Article Text

SP0094 Links between angiogenesis, inflammation and pain in OA
  1. D. Walsh
  1. Arthritis Research UK Pain Centre, Academic Rheumatology, University of Nottingham, Nottingham, United Kingdom


Structural changes in the osteoarthritic joint that lead to pain remain incompletely understood. OA is characterised by synovitis, loss of osteochondral integrity and new nerve growth into structures such as articular cartilage the inner regions of menisci that normally contain no nerves. Each of these features is associated with new blood vessel growth, and each may contribute to pain. Treatments that reduce angiogenesis also reduce pain behaviour in animal models of OA. Inhibiting angiogenesis reduces inflammation, reduces the vascularisation of articular cartilage, and inhibits endochondral ossification at the joint margin. Angiogenesis is quiescent in most normal mature tissues, including the joint, but is an important physiological process in growth, reproduction and tissue repair. Broad spectrum angiogenesis inhibitors used in oncology have predictable adverse events outside the joint that may preclude long term use in chronic non-malignant disease. However, specific molecular mechanisms regulate pathological angiogenesis in the joint, raising the possibility of targeted anti-angiogenic therapies. For example, vascularisation of articular cartilage requires that osteoclasts cut channels from subchondral bone spaces towards the articular surface. Novel treatment approaches that maintain osteochondral integrity can reduce pain in OA.

Disclosure of Interest D. Walsh Consultant for: Pfizer Ltd

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