title: Extracorporeal shock waves promote healing of collagenase-induced Achilles tendinitis and increase TGF-beta1 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-beta1 and IGF-I. Rats with the collagenease-induced Achilles tendinitis were given a single ESW treatment (0.16 mJ/mm(2) 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-beta1 and IGF-I expression. Increasing TGF-beta1 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-beta1 and IGF-I played important roles in mediating ESW-stimulated cell proliferation and tissue regeneration of tendon.
authors.affiliation: Department of Orthopaedic Trauma, Chang Gung University, Linkou, Taiwan.
authors.forename: Yeung-Jen
authors.initials: YJ
authors.lastname: Chen
authors.forename: Ching-Jen
authors.initials: CJ
authors.lastname: Wang
authors.forename: Kuender D
authors.initials: KD
authors.lastname: Yang
authors.forename: Yur-Ren
authors.initials: YR
authors.lastname: Kuo
authors.forename: Hui-Chen
authors.initials: HC
authors.lastname: Huang
authors.forename: Yu-Ting
authors.initials: YT
authors.lastname: Huang
authors.forename: Yi-Chih
authors.initials: YC
authors.lastname: Sun
authors.forename: Feng-Sheng
authors.initials: FS
authors.lastname: Wang
mesh_terms: D000125:Achilles Tendon / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D001696:Biomechanical Phenomena; D017364:Collagenases / Q000009:adverse effects; D004247:DNA / Q000032:analysis; D004195:Disease Models, Animal; D004307:Dose-Response Relationship, Radiation; D006025:Glycosaminoglycans / Q000378:metabolism; D019220:High-Energy Shock Waves / Q000627:therapeutic use*; D006909:Hydroxyproline / Q000378:metabolism; D007334:Insulin-Like Growth Factor I / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D052256:Tendinopathy / Q000139:chemically induced / Q000473:pathology / Q000628:therapy*; D013708:Tendon Injuries / Q000139:chemically induced; D016212:Transforming Growth Factor beta / Q000096:biosynthesis*; D053773:Transforming Growth Factor beta1; D014945:Wound Healing / Q000528:radiation effects*
chemical_list: D006025:Glycosaminoglycans; C508962:Tgfb1 protein, rat; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D007334:Insulin-Like Growth Factor I; D004247:DNA; D017364:Collagenases; D006909:Hydroxyproline