title: Chondrocyte damage and contact pressures following impact on the rabbit tibiofemoral joint.
abstract: Epidemiological studies show that tibial plateau fractures comprise about 10% of all below-knee injuries in car crashes. Studies from this laboratory document that impacts to the tibiofemoral (TF) joint at 50% of the energy producing gross fracture can generate cartilage damage and microcracks at the interface between calcified cartilage and underlying subchondral bone in the tibial plateau. These injuries are suggestive of the initiation for a long term chronic disease, such as osteoarthritis. The disease process may be further encouraged by acute damage to chondrocytes in the cartilage overlying areas of occult microcracking. The hypothesis of the current study was that significant damage to chondrocytes in tibial plateau cartilage could be generated in areas of high contact pressure by a single impact delivered to the rabbit TF joint, without a gross fracture of bone. Three rabbits received a single, 13 J of energy blunt insult to the TF joint, while another three animals were used as controls. Cell viability analyses compared chondrocyte damage in impacted versus control cartilage. Two additional rabbits were impacted to document contact pressures generated in the TF joint. The study showed high contact pressures in uncovered areas of the plateau, with a trend for higher pressures in the lateral versus medial facets. A significantly higher percentage of damaged chondrocytes existed in impacted versus the opposite, nonimpacted limbs. Additionally, more chondrocyte damage was documented in the superficial zone (top 20% of cartilage thickness) of the cartilage compared to middle (middle 50% of thickness) and deep (bottom 30% of thickness) zones. This study showed that a single blunt insult to the in situ rabbit TF joint, generating large areas of contact pressure exceeding 20 MPa, produces significant chondrocyte damage in the tibial articular cartilage, especially in the superficial zone, without gross fracture of bone. Future studies will be needed to investigate the long term, chronic outcome of this blunt force joint trauma.
authors.affiliation: Orthopaedic Biomechanics Laboratories, College of Osteopathic Medicine, Michigan State University, East Lansing, MI 48824, USA.
authors.forename: Daniel I
authors.initials: DI
authors.lastname: Isaac
authors.forename: Eric G
authors.initials: EG
authors.lastname: Meyer
authors.forename: Roger C
authors.initials: RC
authors.lastname: Haut
mesh_terms: D000818:Animals; D019902:Chondrocytes / Q000473:pathology* / Q000502:physiology*; D050724:Fractures, Cartilage / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology*; D007718:Knee Injuries / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology*; D007719:Knee Joint / Q000473:pathology / Q000503:physiopathology; D010812:Physical Stimulation / Q000009:adverse effects*; D011312:Pressure; D011817:Rabbits