Shock wave therapy induces neovascularization at the tendon–bone junction: A study in rabbits

Despite the success in clinical application, the exact mechanism of shock wave therapy remains unknown. We hypothesized that shock wave therapy induces the ingrowth of neovascularization and improves blood supply to the tissues. The purpose of this study was to investigate the effect of shock wave t...

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Published inJournal of orthopaedic research Vol. 21; no. 6; pp. 984 - 989
Main Authors Wang, Ching-Jen, Wang, Feng-Sheng, Yang, Kuender D, Weng, Lin-Hsiu, Hsu, Chia-Chen, Huang, Chun-Shun, Yang, Lin-Cheng
Format Journal Article
LanguageEnglish
Published Hoboken Elsevier Ltd 01.11.2003
Wiley Subscription Services, Inc., A Wiley Company
Blackwell Publishing Ltd
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Abstract Despite the success in clinical application, the exact mechanism of shock wave therapy remains unknown. We hypothesized that shock wave therapy induces the ingrowth of neovascularization and improves blood supply to the tissues. The purpose of this study was to investigate the effect of shock wave therapy on neovascularization at the tendon–bone junction. Fifty New Zealand white rabbits with body weight ranging from 2.5 to 3.5 kg were used in this study. The right limb (the study side) received shock wave therapy to the Achilles tendon near the insertion to bone. The left limb (the control side) received no shock wave therapy. Biopsies of the tendon–bone junction were performed in 0, 1, 4, 8 and 12 weeks. The number of neo-vessels was examined microscopically with hematoxylin–eosin stain. Neovascularization was confirmed by the angiogenic markers including vessel endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) expressions and endothelial cell proliferation determined by proliferating cell nuclear antigen (PCNA) expression examined microscopically with immunohistochemical stains. The results showed that shock wave therapy produced a significantly higher number of neo-vessels and angiogenesis-related markers including eNOS, VEGF and PCNA than the control without shock wave treatment. The eNOS and VEGF began to rise in as early as one week and remained high for 8 weeks, then declined at 12 weeks; whereas the increases of PCNA and neo-vessels began at 4 weeks and persisted for 12 weeks. In conclusion, shock wave therapy induces the ingrowth of neovascularization associated with early release of angiogenesis-related markers at the Achilles tendon–bone junction in rabbits. The neovascularization may play a role to improve blood supply and tissue regeneration at the tendon–bone junction.
AbstractList Despite the success in clinical application, the exact mechanism of shock wave therapy remains unknown. We hypothesized that shock wave therapy induces the ingrowth of neovascularization and improves blood supply to the tissues. The purpose of this study was to investigate the effect of shock wave therapy on neovascularization at the tendon–bone junction. Fifty New Zealand white rabbits with body weight ranging from 2.5 to 3.5 kg were used in this study. The right limb (the study side) received shock wave therapy to the Achilles tendon near the insertion to bone. The left limb (the control side) received no shock wave therapy. Biopsies of the tendon–bone junction were performed in 0, 1, 4, 8 and 12 weeks. The number of neo‐vessels was examined microscopically with hematoxylin–eosin stain. Neovascularization was confirmed by the angiogenic markers including vessel endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) expressions and endothelial cell proliferation determined by proliferating cell nuclear antigen (PCNA) expression examined microscopically with immunohistochemical stains. The results showed that shock wave therapy produced a significantly higher number of neo‐vessels and angiogenesis‐related markers including eNOS, VEGF and PCNA than the control without shock wave treatment. The eNOS and VEGF began to rise in as early as one week and remained high for 8 weeks, then declined at 12 weeks; whereas the increases of PCNA and neo‐vessels began at 4 weeks and persisted for 12 weeks. In conclusion, shock wave therapy induces the ingrowth of neovascularization associated with early release of angiogenesis‐related markers at the Achilles tendon–bone junction in rabbits. The neovascularization may play a role to improve blood supply and tissue regeneration at the tendon–bone junction. © 2003 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.
Despite the success in clinical application, the exact mechanism of shock wave therapy remains unknown. We hypothesized that shock wave therapy induces the ingrowth of neovascularization and improves blood supply to the tissues. The purpose of this study was to investigate the effect of shock wave therapy on neovascularization at the tendon-bone junction. Fifty New Zealand white rabbits with body weight ranging from 2.5 to 3.5 kg were used in this study. The right limb (the study side) received shock wave therapy to the Achilles tendon near the insertion to bone. The left limb (the control side) received no shock wave therapy. Biopsies of the tendon-bone junction were performed in 0, 1, 4, 8 and 12 weeks. The number of neo-vessels was examined microscopically with hematoxylin-eosin stain. Neovascularization was confirmed by the angiogenic markers including vessel endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) expressions and endothelial cell proliferation determined by proliferating cell nuclear antigen (PCNA) expression examined microscopically with immunohistochemical stains. The results showed that shock wave therapy produced a significantly higher number of neo-vessels and angiogenesis-related markers including eNOS, VEGF and PCNA than the control without shock wave treatment. The eNOS and VEGF began to rise in as early as one week and remained high for 8 weeks, then declined at 12 weeks; whereas the increases of PCNA and neo-vessels began at 4 weeks and persisted for 12 weeks. In conclusion, shock wave therapy induces the ingrowth of neovascularization associated with early release of angiogenesis-related markers at the Achilles tendon-bone junction in rabbits. The neovascularization may play a role to improve blood supply and tissue regeneration at the tendon-bone junction.
Despite the success in clinical application, the exact mechanism of shock wave therapy remains unknown. We hypothesized that shock wave therapy induces the ingrowth of neovascularization and improves blood supply to the tissues. The purpose of this study was to investigate the effect of shock wave therapy on neovascularization at the tendon-bone junction. Fifty New Zealand white rabbits with body weight ranging from 2.5 to 3.5 kg were used in this study. The right limb (the study side) received shock wave therapy to the Achilles tendon near the insertion to bone. The left limb (the control side) received no shock wave therapy. Biopsies of the tendon-bone junction were performed in 0, 1, 4, 8 and 12 weeks. The number of neo-vessels was examined microscopically with hematoxylin-eosin stain. Neovascularization was confirmed by the angiogenic markers including vessel endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) expressions and endothelial cell proliferation determined by proliferating cell nuclear antigen (PCNA) expression examined microscopically with immunohistochemical stains. The results showed that shock wave therapy produced a significantly higher number of neo-vessels and angiogenesis-related markers including eNOS, VEGF and PCNA than the control without shock wave treatment. The eNOS and VEGF began to rise in as early as one week and remained high for 8 weeks, then declined at 12 weeks; whereas the increases of PCNA and neo-vessels began at 4 weeks and persisted for 12 weeks. In conclusion, shock wave therapy induces the ingrowth of neovascularization associated with early release of angiogenesis-related markers at the Achilles tendon-bone junction in rabbits. The neovascularization may play a role to improve blood supply and tissue regeneration at the tendon-bone junction.Despite the success in clinical application, the exact mechanism of shock wave therapy remains unknown. We hypothesized that shock wave therapy induces the ingrowth of neovascularization and improves blood supply to the tissues. The purpose of this study was to investigate the effect of shock wave therapy on neovascularization at the tendon-bone junction. Fifty New Zealand white rabbits with body weight ranging from 2.5 to 3.5 kg were used in this study. The right limb (the study side) received shock wave therapy to the Achilles tendon near the insertion to bone. The left limb (the control side) received no shock wave therapy. Biopsies of the tendon-bone junction were performed in 0, 1, 4, 8 and 12 weeks. The number of neo-vessels was examined microscopically with hematoxylin-eosin stain. Neovascularization was confirmed by the angiogenic markers including vessel endothelial growth factor (VEGF) and endothelial nitric oxide synthase (eNOS) expressions and endothelial cell proliferation determined by proliferating cell nuclear antigen (PCNA) expression examined microscopically with immunohistochemical stains. The results showed that shock wave therapy produced a significantly higher number of neo-vessels and angiogenesis-related markers including eNOS, VEGF and PCNA than the control without shock wave treatment. The eNOS and VEGF began to rise in as early as one week and remained high for 8 weeks, then declined at 12 weeks; whereas the increases of PCNA and neo-vessels began at 4 weeks and persisted for 12 weeks. In conclusion, shock wave therapy induces the ingrowth of neovascularization associated with early release of angiogenesis-related markers at the Achilles tendon-bone junction in rabbits. The neovascularization may play a role to improve blood supply and tissue regeneration at the tendon-bone junction.
Author Huang, Chun-Shun
Yang, Lin-Cheng
Wang, Feng-Sheng
Yang, Kuender D
Wang, Ching-Jen
Hsu, Chia-Chen
Weng, Lin-Hsiu
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Keywords Angiogenesis
eNOS
PCNA
Shock wave therapy
VEGF
Neovascularization
Tendon–bone junction
Language English
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Vaterlein N, Lussenhop S, Hahn M, Delling G, Meiss AL. The effect of extracorporeal shock waves on joint cartilage-An in vivo study in rabbits. Acta Orthop Trauma Surg 2000; 120: 403-6.
Ogden JA, Alvarez R, Levitt R, et al. Shock wave therapy (Orthotripsy®) in musculoskeletal disorders. Clin Orthop 2001; 387: 22-40.
Ackerman PW, Ahmed M, Kreicbergs A. Early nerve regeneration after Achilles tendon rupture-a prerequisite for healing. A study in the rat. J Orthop Res 2002; 20: 849-56.
2001; 287
2002; 36
2001; 387
2002; 84B
1996; 78B
2002; 31
1988; 16
2002; 55
2002; 277
1992; 39
1992; 17
1993; 182
1996; 165
2002; 82
1998; 15
1998; 80B
2002; 41
2002; 20
2001; 6
2002; 140
2002; 84
1993; 31
1999; 81B
1995; 21
2002; 22
2002; 387
2001; 19
1994; 57
2000; 120
1994; 18
1995; 321
1998; 7
1996; 115
Rompe JD (e_1_2_1_32_2) 1995; 321
Rompe JD (e_1_2_1_28_2) 1998; 7
Rompe JD (e_1_2_1_27_2) 1998; 80
Haupt G (e_1_2_1_12_2) 1992; 39
e_1_2_1_41_2
e_1_2_1_40_2
e_1_2_1_22_2
e_1_2_1_45_2
e_1_2_1_23_2
e_1_2_1_44_2
e_1_2_1_20_2
e_1_2_1_43_2
e_1_2_1_21_2
e_1_2_1_42_2
Lingeman JE (e_1_2_1_15_2) 1998; 15
e_1_2_1_26_2
e_1_2_1_24_2
e_1_2_1_47_2
e_1_2_1_46_2
Perlick L (e_1_2_1_25_2) 2002; 140
Thiel M (e_1_2_1_38_2) 2002; 387
e_1_2_1_6_2
e_1_2_1_30_2
e_1_2_1_7_2
e_1_2_1_4_2
Archer RS (e_1_2_1_5_2) 1993; 182
e_1_2_1_2_2
e_1_2_1_11_2
e_1_2_1_34_2
e_1_2_1_3_2
e_1_2_1_33_2
e_1_2_1_10_2
e_1_2_1_31_2
e_1_2_1_16_2
e_1_2_1_13_2
e_1_2_1_36_2
e_1_2_1_14_2
e_1_2_1_35_2
e_1_2_1_19_2
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Suhr D (e_1_2_1_37_2) 1992; 17
e_1_2_1_8_2
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e_1_2_1_9_2
Rompe JD (e_1_2_1_29_2) 1996; 78
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SSID ssj0007128
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Snippet Despite the success in clinical application, the exact mechanism of shock wave therapy remains unknown. We hypothesized that shock wave therapy induces the...
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pubmed
crossref
wiley
istex
elsevier
SourceType Aggregation Database
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Enrichment Source
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StartPage 984
SubjectTerms Achilles Tendon - blood supply
Achilles Tendon - pathology
Achilles Tendon - radiation effects
Angiogenesis
Animals
Biomarkers - analysis
Calcaneus - blood supply
Calcaneus - pathology
Calcaneus - radiation effects
Disease Models, Animal
Endothelium, Vascular - metabolism
Endothelium, Vascular - pathology
Endothelium, Vascular - radiation effects
eNOS
High-Energy Shock Waves
Neovascularization
Neovascularization, Physiologic - physiology
Neovascularization, Physiologic - radiation effects
Nitric Oxide Synthase - metabolism
Nitric Oxide Synthase Type III
PCNA
Proliferating Cell Nuclear Antigen - metabolism
Rabbits
Shock wave therapy
Tendon-bone junction
Ultrasonic Therapy
Vascular Endothelial Growth Factor A - metabolism
VEGF
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Title Shock wave therapy induces neovascularization at the tendon–bone junction: A study in rabbits
URI https://dx.doi.org/10.1016/S0736-0266(03)00104-9
https://api.istex.fr/ark:/67375/WNG-XH5FDWWC-4/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1016%2FS0736-0266%2803%2900104-9
https://www.ncbi.nlm.nih.gov/pubmed/14554209
https://www.proquest.com/docview/235109552
https://www.proquest.com/docview/71260783
Volume 21
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