Chapter 2: Osteoarthritis

INTRODUCTION

• Osteoarthritis (OA) is a common, progressive disorder affecting primarily weight-bearing diarthrodial joints, characterized by progressive destruction of articular cartilage, osteophyte formation, pain, limitation of motion, deformity, and disability.

PATHOPHYSIOLOGY

• Primary (idiopathic) OA, the more common type, has no known cause.

• Secondary OA is associated with a known cause such as inflammation, trauma, metabolic or endocrine disorders, and congenital factors.

• OA usually begins with damage to articular cartilage through injury, excessive joint loading from obesity or other reasons, or joint instability. Damage to cartilage increases activity of chondrocytes in attempt to repair damage, leading to increased synthesis of matrix constituents with cartilage swelling. Normal balance between cartilage breakdown and resynthesis is lost, with increasing destruction and cartilage loss.

• Subchondral bone adjacent to articular cartilage undergoes pathologic changes and releases vasoactive peptides and matrix metalloproteinases. Neovascularization and increased permeability of adjacent cartilage occur, which contribute to cartilage loss and chondrocyte apoptosis.

• Cartilage loss causes joint space narrowing and painful, deformed joints. Remaining cartilage softens and develops fibrillations, followed by further cartilage loss and exposure of underlying bone. New bone formations (osteophytes) at joint margins distant from cartilage destruction are thought to help stabilize affected joints.

• Inflammatory changes can occur in the joint capsule and synovium. Crystals or cartilage shards in synovial fluid may contribute to inflammation. Interleukin-1, prostaglandin E₂, tumor necrosis factor-α, and nitric oxide in synovial fluid may also play a role. Inflammatory changes result in synovial effusions and thickening.

• Pain may result from distention of the synovial capsule by increased joint fluid; microfracture; periosteal irritation; or damage to ligaments, synovium, or the meniscus.

CLINICAL PRESENTATION

• Risk factors include increasing age, obesity, sex, certain occupations and sports activities, history of joint injury or surgery, and genetic predisposition.

• The predominant symptom is deep, aching pain in affected joints. Pain accompanies joint activity and decreases with rest.

• Joints most commonly affected are the distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints of the hand, first carpometacarpal joint, knees, hips, cervical and lumbar spine, and first metatarsophalangeal (MTP) joint of the toe.

• Limitation of motion, stiffness, crepitus, and deformities may occur. Patients with lower extremity involvement may report weakness or instability.

• Upon arising, joint stiffness typically lasts less than 30 minutes and resolves with motion.

• Presence of warm, red, and tender joints suggests inflammatory synovitis.

• Physical examination of affected joints reveals tenderness, crepitus, and possibly enlargement. Heberden and Bouchard nodes are bony enlargements (osteophytes) of the DIP and PIP joints, respectively.

DIAGNOSIS

• Diagnosis is made through patient history, physician examination, radiologic findings, and laboratory testing.

• American College of Rheumatology criteria for classification of OA of the hips, knees, and hands include presence of pain, bony changes on examination, normal erythrocyte sedimentation rate (ESR), and radiographs showing osteophytes or joint space narrowing.

• For hip OA, patients must ...