Osteoarthritis and Joint Health Quiz

Arthritis Overview

• Arthritis is a general term for joint inflammation.
• The presentation discusses rheumatoid arthritis (RA) and osteoarthritis (OA).

Rheumatoid Arthritis (RA)

• RA is a chronic, systemic autoimmune disease.
• It causes inflammation in connective tissues, primarily in joints.
• The first tissue affected is the synovial membrane, which then spreads to articular cartilage, fibrous joint capsule, and surrounding ligaments and tendons.
• RA is characterized by inflammation of the synovial membrane, systemic signs and symptoms, and normal synovial fluid.

Joint Disease Classification

• Joint diseases are classified as inflammatory or non-inflammatory.
• Inflammatory joint diseases, like RA, are characterized by inflammation of the synovial membrane.
• Non-inflammatory joint diseases, like OA, are not characterized by this inflammation.
• Joint disease diagnosis involves evaluating synovial membrane inflammation, systemic signs & symptoms, and synovial fluid.

Rheumatoid Arthritis (RA) Key Characteristics

• Rheumatoid factors (autoantibodies) are present in the synovial fluid and synovial membranes of people with RA.
• Around 80% of people with RA are rheumatoid factor positive, while 20% are RF negative.
• The interaction between rheumatoid factor and immunoglobulins initiates an inflammatory reaction.
• The cause of RA is unknown but likely involves a combination of genetic and environmental factors.

Pathogenesis of Rheumatoid Arthritis (RA) Step by Step

• An unknown cause triggers an immune response.
• The immune response becomes abnormal.
• Inflammation starts in the synovium, the synovial membrane where cartilage is present.
• The inflammatory response is perpetuated, leading to continuous inflammation.
• Progressive joint destruction occurs.

Synovial Joint Anatomy

• Ligaments and tendons support the bones and control joint motion.
• Synovial membrane has 2 layers, which facilitate phagocytosis of bacteria and synovial fluid's viscous quality
• Periosteum, the deep layer of bone, contains cells involved in bone formation.
• Articular hyaline cartilage reduces friction within a joint and distributes weight-bearing forces.

Rheumatoid Arthritis (RA): Additional Manifestations

• RA can affect other body systems, including cardiovascular, pulmonary, and gastrointestinal systems.
• Infections and osteoporosis are additional potential manifestations.

Rheumatoid Arthritis (RA): Epidemiology

• In 2015, approximately 300,000 Canadians had RA, with a 0.9% cumulative prevalence.
• The prevalence of RA has been steadily increasing.
• Median life expectancy is reduced by 3-7 years in people with RA.
• Onset typically occurs between the ages of 20 and 50, however men and women are equally affected after the age of 60.

Rheumatoid Arthritis (RA): Diagnosis and Criteria

• Diagnosis is challenging in early stages due to gradual onset and waxing/waning symptoms.
• Joint involvement, blood tests for abnormal immune response (autoantibodies), and duration of symptoms are used to diagnose.
• Radiography and MRI can be used to assess joint changes.
• At least 6 out of 10 classification criteria are required for an RA diagnosis.

Osteoarthritis (OA)

• OA is a slowly progressive articular disease, starting in cartilage and affecting underlying bone, soft tissues and synovial fluid.
• Two classifications:
  • Primary OA: Unknown cause, thought to be related to a defect in articular cartilage.
  • Secondary OA: Known cause (trauma, infection, lower limb alignment issues).

Cartilage

• Cartilage provides friction-free movement within the joint.
• It also absorbs shock, and disperses weight-bearing forces across the joint surface.

Cartilage Characteristics

• Cartilage requires elasticity, regaining form after compression.
• It requires high tensile strength to remain effective.

Cartilage Components

• Chondrocytes produce the collagen and proteoglycans within the cartilage Matrix.
• Water makes up 70-85% of the cartilage matrix.

How Proteoglycans Work

• Proteoglycans are negatively charged, so their aggregation causes them to repel each other, taking up more volume in the matrix.
• The matrix is limited by the collagen framework, contributing to cartilage stiffness.

Cartilage Absorption

• When cartilage is compressed, proteoglycans aggregate together, increasing their repulsive force.
• This contributes to increasing compressive stiffness.

Cartilage Maintenance

• Chondrocytes synthesize matrix (anabolic activity) and secrete matrix-degradation enzymes (catabolic activity) to maintain cartilage's normal turnover
• The health of chondrocytes determines the integrity of joints.

Osteoarthritis (OA): Epidemiology

• OA is the most common joint disease.
• Prevalence increases with age being estimated at 60% in men and 70% in women aged 65+.
• Hip OA is more common in men, while OA of IP joints and thumbs are more prevalent in women.

Osteoarthritis (OA): Etiology

• OA is a multifactorial disease with intrinsic and extrinsic factors.
• Intrinsic factors (non-modifiable): Age, gender, genetic susceptibility and nutritional factors play a role.
• Extrinsic factors (modifiable): Physical activity (repetitive) and obesity.
• Smoking can influence the severity of OA presentations

Osteoarthritis (OA): Pathogenesis

• The pathological process of OA originates in excessive joint loading causing failure of the cartilage (Scenario 1).
• Articular cartilage and subchondral bone are normal but the material properties of either are inferior (Scenario 2).

Osteoarthritis (OA): Pathogenesis of Cartilage

• Degradation of cartilage (OA) is the end result of an imbalance in catabolic and anabolic repair activities.
• Early changes to the cartilage matrix include enzymatic breakdown of the collagen network and proteoglycan aggregation interfering with load bearing abilities affecting mechanical transfer.
• Water and synovial fluid are disrupted, affecting stability.

Osteoarthritis (OA): Later Cartilage Changes

• With loss of cartilage, inflammation occurs with ligamentous laxity and muscle weakness.
• Mechanical stress shifts to subchondral bone.
• New bone called osteophytes form and "joint mice" can be produced from small cartilage fragments which irritate the synovial membrane.

Osteoarthritis (OA): Clinical Presentation

• OA pain is often motion related, not aneural (not arising from cartilage itself).
• Pain can result from nerve endings in the periosteum covering osteophytes, microfractures, joint instability and/or synovial inflammation.

Osteoarthritis (OA): Additional Clinical Presentation Characteristics

• Common symptoms beside pain include:
  • Limited range of motion
  • Crepitus (grinding) in motion.
  • Joint effusion.
  • Joint malalignment and deformities are also possible.
• Stiffness (often less than 30 minutes) after inactivity can occur.

Clinical Presentation of Osteoarthritis (OA)

• Pain and symptoms generally increase or occur with motion.
• Stiffness (often less than 30 minutes) is present after periods of inactivity such as sitting or sleeping.
• Swelling, if presented is generally mild and focal to the affected joint.

OA Affected Joints

• Commonly affected joints include: hips, knees, ankles, feet, hands, wrists, neck and the lower back (lumbar and sacroiliac joints).

Contrast OA and RA

• OA is usually one sided, and primarily affects weight bearing joints, while RA is symmetrical.
• Mornings stiffness is usually decreased by physical activity in OA and remains in RA
• OA can be triggered by factors such as trauma, infection and lower limb alignment issues, while RA has an uncertain, likely multifactorial, cause.
• No systemic symptoms exist for OA, while RA may exhibit these symptoms like fatigue and weight loss.
• RA is associated with rheumatoid factors whilst OA is not.