title: Extracorporeal shock wave therapy ameliorates secondary lymphedema by promoting lymphangiogenesis.
abstract: OBJECTIVE
  Although secondary lymphedema is a common complication after surgical and radiation therapy for cancer, the treatment options for lymphedema remain limited and largely ineffective. We thus studied the effect of extracorporeal shock wave therapy on promoting lymphangiogenesis and improving secondary lymphedema.
  
  
  METHODS
  A rabbit ear model of lymphedema was created by disruption of lymphatic vessels. Two weeks after surgery, the lymphedematous ear was treated with or without low-energy shock waves (0.09 mJ/mm(2), 200 shots), three times per week for 4 weeks.
  
  
  RESULTS
  Western blot analysis showed that the expression of vascular endothelial growth factor (VEGF)-C (1.23-fold, P < .05) and VEGF receptor 3 (VEGFR3; 1.53-fold, P < .05) was significantly increased in the ears treated with shock wave than in the untreated lymphedematous ears. Compared with the control group, shock wave treatment led to a significant decrease in the thickness of lymphedematous ears (3.80 +/- 0.25 mm vs 4.54 +/- 0.18 mm, P < .05). Immunohistochemistry for VEGFR3 showed the density of lymphatic vessels was significantly increased by shock wave treatment (P < .05).
  
  
  CONCLUSIONS
  Extracorporeal shock wave therapy promotes lymphangiogenesis and ameliorates secondary lymphedema, suggesting that extracorporeal shock wave therapy may be a novel, feasible, effective, and noninvasive treatment for lymphedema.
authors.affiliation: Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi, Japan.
authors.forename: Masayuki
authors.initials: M
authors.lastname: Kubo
authors.forename: Tao-Sheng
authors.initials: TS
authors.lastname: Li
authors.forename: Takahiro
authors.initials: T
authors.lastname: Kamota
authors.forename: Mako
authors.initials: M
authors.lastname: Ohshima
authors.forename: Bungo
authors.initials: B
authors.lastname: Shirasawa
authors.forename: Kimikazu
authors.initials: K
authors.lastname: Hamano
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004423:Ear; D007150:Immunohistochemistry; D008096:Lithotripsy; D042583:Lymphangiogenesis; D042601:Lymphatic Vessels / Q000378:metabolism / Q000503:physiopathology*; D008209:Lymphedema / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D008297:Male; D011817:Rabbits; D013997:Time Factors; D015854:Up-Regulation; D042582:Vascular Endothelial Growth Factor C / Q000378:metabolism; D040321:Vascular Endothelial Growth Factor Receptor-3 / Q000378:metabolism
chemical_list: D042582:Vascular Endothelial Growth Factor C; D040321:Vascular Endothelial Growth Factor Receptor-3