title: Healing ligaments have decreased cyclic modulus compared to normal ligaments and immobilization further compromises healing ligament response to cyclic loading.
abstract: Ligaments help maintain joint stability by resisting excessive strain during the repetitive loading experienced during daily activity. Healing ligaments may be less able to fulfill this role, straining more under equivalent loading than normal ligaments. We examined the cyclic stress-strain response of normal and healing ligaments to repetitive low loads (<10% of the normal ligament failure strength). Rabbit medial collateral ligaments (MCLs) were surgically gapped in either a unilateral (right MCL; n=23) or bilateral (right and left MCLs; n=17) fashion with immobilization of the right hindlimb in the bilateral group. These MCL scars were allowed to heal for 3, 6, and 14 weeks and were cyclic creep tested at 2.2, 4.1, and 7.1 MPa, respectively. Creep test stresses were a constant 30% of the failure strength of non-immobilized scars at the different healing intervals. Normal MCLs were creep tested at 4.1 and 7.1 MPa (n=13). The cyclic modulus of the non-immobilized scars was less than that of normal ligaments. The percent increase in modulus during cycling was greater for scars than for normal ligaments, likely related to increased viscous dissipation or material inferiorities in scars. Furthermore, immobilization significantly decreased the ability of scars to resist strain, with a majority of immobilized scars failing during repetitive loading. Such failures were preceded by a reduction in cyclic modulus indicating damage to the healing ligaments that was predictive of eventual total failure. The implications of this study are that joints with healing ligaments may have increased strain in joint structures while they are under stress, potentially leading to joint instability. Although immobilization could be used temporarily to maintain joint stability, remobilization would likely lead to total failure of the healing ligament.
authors.affiliation: Department of Mechanical Engineering, University of Alberta, Edmonton, Alberta, Canada. gail.thornton@ualberta.ca
authors.forename: G M
authors.initials: GM
authors.lastname: Thornton
authors.forename: N G
authors.initials: NG
authors.lastname: Shrive
authors.forename: C B
authors.initials: CB
authors.lastname: Frank
mesh_terms: D000818:Animals; D002921:Cicatrix / Q000503:physiopathology; D005260:Female; D019417:Hindlimb Suspension / Q000009:adverse effects*; D007593:Joint Instability / Q000503:physiopathology; D007719:Knee Joint / Q000503:physiopathology; D017888:Medial Collateral Ligament, Knee / Q000293:injuries* / Q000503:physiopathology* / Q000601:surgery; D011817:Rabbits; D016474:Weight-Bearing; D014945:Wound Healing / Q000502:physiology*