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The limitation of acute necrosis in retro‐patellar cartilage after a severe blunt impact to the in vivo rabbit patello‐femoral joint
Author(s) -
Rundell S. A.,
Baars D. C.,
Phillips D. M.,
Haut R. C.
Publication year - 2005
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1016/j.orthres.2005.06.001.1100230618
Subject(s) - cartilage , medicine , necrosis , patella , osteoarthritis , in vivo , surgery , pathology , anatomy , biology , alternative medicine , microbiology and biotechnology
We have previously shown that surface lesions and acute necrosis of chondrocytes are produced by severe levels of blunt mechanical load, generating contact pressures greater than 25 MPa, on chondral and osteochondral explants. We have also found surface lesions and chronic degradation of retro‐patellar cartilage within 3 years following a 6 J impact intensity with an associated average pressure of 25 MPa in the rabbit patello‐femoral joint. We now hypothesized that cellular necrosis is produced acutely in the retropatellar cartilage in this model as a result of a 6 J impact and that an early injection of the non‐ionic surfactant, poloxamer 188 (P188), would significantly reduce the percentage of necrotic cells in the traumatized cartilage. Eighteen rabbits were equally divided into a ‘time zero’ group and two other groups carried out for 4 days. One ‘4 day’ group was administered a 1.5 ml injection of P188 into the impacted joint immediately after trauma, while the other was injected with a placebo solution. Impact trauma produced surface lesions on retro‐patellar cartilage in all groups. Approximately 15% of retro‐patellar chondrocytes suffered acute necrosis in the ‘time zero’ and ‘4‐day no poloxamer’ groups. In contrast, significantly fewer cells (7%) suffered necrosis in the poloxamer group, most markedly in the superficial cartilage layer. The use of P188 surfactant early after severe trauma to articular cartilage may allow sufficient time for damaged cells to heal, which may in turn mitigate the potential for post‐traumatic osteoarthritis. Additional studies are needed to improve the efficacy of this surfactant and to determine the long‐term health ofjoint cartilage after P188 intervention. © 2005 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved.