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Osteoarthritis treatment: Decreasing pain, improving mobility

Saccomano, Scott J., PhD, RN, GNP-BC

doi: 10.1097/01.NPR.0000544281.05010.86

Abstract: Osteoarthritis (OA) is the most common articular disease. The condition results in bone-on-bone contact, stiffness, pain, and decreased mobility. By the year 2050, 40 million individuals will be severely disabled because of OA, and there will be over 130 million individuals suffering from OA worldwide.

Osteoarthritis is the most common articular disease. The condition results in bone-on-bone contact, stiffness, pain, and decreased mobility. By the year 2050, 40 million individuals will be severely disabled because of osteoarthritis, and there will be over 130 million individuals suffering from osteoarthritis worldwide.

Scott J. Saccomano is an assistant professor at the University of North Carolina, Wilmington College of Health and Human Services School of Nursing, Wilmington, N.C.

The author has disclosed no financial relationships related to this article.



Osteoarthritis (OA) is the most common articular disease. The condition results in bone-on-bone contact, stiffness, pain, and decreased mobility. The common sites for OA include the hands, knees, and hips. The World Health Organization reports that OA affects women more than men. It is estimated that 10% to 18% of adults age 60 and older suffer from OA, with over 80% of these having limitations in movement. According to the United Nations, 40 million individuals will be severely disabled with OA, and there will be over 130 million individuals suffering from OA worldwide by the year 2050.1,2

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Loss of articular cartilage is the predominant deficit in OA. The diseased articular cartilage begins to flake off and develop longitudinal fissures. Eventually, the cartilage thins out, with some areas completely lacking cartilage, exposing the bone and leaving it without protection. Eventually, the exposed bony area becomes thick and hard or sclerotic. Cysts can grow within the bone and interact with the longitudinal fissures. Excessive pressure forces the cysts into the synovial cavity, further invading and eroding the articular cartilage.

The eroded cartilage osteophytes can begin to grow from the underlying bone, eventually changing the shape and contour of the bone. These bony spurs continue to enlarge, eventually breaking off in the synovial membrane, which leads to synovitis and erosion of the joint. (See Osteoarthritis of the knee and hip.) The thickening joint capsule adheres to the bone, leading to movement limitation.3

Articular cartilage is lost through a cascade of cytokine and anabolic growth pathways. Macromolecules of proteoglycans, glycosaminoglycans, and collagen are broken into large, diffusible fragments by enzymatic processes, affecting the strength of the matrix. The loss of articular proteoglycans is the classic sign of OA. There is a loss of proteoglycans and collagen fibers with the destruction of the cellular matrix from enzyme degradation. As a result, proteoglycans are altered, interrupting the mechanism of water control and synovial fluid in and out of the cartilage.

With the loss of pumping action of fluids, excess fluid is absorbed, and the joint is unable to tolerate the stress of bearing weight. Proteoglycan content is decreased and water content is increased, affecting the strength of the cartilage. Inflammatory cytokines induce nitric oxide compounds, which further compound cartilage degradation. Proteolytic and ligninolytic enzymes coupled with cytokine release cause an imbalance of cell responses and growth factor activity.4,5

The synovium contains enzymes that degrade collagen; chondrocyte apoptosis is increased in the cartilage, producing hydroxyapatite crystal deposition. The fibrils, which give the cartilage its strength, are destroyed by collagen breakdown. As collagen is breaking down, chondrocytes are exposed to enzyme infiltration and mechanical stress. The destruction of articular cartilage remains cyclical as it destroys proteoglycans, collagen fibers, and chondrocytes, all of which make up the articular cartilage.6,7

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OA risk factors

OA is slow to develop and will worsen over time; specific risk factors are associated with OA development.

Gender/age. The incidence of OA is higher in women than men. Postmenopausal women have more severe hand and knee arthritis than men. The incidence of OA increases with age, peaking between the ages of 55 to 64. Changes in muscle mass, extracellular matrix, and reduced cell density are age-related factors that contribute to OA development in older adults.8-11



Obesity. The exact mechanism of the relationship between increased weight and OA is not clearly understood. The higher the individual's weight, the greater the risk of OA due to the stress and pressure placed on joints, particularly the weight-bearing joints, such as hips and knees. Adipose tissue contains an overabundance of adipokines that trigger the inflammatory response that plays a role in OA development.12

Race and ethnicity/genetics. Varied incidence of OA is known across race and ethnic groups. Those who identify as minorities have a higher incidence of knee arthritis at a younger age, with increased risk of OA noted in Black individuals. The CDC reports that OA is lower in some Asian populations. There is also a genetic component to OA. It is estimated that approximately 40% to 65% of OA cases have a genetic component, with the genetic risk more common in OA of the hand and hip than in OA of the knee.13 OA is more likely to develop in those who have family members with OA.8,13,14

Occupational risk. OA was originally thought to be a disease of age; recently, it is thought that repetitive movements cause microtrauma to joints, contributing to the development of OA. Joints already at risk from mechanical trauma are the most affected. Common sites of microtrauma include the spine, elbow, and knees.15

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History and physical exam

The hallmark symptoms of OA include stiffness, motor restriction, and pain, which is the most common complaint. OA can be most frequently found in the cervical and lumbar spine, hands, hips, and knees.16 Pain duration may be intermittent, whereas pain intensity can be dull, aching, or nagging, and can vary based on the level of physical exertion. Severe pain is not reported in the early onset of the disease; however, minimal physical activity and even rest can cause pain as OA progresses.

The onset of OA may be sudden or insidious. Stiffness, the most common symptom, is usually reported in the morning, generally lasts for less than 30 minutes, and can be associated with muscle spasms. Pain may also be referred or localized to the affected joint. Examples of referred pain include shoulder pain originating from OA in the cervical joints or buttock/hip pain radiating from OA in a lumbar facet joint. The patient can usually resume activities after a period of rest; however, in later stages, pain can be an ongoing complaint even despite adequate rest. Pain can occur in joints several hours after activity. Complaints of functional loss are related to the joints involved.16



OA manifestations of the hands include involvement of the first carpometacarpal joints and the distal and proximal interphalangeal joints. These joint changes are seen as Bouchard nodes and Heberden nodes. (See Osteoarthritis of the hand.) Loss of motion or deformity in the hand is slow, and OA in the hand can remain stable for years. The most rapid deterioration of OA in the hand is seen in the distal interphalangeal joints. Fine motor skill changes are seen particularly with involvement or swelling of the interphalangeal joints. Patients may report difficulties with writing, opening jars, or grasping objects. Although patients may develop these challenges, hand function remains reasonably adequate.17

Crepitus, grating, or grinding may be present for patients with OA of the knee when the joint is moved. Later, the knee can present with joint deformities, such as bony swelling and limited range of motion (ROM). Additional late symptoms include muscle wasting or weakness, particularly in the quadriceps muscle; bowing of knees and knock-knees can be present.

Patients may attempt to address their symptoms by changing their gait pattern and may assume an unsteady gait in order to prevent pain, in turn causing limping. In addition, a reduction in internal and external rotation of the hip may be seen. Patients may complain of the inability to change positions or gait instability when the hips are affected.17

OA of the spine can cause neuropathy and radiculopathy development as a result of nerve compression. The most frequent complaints of those with OA of the cervical spine include paresthesia and numbness in the upper extremities. Muscle tenderness and restricted motion in the cervical spine may be observed during exam. Lumbosacral spinal involvement produces pain across the lower back that radiates to the buttock and posterior thigh. Pseudoclaudication may be present with nerve root compression causing pain in the lower extremity.18

It is not unusual for multiple joints to be simultaneously affected by OA. Gait evaluation is necessary to observe for any gait disturbances related to OA of the hip and knee. Stiff knees may be present on physical exam. The practitioner can easily recognize bony swelling and deformities, especially in the hands and knees. Inflammation can be present if the patient is having an acute exacerbation.

Common signs of inflammation with OA will include erythema, warmth, and swelling around the joint. Crepitus, limited ROM, and painful joints will be present as the joint is moved through ROM. Joint palpitation can reveal joint tenderness, intra-articular effusions, and synovial thickening. Crepitus is more pronounced in active than in passive ROM. Muscle wasting is predominately seen later in the disease.

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In the early 1990s, the American College of Rheumatology developed diagnostic classification criteria for OA of the Hand, Knee, and Hip.19-21 This classification method continues to be a common approach of classifying OA in primary care and clinical studies. A combination of clinical history, physical exam, imaging, and blood tests is used to diagnose OA. While there is no specific blood test to diagnose OA, lab tests that could be performed include rheumatoid factor, cyclic citrullinated peptide, antinuclear antibody, a complete blood cell count with differential, erythrocyte sedimentation rate, joint aspirate for crystals, uric acid, white blood cell count, and C-reactive protein.

Specialized tests such as rheumatoid factor, antinuclear antibody, and cyclic citrullinated peptide are used to rule out other diseases that may cause joint pain or to find if there is evidence of an autoimmune disease.22,23

Diagnostic studies such as X-ray, MRI, and computed tomography scan are useful to identify joint changes, such as joint space narrowing, the formation of osteophytes, changes in subchondral bone, or synovial effusion. Typically with early OA, no radiologic changes may be seen. On imaging, as the disease progresses, loss of joint space or metabolic changes may become more apparent.24

Differential diagnosis. Differential diagnoses for OA includes multiple myeloma, polymyalgia rheumatica, rheumatoid arthritis (rarely involves proximal interphalangeal joints or the spine), crystalline disease (gout or pseudogout), septic arthritis or postinfectious arthropathy, Reiter syndrome, and bursitis. These diseases should be ruled out when appropriate.25,26

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Comprehensive management of OA

Controlling the patient's symptoms and pain while maximizing his or her independence, mobility, and quality of life are the key management principles. Patient education, self-care, pharmacologic and nonpharmacologic interventions, and surgery are some of the modalities of treatment. Practitioners should monitor the response to therapy and adjust as needed.

Pharmacologic management. Commonly prescribed pharmacologic therapies for OA management include oral agents, such as acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroids. Multimodal analgesia uses a combination of drugs with differing actions, targeting peripheral or central pain pathways to provide additive or synergistic analgesia. Using multimodal analgesia for treatment of OA can lower drug doses, essentially minimizing adverse reactions while maximizing relief.27,28

Acetaminophen is a relatively safe drug that helps to lessen OA discomfort without the additional risks of anti-inflammatory medication. Acetaminophen is the drug of choice in noninflammatory OA. According the FDA, acetaminophen should not exceed 4,000 mg/day because of possible acetaminophen toxicity.

In addition, the FDA recommends caution when using other OTC preparations that may contain acetaminophen. Acetaminophen toxicity is a concern primarily if patients are using other preparations with acetaminophen. Patients should be educated on how to read OTC labels to avoid acetaminophen overdose.29-31

NSAIDs. NSAIDs have been a part of OA treatment for many years and can be used alone or in combination therapy. The inflammatory action of NSAIDs is to inhibit the enzyme cyclooxygenase, which is a prostaglandin-inhibiting enzyme responsible for maintaining homeostatic maintenance of the gastrointestinal (GI) tract, specifically the gastric lining, renal circulation, and platelet aggregation. A decrease in prostaglandins contributes to the well-known adverse reactions of NSAIDs, such as gastric ulceration, kidney dysfunction, and increased bleeding times. Caution must be used when administering an NSAID to older adults, as they are at increased risk for such adverse reactions.

In the older adult population, it is best to “start low and go slow” and to increase the dose as needed. NSAIDS are known to increase the risk of cardiovascular thrombotic events, including myocardial infarction and stroke. Careful cardiac history should be evaluated, especially in older adults who report a history of cardiac disease. When necessary a proton pump inhibitor or histamine-2 blocker may be added when patients report a history of NSAID ulceration or simply to protect the GI tract.

In addition, older adult patients on NSAIDs should have periodic kidney function monitoring, and NSAIDs should not be used in patients with decreased creatinine clearance levels.32-34 Alternative treatment therapies for patients who are at risk for adverse reactions to oral NSAIDs have the option of using topical NSAIDs for treatment. Topical NSAIDs are recommended for patients over the age of 75.32-36

Corticosteroids. Long-term oral corticosteroids are not usually prescribed for OA. Although they may be used for intermittent flare-ups, they are not without their own adverse reactions, such as oral infection, embolism, and bone disorders.37 Intra-articular corticosteroid injections can be used to control pain in mild to severe OA; however, benefit duration varies.

Intra-articular injections are not suggested more than every 3 to 4 months, even with patients with severe OA. Intra-articular injections can produce warmth, pain, or redness at the injection site following treatment. Preferred corticosteroid injections include triamcinolone acetonide and methylprednisolone acetate, as these preparations remain in the joint in solution without leaving particulate crystalline debris.37-39

Intra-articular injections/viscosupplements. Indicated for relief of knee arthritis, intra-articular injections are indicated when conservative measures of pain relief have failed. Viscosupplementation treatment can be used alone or in conjunction with NSAIDs. Hyaluronans are injected into the knee and are effective at lubricating the joint and returning the elasticity and viscosity of the synovial fluid of the joint.

Viscosupplements have been demonstrated to improve pain and function, and results can last up to 4 months. Adverse reactions after the injection can include pain at injection site, swelling, and possibly warmth; allergic reactions are rare. Viscosupplementation is suitable for long-term chronic OA, whereas injectable corticosteroids can be used for short-term flare-ups.40,41

Selective norepinephrine reuptake inhibitors (SNRIs) are available for use in chronic pain management and are typically used for depression. The neurobiology of depression and chronic pain shares the specific neurotransmitters of serotonin and norepinephrine. SNRIs can reduce chronic pain when interacting with cytokines, serotonin, and norepinephrine to modulate the pain response.42-44 The SNRI duloxetine is approved for the treatment of chronic musculoskeletal pain due to OA.

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Nonpharmacologic approaches

The primary goal of treatment in early OA focuses on the management of pain and stiffness to improve functional abilities. It is necessary to educate patients on the promotion of self-care interventions. Patients with OA often have comorbid conditions, such as obesity, sleep apnea, and depression; paying attention to these comorbidities is essential to ensuring a better quality of life. Treatment goals include protection of joints and reduction of the load on joints is critical.

Exercise has a number of benefits in OA management. Evidence suggests that pacing activities, exercise, and weight reduction are all measures to promote healthy joints. A 5% weight loss can reduce the stress on joints that can improve function and decrease pain and disability. Practitioners can refer patients to a nutritionist if weight loss is indicated.

Applications of heat and cold can be beneficial in reducing pain. It is necessary to use ultrasound therapy to reach deeper tissues to alleviate pain. Furthermore, applications of cold are helpful after strenuous exercise or activity to reduce pain and muscle spasms.45-47

There is a role for exercise in the treatment of OA. Physical therapy and OA referrals are recommended to develop a nonpharmacologic approach to treatment to improve muscle strength, maintain ROM, and increase functional ability. Exercise goals are to decrease pain, improve ROM, increase muscle strength, and improve activities of daily living. Muscle strengthening and aerobic exercises are beneficial, especially for muscles surrounding the affected joint.

Isometric exercise is the exercise of choice, as it puts less stress on the joint. Patients should incorporate daily exercise into their routine. Cycling, swimming, and elliptical training are some of the recommended exercises as long as the patient tolerates them. Aqua therapy exercises, which occur in heated therapeutic pools, are shown to have some short-term pain relief, whereas long-term results are inconclusive.45-47

Adults with Medicare Advantage or Medicare Supplemental Health plans receive automatic membership in “Silver Sneakers,” which is available at most gyms or fitness centers and includes a variety of fitness modalities. Available programs include stretching, relaxation, strength training, and yoga. In addition, some facilities may have water activities as well as cardiovascular fitness.48

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Complementary approaches

Pharmacologic treatment of OA has been successful in pain relief and pain management, but it is not without adverse reactions, such as GI and cardiovascular effects; therefore, patients should seek out other methods of treatment to control and manage OA pain and turn to complementary approaches, such as yoga, tai chi, acupuncture, and massage therapy. In addition, natural products such as glucosamine, chondroitin, and capsaicin may also be used.

Yoga positions or poses are generally harmless, but patients should exercise caution not to hyperextend affected joints. Yoga can also reduce anxiety and stress, which can be a challenge for some patients with OA. Tai chi, a series of slow, meditative movements, can improve balance in patients who are at risk for falls due to weakness and instability of the knee.

Acupuncture uses needles at specific anatomical body points to provide local anesthesia or pain relief. Acupuncture has been known to reduce pain intensity, increase functional ability, and increase quality of life in patients with OA. Massage therapy releases endorphins and provides muscle relaxation and can reduce muscle spasms, particularly for patients with knee arthritis. 49-51

Glucosamine and chondroitin receive mixed reviews for their benefit in treating knee and hip OA. These supplements can be taken together or separately and can interact with other prescribed medications; it is suggested that patients discuss options with their practitioner.49-50

Topical capsaicin is an alternative treatment to topical NSAIDs. Capsaicin is the ingredient that causes the burning sensation from eating chili peppers. Topical capsaicin interrupts pain transmission signals by providing pain relief for OA patients. In 2012, the American College of Rheumatology (ACR) Guidelines supported the conditional use of capsaicin for OA of the hand.35 Of note, the ACR 2012 guideline is currently under revision.

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OA is a multifactorial disease of aging and is the most common form of arthritis affecting the hands, knees, hips, and spine. OA is a degenerative disease that worsens over time. The disruption of the cartilage in joints can cause pain, decreased mobility, and can affect activities of daily living. OA affects each individual differently. With treatment, patients can decrease pain, improve mobility, and continue to live active lives.

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                  degenerative joint disease; joint mobility; joint pain; mobility; osteoarthritis; pain

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