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Arthritis or degenerative joint disease (DJD) of the shoulder in young athletes is a disabling condition that often limits sports participation and is extremely challenging to treat. Shoulder arthritis, defined as a degeneration of the articular cartilage of either the humeral head or glenoid, is caused by multiple etiologies, including primary osteoarthritis and secondary causes such as trauma, iatrogenic disease, and rheumatoid disease. Although each subtype has a unique set of considerations and treatment options, all have the same end goal of providing a functional, pain-free shoulder that has the durability to withstand the forces of daily and recreational activities for the duration of the athlete's life—a particularly important and challenging consideration in this young, active, population.
Shoulder DJD begins with loss of mobility and the inability to maintain function because of contracture and pain in and around the shoulder. This condition eventually leads to difficulty in continuing recreational activities, which is a substantial hurdle for individuals who wish to lead an active lifestyle. A wide spectrum of disease can be present, from focal cartilaginous softening to diffuse, full-thickness lesions of both the glenoid and humeral head.
In the United States the overall incidence of glenohumeral chondral lesions and their natural history are largely unknown. These lesions are often found incidentally at the time of arthroscopy for other pathologies. The causes of these lesions range from idiopathic to specific underlying pathologies that eventually lead to osteoarthritis. Chondrolysis, a specific form of osteoarthritis, has been studied in national registries and has an incidence of 5.5 per 10 million person-years. It has an increased incidence in persons with diabetes and in those who have undergone an orthopedic procedure. Nakagawa et al. studied primary osteoarthritis, specifically excluding patients with rheumatoid disease and those with rotator cuff arthropathy, and found an incidence of 0.4% in persons with orthopedic problems versus 4.6% in those with shoulder disease presentation.
Primary osteoarthritis is typically found in persons older than 60 years. In the young, healthy, and active population, the incidence is expected to be much lower, although specific data are lacking in the current literature. Cadaveric studies have shown an increased incidence of chondral lesions associated with rotator cuff tears, with glenoid defects in 32% and humeral defects found in 36% compared with rates of 6% and 7%, respectively, in shoulders without rotator cuff tears.
Posttraumatic osteoarthritis, specifically those related to shoulder dislocations, have been studied extensively to look at chondral injuries. In 1997 Taylor and Arciero reported that 57 of 63 patients had a Hill-Sachs lesion after anterior dislocation; 40% were chondral lesions, and 60% were osteochondral lesions. Furthermore, arthroscopic evaluation of 212 patients demonstrated a 23% incidence of glenoid defects and an 8% incidence of humeral head defects in persons who had one dislocation, whereas persons who reported more than two dislocations had a significantly increased incidence of arthritic lesions (27% and 36%, respectively).
Primary shoulder osteoarthritis is a rare phenomenon in the young athlete; this disease occurs mostly in patients 60 years and older, and its etiology is unknown. It begins with glenohumeral joint stiffness, followed by joint space narrowing and humeral head and inferior glenoid osteophytes, which is considered the classic finding, with an intact rotator cuff. Samilson and Prieto first described radiographic parameters for glenohumeral arthritis in 1983. Since then, the classification has been revised, and in 2002 Guyette et al. further refined this classification, with radiographs evaluated for humeral osteophytes, glenoid changes, and loss of joint space, collectively.
Walch et al. have further noted that fixed posterior humeral head subluxation may precede the development of osteoarthritic changes and may be the first sign of primary glenohumeral arthritis, and Ropars et al. indicated that a spinoglenoid cyst is an even earlier sign of glenohumeral degeneration. Patients often have anterior capsular tightness that causes a static subluxation of the humeral head in relation to the glenoid. As arthritis progresses beyond the 55% humeral subluxation index, described by Kidder, further osteophyte formation develops, including progressive central loss of cartilage on both the glenoid and humeral head.
Although the rates of shoulder arthritis have been demonstrated to be higher in patients who have sustained a shoulder dislocation (so-called dislocation arthropathy ) and in patients who have had that dislocation treated surgically (so-called capsulorrhaphy arthropathy ), we believe that these entities, although deserving of discrete consideration, may have significant overlap and are various points on a spectrum of the same disease process. However, to date, the literature has separated these processes into two distinct entities.
Impaction and shear across the glenohumeral joint causes an articular cartilage lesion during shoulder dislocation, with an incidence of chondral and osteochondral lesions of 47% and 46%, respectively. Initially described by Neer et al. in 1982, Samilson and Prieto classified the condition in 1983. This form of arthritis is associated with increasing age at the initial event, direction of dislocation (with posterior causing more changes than anterior), and associated glenoid fractures. However, the number of dislocations and prior stabilization procedures were not associated with development of shoulder arthritis. Interestingly, Matsoukis et al. reported no difference between patients treated with and without surgery in regard to the severity of arthritis, and the overall incidence of arthritis after shoulder dislocation in patients treated nonoperatively ranges from 10% to 20%. Most recently, 25-year follow-up data, reported by Hovelius and Saeboe in 257 shoulders that sustained primary anterior dislocation, show that shoulders were radiographically normal in only 44% of patients at 25 years and the arthrosis development was related to age at primary dislocation (>25 years), recurrence of instability, participation in high-energy sports causing injury, and an alcohol abuse history. Although the rate of moderate to severe arthritis was 18% in shoulders without a recurrence compared with 26% with surgically stabilized shoulders, the rate of arthrosis in these surgically stabilized shoulders was less than in shoulders that were reported to have “stabilized over time,” raising a significant question regarding the role of recurrent instability in the future development of arthrosis.
Capsulorrhaphy arthropathy, as coined by Matsen and Wirth, is described as arthrosis that is attributed to overtightening of the capsular structures which results in abnormal translation of the humeral head opposite the direction of capsulorrhaphy. Found in male patients at a mean age of 45, it has been linked to length of time since follow-up, amount of external rotation contracture, and the age at initial trauma. Biomechanical testing of selective capsular plication has shown that this mechanism causes alterations in humeral head translation. These translational differences lead to nonanatomic biomechanics, asymmetric cartilage wear, and ultimately arthritis ( Fig. 52.1 ).
Surgical options have evolved as we have come to better understand the effects of biomechanics on shoulder articulation. Surgical options can now be divided into anatomic and nonanatomic procedures. Most nonanatomic repairs have been abandoned, including the Putti-Platt and Magnuson-Stack methods ; however, the Bristow-Latarjet method (although modified from its original description) has continued to be a mainstay of treatment in cases of anterior instability in the setting of bony glenoid deficiency.
In contrast to most nonanatomic repairs, anatomic procedures including Bankart repair and capsulorrhaphy have become the mainstay of treatment and have evolved significantly with use of arthroscopic techniques for primary and revision instability repairs; some persons argue that these procedures are the current standard of care. However, this paradigm shift from primarily open to arthroscopic techniques leaves unanswered questions about the long-term outcomes of open versus arthroscopic procedures, especially with regard to arthritis.
Long-term data indicate the presence of degenerative changes after the Putti-Platt procedure in 30% to 61% of patients at 9 to 26 years of follow-up. These results have led to the abandonment of this procedure; however, the Bristow-Latarjet reconstruction remains part of the current treatment algorithm even though it has a reported incidence of arthritis of as high as 49% at 14 years. It may be argued that several technical details in the techniques used in these procedures (specifically, complete subscapularis takedown) are not currently performed, which may greatly affect outcomes, although few studies refuting this high rate of arthrosis have been reported. However, a more recent study has demonstrated that, despite an overall incidence of arthrosis in 34% of patients, moderate or severe arthrosis was present in only 6% (which correlated with worse outcomes), whereas the patients with only mild arthrosis had no degradation of outcomes from joint damage after the Bristow-Latarjet procedure. These studies have shown that the development of arthrosis may be more closely related to graft malposition than other factors previously thought to be responsible.
Chondrolysis of the glenohumeral joint is a devastating problem that has proven to be one of the most vexing diagnoses faced by shoulder surgeons during the past decade. It has many associated (although not well proven) causes and is characterized by unexpected pain and loss of joint mobility for weeks to months, typically after arthroscopic shoulder surgery. Global dissolution of cartilage occurs on both the glenoid and humeral head, with the characteristic findings of joint space narrowing, periarticular bone edema, and subchondral cystic changes, although without osteophyte formation. Although this condition has been associated with the use of radiofrequency energy in the shoulder, low-grade infection, intra-articular injection of contrast medium, use of bioabsorbable suture anchors, and postoperative pain pump infusion, small case series and case reports have led to difficulty in extrapolating meaningful data with regard to the true etiology of this condition.
Recently, 375 patients who underwent an arthroscopic intra-articular shoulder procedure by an individual community orthopedic surgeon were evaluated specifically with regard to chondrolysis. This cohort demonstrated a 13% incidence of chondrolysis, with all cases associated with an intra-articular postarthroscopic infusion of local anesthetic (bupivacaine or lidocaine); chondrolysis did not develop in any patients who underwent arthroscopy without a postoperative anesthetic infusion and is not present following an intra-articular steroid injection. In addition, Bankart repair, arthroscopic débridement, suture anchor placement in the glenoid, and operative time were associated with this finding. This finding of the association between a postoperative anesthetic infusion and chondrolysis has been further supported by the results of a recent systematic review of 100 cases of chondrolysis in the literature, with this situation demonstrated in 59% of the cases reviewed.
In addition, it has been demonstrated that the development of chondrolysis after a postoperative anesthetic infusion may be a dose-related phenomenon, which has been demonstrated in several basic science studies and supported in a recent clinical cohort. When a high-flow pain pump was used postoperatively, chondrolysis developed in 16 out of 32 patients, whereas it developed in only 2 out of 12 patients with a low-flow pump containing bupivacaine, epinephrine, and infusate.
With regard to low-grade infection as a causative agent, in their systematic review of 100 cases, Scheffel et al. reported that of 91 patients who underwent revision surgery, 41 had microbiologic cultures taken at the time of revision surgery. Growth was reported for only 3 of these 41 cases, with Propionibacterium acnes reported in all 3 cases and no finding of any other positive cultures mentioned.
The possibility that bioabsorbable suture anchors are an etiologic agent has also recently been analyzed; Dhawan et al. performed an evaluation of the 1,072,000 bioabsorbable anchors placed about the shoulder in 2008. Of these cases, 10 suture anchor–related complications were reported to the US Food and Drug Administration, all of which were thought to be related to anchor malposition and typically demonstrated geographic rather than global cartilage loss. This finding was viewed as a best-case scenario, in that many cases of complications may not be reported; however, the authors still concluded that use of bioabsorbable anchors remains a safe practice when they are implanted properly based on the available literature.
Unfortunately, a reliable treatment algorithm or diagnostic modality to definitively identify patients with chondrolysis does not currently exist. Chondrolysis remains largely a diagnosis of exclusion, although surgeons need a high index of suspicion in the setting of failed previous surgery with early, progressive, and advanced arthritic changes of the glenohumeral joint. The outcomes of further definitive treatment of these patients have also been disappointing, and chondrolysis thus remains a major challenge for shoulder surgeons.
Rheumatoid arthritis is an inflammatory arthritic condition that affects the synovial linings of both small and large joints. Although other inflammatory arthritides may affect the young athletic population (particularly psoriatic arthritis, spondyloarthropathy, and reactive arthritis), most is known about rheumatoid disease in this setting. The inflammatory nature of the disease leads to a disabling secondary erosive arthritis. It most commonly affects the small joints of the body but is found in the shoulder in 90% of patients with chronic rheumatoid disease. Rheumatoid disease in the shoulder is progressive in nature, with early symptoms of pain, swelling, and decreasing shoulder motion. With disease progression, extra-articular structures become involved, including the subacromial bursa, acromioclavicular (AC) joint, and rotator cuff. Radiographic progression begins with medial migration of the humeral head into the glenoid with characteristic central erosion of the articular surface ( Fig. 52.2 ). Bone quality is typically osteopenic with periarticular erosions involving the superior and medial humeral head. Cystic formation may occur at the rotator cuff insertion, which, coupled with intrinsic degeneration of the rotator cuff, may lead to functional rotator cuff deficiency, static superior migration, and uneven joint erosion. Late sequelae of the rheumatoid shoulder leads to painful joint destruction, loss of bone stock (which has significant implications for reconstructive options), rotator cuff compromise, and poor overall function. Further evaluation, especially in the preoperative setting, of all patients with rheumatoid arthritis should also include flexion and extension lateral views of the cervical spine to check for cervical instability and further causes of rheumatologic problems that may affect the shoulder joint concomitantly.
Osteonecrosis (also known as avascular necrosis [AVN]) is another form of progressive glenohumeral arthritis that may be encountered during evaluation of the shoulder of a young athlete with arthritic disease. Osteonecrosis is characterized by the development of avascular regions of periarticular bone, resulting in infarction, necrosis, and ultimately collapse of the bony architecture of the subchondral plate with resultant deformity and arthrosis as a result of incongruity. Early workup of this disease should include testing for sickle cell anemia, particularly in the African-American population. Also to be considered etiologically are protein C and S deficiency, factor V Leiden, and hyperlipidemia.
Although many causes of osteonecrosis have been described, including dysbarism, hemoglobinopathies, coagulopathies, Gaucher disease, and connective tissue disorders, steroid use and alcohol abuse predominate clinically. If radiographs reveal a crescent sign and collapse, the contralateral shoulder should be imaged to rule out asymptomatic bilateral disease, and use of the aggravating agent (if identified) should be stopped to prevent further progression of the disease. Collapse of the articular surface is secondary to fractures in weak subchondral bone, and pain is often the most common complaint, specifically with difficulty sleeping and pain interfering with activities of daily living. Pain is usually present with flexed and abducted shoulder positions because of the incongruous central superior position of the humeral head contacting the glenoid in this position.
Classification of osteonecrosis of the humeral head has been described by Cruess ( Table 52.1 ). Osteonecrosis has six stages based on radiograph and magnetic resonance imaging (MRI); these stages are largely based on and parallel the original description in the femoral head by Arlet and Ficat. Indeed, osteonecrosis of the humeral head is similar to that in the femoral head, first with edema visible only on MRI, followed by sclerosis and then development of the crescent sign, with further collapse of the articular surface and finally degeneration on both sides of the joint ( Fig. 52.3 ).
Stage | Description |
---|---|
I | Normal radiograph; changes on magnetic resonance imaging |
II | Sclerosis (wedged, mottled), osteopenia |
III | Crescent sign indicating a subchondral fracture |
IV | Flattening and collapse |
V | Degenerative changes extend to glenoid |
Glenohumeral arthritis has no classic or pathognomonic history but typically presents as a progressive loss of shoulder rotary mobility coupled with pain. Some persons report noise, grinding, crepitus, and a feeling of a point of “clunking with release.” Another suggestive history includes instability without a history of dislocation, with the incongruent articular surfaces having a mechanical catch. In addition, patients may report morning stiffness that improves throughout the day, along with pain during sleeping.
Primary glenohumeral arthritis in the young population (i.e., younger than 50 years) is exceedingly rare and warrants an exhaustive history to identify the underlying primary diagnosis. History should include prior episodes of trauma, current and previous medications, family history, prior surgical procedures, and recreational and social factors. In addition, the patient's desired activity level should be taken into consideration. We have found that the desired activity level is a critical aspect of the evaluation of these patients because outcomes from certain procedures can be perceived as “catastrophic” if patients are not counseled about the longevity and limitations of implants and their ability to meet patients’ expectations.
Examination of the shoulder starts with evaluation of the cervical spine, with notation of deficits in range of motion (ROM) and reproduction of pain with provocative maneuvers, such as the Spurling test. Referred pain from the cervical spine is common; patients with cervical spine pathology are often more comfortable with their hand draped over their head. Although referred pain and findings of cervical spine pathology do not exclude shoulder pain, patients suspected of having cervical pathology should be referred for proper care and the possibility excluded from the differential diagnosis.
The shoulder examination begins with visual inspection for symmetry, muscle atrophy, and previous surgical incisions. It is critical that the entire shoulder be visualized, including the entirety of the scapula, to ensure that the patient is examined for subtle but significant pathology, including scapular winging. Next, palpation of the posterior capsule, AC joint, greater tuberosity, and biceps groove helps to delineate and isolate glenohumeral pathology. Further evaluation includes both passive and active mobility with careful delineation of the painful arc of motion, while looking for the typical finding of an equal limitation of active and passive ROM in all planes. Motion is evaluated in forward flexion, abduction (controlling for scapulothoracic motion), external rotation at zero and 90 degrees of abduction, and internal rotation with regard to the vertebral level reached by the hand behind the back. Findings should be compared with the contralateral (presumably unaffected) side. Decreased rotational movements and mid ROM pain should alert the examiner to the presence of an arthritic process, whereas terminal ROM pain is more typically indicative of impingement, osteophytes, and capsular contraction.
Strength testing and impingement signs aid in the evaluation of rotator cuff pathology. Each tendon of the rotator cuff must be evaluated independently. The supraspinatus is evaluated using the champagne toast test, whereas infraspinatus testing is accomplished via external rotation strength with the arm adducted at the side. Lag signs must be elicited if they are present, and the Hornblower sign (external rotation with the shoulder abducted 90 degrees) tests the integrity of the teres minor. In this patient population, we have found that it is critical to evaluate the integrity of the subscapularis, especially in the setting of capsulorrhaphy arthropathy after an open anterior instability procedure, where we have noticed a high rate of this finding. Subscapularis tear is typically characterized by asymmetric hyperexternal rotation with the arm in adduction with a positive belly press (a test for the upper subscapularis) and lift-off (a test for the lower subscapularis). The implications of these findings are critical because they may play a significant role in surgical decision-making; for example, consideration of procedures such as a concomitant pectoralis major transfer in the setting of subscapularis insufficiency with arthroplasty may be necessary.
A complete evaluation of the dates of individual surgeries, prior imaging, and arthroscopic images should also be undertaken for each patient. Such an evaluation can help differentiate between existing pathology and a new diagnosis. Particular attention to results after prior procedures is imperative to understand if recurrent pathology is present or if further problems have developed. Arthroscopic images help provide a firsthand view of the cartilage surfaces and the previously treated pathology. Previous MRI scans and radiographs can help put together a picture to further understand previous and new pathology. A review of the operative report of previous surgeries can help the surgeon understand the exact surgical procedures and difficulties affecting the surgical outcomes. Patients often understand that they have a problem in their shoulder but do not effectively communicate exact pathologies that may help guide future considerations.
Careful examination of the detailed operative note should include notation of implants, intraoperative findings, and difficulties with the previous procedures. Prior implants could limit the ability to access the canal if, for example, a biotenodesis screw has been previously placed for a biceps tenodesis. Placement of metal suture anchors into the glenoid and greater tuberosity also could be limiting. These anchors may scratch sensitive metal and polyethylene components that would lead to early failure of further implants, without removal of the previous anchors. In addition, certain glenoid anchors have been thought to cause cyst formation, which may make it difficult to place a stable glenoid component on the subchondral surface.
Evaluation of all types of arthritis starts with plain film radiographs. X-ray views should include at a minimum a Grashey anteroposterior view, an axillary lateral view at 45 degrees of abduction, and a scapular Y view ( Fig. 52.4 ). These three views are able to document the position of the humeral head in relation to the glenoid, the presence of osteophytes, bone quality, the glenohumeral joint space, and glenoid bone loss. They should be evaluated for humeral head posterior subluxation, which may be the earliest sign of arthritis found on radiographs.
Further evaluation includes advanced modalities such as computed tomography (CT) and MRI. CT arthrography is extremely helpful in evaluating joints, especially in the setting of prior hardware placement. Glenoid morphology, bone stock and quality, and the status of the cartilage and rotator cuff can be well evaluated with a CT arthrography scan. A glenoid version can be further assessed by the techniques described by Friedman and colleagues ( Fig. 52.5 ). Walch et al. further described the bony anatomy of posterior glenoid wear in the anteroposterior plane, specifically evaluating for biconcavity, which is best evaluated by CT ( Fig. 52.6 ). MRI is especially helpful in evaluating changes to the subchondral bone and associated soft tissue comorbidities. However, the sensitivity and specificity of evaluating chondral lesions is generally regarded as poor; up to 45% of grade IV chondral lesions may be missed. Newer evaluations with 1.5T and 3.0T MRIs have been found to detect glenoid and humeral lesions at 84% and 78%, respectively, with lower-grade lesions often missed.
Treatment goals for the younger athletes with glenohumeral arthritis are resolution of symptoms and restoration of function and mobility. However, patient expectations must be matched to the durability and longevity of the specific treatment chosen. In fact, in 2008 McCarty et al. demonstrated that the most common reason this population pursued treatment was to attempt to return to their previous level of sporting activity. Although older patients have reliable outcomes with shoulder replacement, young glenohumeral arthritis patients have worse arthroplasty outcomes, and their treating surgeons have difficult decisions to make with regards to implant survivability. The Neer-type total shoulder arthroplasty (TSA) implants have demonstrated an 84% survival rate at 15 years, although revision surgery in the area of the shoulder is extremely complex and few implants have been able to compensate for the glenoid bone loss frequently encountered in revision settings. In young patients, nonoperative treatments should be thoroughly pursued and exhausted before surgical interventions are contemplated. The mainstay of successful outcomes, whether surgical or nonsurgical, is related to patient education that clearly outlines the natural history and functional process that is present, along with the provision of acute and chronic pain management.
The initial treatment of symptomatic glenohumeral osteoarthritis involves recommendation of activity modification, supervised physical therapy, and a trial of oral nonsteroidal antiinflammatory medications. Physical therapy should include a daily regimen of exercise with a focus on strengthening periscapular, deltoid, and rotator cuff musculature. Stretching the joint with manual manipulation helps to improve ROM, which counteracts restrictions caused by cartilage damage and resultant capsular contracture. In addition to these modalities, image-guided or blind injection into the glenohumeral joint with a mixture of corticosteroid and lidocaine is an excellent diagnostic and therapeutic tool. However, such an injection may not provide long-term relief for athletic patients engaging in high-demand sports who continue to participate in athletic endeavors, because their symptoms often return with continued activity. In addition, off-label use of viscosupplementation with hyaluronic acid injections has been shown to provide partial symptom relief but has not been shown to provide statistically improved outcomes over saline injections. The relief experienced often involves improvement in overall pain and has been effective in allowing patients to sleep through the night with minimal shoulder pain after treatment.
The diagnosis of glenohumeral arthritis is often made incidentally at the time of arthroscopic intervention aimed at other pathology, unless radiographic changes or underlying conditions are present. However, arthroscopy provides a minimally invasive means to evaluate and treat chondral lesions and concomitant pathology in the shoulder, allowing for early rehabilitation and return to activity in symptomatic patients who have not responded to nonoperative measures. Unfortunately, arthroscopy in this setting remains a temporizing measure that does not alter the underlying disease process; however, it can provide pain relief and functional improvement for a considerable amount of time.
Several authors have reported successful results of arthroscopic débridement for glenohumeral arthritis and isolated cartilage lesions in patients younger than 55 years, and several prominent themes have emerged from this work. Results have been reliable and have correlated with the extent of disease in those younger than 50 years. Risk factors for failure are chondral lesions larger than 2 cm 2 , grade IV bipolar lesions, residual joint space less than 2 mm, the presence of large osteophytes, and Walch B2, C glenoids. Weinstein et al. reported that pain relief and maintenance of function was sustained for 76% of patients at 34-month follow-up, and it was sustained in 88% of patients at 2-year follow-up in the series by Cameron et al. Conversion to arthroplasty was required in 22% of patients at an average of 10.1 months after débridement in one series and in 15% of patients at 20 months in another series.
Several concomitant procedures were performed in the aforementioned series, including bicep tenotomy/tenodesis, distal clavicle resection, subacromial decompression, microfracture, loose body/osteophyte removal, and capsular release. We have found that capsular release is extremely useful, and it has been recommended that capsular release be included in arthroscopic treatment if rotation is limited by greater than 15 degrees in any plane of motion. Significant attention must be given to these aforementioned concomitant pain generators in the setting of arthritic disease, and furthermore, failure to address these pathologies has been demonstrated to produce worse postoperative results.
In addition to débridement, it has been recommended that full-thickness cartilage lesions be managed with use of microfracture, similar to that described in the knee ( Fig. 52.7 ). In 2009 Millett et al. reported on 31 patients (average age: 43 years) with full-thickness cartilage lesions in the glenohumeral joint who underwent treatment using microfracture. At a mean follow-up of 47 months, the patients demonstrated significant improvement in the visual analog scale score, American Shoulder and Elbow Surgeons (ASES) score, and painless use of the arm, as well as improvement in patients’ ability to work, perform activities of daily living, and participate in sports activity, with failure in 19% of patients, who required additional procedures. These investigators demonstrated the greatest improvement in patients with smaller, isolated humeral head lesions and the worst results in patients with bipolar lesions.
More recently, Frank et al. published their experience with a similar cohort of 15 shoulders in 14 patients (average age: 37 years) who underwent glenohumeral microfracture and demonstrated similar results. At an average follow-up of 28 months, these investigators showed significant improvements in the visual analog scale, simple shoulder test, and ASES scores, with 92% of patients stating that they would have the procedure again. The procedure was considered a failure in three patients in this series (20%), who required further operative intervention during the study period.
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