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(Degenerative Joint Disease; Osteoarthrosis; Hypertrophic Osteoarthritis)
Osteoarthritis (OA) is a chronic arthropathy characterized by disruption and potential loss of joint cartilage along with other joint changes, including bone hypertrophy (osteophyte formation). Symptoms include gradually developing pain aggravated or triggered by activity, stiffness lasting < 30 min on awakening and after inactivity, and occasional joint swelling. Diagnosis is confirmed by x-rays. Treatment includes physical measures, rehabilitation, patient education, and drugs.
OA, the most common joint disorder, often becomes symptomatic in the 40s and 50s and is nearly universal (although not always symptomatic) by age 80. Only half of patients with pathologic changes of OA have symptoms. Below age 40, most OA occurs in men and results from trauma. Women predominate from age 40 to 70, after which men and women are equally affected.
OA is classified as primary (idiopathic) or secondary to some known cause.
Primary OA may be localized to certain joints (eg, chondromalacia patellae is a mild OA that occurs in young people). Primary OA is usually subdivided by the site of involvement (eg, hands and feet, knee, hip). If primary OA involves multiple joints, it is classified as primary generalized OA.
Secondary OA results from conditions that change the microenvironment of the cartilage. These conditions include significant trauma, congenital joint abnormalities, metabolic defects (eg, hemochromatosis, Wilson disease), infections (causing postinfectious arthritis), endocrine and neuropathic diseases, and disorders that alter the normal structure and function of hyaline cartilage (eg, RA, gout, chondrocalcinosis).
Normal joints have little friction with movement and do not wear out with typical use, overuse, or most trauma. Hyaline cartilage is avascular, aneural, and alymphatic. It is 95% water and extracellular cartilage matrix and only 5% chondrocytes. Chondrocytes have the longest cell cycle in the body (similar to CNS and muscle cells). Cartilage health and function depend on compression and release of weight bearing and use (ie, compression pumps fluid from the cartilage into the joint space and into capillaries and venules, whereas release allows the cartilage to reexpand, hyperhydrate, and absorb necessary electrolytes and nutrients).
The trigger of OA is most often unknown, but OA sometimes begins with tissue damage from mechanical injury (eg, torn meniscus), transmission of inflammatory mediators from the synovium into cartilage, or defects in cartilage metabolism. The tissue damage stimulates chondrocytes to attempt repair, which increases production of proteoglycans and collagen. However, efforts at repair also stimulate the enzymes that degrade cartilage, as well as inflammatory cytokines, which are normally present in small amounts. Inflammatory mediators trigger an inflammatory cycle that further stimulates the chondrocytes and synovial lining cells, eventually breaking down the cartilage. Chondrocytes undergo programmed cell death (apoptosis). Once cartilage is destroyed, exposed bone becomes eburnated and sclerotic.
All articular and some periarticular tissues become involved in OA. Subchondral bone stiffens, then undergoes infarction, and develops subchondral cysts. Attempts at bony repair cause subchondral sclerosis and osteophytes at the joint margins. The osteophytes seem to develop in an attempt to stabilize the joint. The synovium becomes inflamed and thickened and produces synovial fluid with less viscosity and greater volume. Periarticular tendons and ligaments become stressed, resulting in tendinitis and contractures. As the joint becomes less mobile, surrounding muscles thin and become less supportive. Menisci fissure and may fragment.
OA of the spine can, at the disk level, cause marked thickening and proliferation of the posterior longitudinal ligaments, which are posterior to the vertebral body but anterior to the spinal cord. The result can be transverse bars that encroach on the anterior spinal cord. Hypertrophy and hyperplasia of the ligamenta flava, which are posterior to the spinal cord, often compress the posterior canal, causing lumbar spinal stenosis. In contrast, the anterior and posterior nerve roots, ganglia, and common spinal nerve are relatively well protected in the intervertebral foramina, where they occupy only 25% of the available and well-cushioned space.
Onset is most often gradual, usually beginning with one or a few joints. Pain is the earliest symptom, sometimes described as a deep ache. Pain is usually worsened by weight bearing and relieved by rest but can eventually become constant. Stiffness follows awakening or inactivity but lasts < 30 min and lessens with movement. As OA progresses, joint motion becomes restricted, and tenderness and crepitus or grating sensations develop. Proliferation of cartilage, bone, ligament, tendon, capsules, and synovium, along with varying amounts of joint effusion, ultimately cause the joint enlargement characteristic of OA. Flexion contractures may eventually develop. Acute and severe synovitis is uncommon.
Tenderness on palpation and pain on passive motion are relatively late signs. Muscle spasm and contracture add to the pain. Mechanical block by intra-articular loose bodies or abnormally placed menisci can occur and cause locking or catching. Deformity and subluxations can also develop.
The joints most often affected in generalized OA include the following:
Cervical and lumbar spinal OA may lead to myelopathy or radiculopathy. However, the clinical signs of myelopathy are usually mild. Lumbar spinal stenosis may cause lower back or leg pain that is worsened by walking (neurogenic claudication, sometimes called pseudoclaudication) or back extension. Radiculopathy can be prominent but is less common because the nerve roots and ganglia are well protected. Insufficiency of the vertebral arteries, infarction of the spinal cord, and dysphagia due to esophageal impingement by cervical osteophytes occasionally occur. Symptoms and signs caused by OA in general may also derive from subchondral bone, ligamentous structures, synovium, periarticular bursae, capsules, muscles, tendons, disks, and periosteum, all of which are pain sensitive. Venous pressure may increase within the subchondral bone marrow and cause pain (sometimes called bone angina).
Hip OA causes gradual loss of range of motion and is most often symptomatic during weight-bearing activities. Pain may be felt in the inguinal area or greater trochanter or referred to the knee.
Knee OA causes cartilage to be lost (medial loss occurs in 70% of cases). The ligaments become lax and the joint becomes less stable, with local pain arising from the ligaments and tendons.
Erosive OA causes synovitis and cysts in the hand. It primarily affects the DIP or PIP joints. The thumb carpometacarpal joints are involved in 20% of hand OA, but the metacarpophalangeal joints and wrists are usually spared. At this time, it is uncertain whether erosive interphalangeal OA is a variant of hand OA or whether it represents a separate entity.
OA is usually sporadically progressive but occasionally, with no predictability, stops or reverses.
OA should be suspected in patients with gradual onset of symptoms and signs, particularly in older adults. If OA is suspected, plain x-rays should be taken of the most symptomatic joints. X-rays generally reveal marginal osteophytes, narrowing of the joint space, increased density of the subchondral bone, subchondral cyst formation, bony remodeling, and joint effusions. Standing x-rays of knees are more sensitive in detecting joint space narrowing.
Laboratory studies are normal in OA but may be required to rule out other disorders (eg, RA) or to diagnose an underlying disorder causing secondary OA. If OA causes joint effusions, synovial fluid analysis can help differentiate it from inflammatory arthritides; in OA, synovial fluid is usually clear, viscous, and has ≤ 2000 WBC/μL.
OA involvement outside the usual joints suggests secondary OA; further evaluation may be required to determine the underlying primary disorder (eg, endocrine, metabolic, neoplastic, or biomechanical disorders).
OA treatment goals are relieving pain, maintaining joint flexibility, and optimizing joint and overall function. Primary treatments include physical measures that involve rehabilitation; support devices; exercise for strength, flexibility, and endurance; patient education; and modifications in activities of daily living. Adjunctive therapies include drug treatment and surgery.
Moderate weight loss in overweight patients often reduces pain and may even reduce progression of knee OA. Rehabilitation techniques are best begun before disability develops. Exercises (range of motion, isometric, isotonic, isokinetic, postural, strengthening—see Physical Therapy (PT) ) maintain range of motion and increase the capacity for tendons and muscles to absorb stress during joint motion. Exercise can sometimes arrest or even reverse hip and knee OA. Aquatic exercises are recommended because they spare the joints from stress. Stretching exercises should be done daily. Immobilization for any prolonged period of time can promote contractures and worsen the clinical course. However, a few minutes of rest (every 4 to 6 h in the daytime) can help if balanced with exercise and use.
Modifying activities of daily living can help. For example, a patient with lumbar spine, hip, or knee OA should avoid soft deep chairs and recliners in which posture is poor and from which rising is difficult. The regular use of pillows under the knees while reclining encourages contractures and should also be avoided. However, pillows placed between the knees can often help relieve radicular back pain. Patients should sit in straight-back chairs without slumping, sleep on a firm bed (perhaps with a bed board), use a car seat shifted forward and designed for comfort, do postural exercises, wear well-supported shoes or athletic shoes, and continue employment and physical activity.
In OA of the spine, knee, or thumb carpometacarpal joint, various supports can relieve pain and increase function, but to preserve flexibility, they should be accompanied by specific exercise programs. In erosive OA, range-of-motion exercises done in warm water can help prevent contractures.
Drug therapy is an adjunct to the physical program. Acetaminophen in doses of up to 1 g po qid may relieve pain and is generally safe. More potent analgesics, such as tramadol or rarely opioids, may be required; however, these drugs can cause confusion in older patients. Duloxetine, a serotonin norepinephrine reuptake inhibitor, reduces pain caused by OA. Topical capsaicin has been helpful in relieving pain in superficial joints by disrupting pain transmission.
NSAIDs, including cyclooxygenase-2 (COX-2) inhibitors or coxibs, may be considered if patients have refractory pain or signs of inflammation (eg, redness, warmth). NSAIDs may be used simultaneously with other analgesics (eg, tramadol, opioids) to provide better relief of symptoms. Topical NSAIDs may be of value for superficial joints, such as the hands and knees. Topical NSAIDS may be of particular value in the elderly, because NSAID absorption is reduced, minimizing risk of drug adverse effects.
Muscle relaxants (usually in low doses) occasionally relieve pain that arises from muscles strained by attempting to support OA joints. In the elderly, however, they may cause more adverse effects than relief.
Oral corticosteroids have no role. However, intra-articular depot corticosteroids can help relieve pain and increase joint flexibility in some patients.
Hyaluronans (similar to normal hyaluronic acid, a component of the joint) can be injected into the knee and provide some pain relief in some patients for prolonged periods of time. They should not be used more often than every 6 mo. The treatment is a series of 1 to 5 weekly injections. Efficacy in patients with x-ray evidence of severe disease is absent or limited and, in some patients, local injection can cause an acute inflammatory synovitis.
Glucosamine sulfate 1500 mg po once/day has been suggested to relieve pain and slow joint deterioration; chondroitin sulfate 1200 mg once/day has also been suggested for pain relief. Studies to date have shown mixed efficacy in terms of pain relief.
Other adjunctive measures can relieve pain, including massage, heating pads, weight loss, acupuncture, and transcutaneous electrical nerve stimulation (TENS―see Rehabilitative Measures for Treatment of Pain and Inflammation : Electrical stimulation). Laminectomy, osteotomy, and total joint replacement should be considered if all nonsurgical approaches fail.
Experimental therapies that may preserve cartilage or allow chondrocyte grafting are being studied. It is not clear whether using a lidocaine 5% patch relieves pain. Flavocoxid, a plant-derived compound, can be tried. Little information supports injections of platelet-rich plasma for OA.
OA, the most common joint disorder, becomes particularly common with age.
Key pathophysiologic features include disruption and loss of joint cartilage and bony hypertrophy.
OA can affect particular joints (sometimes secondary to injury or another joint problem) or be generalized (often as a primary disorder).
Symptoms include gradual onset of joint pain that is worsened by weight-bearing or stress and relieved by rest, and stiffness that lessens with activity.
Confirm the diagnosis with x-ray findings such as marginal osteophytes, narrowing of the joint space, increased density of the subchondral bone, bony remodeling, and sometimes subchondral cyst formation and joint effusion.
Treat primarily with physical measures that involve rehabilitation; support devices; exercise for strength, flexibility, and endurance; patient education; and modifications in activities of daily living.
Treat adjunctively with drugs (eg, analgesics, NSAIDs, muscle relaxants) and surgery.
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