Bone loss in shoulder instability: Current concepts and technological advances

Arthroscopic instability repair has overtaken open instability repair for most patients with shoulder instability in the last decade. Technological advances as well as improved understanding of the anatomy and pathology have led to this change in approach. However, increasing awareness of bone loss of the glenoid and humeral head have led to a better understanding of when advanced arthroscopic techniques or bone augmentation procedures are necessary to avoid surgical failure.

We have assembled some of the world’s foremost thought leaders and surgeons in this Orthopedics Today Round Table discussion to share their experiences and insights into bone loss and its role in the unstable shoulder. Our hope is that this will assist our readers in the management and care of patients with shoulder instability and bone loss.

William N. Levine, MD
Moderator

Round Table Participants Moderator William N. Levine, MD Columbia University Medical Center New York, N.Y. Christopher S. Ahmad, MD Columbia University Medical Center New York, N.Y. Augustus D. Mazzocca, MS, MD New England Musculoskeletal Institute University of Connecticut Health Center Farmington, Conn. Edwin R. Cadet, MD Columbia University College of Physicians and Surgeons New York-Presbyterian/Columbia University Medical Center New York, N.Y. Matthew T. Provencher, MD, CDR, MC, USN Naval Medical Center San Diego San Diego, Calif. T. Bradley Edwards, MD Fondren Orthopedic Group Houston, Texas

William N. Levine, MD: How do you evaluate the patient with recurrent anterior instability following prior arthroscopic labral repair?

Christopher S. Ahmad, MD: In general, failed surgery is challenging, and it is helpful as a clinician to develop an organized evaluation approach. I prefer to organize the causes of failure as problems that occur prior to, during or after surgery. Prior to surgery, we are concerned with problems related to misdiagnosis, such as a patient with multidirectional instability (MDI) or posterior instability that undergoes an isolated anterior stabilization procedure, voluntary instability, collagen disorders and osseous deficiencies — with osseous deficiency being on the top of list. Also important prior to surgery is appreciating the patient’s expectations and risk factors such as participation in collision sports.

Problems that occur during surgery focus on technical issues and include failure to address all aspects of capsular and labral injury, poor anchor placement (such as being too medial on glenoid) and use of too few anchors. Problems after surgery are related to non-compliance with rehabilitation and repeat trauma.

History taking, therefore, attempts to determine the patient’s age, activity level, number of dislocations prior to surgery and ability to self-reduce, and number of dislocations after surgery and ability to self reduce. Lack of an interval of symptomatic improvement following surgery suggests the possibility of an incorrect diagnosis or missed pathology. Operative reports often indicate the observed pathology at the time of surgery, the technique of capsulolabral repair, the number of anchors used and if thermal capsular shrinkage was used.

Physical exam should attempt to elicit generalized laxity, translation testing and apprehension. Apprehension at minimal degrees of abduction and external rotation suggests bony deficiency. It is important to obtain plain X-rays with an axillary view and note if anchors are placed inferior (close to 6 o’clock) and lateral on the glenoid.

For failed instability, we routinely obtain an MRI scan with intra-articular gadolinium for soft tissue evaluation. Because of the high incidence of bone loss associated with failed surgery, we always obtain a CT scan with 3-D reconstructions that isolate the humeral head and the glenoid.

Edwin R. Cadet, MD: My approach first begins with a thorough history. I try to exclude preceding trauma as one possible cause for recurrent instability following shoulder stabilization surgery. It is also important to discern whether symptoms of instability are that of frank dislocation or subluxation. Is the patient able to voluntarily dislocate the shoulder, and if not, what activities and what arm positions does that shoulder dislocate or feel unstable? At times you can elicit the direction of instability based on the patient’s subjective description, but often with the patient’s recollection of specific arm positions and activities that induce subjective or objective signs of instability. The previous operative report is critical to determine what was done initially. Was the initial surgery performed arthroscopically or open? That is an important concept as with open approaches as subscapularis deficiency may come into play.

Physical examination must always be conducted with the upper torso disrobed. For me, anterior/posterior load and shift in the supine position is extremely helpful. Downward traction of the arm (sulcus) sign in neutral and external rotation in the upright position will help determine if multidirectional instability exists and test the competency of the rotator interval. The Gagey hyperabduction test has also been a useful tool for me. Abnormal glenohumeral abduction against resisted scapular motion is defined as greater than 105°. This signifies inferior capsular laxity.

In addition to a full series of radiographs including anteroposterior (AP) views in neutral, external and internal rotation and an axillary view (West Point or “standard” axillary is adequate), I order MRI with intra-articular contrast, particularly in the postoperative setting. Three-dimensional CT is an important adjunct as it provides excellent detail regarding the osseous anatomy to identify regions of critical bone loss. CT scans often show the location and number of anchor tracks form prior surgery better than plain radiographs.

T. Bradley Edwards, MD: I first take a thorough history starting with the patient’s chief complaint – instability, pain or both. If instability is a complaint, I ask about frank dislocation requiring a reduction maneuver or subluxation. Just because a patient has had a prior labral repair does not mean recurrent instability is why the prior surgery failed. Patients who complain primarily of pain make me consider other etiologies of failure, not just recurrent instability. The number and type of prior surgeries are reviewed along with operative reports and intraoperative photographs if available. Additionally, other factors such as co-morbidities (Ehlers-Danlos syndrome) or confounding factors (workman’s compensation) are elucidated from the history.

For patients with prior instability surgery, the examination specifically focuses on presence of prior incisions, shoulder mobility, rotator cuff testing, instability testing and neurovascular status. Prior skin incisions are noted and checked for any signs of infection. Both active and passive shoulder mobility are evaluated checking mainly for any signs of capsular stiffness, which can indicate an over-tightened shoulder and the presence of glenohumeral crepitus, which can indicate the presence of instability arthropathy. The rotator cuff is then systematically examined for presence of disease, which is more likely to be present in older patients.

My rotator cuff exam consists of Jobe’s test for the supraspinatus, the external rotation lag sign, external rotation strength for the infraspinatus, the horn blower’s sign for the teres minor, and the lift-off and belly-press tests for the subscapularis. Instability examination begins with looking for signs of hyperlaxity using the sulcus sign and the presence of greater than 90° of passive external rotation with the arm at the side. Standard anterior apprehension and relocation tests are used along with their posterior corollaries. I also use O’Brien’s active-compression test for superior labral pathology, although I find this test rather non-specific. Lastly, I perform a thorough neurovascular examination.

My standard instability radiographic series includes an AP view of the glenohumeral joint with the arm internally rotated to look for a humeral head impaction fracture (Hill-Sachs lesion), and a Bernageau glenoid profile view with a comparative Bernageau view of the unaffected shoulder (Figure 1). If the patient is older and I am suspicious of rotator cuff pathology or arthropathy, I obtain an AP view of the glenohumeral joint with the arm in neutral rotation, an axillary lateral view and a scapular outlet view. These radiographs are performed using fluoroscopy and controlled for magnification. If these radiographs clearly define the problem, for example the presence of anterior glenoid bone loss and a Hill-Sachs lesion, no further imaging is performed unless suspicion exists for additional pathology such as a rotator cuff tear. If radiographs are normal, my secondary imaging modality of choice is magnetic resonance arthrography (MRA).

Figure 1. Bernageau glenoid profile radiograph shows anterior bone loss (arrows) with normal contralateral radiograph. Images: Edwards B

Augustus D. Mazzocca, MS, MD: I look to the initial history of instability that brought the patient to have the surgery in the first place. I consider the type of trauma that originally caused the event and how many times it has happened, including the position of the arm, activity the patient was doing and the amount of force applied to the shoulder. Also, I think that it is important to determine the decisions made by the previous surgeon, i.e., how the original surgery was performed (arthroscopically or open), how many anchors were placed, where the anchors were placed and the overall condition of the intra-articular glenohumeral joint at the time of the initial surgical procedure (cartilage defects, articular-sided rotator problems, etc.).

We then delve into a detailed history of how the patient did postoperatively — the rehabilitation program, how long the patient wore a sling, the type of exercises the patient did in therapy and how long physical therapy was. This information is important for me to know if I think perhaps the rehab was too fast or aggressive, if the exercises done in the beginning stretched out or pulled the capsule or, on the contrary, maybe the anterior labrum was fixed and the inferior labrum was left a little looser and the patient now has a hourglass type of problem.

Once I have this information, I ask the patient questions about mid-range instability. We know that the inferior glenohumeral capsule (both the anterior and posterior bands), as well as the superior and middle glenohumeral ligament, are in effect only at the end ranges of motion. If the patient has a dislocation or subluxation or feels apprehension in mid-range, that would lead me to believe there is more bone abnormality. Does the patient dislocate or have subluxation events while sleeping? Does it take decreasing force to reduce after dislocation or subluxation?

The exam always begins with inspection to observe atrophy or any asymmetry between the deltoid. We then perform a cervical spine exam to ensure that there are no conflicting cervical spine issues. After range of motion, we perform a supine exam – abduction to 90°, external rotation to determine where the apprehension lies, internal rotation with the scapula fixed and a load-shift maneuver.

With the patient in the supine position, I get a better feel and can relax the patient as I sit on a small stool next to him or her. The shoulder hangs over the edge of the table with the scapula stabilized on the edge. This positioning allows for a load to be applied to center the humeral head on the glenoid and then an anteroinferior force is applied and graded 1+ (to the edge), 2+ (over the edge and back) and 3+ (locked). We also do this posteriorly. We will also do a posterior jerk test making sure that the forward elevation is past 140° and the Kim test in a seated position, paying special attention to the posterior aspect to make sure there is no missed posterior inferior problem. As Cadet suggested, we also do a sulcus sign supine and in external rotation to determine competency of the rotator interval. Finally, we look at the strength of the anterior/middle and posterior deltoid, supraspinatus and subscapularis.

We do a series of X-rays including a standard AP, a West Point view, an axillary view, a striker notch view, and I usually add a Zanca view. Following radiographs, we will get a CT scan with 3-D, reconstruction, subtracting the humerus and glenoid to see those bones by themselves and to assess the amount of bone loss. Finally, we get a MRA to assess that there is no humeral avulsion of the glenohumeral ligaments or other missed problem.

Matthew T. Provencher, MD, CDR, MC, USN: The patient with a potentially failed instability repair presents a diagnostic challenge. I try to keep in mind that the index instability procedure may have failed for many different and potentially overlapping reasons (not just recurrent instability or redislocation event), including recurrent instability, persistent pain, weakness or stiffness. Thus, it is important to ascertain what is the main issue for the potential failure after instability repair with a comprehensive history and physical examination.

When taking the patient history, it is important to document the level of energy to cause the recurrence as well as the arm position of the instability event. This provides information regarding the integrity of the repair and position of instability. Patients with a history of hyperlaxity may be at increased risk for recurrence after arthroscopic instability repair secondary to an inability to optimally re-tension the capsule.

One should also investigate the frequency of instability events, determine if there is a progressive ease of instability and what arm positions the patient avoids. In addition, does the patient have a history of bilateral shoulder instability (glenoid hypoplasia), relatively low-energy mechanism (glenoid or humeral bone injury) and superior labrum anterior posterior (SLAP) signs? This will provide information on the level of energy required for an instability event, and to ascertain if glenoid and/or humeral head bone loss may be a contributing factor.

On examination, one should pay attention to hyperlaxity signs, the sulcus test (indicating inferior capsule and/or rotator interval incompetence and the predominant position and direction of instability. As glenoid bone loss is one of the leading causes of arthroscopic instability repair failure, one of the most important examination findings is to determine if the patient has instability in mid-ranges of motion (arm abducted 45° with external rotation), rather than the full apprehension position. In addition, if a patient has limited and asymmetrical external rotation at the side (a seemingly tight shoulder), but recurrent anterior instability findings, one should be suspicious that the anteroinferior structures were either reinjured or inadequately addressed in the primary repair construct.

A comprehensive radiographic evaluation should be performed in the setting of a failed instability repair – including plain radiographs (AP, True AP, supraspinatus outlet and West Point axillary view), a MRI or MRA, and I almost always obtain a 3-D CT scan in order to ascertain for glenoid and humeral head bone loss, version issues, or other bony erosion that may be leading to the recurrence.

Levine: Anything different for the patient who has recurrent anterior instability following prior open Bankart/capsular shift?

Ahmad: A patient who has undergone an open stabilization procedure from the anterior side has unique features that should be evaluated including the integrity of the subscapularis which could be assessed with a lift-off test, belly press, internal rotation strength and increased passive external rotation at the side. In addition, technical aspects of open capsular shift may neglect inferior capsular tensioning. Inferior translation should be assessed with a sulcus sign as well as posterior translation and degree of external rotation. Imaging studies should also look for the possibility of asymmetric tightening, which is evident with posterior translation of the humeral head and the integrity of the subscapularis (axillary view will show anterior subluxation with a deficient subscapularis).

Cadet: The subscapularis comes into play when discussing recurrent anterior instability following an open procedure. Subscapularis deficiency can be a source of anterior instability. How was the subscapularis managed at the initial surgery? This is important information that needs to be elucidated from the operative report. In addition, the type of shift (medial or laterally based), if any, is also important to know as this will affect preoperative planning regarding managing the capsule at the time of revision surgery.

Edwards: I do nothing different for the patient with a failed open repair.

Mazzocca: There would be nothing different. We would spend the same time performing the same exam, history taking, and imaging studies for someone who has had an open or arthroscopic procedure. We would pay close attention to any change in strength between uninvolved and involved subscapularis.

Provencher: The open Bankart repair remains the gold standard for instability repair and has proven effective even in the setting of mild to moderate glenoid bone loss. Thus, if a patient has recurrent anterior instability after an open Bankart repair, one should carefully evaluate for more extensive bone loss with a 3-D CT scan with the humeral head digitally subtracted to optimally visualize the glenoid face. In addition, the subscapularis should be carefully evaluated, both clinically and with MRI, to assess muscle volume, as recurrent instability may be secondary to poor dynamic stabilization of the shoulder joint secondary to subscapularis dysfunction.

If a shoulder is stiff in external rotation at the side and still has instability, particular attention should be paid to the inferior and anteroinferior capsule as these structures may not have been adequately tensioned or reinjured in the recurrent instability event.

Levine: How do you determine how much bone loss has occurred on the glenoid side? How much glenoid bone loss is “too much” and should preclude a soft tissue reconstruction?

Ahmad: Bone loss on the glenoid side is best detected with a CT scan with 3-D reconstructions that allows the percent of glenoid deficiency to be determined. One method is to create a best-fit circle on the inferior two-thirds of the glenoid, and then from the center of that best-fit circle, estimate the amount of anterior bone loss. The average diameter of inferior glenoid approximates 24 mm. Basic science and clinical reports suggest that less than 15% of bone loss, which equates to 3 mm to 4 mm of bone loss, can be managed with a standard soft tissue instability repair. However, greater magnitudes from 15% to 30%, which equates to 4 mm to 9 mm of bone loss, can be significant for some high risk patients and greater than 30% of bone loss, which equates to 8 mm to 9 mm, will be significant in most patients. Diagnostic arthroscopy can confirm the magnitude of bone loss using the bare spot as described by Burkhart et al. In the setting of significant bone loss, especially in failed previous surgery, consideration should be given for bone augmentation procedures such as the coracoid transfer.

Cadet: The amount of bone loss can be determined preoperatively and postoperatively. The pattern of glenoid bone loss also has to be determined. Burkhart’s “inverted pear” description is a nice way to define glenoid bone loss qualitatively. Basically, the shape of a pear is largest at its base, just as with the glenoid. If this relationship is distorted, specifically, if the base of the glenoid has similar or less bone than the superior glenoid, then you are dealing with significant bone loss. Quantitatively, on the sagittal view on CT or MRI scans, one can identify the center of the glenoid, which usually corresponds to the “bare spot” intraoperatively. The shape of the inferior glenoid is considered circular, and one can draw a best-fit circle. The radius (B) is measured from the center to the posterior edge of the glenoid (assuming no posterior glenoid bone loss). 2B represents the diameter of the glenoid undisturbed. Distance A is the distance from the center to the most anterior edge of the glenoid (excluding the Bankart fragment). Thus, I calculate the percentage bone loss based on the formula described by Sugaya et al.

Percent bone loss = [(B-A)/2B] X 100

Intraoperatively, I use the “bare spot” as my reference point for the center of my measurement. The greatest diameter of the glenoid at this point should be approximately 24 mm (radius is 12 mm from the point of the “bare spot” to the anterior or posterior edge). The diameter of the probe is generally 3 mm. Thus, greater than 6 mm of bone loss from the bare spot would be 25%. Greater than 25% is what I consider to be “too much” and would preclude an isolated “soft tissue reconstruction.”

Edwards: I compare the Bernageau glenoid profile views and make measurements of the anteroposterior glenoid diameter using a digital caliper. We do not know how much bone loss is “too much,” but we are currently researching use of a ratio created from these measurements to help guide our decision-making.

Mazzocca: We use CT scan with 3-D reconstruction as our primary imaging to determine bone loss. This method of imaging provides an idea of the area and significance of the bone loss.

Yamamoto et al and Detterline et al have described the clinically significant combined lesions called the glenoid track. In general, the width of the glenoid track is 85% of the glenoid with no defect. The take-home point is if the medial margin of the humeral head defect is greater than the glenoid tract, the humeral head is likely to engage. We really believe in this, so we will measure the distance of the Hill-Sachs lesion and the glenoid and take 85% of that and look to see. We also will assess with Gerber’s method and Sugaya’s method to get a sense of bone loss. We spend a lot of time speaking with the patient regarding the risks and benefits of bone augmentation with hardware vs. arthroscopic soft tissue repair.

Provencher: The gold standard to determine glenoid bone loss is with a 3-D CT scan with the humeral head digitally subtracted so you can view the glenoid directly en face (Figure 2). As discussed by the other faculty, the inferior two-thirds of the glenoid is a well-conserved circle, so with simple measurement by placing a circle in the bottom of the glenoid (either electronically or with pencil), you can determine the amount of glenoid bone loss across the diameter of the circle. When measuring in the lab, or for clinical studies, we have measured the surface area of bone loss and expressed in mm², although this is likely too cumbersome for routine clinical use. If there is concern about the radiation associated with a CT scan, a MRA, especially with a reasonable magnet strength (>1.5 Tesla) can also measure the amount of bone in a similar fashion. I think that plain radiographs are inadequate to determine the amount of glenoid bone loss for treatment decisions.

Figure 2. Sagittal 3-D CT reconstruction with humerus removed in a 25-year-old male after arthroscopic instability repair with recurrent anteroinferior instability. Note the glenoid bone deficiency and the “inverted pear” deformity. Image: Columbia University Center for Shoulder, Elbow and Sports Medicine

An additional and simple way to measure bone loss is arthroscopically with the glenoid bare spot technique. With the arthroscope in the anterosuperior portal, a graduated probe is brought in from the back, and the relative amount of bone loss anterior to the bare spot is measured vs. the amount of bone that is present from the bare spot posteriorly and expressed as a percentage of loss.

Clinical evidence would suggest that there is no “hard” number of the amount of glenoid bone loss that would preclude a soft tissue repair. The main reason for this is that there are many complexities involved in recurrent shoulder instability associated with glenoid bone loss. For example, a patient who skydives for a living cannot dislocate when jumping out of an airplane. The amount of glenoid bone loss that a skydiver or wrestler may tolerate may be less than say someone who participates in recreational sports, is an older instability patient or one who has lesser demands. That being said, in general, patients with 15% of less of glenoid bone loss, a soft tissue repair is a reasonable approach, especially if there is a bone fragment that can be incorporated into the repair construct. For this type of patient, an open repair may also add additional stability over an arthroscopic repair. For patients with 15% to 25% bone loss, this represents a level in which an arthroscopic repair should be approached with caution. Patients with a bony fragment that can be incorporated into the repair may have better outcomes in terms of stability as the glenoid can effectively be anatomically restored. For patients with more than 25% loss, a bone augmentation procedure is generally recommended.

Levine: How do you determine how much bone loss has occurred on the humeral side? How much humeral bone loss is “too much” and would lead you to consider addressing it?

Cadet: I consider a Hill-Sachs lesion greater than 40% with less than 20% glenoid bone loss to be too much. However, an engaging Hill-Sachs lesion that is less than 40% but is deep may also be too much. Quantifying the Hill-Sachs preoperatively can sometimes be difficult. I will quantify it based on a percentage of the diameter of the humeral head on axial and coronal sections at the Hill-Sachs largest diameter and width.

Edwards: In the absence of a fixed glenohumeral dislocation, humeral bone loss that significantly affects stability is very rare in my practice. To this point, I have only used radiographs to evaluate humeral bone loss, specifically the AP internal rotation view and the axillary lateral view. I have addressed the vast majority of large Hill-Sachs lesions in my practice via the glenoidplasty effect provided by the Latarjet. The Latarjet increases the AP diameter of the glenoid prohibiting sufficient anterior translation to allow engagement of the humeral head lesion.

Mazzocca: Once again, we use the glenoid track but, in general, we use the 30% rule where we will measure that off of a CT scan.

Provencher: Humeral bone loss determination remains a challenge. This is due to the fact that the humeral head defect is 3-D and usually in the shape of an orange slice. The best way to identify and measure a Hill-Sachs is with either ultrasound, MRI or CT scan. Plain radiographs may also identify the presence of a Hill-Sachs lesion.

It is a rare case to have a large amount of humeral head bone loss without a corresponding significant glenoid bone injury. However, the relatively harder anterior glenoid bone may cause a significant impaction on the humeral head without glenoid bone loss. The more usual case is that the glenoid and humeral head have concomitant bone injuries, which are usually addressed on the glenoid side with either a soft tissue repair or a bony augmentation case. As Mazzocca mentioned above, we have learned that the glenoid track is an important emerging concept to look at the size of the Hill-Sachs lesion relative to the glenoid.

Unless the humeral head easily “engages” on the glenoid, a soft tissue procedure is generally adequate. However, in larger defects (Hill-Sachs lesions greater than 20% to 25% depth of the humeral head) that easily engage, a combination of procedures may be performed – including capsulolabral soft tissue repair and potential remplissage (tenodesis of the infraspinatus into the humeral head defect) vs. a glenoid bone augmentation procedure that effectively prevents the humeral head engagement. In general, I prefer a bone augmentation procedure if there is humeral head bony engagement, which usually suggests a combined humeral head and glenoid bone injury.

A note from the editors:

Look for Part 2 of this Round Table discussion in the June issue.

References:

• Burkhart SS, de beer JF, Tehrany AM, Parten PM. Quantifying glenoid bone loss arthroscopically in shoulder instability. Arthroscopy. 2002;18:488-491.
• Detterline AJ, Provencher MT, Ghodadra N, et al. A new arthroscopic technique to determine anterior-inferior glenoid bone loss: validation of the secant chord theory in a cadaveric model. Arthroscopy. 2009;25:1249-1256.
• Lo IK, Parten PM, Burkhart SS. The inverted pear glenoid: an indicator of significant glenoid bone loss. Arthroscopy. 2004;20:169-174.
• Pagnani MJ. Open capsular repair without bone block for recurrent anterior shoulder instability in patients with and without bony defects of the glenoid and/or humeral head. Am J Sports Med. 2008;36:1805-1812.
• Sugaya H, Kon Y, Tsuchiya A. Arthroscopic repair of glenoid fractures using suture anchors. Arthroscopy. 2005;21:635.
• Yamamoto N, Itoi E, Abe H, et al. Contact between the glenoid and the humeral head in abduction, external rotation, and horizontal extension: A new concept of glenoid track. J Shoulder Elbow Surg. 2007;16:649-656.

• Christopher S. Ahmad, MD, can be reached at the Center for Shoulder, Elbow and Sports Medicine, Columbia University, 622 W. 168th St., New York, NY 10032; 212-305-5561; email: csa4@columbia.edu.
• Edwin R. Cadet, MD, can be reached at Columbia University Medical Center, 622 W. 168th St., PH-1117 Center, New York, NY 10032; 212-305-4626; email: ec2195@columbia.edu.
• T. Bradley Edwards, MD, can be reached at Fondren Orthopedic Group LLP, 7401 South Main St., Houston, TX 77030; 713-799-2300; email: bemd@fondren.com.
• William N. Levine, MD, can be reached at Columbia University Medical Center, 622 W. 168th St., PH-1117r, New York, NY 10032; 212-305-0762; email: wnl1@columbia.edu.
• Augustus D. Mazzocca, MS, MD, can be reached at New England Musculoskeletal Institute, Medical Arts and Research Building, Room 4017, University of Connecticut, 263 Farmington Ave., Farmington, CT 06034-4037; 860-679-6633; email: admazzocca@yahoo.com.
• Matthew T. Provencher, MD, MC USN, can be reached at the U.S. Naval Medical Center, San Diego, Department of Orthopaedic Surgery, 34800 Bob Wilson Drive, San Diego, CA 92134; 619-532-8427; email: matthew.provencher@med.navy.mil.
• Disclosures: Ahmad is a paid consultant for Arthrex and Acumed, and receives research support from Stryker, Zimmer and Arthrex. Cadet previously received research support in the form of research materials from Smith & Nephew. Edwards has no relevant financial disclosures. Levine and Provencher have no relevant financial disclosures. Mazzocca is consultant for and receives research funding from Arthrex Inc.