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Abstract
This study investigated the effect of shock-wave therapy (SWT) on collagenase induced tendinopathy in the rabbit patellar tendon. Eighteen rabbits were treated by ultrasonography-guided injection of 0.025 ml collagenase into the patellar tendon in both knees. After tendinopathy was confirmed at 3 weeks post-treatment by the histological examination, SWT was initiated to the right patellar tendon involving 1500 cycles at 0.29 mJ/mm^sup 2^ in two separated weekly courses from 4 weeks post-treatment. The rabbits were randomly divided into two groups, which were sacrificed at the 4th and 16th week after SWT, respectively. The histological examination, the mechanical and biochemical tests then were performed. The ultimate tensile load in the SWT tendon increased 7.03% at 4 week and 10.34% at 16 week after treatment as compared to the sham group. Hydroxyproline concentrations increased in the SWT tendons over both the 4 and 16 weeks after treatment. Moreover, the pyridinoline concentration increased at the 4th week but decreased at 16th week as compared to the sham group. The histological examination demonstrated increased blast-like tenocyte at the 4th week, while more mature tenocyte with neovasculization at the 16th week. The result obtained here validates the effectiveness of the SWT in the established tendinopathy. SWT may increase collagen synthesis and collagen crosslink formation during early healing process.
© 2003 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved.
Introduction
Since early 1980s in Europe, shock-wave therapy (SWT) has received enthusiastic attention regarding its clinical application for various soft-tissue pathologies, including lateral humeral epicondylitis, Achilles tendinitis, rotator cuff calcifying tendinopathy, and plantar fasciitis [11-13,25,26]. Outcomes have been favorable, but the exact mechanism inducing accelerated soft-tissue healing remains unclear. Tendinopathy is a condition of tendon degeneration, and has been attributed to various causes, including local injury, hormone, aging, chemicals, vascular insufficiency and overuse [2,4,5,16,19,23]. Immediately following tendon injury, firstly neutrophil aggregates, then macrophage ensues to phagocyte the necrotic debris and release collagenase, thus causing significant inflammation [18]. Injection of collagenase into the tendon mimics this situation and has been widely employed as a animal tendinopathy model since being reported by Silver et al. in the late 1970 [2,5,6,29].
In a tendon regeneration process, the reparative cell is tenocyte, which when activated behaves like a modified form of...