Abstract

BackgroundAchilles 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.AimThe 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.MethodsA 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.ResultsExpression 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.ConclusionGene 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.

Highlights

  • Adipose tissue has multiple functions including insulation and structural support, but is first and foremost a key metabolic tissue with profound influence on whole-body homeostasis [1]

  • Expression of the majority of analyzed inflammatory marker genes was increased in patients with Achilles tendinopathy compared to that in healthy controls

  • The pain-signaling neuropeptide substance P was found to be present in PLOS ONE | DOI:10.1371/journal.pone

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Summary

Introduction

Adipose tissue has multiple functions including insulation and structural support, but is first and foremost a key metabolic tissue with profound influence on whole-body homeostasis [1]. Kager’s fat pad, described as the pre-Achilles fat pad, is a sharply enclosed radiolucent triangle delineated by the flexor halluces longus muscle and tendon (anterior border), the superior cortex of the calcaneus (inferior border) and the Achilles tendon (posterior border) [5]. It has been suggested that the flexor halluces longus part of Kager’s fat pad contributes to moving the bursal wedge during plantar flexion, that the Achilles-associated part protects blood vessels passing through it to supply the Achilles tendon, and that the region near the bursal wedge minimizes pressure changes in the retrocalcaneal bursa [6]. 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.

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