Glenohumeral osteoarthritis (OA) is a common musculoskeletal condition in the aging population. It is classified as a degenerative disorder of the shoulder. Although OA is diagnosed less often in the shoulder than in weight-bearing joints such as the knee or hip, approximately 20% of older adults experiences shoulder OA.1,2 In the case of primary glenohumeral osteoarthritis (OA not due to trauma) women and patients older than 60 are more commonly affected.3
As the baby boomers age, clinicians may be faced with a parallel increase in the prevalence of shoulder pain due to osteoarthritic changes. Studies show that the number of hemiarthroplasties and total shoulder arthroplasties has increased substantially over the past decade, with approximately 10,000 shoulder arthroplasties in 1990 and 20,000 in 2000. In 2008, approximately 27,000 total shoulder arthroplasties and 20,000 hemiarthroplasties were performed; more than 43% of the patients had a primary diagnosis of osteoarthritis.4
It is imperative that clinicians recognize the signs of early changes in glenohumeral OA, so that they can act to reduce pain and morbidity for patients and decrease healthcare costs by delaying the need for surgical treatments.5
Glenohumeral osteoarthritis can be classified as primary or secondary. Primary OA is diagnosed in patients who have no predisposing risk factors that could lead to joint failure, meaning OA could be due to advancing age alone. Secondary OA includes changes associated with predisposing risk factors such as age older than 60, previous rotator cuff tear, systemic arthritis, congenital malformation, repetitive use, previous fractures of the joint surface, or recurrent shoulder dislocations.6,7 Other risk factors include obesity, female gender, genetic predisposition, chronic or repetitive use of the joint, joint infection, and occupations that require heavy lifting or overhead sports. As the population ages, the prevalence of shoulder osteoarthritis increases.8
Shoulder pain can develop over time due to failure of the joint's protective structures. These structures include the joint capsule and its ligaments, muscles and underlying bone. Synovial fluid that surrounds the glenohumeral joint reduces friction and minimizes shear stress during motion between articulating cartilage surfaces, which begins to degrade as a result of overactivity or previous injury.
Once this occurs, pathologic changes within the cartilage arise due to friction-induced cartilage wear, which is the earliest change associated with OA.9 Over time, the cartilage forms focal lesions that extend into the underlying bone and activate osteoclasts and osteoblasts in the subchondral bony surface. This activation causes an increase in subchondral bone thickness and leads to a narrowing of joint space and further loss of shoulder rotation. In more progressive forms of OA, osteophytes develop at the marginal surface of the joint, near areas of cartilage loss, and are a hallmark sign of OA on radiographs.9
Signs and Symptoms
The most common presenting complaint associated with glenohumeral OA is pain in the posterior shoulder. This pain is characterized as gradual and progressive, and it becomes worse with activity and is alleviated with rest.10 In the early stage, glenohumeral OA may present as mild pain with an unremarkable physical exam. As the disease progresses, the following signs and symptoms may be present: morning stiffness that subsides within 30 minutes; proximal muscle weakness; decreased range of motion (ROM) most often noted on external rotation and abduction; pain with passive movement (particularly on internal rotation); and/or painful crepitus with arm motion.8,11
During the physical examination, the patient with glenohumeral OA shows signs of pain when the examiner palpates over the glenohumeral joint, most notably in the posterior glenohumeral joint space. In the advanced stage, nighttime pain and stiffness may interfere with sleep and the patient may lose function in the affected joint.11
The physical examination should assess shoulder appearance, tenderness to palpation, strength, neurovascular status, and both active and passive range of motion. Because the shoulder joint has the largest ROM, it is important to assess the patient's active and passive ROM to exclude other possible causes of shoulder pain.
Motion testing includes active ROM with the shoulder in forward elevation (flexion), abduction, external rotation and internal rotation. These motions should then be performed passively by the provider.8,12
The physical examination should identify where the pain is localized and whether the tenderness is over the joint line or just distal to it.9 Special tests such as Neer's impingement sign, Hawkins impingement sign and the apprehension test should also be included to rule out possible impingement syndrome or rotator cuff disease.
Diagnosing Glenohumeral OA
Diagnosis of glenohumeral OA can be made based on a thorough history, physical examination and radiographic imaging. The history should include questions about the patient's occupation, hobbies and daily activities, since these may contribute to chronic wear and tear of the shoulder joint. Possible risk factors are age, sex, body habitus, previous injuries, infections or surgery to the shoulder.9
Imaging is a necessary diagnostic tool for detecting glenohumeral OA. The initial choice is radiographic imaging of the shoulder in three views: axillary, anteroposterior (AP) and impingement. In the early stage of disease, radiography will show mild narrowing of the glenohumeral joint space, small osteophytes, subchondral sclerosis, cysts and eburnation or advanced articular cartilage loss.7,8 Axial and AP views allow better visualization of joint space narrowing.8 However, an unremarkable radiograph does not rule out the presence of OA (see image).
If further imaging is needed, computed tomography arthrograms are used to identify any osseous structural abnormalities, such as the humeral head and glenoid, and to assist surgeons in determining which surgical approach may be needed. Magnetic resonance arthrography is a better imaging study for soft tissue abnormalities in the shoulder. It allows better visualization of subtle changes in articular cartilage, pathology of the rotator cuff, glenohumeral ligaments, and subchondral edema.12,13
X-ray of a 74-year-old woman with mild osteoarthritis of the left shoulder with marginal osteophytes. There are small subchondral cysts within the lateral humeral head, mild degenerative changes at the glenohumeral joint and acromioclavicular joint, with small spurs from the lateral acromion. Image courtesy the author .
Because these imaging studies may be inconclusive for chondral lesions and injury, the gold standard for diagnosing glenohumeral OA is arthroscopy. This may be needed when noninvasive imaging and conservative treatment fail to produce a conclusive diagnosis.13
Laboratory testing is not useful in diagnosing glenohumeral osteoarthritis, only for ruling out other possible causes of shoulder pain, such as rheumatoid arthritis, gout or infection that can mimic osteoarthritis.
For glenohumeral OA, the main goals of treatment are pain control and the restoration of function.11 The course of treatment depends on the progression of the disease, how it is affecting the patient's quality of life, and adherence. Radiography is one way to assess the best option for treatment. For patients with mild joint changes and less pain, the initial approach of physical therapy in conjunction with over-the-counter analgesics or anti-inflammatory medication may be all that is needed. Physical therapy should include strength training exercises as well as aerobic exercises to increase ROM and alleviate symptoms.
Many studies have suggested that acetaminophen should be the initial drug of choice when treating OA because it has less toxic effects on the body.11,12 The recommended dose of acetaminophen is 1 g by mouth four times daily (patient should not exceed 4 g daily). For patients who do not respond to acetaminophen, NSAIDs (e.g. ibuprofen, fenoprophen, naproxen, diclofenac) may provide relief. NSAIDs are a mainstay treatment for OA, but patients should be cautioned about long-term use due to their side effects (gastrointestinal irritation, gastric ulcers or renal failure). Alternative analgesics include tramadol, topical NSAIDs such as diclofenac gel 1%, or a COX-2 inhibitor such as celecoxib.11,14
As the disease progresses, patients may no longer respond to medication. When pain is not well managed with physical therapy and medication alone, a corticosteroid injection into the affected glenohumeral joint may be warranted to reduce pain and swelling within the joint. A variety of techniques may be used to inject the glenohumeral joint (anterior, posterior or superior approaches); the anterior approach is chosen most often.15 Possible injection combinations include 5 mL to 7 mL of 1% lidocaine/1 mL to 2 mL betamethasone sodium phosphate and acetate or 0.25% or 0.5% bupivacaine/ 1 mL to 2 mL methylprednisolone, 40 mg/mL.15 Corticosteroid injections are used for short-term relief from pain and usually last 4 to 8 weeks; no more than four injections should be given per year.16
Surgical treatment is reserved for patients who do not respond to conservative therapies. Arthroscopy is an appropriate option for patients in the early stage of disease who have not experienced sufficient symptom improvement with nonsurgical treatment or have no desire for joint replacement.11 Depending on the pathologic cause of pain, an arthroscopic procedure can provide treatment or pain relief by lavage, debridement of degenerative labral tears and chondral lesions, loose body removal, and partial synovectomy and osteophytectomy.3 Arthroscopic debridement can not only improve pain, but also restore range of motion and shoulder function, research shows.
For the most advanced cases of glenohumeral OA, a shoulder arthroplasty may be recommended. Indications for shoulder arthroplasty include: loss of function that is unresponsive to conservative treatment; end-stage rotator cuff tear arthropathy; osteonecrosis; and a previously failed joint-sparing surgery or total shoulder arthroplasty.8 Today, two procedural options are used most often for shoulder arthroplasty: hemiarthroplasty, which entails replacement of the humerus only, and total shoulder arthroplasty, which involves replacing the glenoid and humerus.8 These procedures are not recommended for patients younger than 45. This is because younger patients are likely to lead more active lifestyles that will necessitate the need for more for revisions during their lifetime.2 With each revision comes more risk of surgical complications, hardware failure and infection. These interventions are also contraindicated in patients with osteonecrosis of the joint, irreparable shoulder instability, paralysis of proximal muscles, infection or poor medical status.8
Severity Influences Outcome
Glenohumeral osteoarthritis is a progressive and chronic disease. Its prognosis depends on the severity of the disease and the amount of degeneration the glenohumeral joint has undergone. Although the effects of OA on the glenohumeral joint cannot be reversed with treatment, the progression of the disease may be slowed. Mild to moderate degenerative changes may not affect a patient's functioning or quality of life and may improve with conservative treatment alone.8,11
For patients in the most advanced stage of disease, loss of function may be their greatest concern. Glenohumeral OA is not a systemic or fatal disease, but due to the loss of function and decreased quality of life, patients may experience depression, anxiety, limitation of activities and decreased job performance that could lead to termination of employment. For patients with severe glenohumeral OA, joint replacement may be their only option for relief.8,11
Janna L. Brown is a student in the physician assistant program at Georgia Regents University in Augusta. She has completed a disclosure statement and reports no relationships related to this article.
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