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Acute and late changes in intraarticular cytokine levels following anterior cruciate ligament injury

Authors :
Marco, Bigoni
Paola, Sacerdote
Marco, Turati
Silvia, Franchi
Marta, Gandolla
Diego, Gaddi
Sarah, Moretti
Daniele, Munegato
Carlo A, Augusti
Elena, Bresciani
Robert J, Omeljaniuk
Vittorio, Locatelli
Antonio, Torsello
Bigoni, M
Sacerdote, P
Turati, M
Franchi, S
Gandolla, M
Gaddi, D
Moretti, S
Munegato, D
Augusti, C
Bresciani, E
Omeljaniuk, R
Locatelli, V
Torsello, A
Publication Year :
2013

Abstract

Surgical reconstruction of the anterior cruciate ligament (ACL) does not necessarily decrease the risk of developing osteoarthritis (OA). The inflammatory response and relative changes in pro- and anti-inflammatory cytokines could participate in triggering the development of OA. To test this hypothesis we measured the concentrations of IL-1β, IL-1ra, IL-6, IL-8, IL-10, and TNF-α at different times after ACL rupture. The sample population consisted of 48 patients with ACL tear which were assigned to different groups according to the time elapsed from the injury: 22 acute (A), 7 early sub-acute (ESA), 11 late sub-acute (LSA), and 8 chronic (C). In group A, there were high levels of IL-1β, IL-6, and IL-8, whereas levels of IL-1ra and TNF-α were significantly lower than usually reported. IL-1β and IL-8 concentrations returned with time to normal levels in the ESA group. Interestingly, IL-1ra levels remained always significantly lower than normally reported levels, and TNF-α levels did not increase after trauma. Our data show increased level of pro-inflammatory cytokines (IL-6 and IL-8) in the acute phase of inflammation which could be responsible for triggering cartilage catabolism and suggest that prompt neutralization of IL-6 and IL-8 accumulations in synovial fluid could help prevent development of OA in ACL-injured knees. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31: 315-321, 2013 Copyright © 2012 Orthopaedic Research Society.

Details

Language :
English
Database :
OpenAIRE
Accession number :
edsair.pmid.dedup....e0fcca360c15e9639888e6d6e9727e1e