How ACLs Tear

Anterior cruciate ligament (ACL) injury is the number one reason for time missed in sport with 100,000 -250,000 occurring every year in the U.S. alone (Hewett, 2016.) These injuries carry huge financial ramifications and increases rate of post-traumatic arthritis. Fortunately, risk of ACL injury can be quite accurately predicted and prevention strategies are shown to work well at reducing the incidence of injury and re-injury this.

–an important note: this risk is in reference to populations and not individuals; it is impossible to say exactly who will tear an ACL, but you can estimate risk within populations–

About 80% of ACL ruptures are non-contact injuries, with the athlete’s own movement strategies and muscle recruitment patterns causing the injury. Neuromuscular control programs indicate that at least 1/2 of non-contact ACL injuries can be prevented with neuromuscular training oriented at altering movement strategies (Gagnier, 2013)(Hewett, 2016.) These neuromuscular training programs are especially beneficial for at-risk females, as females are known to have altered neuromuscular control which places them at higher risk of ACL injury than men.

Non-contatct ACL injuries happen with rapid deceleration movements such as which happens with change of direction cutting, pivoting, and landing movements, especially when occurring in a single leg stance position. The ACL primarily restricts anterior translation of the tibia on the femur but also helps prevent hyperextension of the knee and gives rotational stability of the knee restricting tibial internal rotation (IR) more so than external rotation (ER.)

The amount of force required to rupture an ACL will vary individual to individual based on size of the ACL (larger individuals have larger ACLs) and likely genetic components. A study by Woo et al. showed younger cadaveric subjects, aged 22-35, had higher average strengths of the ACL with failure occurring around 2200 N of force as compared to 1500N and 660N for subjects aged 40-50 and 60-97, respectively. To put this into perspective 2200N (newton) is the force of about 220 kilograms with the accerleration due to gravity (roughly 10m/s^2.) Which is approximately the force of 485 lbs. This may seems like a lot of force, but consider that straight-line running can create ground reaction forces up to 3x bodyweight. Which means that a 200-lb male would create sufficient force to rupture an ACL with every step if it were to be transmitted into the ACL. Furthermore, the ground reaction forces within sporting events can be much greater than this. When these forces are directed into the ACL, it tears. Video analysis, computer modeling, and cadaveric studies have given us pretty solid evidence on how the ACL ruptures.

There is extensive evidence that now widely supports a triplanar ACL mechanism with knee valgus the common denominator. A 2014 study by Carmen Quatman revealed that loading of the ACL was greatest with triplanar motion involving tibial internal rotation, tibial abduction, and anterior tibial shear, though loads in her simulated falls using cadaver limbs were not sufficient to strain the MCL (Quatman, 2014.) This helps explain why only 4-17% of ACL ruptures occur with a concomitant MCL injury despite the MCL being the primary restraint to tibial abduction.

Video analysis of ACL injuries reveal they nearly always occur at knee flexion positions of around 20-30 degrees, which is actually quite a straight knee when viewed in the context of athletic performance (Koga, 2010.) It is not coincidental that this is the same angle we perform Lachman testing as ACL tension is greater in these positions of lesser knee flexion angles than when the knee is flexed more. An ACL rupture has been found to occur within 40 milliseconds of ground contact (Koga, 201o.) This is incredibly fast. About 3-4 times faster than the average reaction time for auditory and visual stimulus, and therefore, faster than what would be possible to sense and correct the risky position. This reveals the importance of appropriate preparatory movement and motor recruitment patterning. Observations of ACL injuries show the tibia internally rotating quickly in the first 40 milliseconds but then subsequently externally rotating. This change from tibial internal rotation to tibial external rotation is hypothesized to occur because of the loss of the ACL. A loss in the ACL’s ability to resist tibial anterior translation would cause the medial femoral condyle to shift backwards relative to the tibia with concomitant tibial external rotation (Koga, 2010.)

Muscle recruitment patterns can also help identify increased risk of ACL injury. Hamstring to quadriceps ratios (H:Q) have been used in the past as it is acknowledged that the co-contraction of the hamstring muscles create a posterior shear which offsets the anterior shear of the quadriceps and can decrease risk of knee injury, especially to the ACL. A quadriceps dominant landing strategy has been linked to increases in ACL injury (Zebis, 2009) Landing with a quadriceps dominant landing strategy not only increases the anterior shear of the tibia on the femur because of the line of pull of the quads, but it also is a strategy associated with landing on a stiffer leg and thus less knee flexion, which we also understand to be correlated with increased ACL loading and injury. Stiffer leg landing strategies are associated with greater relative quadriceps to hamstrings ratio and less overall hamstrings recruitment (Boling, 2013.)

Historically, hamstring to quad ratios (H:Q) have been used in terms of isometric strength but it may be more appropriate to consider the rate of torque development of the hamstrings as it is noted above and the quickness of ACL tear in response to GRF. It is observed that high peak concentric H:Q tend to be correlated to rate of torque development H:Q but the relationship is not always consistent(Greco, 2012.)

Side-cutting strategies have also been linked with increase rates of ACL rupture. Strategies of cutting in a wide stance and with trunk lean over stance leg show an increase in knee abduction moments and thus increase risk to the ACL (Kristianslund, 2014.) When the trunk flexes laterally over a plant leg the laterally displacement of the COM causes the ground reaction force, which is directed towards the COM, to pass now lateral to the knee which causes an increased knee abduction moment and predisposes to valgus collapse. Furthermore, landing with the center of mass located further from the base of support in the sagittal plane and with a greater limb angle (limb further from the vertical) is associated with increases in ACL rupture (Sheehan, 2012.)

It has been hypothesized that ACL tears could come from tissue fatigue failure, different from a traditional view of fatigue, whereby continual stress applied to tissue may cause eventual failure at the same amount of load which previously caused no harm. Fatigue failure has been demonstrated in MCLs of rabbits(Zek, 2010) and human extensor digitorum longus tendons (Schechtman, 1997.) A study in 2015 out of AJSM by Melanie Beaulieu suggests that ACLs can also fail from tissue fatigue which increases with limited femoral internal rotation with repeated landings (Beaulieu, 2015.) If the femur is not allowed to internally rotate then the relative internal rotation of the tibia on the femur will be much greater. Typically we want the amount of tibial rotation to be matched with the amount of femoral internal rotation. When the tibia accelerates into internal rotation relative to the femur then we increase loading of the ACL. The large valgus collapses we see in ACL injuries likely happen after the ACL has torn and partly because it has torn.

The best screening strategy would be do identify individuals using these movement patterns during dynamic activities. Four variables we are looking for during screening were summarized by Dr. Tim Hewett as ligament dominance, quadriceps dominance, trunk dominance, and leg dominance. Ligament dominance can be observed with inappropriate absorption of GRFs using a stiff legged landing and landings that are observed to coincide with increases in valgus collapse of the knee as mentioned above. Quad dominance is often observed with stiff legged landing strategies but can also be assessed with muscle testing and potentially with observation of movement patterns. Quad dominant individuals may display reduction in ability to hip hinge especially of note when the individual does not posterior shift their center of mass with athletic positions, but instead simply flexes the knee to achieve a lower COM. Trunk dominance, also termed core dysfunction, can be observed with single leg balance and cutting tasks. Tendencies for individuals to maintain balance on a single limb by laterally flexing their spine can cause ground reaction forces to pass lateral of the knee creating a knee abduction moment which can cause valgus collapse. When implementing return to sport/activity tests for patients returning from ACL reconstruction it is important to know how the ACL is torn and positions and movements which could load the ACL so we can appropriately screen for elevated risk. Keep these ideas in mind when rehabbing ACL patients.

 

 

Beaulieu ML, Wojtys EM, Ashton-miller JA. Risk of anterior cruciate ligament fatigue failure is increased by limited internal femoral rotation during in vitro repeated pivot landings. Am J Sports Med. 2015;43(9):2233-41.

Boling M, Padua D. Relationship between hip strength and trunk, hip, and knee kinematics during a jump-landing task in individuals with patellofemoral pain. Int J Sports Phys Ther. 2013;8(5):661-9.

Gagnier JJ, Morgenstern H, Chess L. Interventions designed to prevent anterior cruciate ligament injuries in adolescents and adults: a systematic review and meta-analysis. Am J Sports Med. 2013;41(8):1952-1962.

Greco CC, Da silva WL, Camarda SR, Denadai BS. Rapid hamstrings/quadriceps strength capacity in professional soccer players with different conventional isokinetic muscle strength ratios. J Sports Sci Med. 2012;11(3):418-22.

Hewett TE, Ford KR, Hoogenboom BJ, Myer GD. Understanding and preventing acl injuries: current biomechanical and epidemiologic considerations – update 2010. N Am J Sports Phys Ther. 2010;5(4):234-51.

Hewett TE, Myer GD, Ford KR, Paterno MV, Quatman CE. Mechanisms, prediction, and prevention of ACL injuries: Cut risk with three sharpened and validated tools. J Orthop Res. 2016;34(11):1843-1855.

Koga H, Nakamae A, Shima Y, et al. Mechanisms for noncontact anterior cruciate ligament injuries: knee joint kinematics in 10 injury situations from female team handball and basketball. Am J Sports Med. 2010; 38(11):2218–2225. [PubMed: 20595545]

Kristianslund E, Faul O, Bahr R, Myklebust G, Krosshaug T. Sidestep cutting technique and knee abduction loading: implications for ACL prevention exercises. Br J Sports Med. 2014;48(9):779-83.

Schechtman H, Bader DL. In vitro fatigue of human tendons. J Biomech. 1997; 30(8):829–835. [PubMed: 9239568]

Sheehan FT, Sipprell WH, Boden BP. Dynamic sagittal plane trunk control during anterior cruciate ligament injury. Am J Sports Med. 2012;40(5):1068-74.

Woo SL, Hollis JM, Adams DJ, Lyon RM, Takai S. Tensile properties of the human femur-anterior cruciate ligament-tibia complex. The effects of specimen age and orientation. Am J Sports Med. 1991;19(3):217-25.

Zebis MK, Bencke J, Andersen LL, et al. Acute fatigue impairs neuromuscular activity of anterior cruciate ligament-agonist muscles in female team handball players. Scand J Med Sci Sports. 2011;21(6):833-40.

Zec ML, Thistlethwaite P, Frank CB, Shrive NG. Characterization of the fatigue behavior of the medial collateral ligament utilizing traditional and novel mechanical variables for the assessment of damage accumulation. J Biomech Eng. 2010; 132(1):011001. [PubMed: 20524739]

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Author: Landon Booker, PT, DPT, CSCS

I am a doctor of physical therapy and strength and conditioning specialist practicing in an orthopedic and sports medicine physical therapy clinic in Omaha, Nebraska.

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