Osteoarthritis

Presentation

• Intermittent pain – worse on or after movement
  
• Stiffness – In the morning, after activity or the evening.
  
• Loss of movement – Difficulties climbing stairs or walking etc.
  
• Joint inflammation.

Arthritis Definition

• Inflammation of one or more joints. Pro-inflammatory mediators (IL-1, TNFalpha, prostaglandins) interact to promote chronic inflammation and damage to articular cartilage and other joint tissue.

Arthritis Types

• Osteoarthritis – 80%
  
• Rheumatoid arthritis – 10%
  
  • Inflammation of the membrane around the joint.
    
• Goutry arthritis – 5%
  
  • Rich diet, Crystals of uric acid accumulate in joints causing inflammation.
    
• Ankylosing spondylitis (2%)
• Juvenile (1%)
• Suppurative (1%) arthritis

Osteoarthritis Definition

• Thinning of articular cartilage and thicker bone with nodules (osteophytes). Atrophy of muscle, damage to meniscus, ligament dysfunction and changes to fat metabolism to increase fat accumulations.
  
• Most common form of arthritis which increases in prevalence with age.
  
• Principally affects weight bearing joints.

Pathophysiology

• Normal Process of Articular Cartilage
  • Chondrocytes produce the matrix and secrete proteolytic enzymes.
  • Collagen fibres (type 2) form a network to provide tensile strength.
  • Proteoglycans (bottlebrush shaped proteins) bind water to provide jelly like, shock absorbing substance.
  • There are no nerves or lymphatics. No blood vessels so slow cell turnover and no nerves meaning cartilage doesn’t cause pain.
• Normal Process of Synovium
  • Synovial membrane – Lines joint capsule, Cellular layer = macrophages/fibroblasts. Deeper layer = loose connective tissue, capillaries.
    
  • Synovial fluid – Small volume (0.5 ml in the knee). High protein content ~30% of plasma (hyaluronate for viscosity and glycoproteins for lubrication secreted by cells in synovial intima.)
• Normal Process of Subchondral Bone
  • Bone underlying articular cartilage. Responds to loading -> Highly metabolically active and adapts to levels of loading and inflammatory markers.
• In Osteoarthritis
  • Articular Cartilage:
    • In early stages areas of chondrocytes increase protein synthesis due to increased load.
    • Increased production of proteinases leads to cartilage destruction
    • Therefore chrondrocyte apoptosis and reduced synthesis -> weaker, thinner cartilage.
    • Inflammatory mediators -> Inflammatory cytokines,
    • Prostaglandins (produced by chondrocytes) enhance degradation,
    • ROS promote chondrocyte apoptosis, nitric oxide produced by chondrocytes in response to inflammatory cytokines.
  • Synovium:
    • Inflammation – Macrophages (from synovial membrane) infiltrate synovial fluid.
    • This produces catabolic and proinflammatory mediators that contribute to cartilage destruction.
      
    • Synovitis is what contributes to the pain associated with osteoathritis.
  • Subchondral Bone:
    • Formation of osteophytes – bony nodules at joint margins, possibly stimulated by growth factors, may be responsible to stabilise damaged structures.
      
    • Subchondral bone sclerosis (abnormal hardening of body subchondral bone) – Thickened cortical bone and reduced trabecular bone.
      
    • Bone lesions – Areas of bone death (necrosis)
      
    • Also my contribute to pain
  • Other structures:
    • Skeletal muscle – Muscle weakness which can put excess force on a joint or pain means joint is used less. Cause or effect unknown.
    • Menisci – (Fibrocartilage pads in knee) susceptible to matrix destruction, cell clusters and calcification and cell death. Increased vascular and sensory nerve infiltration in OA.
    • Ligaments – Matrix destruction and collagen fibre disruption of some ligaments.

Most Common

• Increases in prevalence with age however doesn’t necessarily become worse with age and isn’t a necessary part of aging.
  
• Increases in Incidence with age up until after 70 which it decreases as there is less new cases in this age group.
• Highest in American Indian
• High in Caucasian and African American
• Reduced in Asian and Hispanic

Most Affected Body Part

• Knee
• Hip
• Hand

Risk Factors

• Systemic – Age, gender, ethnicity, genetics.
  
• Local – Injury (trauma/overuse), obesity, joint malalignment, bone shape

Signs and Symptoms

• Morning stiffness for less than 30 minutes
• Hard and bony joints
• Crepitus
• Heberden’s Node
• Bouchard’s Node
• Usually joints affected:
  • DIP (distal interphalangeal) joints
    
  • CMP (carpometacarpal) joints

Diagnoses

• Symptomatic – NICE states diagnose as OA if >45 years, activity related joint pain, No (<30 minutes) morning stiffness – to differentiate to RA. May also use pain scored.
• Labs are normal
• X-Ray – Scoring system to quantify based on
  • Joint space (cartilage thickness)
  • pathology e.g. osteophytes, subchondral bone thickness.
• MRI – Can visualize cartilage to quantify thickness of volume.

Treatment

• Clinical management
  • Exercise, weight lost, aids such as walking stick or insoles.
  • Walking, water aerobics, stationary bike riding along with strengthen training (lifting weights: helps strengthen muscles around the joint)
  • ROM: improves the mobility of the joint and decreases stiffness.
  • It is important patients with OA avoid high impact exercises that will increase stress on weight bearing joints such as running/jogging, jump rope, tennis, or any type of exercise with both feet off the ground.
• Pharmaceutical treatment
  • Pain killers and anti inflammatory
  • Voltaren Gel (Diclofenac)
  • Tylenol Arthritis
  • Mobic
  • Meloxicam
• Injections
  • Steroids
• Surgical treatment
  • Joint replacement, affected joint structures removed with prosthesis. Increases mobility, reduces pain, major surgery and prosthesis has limited life.