In vivo microdialysis and immunohistochemical analyses of tendon tissue demonstrated high amounts of free glutamate and glutamate NMDAR1 receptors, but no signs of inflammation, in Jumper's knee.
This investigation describes, to our knowledge, the first experiment where the microdialysis technique was used to study certain metabolic events in human patellar tendons in combination with immunohistochemical analyses of tendon biopsies. In five patients (four men and one woman) with a long duration (range 12-36 months) of pain symptoms from Jumper's knee (localized tenderness in the patellar tendon verified as tendon changes with ultrasonography or MRI), and in five controls (four men and one woman) with normal patellar tendons, a standard microdialysis catheter was inserted into the patellar tendon under local anestesia. The local concentrations of glutamate (excitatory neurotransmitter) and prostaglandin E2 (PGE2) were registered under resting conditions. Samplings were done every 15 min during a 2 h period. In all individuals (patients and controls) biopsies were taken for immunohistochemical analyses. The results showed that it was possible to detect and measure the concentrations of glutamate and PGE2 in the patellar tendon with the use of microdialysis technique. There were significantly higher concentrations of free glutamate, but not PGE2, in tendons with tendinosis compared to normal tendons. In the biopsies, there were no inflammatory cell infiltrates, but, for the first time, it was shown that there was immunoreaction for the glutamate receptor NMDAR1 in association with nerve structures in human patellar tendons. These findings altogether indicate that glutamate might be involved in painful Jumper's knee, and further emphasizes that there is no chemical inflammation (normal PGE2 levels) in this chronic condition.
Alfredson
H
H
Department of Surgical and Perioperative Sciences, University of Umeå, Sweden. hakan.alfredson@idrott.umu.se
Forsgren
S
S
Thorsen
K
K
Lorentzon
R
R
D000328:Adult; D001706:Biopsy; D015232:Dinoprostone / Q000032:analysis / Q000378:metabolism; D005260:Female; D018698:Glutamic Acid / Q000032:analysis / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D007718:Knee Injuries / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D017551:Microdialysis; D016194:Receptors, N-Methyl-D-Aspartate / Q000032:analysis / Q000378:metabolism*; D052256:Tendinopathy / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D013710:Tendons / Q000737:chemistry / Q000378:metabolism* / Q000473:pathology
D015232:Dinoprostone; D018698:Glutamic Acid; D016194:Receptors, N-Methyl-D-Aspartate