Vascular pathology and osteoarthritis

• Published in: Rheumatology Vol. 46; no. 12; pp. 1763 - 1768
• Main Author: Findlay, D. M.
• Format: Book Review Journal Article
• Language: English
• Published: Oxford Oxford University Press 01-12-2007; Oxford Publishing Limited (England)
• Subjects: Arterial hypertension. Arterial hypotension; Biological and medical sciences; Blood and lymphatic vessels; Blood Coagulation Disorders - complications; Blood Coagulation Disorders - diagnosis; Blood vessels; Bone and Bones - blood supply; Bone Remodeling - physiology; Cardiology. Vascular system; Diseases of the osteoarticular system; Edema - complications; Edema - diagnosis; Female; Fibrinolysis; Hematologic and hematopoietic diseases; Humans; Hypercoagulability; Hypertension; Hypertension - complications; Hypertension - diagnosis; Hypoxia; Ischemia - complications; Ischemia - diagnosis; Joints - blood supply; Male; Medical sciences; Osteoarthritis; Osteoarthritis - etiology; Osteoarthritis - physiopathology; Osteoclast; Osteocyte viability; Platelet diseases and coagulopathies; Prognosis; Risk Factors; Subchondral bone; Vascular Diseases - diagnosis; Venous stasis; Hypertension; Hypercoagulability; Subchondral bone; Venous stasis; Blood vessels; Hypoxia; Osteoclast; Osteoarthritis; Osteocyte viability; Oxygen; Diseases of the osteoarticular system; Cardiovascular disease; Hemopathy; Blood vessel; Arthropathy; Degenerative disease; Bone; Vein; Osteocyte; Coagulopathy
• DOI: 10.1093/rheumatology/kem191
• EISSN: 1462-0332
• ISSN: 1462-0324

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.