humeral avulsions of the glenohumeral ligament (HAGL lesion), and capsular injuries. Injury to any of these structures can reduce the effectiveness of the static stabilizing mechanism of the joint and predisposes a patient to recurrent instability. Osseous injuries to the glenoid and humeral head also can occur and will be the focus of this discussion. Glenoid bone loss is an increasingly recognized pathology associated with anterior instability. [26] Once overlooked, osseous injuries to the glenoid have been reported in a high percentage of initial traumatic dislocations and nearly all patients with recurrent dislocations. [26] Evidence also suggests an increased rate of glenoid bone loss in contact athletes, presumably due to higher energy mechanisms of injury. [19] Glenoid bone loss can occur as a result of acute glenoid rim fractures (“bony Bankart” lesions) or attritional erosive bone loss from recurrent dislocations, resulting in the classic “inverted pear” glenoid appearance. [19] Additionally, fracture fragments may resorb over time. In their study utilizing 3-D CT to evaluate morphology

of 100 consecutive patients with recurrent instability, Sugaya et al. reported that 50% had acute bony Bankart lesions while an additional 40% demonstrated erosive changes. [26] Osseous deficiency decreases the available articular glenoid arc and depth, resulting in a loss of a portion of the static stabilization in an inherently unstable joint, and predisposes the patient to recurrence. Additional instability events potentially result in further bone loss, compounding the problem. Researchers have attempted to identify a level of “critical” bone loss that jeopardizes the outcomes of soft-tissue stabilization techniques. In a cadaveric biomechanical study, Itoi demonstrated that a loss of 21% of the anteroinferior glenoid radius significantly compromised stability with soft tissue repair alone. [27] In a similar study, Yamamoto found the force required for glenohumeral translation to be inversely proportional to the size of the glenoid osseous defect and considered a defect of 19% of the glenoid width at risk for failure after soft tissue repair. [28] Currently, a loss of 20-30% inferior glenoid surface area or 6-9mm width at the level of the bare area is considered significant. [29] Failure to recognize and address this glenoid deficiency at the time of surgery results in increased failure rates with soft-tissue stabilization. [19] [20] [21] In addition, a lower percentage of bone loss, termed “sub-critical”, may result in poorer clinical outcomes in the setting of soft-tissue stabilization, even without true recurrence. [24] Humeral bony injury results in a characteristic posterosuperolateral impaction fracture of the humeral head against the denser anterior glenoid rim during an anterior dislocation. This depression was termed the Hill-Sachs lesion for the radiologists that described it in 1940. [30] While the exact incidence is unknown, Hill-Sachs lesions have been reported in 40-90% of shoulders after initial anterior dislocations. [30] They may occur in nearly 100% of patients with recurrent instability. [4] As the arm is brought into abduction and external rotation, the depression may “engage” the anterior glenoid rim, levering the humeral head to dislocate. [19] The presence of concurrent glenoid and humeral-sided bone loss, termed the “bipolar lesion”, may be present in the majority of recurrent anterior shoulder instability cases. Nakagawa et al. demonstrated 56.3% of patients who underwent labral repair had evidence of a bipolar lesion on CT scan, including 33.3% of those with primary instability and 61.8% with recurrent instability. [31] The prevalence of bipolar lesions correlated with the number of instability events. Arciero, et al. examined the effect of bipolar lesions on stability in a biomechanical study. [22] Sequential glenoid defects were created and translational stability was

tested using representative small- and medium-sized Hill-Sachs defects, demonstrating the additive effect of combined glenoid and humeral bone loss in recurrent instability and its potential to jeopardize soft tissue repair. These findings were reaffirmed in similar subsequent cadaveric and computer-simulated models. [32] [33] The “glenoid track” concept was developed by Yamamoto, et al. in 2007 in an attempt to better understand the interplay between humeral and glenoid-sided bone loss and its contribution to recurrent instability. [23] As the arm is raised into abduction and external rotation, glenoid contact area shifts from inferomedial to superolateral on the humeral head, creating a zone of contact termed the “glenoid track”. The true contact zone was shown to include 84% of the glenoid diameter due to lateral overlap with the rotator cuff attachment. With an intact glenoid track, stability is maintained. A Hill-Sachs lesion is at higher risk of engagement if it extends medially over the boundary of the glenoid track. [34] [35] Glenoid bone loss decreases the width of the glenoid track, increasing the potential for engagement and dislocation. [34]

Posterior Instability Posterior glenohumeral instability occurs with the arm in a position of flexion, adduction, and internal rotation. Compared with anterior dislocations, acute traumatic posterior dislocations are relatively rare, particularly in an athletic population. The majority of posterior instability cases seen in athletes are acquired due to repetitive microtrauma to the posterior capsulolabral structures from activities such as weightlifting and blocking in football. Patients often experience pain and subluxations in provocative positions that result in posterior loading of the glenohumeral joint. Although less common due to the lower incidence of traumatic posterior instability, posterior glenoid bone loss can occur. [36] Posterior glenoid rim fractures (reverse bony Bankart lesions) are reported in 31% of initial posterior dislocations. [37] The posterior glenoid is also subject to attritional erosive bone loss with recurrent instability. As with the anterior glenoid, posterior bone loss increases the risk of recurrence by decreasing the articular arc. Humeral bone loss involves an anterosuperomedial impaction fracture of the humeral head caused by contact with the posterior glenoid rim. Described by McLaughlin, [38] this reverse Hill-Sachs lesion is seen in up to 86% of patients after posterior dislocation. [37] Classified by Robinson as small (<25%), medium

(25-50%), or large (>50%),[39] reverse Hill-Sachs lesions generally involve much greater articular cartilage injury then traditional lesions. Large lesions are a risk factor for engagement of the posterior glenoid rim in internal rotation and subsequent recurrence.

Clinical Evaluation History & Presentation A thorough history is critical when evaluating a patient with suspected glenohumeral instability to ensure proper diagnosis, classification, and treatment. The circumstances surrounding both the initial event and recurrences should be elicited. Key factors include the mechanism of injury (traumatic vs. atraumatic), degree (dislocation requiring reduction vs. subluxation), number of events, and frequency of symptoms. Arm position at the time of the event and provocative positions can be helpful in determining directionality. In the setting of bony deficiency, the patient may report experiencing symptoms in more mid-range motions and with progressively lower energy activities of daily living. In athletes, complete understanding of the patient’s sport, position, time in season, and future career goals are critical in formulating a treatment plan and timeline.

Physical Examination A comprehensive physical examination of both shoulders should be performed in all patients with suspected shoulder instability. The shoulder girdle is thoroughly inspected for symmetry, atrophy, deformity, and previous incisions. Bony prominences are palpated to assess for possible associated fracture. Active and passive range of motion is recorded in all planes and scapulothoracic motion is observed for dyskinesis or winging. Rotator cuff strength testing is performed to individually assess for supraspinatus, infraspinatus, teres minor, and subscapularis function. A thorough neurovascular exam should be conducted, especially after an acute dislocation, with particular attention to axillary nerve sensorimotor function. Numerous specialized provocative maneuvers have been developed to detect the specific pathology associated with anterior, posterior, and multidirectional instability (MDI). Anterior instability maneuvers include the anterior load-and-shift, and anterior apprehension, relocation, and release tests. Patients with bone loss often experience apprehension in positions of mid-abduction. Posterior maneuvers include the posterior load-and-shift, posterior apprehension, and jerk tests. Finally, the patient is

assessed for clinical signs of MDI, including a sulcus sign, generalized ligamentous laxity, hypermobility, and possible connective tissue disorder.

Imaging A thorough radiologic evaluation is critical in evaluating patients with instability. A detailed account of the imaging workup in the contact athlete is available in an article earlier in this issue. Imaging begins with a plain radiographic series, including anteroposterior (AP), axillary, and scapular Y views. Orthogonal views are assessed for concentric reduction and associated fracture, bone loss, or impaction deformity. The West Point view is a medially directed oblique projection obtained with the patient prone at 90 degrees of abduction to evaluate the anteroinferior glenoid. Hill Sachs deformities are best evaluated using the Stryker notch view, obtained in a supine patient with the arm abducted and externally rotated. However, these supplemental radiographs have largely been replaced by advanced imaging. Magnetic resonance imaging (MRI) is the current standard for assessment of soft tissue pathology associated with instability. Magnetic resonance arthrography (MRA) with intra-articular gadolinium has been shown to increase its sensitivity and specificity to greater than 90% in detection of lesions of the capsulolabral complex. [40] Distention with contrast may reveal a patulous capsule and increased intra-articular volume in cases of MDI. Well-described normal variants of the anterior capsulolabral complex can often be mistaken for pathologic lesions when reviewing MRAs. With increasing attention to the contribution of osseous lesions to recurrent instability, computed tomography (CT) scan has become an important assessment tool in both glenoid and humeral-sided lesions. Threedimensional (3-D) CT reconstructions with the humeral head digitally subtracted are now considered the most accurate for evaluation of glenoid deficiencies. [26, 41] Multiple methods for measuring glenoid bone loss with 3-D CT have been described, including computer software-assisted techniques. [42] They generally quantify the percentage of bone loss using an estimated normal inferior glenoid surface area and are detailed in an article in this issue. [43] [44] [45]

Bony Augmentation for Anterior Glenoid Defects Coracoid Transfer Coracoid process transfer to the anteroinferior glenoid has long been utilized to treat recurrent anterior glenohumeral instability. Numerous early variations of this technique were described. While Michel Latarjet is often credited with its original description in 1954, [46] his contemporary Trillat published a nearly identical technique in the same year. [47] In 1958, Helfet reported a technique utilizing a smaller coracoid fragment with a different orientation perpendicular to the articular surface that he attributed to his mentor Bristow. [48] Today, coracoid transfer, particularly the Latarjet procedure, has become the treatment of choice for deficiencies greater than 20-30% of the glenoid surface area. Some surgeons advocate its use as a first line treatment for anterior instability even with limited osseous deficiency, particularly in contact athletes at high risk of failing soft tissue repair. Although it continues to be modified and refined, the modern technique for coracoid transfer is remarkably similar to its original description by Latarjet. [46] Utilizing a deltopectoral exposure, the pectoralis minor and coracoacromial ligaments are released from the coracoid, leaving the conjoined tendon origin intact. A coracoid osteotomy is performed, preserving the coracoclavicular ligaments. The graft is then typically transferred through a longitudinal subscapularis split and secured flush to the glenoid margin with screws. It can be positioned with the posterior surface facing the glenoid or rotated 90 degrees so the posterior surface is parallel to the articular surface to maximize its surface area (“congruent arc” technique). [49] Over the last decade, arthroscopic approaches have been developed and subsequently gained popularity. [50, 51] However, concerns exist regarding increased technical complexity and operative time, the need for specific instrumentation, and significantly higher costs. [52, 53] Coracoid transfer reliably restores glenohumeral biomechanical stability in the setting of glenoidbased soft tissue and bony pathology both in-vitro and in-vivo. [54] [55] Three distinct stabilizing mechanisms have been identified to contribute to its efficacy. Static stabilization is provided through an increased articular arc and greater surface area for contact from the graft itself. Repair of the coracoacromial ligament stump to anterior capsule may also provide additional static stability. However, recent biomechanical data has questioned the use of this capsular repair, citing the potential for limiting range of

motion due to over-constraint without providing any significant additional translational stability. [56] [57] Finally, a dynamic “sling effect” that resists dislocation is produced by the conjoined tendon reinforcing the tensioning of the lower subscapularis muscle fibers in abduction and external rotation. This has been shown to be the most important biomechanically in both mid-range and end-range positions, contributing over 75% of the stability in the extremes of the apprehension position. [54] Recent biomechanical evidence suggests that the Latarjet procedure results in more stability than the Bristow variation. [58] Many authors have reported excellent outcomes and reliably low recurrence rates with coracoid transfer, including a predictably shorter rehabilitation and faster return to sport. [59] Mizuno et al. reported a 5.9% recurrence rate with 90.9% subjective shoulder value at 20-year follow-up. [60] Similarly, Hovelius et al. reported 98% patient satisfaction with a 3.4% recurrence at 15 year follow-up. [61] An, et al. [62] conducted a systematic review and meta-analysis of studies comparing coracoid transfer with open or arthroscopic soft-tissue stabilization. Compiled data from 8 studies (795 shoulders) demonstrated significantly lower recurrence rates with coracoid transfer (11.6% vs. 21.1%). Many reservations concerning coracoid transfer exist due to high reported complication rates. Early perioperative complication rates are generally quoted to be in the 15-30% range. These include infection, hematoma, intraoperative graft fracture, graft malposition or malunion, hardware complications including screw breakage, nonunion, and neurovascular injury. [63] Iatrogenic neurologic injuries are perhaps the most alarming, with high rates of intraoperative nerve changes on EMG and postoperative clinically detectable deficits in the axillary and musculocutaneous nerves reported. [64] [63]. Late graft resorption is increasingly recognized, although the clinical significance of this is unclear. [65] Long-term longitudinal studies have demonstrated high rates of postoperative glenohumeral arthropathy, [66] with one report showing a 34% rate of moderate to severe degenerative changes at 30 years follow-up. [67] Failure to position the coracoid graft flush to the glenoid margin with lateral overhang results in abnormal contact pressures in cadaveric models and may contribute to arthropathy in the long term. [68] Other authors have shown arthropathy rates to be similar to the natural history of recurrent instability and soft tissue repair, suggesting degenerative changes to be the result of the initial injury rather than the method of surgical intervention. [69] [67] Early reports have not consistently demonstrated increased complication rates with arthroscopic techniques. [70]

Autograft Reconstruction Free autograft reconstruction for anterior glenoid augmentation predates coracoid transfer by several decades. In 1917, Eden described transferring a tibial corticocancellous block to the scapular neck to extend the anterior glenoid. [71] Use of a tricortical iliac crest bone block was later proposed by Hybinette. [71] Today, iliac crest autograft transfer is commonly referred to as the Eden-Hybinette procedure. The precise indications for autograft transfer are controversial; however, this option has been recommended in the setting of extremely large glenoid defects and failed coracoid transfer. In the modern Eden-Hybinette technique, a tricortical iliac crest graft is harvested and secured congruous with the anterior glenoid with screws in similar fashion to a coracoid transfer. The cortical inner table of the ilium effectively extends the articular glenoid arc and restores static stability. [72] Willemot et al. demonstrated that a graft positioned 50-75% below the glenoid equator is ideal in a biomechanical model. [73] Recently, arthroscopic-assisted techniques have also been described. [74, 75] [76] Multiple authors have reported results after iliac crest bone grafting procedures, although outcome reports are not nearly as extensive as with coracoid transfer. [77, 78] [79] [80, 81] [82] [83] Longo et al. conducted a systematic review that revealed similar clinical outcomes when comparing coracoid with iliac crest autograft transfer. [84] Both demonstrated lower recurrence rates than soft tissue repairs, with a slightly higher rate of recurrence with iliac bone graft (9.8%) compared to coracoid transfer (7.5%). Iliac crest graft also demonstrated a nominally higher overall complication rate (17.6 vs 15%). However, generally low-level evidence and a lack of randomized direct comparison studies make these assessments less then definitive.

Allograft reconstruction The use of several fresh or fresh frozen osteochondral allografts have been attempted as an alternative to iliac crest autograft for large glenoid defects or revision settings, including glenoid [85], femoral head [86], and distal tibial plafond [87] [88]. Authors cite decreased donor site morbidity and the introduction of a more natural chondral surface as advantages over iliac crest autograft. Potential

disadvantages associated with allograft use include limited availability, the potential for disease transmission, increased infection rates, possible less predictable graft healing, and increased cost. Glenoid reconstruction with the distal tibia has been of particular interest recently, as the lateral distal tibial articular surface provides a similar contour to the intact glenoid. [87] [88] It also may provide denser subchondral bone than other options. [87] Sayegh et al. conducted a recent review of 8 available studies (70 shoulders) reporting on the results of the use of osteochondral allograft for glenoid reconstruction. [89] Combined data revealed 93.4% satisfaction, 100% union, and 2.9% recurrent dislocation at mean 44.5 months follow up. However, larger series and comparative studies are needed before conclusive statements can be made regarding osteochondral allograft reconstruction.

Bony Augmentation of Hill Sachs Lesions Procedures targeting the Hill-Sachs lesion historically have attempted to fill the defect to restore native anatomy and prevent engagement. Iliac crest autograft, matched humeral osteochondral allograft, and talar allograft (unpublished) have been used through anterior deltopectoral and posterior open approaches. [90] [91] [92] However, these invasive procedures are not ideal for high-level athletes attempting to return to sport, and outcomes studies are limited to small case series. Disimpaction and bone grafting through a cortical window has also been attempted, but is not routinely performed. [93] [94] Currently, the remplissage procedure is most popular for addressing clinically significant Hill-Sachs lesions. [95] Meaning “to fill”, remplissage involves an arthroscopic infraspinatus capsulotenodesis, converting the defect into an extraarticular lesion and preventing engagement. However, concerns exist regarding decreased range of motion, particularly in an athletic population. [96] [95] Bony procedures addressing the Hill-Sachs lesion may be utilized on a selective basis, although there is no clear consensus for the “critical” point at which humeral-sided defects need to be addressed surgically. Traditionally, lesions <20% of the humeral head articular arc were considered clinically insignificant while lesions greater than 40% were considered nearly always significant. [30] The relevance of lesions consisting of 20-40% of the articular surface was unclear. The glenoid track concept sought to better define their significance with regard to their location and interplay with glenoid deficits. Authors have suggested a ratio

between the Hill-Sachs width and glenoid diameter, termed the Hill-Sachs interval, to determine if the lesion should be addressed at the time of surgery. [97] Glenoid-based treatments remain first line for treating humeral sided defects by normalizing the glenoid track and preventing engagement. However, this strategy may not be applicable in all cases. A biomechanical study suggested coracoid transfer alone might be inadequate in restoring stability with humeral defects great than 31%. [98] Clinical decision-making will likely evolve as the glenoid track concept continues to be refined with further research.

Bony Augmentation for Posterior Glenoid Defects Fried described augmentation of a posterior glenoid deficiency with a bone block in 1949. [71] Analogous to an anterior graft, posterior grafting generally involves a large open posterior exposure, but arthroscopic-assisted techniques have been described recently. [99] [100] [101] Traditionally, iliac crest autograft has been utilized, [102] but the use of distal tibial osteochondral allograft has been reported recently as well. [103] [100] As the need for posterior glenoid bone grafting is rare and evidence regarding the procedure is limited, its specific indications are not precisely defined. Cerciello, et al. conducted a systematic review of the available literature on bone grafting procedures for posterior instability. [104] Only seven studies involving grafting to treat posterior glenoid bone loss were identified. [105] [106, 107] [101] [102, 103] All consisted of small retrospective case series. While low levels of recurrence were reported, graft lysis and progressive osteoarthritis were common in long-term follow-up.

Bony Augmentation of Reverse Hill Sachs Lesions Large reverse Hill-Sachs lesions were historically treated with transposition of the subscapularis tendon or lesser tuberosity into the defect, as originally described by McLaughlin.[38] Disimpaction and grafting has also been described for acute lesions. [108] Generally, osteochondral allograft options are often preferred due to the large chondral involvement of the humeral head commonly seen. The use of humeral [109], femoral head [110], and talar (unpublished) allografts have been described. Involvement of greater than 20% of humeral articular surface is generally cited as requiring surgical intervention due to the risk of recurrence and large articular involvement. However, this figure is based on clinical experience and expert

opinion. In the review by Cerciello, et al., [104] only 5 studies reported outcomes of the use of allograft to treat reverse Hill-Sachs defects. [110] [111] [112] [109] [113]

Conclusion Glenohumeral instability is a common pathology affecting young athletes. Individuals involved in contact sports generally expose the joint and its stabilizing structures to greater amounts of trauma, resulting in more extensive injury and disrupted anatomy. Anterior glenoid bone loss and Hill-Sachs lesions are an increasingly recognized cause for recurrent anterior instability and failure of soft tissue stabilization techniques. Although less common in an athletic population, significant bone loss also occurs as a result of episodes of posterior instability. This review highlights bony augmentation procedures utilized for the treatment of recurrent anterior and posterior glenohumeral instability.

Figures Figure 1: Viewing from a superior portal, an arthroscopic probe is used to estimate anterior glenoid bone loss

Figure 2: A best fit circle is drawn on 3-dimensional CT scan with the humeral head subtracted to estimate the percentage of glenoid bone loss.

Figure 3: Axial MRI demonstrating a reverse Hill-Sachs lesion after a posterior dislocation.

Figure 4: Axial CT demonstrating severe attritional posterior glenoid bone loss with retroversion.

Figure 5: A distal tibial osteochondral allograft is prepared for reconstruction of an anterior glenoid defect.

Figure 6: An oscillating saw is used to fashion a matched osteochondral graft from a fresh talar allograft

Figure 7: Postoperative X-ray in true anterior-posterior view after reconstruction of a large reverse HillSachs lesion with talar allograft.

Figure 8: Three-dimensional computed tomography scan demonstrating a large reverse Hill-Sachs lesion.

Figure 9: Intraoperative photograph of the coracoid process graft prior to fixation during a Latarjet procedure.

Figure 10: Postoperative X-ray in axillary view following Latarjet reconstruction. Please note the use of two screws for fixation of the coracoid process graft to the glenoid bone.

Figure 11: Postoperative X-ray in axillary view at 27 months after Latarjet reconstruction demonstrating two bent screws originally used for fixation of the coracoid process graft. This requires screw removal and revision surgery.

Tables Table 1. Physical exam and imaging findings of patients with bone loss. Anterior Instability Posterior Instability Physical Exam Findings High grade anterior load & shift High grade posterior load & shift Anterior apprehension (often in midPosterior Apprehension abduction) Jerk Test Imaging Findings Anterior glenoid rim fractures (Bony Posterior glenoid rim fractures (reverse Bankart lesions) Bony Bankart lesions) Attritional anterior glenoid bone loss Attritional posterior glenoid bone loss Hill-Sachs lesions Reverse Hill-Sachs lesions References

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