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The Scientific World Journal
Volume 2013 (2013), Article ID 514743, 8 pages
Clinical Study

Patellar Tendon Properties and Lower Limb Function in Rheumatoid Arthritis and Ankylosing Spondylitis versus Healthy Controls: A Cross-Sectional Study

1School of Sport, Health and Exercise Sciences, Bangor University, Bangor LL57 2DG, UK
2Department of Rheumatology, Betsi Cadwaladr University Health Board, Llandudno Hospital, Llandudno LL30 1LB, UK
3CERN, European Organization for Nuclear Research, 1211 Geneva 23, Switzerland

Received 30 March 2013; Accepted 15 May 2013

Academic Editors: S. Ruta and E. R. Soriano

Copyright © 2013 Verena Matschke et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objective. Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) lead to inflammation in tendons and peritendinous tissues, but effects on biomechanical tendon function are unknown. This study investigated patellar tendon (PT) properties in stable, established RA and AS patients. Methods. We compared 18 RA patients (13 women, 59.0 ± 2.8 years, mean ± SEM) with 18 age- and sex-matched healthy controls (58.2 ± 3.2 years), and 12 AS patients (4 women, 52.9 ± 3.4 years) with 12 matched controls (54.5 ± 4.7 years). Assessments with electromyography, isokinetic dynamometry, and ultrasound included quadriceps muscle force and cross-sectional area (CSA), PT stiffness, and PT CSA. Additionally, measures of physical function and disease activity were performed. Results. PT stiffness and physical function were lower in RA and AS patients compared to healthy controls, without a significant difference in force production. PT CSA was significantly larger leading to reduction in Young’s modulus (YM) in AS, but not in RA. Conclusion. The adverse changes in PT properties in RA and AS may contribute to their impaired physical function. AS, but not RA, leads to PT thickening without increasing PT stiffness, suggesting that PT thickening in AS is a disorganised repair process. Longitudinal studies need to investigate the time course of these changes and their response to exercise training.