1. OA vs RA Alastair Stephens Matt Vreugde

2. What are the 5 functions of bone? Function SupportProtection Movement Haematopoiesis Mineral Homeostasis

3. Describe the pathogenesis of RA. Genetic predisposition and an immunologic trigger initiates T-cell mediated immune response leads to cytokine release which reduces cartilage formation and activates osteoclasts Rheumatoid factor binds to antigen on the synovium, with complement, which initiates an inflammatory response This recruits inflammatory cells, which release enzymes causing degradation of the hyaline cartilage and subchondral bone The synovium undergoes hyperplasia as a result of the inflammation A pannus is fibrovascular granulation tissue that invades the joint in an attempt to aid healing but releases cytokines that degrade hyaline cartilage and subchondral bone further Angiogenesis is necessary to increase vascular supply to the hyperplased synovium and pannus but vessels are leaky which leads to joint swelling Movement at the joint damages the new vessels causing fibrous then bony ankylosis

4. What are the risk factors for RA? Genetic predisposition: HLA-DR4 associated 2-3x more women than men Increases with age Caucasians What type of arthropathy is RA? Seropositive Symmetrical Polyarthritis

5. What are some of the clinical features of RA in the hands? MCP and PIP joints are swollen, stiff (morning) and painful Bouchard’s nodes Swan neck deformity Z line deformity of the thumb Ulnar deviation

6. What are some of the extra-articular symptoms of RA? Heart : pericarditis, valve problems, atherosclerosis → IHD & CVA Lungs : pleural effusions, rheumatoid nodules, pulmonary fibrosis Blood : anaemia, splenomegaly Orthopaedic : osteoporosis Skin : rheumatoid nodules, vasculitis, leg ulcers Neurological : C1/C2 atlanto-axial subluxation, nerve compression Eyes : scleritis, xerophthalmia (2° Sjögren's syndrome) 20%

7. Briefly, what are the management options for RA? Exercise/physiotherapy Symptomatic relief Pain killers: NSAIDs Glucocorticosteroids Treatment of underlying disease DMARDs: Anti-proliferatives, suppressive and gold injection Biological agents Surgery Mode of action? Folic acid antagonists Purine analogues

8. So now OA More common than RA Risk factors: Age, family history, previous trauma, joint defects, gender, race, bone mass and obesity. Presentation Aching joint, enlarged, hard, limited movement, grinding (crepitation) Other joints might be affected due to compensation Does come and go; occurs in flare ups

9. Pathogenesis of OA Destruction Cartilage slowly becomes cracked, exposing the bone. Bone becomes burnished from wear: eburnation Bone and cartilage fragments in joint cavity Repair Osteophytes: abnormal bony, outgrowths form Alteration in composition of cartilage Reduced proteoglycans and collagen increased water, chondrocyte hypertrophy. Alteration of mechanical properties, bone shock absorbing properties reduced

10. Changes in OA

11. OA vs. RA