• Clinical science

Osteoarthritis (Osteoarthrosis)

Abstract

Osteoarthritis (OA) is a disabling joint disease characterized by a noninflammatory degeneration of the joint complex (articular cartilage, subchondral bone, and synovium) that occurs with old age or from overuse. It mainly affects the weight-bearing and high-use joints, such as the hip, knee, hands, and vertebrae. Despite the widespread view that OA is a condition caused exclusively by degenerative “wear and tear” of the joints, newer research indicates a significant heterogeneity of causation, including pre-existing peculiarities of joint anatomy, genetics, local inflammation, mechanical forces, and biochemical processes that are affected by proinflammatory mediators and proteases.Major risk factors include advanced age, obesity, previous injuries, and asymmetrically stressed joints. In early-stage osteoarthritis, patients may complain of reduced range of motion, joint-stiffness, and pain that is aggravated with heavy use. As the disease advances, nagging pain may also occur during the night or at rest. Diagnosis is predominantly based on clinical and radiological findings. Classic radiographic features of OA do not necessarily correlate with clinical symptoms and appearance. If lifestyle changes (moderate exercise, weight loss) and physical therapy fail to improve symptoms, nonsteroidal anti-inflammatory drugs (NSAIDs) in particular, are used to for the management active osteoarthritis. If medical interventions fail to improve the patient's quality of life, surgical procedures such as joint replacement may become necessary.

For more information on osteoarthritis of the hip and knee, see the respective learning card.

Epidemiology

  • Most common joint disorder in the USA, affecting more than 20 million adults
  • Incidence: increases with age
  • Sex: > , especially in patients older than 50 years
  • Incidence rates in specific joints: knee > hip > hand

References:[1][2]

Epidemiological data refers to the US, unless otherwise specified.

Etiology

Modifiable risk factors
  • Obesity
  • Excessive joint loading or overuse
Nonmodifiable risk factors
  • Age (> 55 years)
  • Familial history
  • History of joint injury or trauma
  • Anatomic factors causing asymmetrical joint stress
  • Hemophilic hemarthroses and deposition diseases that stiffen cartilage
  • Gender (see “Epidemiology” above)

References:[3][2]

Classification

References:[4]

Pathophysiology

Joint damage/stress → cartilage damage → decreased proteoglycans levels cartilage becomes friable and inelastic and starts to degrade → loss of joint space and bony surface → subchondral bone becomes thickened and sclerotic.

References:[5][6]

Clinical features

  • Early clinical findings
    • Pain on exertion, which is relieved with rest
    • Pain in both complete flexion and extension
    • Crepitus on joint movement
    • Joint stiffness and restricted range of motion
    • Radiating or referred pain (e.g., coxarthrosis may lead to knee pain)
  • Late clinical findings
    • Constant pain (including at night)
    • Morning joint stiffness usually lasting < 30 minutes
    • More severely restricted range of motion

References:[3]

Subtypes and variants

In contrast to osteoarthritis, rheumatoid arthritis does not affect the DIP joints.

References:[4]

Diagnostics

Osteoarthritis is usually diagnosed on the basis of clinical and radiographic evidence of joint degeneration.

Radiological signs of osteoarthritis

General radiological classification of osteoarthritis according to the Kellgren-Lawrence Grading Scale

Grade Conventional x-ray findings
Subchondral sclerosis Joint space narrowing Formation of osteophytes
I Mild None None
II Irregular articular surface suggested Mild Mild
III Irregular articular surface visible Severe Severe
IV Extensive degenerative changes to complete destruction of the articular joint. Deformation/necrosis of the joint visible.

The patient's history and clinical diagnosis are essential for the assessment and treatment of osteoarthritis! Radiographic signs often do not correlate with the patient's perception and clinical findings!

References:[3][7]

Differential diagnoses

See “Differential diagnoses” section in inflammatory arthritis

The differential diagnoses listed here are not exhaustive.

Treatment

  • General
    • Weight loss
    • Regular exercise
    • Shoe inserts (e.g., buffer insoles) in, e.g., valgus deformity of the knee
    • Targeted muscle growth, physiotherapy, and medical training therapy
    • Topical and heat therapy
  • Pharmacotherapy
  • Interventional therapy
    • In severe courses: intraarticular glucocorticoid injections (not a long-term treatment!)
  • Surgical therapy: if conservative and interventional measures fail
    • Endoprosthesis (joint replacement)
    • In case of failure of endoprosthesis or in select OA subtypes (e.g., Heberden's OA): arthrodesis (operative ankylosis)

Pharmacotherapy should be used as acute and symptomatic therapy only; long-term NSAID therapy should be avoided due to its many side effects!

References:[8][9][3]