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Int J Mol Sci. 2018 Jan 30;19(2). pii: E404. doi: 10.3390/ijms19020404.

Different Achilles Tendon Pathologies Show Distinct Histological and Molecular Characteristics.

Author information

1
Julius Wolff Institute, Center for Musculoskeletal Surgery, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 13353 Berlin, Germany. Franka.Klatte@charite.de.
2
Berlin-Brandenburg Center for Regenerative Therapies, Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany. Franka.Klatte@charite.de.
3
Julius Wolff Institute, Center for Musculoskeletal Surgery, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 13353 Berlin, Germany. Susann.Minkwitz@charite.de.
4
Berlin-Brandenburg Center for Regenerative Therapies, Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany. Susann.Minkwitz@charite.de.
5
Julius Wolff Institute, Center for Musculoskeletal Surgery, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 13353 Berlin, Germany. Aysha.Schmock@charite.de.
6
Julius Wolff Institute, Center for Musculoskeletal Surgery, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 13353 Berlin, Germany. Nicole.Bormann@charite.de.
7
Berlin-Brandenburg Center for Regenerative Therapies, Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany. Nicole.Bormann@charite.de.
8
Julius Wolff Institute, Center for Musculoskeletal Surgery, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 13353 Berlin, Germany. Alper.Kurtoglu@charite.de.
9
Julius Wolff Institute, Center for Musculoskeletal Surgery, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 13353 Berlin, Germany. Serafeim.Tsitsilonis@charite.de.
10
Julius Wolff Institute, Center for Musculoskeletal Surgery, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 13353 Berlin, Germany. Sebastian.Manegold@charite.de.
11
Julius Wolff Institute, Center for Musculoskeletal Surgery, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 13353 Berlin, Germany. Britt.Wildemann@charite.de.
12
Berlin-Brandenburg Center for Regenerative Therapies, Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany. Britt.Wildemann@charite.de.

Abstract

Reasons for the development of chronic tendon pathologies are still under debate and more basic knowledge is needed about the different diseases. The aim of the present study was therefore to characterize different acute and chronic Achilles tendon disorders. Achilles tendon samples from patients with chronic tendinopathy (n = 7), chronic ruptures (n = 6), acute ruptures (n = 13), and intact tendons (n = 4) were analyzed. The histological score investigating pathological changes was significantly increased in tendinopathy and chronic ruptures compared to acute ruptures. Inflammatory infiltration was detected by immunohistochemistry in all tendon pathology groups, but was significantly lower in tendinopathy compared to chronic ruptures. Quantitative real-time PCR (qRT-PCR) analysis revealed significantly altered expression of genes related to collagens and matrix modeling/remodeling (matrix metalloproteinases, tissue inhibitors of metalloproteinases) in tendinopathy and chronic ruptures compared to intact tendons and/or acute ruptures. In all three tendon pathology groups markers of inflammation (interleukin (IL) , tumor necrosis factor α, IL6, IL10, IL33, soluble ST2, transforming growth factor β1, cyclooxygenase 2), inflammatory cells (cluster of differentaition (CD) 3, CD68, CD80, CD206), fat metabolism (fatty acid binding protein 4, peroxisome proliferator-activated receptor γ, CCAAT/enhancer-binding protein α, adiponectin), and innervation (protein gene product 9.5, growth associated protein 43, macrophage migration inhibitory factor) were detectable, but only in acute ruptures significantly regulated compared to intact tendons. The study gives an insight into structural and molecular changes of pathological processes in tendons and might be used to identify targets for future therapy of tendon pathologies.

KEYWORDS:

acute rupture; chronic tendon pathologies; fat; human; inflammation; innervation; matrix; modeling/remodeling; tendon structure

PMID:
29385715
PMCID:
PMC5855626
DOI:
10.3390/ijms19020404
[Indexed for MEDLINE]
Free PMC Article

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