Rheumatic disease, commonly known as arthritis, is a term used to describe a collection of diseases affecting the joints and soft tissues. Arthritis-related musculoskeletal disorders contribute significantly to disability globally (Vos et al., 2012) and in the United States of America (Hootman et al., 2006). Predictions indicate that by the year 2030, arthritis will affect one-quarter of the US population, with women being more often affected than men (Cheng et al., 2010). A diagnosis of arthritis may be established following careful attention to clinical manifestations, laboratory tests, radiographic and imaging studies, and responses to drug therapy. Although arthritis can affect anyone, certain types of arthritis are commonly associated with aging. Discussed below is the pathophysiology, medical management and recommended therapy for the following rheumatic conditions: osteoarthritis, rheumatoid arthritis, systemic lupus erythematosus, gout, pseudogout, polymyalgia rheumatica, bursitis and tendinitis.

Osteoarthritis (OA), also called osteoarthrosis or degenerative joint disease, is the most common joint disorder and one of the leading causes of disability in the elderly. The condition involves cartilage degeneration, the remodeling of subchondral bone and overgrowth of bone at joint margins. Joint effusion and thickening of the synovium and capsule also may occur. OA affects women more than men, though both genders are affected with severity increasing with age (Deyle et al., 2012). The most affected joints are the weight-bearing synovial joints of the lower extremity, the spine and the carpometacarpal and distal interphalangeal joints of the hand (CDC, 2013a).

OA occurring without a predisposing condition is called ‘primary OA’, whereas ‘secondary OA’ results from a local or systemic factor such as trauma, developmental deformity, infection, or following cartilage damage due to another disease or another form of arthritis. The disease process of OA affects the entire joint, including the articular cartilage, synovium, subchondral bone and surrounding supportive connective tissues. The most marked changes in OA involve the articular cartilage. In an unaffected joint, the articular cartilage provides a smooth, almost frictionless weight-bearing joint surface which spreads and minimizes local loads. Repeated excessive loading of normal cartilage and subchondral bone, or normal loading of biologically deficient cartilage and subchondral bone, may lead to microcracks and uneven distribution of chondrocytes. The degenerating, thinning cartilage is less able to redistribute forces, leading to greater force transference to the subchondral bone (Egloff et al., 2012). The reaction is subchondral bone hardening and the formation of osteophytes (bone spurs) at joint margins. As the joint surface deteriorates, the joint capsule may become lax, leading to joint instability. OA is evidenced on radiographs by decreased joint space, osteophyte formation, subchondral sclerosis and subchondral trabecular fractures. Radiographic evidence of OA is present in the majority of older individuals, though not all individuals are symptomatic. Generally, however, a positive correlation exists between clinical and radiographic findings. Factors contributing to OA include aging, excess body weight, occupational or sport joint injury, and metabolic or endocrine disorders (Deyle et al., 2012).

Clinical characteristics include joint pain, stiffness, tenderness, instability and enlargement. Periarticular muscle atrophy and weakness occur, contributing to disability. Early in the disease course, pain is worsened by activity and relieved by rest. With disease progression, pain is often present even at rest and may lead to significant functional impairment. Articular cartilage is devoid of nerve endings, thus the pain associated with OA arises from innervated intraarticular and periarticular structures. In the spine, bony overgrowth may encroach on emerging nerve roots, causing pain. Stiffness, usually occurring in the mornings and following periods of rest, is relieved by movement. Motion limitation may be caused by irregular joint surface movement due to cartilage degeneration, muscle spasms due to pain, muscle weakness due to disuse and osteophyte formation. Crepitus, a clicking or crackling sound, may occur as the joint is moved. Joints may enlarge due to synovitis, joint effusion, connective tissue overgrowth, or osteophyte formation. Joint deformity may occur, as forces are inappropriately distributed between joint structures.

Inflammation is not a typical characteristic of OA, but may occur as the irritated synovium contributes to the activation of chondrocytes causing production of a wide range of inflammatory mediators that release cartilage-damaging products. The imbalance between chondrocyte synthesis and degradation stimulates further production of proinflammatory mediators and proteinases. The naturally occurring tissue inhibitors become overwhelmed and crystals may be deposited in the degenerating cartilage, sometimes breaking off into the joint and creating acute or chronic inflammation (Walker, 2004).

The aim of therapeutic intervention is to relieve symptoms, maintain and improve function, and limit the degree of functional impairment. Typical therapeutic interventions for OA include education, rest, pharmacologic agents, exercise, weight reduction and possibly surgery. Patients should be instructed in joint protection and energy conservation techniques to help prevent acute flare-ups and to help minimize joint stress and pain. Regularly administered pharmacologic agents include analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs). Intraarticular corticosteroid injections may benefit acute joint inflammation.

Rehabilitation should include appropriate weight-bearing and non-weight-bearing exercise. The Ottawa Panel Evidence-Based Clinical Practice Guidelines recommends therapeutic exercise, particularly strengthening and general activity, with or without manual therapy, in managing pain and functional impairment of OA (Ottawa Panel, 2005), though manual therapy in addition to exercise may enhance pain relief (Jansen et al., 2011). Individualized programs should include strengthening, range of motion and cardiovascular fitness. To minimize stress on the joints, the design of the strengthening program should be one using low weight and high repetitions. Aquatic therapy, elliptical training and cycling are examples of therapeutic exercise that allow patients to place decreased stress through their affected joints while allowing for aerobic training (Ottawa Panel, 2005; Sinusas, 2012). Exercise in water is an excellent activity since buoyancy in water reduces the effect of gravity and the loading effect on joints. Resistive exercise producing increased joint pain during or following exercise probably indicates too much resistance is being used, stress is being placed at an inappropriate part of the range of motion, or the exercise is being incorrectly performed. Stretching exercises incorporating a low load, prolonged stretch, performed three or more times a day, will lead to more appropriate length– tension relationship for the muscles surrounding the affected joints and may lead to decreased stress in the intraarticular and periarticular joint structures. Home exercise programs must be carefully planned and monitored. Heat may decrease pain and stiffness and cold may decrease pain and inflammation. Splints, braces and gait devices, such as crutches, a walker or rolling walker, may be helpful to decrease joint stress. If excess weight is present, weight loss may alleviate or even prevent the onset of symptoms, and should always be incorporated into the patient’s therapeutic program.

Surgical interventions such as arthroscopy, arthroplasty and angulation osteotomy may provide symptomatic relief, improved motion and improved joint biomechanics. The most common major orthopedic procedure performed in the elderly is hip surgery, the indications being fracture or pain due to OA. A large percentage of hip and knee replacements are for OA. While elderly patients are at higher risk for complications than younger patients, most have a satisfactory outcome and significant relief of pain. Experimental surgical techniques to stimulate cartilage repair or transplant cartilage are generally not successful, though select patient populations with focal defects may benefit (Kreuz et al., 2009).

The prevalence of RA increases with age, is 2–3 three times higher in women than men, and has a peak incidence in the sixth decade (CDC, 2013b). The onset of RA may be acute, but is usually insidious. The clinical course of RA is variable and unpredictable. Patients with RA who smoke, have diabetes, or are physically inactive tend to be at higher risk for developing comorbidities such as cardiovascular or respiratory disease (Verstappen & Symmons, 2011). In the initial stages, joint pain and stiffness are prevalent, especially in the mornings. With disease progression, motion becomes more limited and ankylosis may develop. Radiographic evidence of the disease becomes apparent over time. Treatment effectiveness may be difficult to determine due to spontaneous exacerbations and remissions. Testimonials of ‘cures’ with unproven remedies are common, as certain treatment approaches may have been initiated during the initial stages of a spontaneous remission.

The etiology of RA is unknown. Evidence exists for a genetic predisposition for the disease that may be triggered by bacteria or viruses. The pathogenesis of RA is better understood than the etiology. The characteristic chronic inflammatory process begins with synovitis, developing as microvascular endothelial cells become swollen and congested. As the disease advances, the synovium becomes progressively thickened and edematous, with projections of synovial tissue invading the joint cavity. Pannus, tumor-like thickened layers of granulation tissue, infiltrates the joints destroying periarticular bone and cartilage. Fibrotic ankylosis may eventually occur, with bony malalignment, visible deformities, muscle atrophy and subluxation of joints. In advanced RA, bony ankylosis and significant disability may occur.

A definitive diagnosis is based on a combination of clinical manifestations and laboratory findings, as there is no laboratory test specific for RA. Frequent laboratory findings in persons with RA include decreased red blood cell count, increased erythrocyte sedimentation rates (ESR) and positive rheumatoid factor (RF). A positive test of RF is not diagnostic, as RF is found in a small percentage of normal individuals and in persons with other autoimmune diseases. However, high concentration of RF is associated with greater long-term risk of RA (Nielsen et al., 2012).

Joint manifestations occur bilaterally, affecting principally the small joints of the hands and feet, ankles, knees, wrists, elbows and shoulders. Typically, the metacarpophalangeal and proximal interphalangeal joints of the hand are affected, with sparing of the distal interphalangeal joints. RA can affect the hip, knee, ankle and small joints of the foot. In axial involvement, the upper cervical spine is most affected. Tenosynovitis of the transverse ligament of the first cervical vertebra and disease of the cervical apophyseal joints may lead to instability and cord compression. A thorough neurological examination should be conducted to determine involvement. Most of the joints ultimately affected by RA will be involved during the first year of the disease.

Joint deformities result from synovitis, pannus formation, cartilage destruction and voluntary joint immobilization due to pain. The change in joint mechanics from cartilage degeneration and the erosive effect of chronic synovitis may lead to ligament laxity. The changed mechanics result in abnormal lines of pull from tendons, leading to joint deformity. Additionally, tenosynovitis may occur, causing an obstruction of tendon movement within the tendon sheath and/or tendon rupture. Nodular thickening may occur, leading to a ‘locking’ sensation or rupture of the tendon. Synovitis can lead to compression of nerves, particularly in the carpal tunnel and, less commonly, the tarsal tunnel. The ulnar nerve may be compressed at the elbow or in the hand.

Common deformities of the hand include radial deviation of the wrist, ulnar deviation at the metacarpophalangeal joints, and deformities in the fingers. Flexion deformity of the elbow and loss of shoulder motion is common. Due to the weight-bearing nature of the lower extremity, major disability can result, particularly in the toes and ankle. Cock-up deformities of the toes and subluxation of the metatarsal heads with concurrent migration of the metatarsophalangeal fat pad result in significant pain in walking.

Effective treatment of RA attempts to reduce the inflammation, provide pain relief, maintain and restore joint function, and decrease the development of joint deformity. Medications include NSAIDs, corticosteroids, slow-acting antirheumatic drugs, and disease-modifying antirheumatic drugs (DMARDs) (Singh & Cameron, 2012). Patients must balance activity and rest. Fatigue may be decreased with appropriate rest, which may include 8–10 hours of sleep at night and an afternoon nap. Energy should be conserved for daily activities. Prolonged bed rest has not proven to be beneficial. Therapeutic exercise cannot alter the course of the disease, but can help prevent deformity and loss of motion and muscle strength. Clinical practice guidelines developed by the Ottawa Panel emphasize shoulder, hand, knee and whole body functional strengthening at low intensities (Ottawa Panel, 2004a). Active and passive range of motion exercise, pain-free isometrics, proper positioning and posture should be performed regularly to achieve functional goals. Joint-stressing activities should be avoided. Aquatic therapy is an excellent medium for active individual or group structured exercise, though the water temperatures for patients with RA may need to be higher than usual. Splints and assistive devices should be used as needed to protect the joints. During active inflammatory periods, exercise should be performed carefully, with special care taken to protect the joints. Heavy resistive exercise should be avoided, as the joint compression that occurs with this exercise could increase pain and contribute to joint damage. Since the limitation of motion is due to distended joint capsules and not to adhesions, forceful stretching should be avoided. During times of remission, non- or low-impact aerobic conditioning such as swimming or stationary bicycling can be performed within the patient’s tolerance. Gentle stretching can be performed. Relaxation exercises often help to decrease muscle tension and stress.

Clinical evidence exists for the inclusion of low-level laser therapy (Brosseau et al., 2005; Alves et al., 2011; Bálint et al., 2012), therapeutic ultrasound, thermotherapy and transcutaneous electrical stimulation in the management of RA (Ottawa Panel, 2004b). Surgical procedures may be performed with goals to reduce pain, improve function, and correct instability or deformity. Common surgical procedures include tenosynovectomy, tendon repair, synovectomy, arthrodesis and arthroplasty.

Systemic lupus erythematosus (SLE) is an autoimmune disease primarily affecting young women. The peak incidence of SLE occurs between the ages of 15 and 40, but the disease may affect both younger and older persons, with a female to male ratio of approximately 10:1. The disease course varies widely from a relatively benign to life-threatening illness (Robbins, 2001). Most deaths occur due to infection (Chen et al., 2008).

The etiology of SLE is unknown, but may involve immunologic, environmental, hormonal and genetic factors. The prime causative mechanism is thought to be autoimmunity in which tissues are damaged as antibodies are produced against many body tissues and tissue components such as blood vessels, red blood cells, lymphocytes and various organs. Antibodies directed against components of the cell nucleus, antinuclear antibodies (ANA), are found in most SLE patients.

Two ANA molecules, ANA-DNA and ANA-Sm, are unique to SLE and are used as diagnostic criteria. The diagnosis of SLE is based on clinical manifestations supported by laboratory tests. Clinical criteria to classify SLE include skin rash, renal dysfunction, blood disorders, arthritis, cardiopulmonary dysfunction, neurological/psychiatric problems and abnormal immunologic tests (Petri et al., 2012). Clinically apparent nephritis develops in many cases and biopsies may be used to assess the degree of kidney damage. Photosensitive skin disorders are common, especially acute inflammatory rash on the malar regions of the face, known as ‘butterfly rash’, or on the upper extremities or trunk. Subacute symmetrical and widespread lesions or chronic disc-shaped, scaly lesions may appear. Pleurisy, pericarditis, chronic interstitial lung inflammation, heart valve abnormalities, and thromboses are common with varying degrees of severity. Neurological and psychiatric manifestations include seizures and psychosis. Gastrointestinal manifestations include diffuse abdominal pain, nausea and vomiting, and anorexia. The arthritis associated with SLE may be symmetrical or nonsymmetrical and typically affects the small joints of the hands, wrists and knees. Typically, the arthritis is non-erosive, but deforming arthropathy, particularly of the hands, can develop as a consequence of recurrent inflammation.

While the short-term prognosis has improved in recent years, the long-term outlook for patients with SLE is generally poor, with complications resulting from either the disease itself or as a consequence of treatment. Late complications of SLE include end-stage renal disease, atherosclerosis, pulmonary emboli, venous syndromes, avascular necrosis, and neuropsychological dysfunction and bactericemia (Chen et al., 2008).

Treatment of SLE is determined by disease activity and severity. Drugs that suppress inflammation and interfere with immune system functioning are commonly prescribed. NSAIDs may be used to treat musculoskeletal complications. Skin lesions may be treated with corticosteroids and antimalarial agents. Corticosteroids are used in the treatment of systemic symptoms of SLE such as pericarditis, nephritis, vasculitis and CNS involvement. In some patients, cytotoxic drugs such as methotrexate, azathioprine and cyclophosphamide are prescribed. In the absence of lupus nephritis or neuropsychiatric lupus, the drug belimumab appears effective and well tolerated (Boyce & Fusco, 2012).

Patient education is paramount in the treatment of SLE. The patient must understand that periods of remission and exacerbation are typical. Many patients with SLE are photosensitive and must be reminded to avoid or reduce sun exposure when possible. Due to the increased risk of infection, emphasis should be placed on prompt evaluation for unexplained fever. The fatigue associated with SLE may be reduced through cardiovascular fitness and muscular strengthening interventions (Ayan & Martin, 2007; Yuen et al., 2011). Heat may be used to relieve joint pain and stiffness. Regular active exercise may prevent contractures.

Gout is a metabolic disease characterized by the deposition of monosodium urate crystals in connective tissues, resulting in painful arthritis. The hyperuricemia associated with gout may result from a variety of factors, including a genetic defect in purine metabolism, leading to an overproduction and/or undersecretion of uric acid. Other associated factors include obesity, diet, lifestyle, renal dysfunction and hemoglobin levels. Diuretics can lead to an underexcretion of uric acid and may play a role in the pathogenesis of gout (Rakieh & Conaghan, 2011). Primary gout typically occurs in men, with peak incidence in the fifth decade, and commonly causes short-term disability. Gout may also occur in postmenopausal women, especially when diuretics are used. Secondary gout occurs primarily in the elderly and results from the hyperuricemia associated with diseases such as diabetes mellitus and hypertension. The mechanisms are not fully defined, but are likely due to diminished renal function, dehydration, decreased tissue perfusion, and the effect of certain drugs leading to uric acid overproduction or underexcretion. Gout is relatively common in organ transplant recipients due to the use of cyclosporine and reduced renal function, regardless of the organ transplanted.

The clinical course of gout typically follows four stages: asymptomatic, acute, intercritical and chronic. An asymptomatic period of urate crystal deposition in connective tissue often appears prior to the first episode of gouty arthritis. The initial episode of gout is typically sudden, often occurring during the night. The patient awakes with severe unexplained joint pain and swelling. The first metatarsophalangeal joint is commonly affected. The ankle, tarsal joints and knee may also be involved. Trauma, alcohol, drugs, or acute medical illness may precipitate acute attacks. The intercritical stage is characterized by symptom-free periods which may last from months to years. The presence of crystal deposition persists during these asymptomatic periods and aspiration of synovial fluid may confirm the diagnosis. The chronic stage of gout is characterized by tophi, large masses of urates within the subarticular bone or surrounding soft tissues. Less commonly, tophi form in the internal organs. Tophi deposits precipitate joint erosion and tendon rupture. The arthritic clinical manifestation of chronic gout may resemble RA, though gout is usually more asymmetrical and can involve any joint.

Not all persons with hyperuricemia will develop gout. The presence of monosodium urate crystals in synovial fluid is generally considered necessary to establish a definitive diagnosis. Even during asymptomatic periods, monosodium urate crystals may be demonstrated in synovial fluid aspirated from previously involved joints, as well as from joints that have never been involved. Serum uric acid levels are less helpful in definitive diagnosis, especially in the acute phase, but will eventually become elevated.

Treatment of gout is aimed at early intervention for acute attacks, reducing hyperuricemia, preventing recurrence, and preventing erosive joint damage and kidney complications. During acute attacks, NSAIDs, colchicines or corticosteroids may be used to relieve symptoms. Urate-lowering therapy may be used for long-term control (Doghramji et al., 2012). Included in the treatment regimen are bedrest, joint immobilization and local cold application to inflamed joints. Attack frequency may be decreased by certain dietary and lifestyle changes. Recommended dietary modification includes the avoidance of alcohol and a restriction of purine-rich foods, such as liver, kidneys, shellfish, salmon, peas, beans and spinach. Weight loss and the avoidance of repetitive trauma are helpful prophylactic measures that may allow one to avoid drug therapy during intercritical periods. Infected or ulcerated tophi may require excision.

Practical considerations include the use of a bed cradle to keep bed covers off inflamed joints, the intake of plenty of fluids to prevent the formation of kidney stones, prompt treatment of acute attacks, and rapid attention to the side-effects of drug therapies. Assistive devices may also be used to decrease stress on inflamed joints.

Polymyalgia rheumatica (PMR) is a common systemic inflammatory disorder in the elderly and is characterized by the gradual development of persistent pain, weakness and stiffness in proximal muscles, in combination with fever, weight loss and high ESR. More common in women than men, PMR occurs mostly in those over 50 years of age, with peak incidence between 60 and 75 years of age (Charlton, 2008). Symptoms are usually symmetric and onset may be abrupt. Stiffness is typically worse in the morning. Tenderness and stiffness is most common in the muscles of the shoulder, pelvic girdles and neck, but may be present in the knees, wrists and hands. Differential diagnosis of PMR from hypothyroidism, malignancies, RA, SLE and infectious diseases, is critical. Giant cell arteritis (GCA), also known as temporal arteritis, is a systemic inflammatory disorder affecting large and medium-sized blood vessels. The pain presentation may be similar to that in PMR and the conditions may coexist in some persons. The vasculitis associated with GCA may lead to severe occlusive disease and result in stroke and blindness (Weyand et al., 2012). Symptoms include headache, visual disturbance, scalp tenderness and abnormalities in the temporal arteries.

The diagnosis of PMR is based on clinical manifestation supported by laboratory tests such as high ESR and C-reactive protein. Results of muscle enzyme tests and biopsies and plain film radiographs do not contribute to differential diagnosis. PMR responds dramatically to prednisone therapy; thus, the response is used in diagnosis as well as treatment. The lowest dose of prednisone to control symptoms is optimal, and long-term side-effects such as osteoporosis, diabetes, hypertension and gastrointestinal problems should be monitored and treated. The disease is typically self-limiting, lasting 2–7 years. Patients should be warned of the signs and symptoms of GCA. Later in the course of the disease, stretching and strengthening exercises may be helpful. Modalities such as ice and electrical stimulation may be used to decrease pain. The use of assistive devices may decrease the risk of falls.

Typical therapeutic interventions for acute tendinitis include protection and rest of the area, ice and anti-inflammatory medications. Also essential is relieving any possible causes of the tendinitis by altering or modifying work and/or environmental factors that may be contributing to the problem, such as an office worker with extensor carpi ulnaris tendinitis who may further aggravate the condition by continuing to type. Corticosteroid injection into the tendon or tendon sheath may be beneficial in acute cases, but is not indicated for chronic lesions (Jacobs, 2009).

As the acute inflammation subsides, painfree active motion is encouraged to help provide nutrition to the area and decrease swelling. In cases of chronic tendinitis, determining the cause of the problem becomes the most important factor in successful treatment. If a patient has a chronic supraspinatus tendinitis, the cause, such as weak shoulder external rotators or a bone spur on the inferior side of the acromion, needs to be identified. Chronic tendinitis is usually the result of poor blood flow to the injured area combined with a continued stress that does not allow for adequate maturation of the healing tissue. Transverse friction massage may be used in chronic tendinitis to increase the mobility of the scar and stimulate healing of the scar tissue with normal fiber alignment. Surgical intervention is only performed when conservative measures have not improved the condition. These procedures usually have the goal of creating more area for structures to move, such as an acromioplasty or removal of osteophytes from the undersurface of the acromion process and acromioclavicular joint in impingement syndrome.