title: Pathogenesis of tendinopathies: inflammation or degeneration?
abstract: The intrinsic pathogenetic mechanisms of tendinopathies are largely unknown and whether inflammation or degeneration has the prominent role is still a matter of debate. Assuming that there is a continuum from physiology to pathology, overuse may be considered as the initial disease factor; in this context, microruptures of tendon fibers occur and several molecules are expressed, some of which promote the healing process, while others, including inflammatory cytokines, act as disease mediators. Neural in-growth that accompanies the neovessels explains the occurrence of pain and triggers neurogenic-mediated inflammation. It is conceivable that inflammation and degeneration are not mutually exclusive, but work together in the pathogenesis of tendinopathies.
authors: Postgraduate School of Physical Medicine and Rehabilitation, University G d'Annunzio, Chieti-Pescara, 66013 Chieti Scalo, CH, Italy. m.abate@unich.it.
authors: Michele
authors: M
authors: Abate
authors: Karin Gravare
authors: KG
authors: Silbernagel
authors: Carl
authors: C
authors: Siljeholm
authors: Angelo
authors: A
authors: Di Iorio
authors: Daniele
authors: D
authors: De Amicis
authors: Vincenzo
authors: V
authors: Salini
authors: Suzanne
authors: S
authors: Werner
authors: Roberto
authors: R
authors: Paganelli
mesh_terms: D000818:Animals; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D018836:Inflammation Mediators / Q000378:metabolism / Q000502:physiology*; D009389:Neovascularization, Pathologic / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D052256:Tendinopathy / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*
chemical_list: D018836:Inflammation Mediators