title: Tenocyte hypercellularity and vascular proliferation in a rabbit model of tendinopathy: contralateral effects suggest the involvement of central neuronal mechanisms.
abstract: OBJECTIVE
  To determine whether there are objective findings of tendinosis in a rabbit tendinopathy model on exercised and contralateral (non-exercised) Achilles tendons.
  
  
  METHODS
  Four groups of six New Zealand white rabbits per group were used. The animals of one (control) group were not subjected to exercise/stimulation.
  
  
  METHODS
  Animals were subjected to a protocol of electrical stimulation and passive flexion-extension of the right triceps surae muscle every second day for 1, 3 or 6 weeks.
  
  
  METHODS
  Tenocyte number and vascular density were calculated. Morphological evaluations were also performed as well as in-situ hybridisation for vascular endothelial growth factor (VEGF) messenger RNA.
  
  
  RESULTS
  There was a significant increase in the tenocyte number after 3 and 6 weeks of exercise, but not after 1 week, in comparison with the control group. This was seen in the Achilles tendons of both legs in experimental animals, including the unexercised limb. The pattern of vascularity showed an increase in the number of tendon blood vessels in rabbits that had exercised for 3 weeks or more, compared with those who had exercised for 1 week or not at all. VEGF-mRNA was detected in the investigated tissue, with the reactions being more clearly detected in the tendon tissue with tendinosis-like changes (6-week rabbits) than in the normal tendon tissue (control rabbits).
  
  
  CONCLUSIONS
  There were bilateral tendinosis-like changes in the Achilles tendons of rabbits in the current model after 3 weeks of training, suggesting that central neuronal mechanisms may be involved and that the contralateral side is not appropriate as a control.
authors.affiliation: Department of Integrative Medical Biology, Anatomy, Umeå University, Sweden.
authors.forename: Gustav
authors.initials: G
authors.lastname: Andersson
authors.forename: Sture
authors.initials: S
authors.lastname: Forsgren
authors.forename: Alexander
authors.initials: A
authors.lastname: Scott
authors.forename: James Edmund
authors.initials: JE
authors.lastname: Gaida
authors.forename: Johanna Elgestad
authors.initials: JE
authors.lastname: Stjernfeldt
authors.forename: Ronny
authors.initials: R
authors.lastname: Lorentzon
authors.forename: Håkan
authors.initials: H
authors.lastname: Alfredson
authors.forename: Clas
authors.initials: C
authors.lastname: Backman
authors.forename: Patrik
authors.initials: P
authors.lastname: Danielson
mesh_terms: D000125:Achilles Tendon / Q000098:blood supply / Q000473:pathology*; D000818:Animals; D049109:Cell Proliferation; D002490:Central Nervous System / Q000502:physiology*; D004558:Electric Stimulation; D005260:Female; D009119:Muscle Contraction / Q000502:physiology; D018482:Muscle, Skeletal / Q000502:physiology; D009389:Neovascularization, Pathologic / Q000473:pathology; D009474:Neurons / Q000502:physiology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits; D052256:Tendinopathy / Q000473:pathology*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A