Shoulder Arthritis and Arthroplasty

Vahid Entezari, MD, MMSc

Eric T. Ricchetti, MD

Dr. Entezari or an immediate family member serves as a paid consultant to or is an employee of DJ Orthopaedics and has received research or institutional support from OREF. Dr. Ricchetti or an immediate family member has received royalties from DJ Orthopaedics; is a member of a speakers’ bureau or has made paid presentations on behalf of DJ Orthopaedics; serves as a paid consultant to or is an employee of DJ Orthopaedics; and serves as a board member, owner, officer, or committee member of the American Academy of Orthopaedic Surgeons, the American Board of Orthopaedic Surgery, Inc., and the American Shoulder and Elbow Surgeons.

ABSTRACT

The shoulder encompasses two diarthrodial joints—the glenohumeral (GH) joint and the acromioclavicular joint (AC)—and either can develop arthritis. Arthritic changes in the AC joint are common in patients older than 60 years with a low correlation between imaging and patient symptoms. Cortisone injection is effective in alleviating pain, and in patients who do not have lasting relief, distal clavicle excision (DCE) is an effective surgical treatment for symptomatic AC arthritis. One-third of patients older than 60 years with shoulder pain have GH arthritis. Primary GH osteoarthritis (OA) is common in elderly females and younger patients with manual labor and heavy weight-lifting habits. In addition to primary GH OA, secondary forms of GH arthritis include posttraumatic arthritis after proximal humerus or glenoid fracture, inflammatory arthritis (including rheumatoid arthritis, psoriatic arthritis, gout, and others), instability arthropathy and capsulorrhaphy arthropathy, osteonecrosis of the humeral head, cuff tear arthropathy in patients with long-standing rotator cuff failure, Charcot arthropathy, and arthropathy of hemophilia. In addition to a history and physical examination, evaluation of GH arthritis starts with plain radiographs. Advanced imaging such as CT and/or MRI may be ordered to assess glenoid and humeral morphology, rotator cuff integrity, and for preoperative planning. The modified Walch classification uses axial CT imaging to categorize primary GH OA based on glenoid erosion and humeral head subluxation. When arthritic changes are mild in young and active patients, arthroscopic débridement can be effective in delaying reconstructive surgery. Hemiarthroplasty is associated with high rate of glenoid erosion and revision, and its use should be limited to young patients with severe GH arthritis and high level of activity or patients with unipolar arthritic disease (eg, osteonecrosis of the humeral head with collapse but without significant glenoid chondral involvement). Anatomic total shoulder arthroplasty (ATSA) is the benchmark for surgical treatment of GH arthritis with an intact cuff with excellent mid-to long-term outcomes. There is a growing trend in performing ATSA with short stem and stemless humeral components and using augmented glenoid components to address glenoid bony deficiency. Reverse total shoulder arthroplasty (RTSA) has gained popularity in recent years for surgical treatment of rotator cuff arthropathy, comminuted proximal humerus fractures, irreparable rotator cuff tears without arthritis, and revision arthroplasty. Overall complications rate of anatomic and RTSA are reported as 10% and 16%, respectively. Glenoid component loosening, instability, and rotator cuff failure are the most common complications after ATSA, and instability, periprosthetic fracture, and infection are the most common complications after RTSA.

Keywords: Acromioclavicular arthritis; hemiarthroplasty; reverse shoulder arthroplasty; shoulder arthritis; shoulder arthroplasty

Introduction

Shoulder arthritis is a degenerative process resulting in a loss of cartilage, synovitis, and capsular thickening, which frequently reduces joint mobility. With an aging population and a trend toward a more active lifestyle, the
prevalence of symptomatic shoulder arthritis is rising. This chapter reviews and presents the current literature on presentation, evaluation, and treatment of acromioclavicular (AC) and glenohumeral (GH) arthritis.

Acromioclavicular Arthritis

The AC joint is a diarthrodial joint between the distal clavicle and acromial process. This joint is subjected to motion with hinging and translation during arm abduction and rotation around the long axis of the clavicle with forward elevation. The AC joint contains an intra-articular fibrocartilage disk which shows signs of degeneration starting in the second decade of life.¹ Radiographic AC joint narrowing is commonly seen in patients older than 60 years. Arthritis is the most common cause of pain in the AC joint and can be caused by degenerative, posttraumatic (prior AC dislocation, distal clavicle fracture or heavy lifting), septic, or inflammatory etiologies. Distal clavicle osteolysis is a distinct presentation of AC arthritis in young adults who frequently engage in overhead sports or repetitive heavy lifting.²

Presentation/Evaluation

Patients with AC arthritis generally present with pain localized to the AC joint, with occasional referred pain radiating into the trapezius, which is worse at night and aggravated by overhead and cross-body adduction activities. On examination, tenderness over the AC joint and positive provocative tests such as cross-body adduction (maximum adduction with the arm in 90° of forward flexion) or O’Brien compression test (resisted forward elevation causing pain only in internal rotation with arm in 90° of forward elevation and 10° of adduction) are highly suggestive of AC joint pathology.³ Radiographic evaluation should include a Zanca view (AP view with 10° cephalad tilt), which avoids overlapping of the clavicle and the acromion. Common radiographic findings are joint space narrowing, osteophyte formation, and possibly joint malalignment in those patients with a history of AC dislocation. While radiographic findings are frequently asymptomatic, significant bone edema on MRI has a better correlation with symptomatic AC arthritis.⁴ Despite this, the false-positive rate of MRI for true AC arthritis is reported to be as high as 82%.⁵ Therefore, clinical correlation of any imaging findings is critical.

Treatment

The first-line of treatment for AC arthritis is nonsurgical, including rest, activity modification (avoiding repetitive overhead activities and heavy lifting), anti-inflammatory medications, cortisone injections, and physical therapy. Cortisone injections are highly effective in improving patients’ pain and function in the short-term and although they commonly need to be repeated, studies show benefit for up to 5 years.⁶ When nonsurgical interventions fail, open or arthroscopic DCE can be performed. There has been a trend toward arthroscopic DCE in recent years due to presumed lower complication rate, better cosmesis, and ability to evaluate other shoulder pathologies which are present in 98% of patients with symptomatic AC arthritis.⁷ A biomechanical study demonstrated that DCE of more than 5 mm is sufficient to avoid any bony contact and resection of more than 15 mm risks causing coracoclavicular ligament incompetency.⁸ A randomized clinical trial showed adding DCE to an arthroscopic rotator cuff repair in patients with symptomatic AC arthritis did not change patient reported outcomes at minimum 2-year follow-up.⁹ This emphasizes the importance of having sound indications to perform DCE. Complications of DCE, although uncommon, include persistent pain, over resection causing instability, infection, heterotopic ossification, suprascapular nerve injury, and failure to completely address the pathology—most commonly with underresection of the posterosuperior distal clavicle.

Glenohumeral Arthritis

The glenohumeral (GH) joint is a diarthrodial, ball and socket type joint with the largest mobility of any joint in the body. GH arthritis is defined by degradation of articular cartilage and adaptations in the bone, labrum, and capsule that lead to increased joint friction and progressive loss of motion. Prevalence of GH arthritis in the general population is far less common than lower extremity weight-bearing joints. However, radiographic findings of GH arthritis are present in up to one-third of patients older than 60 years who have shoulder pain.¹⁰ Risk factors for GH arthritis include genetic predisposition, age older than 70 years, female sex, occupation (eg, repetitive, heavy manual labor), inflammatory disease, prior shoulder dislocation, fracture, osteonecrosis, infection, rotator cuff tear, certain medical conditions (eg, hemophilia), and prior surgical procedure. A classification of GH arthritis and its common etiologies are presented in Table 1. We will briefly review the common etiologies of secondary GH arthritis.

Post-traumatic

A history of major or repetitive injury to the shoulder joint has been recognized as one of the leading causes
of GH arthritis. Repetitive injury may occur from heavy manual labor or excessive weight-lifting, while major injury most commonly occurs from intra-articular fracture (proximal humerus or glenoid) with joint incongruity that ultimately leads to GH arthritis. The incidence of posttraumatic arthritis is not well defined, possible due to a lack of specific features to distinguish it from primary GH OA if malunion is not present and slow progression of the disease. In addition to potential joint incongruity after healing, proximal humerus or intra-articular glenoid fractures may be associated with full-thickness cartilage loss that contributes to the development of long-term arthritic changes.

Table 1 Classification of Glenohumeral (GH) Arthritis Etiology

Type		Etiology
Primary		Idiopathic
Secondary
	Posttraumatic	Proximal humerus fracture Dislocation/recurrent instability Microtrauma (manual labor, heavy lifting)
	Inflammatory	Crystal induced Rheumatoid arthritis (RA) Systemic lupus erythematous (SLE) Seronegative osteoarthropathies
	Postsurgical	Capsulorrhaphy Rotator cuff repair Intra-articular hardware
	Osteonecrosis	Corticosteroids Alcohol Chemo/radiation Sickle cell disease Metabolic disease (eg, Gaucher disease) Malignancy (eg, multiple myeloma) Trauma/dislocation
	Septic	Acute purulent infection Chronic indolent infection
	Cuff arthropathy	Massive rotator cuff tear
	Neuropathic arthropathy	Syringomyelia Diabetes mellitus
	Other	Arthropathy of hemophilia Chondrolysis from intra-articular pain pump

Inflammatory Arthritis

Rheumatoid arthritis (RA) is the most common inflammatory arthritis of the shoulder joint. RA affects 1% to 3% of the general population and is characterized by progressive joint destruction. The common features of RA and other inflammatory arthropathies (psoriatic arthritis, ankylosing spondylitis, etc.) include osteopenia, absence of typical osteoarthritic osteophytes, bipolar cystic changes, and joint space narrowing with joint line medialization from glenoid erosion in advanced phases of the disease.¹¹ The inflammatory changes can also lead to rotator cuff tendon attenuation and muscle atrophy. Widespread use of disease modifying agents have revolutionized the medical treatment of RA and other inflammatory arthropathies, helping patients to live with lower disease burden. Crystal induced arthropathies also fall under the category of inflammatory arthritis and are commonly reported in middle to advanced-age patients and are associated with poor kidney function or use of medications that affect production or excretion of uric acid in the body. Deposition of calcium hydroxyapatite (Milwaukee shoulder), calcium pyrophosphates (pseudogout), or monosodium urate monohydrate (goat) crystals into the joint results in an intense inflammatory reaction that can cause destructive GH arthritis. Milwaukee shoulder affects elderly women and has features of a rapidly progressive cuff tear arthropathy.¹²

Instability Arthropathy and Capsulorrhaphy Arthropathy

Neer identified shoulder dislocation as a cause of shoulder arthritis originally in 1982,¹³ and later the term “dislocation arthropathy” was coined and linked to chronic recurrent instability. Marx et al reported a 10-fold increase in the risk of developing GH arthritis requiring shoulder arthroplasty in patients who had a history of prior shoulder dislocation.¹⁴ Hovelius and Saeboe followed 223 patients with anterior dislocation for 25 years and reported age more than 25 years at the time of dislocation, high-energy sport, and alcohol use were linked to development of GH arthritis.¹⁵ Besides dislocation itself, surgical treatment of instability can also lead to arthritic changes. Rapid loss of cartilage has been observed after arthroscopy and is referred to as postarthroscopic glenohumeral chondrolysis (PAGCL).¹⁶ Overtightening of the anterior capsule
and possible excessive compression on the cartilage have been implicated in development of this complication. More commonly over the long term, overtightening of the anterior capsule can lead to contracture and abnormal GH mechanics that cause capsulorrhaphy arthropathy. The degenerative changes of capsulorrhaphy arthropathy are characterized by GH arthritis with eccentric posterior glenoid wear and posterior subluxation of the humeral head if the anterior capsule was overtightened. Prominent intra-articular hardware from surgical treatment (screws or anchors) can also cause cartilage destruction that leads to GH arthritis.¹⁷

Osteonecrosis of the Humeral Head

The humeral head is the second most common site for developing osteonecrosis in the body after the femoral head, but it is a relatively uncommon cause of GH arthritis. Osteonecrosis has a multifactorial etiology that leads to loss of blood supply to the humeral head and ultimately necrosis and articular collapse. Atraumatic osteonecrosis can be idiopathic or secondary to sickle cell disease, systemic lupus erythematosus, corticosteroid use, chemotherapy, alcohol use, and Caisson disease.¹⁸ Traumatic osteonecrosis most commonly occurs following proximal humerus fractures but can also happen after shoulder dislocation or surgical fixation. Osteonecrosis is reported after zero to 34% of three-and four-part proximal humerus fractures and with a higher rate after surgical fixation of these fractures.¹⁹ Hertel et al identified anatomic neck involvement, posteromedial metaphyseal extension of greater than 8 mm, and a disrupted medial hinge as prognostic factors for ischemia in proximal humerus fractures treated with open reduction and internal fixation.²⁰ Treatment of osteonecrosis depends on the disease stage and extent of humeral head collapse and involves nonsurgical management or arthroscopic débridement with core decompression for early stages without humeral head collapse, versus shoulder arthroplasty for more advanced stages of the disease with humeral head collapse. A resurfacing or standard hemiarthroplasty can be performed when collapse is present based on the extent of necrosis, with the goal of removing all of the necrotic bone with the implant. If arthritic changes also develop on the glenoid, TSA should be performed.

Rotator Cuff Tear Arthropathy

Rotator cuff tear arthropathy is defined as a constellation of soft tissue (eg, rotator cuff muscle atrophy and fatty infiltration) and bony (eg, femoralization of the humeral head and acetabulization of the acromial arch) adaptations that develop in response to a long-standing rotator cuff tear.²¹ When the rotator cuff no longer provides dynamic stabilization of the humeral head in a large or massive rotator cuff tear and the GH joint cannot function as a stable fulcrum, the humeral head migrates upward, contacting the undersurface of the acromion and ultimately leading to the above-mentioned bony changes. The term cuff tear arthropathy was coined by Neer in 1983, and it was used to describe the end result of a chronic massive rotator cuff tear.²²

Other Forms of Secondary Glenohumeral Arthritis

Neuropathic (Charcot) arthropathy can results in unexplained and severe joint destruction which is thought to be due to loss of protective and proprioceptive sensation of the GH joint. These patients should undergo evaluation for underlying diabetes mellitus or a syringomyelia of the cervicothoracic spine. Hemophilia is a rare inherited bleeding disorder that results in spontaneous bleeding into the joints and commonly affects the knee, ankle, elbow, and shoulder.²³ Recurrent intra-articular bleeding results in hemophilic arthropathy which involves synovial hyperplasia, fibrosis, and precipitation of iron product within the synovium in the first two decades of life. The use of continuous intra-articular pain pumps was found to be associated with a rapidly progressive GH arthritis that had features of PAGCL and was linked to the cytotoxic effect of bupivacaine analgesic on chondrocytes.²⁴ Since this discovery, the use of pain pumps has been abandoned, and evidence has shown that even a single injection of bupivacaine can result in reduction of chondrocyte cell population.

Presentation/Evaluation

Primary GH osteoarthritis commonly presents with activity-related joint pain which can radiate posteriorly with associated crepitus and a catching sensation with certain movements. With disease progression, patients usually report morning pain and stiffness and difficulty sleeping on the affected side. Surgeons should obtain information about the nature and pattern of pain, its location and relation to movement and sleep, timing of symptoms, comorbidities, and prior treatment including medications, cortisone injection, physical therapy, or surgeries.

On physical examination, the shoulder is inspected for any asymmetry, muscle atrophy (deltoid and posterior rotator cuff muscles), swelling or joint effusion, and the location of scars from prior surgeries should be noted. The examiner should palpate the AC joint, bicipital groove, and the anterior and posterior GH
joint line for signs of tenderness. Active and passive range of motion (ROM) are tested to assess stiffness in all planes and should be compared with the contralateral side, which may also not be normal. Patients with cuff tear arthropathy can develop loss of the stable fulcrum of the GH joint with superior migration of the humeral head and loss of containment of the humeral head within the coracoacromial arch, leading to the examination findings of “anterosuperior escape,” in which the humeral head becomes prominent anterosuperiorly with attempted active shoulder elevation, and “pseudoparalysis,” in which active shoulder elevation is limited despite full passive shoulder ROM and intact neuromuscular function. Neurovascular status of the extremity including normal distal pulses and motor and sensory function of the axillary (by firing of all three heads of the deltoid muscle), median, ulnar, radial and, musculocutaneous nerves should be documented.

Imaging

Radiography

Initial imaging studies for GH arthritis should at minimum include true AP (Grashey view) and axillary views. Plain radiographs provide information about the type and severity of GH arthritis based on the degree of joint space narrowing, size and location of osteophytes, morphology of the glenoid, humeral head subluxation in any plane, and presence of calcifications, loose bodies, or implant/hardware from prior surgeries. Primary osteoarthritis typically demonstrates prominent osteophyte formation in advanced cases (Figure 1A). Surgeons should also take note of the overall bone quality, size of the intramedullary canal, and presence of an os acromiale or acromial erosion/stress fracture as they will have implications for surgical planning. Cuff tear arthropathy usually presents with GH arthritis and superior humeral head migration that in severe and long-standing arthritic cases results in AC arch erosion with concave deformity of the acromial undersurface known as “acetabulization” and rounding off of the greater tuberosity or “femoralization” of the proximal humerus (Figure 1B). Inflammatory arthritis can present in advanced cases with osteopenia, lack of osteophyte formation, cystic changes, central glenoid erosion, and joint line medialization (Figure 1C). The quality of plain radiographs is subjected to wide variation based on technique, patients’ body habitus, and positioning of the shoulder relative to the radiograph beam. Measurements done on plain radiograph show 10% to 50% variation with only a 20° change in the angle of the radiograph beam.²⁵ Several studies have documented limitations of two-dimensional radiograph imaging in assessment of glenoid version, morphology, and quantifying the degree of glenoid bone loss.²⁶

CT Scan

CT is a commonly utilized advanced imaging tool for evaluation of GH arthritis. CT allows for better assessment of glenoid version, inclination, morphology, and bone loss than plain radiographs and is commonly used for planning prior to shoulder arthroplasty. To achieve the best accuracy, CT images should be reconstructed in the scapular plane.²⁷

Walch et al²⁸ used CT to classify glenoid morphology in primary GH osteoarthritis based on the pattern of glenoid wear and the subluxation of the humeral head relative to the scapular axis on the axial cuts (Figure 2A). Type A (59%) shows a well-centered humeral head with no subluxation and symmetric central glenoid wear, type B (32%) presents with posterior humeral head subluxation and posterior glenoid wear, and type C (9%) is a dysplastic glenoid with more than 25° of retroversion. Type A and B were further categorized as A1 and B1 if bony erosion was mild and A2 and B2 (biconcave) if bony erosion was advanced. Studies showed only fair interobserver reliability of the original Walch classification.²⁹ The classification was updated in 2016 by adding a type B3 glenoid with a monoconcave and posteriorly worn glenoid and a type D glenoid with anterior humeral head subluxation or glenoid anteversion (Figure 2B).³⁰ They demonstrated that both inter- and intraobserver reliability improved with the modified classification. Further modification of the Walch classification has included the addition of a C2 glenoid, in which a dysplastic C glenoid develops biconcavity from posterior glenoid wear.³¹ It has been shown that the Walch classification has value in predicting natural history of GH osteoarthritis with A1 glenoids rarely developing posterior glenoid wear.³² Also, surgical reconstruction of a glenoid with significant posterior glenoid bone loss can be technically challenging and ATSA without augmented glenoid components in these patients may have a less reliable outcome.³³

Goutallier et al used CT to classify fatty infiltration of the rotator cuff muscles based on axial cuts as a surrogate for rotator cuff integrity and function.³⁴ Although the role of rotator cuff fatty infiltration in shoulder arthroplasty is not well understood, there are data to suggest that fatty infiltration negatively impacts patients’ postoperative ROM and functional outcome.³⁵

Figure 1 Radiographic appearance of glenohumeral (GH) arthritis. A, AP and axillary radiographs of primary GH arthritis with joint space narrowing and large osteophyte formation. In this particular case, the glenoid has B2 (biconcave) morphology with posterior glenoid wear. B, AP and axillary radiographs of cuff tear arthropathy with superior humeral head migration, anterosuperior glenoid wear, acetabularization of the acromion, and femoralization of the greater tuberosity. C, AP and axillary radiographs of inflammatory arthritis with joint space narrowing, minimal osteophyte formation, central glenoid erosion, and joint line medialization. D, AP and axillary radiographs and MRI of a steroid induced osteonecrosis of the humeral head with no collapse of the subchondral plate. E, AP and axillary radiographs of GH arthritis in a patient with a prior history of instability who underwent both arthroscopic and open anterior capsulorrhaphy. The axillary radiograph shows eccentric posterior glenoid wear and posterior subluxation of the humeral head that develops as a consequence of the anterior capsule being overtightened.

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