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Review
. 2009;11(3):235.
doi: 10.1186/ar2723. Epub 2009 Jun 30.

Pathogenesis of tendinopathies: inflammation or degeneration?

Michele Abate  1 , Karin Gravare Silbernagel, Carl Siljeholm, Angelo Di Iorio, Daniele De Amicis, Vincenzo Salini, Suzanne Werner, Roberto Paganelli
Affiliations
Review

Pathogenesis of tendinopathies: inflammation or degeneration?

Michele Abate et al. Arthritis Res Ther. 2009.

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.

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Figures

Figure 1
Figure 1
Mechanisms of damage. EGF, epidermal growth factor; HIF, hypoxia inducible factor; MMP, matrix metalloproteinase; PDGF, platelet-derived growth factor; TIMP, tissue inhibitor of metalloproteinase; VEGF, vascular endothelial growth factor.
Figure 2
Figure 2
From neovascularization to neurogenic inflammation. CGRP, Calcitonin gene related peptide; NMDA-R, N-methyl-D-aspartic acid receptor.
Figure 3
Figure 3
The iceberg theory.
See this image and copyright information in PMC

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