ABSTRACT: Glenohumeral joint osteoarthritis may result from trauma, concomitant shoulder pathology, or crystal deposition disease, or it may have no discernible cause. The physical examination reveals muscular atrophy, abnormalities during palpation, and limited range of motion, particularly in external rotation and flexion. Treatment includes both nonpharmacologic and pharmacologic interventions. Nonpharmacologic strategies include patient education, activity modification, and structured rehabilitation followed by transition to a long-term home exercise program. Pharmacologic treatment may involve progressively potent oral analgesics and perhaps corticosteroid injections. Surgical procedures, such as shoulder arthroplasty and arthroscopic debridement, are indicated for intractable pain and loss of function.
Shoulder pain may result from a variety of specific acute, traumatic events or overuse activities. However, it is not uncommon for a patient to present with shoulder pain that is unrelated to a specific injury.
Because many activities of daily living involve the use of the shoulder, proper diagnosis and treatment of shoulder pain is necessary for improved function and health. Determining the causes and precipitating factors of shoulder pain helps guide treatment and maximize functional ability.
Glenohumeral joint osteoarthritis (GHJOA) should be included in the differential diagnosis of shoulder pain and loss of function; however, it is often overlooked because subacromial bursitis/rotator cuff tendinitis is much more common. Although pain, decreased range of motion (ROM), and loss of function are common to both disorders, the prognosis and treatment are different.
In this article, we review the causes of GHJOA and offer guidelines on diagnosis and management.
Shoulder pain is a common complaint in primary care. In one study, 46% of patients seen in a primary care practice had at least one episode of shoulder pain during the course of a year.1 Another study found that the prevalence of shoulder pain was 45% and the incidence was 8% in a group of workers engaged in repetitive activities.2
GHJOA can be classified as primary or secondary. Primary GHJOA, which has no specific cause, is more common in women and in persons older than 60 years.3 The disorder is believed to develop in part from many years of overuse that eventually contribute to symptomatic wear and tear of the articular cartilage between the head of the humerus and the glenoid fossa of the scapula. Primary GHJOA is believed to be far less common than primary osteoarthritis (OA) in weight-bearing joints, such as the knee and hip.
Secondary GHJOA, which occurs much more frequently than the primary form, usually results from trauma, concomitant intrinsic shoulder pathology, or crystal deposition disease. Because there can be significant overlap among these processes, a single cause often cannot be discerned. All of these conditions cause GHJOA by disrupting the spherically congruent articular surfaces of the humeral head and the glenoid labrum, which results in an abnormal load distribution across the glenohumeral joint.4
Trauma. One major traumatic event is sometimes sufficient to cause significant degenerative changes in the glenohumeral joint. Trauma can take the form of a shoulder dislocation with or without involvement of thehumeral head and/or fracture of the bony labrum, proximal humeral fractures, and rotator cuff tear. For example, in one study, approximately 20% of patients who sustained an anterior shoulder dislocation had mild to severe degenerative joint changes during the subsequent 10-year period.5 These changes occurred equally in shoulders with one dislocation recurrence and in shoulders with recurrent instability. Degenerative articular changes may also occur after malunion of comminuted and displaced fractures of the proximal humerus.6
Rotator cuff arthropathy may develop in patients with a traumatic rotator cuff tear. This condition is particularly common in elderly women. The mechanism of joint destruction is thought to include both mechanical and nutritional alterations in the shoulder. When a macroscopic rotator cuff tear occurs, there is loss of stabilization of the humeral head, which allows for superior subluxation of the humeral head and narrowing of the acromiohumeral interval.7 Articular cartilage nutrition is compromised because of synovial fluid leakage and joint immobility. The result is articular cartilage degeneration and subchondral osteoporosis. In a study of cadaveric shoulder joints, articular degeneration was almost twice as frequent in joints with macroscopic rotator cuff tears as in those without tears.8
Concomitant shoulder pathology. In one study, the incidence of primary GHJOA with concomitant shoulder pathology was 4.6%.3 The incidence increased with age; it was 8.7% in patients older than 80 years.
Crystal deposition disease. This entity, also known as Milwaukee shoulder syndrome, is a crystalline-induced arthropathy in which inflammatory mediators progressively destroy periarticular glenohumeral joint tissue, including the rotator cuff. The appearance of hydroxyapatite crystals in synovial fluid is believed to lead to the production of detrimental inflammatory mediators, such as active collagenase and neutral proteinase. The clinical features of crystal deposition disease are identical to those of rotator cuff tear arthropathy. It is still unclear whether a rotator cuff defect develops first and abnormal joint mechanics then cause crystals to appear in the synovial fluid, or whether hydroxyapatite crystals appear first in the subsynovial layers and generate the cytokines that lead to a rotator cuff tear.9
History. Consider GHJOA in patients who present with shoulder pain, particularly if the pain is localized to the posterior shoulder region and is accompanied by tenderness in the upper arm. Patients sometimes report a history of shoulder region trauma or large rotator cuff tear.
As is often the case with OA in other parts of the body, the pain is typically described as constant, dull, vague, and diffuse; it is aggravated by activity and relieved by rest. Stiffness on waking, weakness, and fatigue are also common. Patients sometimes complain of instability. Symptoms usually develop gradually and worsen progressively. Night pain, which may develop eventually, makes sleeping difficult. In later stages of the disease, the pain may not respond to activity modification, oral analgesics, or physical therapy. Symptoms may be present for months to years.10,11
Patients may report a gradual decrease in glenohumeral joint ROM; the most profound effects are loss of forward flexion and external rotation because of contraction of the anterior capsule, which causes posterior subluxation of the humeral head into the glenoid labrum. As a result, patients may report difficulty in reaching overhead, placing objects on shelves, and combing their hair.4 Muscular weakness attributable to disuse atrophy because of pain and stiffness often ensues.
Examination. Physical examination abnormalities are listed in Table 1.A thorough evaluation of the neck, shoulder, and thorax is warranted in all patients who present with shoulder pain. Examination of the shoulder involves inspection, palpation, active and passive ROM testing, manual muscle testing, specialized test maneuvers, and neurovascular assessment. The uninvolved shoulder can serve as a baseline for comparison during examination.
In patients with GHJOA, inspection may reveal disuse muscular atrophy that manifests as mild flattening of the deltoid, especially anteriorly; it can also be seen laterally and posteriorly. Have the patient place his or her hands on the hips to facilitate comparison of shoulders for asymmetry and to better visualize muscular atrophy.
Palpation may reveal anterior glenohumeral joint line tenderness just below the coracoid process and, occasionally, mild anterior joint swelling. Crepitus may be noted during active and passive ROM. Glenohumeral crepitus is best palpated along the posterior aspect of the humeral head below the angle of the acromion as the adducted arm is rotated.
Complete evaluation of shoulder ROM includes forward flexion, external rotation, internal rotation, abduction, and cross-body adduction. Assess active ROM before passive ROM to avoid potential injury. Asynchronous glenohumeral movement may be observed when assessing active ROM of both arms simultaneously. In addition to painful restricted ROM, patients also manifest end point stiffness. Contractures and adhesions may result in additional stiffness and loss of motion in several planes of shoulder movement.4
Provocative maneuvers are helpful in detecting other potential pain generators in patients with GHJOA. The Neer and Hawkins-Kennedy tests may help detect impingement of the supraspinatus tendon. Note that the Neer test can be difficult to interpret because it requires at least 140 degrees of forward flexion for validity. Many patients with GHJOA cannot achieve this. Furthermore, patients experience pain with this maneuver because of the OA per se, rather than as a result of subacromial impingement. Patients with GHJOA usually have exaggerated impingement signs as a result of narrowing of the joint space, bony irregularities of the glenoid fossa, and spurring of the humeral head. Manual muscle testing of the rotator cuff muscles is necessary to assess the degree of shoulder stabilization that these muscles are capable of providing.
Imaging studies. Plain radiographs are generally necessary to confirm the diagnosis. Radiographs can also help assess disease severity.11
Complete radiographic evaluation of the glenohumeral joint includes a true anteroposterior (AP) (Grashey) view, as well as an axillary view of the shoulder.12 The true AP view is taken within the plane of the scapula, which is approximately 30 degrees oblique to the coronal plane of the body. The resulting radiograph presents a true AP projection of the shoulder girdle, with the glenoid labrum seen in profile and the glenohumeral joint space open in a nonpathologic shoulder. This view is necessary to accurately gauge the degree of joint-space narrowing; the glenohumeral joint space is obscured in a routine AP shoulder position because the shoulder girdle is in an oblique orientation (Figure 1).12 An axillary view is required to assess posterior subluxation and glenoid wear as well as joint-space narrowing.11 A summary of radiographic findings in GHJOA is listed in Table 2.11 Typical true AP and axillary view radiographs of a patient with GHJOA are shown in Figures 2 and 3.
If you suspect GHJOA, order a degenerative shoulder radiographic series if available, or specify that GHJOA is to be ruled out. GHJOA may be missed if the patient undergoes only traditional AP and lateral radiography.
Neither CT nor MRI is usually needed to detect GHJOA. However, CT is useful in preoperative planning to analyze posterior glenoid wear. MRI helps evaluate possible concomitant soft tissue pathology, especially that which involves the rotator cuff.
When more than one radiographic area of pathology is found, a diagnostic intra-articular glenohumeral joint injection of local anesthetic may help confirm that a structural lesion in the glenohumeral joint is the primary pain generator. Nonfluoroscopic and fluoroscopic-guided injection techniques have been described for the glenohumeral joint, using either an anterior or posterior approach (Figure 4).13 Fluoroscopic guidance assures injection accuracy. Referral to a specialist in musculoskeletal medicine (such as a physiatrist) who has extensive experience with fluoroscopic-guided injection procedures may be warranted.
The goals of treatment are to reduce pain and improve function. Because there is wide variability in presentation, therapy must often be individualized.4 Initial treatment generally consists of a combination of nonpharmacologic and pharmacologic modalities (Table 3). Pharmacologic agents are thought to be most successful when used in conjunction with nonpharmacologic treatment.11
Nonpharmacologic interventions-including patient education, activity modification, and rehabilitation-are the foundation of effective management of OA. Although patient education for GHJOA has not been systematically studied, it is generally regarded as an effective intervention for hip and knee OA.14 The goals of activity modification are to avoid large stress loads across the glenohumeral joint and to limit repetitive overhead activity.15 A comprehensive rehabilitation program can be guided by a physiatrist, who can order and monitor physical therapy and ultimately transition the patient to a home exercise program. The rehabilitation program should focus on the restoration of endurance, flexibility, and strength of the shoulder-girdle muscles. Strengthening of these muscle groups helps reduce associated shoulder instability and/or impingement. The restoration of normal movement patterns and muscle strength also allows for appropriate force generation and dissipation.15,16
After the patient has been discharged from physical therapy, a simple home program can be designed to focus on stretching and low-resistance isometric rotator cuff strengthening. Gentle stretching, ideally performed up to 5 times a day, is done to avoid the application of large torques to the arm. Nonimpact repetitive shoulder motion also helps maintain flexibility. Exercises such as swimming, power walking, and stationary cycling help improve flexibility and maintain cardiovascular conditioning.4
Because OA is a chronic condition that requires long-term treatment, the benefits of pharmacologic therapy must be weighed against potential side effects.11 A general approach to medication selection has been developed for OA of the knee and hip; this can be applied to GHJOA.14
Oral analgesics. A variety of progressively potent oral agents are available.
Acetaminophen.Regularly dosed acetaminophen is an effective first-line analgesic that reduces mild to moderate pain sufficiently to allow participation in a rehabilitation program. It has a safer GI profile than NSAIDs. To minimize the risk of hepatotoxicity, patients with normal hepatic function should not exceed a daily dose of 4 g.16 Acetaminophen and NSAIDs are similarly effective in improving functional status in patients with knee OA, but these agents have not been compared specifically in GHJOA.17
NSAIDs and COX-2 inhibitors. NSAIDs are more effective than acetaminophen in the treatment of moderate to severe osteoarthritic pain.18 Cyclooxygenase (COX)-2 inhibitors are as effective as traditional NSAIDs in relieving pain and reducing inflammation and are significantly less harmful to the GI tract. COX-2 inhibitors are probably still considered the oral anti-inflammatory drugs of choice in patients at high risk for GI toxicity or bleeding.19-21 This general sentiment may change, however, in light of the recent withdrawal of rofecoxib from the market and the controversy surrounding both valdecoxib and celecoxib.
Tramadol. The American College of Rheumatology guidelines for knee and hip OA recommend tramadol in patients whose pain is not adequately relieved with acetaminophen, NSAIDs, or COX-2 inhibitors.14 Although tramadol has not been specifically studied in GHJOA, its efficacy in knee and hip OA management is well established.22 Tramadol provides additive analgesic effects when combined with NSAIDs.23 The combination of low-dose tramadol and acetaminophen in a single tablet is convenient and lessens the chance of tramadol-related side effects.
Opioid analgesics. These agents may be considered for patients who fail to respond to or cannot tolerate tramadol. Pure opioid analgesics are not associated with GI bleeding or hepatic or renal side effects; however, some patients experience physical dependence, psychological addiction, or tolerance that requires dose escalation. Short-acting opioid analgesics can be used as premedication for therapeutic exercises, particularly if stretching is painful but believed to be an important component of the program.
Therapeutic injections. Some physiatrists who specialize in musculoskeletal medicine are particularly adept at fluoroscopic-guided injection procedures.
Intra-articular corticosteroid injections.These may be administered following or as an adjunct to other pharmacologic interventions.24 They may be particularly useful in patients with renal dysfunction or other contraindications to oral anti-inflammatory agents. Patients who wish to delay surgical intervention may also benefit from injections.11,25
Viscosupplementation. This treatment involves the intra-articular injection of a hyaluronate solution. It is approved for the knee only in settings in which it has been shown to relieve pain, improve function, and possibly protect cartilage from further breakdown. Preliminary results of glenohumeral joint viscosupplementation have been promising.26,27
Other agents. These include supplements and topical analgesics.
Glucosamine and chondroitin sulfate.In some studies,these supplements showed moderate to significant benefit for osteoarthritic pain and mobility limitations.28 A 3-year study found that patients with knee OA given glucosamine had significant improvement in knee pain and less radiographic joint-space narrowing.29 Although glucosamine and chondroitin sulfate have not been specifically studied in GHJOA, it is probably reasonable to consider a trial of these agents in patients with this condition.
Topical analgesics.Agents such as capsaicin, salicylates, and NSAIDs may be helpful for relieving osteoarthritic knee and hand pain.30 However, they are unlikely to be of benefit in GHJOA because the glenohumeral joint is quite deep.
Surgery is indicated for intractable pain and loss of function despite nonpharmacologic and pharmacologic therapy. The most effective and widely accepted treatment is shoulder arthroplasty; however, other procedures, such as arthroscopic debridement, are also used.11 These procedures may be particularly beneficial for younger patients with post-traumatic arthritis who wish to delay shoulder arthroplasty and for elderly patients who want to avoid extensive surgery and prolonged rehabilitation.31 In patients with severe disease for whom surgery is imminent, therapeutic exercises may help improve preoperative conditioning.4
REFERENCES:1. Bruusgaard D, Natvig B, Nessioy I, et al. Musculoskeletal symptoms in a local community. Eur J Gen Pract. 1995;1:25-28.
2. Leclerc A, Chastang JF, Niedhammer I, et al; Study Group on Repetitive Work. Incidence of shoulder pain in repetitive work. Occup Environ Med. 2004;61:39-44.
3. Nakagawa Y, Hyakuna K, Otani S, et al. Epidemiologic study of glenohumeral osteoarthritis with plain radiography. J Shoulder Elbow Surg. 1999;8: 580-584.
4. Parsons IM 4th, Weldon EJ 3rd, Titelman RM, Smith KL. Glenohumeral arthritis and its management. Phys Med Rehabil Clin N Am. 2004;15:447-474.
5. Hovelius L, Augustini BG, Fredin H, et al. Primary anterior dislocation of the shoulder in young patients. A ten-year prospective study. J Bone Joint Surg Am. 1996;78:1677-1684.
6. Zyto K, Kronberg M, Brostrom LA. Shoulder function after displaced fractures of the proximal humerus. J Shoulder Elbow Surg. 1995;4:331-336.
7. Jensen KL, Williams GR Jr, Russell IJ, et al. Rotator cuff tear arthropathy. J Bone Joint Surg Am. 1999; 81:1312-1324.
8. Feeney MS, O'Dowd J, Kay EW, et al. Glenohumeral articular cartilage changes in rotator cuff disease. J Shoulder Elbow Surg. 2003;12:20-23.
9. Antoniou J, Tsai A, Baker D, et al. Milwaukee shoulder: correlating possible etiologic variables. Clin Orthop. 2003;407:79-85.
10. Goldstein B. Shoulder anatomy and biomechanics. Phys Med Rehabil Clin N Am. 2004;15: 313-349.
11. Wiater JM, Levine WN, Bigliani LU. Upper extremity shoulder considerations. In: Moskowitz RW, Howell DS, Altman RD, et al, eds. Osteoarthritis Diagnosis and Medical/Surgical Management. Philadelphia: WB Saunders; 2001:469-475.
12. Long BW, Rafert JA. The shoulder. In: Long BW, Rafert JA, eds. Orthopaedic Radiology. Philadelphia: WB Saunders; 1995:164-218.
13. Stitik TP, Foye PM, Fossati J. Shoulder injections for osteoarthritis and other disorders. Phys Med Rehab Clin N Am. 2004;15:407-446.
14. American College of Rheumatology Subcommittee on Osteoarthritis Guidelines. Recommendations for the medical management of osteoarthritis of the hip and knee. Arthritis Rheum. 2000;43: 1905-1915.
15. Shiller AD. Osteoarthritis. In: Frontera WR, Silver JK, eds. Essentials of Physical Medicine and Rehabilitation. St Louis: Hanley and Belfus; 2002:638-644.
16. Dugan S, Weber K. Selected topics in sports medicine. Disease-A-Month. 2002;48:572-616.
17. Towheed TE, Judd MJ, Hochberg MC, et al. Acetaminophen for osteoarthritis. Cochrane Database Syst Rev. 2003;2:CD004257.
18. March L, Irwig L, Schwarz J, et al. n of 1 trials comparing non-steroidal anti-inflammatory drug with paracetamol in osteoarthritis. BMJ. 1994;309: 1041-1046.
19. Kuritzky L, Weaver A. Advances in rheumatology: coxibs and beyond. J Pain Symptom Manage. 2003;25(2 suppl):S6-S20.
20. Ruoff G, Lema M. Strategies in pain management: new and potential indications for COX-2 specific inhibitors. J Pain Symptom Manage. 2003;25 (2 suppl):S21-S31.
21. Schnitzer TJ. American College of Rheumatology. Update of ACR guidelines for osteoarthritis: role of the coxibs. J Pain Symptom Manage. 2002; 23(4 suppl):S24-S30.22. Babul N, Noveck R, Chipman H, et al. Efficacy and safety of extended-release, once-daily tramadol in chronic pain: a randomized 12-week clinical trial in osteoarthritis of the knee. J Pain Symptom Manage. 2004;28:59-71.
23. Schnitzer TJ, Kamin M, Olson WH. Tramadol allows reduction of naproxen dose among patients with naproxen-responsive osteoarthritis pain: a randomized, double-blind, placebo-controlled study. Arthritis Rheum. 1999;42:1370-1377.
24. Tallia AF, Cardone DA. Diagnostic and therapeutic injection of the shoulder region. Am Fam Physician. 2003;67:1271-1278.
25. Creamer P. Intra-articular corticosteroid treatment in osteoarthritis. Curr Opin Rheumatol. 1999; 11:417-421.
26. Kelly MA, Moskowitz RW, Lieberman JR. Hyaluronan therapy: looking toward the future. Am J Orthop. 2004;33(2 suppl):23-28.
27. Hamburger MI, Lakhanpal S, Mooar PA, et al. Intra-articular hyaluronans: a review of product-specific safety profiles. Sem Arthritis Rheum. 2003;32: 296-309.
28. McAlindon TE, LaValley MP, Gulin JP, et al. Glucosamine and chondroitin for treatment of osteoarthritis. JAMA. 2000;283:1469-1475.
29. Reginster JY, Deroisy R, Rovati LC, et al. Long-term effects of glucosamine sulphate on osteoarthritis progression: a randomised, placebo-controlled clinical trial. Lancet. 2001;357:251-256.30. Moore RA, Tramer MR, Carroll D, et al. Quantitative systematic review of topically applied NSAIDs. BMJ. 1998;316:333-338.
31. Bishop JY, Flatow EL. Management of glenohumeral arthritis: a role for arthroscopy? Orthop Clin North Am. 2003;34:559-566.