Rundell S; Baars D; Phillips D; Haut RC

Abstract:

Our laboratory has previously shown that severe levels of blunt mechanical load, generating contact pressures greater than 25 MPa, on chondral and osteochondral explants produce surface lesions and acute necrosis of chondrocytes. In vivo studies by our laboratory also show surface lesions and chronic degradation of retro-patellar cartilage within 3 years following a 6 Joule impact intensity with an associated average pressure of 25 MPa in the rabbit patello-femoral joint. A hypothesis of the current study was that significant cellular necrosis is produced acutely in the retro-patellar cartilage of the aforementioned rabbit model as a result of a 6 Joule impact. Another hypothesis of the study was that an early injection of the non-ionic surfactant, poloxamer 188 (P188) would significantly reduce the percentage of necrotic cells in the traumatized retro-patellar cartilage.

In the current study eighteen rabbits were equally divided into 3 groups. One group was termed ‘time zero’, and the other groups were 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 in all groups. Approximately 18% of retro-patellar chondrocytes suffered acute necrosis in the ‘time zero’ and ‘4 day no poloxamer’ groups. In contrast, significantly fewer (7%) cells suffered necrosis in the ‘4 day poloxamer’ group. The effect of this treatment was most significant in the superficial layer of the cartilage.

These data suggest the need to address acute damage to chondrocytes (via necrotic death) following a severe blunt joint impact. The study further indicated the potential use of P188 surfactant in the acute repair of mechanically damaged cell membranes in the in vivo setting. Its use early after severe trauma to articular cartilage may allow sufficient time for damaged cells to heal or to treat other types of cell death (i.e., apoptosis) and/or the production of degradation enzymes, etc., to help mitigate the potential for a post-traumatic osteoarthritis in the joint. Additional studies are needed to improve the efficacy of this surfactant and to determine the long-term health of joint cartilage after P188 intervention.

Orthopaedic Biomechanics Laboratories,

College of Osteopathic Medicine,

Michigan State University,

East Lansing, Michigan 48824

Please address correspondence to:

Roger C. Haut, Ph.D.,

Orthopaedic Biomechanics Laboratory,

College of Osteopathic Medicine,

A414 East Fee Hall,

Michigan State University,

East Lansing, MI 48824,

Tel: (517)355-0320,

Fax: (517)353-0789,

E-mail: haut@msu.edu