USPharm. 2011;36(10)22-26.

Musculoskeletal problems cause a great burden in older adults due to a combination of pain and functional impairment.1 The aging process of tissues, such as articular cartilage and bone, contributes to this burden.1 Arthritis—both osteoarthritis and rheumatoid arthritis—affects approximately 50% of all people aged 65 years and over, and has been characterized as the leading cause of functional limitation, physician visits, and missed work days, according to public health data.2,3 Arthritis-associated mobility impairment increases the risk for numerous other conditions, and as a result, decreases disability-free life expectancy.2

Osteoarthritis (OA), also referred to as degenerative arthritis or degenerative joint disease, is the most common form of arthritis in the United States and Europe.4,5  This condition is associated with impaired quality of life and high economic costs.6 OA is characterized by degeneration of joint cartilage and its underlying bone; bony overgrowth also occurs.4 When breakdown of these tissues eventually occurs, pain and joint stiffness ensue.4 The joints most commonly affected by OA are the knees, the hips, and those in the hands and spine.4

About 80% of patients with OA have some degree of movement limitation, and 25% cannot perform major activities of daily living.4 Knee OA is one of five leading causes of disability among non-institutionalized adults.4,7 Even mild or moderate OA hand pain may negatively impact an individual’s physical and emotional status, with the potential to significantly reduce quality of life.

While the exact causes of OA are uncertain, they are believed to be secondary to a combination of both mechanical and molecular events—it is likely that multiple causes and many factors influence disease expression (TABLE 1).4,5,8,9 The onset of OA is gradual and usually begins after 40 years of age.4 Symptoms include pain, swelling, and stiffness of the affected joint.4 Zhang et al noted, in a study of elderly persons aged 71 years or older, that symptomatic hand OA occurred more frequently among distal interphalangeal (DIP), proximal interphalangeal (PIP), and base-of-thumb joints.10 When compared with persons without symptomatic OA, participants with symptomatic hand OA reported greater difficulties in the following: 1) writing; 2) carrying a bundle; and 3) manipulating or handling small objects.10

Currently, there is no cure for OA; however, careful and proper management of the condition can prevent further disease-induced functional disability.2,4 Because no single therapy is adequate in OA, the major clinical guidelines for management of OA generally agree that therapy should involve a combination of nonpharmacologic and pharmacologic therapies, referred to as multimodal therapy (TABLE 2).6 For example, a combination of patient education, physical therapy, weight control, and use of medications would be included in the comprehensive treatment plan.4

Risk Factors

Advancing age is the strongest risk factor for virtually all types of OA.11-13 Musculoskeletal aging—that is, age-related changes affecting joint tissues and age-related changes affecting joint functions—increases the susceptibility to OA.9 Additional factors are also typically present that lead to the manifestation of symptomatic OA. According to Loeser et al, these “OA factors” include obesity, joint injury/instability, genetics (i.e., abnormal cartilage matrix proteins), and abnormal joint anatomy (TABLE 1).9 Furthermore, they explain the most likely scenario that one or more of these factors produce abnormal effects on the structure and function of the joint, and in concert with aging, result in the development of OA and the manifestation of symptoms and disability.9

Obesity is a risk factor that is common to knee, hip, and hand OA; it presents the greatest risk in knee OA, less of a risk in hip OA, and the least risk in hand OA.12-14 Another risk factor for hand, knee, and hip OA is elevated bone density.12,13,15 Women are noted to have an increased risk of OA, particularly for knee and hand OA, while men appear more likely to experience OA of the cervical spine.16 With regard to OA of the hand, factors conferring greater risk include family history, previous hand injury, work-recreational-related activity, elevated bone density, menopausal status, and joint laxity.13


Pathology is indicated by radiographic changes showing joint space narrowing, osteophytes, and bony sclerosis.4 The cause of OA—a chronic and progressive articular pathology—is based on a variety of factors characterized by cartilage deterioration (hallmark sign) and the formation of subchondral bone abnormalities secondary to the disease.3,8,9 A decrease in articular cartilage cellularity, secondary to aging, has been associated with cartilage fibrillation, cartilage thinning, and an increased prevalence of OA in the elderly.1,14,15 While OA invariably involves articular cartilage, it is currently considered a disease of the entire joint.6 With regard to cartilage aging and OA pathogenesis, chondrocyte apoptosis currently appears to be a crucial event.1

In the early stages of OA, there is an increase in cell proliferation and synthesis of matrix proteins, proteinases, growth factors, and cytokines.8 Also contributing to the pathogenesis of OA are other types of cells and tissues such as the synovium; focal synovial inflammation can also be observed.5,8 Although OA has classically been referred to as a noninflammatory condition, accumulating evidence supports the relevance of inflammation in its pathogenesis.17


The American College of Rheumatology criteria used for the diagnosis of hand OA (sensitivity 92%, specificity 98%) requires the presence of all of the following:

• Hand pain, aching, or stiffness

• Hard tissue enlargement of at least 2 of 10 selected joints

• Fewer than 3 swollen metacarpophalangeal joints

• Either hard tissue enlargement of at least 2 DIP joints or deformity of at least 1 of 10 selected joints6,18

In patients who exhibit diffuse pain despite maximal medical adjunctive therapy, conditions other than OA should be considered (including osteomalacia and vitamin D deficiency, infectious arthritis, tendinitis, polymyalgia rheumatica, lupus, diabetes, malignancy).5 Metabolic disturbances that affect bone (e.g., vitamin D deficiency, hyperpara- 
thyroidism) may present with persistent pain and diffuse tenderness of periarticular regions and warrant evaluation.5 Patients with fibromyalgia, which is more prevalent in late life and characterized by soft tissue tenderness, pain, fatigue, and nonrestorative sleep, respond poorly to conventional management of OA.5

Multimodal Management

The goal of OA management focuses on lessening painful symptoms and improving function and quality of life.5 Response to pain management varies greatly, therefore, therapy must be individualized.3 Most likely, it will integrate physical therapy and occupational therapy into a medication regimen.3 Goals should be revised as needed to maximize patient benefit and comfort. Allergies, concomitant medications, and the presence or absence of comorbidities may affect the general approach to treatment. Obesity is an important risk factor for the development and progression of knee, hip, and even hand OA.5 Further, patients with OA of the hand are candidates for the development of OA of the knees and hips; weight loss and exercise may be an important consideration based on these findings.3

In general, pharmacologic treatments for OA include, but are not limited to, analgesics such as acetaminophen, opioids, and capsaicin, and anti-inflammatory agents with analgesic properties (e.g., nonselective nonsteroidal anti-inflammatory drugs [NSAIDs], cyclooxygenase [COX]-2 inhibitors, topical NSAIDs, and intra-articular corticosteroids).6 Slower-acting options include intra-articular hyaluronate (FDA-approved for knee OA), as well as glucosamine sulfate and chondroitin sulfate.6

The major clinical guidelines recommend that pharmacologic treatment of pain secondary to mild-to-moderate OA should initiate with acetaminophen, based on its efficacy and safety.19-23 Of note, on July 28, 2011, the McNeil Consumer Healthcare Division of McNEIL-PPC, Inc., announced a new maximum daily dose for their OTC acetaminophen products from 4,000 mg per day to 3,000 mg per day; the change was designed to help encourage appropriate acetaminophen use and reduce the risk of accidental overdose, which can cause liver damage.24 This action was subsequent to the January 13, 2011, announcement by the FDA to limit acetaminophen in prescription combination products to 325 mg per tablet or capsule to reduce the risk of liver toxicity, which primarily occurs when patients take multiple products containing acetaminophen at one time and exceed the current maximum daily dose of 4,000 mg within a 24-hour period.25

In combination with oral analgesics, or as alternatives to them, topical NSAIDs (e.g, diclofenac gel) and capsaicin are recommended.6,19-21 If sufficient pain relief is not provided by acetaminophen, a trial of an oral NSAID, at the lowest effective dose, is recommended; long-term use should be avoided whenever possible due to gastrointestinal (GI) side effects associated with these agents.6,19,20 Of note, the elderly are a high-risk population for adverse effects from NSAIDs; up to 60% of the elderly can develop peptic ulceration and/or hemorrhage asymptomatically.26 The concomitant use of H2 blockers and sucralfate is not effective as prophylaxis, except for NSAID-induced duodenal ulcers, which may be prevented by the use of ranitidine.26 The only agents proven to help prevent the development of NSAID-induced ulcers are proton pump inhibitors and misoprostol.26

Also contributing to the risk of NSAID-associated GI adverse effects are comorbidities and concomitant medication therapy.26 When necessary, NSAIDs should be used at the lowest effective dose, for the shortest period possible. Age-related renal function impairment should be considered, as well as the potential for NSAIDs to compromise existing renal function, especially when creatinine clearance is less than or equal to 30 mL/minute.26 While NSAID-associated central nervous system adverse effects (including confusion, agitation, and hallucination) are generally seen with high doses or toxicity, the elderly may demonstrate these adverse effects at lower doses than their younger counterparts; tinnitus is an unreliable indication of toxicity.26

If pain is insufficiently relieved with acetaminophen, nonselective NSAIDs, or COX-2 inhibitors, or if any of these agents is intolerable, the clinical guidelines suggest the use of intra-articular injections (e.g., corticosteroids and/or hyaluronate [FDA-approved for knee OA]), glucosamine sulfate, or chondroitin sulfate.6,20,21,23

Opioids may also be used, with or without acetaminophen, if other oral analgesics fail; more potent opioids are discouraged except when very severe pain is present that cannot be treated with other analgesic agents.6,19,20,23 The elderly may be particularly susceptible to narcotic-associated CNS depression, confusion, and constipation.26

Role of Exercise

Exercise is beneficial in arthritis. Several randomized, controlled trials have demonstrated that exercise—even vigorous exercise—results in beneficial functional status outcomes for both young and older adult patients with mild-to-moderate arthritis (i.e., OA and rheumatoid).27 Improvement in functional status outcomes of 10% to 25%—persisting for as long as 9 months after discontinuation of a supervised exercise program—include 1) lower level of subjective pain; 2) less frequent use of pain medications; 3) faster gait; 4) improved performance of physical function; and 5) lower scores for depression.27 The type of exercise studied includes both strength training (i.e., using weights) and endurance training, such as stationary bicycling.27 The positive effects of exercise may help to sustain independence; patients with arthritis have shown a reduced loss of activities of daily living with resistance or endurance exercise.27


OA of the hands poses a threat to an individual’s functional ability and quality of life. While this chronic condition cannot be cured, proper management can prevent further disease-associated functional loss. Clinical consensus supports a multimodal management approach, including pharmacologic and nonpharmacologic therapies tailored to the individual and his or her response to therapy.


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