Osteoarthritis Academic Notes

Osteoarthr itis     Osteoarthritis is a heterogenous group of conditions leading to joint signs and symptoms which are associated with defective integrity of articular cartilage, in addition to related changes in the underlying bone at the joint margins Pathologically, there is an alteration in cartilage structure, radiologically there are osteophytes and joint space narrowing, and clinically some complains of pain and disability It is the most common joint disease in the world, affecting the majority of people over the age of 65. The prevalence increases with age, where 80% of people over the age of 75 are affected It affects both the small joints (distal & proximal inter-phalangeal and base of thumb), with node formation, redness and cyst formation, as well as the weight bearing joints (spine, hips and knees), causing creaking/clicking and cool joint swelling. Components of cartilage     Fibrillar collagen (Type II, IX, and XI) – structurally important component that also have a function in holding proteoglycans and water gel. It has a slow turnover rate. Proteoglycans – major component of extracellular matrix, the "filler" substance existing between cells in an organism. Here they form large complexes, both to other proteoglycans, to hyaluronan and to fibrous matrix proteins (e.g. collagen). o Consists of 90% aggrecan, and also contain hyaluronan (repeating glucosamine and glucuronic acid, with viscoelastic function) o Aggrecan consists of keratan sulfate and chondroitin sulfate (which is a repeating glucuronic acid and galactosamine chain). They provide resistance to tension Chondrocytes – the only cells found in cartilage, which produce and maintain the cartilaginous matrix (consists of collagen + proteoglycans) No nerves or blood vessels in articular cartilages Factors leading to development of OA     Genetics o Genetics has a 50% influence in affecting the hand and hip, less so for the knee joints. Some components include insulin-like growth factor, collagen defects and production, proteoglycan defects and production, and problems with some enzymes Biomechanics o These factors include occupation, obesity, trauma, sports injuries, muscle bulk and position sense Inflammation o Mainly via inflammatory synovitis, involving collagenases, stromelysin, hyaluronidase and aggrecanase Age o With increasing age, there is impaired chondrocytes function, with cumulative trauma and decreases in strength and position sense Pathogenesis of OA       Healthy articular cartilage provides a resilient, slippery surface that is able to bear weight. Degeneration of articular surface in osteoarthritis begins with loss of proteoglycans and an increase in the water content associated with softening of the cartilage matrix. This is also with death of many chondrocytes as well. The softened cartilage matrix begins to undergo fibrillation (the surface breaks up into a series of fine parallel cracks), which larger defects gradually begin to develop and pieces of articular cartilage may dislodge from surface. The surviving chondrocytes attempt to repair the damage by proliferating, and forming clusters. In addition, there are production of fibrocartilage to replace the lost hyaline cartilage (less resilient) Defects in the articular cartilage that had extended beyond the tide mark stimulates new bone formation with a thickening of subcondral bone plate, activation of osteoblasts + osteoclasts, and an ingrowth of new blood vessels (also called neovascularisation) Following the loss of articular cartilage, the adjacent subcondral bone plates rub on each other producing a polished, ivory-like appearance – “eburnation”. Osteocytes necrosis occurs and the thickened and less flexible subcondral bone plates become more prone to developing cracks. Synovial fluid also may leak through cracks, stimulating the formation of subcondral bone cysts. Treatment and management of OA  Joint protection: decrease weight (weight loss benefits biomechanics of the knee), occupation, trauma, orthopaedic repair, footwear, splints, musculature. Moderate exercise is important as it increase GAG content in knee cartilage     Reduce inflammation: ↓ enzyme induction, ↑ enzyme inhibition, viscosupplementation (using high molecular weight hyaluronan to increase viscoelastic functions such as lubrication and shock absorption) Relieve pain and associated symptoms: use of NSAID for anti-inflammation and pain relief Relieve stiffness and swelling Minimise/improve disability – maintain function of joint Radiographic comparison of OA and RA