Theories posit complex mechanisms
By Jordana Bieze Foster
In recent years, discussions of anterior cruciate ligament injury biomechanics have increasingly concluded that the mechanism of such injuries is likely multifactorial, with a number of different lines of research each contributing a piece of the puzzle. Now some investigators are beginning to articulate just what these multifactorial mechanisms might entail.
In a “perspective article” e-published on Dec. 6 by the Journal of Biomechanics, researchers from Texas Tech University and four other institutions proposed a mechanism in which four distinct but related factors converge to set the stage for noncontact ACL injury. Many of the same themes, in particular the potential interactions between morphological and mechanical risk factors, were also discussed in a University of Michigan article published just two months earlier in Exercise & Sports Sciences Reviews.
The Journal of Biomechanics article theorized that noncontact ACL injury during a deceleration task occurs when all four of the following criteria are met: co-activation of the quadriceps and hamstrings muscles is slow and/or delayed, a dynamic ground reaction force is experienced while the knee is near full extension, the athlete has a shallow medial tibial plateau and a steep posterior tibial slope, and the hip flexes more slowly than the knee.
Each of these factors has been linked to ACL injury risk in previous studies, but no other researchers had yet offered a detailed hypothesis for how they all might interact. The authors proposed that the inciting event would be the delayed co-activation of quadriceps and hamstrings, which could occur as a result of fatigue or a sudden decrease or increase in muscle load. The delayed co-activation would diminish active tibiofemoral stabilization, meaning that joint stability would be at the mercy of passive structures.
Even in the presence of a potentially injurious ground reaction force, several remaining variables still have the potential to protect the joint from injury: these include a gradual tibial slope, a deep medial tibial plateau, and a synchronicity between hip flexion velocity and knee flexion velocity. Failure of those protective mechanisms, however, increases the risk of injury significantly.
The Michigan researchers also underscored the likelihood that a noncontact ACL injury mechanism involves both morphological (e.g., tibial slope, tibial plateau depth, knee laxity) and mechanical (e.g., postural alignment) contributing factors. Although their paper stopped short of proposing a detailed integrated mechanism of injury, it did broaden the discussion to address issues of clinical relevance.
The fact that high rates of ACL injury are still being reported despite implementation of neuromuscular training programs suggests that morphological risk factors may play a more significant role in the multifactorial injury mechanism than previously thought, the Michigan authors hypothesized. Injury prevention programs that could theoretically account for athlete-specific morphological variables – or, more specifically, the interaction between morphologic and mechanical variables – would potentially be more effective, particularly in female athletes.
They went on to point out that, although morphological characteristics are not modifiable with training, some of these characteristics do change during the process of maturation, even as gender-specific differences in neuromuscular control are also emerging. If the neuromuscular control patterns that evolve in female athletes are actually compensating for morphological risk factors, then the current practice of training athletes of both genders in typically “male” neuromuscular strategies may have the opposite of its intended protective effect.
It’s also possible, however, that morphological risk factors may in fact be modifiable, the Michigan researchers noted. Preliminary findings from Germany suggest that an individual’s “loading history,” based on intensity of physical activity over time, can affect knee joint structure. If the specific structural variables contributing to ACL injury risk are also affected by loading history, then interventions could theoretically be implemented to modify those longitudinal loading patterns and reduce the injury risk.