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FOUNDATION OVERVIEW

Osteoarthritis (OA) is a joint disease arising from different pathophysiological causes with manifestations of joint damage, mechanical stress, and loss of articular cartilage. A normal joint is composed of subchondral bone covered by a thin layer of articular cartilage. The interarticular space separates the adjoining subchondral bone and is cushioned with synovial fluid. Articular cartilage allows frictionless movement and uniform load distribution. Muscles, ligaments, and tendons surround the joint providing strength, maintaining stability, and absorbing load. However, there are several physiologic changes that lead to a weakened joint, instability with loss of dexterity, development of pain, and decreased mobility. Weight-bearing joints such as the knee and hip are mainly affected in OA; however, joints of the hand, foot, lumbar, and cervical spine may also be involved.

Patients with OA present with joint pain and tenderness, limited mobility, instability, and crepitus with joint movement. Symptoms may progress from absence of pain, to joint pain upon movement relieved by rest, to pain with rest. Advanced disease will manifest with joint space narrowing, formation of new bone at joint margins (osteophytosis), and subchondral sclerosis on radiographs. Risk factors associated with OA include advanced age, female gender, genetics, obesity, history of joint trauma, repetitive movement, excess mechanical stress, misalignment, and quadriceps weakness. Diagnosis of OA is based on patient history, physical examination, radiographic evidence, and laboratory testing. The American College of Rheumatology criteria for classification of OA of the knee and hip share common elements including: age more than 50 years, joint-specific pain, and joint stiffness. Diagnosis of knee or hip OA also includes bone tenderness and enlargement with radiographic evidence of osteophytes. Pain with internal rotation of the hip joint validates OA diagnosis. Hard tissue enlargement, swollen joints, and deformity in addition to hand pain with aching or stiffness, are criteria used to diagnose OA of the hand.

PREVENTION

Addressing risk factors such as obesity with weight loss, potential joint injury with joint protection, and muscle weakness with exercise are strategies for prevention of OA. Increased body mass is associated with muscle weakness, altered gait, decreased function, and fall risk and weight loss reduces the probability of developing OA. Joint injury predisposes patients for OA later in life. Current treatment of injury in those without OA may include surgery, joint rehabilitation, and muscle strengthening. Regular physical activity and muscle strengthening through resistance exercise in those without OA may be a preventative strategy. Because muscles provide movement, absorb load, and stabilize the joint, strengthening can improve muscle function.

TREATMENT

Treatment goals for OA include disease state awareness, relieving pain and stiffness, improving musculoskeletal movement and function, protecting affected joints, and maintaining and improving quality of life. These goals are accomplished by lifestyle changes, orthotics, physical and occupational rehabilitation, and pharmacologic therapy. Regular contact should be established with the patient through office visits or telephone contact to discuss pain ...

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