title: [Overload damage to the Achilles tendon: the importance of vascularization and angiogenesis].
abstract: In the Achilles tendon, degenerative changes mostly occur in regions that are hypo- or avascular. Angiogenesis is mediated by angiogenic factors and recent studies have shown that vascular endothelial growth factor (VEGF) is highly expressed in degenerative Achilles tendons, whereas VEGF expression is nearly completely downregulated in healthy tendons. VEGF expression in tendon fibroblasts is regulated by the transcription factor hypoxia inducible factor 1 (HIF-1). Several factors are able to upregulate VEGF expression in tenocytes: hypoxia, inflammatory cytokines and mechanical load. Angiogenesis plays an important role in the tendinotic process. The neovessels are accompanied by small glutamate positive neural structures. This finding suggests that angiogenesis plays an important role in the pain experienced during the degenerative tendon disease. On the other hand, there is some evidence that HIF-1/VEGF induced angiogenesis has an effect on the material properties of the tendinotic tendon tissue. Since VEGF has the potential to stimulate the expression of matrix metalloproteinases and inhibits the expression of tissue inhibitors of matrix metalloproteinases (TIMP) in various cell types this cytokine might play a significant role in the pathogenetic processes during degenerative tendon disease. These experimental findings are in accordance with clinical results which show that eccentric training leads to a regression of neovessels and decrease of pain. Another strategy is the local administration of a sclerosing agent (Polidocanol) to destroy neovessles. Preliminary results show that both strategies are effective in reducing vascular density and pain.
authors.affiliation: Klinik für Unfall-, Hand- und Wiederherstellungschirurgie Universitätsklinikum Münster. wolf.petersen@ukmuenster.de
authors.forename: W
authors.initials: W
authors.lastname: Petersen
authors.forename: T
authors.initials: T
authors.lastname: Pufe
authors.forename: S
authors.initials: S
authors.lastname: Pfrommer
authors.forename: B
authors.initials: B
authors.lastname: Tillmann
mesh_terms: D000125:Achilles Tendon / Q000098:blood supply* / Q000293:injuries* / Q000378:metabolism; D012090:Cumulative Trauma Disorders / Q000503:physiopathology*; D004268:DNA-Binding Proteins / Q000378:metabolism*; D006801:Humans; D051793:Hypoxia-Inducible Factor 1; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D020782:Matrix Metalloproteinases / Q000378:metabolism*; D009389:Neovascularization, Pathologic / Q000503:physiopathology*; D009687:Nuclear Proteins / Q000378:metabolism*; D013708:Tendon Injuries / Q000503:physiopathology*; D014157:Transcription Factors / Q000378:metabolism*; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
chemical_list: D004268:DNA-Binding Proteins; C497442:HIF1A protein, human; D051793:Hypoxia-Inducible Factor 1; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D009687:Nuclear Proteins; D014157:Transcription Factors; D042461:Vascular Endothelial Growth Factor A; D020782:Matrix Metalloproteinases