Original scientific articleSynovial Hypoxia as a Cause of Tendon Rupture in Rheumatoid Arthritis
Section snippets
In Vivo Oxygen Tension Measurements
All of the patients had clinically apparent rheumatoid hand disease at the time of surgery and met the American College of Rheumatology (formerly the American Rheumatism Association) 1987 criteria for RA.29 Patients having elective hand surgery for indications other than inflammatory synovitis (eg, surgery for Dupuytren’s contracture and carpal tunnel release for median nerve compression) were recruited as non-RA controls. Patients with concurrent illnesses that could affect tissue oxygenation
Invasive RA Tenosynovium Is Significantly Hypoxic
Oxygen measurements were carried out in 21 patients with RA and in 10 patients without RA. The measurements were taken at the start of each surgical procedure, while each patient was under general anesthesia but before application of a tourniquet. The number of separate oxygen tension recordings taken from each area was dependent on the size of the tissue being sampled and the degree of trauma caused by insertion of the electrode into the tissues. Between 1 and 4 measurements were possible at
Discussion
Despite dramatic improvements in the medical treatment of RA, it has been our clinical experience that (for many patients) destructive changes in the hand continue even when patients are on maximum therapy. The cause of tendon rupture in RA has been variously attributed to attrition over bony prominences and/or invasion of the tendons by synovium.3 Looked at more closely, attrition over a bony prominence is probably an overly simplistic explanation. In our hands, inspection of the bed in which
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The Kennedy Institute of Rheumatology receives a core grant from arc (Registered Charity No. 207711). The authors are grateful for the support of the Restoration of Appearance and Function Trust (B.S., M.A.A.) and the Royal College of Surgeons of England and The Dunhill Medical Trust (M.A.A.). B.S. was a recipient of a Research Fellowship from the Royal College of Surgeons of England. The authors are grateful to Dr. Serafim Kiriakidis (Faculty of Medicine, Imperial College London) for advice, to Mr. David Peston and Mr. David Essex (Department of Histopathology, Charing Cross Hospital, London) for immunohistochemistry expertise, and to Dr. R.E. Ellis (School of Physics, University of Exeter) for help in constructing the electrodes.
No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article.