Chapter 184

Osteoarthritis

Joanne Sandberg-Cook

Definition and Epidemiology

Osteoarthritis (OA) is a progressive degenerative joint process. It involves degeneration of the articular (hyaline) cartilage layer on the ends of bones at the joints as well as increasing thickness and sclerosis of the bone plate and subsequent involvement of joint protective mechanisms including ligaments and muscle. OA manifests as a monoarticular or polyarticular phenomenon and is often asymmetric. It can occasionally appear as a more generalized disease. OA is the most common type of arthritis, and it usually begins asymptomatically in the second or third decade of life. By the fourth decade, most people have some degree of pathologic (radiologic) change on articular weight-bearing surfaces. Symptoms typically begin to appear in the fourth through sixth decades of life. Some degree of symptomatic arthritis is extremely common by the seventh decade. OA occurs more commonly in women, at least in middle-aged and elderly persons. Risk factors include age, obesity, prior trauma, genetics, repetitive activities, metabolic disorders, neurologic diseases, and hematologic conditions.¹

The carpometacarpal joints of the thumbs, distal interphalangeal joints of the fingers, first metatarsophalangeal joints of the feet, cervical and lumbar spine, and weight-bearing joints such as the hips and knees are most commonly affected. OA can also affect previously injured joints. Pain, stiffness, and limited range of motion are the most common reasons for seeking medical care. The degenerative effects of OA result in physical disability and can have a profound impact on the quality of life.¹^,²

Pathophysiology

Initially, the cartilage softens and becomes overhydrated and boggy, with decreased quantity and size of proteoglycans within the matrix. Collagen also loses its stiffness, with fewer cells and loss of cross-links as degradation continues.³^,⁴ The surface layers fibrillate, and the cartilage loses its thickness, develops surface crevices, and then loses integrity. Loose cartilaginous fragments (known as loose bodies) can flake off, blocking range of motion and contributing to pain and disability.⁴

Chondrocytes proliferate with increased metabolic activity as the subchondral bone scleroses under the damaged areas. The bone thickens, stiffens, and then produces cysts, microfractures, and osteophytes at the joint margins,⁴ findings that are often seen on imaging. The associated increased metabolic activity can be detected on a bone scan.

The cartilage surface is completely aneural, making the pathogenesis of pain from OA speculative. It is now thought to be a whole-joint disease with significant inflammatory soft tissues changes including synovitis as well as bone marrow lesions. Changes in joint nociceptors have been identified, and some researchers have suggested neuropathic pathways as contributors to pain.⁴ Joint effusions are not uncommon, especially in the knee, causing stiffness and difficulty walking.

Clinical Presentation and Physical Examination

Insidious, progressive pain or stiffness of one or more joints may be the initial presenting complaint. Symptoms are most prevalent on arising, with a duration of less than 1 hour, and after a prolonged activity and are relieved by rest.³ Weight-bearing activities, such as going up or down stairs, getting up from a sitting position, walking, prolonged standing, or changing activity level, can be particularly troublesome. The patient may also complain of crepitus (grinding), swelling, joint deformity, and gradual loss of motion as the disease progresses.⁵

When OA involves the cervical or lumbar spine, neuropathy and radiculopathy may develop as nerves are compressed. OA involving the hip manifests with groin or buttock pain that can radiate to the knee. The pain can cause the patient to “favor” the hip, which in turn can contribute to specific muscle weakness. The resultant gait is known as Trendelenburg gait. OA of the knee involves the medial joint compartment 70% of the time, leading to a varus deformity of the extremity. It can then progress to include the lateral joint compartment and patellofemoral articulations as well. Pain on palpation of the medial and lateral joint lines and joint effusions are often seen. Quadriceps muscle atrophy is common on the affected side.⁵

OA of the hands manifests as Heberden nodes (deformity of the distal interphalangeal joints) and Bouchard nodes (deformity of the proximal interphalangeal joints). A compression test as well as pain with palpation of the joint can detect OA of the carpometacarpal joint. Contracture, deformity, and even joint fusion are common as the disease progresses.⁵ Fortunately, OA of the hands is seldom completely disabling.

Diagnostics

In the early stages of OA, radiographic findings may not be evident.³ As the disease progresses and joint space is lost, radiographic changes become more prominent. Plain radiographs are often all that are needed to confirm the diagnosis. Magnetic resonance imaging (MRI) helps to identify changes in surrounding soft tissue. A bone scan may show increased metabolic activity within an arthritic joint.⁴

OA is a nonsystemic disease. There are no serologic markers for OA as yet, but serologic tests are commonly performed to rule out other disorders. Examination of the joint fluid may be helpful in ruling out crystalline, infectious, or inflammatory conditions. See the the diagnostics box for optional testing.

Diagnostics

Osteoarthritis

Laboratory

Rheumatoid factor ^*

Cyclic citrullinated peptide ^*

Antinuclear antibodies ^*

CBC and differential ^*

ESR ^*

Uric acid ^*

Joint aspirate for crystals, white blood cells ^*

C-reactive protein ^*

Imaging

CBC, complete blood count; CT, computed tomography; ESR, erythrocyte sedimentation rate.

Differential Diagnosis

The differential diagnosis box lists other diseases that should be considered and excluded when appropriate. Other arthritic conditions, such as rheumatoid arthritis (see Chapter 218), gout and pseudogout (see Chapter 176), and psoriatic arthritis (see Chapter 215), are commonly seen with OA.⁵

Differential Diagnosis

Osteoarthritis