By James R. Slauterbeck, MD, David E. Hassinger, MD, and Dan M. Hardy, PhD
Females tear their ACLs 3-10 times more frequently than males participating in similar athletic events. The reasons for this disparity are not known and are probably due to several causative factors. Extrinsic factors relate to those outside the body such as training and conditioning. Intrinsic factors within the body include intercondylar notch configuration, ligamentous laxity, anatomic alignment, femoral anteversion, genu valgum, and finally hormonal differences. The cross-sectional area of the female ACL normalized by body weight is smaller than that of the male ACL. Thus, the same tensile force may be sufficiently large enough to rupture the female ACL but not large enough to rupture the male ACL.
In female athletes, the tensile loads on the ACL may reach higher levels than in males. The dynamic resistance to translation is termed the sagittal plane shear stiffness, and is due to maximal co-contraction of quadriceps and hamstrings muscles around the knee.1 Co-contraction of muscle groups occurs during running, cutting, and landing. Because women have less sagittal plane stiffness than men, activities producing high shear forces will place a greater percentage of the force on the ACL.
According to Wolff’s Law, the increased load on the female ACL should invoke a remodeling response to increase its strength. Tissue remodeling occurs continuously in both normal and injured tissues. Indeed, a cyclic tensile load on the ACL in culture results in increased collagen synthesis.2 However, increasing estrogen concentration in tissue culture decreases ACL collagen synthesis3 and has shown a decreased load to failure in rabbit ACLs.4 Also, an increase in a matrix degredadive enzyme, MMP3, without a concomitant increase in its inhibitor, TIMP-1, has been reported.5 Collectively, these factors decrease the ability of the female ACL to remodel over time with elevated stress levels.
Prophylactic treatment recommendations for female athletes are being considered based on inconclusive data from both animal and human studies. Some physicians are already recommending control of the menstrual cycle for injury prevention without sound science to support treatment. We do not support this approach but rather are investigating if a correlation between gender, ligament remodeling, and ACL strength exists. If so, perhaps a medication could be formulated that shifts the remodeling process in favor of ACL repair. Clearly, no one factor has been shown to be the cause for the gender disparity of ACL injury. We submit that a multi-factorial integrated approach combining biomechanical, neuromuscular, and molecular theories is required to address the gender-based disparity of ACL injury in humans.
Males and females demonstrate different neuromuscular responses to landing from a height. Females respond with greater dynamic knee valgus, such that the knees may actually collapse together and touch. Neuromuscular-based training programs have been implemented to limit knee valgus during jumping and landing and have been successful in decreasing ACL injuries. These training programs use plyometric techniques to change muscular firing strategies in athletes.6
Regarding operative treatment of ACL deficient knees, most controversy today centers around graft choice and fixation options. When autograft is chosen, the primary choices are hamstring and patellar tendon. Clinical results are slightly better with patellar tendon graft with 93% of patients returning to their same level of sports activity vs. 88% in hamstring patients.7 There is also slightly increased laxity in hamstring graft patients as measured with KT-2000 arthrometry. Hamstring graft patients had 3 mm or less side-to-side difference in 83% vs. 93% for patellar tendon graft in one large randomized, prospective study.7 The hamstring muscle group is an agonist to ACL function by acting as a dynamic constraint resisting anterior translation of the tibia on the femur. Their harvest for graft may impair this stabilizing role during the recovery period, although a growing body of evidence supports regrowth of the hamstring tendons over time.
Patellofemoral pain after patellar tendon autograft occurs in up to half of patients. Although there may be less graft site morbidity with hamstring autograft, longer incorporation time remains problematic, although initial fixation methods are improving. Allograft reconstructions are selected primarily because of their lack of graft site morbidity. The main risk with allograft reconstruction is the possibility of disease transmission. The HIV transmission risk has been estimated at 1 in 1.7 million.8 Functional results are somewhat similar to autograft with good-to-excellent results in 70-90% and laxity testing of 3 mm or less in 71%.9
A final controversy in ACL surgery involves fixation choice. The fixation needs to be able to withstand forces seen by the ACL during the rehabilitation period until adequate graft interface healing has occurred. These forces are approximately 500 N and can involve 125,000-250,000 cycles.10 There are many options available (26 in 1 review). Femoral fixation with a post provides greater than 1000 N of fixation strength and several tibial fixation systems produce similar results. Traditional interference screw fixation gives up to 640 N of fixation strength.11 All of these are viable options at physiologic loads.
I recommend patella tendon autograft as my graft of choice because I believe it is important to keep the muscles that counter anterior tibial translation strong during the early rehabilitation process. I accept that some athletes may have a small amount of nondebilitating anterior knee pain but will have less anterior tibial excursion. I will consider hamstring grafts for female athletes with exaggerated Q-angles or significant preinjury anterior knee pain. Finally, I avoid allografts in young athletes, reserving these for older athletes with limited exercise goals or a need to return to sedentary type work fast.
Dr. Slaughterbeck, Associate Professor, Department of Orthopedic Surgery, Texas Tech University Health Sciences Center, Lubbock, TX, is Associate Editor of Sports Medicine Reports. Dr. Hassinger is a PGY-V Resident in the Department of Orthopedic Surgery at the Texas Tech University Medical Center. Dr. Hardy has a Joint Appointment as an Associate Professor in the Cell and Molecular Biology and Department of Orthopedic Surgery at the Texas Tech University Medical Center, Lubbock, Tex.
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11. Pena F, et al. Am J Sports Med. 1996;24(3):329-334.
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