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Rheumatology Advance Access originally published online on August 3, 2004
Rheumatology 2005 44(1):7-16; doi:10.1093/rheumatology/keh344
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Rheumatology Vol. 44 No. 1 © British Society for Rheumatology 2004; all rights reserved

REVIEW

Osteoarthritis, angiogenesis and inflammation

C. S. Bonnet and D. A. Walsh

Academic Rheumatology, University of Nottingham, Nottingham City Hospital, Nottingham, UK.

Correspondence to: D. A. Walsh, Academic Rheumatology, University of Nottingham, Clinical Sciences Building, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, UK. E-mail: David.Walsh{at}nottingham.ac.uk

Angiogenesis and inflammation are closely integrated processes in osteoarthritis (OA) and may affect disease progression and pain. Inflammation can stimulate angiogenesis, and angiogenesis can facilitate inflammation. Angiogenesis can also promote chondrocyte hypertrophy and endochondral ossification, contributing to radiographic changes in the joint. Inflammation sensitizes nerves, leading to increased pain. Innervation can also accompany vascularization of the articular cartilage, where compressive forces and hypoxia may stimulate these new nerves, causing pain even after inflammation has subsided. Inhibition of inflammation and angiogenesis may provide effective therapeutics for the treatment of OA by improving symptoms and retarding joint damage. This review aims to summarize (i) the evidence that angiogenesis and inflammation play an important role in the pathophysiology of OA and (ii) possible directions for future research into therapeutics that could effectively treat this disease.

KEY WORDS: Osteoarthritis, Synovitis, Angiogenesis, Innervation, Osteophyte, Macrophage, Chondrocalcinosis


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