Management of Osteoarthritis

Although there is no cure for OA, preventive measures can be taken to slow down the progression of the disease or better manage the symptoms. Obesity places extra stress on joints and is a key risk factor that can be prevented or remedied with proper diet and exercise.19,24 The addition of vitamin D and calcium to a patient’s diet can also reduce the occurrence and progression of OA.¹⁹ Muscle weakness and repetitive motions or trauma contribute to the onset of OA.²⁴ Studies also have shown that immobilizing the joint for longer than 30 days can increase the risk of cartilage damage.⁴ Given the positive and negative effects of changes in behavior it is imperative to educate the patient on joint protection, health behavior changes, and the importance of exercise to the management of arthritis.

Education is the most important component to the management of OA. Patients must be educated on the progression of the disease and management of pain with supportive devices, alteration in activities of daily living (ADLs), or thermal modalities. Exercise and weight control are key components to a patient’s success with OA.2,24

Research has shown that every pound of body weight increases the forces in the knee by 2 to 3 pounds during single leg stance.³⁸ Exercise, specifically flexibility, and strength training, has been shown to decrease pain and improve function in individuals with OA.²⁴ Maintaining flexibility is an important first step because it helps decrease stiffness and allows for more comfortable movement.² Slow progression of the exercise program is important so as to not exacerbate symptoms. Patients should be progressed to 15 minutes of stretching without an increase in symptoms before initiating strength training.^2,24 Strength training improves the ability to absorb shock, support joints, and protect from injury.^2,26 When choosing an appropriate exercise it is important to keep in mind how much stress in being placed on the joint. Closed-chain weight-bearing exercises can create shear and compressive forces across the lower extremity joints and may be a contraindication pending severity of OA. Open-chain exercises, therefore, are encouraged in patients with OA.

Rheumatoid Arthritis

Rheumatoid arthritis is the second most common form of arthritis, and while it can be equally disabling as OA, it can also lead to increased mortality. This increased mortality has been shown in some research to have systemic causes.¹² The progression of RA also leads to difficulty with ADLs and disability. Along with most arthritic conditions, RA affects women more commonly than men and occurs at 20 to 40 years of age.^2,14,19 Both genetic and environmental factors have been linked as causes of RA.^14,19

Although the exact etiology of RA is unknown, it is believed to start with a viral or bacterial infection that triggers an autoimmune response.2,14 The immune response causes the body to attack its own tissue, leading to breakdown of joints.^2,14 RA affects the synovium lining, which then expands, damaging the extracellular matrix, cartilage, and bone.^2,14,26 This autoimmune response also activates T cells, which secrete cytokines, causing expansion of the synovial layer. Cytokines increase activation of fibroblast-like cells and macrophages leading to breakdown of cartilage and bone (Fig. 24-3).^2,14

Early signs and symptoms associated with RA include fatigue, weight loss, fever, and musculoskeletal pain. Later signs or symptoms include pain, tenderness, swelling, redness, and stiffness in specific joints.2,7,14,19 Unlike OA, RA morning stiffness can last hours and even all day. Fatigue in patients with RA may cause the patient to need to rest through the day.² Extraarticular manifestations can affect the lungs, heart, blood vessels, eyes, skin, and other organs.^2,7,19 It is important for the physical therapist assistant (PTA) to be able to distinguish the main differences between OA and RA (Table 24-1).

A unique feature of RA is the rheumatoid nodules, which occur on bony prominences, extensor surfaces, or pressure points.2,19 There are several common physical changes that occur³⁶:

Reactive Arthritis

Reactive arthritis, or Reiter syndrome, is most commonly an abrupt onset of arthritis in young men presenting with the triad, conjunctivitis, urethritis, and oligoarticular arthritis.7,18,19 Conjunctivitis is also known as pinkeye, which is inflammation of the conjunctiva (outermost layer of eye and inner surface of eyelid). Urethritis is inflammation of the urethra and presents as painful urination. Oligoarthritis is a form of arthritis with inflammation in two to four joints. Reiter syndrome usually presents within days or weeks of a dysenteric or sexually transmitted infection.^18,19 The arthritis is usually asymmetrical and involves the weight-bearing joints, such as the toes, ankles, and knees, then ascends to the axial skeleton and upper extremities.^7,18,19 Other symptoms present with Reiter syndrome are oral ulcers, penile lesions, keratoderma blennorrhagicum, and plantar heel pain.^7,19 Approximately 80% of individuals with Reiter syndrome are positive for human leukocyte antigen B27 (HLA-B27).^7,19 The human leukocyte antigen system is the name of the major histocompatibility complex in humans. The major HLA antigens are essential elements in immune function. Sacroiliitis is observed in about 60% of patients with chronic Reiter syndrome. Management of Reiter syndrome includes NSAIDs and physical therapy similar to that used to treat ankylosing spondylitis.

Psoriatic Arthritis

Psoriatic arthritis is a seronegative inflammatory joint disease affecting a small percentage of people with psoriasis.13,19 Psoriasis is an inherited chronic inflammatory skin disease that is characterized by silvery scales on a bright red plaque (Fig. 24-4).^5,13 In most cases the skin disease precedes the arthritis symptoms by several months to years.⁹ Psoriatic arthritis closely resembles rheumatoid arthritis, but has differences such as DIP involvement, psoriasis or family history, nail pitting, and “sausage” appearance of digits.^7,14,19 Gender does not appear to predispose one to psoriatic arthritis, but it generally begins at ages 30 to 50 years.^9,13,18 Psoriatic arthritis is usually asymmetric and involves the small joints of hands and feet.^7,13,32 However, larger axial joints such as the sacroiliac joint can be affected in later phases of disease. Sacroiliitis usually occurs unilaterally, whereas ankylosing spondylitis is bilateral.^13,18 Imaging reveals a “pencil-in-cup” deformity caused by erosion and destruction of the phalanx bones that makes them look like a sharpened pencil at the end of the bone (Fig. 24-5).^5,7,32 Furthermore, psoriatic arthritis can cause fingernail thickening, pitting, and separation from the nail bed.⁹ Finally, periosteal reactions (formation of new bone) can be seen on x-rays.

Management for psoriatic arthritis is similar to that of rheumatoid arthritis.7,18,32 Although there is no cure for psoriatic arthritis, NSAIDs can be used to treat inflammatory symptoms.^5,13 Most of the time the disease is mild and not destructive; therefore treatment consists of symptom management.^5,13

Juvenile Rheumatoid Arthritis

Many rheumatic diseases in children exist, consisting of both acute and chronic conditions, with juvenile rheumatoid arthritis (JRA) being one of the most common.⁴⁴ JRA, a chronic inflammatory disease, actually covers three types of childhood arthritis: pauciarticular, polyarticular, and systemic.^7,13,32,44 The etiology of JRA is unknown, but is thought to be triggered by environmental factors or infection in children with genetic predisposition.^13,44 “JRA is similar to adult RA in the fact that the immune system mistakenly attacks the joints and organs, causing inflammation, destruction, fatigue, and other local and systemic effects.”¹³ JRA occurs before the age of 16 years and affects girls more commonly.^7,13,44 To confirm diagnosis the child must have the arthritis for at least 6 consecutive weeks.⁴⁴ Other symptoms of JRA are fever, rash, fatigue, anemia, loss of appetite, stiffness, irritability, altered mobility, and change in ADLs.⁴⁴

Pauciarticular JRA is characterized by asymmetric synovitis of four or less joints.7,13,44 There are usually no systemic features and it most commonly affects the knee, elbow, and ankle (Fig. 24-6).^13,44 Two subtypes of pauciarticular JRA exist: early onset and late onset.^7,13,44 Early onset pauciarticular JRA occurs before the age of 5 years and usually affects girls. Early onset pauciarticular JRA left untreated can result in iridocyclitis that can lead to visual impairments.^7,13,44 The second subtype, late onset pauciarticular JRA, occurs between the ages of 10 and 12 years and is more common in boys. This subtype affects large weight-bearing joints and entheses (insertion point of tendon into bone).⁴⁴ These children often have spinal involvement that may develop into a spondyloarthropathy.^13,44

Polyarticular JRA is synovitis in more than four joints and is more common in girls.7,13,44 It usually manifests with symmetrical involvement of the small joints of the hands or feet, wrists, elbows, shoulders, knees, hips, ankles, cervical spine, and temporomandibular joints.^13,44 Bursitis and tendinitis can occur because they too are lined with synovial tissue. Unlike pauciarticular JRA, polyarticular JRA can have systemic features, including low grade fever, anemia, leukocytosis, mild hepatosplenomegaly, and lymphadenopathy.⁴⁴

The last type of JRA is systemic JRA (Still disease) which can occur at any age and does not favor girls or boys.13,44 Systemic JRA is characterized by a rash, synovitis in one or more joints, and an intermittent high grade fever.^7,13,44 The fever usually occurs in the afternoon and evenings and will return to normal with the child feeling better.^13,44 Because the fever can precede all other symptoms these children are often initially evaluated for fever of unknown origin.⁴⁴ The rash usually appears with the fever and is salmon pink, 2 to 5 mm in diameter, and has an erythematous perimeter.⁴⁴ Other signs and symptoms of systemic JRA include malaise, irritability, anemia, hepatitis, peptic ulcer disease, leukocytosis, thrombocytosis, lymphadenopathy, hepatomegaly, splenomegaly, pericarditis, and pleuritis.^13,44

Septic Arthritis

Septic arthritis is the invasion of a joint by an infectious agent causing arthritis. Septic arthritis usually occurs from a bacterial infection, but can be viral, mycobacterial, or fungal. Bacteria are introduced into the joint by the bloodstream from an infection elsewhere or from direct penetration after a wound, surgery, or local infection.⁴² Two common types of septic arthritis are gonococcal and nongonococcal.^19,42

Arthritic Conditions of the Spine

Arthritic conditions of the spine, otherwise known as spondyloarthropathies, have their main effect on the axial skeleton. Clinically the patient will have low back pain that increases with rest and improves with activity. Spondyloarthropathies have the following characteristics:

Ankylosing Spondylitis

Ankylosing spondylitis is a type of inflammation that affects the synovium of the spinal arthrodial joints as well as all the joint ligaments of the spine at their insertion points into the bone (enthesitis). It begins in the sacroiliac joints in nearly all patients and spreads superiorly up the spine.¹⁸ As the disease progresses the spine becomes more rigid (ankylosed) and develops flexion deformities.¹⁸ The disease also leads to formation of bony bridges called syndesmophytes between the vertebra. Structurally the patients will lose the lumbar curve, have reduced chest expansion, and have an increase in thoracic kyphosis.^18,22 Other changes noted in radiographic imaging are squaring of vertebrae and destruction of the sacroiliac joints³² (Fig. 24-7).

Ankylosing spondylitis has a greater incidence in men and the age of onset is usually in the late teens to early 20s.¹⁸ Hypomobility is likely to be seen in men between ages 40 and 50 years and in women older than 50 years.²⁷ Patients with ankylosing spondylitis usually will complain of alternating buttock pain that radiates down the thigh and that increases with rest but decreases with activity, a hot bath, or a shower.¹⁸ Patients may show signs of peripheral arthritis such as swelling, redness, and tenderness. Constitutional symptoms include fever, fatigue, weight loss, and elevated erythrocyte sedimentation rate (ESR).¹⁸ Ankylosing spondylitis can often be confused with sacroiliac arthritis, however there are several differences between these two diseases (Table 24-2).

Table 24-2

Differential Diagnosis between Ankylosing Spondylitis and Sacroiliac Arthritis

Differential	Ankylosing Spondylitis	Sacroiliac Arthritis
History	Bilateral sacroiliac pain that may refer to posterior thigh Morning stiffness Male predominance	Bilateral sacroiliac pain referring to gluteal area (S1-S2 dermatomes) Morning stiffness (prolonged) Coughing painful
Observation	Stiff, controlled movement of pelvis	Controlled movement of pelvis
Active movement	Decreased	Side flexion and extension full Slight limitation of flexion
Passive movement	Decreased	Normal
Resisted isometric movement	Pain and weakness, especially if sacroiliac joints are stressed	Pain, especially if sacroiliac joints are stressed
Special tests	Sacral stress tests probably positive	Sacral stress tests probably positive
Sensation and reflexes	Normal	Normal
Palpation	Tender over sacroiliac joints	Tender over sacroiliac joints
Diagnostic Imaging	X-rays diagnostic	X-rays diagnostic
Lab tests	Erythrocyte sedimentation rate increased HLA-B27 human leukocyte antigen present in 80%	Normal

From Magee DJ: Orthopedic physical assessment, ed 5, St Louis, 2008, Saunders.

Management of ankylosing spondylitis

Management for ankylosing spondylitis includes both physical therapy and drug therapy. Early rehabilitation of ankylosing spondylitis is crucial because it has been shown to significantly reduce the impact of disability.¹⁸ Therapeutic exercise along with antiinflammatory drug therapy is important in managing ankylosing spondylitis. Benefits of exercise include improved mobility, posture, and function. Education is key to starting management of patients with ankylosing spondylitis. Patients should try to exercise when pain level is low and they are least tired. Starting an exercise session with heat application and light motion exercises can help loosen the joints and decrease pain for exercise.¹⁸ Before starting the patient on a strengthening regimen, the therapist should always try to improve mobility of the spine, which can reduce pain and stiffness in the patient.¹⁸ Physical therapy should focus on stretching the anterior flexor muscles and strengthening the extensors. Specifically, therapy should focus on strengthening the postural muscles, back and neck extensors, shoulder retractors, and hip extensors and abductors.¹⁸ A prone program is a good management option to stretch the anterior muscles.¹⁸ Postural exercises are also beneficial, including standing against a wall with heels, buttocks, and shoulders touching the wall. Also, patients should try to sleep with as much extension as tolerable and lay prone at least 15 minutes a day.¹⁸ Aquatic therapy is another management option that can help reduce discomfort and provide an avenue for relaxation, stretching, and strengthening.¹⁸ Finally, breathing exercises are important because of the decreased chest expansion that occurs with ankylosing spondylitis.

Pharmacologic intervention is usually NSAIDs to help decrease pain and stiffness, allowing for normal ADLs and exercise. Indomethacin is the most effective NSAID used with ankylosing spondylitis for decreasing night pain and morning stiffness.18,19 Sulfasalazine, which reduces the levels of acute phase reactants, may act as a “disease-modifying” agent. Sulfasalazine can decrease the peripheral symptoms associated with ankylosing spondylitis. Immunosuppressant drugs are reasonable for the severe cases when a patient cannot participate in physical therapy.^18,19

Management of Gout

Management of acute gout focuses on the arthritis and then addresses the hyperuricemia.13,19 NSAIDs are the most common management for acute gout decreasing both inflammation and pain.^13,19,42 Corticosteroids are also used, but mainly when a patient has a contraindication for NSAIDs.¹⁹ Another management option is to use drugs to inhibit tubular reabsorption of uric acid to promote urinary excretion.³⁹ Furthermore, rest, elevation, and joint protection are important during acute gout to further promote decreased inflammation.^13,42 Between or after the acute attacks hyperuricemia is addressed to help prevent future episodes.^13,19,42 Management when symptom free includes changes in diet, avoidance of hyperuricemic medications, colchicine, and reduction of serum uric acid. Dietary changes that can decrease the risk of gout are weight loss, moderation of alcohol, and avoidance of high purine foods.^13,19 Controlling the hyperuricemia is important to prevent gout from becoming chronic.¹³

Fibromyalgia

Fibromyalgia is a chronic widespread muscle pain syndrome.8,13,19,21 By definition fibromyalgia is widespread pain lasting at least 3 months with physical findings of 11 to 18 tender points (Fig. 24-9).^8,13,21 Common characteristics of fibromyalgia are chronic widespread pain, aching, fatigue, and stiffness. Patients may also complain of headaches, sleep disorders, mood disorders, irritable bowel syndrome, and paresthesias.²⁸ Fibromyalgia is most common in women aged 20 to 50 years.^8,13,19 The exact etiology and pathogenesis of fibromyalgia is not fully understood, but is thought to be disturbances in different systems of the body. One common thought is that pain results from abnormalities of central sensory processing.⁸ New research characterizes fibromyalgia as a biological disorder associated with neurohormonal dysfunction of the autonomic nervous system (ANS) because of the objective biochemical, endocrine, and physiologic abnormalities.¹³ Furthermore, abnormalities in the hypothalamic–pituitary–adrenal axis, reproductive hormone axis, ANS, and immune system have been found in patients with fibromyalgia.¹³ The onset of fibromyalgia may be due to prolonged stress or anxiety, trauma, rapid steroid withdrawal, hypothyroidism, and viral and nonviral infections.^8,13 Fibromyalgia may start as localized pain and after months or years become widespread.⁸ The pain associated with fibromyalgia is often described as burning or aching, and sometimes tender, stiff, throbbing, and sore.^8,13 Even though fibromyalgia pain is widespread, patients will have one or two locations that are the worst, which are usually the neck, shoulders, and back.^8,19,21 Sleep disturbance is one of the other more common symptoms in fibromyalgia.^8,13,19 Patients will complain of exhaustion even after a night of sleep, which is because of the disordered non-rapid eye movement sleep.³⁵ Also, patients with fibromyalgia have increased motor activity and restlessness during sleep, which accounts for increased fatigue.³⁵ Other common symptoms are fatigue, subjective numbness, chronic headaches, dizziness, Raynaud phenomenon, and irritable bowel and bladder.^8,13,19,21 Symptoms tend to be exacerbated with noise, stress, tiredness, weather changes, trauma, noxious smells, and too much or too little exercise.^8,13,28

Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disorder that may affect multiple organ systems.7,13,19,37 SLE is most common in women during their childbearing years and is rarely found in older individuals.^7,13,19,37 In SLE the body produces antibodies against itself.¹³ The antigen–antibody complexes in tissues suppress the body’s immunity and damage tissues. The etiology of SLE is unknown, but environmental and genetic factors are believed to be the most related with evidence also supporting interrelated immunologic and hormonal factors.¹³ Many risk factors exist for SLE with hereditary factors at the forefront, along with physical and mental stress, streptococcal or viral infections, exposure to sunlight or ultraviolet light, and abnormal estrogen metabolism.¹³ Diagnosis for SLE is not difficult if the patient presents with common symptoms associated with SLE. The American Rheumatism Association has diagnosis criteria for SLE in which the patient needs to show 4 or more of the 11 symptoms. If the patient shows a few symptoms then diagnosis is made using clinical judgment along with supportive laboratory testing.^19,37

The clinical symptoms of patients with SLE are variable and most will not present with exactly the same symptoms. The severity of SLE can vary drastically from a treatable rash or fatigue to a life-threatening illness.19,37 The skin, joints, lungs, kidneys, blood, and other organs and tissues can be affected.^13,19,32,37 General signs of SLE include fever, fatigue, anorexia, weight loss, and myalgias.^19,37 Joint involvement is one of the earlier symptoms and occurs in more than 90% of patients.¹⁹ Symmetrical polyarthritis is common in any joint, but is usually found in small joints of hands, wrists, and knees.^13,37 SLE presents like RA, but is not usually destructive or deforming.^13,19,32,37 When deformities are present, ulnar deviation, swan neck deformity, fixed subluxations of fingers, tenosynovitis, and tendon ruptures can occur.^13,37 Recurrent inflammation of tendons and other supportive structures of the joints can lead to ulnar deviation of the second to fifth fingers and subluxation of the metacarpophalangeal joints, which is referred to as Jaccoud arthropathy.^37,45 Jaccoud arthropathy is correctable with no radiographic signs of erosion.³⁷ Also, observe patients for signs of osteonecrosis or septic arthritis, which will present as persistent monoarthritis primarily in the shoulders, hips, or knees.³⁷

Another common symptom in SLE is skin rashes over areas exposed to sunlight. Butterfly rash is an acute inflammatory rash over the nose and checks.13,19,32,37 Discoid lupus is characterized by raised, red, scaly, and scarring rashes that can develop around the face, scalp, ears, and upper extremities (Fig. 24-10).^13,19,37 Other cutaneous manifestations include alopecia, oral ulcers, fingertip lesions, periungual erythema, nail fold infarcts, splinter hemorrhages, livedo reticularis, urticaria, panniculitis, and Raynaud phenomenon.^13,19,37 Other clinical findings in SLE are associated with the renal, hematologic, cardiopulmonary, immune, and central nervous systems.^13,19,37

Modalities are not a cure for disease, but application of both cold and heat can help decrease symptoms and allow for better function.

Electrical stimulation

Transcutaneous electrical nerve stimulation (TENS) is an effective management to decrease pain (Fig. 24-12).¹⁷ A TENS units should never be placed close to the heart in a patient with a pacemaker.¹¹ TENS uses the gate theory to block pain by stimulating larger sensory fibers, which then block the smaller pain C fibers. C fibers innervate the synovium and joint capsule, so blocking pain perception in these fibers is beneficial to decreasing pain in patients suffering from arthritis.¹⁷ One study has shown decreased inflammation, joint volume, and joint pressure from use of TENS.¹⁷

Analgesics

The main role of an analgesic is to decrease pain, which is prevalent in patients with rheumatic disorders. Analgesics are primarily used with OA or in the early phases of RA, where inflammation is not as prevalent.³¹ There are several analgesics available to patients with rheumatic disorders, most notably acetaminophen, oxycodone, propoxyphene, and tramadol. Acetaminophen is one of the safest and most cost-effective drugs available. Other pain reducers, such as propoxyphene, oxycodone, and tramadol, are often used but have more side effects and higher risk of dependence. Tramadol is the least likely to cause dependence and is therefore often used first; however, tramadol does contain opioids, which decrease the sensation of pain through the central nervous system. Opioids can cause sleepiness, dizziness, and constipation.³¹ Education on the side effects is important so patients can report any side effects.

Nonsteroidal Antiinflammatory Drugs

NSAIDs have both analgesic and antiinflammatory effects but have no effect on arthritis progression.¹³ There are many NSAIDs, including ibuprofen (Motrin), aspirin, naproxen, indomethacin, meloxicam (Mobic), choline, and magnesium salicylates.^9,31 NSAIDs inhibit cyclooxygenase (COX), which is an enzyme that converts arachidonic acid to prostaglandin, a molecule that has many roles including the promotion of inflammation and pain. COX has two different isomers: COX-1 and COX-2. COX-1 may be the main contributor in the adverse side effect of gastric bleeding and ulcers. COX-2 is mainly involved in inflammation of tissues; therefore, COX-2 inhibition may be the key factor in the use of NSAIDs.^19,31

NSAIDs given at a lower dosage act more as an analgesic, but NSAIDS given at a higher dosage have more of an antiinflammatory effect. Low doses of NSAIDs may therefore be more appropriate with OA and early phase RA.⁶ Late phase or severe RA may require a higher dosage. Educating the patient on the importance of regularly taking their NSAID to get proper dosage is important. Symptoms should decrease in the first 2 to 3 weeks of NSAID use, however some patients will respond better to different medications, so a different NSAID should be tried if the patient does not feel any improvement after 3 weeks.¹⁹ Side effects to watch for include gastrointestinal bleeding and ulcers, dizziness, headaches, and drowsiness. Nausea and abdominal irritation are common and can be reduced by taking medication with food.³¹

Corticosteroids

Patients with inflammation as a primary symptom or who do not respond to NSAIDs are good candidates for corticosteroids.⁶ Several corticosteroids are available including prednisone, dexamethasone, hydrocortisone, and betamethasone.^19,31 Corticosteroids are primarily used on a short-term basis to decrease symptoms and allow for other management methods to be used, such as physical therapy. Though corticosteroids usually provide the fastest and most effective antiinflammatory response long term usage has been shown to increase the risk of osteoporosis. Patients using corticosteroids should take precautions to make sure they get adequate calcium and vitamin D. Corticosteroids given by intraarticular injection should not be repeated more than three to four times in a year because of increased loss of blood supply to the bones. Oral and intravenous options are also available for giving corticosteroids. Most patients will feel a decrease in symptoms within 24 hours of dosage. Corticosteroids are often given along with NSAIDS or DMARDs.¹³

Disease-Modifying Antirheumatic Drugs

DMARDs are generally started as soon as a definite diagnosis of rheumatoid disease is made because they work in the early phases of the inflammatory process, can decrease arthritic symptoms, and possibly decrease the rate of damage to bone and cartilage.13,19,31 DMARDs decrease this damage by suppressing the immune system, but generally take several weeks to months to produce effects.⁹ DMARDs are primarily used with patients diagnosed with RA and systemic lupus erythematosus, but DMARDs may also used for psoriatic arthritis and ankylosing spondylitis.^9,31

There are several types of DMARDs, including methotrexate, oral gold, penicillamine, sulfasalazine, and antimalarial drugs. Methotrexate is generally the first option for severe RA because of its long-term efficiency and its antiinflammatory and immunosuppressant effects.9,19,31 Methotrexate tends to produce results within 2 to 6 weeks, as opposed to other DMARDs that can take up to 6 months.^19,31 As stated earlier, it is important for the PTA to be cognitive of side effects for each drug. Methotrexate side effects include nausea, vomiting, diarrhea, mouth ulcers, decreased white blood cell count, megaloblastic anemia, and liver fibrosis or cirrhosis.³¹

Oral gold was one of the first DMARDs that showed improved symptoms in the majority of patients, but it has several side effects that start to negatively impact the risk-to-benefit ratio. Penicillamine was another DMARD used; it has many adverse side effects with about the same amount of beneficial results as oral gold. Sulfasalazine has been shown to be effective in treating spondyloarthropathies and juvenile RA.9,31 Sulfasalazine has antibacterial, antiinflammatory, and immunomodulatory properties and has been shown to inhibit tumor necrosis factor-alpha which coordinates the autoimmune process.^31,41

Biological Response Modifiers

The main purpose of biological agents is to inhibit the chemicals that are key factors in the inflammation and autoimmune processes. Unlike DMARDs, biological response modifiers target specific components of the immune system, thereby avoiding its widespread suppression.⁹ Two chemicals that current RA drugs are addressing are tumor necrosis factor (TNF) and interleukin-1 (IL-1). TNF is a cytokine that activates lymphocytes and leukocytes, two inflammatory cell types that destroy the synovium of joints.^19,31 TNF inhibitors can be more effective than methotrexate in early phases of RA, but the two have been used in combination with favorable results.¹⁹ Side effects are minimal with TNF inhibitors, but can include fever, chills, dyspnea, hypotension, and possibly higher chances of infection.³² IL-1 receptor antagonist is designed to slow the rate of joint damage. This is done by blocking interleukin-1 alpha and beta, which play a role in immune and inflammatory responses in the body.

Supplements

Glucosamine and chondroitin sulfate are two safe supplements widely used for pain with arthritis.³¹ Glucosamine is a natural substance that is a precursor in the synthesis of glycosaminoglycans, which are present in cartilage. Glucosamine therefore helps the body build and repair cartilage.²⁰ Chondroitin sulfate is a glycosaminoglycan and is thought to draw fluid into the cartilage, allowing for better joint function and protection from destructive enzymes.^20,31 There are no serious side effects documented with either of these supplements and they are readily available.^20,31,40 According to Richy and colleagues,⁴⁰ patients taking glucosamine and chondroitin reported improved scores on a visual analog scale for both pain and mobility. These two supplements have an excellent safety record and have been shown to be effective in managing the symptoms of arthritis in the knee and hip.³⁰

Synovectomy

A synovectomy is the removal of synovium infected with inflammation. Removing the inflamed synovium can decrease symptoms and prevent or slow destruction of a joint.⁹ Patients who continue to have inflammation after pharmacologic intervention are good candidates for this procedure; however, if the joint is degenerative without synovial inflammation then a synovectomy will not be beneficial. Synovium does grow back so the long-term benefits of a synovectomy are unknown.¹⁹

Osteotomy

An osteotomy is a procedure during which bone is cut to change the alignment of the joint to a better position (Fig. 24-14). Osteotomy can improve weight-bearing position of the lower extremities to aid in ambulation and is commonly used to correct coax vera, genu valgum, and genu varum.⁹ Osteotomy is one option that can be used to delay the need for a total joint replacement. During the rehabilitation of a patient after an osteotomy the therapist needs to be careful to not cause trauma or torque on the extremity. Stretching and exercise should be done in a gentle manner, and pain in these activities should last no longer than 1 hour. Osteotomy may be used for a patient with a spondyloarthropathy disease who has severe deformities of the lumbar spine.¹⁸

Resection

Resection is a procedure during which part or all of a bone is removed from a stiff or immobile joint, creating a space between the bones (Fig. 24-15). The empty space fills with scar tissue, which can be more flexible.⁹ Patients with severe arthritis of the foot can have bone resection in the foot to improve walking and pain. Other common sites for resections are the wrist, thumb, and elbow. The main goal of the surgery is to improve function and decrease pain.

Arthrodesis

Arthrodesis is the artificial ossification between two bones or a bone fusion (Fig. 24-16). By fusing, the joint pain is decreased and the joint can better sustain weight. The two bones lose flexibility but are pain-free and sturdy.⁹ Common sites for arthrodesis are the ankles, wrists, fingers, and thumbs. Arthrodesis is used less commonly, but can be beneficial for a chronically infected and painful joint.¹⁹

Arthroplasty

Arthroplasty is a procedure for rebuilding joints that have been damaged, become painful, and are less functional (Fig. 24-17). Total joint replacement is a very successful method for decreasing pain and improving the functional ability of individuals, but generally the surgery is used in people older than the age of 65 years because the new joint only lasts about 10 to 15 years. The arthritic joint is replaced with metal, ceramic, and plastic parts. The two most common joint replacements are knee and hip, but shoulder, elbow, ankle, and knuckles also can be replaced.¹⁹ In general, patients are expected to return to normal function, strength, mobility, and ROM after 6 months.³ Hip and knee arthroplasties are common surgical interventions in patients with OA²⁴; total hip arthroplasty is the most common procedure in patients with ankylosing spondylitis.¹⁸

Arthroscopy

Arthroscopy is not a procedure but rather a means of performing a procedure. The arthroscope is a thin tube with a light at the end connected to a screen. Arthroscopic surgery allows for exploration of a joint to determine what is wrong and to determine how extensive the damage is. Biopsies, cutting loose tissue, repairing cartilage, or smoothing rough surfaces can all be done arthroscopically. Arthroscopic surgery can have a faster recovery time than more invasive procedures, because only small incisions are required and minimal anesthesia is used. Surgeries commonly performed arthroscopically are meniscus repairs, rotator cuff repairs, cartilage damage repairs, and labral tear repair.