Extracorporeal shock waves promote healing of collagenase‐induced Achilles tendinitis and increase TGF‐β1 and IGF‐I expression

Abstract

Extracorporeal shock waves (ESW) have recently been used in resolving tendinitis. However, mechanisms by which ESW promote tendon repair is not fully understood. In this study, we reported that an optimal ESW treatment promoted healing of Achilles tendintis by inducing TGF‐β1 and IGF‐I. Rats with the collagenease‐induced Achilles tendinitis were given a single ESW treatment (0.16 mJ/mm² energy flux density) with 0, 200, 500 and 1000 impulses. Achilles tendons were subjected to biomechanical (load to failure and stiffness), biochemical properties (DNA, glycosaminoglycan and hydroxyproline content) and histological assessment. ESW with 200 impulses restored biomechanical and biochemical characteristics of healing tendons 12 weeks after treatment. However, ESW treatments with 500 and 1000 impulses elicited inhibitory effects on tendinitis repair. Histological observation demonstrated that ESW treatment resolved edema, swelling, and inflammatory cell infiltration in injured tendons. Lesion site underwent intensive tenocyte proliferation, neovascularization and progressive tendon tissue regeneration. Tenocytes at the hypertrophied cellular tissue and newly developed tendon tissue expressed strong proliferating cell nuclear antigen (PCNA) after ESW treatment, suggesting that physical ESW could increase the mitogenic responses of tendons. Moreover, the proliferation of tenocytes adjunct to hypertrophied cell aggregate and newly formed tendon tissue coincided with intensive TGF‐β1 and IGF‐I expression. Increasing TGF‐β1 expression was noted in the early stage of tendon repair, and elevated IGF‐I expression was persisted throughout the healing period. Together, low‐energy shock wave effectively promoted tendon healing. TGF‐β1 and IGF‐I played important roles in mediating ESW‐stimulated cell proliferation and tissue regeneration of tendon. © 2003 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved.