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In recent years much effort has been devoted to finding a satisfactory replacement for the injured ACL. None of the reconstruction techniques used in the past can be considered ideal because of their inability to dupli cate the complex geometry, structure, and function of the ligament. Current advances in allograft transplan tation and cryopreservation have led us to design and implement an experimental model for testing the feasi bility of cryopreserved ACL allotransplantation. Groups of dogs were used to evaluate the effect of cryopreservation on ligament strength and to compare the relative performance of both autograft and allograft ACL transplants up to 18 months after implantation. The ligaments were examined mechanically, histologi cally, and microangiographically. The cryopreservation process and duration of stor age had no effect on the biomechanical or structural properties of the ligament. The mechanical integrity of the allografts was similar to that of the autografts, with both achieving nearly 90% of control ligament strength by 36 weeks. Revascularization approached normal by 24 weeks in both autograft and allograft. No evidence of structural degradation or immunological reaction was seen. Based on these results, we believe that a cryopre served ACL allograft can provide the ideal material for ACL reconstruction. We have outlined a surgical tech nique for harvesting and implanting this graft clinically.

This study correlates force generation and healing in muscle after controlled strain injury. Right tibialis ante rior (TA) muscles from 30 rabbits were strained to approximately 80% of failure while the left TA muscles served as control. Both injured and control muscles were then tested for ability to generate force. Seven animals were sacrificed immediately after testing and the muscles were examined grossly and histologically. Remaining animals were retested at 24 hours (N = 7), 48 hours (N = 8), and 7 days (N = 8). Contractile ability following injury was 70.5% of control immediately, 51.1% at 24 hours, 74.5% at 48 hours, and 92.5% at 7 days. Immediate histology showed limited distal fiber rupture and hemorrhage. By 24 hours, histology showed fiber necrosis, infiltration of inflammatory cells, edema, and hemorrhage. At 48 hours there was com plete fiber breakdown and intense inflammatory cell proliferation. At 7 days inflammation was reduced and collagen fibrosis more advanced. Our findings demon strate that injured muscle begins functional recovery by 48 hours despite inflammation and active healing. This suggests that decreasing muscle function seen clinically between 24 and 48 hours following strain injury may result from pain due to inflammation. Scarring and fibrosis seen at 7 days may explain the frequent recur rence of injury to strained muscles.

This study investigates the biomechanical failure prop erties of five architecturally different skeletal muscles and examines the role muscle structure plays in the passive extension characteristics of musculotendinous units. The muscles used in this study fall into four morphologic categories: fusiform, unipennate, bipen nate, and multipennate.Each muscle was pulled to failure at three different rates of strain (1, 10, and 100 cm/min). Specimens of fusiform, unipennate, and bipennate muscles were pulled from their proximal as well as distal attachments. The relationship of elongation to failure of the entire musculotendinous unit to resting muscle fiber length was examined to determine the effect of angle of pennation and fiber length on the failure properties.Our results demonstrate that all four muscle types tested show injury and rupture at the musculotendinous junction whether pulled from proximal or distal attach ment, regardless of muscle structure and rate of strain. There was a statistically significant difference (P < 0.005) in the degree of elongation to failure relative to resting muscle fiber length, with a tendency to greater elongation relative to fiber length for muscles with more pennate structure (tibialis anterior, 72.7% ± 1.0%; ex tensor digitorum longus, 113.1% ± 3.5%; rectus fem oris, 225.5% ± 3.7% elongation in percent resting fiber length).

Acute hamstring muscle strains occurring in ten college athletes were evaluated using computed tomography to identify the location and characteristics of these common injuries. Acute muscle strains appeared as areas of hypodensity within the muscle 1-2 d following injury. This suggests that inflammation and edema are the major component of injury, not bleeding as commonly assumed. Injuries were seen most commonly in the proximal and lateral portions of the hamstring muscle group, particularly in the biceps femoris.