OsteoarthritisDz

Synonyms: OA, degenerative joint disease, osteoarthrosis.

ICD-9 Codes: 715.9 (multiple sites); hand, 715.4; hip, 715.5; knee, 715.6; spine,
721.90.
ICD-10 Codes: M15-M19;M47

Definition: OA is the most common arthropathy seen in adults. This noninflammatory condition arises from degenerative changes and progressive loss of cartilage with resultant hypertrophic changes in surrounding bone.

Etiology: Cause is unknown. Mechanical (e.g., trauma, repetitive stress), biochemical, and inflammatory factors contribute to its pathogenesis. A genetic predisposition exists for women with OA of the distal interphalangeal joints (Heberden nodes).

Pathology: Biochemical changes in cartilage result in a loss of water content, loss of proteoglycan and collagen, and a decreased number of chondrocytes, changes that soften cartilage and make it more prone to damage. Grossly, there is evidence of cartilage damage, with fissuring, pitting, ulceration, and (eventually) denuded bone. Adjacent to cartilage loss is the development of reactive or hypertrophic bone, most often manifest as osteophyte (or spur) formation. Underlying subchondral bone may remodel and show sclerosis or bony cysts. The synovium in OA may be normal or show mild to moderate inflammatory changes, similar to those seen in RA, although not as intense. It is possible that intermittent inflammatory synovial disease may further contribute to degeneration of articular cartilage.

Demographics: OA has a prevalence of 12% in the U.S. population and is most common in those older than age 65. Radiographic changes of degenerative joint disease are seen in >80% of those older than age 75. OA is most common in women. Isolated hip OA is most common in men. All races are affected.

Risk Factors: OA is either primary/idiopathic or secondary. Secondary causes of OA include trauma, obesity, congenital or metabolic disorders (Wilson’s disease, alcaptonuria, hemochromatosis), inflammatory arthritis (i.e., RA, septic arthritis), neuropathic arthritis, and hemophilia. Obesity increases the risk of knee OA (especially in women) but does not increase risk of hand or hip OA. With structurally normal knees, there is no added risk of OA in long-distance runners. There is an inverse relationship between OA and bone mass.

Cardinal Findings: Most patients note the insidious onset of pain in affected joints. This mechanical or degenerative pain is worsened by activity and improved with rest. It is maximal at the end of the day or during the night and may interfere with sleep. Stiffness tends to be minor in the morning, yet it recurs during periods of sedentary rest throughout the day and is described as “gel phenomenon.” Inflammatory swelling or effusions are unusual. Instead, bony swelling (or hypertrophy) may develop and interfere with normal range of motion. Bony hypertrophy is most obvious in the distal interphalangeal joints (Heberden’s nodes), proximal interphalangeal joints (Bouchard’s nodes), and first carpometacarpal joints (base of the thumb), often in a symmetric fashion. Heberden’s nodes are primarily found in women. Once the hypertrophic changes have fully evolved in affected hand joints, the pain often subsides. Beyond the hand, asymmetric joint disease is most common and typically affects the hip, knees, metatarsophalangeal joints, and cervical and lumbar spine. Shoulders, elbows, ankles, and tarsal joints tend to be spared unless traumatic or occupational events predispose the patient to degenerative changes in these joints. For example, tarsal OA is a common finding in ballerinas. Coarse crepitus may be felt in joints of those with moderate to severe OA.

—Primary generalized OA (nodal OA): Occurring predominantly in middle-aged women, primary generalized OA affects the distal and proximal interphalangeal joints, first carpometacarpal joint, knee, metatarsophalangeal joint, hips, and spine.
—Chondromalacia patellae: Chondromalacia patellae is a form of degenerative arthritis that affects the patellofemoral joint and is often caused by malalignment of the patella within the intercondylar groove. The underside of the patellar cartilage develops degenerative features and manifests with pain that is worsened by walking, running, squatting, or climbing stairs. Such patients are often treated conservatively with NSAIDs, analgesics, and quadriceps-strengthening exercises.
—Inflammatory OA: Erosive or inflammatory OA typically affects post- menopausal women with inflammatory changes and erosions at nodal sites, the proximal or distal interphalangeal joints. Medial or lateral subluxation at the proximal or distal interphalangeal joint is common in this variant of OA. Radiographic changes include loss of joint spaces, sclerosis, and osteophytes, with erosions and occasional ankylosis. In the fingers, these central erosions and peripheral osteophytes may give rise to a “seagull” sign on radiography. Inflammatory OA must be distinguished from psoriatic arthritis. Uncommonly, inflammation arising in Heberden or Bouchard nodes may be caused by gout. This usually occurs in older women on diuretics with renal insufficiency.

Uncommon Findings: OA uncommonly affects the MCP (usually the second and third) joints but, if present, may be idiopathic or secondary to trauma or hemochromatosis (see p. 199).

Diagnostic Testing: Laboratory tests (e.g., CBC, ESR, SMA12) tend to be normal for age. Serologic testing for ANA and RF is not necessary. Synovial fluid is usually amber, clear, and noninflammatory (WBCs <2,000 cells/mm3), with normal viscosity.

Imaging: Conventional radiography may help establish OA as a diagnosis. Typical radiographic changes include loss of joint space, subchondral sclerosis, bony cysts, and reactive osteophytes. Articular erosions and osteoporosis are rare. It is important to note that radiographic findings do not correlate with clinical symptoms.

Keys to Diagnosis: Two primary patterns are seen: (a) patients with Heberden and Bouchard nodes (with or without first carpometacarpal hypertrophy) or (b) patients with a noninflammatory asymmetric oligo- or monarthritis af- fecting the hip, knee, metatarsophalangeal joints, or spine.

Differential Diagnosis: Disorders commonly confused with OA include psoriatic arthritis, reactive arthritis, hemochromatosis, osteonecrosis, gout, pseudogout, or hydroxyapatite deposition disease.

Therapy: The primary goals of therapy are to relieve pain and maintain function. The initial approach to treatment should always include patient and family education regarding the nature of the disorder and the prognosis. Physical and occupational therapy should be periodically encouraged to optimize joint protection, mobility, and function. Use of weight loss, splinting, ambulatory assist-devices, and vocational rehabilitation should also be considered.
Several studies have shown that regular low-impact aerobic exercise (i.e., stationary bicycling, swimming) and isometric exercise can substantially reduce pain, increase mobility, and (in some patients) even retard progression to joint replacement surgery.

Initial pharmacologic attempts at pain control should rely on the use of safe therapies, such as nonnarcotic analgesics (e.g., acetaminophen), topical therapies (e.g., ice, heat, capsaicin cream), and nonacetylated salicylate (e.g., salsalate). Low-dose NSAIDs may be used if not contraindicated. Patients who do not respond well to these conservative measures may try other or higher dose NSAIDs, add other analgesic agents (e.g., propoxyphene, tramadol, nightly tricyclic antidepressants), or be considered for intraarticular injection. Use of strong narcotics and oral corticosteroids should be discouraged.
Intraarticular corticosteroid injection may provide temporary or sustained relief of pain. Intraarticular injection of hyaluronate (usually given as a series of three to five weekly injections) has a modest to moderate effect in patients with OA of the knees. Because of equivocal results, joint lavage is not routinely recommended for the treatment of knee OA. Intraarticular hyaluronic acid injections.

Glucosamine and chondroitin sulfate have been advocated by lay individuals as beneficial. Recent reports suggest this combination has a modest effect on pain and long-term use may be associated with a delay in cartilage loss over time in the knees.

Surgery: For those with advanced disease, joint replacement surgery may dramatically improve the quality of life. Surgery should be considered for patients who experience intractable/refractory pain, loss of function or mobility, and radiographic evidence of advanced degenerative changes in the joint. Arthroplasty (joint replacement surgery) is routinely recommended for advanced OA involving the hip or knee. More than 265,000 knee and >165,000 hip replacements are performed yearly in the United States. Relative contraindications to arthroplasty include obesity, multiple medical disorders (that impart a high perioperative risk of death), and a lack of motivation or inability to participate in a postoperative rehabilitation program.

BIBLIOGRAPHY

Bradley JD, Brandt KD, Katz BP, et al. Comparison of an antiinflammatory dose of ibuprofen, an analgesic dose of ibuprofen and acetaminophen in the treatment of patients with osteoarthritis of the knee. N Engl J Med 1991;325:87–91. PMID:2052056

Felson DT. The epidemiology of knee osteoarthritis: results from the Framingham Osteoarthritis Study. Semin Arthritis Rheum 1990;20:42–50.PMID:2287948

Hochberg MC, Altman RD, Brandt KD, et al. Guidelines for the medical management of osteoarthritis. Part I: Osteoarthritis of the hip. PartII: osteoarthritis of the knee. Arthritis Rheum 1995;38:1535–1546.PMID:7488272

Roddy E, Doherty M. Guidelines for management of osteoarthritis published by the American College of Rheumatology and the European League Against Rheumatism: why are they so different? Rheum Dis Clin North Am 2003;29:717–731.PMID:14603579

Wang CT. Therapeutic effects of hyaluronic acid on osteoarthritis of the knee. A meta-analysis of randomized controlled trials. J Bone Joint Surg Am 2004;86A:538–545.PMID:14996880