Musculoskeletal disorders have had a significant impact on the world’s population. Arthritis and chronic joint symptoms affect one of three adults, which is why it is the most widespread disease in America. The prevalence of arthritis for all joints is higher in whites, men older than 45 years, women older than 55 years, overweight and inactive persons, and persons with less than eight years of education (Millett et al., 2008). Nearly 60% of those affected by osteoarthritis are older than 65 years, and the incidence is increasing (Millett et al.). Shoulder OA is not as common as other joint OA, but it is just as debilitating. The loss of shoulder function can lead to a variety of conditions, including depression, anxiety, activity limitations, and job-performance problems. The causes of shoulder OA can be classified into primary and secondary causes. Primary OA does not have a specific cause but is more prevalent and is not isolated to only older Evaluation of shoulder OA A shoulder OA diagnosis involves a specific set of symptoms, physical examination findings, and changes to the bone, which are visible by imaging. The typical presenting symptoms are progressive activity-related pain often described as being deep in the joint and often is localized to the posterior aspect of the shoulder. As the disease progresses, the patient may complain of pain at rest and disruption of sleep because of pain. In the advanced cases, the stiffness creates functional limitations. In younger patients, a history of prior trauma, dislocation, or previous surgery for shoulder instability may be reported and are all factors associated with the development of osteoarthritis. Patients in the early stages of this disease may complain of mild pain and may have an unremarkable examination. Radiography may show only subtle changes to the bone until the disease progresses and there is destruction that is more advanced. The only objective evidence of the disease is articular cartilage wear, which may be shown on a magnetic resonance image (MRI). Physical examination of a patient with shoulder OA will reveal painful crepitus, joint enlargement, and swelling. In more severe cases, audible and palpable grinding may occur when a mechanical stress is placed on the shoulder. During the evaluation, it is important to exclude other shoulder pathologies that cause pain besides OA. ● Pain not induced by joint palpation or passive range of motion (PROM) is more suggestive of bursitis, rotator cuff disease, or biceps tendinitis. ● Loss of PROM and active range of motion (AROM) can also occur with calcific tendinitis or idiopathic adhesive capsulitis.
individuals. Secondary OA has a known cause or a predisposing factor, such as major shoulder trauma, chronic dislocations, infection, congenital malformation, or chronic rotator cuff tear (Millett et al., 2008). Secondary atraumatic osteonecrosis may be caused by excessive alcohol consumption, corticosteroid therapy, cytotoxic drugs, Gaucher’s disease, lipid metabolism disorders, obesity, radiation, or sickle cell disease. Postinflammatory secondary OA may be caused by crystal arthropathies, postinfection arthritis, rheumatoid arthritis, or rotator cuff arthropathy. Postsurgical causes of secondary OA include capsulorrhaphy arthropathy, intra-articular hardware, and an overtightened anterior joint capsule. Post-traumatic causes include dislocation, malunion of the proximal humerus, post-traumatic avascular necrosis, and shoulder subluxation. ● Morning stiffness may more likely indicate rheumatoid arthritis. ● Joint effusion may indicate OA, rheumatoid arthritis, or septic arthritis. ● Pain at night may indicate rotator cuff disease. ● Pain or a “clunking” sound with overhead motion may indicate a labral disorder. ● Pain that radiates down the arm may be caused by cervical disc disease. ● Upon physical examination, if there is shoulder joint line tenderness, this is more likely to indicate shoulder OA. ● Warmth and erythema of the joint is more likely to indicate septic or rheumatoid arthritis. ● Decreased ROM, specifically external rotation and abduction, indicates shoulder OA or a soft tissue injury or frozen shoulder. ● Crepitus can be a sign of shoulder OA or rheumatoid arthritis. ● Decreased cervical ROM usually provides information about a cervical disk disease. ● Radiographic imaging can also help in the differential diagnosis of shoulder OA. ● Joint space narrowing can indicate cuff-tear arthropathy, OA, or rheumatoid arthritis. ● Marginal joint erosions generally point to rheumatoid arthritis. ● A normal joint on radiographic imaging is generally part of the diagnosis of either frozen shoulder or septic arthritis. ● An osteophyte or subchondral sclerosis generally indicates shoulder OA when seen on imaging.
TREATMENT STRATEGIES FOR SHOULDER OA
Nonsurgical treatment No known interventions can alter the natural history of early osteoarthritis, but there are treatments that can control pain and restore function. The initial approach to treatment of shoulder osteoarthritis begins with activity modification, rest, and ice. Physical therapy interventions can help control pain and restore function, which include strength training and aerobic exercises to help alleviate symptoms. Acetaminophen can be used to manage pain, and nutritional supplements, such as glucosamine and chondroitin, can be used as alternatives to acetaminophen— although only anecdotal evidence supports their use for shoulder osteoarthritis. Other pharmacotherapy for degenerative joint disease includes nonselective and selective cyclooxygenase-2 (COX-2) inhibitors or nonsteriodal anti-inflammatory drugs (NSAIDS). Nonselective COX-2 inhibitors—including ibuprofen, diclofenac, naproxen, and selective COX-2 inhibitors—have been effective in alleviating symptoms of osteoarthritis—but they can also have side effects.
The definition of failure of conservative treatment of shoulder OA varies from surgeon to surgeon. Nonsurgical management for the treatment of shoulder OA information is limited in the literature. Comprehensive conservative management of shoulder OA can produce satisfactory midterm outcomes in unilateral shoulder OA patients according to one study. Nonsurgical management of shoulder OA can temporarily relieve symptoms; however, it will not alter the natural history of shoulder OA or shoulder joint degeneration and can have unsatisfactory results. Nonpharmacologic measures, such as aerobic exercise and strengthening, are not proven successful for shoulder OA. One study showed that acetaminophen was more effective than placebo in pain reduction but less effective than NSAIDS. Pharmacological results have shown that newer COX-2 selective inhibitors are not more effective than NSAIDS are for treating knee and hip OA. Another study showed that COX-2 inhibitors caused fewer gastrointestinal problems than NSAIDS did. More
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