Osteoarthritis

Osteoarthritis (OA) is the most common form of arthritis, and is due to cartilage destruction and changes of the subchondral bone. The risk of developing this disorder increases with age, obesity, and repetitive joint use or trauma. Patients develop gradual joint pain, stiffness lasting < 30 minutes, and decreased range of motion. Physical exam may reveal crepitus with joint motion and osteophyte formation (Heberden’s and Bouchard’s nodes). The diagnosis is clinical and supported with radiographic joint findings. Management includes conservative measures, analgesic medications, glucocorticoid intra-articular injections, and surgery for advanced disease.

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Epidemiology and Etiology

Epidemiology

  • Most common arthropathy (> 70% of all arthritis)
  • Incidence: approximately 195 cases per 100,000 people worldwide
  • Prevalence increases with age.
    • 80%–90% of individuals < 65 years have radiographic osteoarthritis (OA).
    • Symptoms are generally not noticed until after the age of 50.
  • Women are more commonly affected.

Classification and etiology

  • Primary OA: 
    • Idiopathic
    • Nodal OA
  • Secondary OA: 
    • Trauma or surgery
    • Congenital disorders
      • Scoliosis
      • Epiphyseal dysplasia
      • Legg-Calve-Perthes disease
      • Joint hypermobility
      • Slipped femoral capital epiphysis
      • Congenital hip dislocation
    • Metabolic disorders
      • Hemochromatosis
      • Wilson’s disease
      • Crystal deposition disease (gout)
      • Hemoglobinopathies (thalassemia)
    • Infection
    • Bone disorders
      • Paget’s disease
      • Osteonecrosis
    • Neuropathic (Charcot’s joint)
      • Diabetes mellitus
      • Syphilis

Risk factors

  • Age
  • Obesity
  • Sex
  • Genetics and family history
  • Physical activity and repetitive use
  • Muscle weakness or dysfunction

Pathophysiology

  • Hypertrophic repair of articular cartilage: mechanical stress → cartilage damage → ↑ proteoglycan and collagen synthesis → swelling of joint cartilage
  • Cartilage destruction:
    • Continued damage → ↑ chondrocyte proliferation and activity → matrix metalloproteinase production → matrix degradation
      • Inflammatory mediators and matrix protein fragments continue chondrocyte stimulation.
      • Ultimately leads to chondrocyte death
    • ↓ collagen and proteoglycans → ↓ cartilage elasticity → ↓ joint integrity
    • Loss of cartilage → ↓ joint space → bone becomes denuded
  • Subchondral bone response:
    • Articulation of exposed bone with an opposing surface → ↑ stress on the bone
    • Vascular invasion and ↑ cellularity → bone becomes thickened and dense (subchondral sclerosis)
    • Chronic impaction and osseous necrosis → cystic degeneration (subchondral cysts)
    • Osseous metaplasia and ossification of connective tissue → outgrowth of new bone (osteophytes)

Pathology of osteoarthritis
Destruction of cartilage leads to decreased joint space. With severe destruction, bone becomes denuded.

Image: “” by Phil Schatz. License: CC BY 4.0

Clinical Presentation

Commonly affected joints

  • Hands:
    • Proximal interphalangeal (PIP) joints
    • Distal interphalangeal (DIP) joints
    • 1st carpometacarpal (CMC) joints
  • Hips 
  • Knees
  • Spine:
    • Intervertebral discs
    • Zygapophyseal (facet) joints
  • Feet: 1st metatarsophalangeal (MTP) joints

Symptoms

  • Joint pain
    • Gradual onset
    • Asymmetric
    • More severe with: 
      • Activity
      • Weight bearing
    • Relieved with rest
    • Later in the disease: 
      • Pain is more constant.
      • Affects sleep and level of activity
  • Morning stiffness
    • Duration < 30 minutes
    • Improves with movement
  • Inguinal pain due to hip involvement
  • Restricted joint movement
  • Sensation of joint instability and locking
  • Radicular pain results from:
    • Spondylolisthesis
    • Nerve impingement

Physical exam

  • Joint line tenderness
  • Limited range of motion (ROM)
  • Crepitus with passive ROM
  • Evidence of osteophytes
    • DIP joints: Heberden’s nodes
    • PIP joints: Bouchard’s nodes
    • First CMC joint: thumb squaring
  • Synovitis 
    • Seen in erosive OA
      • An inflammatory subset of primary OA
      • Etiology is unknown.
    • Signs:
      • Soft-tissue swelling
      • Warm
  • Popliteal or Baker’s cyst
  • Knee varus or valgus deformities

Diagnosis

Imaging

Osteoarthritis is a clinical diagnosis that is confirmed with imaging.

  • Radiography
    • Classic findings:
      • Joint space narrowing
      • Subchondral sclerosis
      • Subchondral cysts
      • Osteophytes
      • “Seagull wing” appearance in erosive OA (due to central subchondral erosions)
    • Insensitive for early disease
    • Findings do not correlate well with symptoms.
  • Magnetic resonance imaging (MRI)
    • More sensitive for early disease
    • Additional findings:
      • Cartilage defects
      • Bone marrow lesions
      • Joint effusions

Supporting workup

The following tests are not used for the diagnosis of OA, but are used to exclude other causes of arthritis.

  • Arthrocentesis with synovial fluid analysis
    • Non-inflammatory with a WBC count < 2,000 cells/μL
    • Crystal analysis to rule out gout and pseudogout
  • Laboratory testing 
    • Negative rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP)
    • Normal erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP)
    • Negative antinuclear antibody (ANA)

Management

The goals of management include alleviating pain and minimizing the loss of physical function.

Osteoarthritis management flowchart
Patients start with conservative measures (weight loss and physical therapy). If symptoms do not improve, or if they worsen, management progresses through this flowchart. Surgery is reserved for patients with severe, unrelenting disease.

Image by Lecturio.

General conservative measures

  • Lifestyle modifications: 
    • Minimize weight bearing.
    • Avoid a slumping posture while sitting.
    • Sleep on a firm bed.
    • Wear supportive shoes or orthoses.
  • Weight loss
  • Physiotherapy to increase: 
    • Strength
    • Flexibility
    • Range of motion
    • Endurance
  • Assistive devices: 
    • Unload or redistribute the load on the joint.
    • Cane, brace, splints, and taping
  • Hot and cold therapy

Medical management

  • Topical capsaicin
  • Acetaminophen
  • Oral and topical nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Muscle relaxants
    • Cyclobenzaprine, methocarbamol
    • Relieve pain from strained muscles
    • Use caution in elderly patients.
  • Duloxetine
    • Can be used in patients with contraindications to NSAIDs
    • Alternative for those who do not respond to the above interventions
  • Corticosteroids
    • Should not be used chronically
    • Can be used orally or as an intra-articular injection
  • Hyaluronic acid
    • Intra-articular injection
    • Controversial, and evidence is limited
  • Supplements
    • Glucosamine, chondroitin
    • Evidence is limited.
  • Opioids
    • Can be considered for short-term use
    • For patients who fail or are not candidates for other treatments
    • Consider referral to a chronic pain management clinic.

Surgical management

  • Reserved for patients with advanced disease who have failed other treatments
  • Total joint arthroplasty (replacement) is the most common procedure.

Differential Diagnosis

  • Rheumatoid arthritis: an autoimmune disease of the joints, causing an inflammatory and destructive arthritis. Patients typically have swelling and pain of the peripheral joints (e.g., hands, wrists, knees, ankles). The DIP joints are generally spared, and morning stiffness typically lasts > 60 minutes. Diagnosis is based on the clinical picture, inflammatory markers, RF, and anti-CCP. Management starts with glucocorticoids, disease-modifying antirheumatic drugs (DMARDs), and NSAIDs.
  • Reactive arthritis: a spondyloarthropathy that is often precipitated by a gastrointestinal or genitourinary infection. Patients may present with an asymmetric arthritis, typically of the lower extremities. Reactive arthritis can be associated with fever, tendinitis, enthesitis, mucocutaneous ulcers, and conjunctivitis. Diagnosis is clinical. Management includes NSAIDs, DMARDs, and treatment of the infection. 
  • Psoriatic arthritis: a spondyloarthropathy that occurs in patients with psoriasis. This inflammatory arthritis is frequently asymmetric. Small and large joints are involved, including the DIP joints and the sacroiliac spine. Enthesopathy and dactylitis are also seen. The diagnosis is clinical, and should be suspected in patients with psoriasis. Management includes DMARDs and biologic agents.
  • Gout: a disease caused by hyperuricemia that leads to arthritis from precipitation of monosodium urate crystals in the joints. Gout is often monoarticular, and usually involves pain, tenderness, swelling, erythema, and warmth of the first MTP joint. The diagnosis is made with identification of negatively birefringent, needle-shaped crystals in the synovial fluid. Management includes NSAIDs, colchicine, corticosteroids, and uric acid reduction with allopurinol.
  • Pseudogout: intra-articular calcium pyrophosphate deposition. The etiology is not clear. Patients present with acute flares of joint swelling, warmth, and pain. Pseudogout usually affects larger joints, such as the knee. Diagnosis is with identification of positively birefringent, rhomboid crystals in the synovial fluid. Management includes NSAIDs, corticosteroids, and colchicine.
  • Septic arthritis: a joint infection due to bacteria (rarely, viruses) in the synovial or periarticular tissues. Patients present with an acute onset of monoarticular swelling, pain, erythema, and warmth. Fever may also be present. Diagnosis is made with synovial fluid analysis, including Gram stain, culture, and WBC count > 20,000 cells/μL. Management includes intravenous antibiotics and drainage of pus from the joint.

References

  1. March, L., and Cross, M. (2020). Epidemiology and risk factors for osteoarthritis. In Ramirez Curtis, M. (Ed.), UpToDate. Retrieved January 11, 2021, from https://www.uptodate.com/contents/epidemiology-and-risk-factors-for-osteoarthritis
  2. Loeser, R.F. (2020). Pathogenesis of osteoarthritis. In Ramirez Curtis, M. (Ed.), UpToDate. Retrieved January 11, 2021, from https://www.uptodate.com/contents/pathogenesis-of-osteoarthritis
  3. Doherty, M., and Abhishek, A. (2019). Clinical manifestations and diagnosis of osteoarthritis. In Ramirez Curtis, M. (Ed.), UpToDate. Retrieved January 11, 2021, from https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-osteoarthritis
  4. Deveza, L.A. (2020). Overview of the management of osteoarthritis. In Ramirez Curtis, M. (Ed.), UpToDate. Retrieved January 11, 2021, from https://www.uptodate.com/contents/overview-of-the-management-of-osteoarthritis
  5. Kontzias, A. (2020). Osteoarthritis (OA). [online] MSD Manual Professional Version. Retrieved January 11, 2021, from https://www.msdmanuals.com/professional/musculoskeletal-and-connective-tissue-disorders/joint-disorders/osteoarthritis-oa
  6. Lozada, C.J., and Culpepper Pace, S.S. (2020). Osteoarthritis. In Diamond, H.S. (Ed.), Medscape. Retrieved January 11, 2021, from https://emedicine.medscape.com/article/330487-overview
  7. Sen, R., and Hurley, J.A. (2020). Osteoarthritis. [online] StatPearls. Retrieved January 12, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK482326/

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