Inflammatory and metabolic alterations of Kager's fat pad in chronic achilles tendinopathy

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Jessica Pingel, Marie Christine Helby Petersen, Ulrich Fredberg, Søren G. Kjær, Bjørn Quistorff, Henning Langberg, Jacob B. Hansen

BACKGROUND: Achilles tendinopathy is a painful inflammatory condition characterized by swelling, stiffness and reduced function of the Achilles tendon. Kager's fat pad is an adipose tissue located in the area anterior to the Achilles tendon. Observations reveal a close physical interplay between Kager's fat pad and its surrounding structures during movement of the ankle, suggesting that Kager's fat pad may stabilize and protect the mechanical function of the ankle joint.

AIM: The aim of this study was to characterize whether Achilles tendinopathy was accompanied by changes in expression of inflammatory markers and metabolic enzymes in Kager's fat pad.

METHODS: A biopsy was taken from Kager's fat pad from 31 patients with chronic Achilles tendinopathy and from 13 healthy individuals. Gene expression was measured by reverse transcription-quantitative PCR. Focus was on genes related to inflammation and lipid metabolism.

RESULTS: Expression of the majority of analyzed inflammatory marker genes was increased in patients with Achilles tendinopathy compared to that in healthy controls. Expression patterns of the patient group were consistent with reduced lipolysis and increased fatty acid β-oxidation. In the fat pad, the pain-signaling neuropeptide substance P was found to be present in one third of the subjects in the Achilles tendinopathy group but in none of the healthy controls.

CONCLUSION: Gene expression changes in Achilles tendinopathy patient samples were consistent with Kager's fat pad being more inflamed than in the healthy control group. Additionally, the results indicate an altered lipid metabolism in Kager's fat pad of Achilles tendinopathy patients.

OriginalsprogEngelsk
Artikelnummere0127811
TidsskriftP L o S One
Vol/bind10
Udgave nummer5
Antal sider13
ISSN1932-6203
DOI
StatusUdgivet - 2015

Bibliografisk note

CURIS 2015 NEXS 427

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