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Rheumatology Advance Access published online on August 10, 2007

Rheumatology, doi:10.1093/rheumatology/kem191
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


Review

Vascular pathology and osteoarthritis

D. M. Findlay

Discipline of Orthopaedics and Trauma, The University of Adelaide and The Hanson Institute, Adelaide, South Australia, Australia.

Correspondence to: D. M. Findlay, Professor of Orthopaedic Research, Discipline of Orthopaedics and Trauma, University of Adelaide, Level 4, Bice Building, Royal Adelaide Hospital, Adelaide, South Australia 5000, Australia. E-mail: david.findlay{at}adelaide.edu.au


   Abstract

There is mounting evidence that vascular pathology plays a role in the initiation and/or progression of the major disease of joints: osteoarthritis (OA). Potential mechanisms are: episodically reduced blood flow through the small vessels in the subchondral bone at the ends of long bones, and related to this, reduced interstitial fluid flow in subchondral bone. Blood flow may be reduced by venous occlusion and stasis or by the development of microemboli in the subchondral vessels. There are several likely effects of subchondral ischaemia: the first of these is compromised nutrient and gas exchange into the articular cartilage, a potential initiator of degradative changes in the cartilage. The second is apoptosis of osteocytes in regions of the subchondral bone, which would initiate osteoclastic resorption of that bone and at least temporarily reduce the bony support for the overlying cartilage. It may be important to recognize these potential aetiological factors in order to develop more effective treatments to inhibit the progression of OA.

KEY WORDS: Osteoarthritis, Blood vessels, Subchondral bone, Venous stasis, Hypertension, Hypercoagulability, Hypoxia, Osteocyte viability, Osteoclast

Submitted 27 February 2007; revised version accepted 21 June 2007.
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[Abstract] [Full Text] [PDF]



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