Medial collateral ligament autografts have increased creep response for at least two years and early immobilization makes this worse.
Recent evidence has shown that 10-40% of knee joints reconstructed with soft-tissue autografts have a recurrence of abnormal joint laxity over time. One possible explanation is the "stretching out" (or unrecovered creep) of the graft tissue. To test in vitro creep and creep recovery of fresh anatomic ligament autografts in an extra-articular environment, 16 rabbits underwent an orthotopic medial collateral ligament (MCL) autograft procedure to one hindlimb. Three subgroups of animals had either unrestricted cage activity for 1 year (n = 5) or 2 years (n = 5) or pin-immobilization for the first 6 weeks followed by cage activity for the remainder of 1 year (n = 6). Following laxity measurements, to test their creep response, isolated MCL grafts were cyclically and then statically creep tested in vitro at 4.1 MPa, allowed to recover at zero load for 20 min, and finally elongated to failure. Due to differences in cross-sectional area between the grafts and normal MCLs, two normal control groups were tested: stress-matched tested at 4.1 MPa (16.2 N; n = 7) and force-matched tested at 29.1 N (7.1 MPa; n = 6). Ligament grafts had normal laxity but significantly increased creep and decreased creep recovery compared to normal MCLs after I and 2 years of healing (p < 0.0004). Graft failure stress was also significantly less than normal (p < 0.0001). Immobilized grafts had significantly greater creep compared to non-immobilized grafts at 1 year of healing (p < 0.05). These results support previous observations concerning material inferiority of fresh anatomic rabbit MCL autografts, but add the concept that such grafts also have increased potential to creep with either slower or incomplete recovery when subjected to low stresses in vitro. Joint and ligament laxities in situ were normal in this model, however, suggesting either that in vivo MCL graft stresses are lower than those used here in vitro or that these tissues have other mechanisms by which they can recover their functional length in vivo.
Thornton
G M
GM
McCaig Centre for Joint Injury and Arthritis Research, University of Calgary, Alberta, Canada.
Boorman
R S
RS
Shrive
N G
NG
Frank
C B
CB
D000818:Animals; D004195:Disease Models, Animal; D004548:Elasticity; D005593:Fracture Fixation, Internal; D006614:Hindlimb / Q000503:physiopathology; D007103:Immobilization / Q000009:adverse effects; D066298:In Vitro Techniques; D007593:Joint Instability / Q000209:etiology* / Q000503:physiopathology; D017888:Medial Collateral Ligament, Knee / Q000503:physiopathology / Q000637:transplantation*; D011183:Postoperative Complications; D011817:Rabbits; D019651:Plastic Surgery Procedures; D013314:Stress, Mechanical; D014182:Transplantation, Autologous; D016474:Weight-Bearing; D014945:Wound Healing / Q000502:physiology