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Review
. 2020 Jan 28;21(3):844.
doi: 10.3390/ijms21030844.

Spectrum of Tendon Pathologies: Triggers, Trails and End-State

Affiliations
Review

Spectrum of Tendon Pathologies: Triggers, Trails and End-State

Sara Steinmann et al. Int J Mol Sci. .

Abstract

The biggest compartment of the musculoskeletal system is the tendons and ligaments. In particular, tendons are dense tissues connecting muscle to bone that are critical for the integrity, function and locomotion of this system. Due to the increasing age of our society and the overall rise in engagement in extreme and overuse sports, there is a growing prevalence of tendinopathies. Despite the recent advances in tendon research and due to difficult early diagnosis, a multitude of risk factors and vague understanding of the underlying biological mechanisms involved in the progression of tendon injuries, the toolbox of treatment strategies remains limited and non-satisfactory. This review is designed to summarize the current knowledge of triggers, trails and end state of tendinopathies.

Keywords: risk factors; tendinitis; tendinopathy; tendinopathy management; tendinosis; tendon pathologies; tendon rupture.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Histopathological changes in tendinopathy. (a) Normal tendon tissue, (b) fiber crimping and kinking, loosening of collagenous matrix, (c) increased proteoglycan (PG)/glycosaminoglycan (GAG) production and changed cytokine profiles, (d) hypercellularity, (e) apoptosis, (f) presence of other cell types such as chondrocytes (fibrochondrogenesis), (g) osteocytes (calcification), h) adipocyte accumulation, i) hypervascularization and j) innervation. Based on Järvinen et al. [25].
Figure 2
Figure 2
Tendinopathy-related histopathological characteristics in human tendon tissue. Hematoxylin–eosin staining of (a) normal tendon tissue and abnormalities such as the (b) presence of chondrocytes, (c) ossification, (d) calcification of the Achilles tendon (X-ray image), (e) accumulation of adipocytes, (f) myxoid (or mucoid) degeneration and (g) hypervascularization. (h) Image g) 10 x zoomed in. Scale bars: 200 µm. Arrows indicate the corresponding feature per image. Images derived from the histopathological archive of Prof. Christoph Brochhausen, Institute of Pathology, University Regensburg.
Figure 3
Figure 3
Schematic representation of tendinopathy pathogenesis. It is hypothesized that various risk factors including mechanical overuse as well as intrinsic and extrinsic factors can trigger the development of tendinopathy in a continuous way. The first step is that these risk factors impair proper tendon repair leading to early reactive tendinopathy, which still harbors the capacity for healing. Furthermore, accumulation and increase of risk factors lead to tendon disrepair, that subsequently results in tendon degeneratione. Poor function and load capacity of the tendon finally end up in the end-state of tendinopathy, that leads to tendon tearing or rupture. Based on Cook and Purdam [11] and Shearn et al. [89].

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