| Increases in anterior laxity occur following anterior cruciate ligament (ACL) reconstruction caused by an increase in length of the graft-fixation-bone-construct. A millimeter-for-millimeter relation exists between the increase in length of the graft-fixation-bone-construct and an increase in anterior laxity in vitro; however, in vivo the relation remains controversial because other factors such as biological healing might increase the stiffness and decrease the contribution to anterior laxity. Because lengthening at the sites of fixation could cause an increase in anterior laxity, the primary objectives of this dissertation were (1) to develop and validate methods to measure lengthening at the sites of fixation and the increase in anterior laxity and (2) to apply these methods in an in vivo study to determine whether the increase in anterior laxity following ACL reconstruction is caused by lengthening at the sites of fixation. To satisfy these objectives, Roentgen stereophotogrammetric analysis (RSA) was used to measure the lengthening at the sites of fixation and the increase in anterior laxity. For the first objective, tantalum markers were implanted into the bones, graft, and fixation devices during ACL reconstruction on 6 cadaveric legs. The knees were cyclically loaded in the anterior-posterior direction for 1500 cycles and both the lengthening at the sites of fixation and the increase in anterior laxity were measured. Because the lengthening at the sites of fixation and the increase in anterior laxity were determined successfully using RSA in vitro, similar methods were used in an in vivo longitudinal study. Nineteen subjects were treated with a soft-tissue allograft and slippage-resistant fixation. Tantalum markers were injected into the bones, graft, and fixation devices. On the day of surgery and at 1, 2, 3, 4, 6, and 12 months, RSA was used to measure lengthening at the sites of fixation and the increase in anterior laxity. It was determined that although lengthening at the sites of fixation did occur, it was not related to the increase in anterior laxity and that it was offset by an increase in stiffness at the sites of fixation most likely due to biological healing of the graft into the tunnel wall. |
