Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/42257
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Type: Journal article
Title: Vascular pathology and osteoarthritis
Author: Findlay, D.
Citation: Rheumatology, 2007; 46(12):1763-1768
Publisher: Oxford Univ Press
Issue Date: 2007
ISSN: 1462-0324
1462-0332
Statement of
Responsibility: 
D. M. Findlay
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.
Keywords: Bone and Bones; Joints; Humans; Osteoarthritis; Vascular Diseases; Hypertension; Ischemia; Blood Coagulation Disorders; Edema; Prognosis; Risk Factors; Bone Remodeling; Fibrinolysis; Female; Male
Description: © The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved.
RMID: 0020073740
DOI: 10.1093/rheumatology/kem191
Appears in Collections:Orthopaedics and Trauma publications

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