Episode 146: RA vs OA

Episode 146: RA vs OA    Future Dr. Magurany explains how to differentiate rheumatoid arthritis from osteoarthritis.  Written by Thomas Magurany, MSIV, Ross University School of Medicine. Comments by Hector Arreaza, MD. You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.1. Etiology:<br /><br /> Rheumatoid Arthritis (RA):<br /><br /> RA is an autoimmune disease wherein the immune system mistakenly attacks healthy tissues, particularly the synovial joints, usually between the ages of 30-50. Genetic predisposition, environmental factors such as smoking or infections, hormonal imbalances, and lower socioeconomic status have been associated with an increased risk of developing RA(1).<br /><br />Osteoarthritis (OA):<br /><br /> OA primarily arises due to mechanical stress on the joints over time. Factors contributing to OA include age, obesity, joint injury or trauma, repetitive joint use or overuse, genetic abnormalities in collagen structure, and metabolic disorders affecting cartilage metabolism (2).The greatest risk factor for the development of OA is age with most patients presenting after 45 years of age. The greatest modifiable risk factor for OA is weight. People with a BMI >30 were found to have a 6.8 times greater risk of developing OA. (3) Primary OA is the most common and is diagnosed in the presence of associated risk factors such as: older age, female gender, obesity, anatomical factors, muscle weakness, and joint injury (occupation/sports activities) in the absence of trauma or disease. Secondary OA occurs alongside a pre-existing joint deformity including trauma or injury, congenital joint disorders, inflammatory arthritis, avascular necrosis, infectious arthritis, Paget disease, osteopetrosis, osteochondritis dissecans, metabolic disorders (hemochromatosis, Wilson’s disease), Ehlers-Danlos syndrome, or Marfan syndrome.2. Pathogenesis:Rheumatoid Arthritis (RA):In some patients, RA is triggered by some sort of environmental factor in a genetically predisposed person. The best example is tobacco use in a patient with HLA-DRB1. The immune response in RA starts at sites distant from the synovial joints, such as the lung, gums, and GI tract. In these tissues, modified proteins are produced by biochemical reactions such as citrullination. (4)<br />In RA, an abnormal immune response leads to chronic inflammation within the synovium lining the joints. The inflammatory cytokines released cause synovitis and lead to the destruction of articular cartilage and bone erosion through pannus formation. Immune cells infiltrate the synovium causing further damage. (4) In summary: formation of antibodies to citrullinated proteins, these antibodies begin attacking wrong tissues.Osteoarthritis (OA):<br />The primary pathological feature of OA is the degeneration of articular cartilage that cushions the joints causing surface irregularity, and focal erosions. These changes progress down the bone and eventually involve the entire joint surface. Mechanical stress triggers chondrocyte dysfunction, leading to an imbalance between cartilage synthesis and degradation that cause cartilage outgrowths that ossify and form osteophytes. This results in the release of enzymes that degrade the extracellular matrix, leading to progressive cartilage loss. As more of the collagen matrix is damaged, chondrocytes undergo apoptosis. Improperly mineralized collagen causes subchondral bone thickening; in advanced disease,