After rupture of the anterior cruciate ligament (ACL), passive anterior laxity on examination and the knee's behavior during activity often diverge. A patient with obvious passive anterior laxity may, once acute swelling and pain have settled, still manage a slow step-up or pass short-term screening with single-leg hop tests. A patient with only a small side-to-side difference on passive anterior pull may still give way repeatedly during a sudden stop, a change of direction, or a deceleration landing [7,8]. Calling both "good anterior stability" or "poor anterior stability" puts the clinical judgment out of focus from the start. The examination table measures tibial displacement under a stated external force. Activity tests whether the passive structures, the geometry of articular contact, and muscle control can together resist high-speed shear. These are different physical processes.
Anterior laxity, functional instability, and four mechanical quantities often conflated
"Anterior stability," as clinicians use the phrase, covers two different kinds of finding. Passive anterior laxity is the magnitude of anterior displacement of the tibia relative to the femur under a stated flexion angle, rotational constraint, and external force. When that displacement exceeds the contralateral reference or the physiologic range, the sign is abnormal passive anterior laxity. Functional instability is the sense that the joint has shifted, and giving way, during a sudden stop, a change of direction, single-leg landing, or deceleration with rotation. What an ACL rupture directly weakens is the passive anterior restraint of the joint, seen on examination as an increase in passive anterior laxity. Whether the patient can complete a particular dynamic task is functional stability. The two are closely related in mechanism. There is no conversion that turns millimeters into functional performance [8].
Four physical quantities are also often conflated in laboratory and clinical measurements of anterior knee mechanics:
Anterior tibial position and displacement have to be defined against an explicit zero or reference path. In the cadaver, the neutral starting point can be placed at the point of lowest stiffness on the curve of anterior-posterior loading and unloading [1]. A six-degree-of-freedom robot can also find the passive flexion-extension path under no external load on which the residual force in each direction is less than 2.0 N and the residual moment is less than 0.2 N·m, and that path can serve as the reference [3]. Once the reference origin shifts, the "anterior translation" read from it is distorted. A typical clinical pitfall occurs after rupture of the posterior cruciate ligament (PCL). In cadaver knees, Butler et al. found that the PCL supplied about 95% of the passive restraint to the posterior drawer at 90° and at 30° of flexion, and 0% of the restraint to the anterior drawer [1]. After the PCL fails, the tibia sags posteriorly under gravity at 90° of flexion. The examiner's pull, bringing that sagged tibia forward to the normal neutral position, is easily felt as a positive anterior drawer, although the ACL is intact.
Anterior laxity under a stated external load is the anterior tibial translation, in millimeters, measured at 88 N, 110 N, 130 N, 150 N, or the examiner's maximum manual anterior pull [2-5,8]. Joint soft tissue is not a linear spring. The same knee gains different increments of displacement at low load and at high load. A millimeter value reported apart from the size of the load, the flexion angle, and the rotational constraint has no comparative meaning.
The nonlinear load-displacement curve, and stiffness, show how resistance changes as the external force rises. Stiffness is the rate of change of restraining force relative to the change in displacement, the slope of the load-displacement curve, in N/mm. An intact knee pulled anteriorly first passes through a low-stiffness initial region as collagen fibers straighten, then enters a high-stiffness linear region of resistance. On palpation this is often a crisp stop as resistance rises quickly, a firm endpoint. After the ACL is lost, the initial low-stiffness slip lengthens. Stretch in the peripheral capsule, the menisci, and the collateral ligaments increases as displacement increases, and the hand often meets a soft endpoint in which resistance rises gradually [1]. The feel of the endpoint is the examiner's clinical palpation, not an absolute mechanical lock, and it is a real help in recognizing the functional state of the ligament. Using the load-displacement curve of a single knee, Butler et al. showed that if the bedside pull is small, or if muscle tension limits the force that can be applied, the difference in displacement between the intact knee and the ACL-cut knee in the low-force region may be only a few millimeters, while at high force the difference widens markedly [1].
ACL in situ force is the resultant tension the intact ACL actually carries, in newtons, when the joint is at a stated three-dimensional position and under external or muscle load [3,6]. Its magnitude depends at once on the direction of that in situ force in space, on how fibers within the ligament are recruited, and on load shared by the other joint structures. It does not rise and fall in a fixed proportion to the millimeters of anterior tibial translation. Sakane et al. found that the sagittal elevation angle of the whole-ACL in situ force vector, relative to the tibial plateau, became markedly smaller at 60° and greater flexion, and the vector lay closer to parallel with the plateau [3]. In the quadriceps-pull experiments of Li et al., anterior tibial translation peaked at 30° of flexion and ACL in situ force peaked at 15° [6]. The angle of greatest displacement is not the angle of greatest ligament force.
The degrees of freedom the apparatus allows also change these readings. From the medial surface of the lateral femoral condyle, the ACL runs obliquely forward, medially, and distally to the anterior intercondylar area of the tibia, and its internal fibers twist in space with flexion and extension. When the rig locks tibial internal and external rotation in neutral and allows only single-plane anterior-posterior translation, a single-degree-of-freedom drawer, the internal rotation that naturally accompanies anterior tibial translation is blocked by the machine. When the other five degrees of freedom are left free at a fixed flexion angle, anterior tibial translation occurs together with coupled internal rotation, and both the three-dimensional relation between the femoral and tibial attachments and the order in which the peripheral structures are stretched then change [1-4]. Unless it is clear which motions an experiment locked and which it freed, numbers from different rigs will be forced into one series.
Experimental evidence for the primary passive restraint, and the conditions under which the proportions hold
The conclusion that the ACL is the main passive structure limiting anterior tibial translation rests on two kinds of cadaveric biomechanical experiment. They run in opposite directions, and each supports the other. One holds the external force constant and measures free displacement. The other reproduces a displacement and measures the difference in resisting force.
In constant-load, free-motion tests, a constant anterior force is applied to the intact knee, motion in several degrees of freedom is recorded, the ACL is cut, and the same anterior force is applied again. On an optical kinematic rig (10 knees analyzed, tibial internal and external rotation free), Willinger et al. applied an 88 N anterior tibial force. After arthroscopic transection of the ACL, anterior tibial translation rose sharply at every tested angle from 0° to 100° (P < .001). Under these cadaveric conditions, with the muscles relaxed, the mean increase was largest near 20° of flexion, about 9 mm [4]. On a six-degree-of-freedom robotic system (8 knees, the other 5 degrees of freedom free), Seon et al. applied a 130 N anterior force. Cutting the ACL likewise increased anterior translation significantly at each tested angle from 0° to 90° (P < .05) [5]. Under these anterior loads, from 88 N to 130 N, loss of the ACL leaves the remaining passive tissues unable to hold the tibia within the anterior translation of the intact knee.
A large increase in displacement after cutting still does not give the share of restraining force the ACL carried in the intact knee at the small anterior translation that knee normally reaches. Once the ACL is torn, the tibia slides out to a large-displacement position the intact knee would not have reached, and the other soft tissues are loaded passively at that abnormal position. The biomechanical answer is the force-difference method that reproduces the same kinematic path (principle of superposition). The intact knee is first driven to a specified anterior translation, or its six-degree-of-freedom path under a given external load is recorded. After the ligament in question is cut, a servo system or a robot reproduces that same bony path strictly. The difference between the total joint restraining-force vectors measured on the two passes is the restraining force, or the in situ force, that ligament contributed while intact [1,3,4]. The method holds on three conditions. The bone segments can be treated as rigid, or bending of the bone has been calibrated and compensated. The soft tissues do not wrap and press on one another in a way that passes force between them. The mechanism reproduces position to submillimeter accuracy, as with the robot used by Sakane et al., whose reproduction error was less than 0.02 mm [3].
The statement often quoted in clinic, that the ACL carries about 85% of the anterior restraint, comes from the displacement-controlled study Butler, Noyes, and Grood published in 1980 [1]. They tested 14 human cadaver knees: 11 at 90° of flexion and another 3 at 30°. The same 14 knees were not measured as pairs at both angles. The test was limited to a single-plane anterior-posterior drawer, with tibial rotation locked in neutral, no active muscle loading, and very small axial compression, less than 1% of the total restraining force within 5 mm of displacement. The menisci were not excised on their own. Their mechanical effect was counted together with the capsule to which they were attached. The denominator of the percentages was the sum of the force drops after the ligaments and the capsule had been cut. At 5 mm of anterior tibial displacement (original Table I; mean ± standard error), the ACL carried 85.1 ± 1.9% of the total soft-tissue restraining force at 90° (11 knees, range 69.3%–92.4%) and 87.2 ± 1.6% at 30° (3 knees, range 84.2%–89.7%; the abstract summarizes these as a mean of 86%) [1]. Reversing the cutting order at 90°, with the ACL cut first or last, did not change these proportions. At that single-plane displacement, mechanical interaction among the structures was small.
Inconsistent sample size in the original report: On page 261, in the methods, Butler et al. state that the effect of loading rate (1 to 40 mm/s) was tested in 8 intact knees. On page 265, in the results, they report the mean result from 9 knee specimens. The exact sample size of that rate comparison is unclear, so the specific rate-effect values are not used. The anterior-restraint proportions at 90° (11 knees) and at 30° (3 knees), which original Table I lists explicitly, are unaffected [1].
Later work confirms the same dominant place of the ACL. The percentages or the newton values cannot be converted into one another as if they were one measure. The specimens, the denominators, the size of the displacement, and the degrees of freedom differ (Table 1). Amis and Dawkins applied a cyclic anterior force of 150 N with the intermediate position of rotation locked. In the single typical specimen they display at 20° of flexion (original Figure 7, peak anterior translation 4.3 mm), secondary restraints retained 22% of the load at the original peak displacement after the ACL had been cut completely, which corresponds to a 78% share for the ACL. That value takes the applied load of 150 N as its denominator, and it represents one specimen [2]. Willinger et al. (funded by the German Society for Arthroscopy and Joint Surgery, the DFG, and Smith & Nephew through a research account at Imperial College London) included 22 unpaired cadaver knees. Ten were used for six-degree-of-freedom robotic tests by the principle of superposition (88 N anterior force, 0°–90°). Another 12 were used for optical kinematic tests; after 2 were excluded for technical error, 10 were analyzed, and they were not the same specimens. In the robotic tests, of the four structures examined, the ACL, the Kaplan fibers, the anterolateral capsule/ligament, and the lateral meniscus posterior root, only the ACL provided a statistically significant anterior restraint at every angle from 0° to 90° (P < .001). The 88%–94% written in the paper uses as its denominator only the sum of the resisting forces of these four examined structures, not every soft tissue in the knee [4].
Sakane et al., in 9 cadaver knees with a mean age of 71 years, used a six-degree-of-freedom robot and a universal force-moment sensor (UFS). The other 5 degrees of freedom were free, anterior force was applied from 22 to 110 N, and they reported the three-dimensional resultant in situ force directly, not a percentage. Under 110 N of anterior force, anterior translation of the intact knee lay between 3.1 ± 1.0 mm at 0° and 7.4 ± 2.5 mm at 60° (mean ± standard deviation). Resultant ACL in situ force was highest at 15° of flexion (110.6 ± 14.8 N) and lowest at 90° (71.1 ± 29.5 N) [3]. The magnitude of the resultant in situ force at 15° (110.6 N) is slightly higher than the pure anterior force applied (110 N) because the ACL crosses three-dimensional space on a slant. While it resists the anterior force, it also carries vertical and lateral components produced by the coupled motion. The magnitude of the spatial resultant is then larger than the component along the anterior-posterior axis alone. Dividing 110.6 N by 110 N does not yield a load share. These studies changed the specimens, the definition of the denominator, the displacement amplitude, and the rotational constraint at the same time. Compared with one another, they agree that the ACL is the primary passive anterior restraint. They do not identify how many percentage points any one of those experimental conditions produced by itself. The "85%" is the experimental proportion under one particular single-plane, small-displacement condition. It is not a constant of the body in daily activity.
The statistical methods contradict the results as written: In the statistical-methods paragraph on page 1139, Willinger et al. state that the change in laxity after any one secondary structure was cut in the kinematic experiment, with only 3 to 4 knees in each cutting order, was not tested statistically and was presented only descriptively. The results paragraph on the same page says that cutting the Kaplan fibers, the anterolateral capsule/ligament, or the lateral meniscus posterior root alone "did not significantly increase" anterior tibial translation. That untested "no significant increase" cannot be taken as statistical evidence that a single lateral structure has no role. The effect of cutting the whole ACL, which was tested (P < .001), and the effect of cutting the lateral structures together (P < .05 at 70°–100°), can still be used [4].
Table 1. Comparison of key cadaveric biomechanical studies of the passive anterior restraint provided by the ACL
| Study and sample | Loading and degrees of freedom | Restraint measure and denominator | Main anterior mechanical result |
|---|---|---|---|
| Butler et al. 1980 [1] (11 knees at 90°; another 3 knees at 30°) | Single-plane anterior-posterior drawer, neutral rotation locked; the intact knee was driven to 5 mm of anterior translation | Force drop on reproduction of the displacement; the denominator is the sum of the force drops from the ligaments and the capsule (menisci not excised separately) | At 5 mm of anterior translation the ACL accounted for 85.1 ± 1.9% of the restraining force at 90° and 87.2 ± 1.6% at 30° (mean ± SEM). After the ACL was cut, secondary restraints were also assessed at a large displacement of 12.2–16.3 mm |
| Amis and Dawkins 1991 [2] (bundle sectioning in 9 knees) | Cyclic anterior pull to 150 N at 20° and at 90°, intermediate rotation locked | Force drop on reproduction of the intact knee's peak anterior translation; bundle shares use the total ACL resisting force as the denominator | No bundle was isometric under no external load. Under a 150 N anterior pull the PLB share was highest at 20°, and the AMB predominated at 90° |
| Sakane et al. 1997 [3] (9 knees) | Anterior force of 22–110 N from 0° to 90°, the other 5 degrees of freedom free | Resultant ACL in situ force (N) along the reproduced three-dimensional path; the force of each bundle projected onto the whole-ACL force vector | Under 110 N, resultant ACL in situ force was 110.6 ± 14.8 N at 15° and still 71.1 ± 29.5 N at 90°. PLB force fell sharply with flexion; projected AMB force changed little |
| Li et al. 1999 [6] (10 knees) | Quadriceps force of 200 N from 0° to 120°, compared with an added hamstring force of 80 N; 5 degrees of freedom free | Anterior translation (mm) relative to the unloaded path, and resultant ACL in situ force (N) | With the quadriceps loaded alone, translation peaked at 30° (5.3 ± 2.1 mm) and ACL force peaked at 15° (44.9 ± 13.8 N). Adding the hamstrings lowered in situ force from 15° to 60° and had no significant effect at 0° |
| Seon et al. 2009 [5] (8 knees) | From 0° to 90°, a 130 N anterior force and a 400 N quadriceps force applied separately; 5 degrees of freedom free | Anterior translation (mm) for the intact knee, after ACL section, after subtotal excision of approximately the inner 80% of the medial meniscal body/posterior horn, and after single-bundle reconstruction | After ACL section, translation under 130 N increased at every angle. Further meniscal excision increased it significantly from 15° to 90° under 130 N (an additional 7.4 ± 3.3 mm at 60°) and, under 400 N, significantly only from 0° to 30° |
| Willinger et al. 2023 [4] (10 knees in the robot tests; 10 other knees analyzed kinematically) | 88 N anterior force; the kinematic tests allowed free internal and external rotation | In the robot tests the denominator is the sum of the force drops of the 4 structures examined; the kinematic tests measured free anterior translation (mm) | In the robot tests only the ACL provided a significant anterior restraint (P < .001). After ACL section in the kinematic tests, translation increased from 0° to 100° (mean increase about 9 mm near 20°). Combined section of the lateral structures added up to a further 4 mm at 70°–100° |
Flexion angle, fiber recruitment, and secondary restraints
In cadaveric tests under a passive anterior force of 88–130 N, the ACL contributes to restraint throughout the arc of flexion and extension, yet the added anterior translation after the ACL is cut is most marked near 15°–30° of flexion [4,5]. Resultant ACL in situ force under 110 N of anterior force also falls from its peak at 15° to about 71 N at 90° [3]. This change with flexion angle follows both the way fibers inside the ACL are recruited and the geometry by which secondary restraints share load as displacement and flexion change.
Bundle function has to be read as two separate measurements: change in the length of the fiber path during unloaded passive flexion and extension, and the share of resisting force under an anterior load. Amis and Dawkins stated directly that ACL fibers twist during flexion and extension and do not run straight. They passed a fine wire along the fiber-bundle paths inside the ligament and measured the change in length from 0° to 130° under a minimal tension of 1 N, with no external anterior-posterior drawer force (original Figure 5; 9 knees, full extension taken as an arbitrary zero). No fiber bundle inside the ACL is strictly isometric. Over the last 30° of extension, the anteromedial bundle (AMB), the intermediate bundle (IB), and the posterolateral bundle (PLB) all lengthen. Moving from 0° toward flexion, the PLB keeps shortening and slackening. The AMB shortens slightly from 0° to about 30°, then lengthens progressively with further flexion as the femoral attachment turns and the fibers twist. A rotation moment of ±1 N·m had no significant effect on length [2].
Once an external anterior force is applied, anterior translation of the tibia itself draws some fibers tight again. The way the ligament is divided into bundles, the quantity measured, and the rotational constraint each show a different face of the experiment. With intermediate rotation locked and a cyclic anterior force of 150 N (original Figure 8; 9 knees), Amis and Dawkins divided the ACL into three bundles and calculated each bundle's percentage of the total ACL resisting force. At 20° of flexion the PLB share was the highest, and the IB and AMB shares were relatively lower. In the single typical specimen at 20° in original Figure 7, the PLB accounted for 47%, the AMB for 32%, and the IB for 21%. By 90° of flexion the AMB had risen to about 60% and the PLB had fallen to about 10% [2]. With the other 5 degrees of freedom free and an anterior force of 110 N (original Figure 6; 9 knees), Sakane et al. divided the ACL into two bundles and measured the in situ force of each bundle projected onto the direction of the whole-ACL force vector. Projected PLB force fell sharply with flexion, from 75.2 ± 18.3 N at 15° to 26.2 ± 14.4 N at 90°, and it was higher than the AMB at 0° and at 15°. Projected AMB force changed little from 0° to 90° (32.6 ± 13.3 N at 0°, 47.4 ± 34.2 N at 60°; 15° compared with 90°, P = .548) [3]. The two results are not slopes running in opposite directions. When the load carried by the PLB falls sharply in deep flexion, the AMB's percentage of the whole ACL's contribution rises even if the AMB's own absolute tension stays level. The studies also used a three-bundle percentage and a two-bundle vector projection. They did not, in the same specimens, change rotational freedom alone as a paired check. The difference in the numbers cannot be assigned to one experimental variable.
Two points govern the clinical reading. First, the fall in in situ force that Sakane et al. measured at 90°, relative to near extension, is misread if it is taken to mean that "the ACL loses function at 90° of flexion." Under an external force of 110 N it still carried about 71 N of resultant in situ force. Together with the share of about 85% of the soft-tissue resisting force that Butler et al. measured at 90° and 5 mm of displacement [1], that force shows that the ACL is still the primary anterior restraint at 90°. Second, from the difference in bundle contribution at the two angles, Amis and Dawkins proposed that a partial tear at the corresponding site may be suggested when, against the normal contralateral knee, only the Lachman test is positive or only the 90° anterior drawer is positive. They also noted that anterior laxity in the normal population has a wide range, and that a complete rupture sometimes remains inside the normal absolute range [2]. Their cadaveric conditions locked rotation and removed the extensor mechanism. In the awake examination, hamstring tension and blocking by the meniscus interfere as well. At the bedside, the difference in slackness between the two tests is a poor basis for deciding which single bundle is torn.
After the whole ACL is gone, the anterior restraint carried by the capsule, the peripheral ligaments, and the menisci rises as displacement increases. In the intact knee the peripheral tissues already take a small part at smaller displacement: non-ACL tissues supplied about 15% of the total soft-tissue restraining force at 5 mm in Butler et al. [1], while secondary restraints supplied 22% of the applied load at 4.3 mm in the single typical knee of Amis et al. [2]. As the tibia continues forward, fibers that were poorly aligned for this pull are drawn oblique and tight, and the share taken by secondary resistance grows. The superficial medial collateral ligament (MCL) is an example. At 90° of flexion it lies nearly perpendicular to the tibial plateau, so at a small anterior translation its posterior horizontal component is small. After a large displacement has pulled it into a backward slant, its resistance rises clearly [1]. Because Butler et al. saw initial damage to the ACL at 7–10 mm of anterior translation in some intact knees, they assessed secondary restraints, after cutting the ACL, at a separate and larger anterior translation of 12.2–16.3 mm (mean about 14 mm) in 6 knees flexed to 90° (original Table II; mean ± standard error). The iliotibial band accounted for 24.8 ± 4.7% (range 9.8%–44.4%), the mid-medial capsule for 22.3 ± 6.9%, the mid-lateral capsule for 20.8 ± 5.4%, the superficial MCL for 16.3 ± 2.9%, and the lateral collateral ligament for 12.4 ± 3.3%. Scatter among specimens was large, and the differences among the structures were not statistically significant [1]. These large-displacement percentages cannot be set in the same table as the shares at 5 mm in the intact knee. Acute cutting in the cadaver cannot show later remodeling of the tissues. From this relation of the forces it can be inferred that if, after loss of the ACL, the peripheral capsule and the menisci are left for a long period to check the tibia repeatedly at a larger anterior position, those accessory tissues will carry shear far beyond their physiologic state.
On the medial and lateral secondary restraints in particular, Seon et al. [5] and Willinger et al. [4] show how an accompanying structural defect changes anterior translation with the way the knee is loaded and with the flexion angle. In 8 ACL-deficient knees, Seon et al. added a subtotal excision removing approximately the inner 80% of the medial meniscal body and posterior horn. This is a model of a large defect. It is not the same thing as every small peripheral tear or every radial tear. Under a passive anterior tibial force of 130 N, the subtotal excision further increased anterior translation, beyond the ACL-deficient state, at 15°, 30°, 60°, and 90° (P < .05). The added increase was especially large in deeper flexion: a further 7.4 ± 3.3 mm at 60° and a further 6.4 ± 2.7 mm at 90°. At 0° the added increase was only 1.4 ± 1.0 mm and was not statistically significant. When the same specimens were tested with a 400 N quadriceps pull and no added anterior drawer force, the significant extra anterior translation from the subtotal excision appeared only in slight flexion, from 0° to 30° (P < .05), and was not seen at 60° or at 90° [5]. A passive anterior force points forward at every angle. As flexion deepens, the femoral condyle moves posteriorly and the posterior wedge of the medial meniscal posterior horn and body stands out more as a block. Quadriceps force is transmitted through the patellar tendon. With deeper flexion the anterior component of the patellar tendon grows smaller and can turn to point posteriorly. In this 400 N model, the anterior difference associated with meniscal excision was no longer apparent at 60° and above.
In the same study, single-bundle reconstruction with a 10 mm bone–patellar tendon–bone (BPTB) graft, in knees that combined ACL loss with subtotal medial meniscectomy, significantly reduced the abnormal anterior translation at each angle. At 30° under 130 N, for example, translation fell from 25.6 ± 2.7 mm to 13.3 ± 2.0 mm. It remained higher than in the intact knee (P < .05) [5]. There was no control in which the same BPTB reconstruction was done with the meniscus intact, and in situ force in the graft was not measured. This residual laxity should not be laid simply on loss of the meniscus. This does not establish that all modern reconstruction techniques fail to restore anterior restraint.
Inconsistent significance symbols in the archived manuscript: In the PMC author manuscript of Seon et al. (PMC3173766), two sentences at the end of the results state that the effect of reconstruction on tibial internal rotation had "no statistical significance," while the parentheses mark P < 0.05. The titles of original Tables 2 and 3 both confirm that differences in internal rotation among the states were not statistically significant. Those two instances of P < 0.05 are inequality signs written the wrong way, and they cannot be used as evidence that rotation improved [5].
Lateral and anterolateral structures also limit the ACL-deficient knee in a way that depends on flexion angle. Under a passive anterior force of 88 N, Willinger et al. found that cutting the Kaplan fibers, the anterolateral capsule/ligament, and the lateral meniscus posterior root together, after the ACL had already been cut, added as much as 4 mm of anterior tibial translation at 70°–100° of flexion (P < .05) [4]. Across the passive-loading results of Seon et al. and Willinger et al. at 88–130 N, the added translation from cutting the ACL alone is mostly larger near 20°–30° and falls off toward 90°. If a patient with an ACL rupture shows, on examination, anterior slip in deeper flexion (the anterior-drawer position at 60°–90°) that is abnormally marked, as prominent as in slight flexion or more marked still, the finding should raise specific concern for substantial loss of function of the medial meniscal posterior horn or body, or for injury of the lateral meniscus posterior root together with the anterolateral structures, and those structures should be checked on MRI and at arthroscopy. The cadaveric tests used wide excision without muscle tone, and the specimens differed widely at baseline. The pattern gives a direction for that search. It cannot be reduced to a quantitative rule on which anterior translation past some number of millimeters, at a given angle, confirms a particular concomitant injury.
Active muscle pull, everyday weight-bearing movement, and early screening of dynamic stability
In the living, moving joint, contraction of the muscles that cross the joint, and contact under load, change the net shear on the tibia from moment to moment. Cadaveric experiments with muscle loading [6], fluoroscopic kinematics of one closed-chain movement [7], and a clinical cohort screened for function in the acute phase [8] each examine a different part of that question.
1. Quadriceps anterior pull, and the flexion angles at which hamstring co-contraction opposes it
In 10 cadaver knees, with the skin around the joint kept and the other 5 degrees of freedom free, Li et al. compared an isolated quadriceps pull of 200 N with a combined pull of 200 N through the quadriceps and 80 N through the hamstrings, 40 N each through semimembranosus and biceps femoris, directed parallel to the femoral shaft [6]. The isolated 200 N quadriceps pull drew the tibia forward from 0° to 60°. Anterior translation reached its peak at 30° of flexion, 5.3 ± 2.1 mm (mean ± standard deviation), and at 120° it had become a slight posterior translation (−0.8 ± 1.1 mm). Resultant ACL in situ force reached its peak at 15° of flexion, 44.9 ± 13.8 N, higher than at the other angles (P < .05). It was 27.8 ± 9.3 N at 0° and about 10 N from 90° to 120°. After the added 80 N hamstring pull, anterior tibial translation decreased significantly from 30° to 120° (P < .05). At 30° it fell to 4.3 ± 1.5 mm, an 18% reduction as the paper reports. The decrease in translation at 0° and at 15° did not reach statistical significance. ACL in situ force decreased significantly at 15°, 30°, and 60° (P < .05). At 15° it fell to 34.7 ± 11.8 N, a reduction of 23%. At full extension (0°) the hamstrings did not significantly lower ACL in situ force. From 90° to 120° the baseline in situ force was already low, and it did not change significantly there either [6].
The abstract does not match the results in the body: The abstract of Li et al. says that adding 80 N of hamstring force lowered ACL in situ force at 15° by 30%, and that anterior translation decreased significantly at every tested angle except full extension. Section 3 of the body, and original Figures 3 and 6, show that in situ force at 15° fell from 44.9 ± 13.8 N to 34.7 ± 11.8 N, a reduction of about 22.7% calculated from the means, which the body states as 23%. They also show that the change in anterior translation was not significant at 0° or at 15°, and reached significance only from 30° to 120°. Interpretation should follow the body. The abstract's "30%," and its "significant decrease in anterior translation at 15°," are not used [6].
These data show that from 0° to 60° of flexion the quadriceps is the main active pull driving the tibia forward and loading the ACL. Hamstring co-contraction significantly reduces ACL in situ force from 15° to 60°. At 15°, translation had not decreased significantly, and ACL force had already fallen by 23%. At full extension (0°) the hamstrings lose that mechanical advantage: their tendon direction lies close to the long axis of the tibia, and the posterior shear component becomes smaller [6]. The 200 N and the 80 N are fixed cadaveric loads, without axial compression from body weight. They do not test what long-term strength training achieves in patients. What they show is that muscle contraction can only adjust active load as the angle and the state of activation change. It cannot restore the passive mechanical restraint of the ligament that is missing.
2. Kinematics of a slow step-up, and confounding by time since injury
Hosseini et al. registered three-dimensional bone models from 3.0-T MRI to a biplane fluoroscopy system at 30 Hz. They recorded 21 preoperative patients with a unilateral ACL injury and a positive clinical Lachman test, using the uninjured knee as the reference, as they climbed a single step slowly. The record covered the second half of knee extension, 50%–100%, from about 30° of flexion out to 0°, with one acquisition on each side. Five patients had an isolated ACL injury, eight a concomitant medial meniscal injury, and eight a concomitant lateral meniscal injury [7]. Every patient had a positive Lachman test at the bedside. During the slow step-up, the mean anterior translation of the injured side relative to the uninjured side was small. At the end of extension (100%) it was 2.3 ± 2.9 mm in the isolated ACL group (P = .144) and 3.5 ± 4.7 mm in the group with a lateral meniscal injury (P = .076). In the group with a medial meniscal injury the mean side-to-side difference remained below 0.5 mm throughout the motion (P > .05). One-way analysis of variance found no statistically significant difference among the three groups in the anteroposterior translation difference at any flexion angle along the motion [7].
The observation shows that a slow, predictable, everyday closed-chain step-up does not have to display the passive anterior laxity measured on the examination table. Loaded contact of the joint surfaces, co-contraction of the muscles that cross the joint, or an adjustment of gait are reasonable mechanical explanations. The study measured neither muscle force, nor electromyography, nor joint contact force, and the effect of axial load itself on anterior translation is also constrained by the geometry of the tibial plateau and by the direction of muscle force. Those mechanisms cannot be written down as causes this study has established. The comparison is also observational, with only 5 to 8 patients in each subgroup, and original Table 1 shows obvious differences in time since injury and in age. The isolated ACL group was a mean of 2.2 ± 1.1 months after injury (mean age 27.0 years), the lateral-meniscus group 6.2 ± 8.7 months (age 36.5 years), and the medial-meniscus group reached 43.2 ± 66.1 months (age 39.6 years), including two patients more than 10 years after injury and one whose duration was missing [7]. The between-group analysis of variance was nonsignificant throughout, and the patients with chronic injuries had had longer to adjust the way they moved. Under those conditions, a mean difference below 0.5 mm in the medial-meniscus group is no evidence that "a medial meniscus tear protects anterior stability." A small sample in which no significant difference was detected is also no evidence that joint kinematics have returned to normal.
Recalculation of the published table does not match the P value in the text: The individual differences published in original Table 2 were recalculated with the paired t test specified in the methods of Hosseini et al. For the 8 patients with a concomitant medial meniscal injury, the mean lateral tibial displacement at the 100% point of the step-up was about 1.05 ± 2.80 mm. The negative sign in the table marks the lateral direction, and the magnitude is compatible with the lateral translation of 1.1 ± 2.8 mm reported in the text. The two-sided P is approximately .323. That does not match the P = .019 reported in the paragraph on mediolateral translation, and rounding cannot explain the difference. The conclusion of "significant lateral translation" in that group cannot be used. For the 5 patients in the isolated ACL group, the recalculated two-sided P for anterior translation at the 90% point is approximately .031. The number differs from the P = .019 in the text, and both are below .05. The recalculated P at the 100% point is approximately .146, close to the P = .144 in the text. The observation that anteroposterior translation during the step-up did not differ significantly among the groups can still be used [7].
3. Where passive anterior laxity and early dynamic screening separate
The clinical evidence that tests passive anterior laxity directly against early dynamic function comes from the prospective screening study of Hurd, Axe, and Snyder-Mackler in 345 highly active patients with an acute unilateral isolated complete ACL rupture [8]. Those enrolled, 216 men and 129 women, age 27 ± 10.3 years, had all taken part before injury in IKDC level I or level II sports of sudden stopping, change of direction, or jumping, for more than 50 hours a year. MRI and a knee arthrometer confirmed a complete ACL rupture. The injury was no more than 7 months old. Concomitant laxity of the other ligaments, repairable meniscal tears, and full-thickness cartilage injury were excluded. Every patient first had to be past the acute picture of injury: motion restored in full, no obvious effusion, a normal gait, and the ability to hop on one leg without pain. The Discussion further states that the quadriceps strength index had to reach at least 70% of the uninjured side. At a mean of 6 ± 5 weeks after injury, wearing an anti-rotation functional brace, they completed four single-leg hop tests. Patients who met all of the following were classed as potential copers (146 patients, 42%): a 6-m timed hop index ≥80%, a Knee Outcome Survey Activities of Daily Living Scale (KOS-ADLS) score ≥80%, a global rating of function ≥60%, and no more than one giving-way episode since the injury. Patients who missed any one of these were classed as non-copers (199 patients, 58%) [8].
The distributions of the side-to-side difference under maximum manual anterior pull were almost the same in the two groups (Table 2). The between-group difference was not statistically significant. In a regression that entered the variables one after another in a predetermined order, the incremental variance in the four single-leg hop scores explained by passive anterior laxity was close to zero (original Table 2; R² increment .001–.008, P = .108–.470). The incremental variance explained in the patient's global rating of knee function was 0.000 (original Table 3, P = .669). The quadriceps strength index explained only 3.8%–7.5% of the variance in the single-leg hop [8].
The archived manuscript is inconsistent on the arthrometer model and on the regression variables: In the PMC author manuscript of Hurd et al. (PMC2891104), the methods and the caption of original Figure 1 name the knee arthrometer as a KT-1000, while the notes to original Tables 2 through 4 name a KT-2000. Both places state that a maximum manual anterior pull and the side-to-side difference were used. The test angle of 20°–30° of flexion appears only in the methods. The difference in the model label does not affect the analysis relating laxity to function. The abstract of the same archived manuscript says that only the 6-m timed hop affected the patient's global rating of function. The results in the body, and original Table 3, show that preinjury activity level, once entered in the model, was also statistically significant (R² increment = .020, P = .007). The phrasing "the only related variable" is not used [8].
Table 2. Early functional-screening class and the distribution of passive anterior laxity in highly active patients with an acute isolated complete ACL rupture (from original Table 4 of Hurd et al. [8]; n = 345)
| Item | Potential copers (n = 146, 42%) | Non-copers (n = 199, 58%) | Conditions of assessment and between-group comparison |
|---|---|---|---|
| Criteria met on screening | 6-m timed hop ≥80%, KOS-ADLS ≥80%, global rating ≥60%, and ≤1 giving-way episode since injury | Any criterion not met, or more than one giving-way episode since injury | Tested in a functional brace at a mean of 6 ± 5 weeks after injury, after the swelling had settled and quadriceps strength was ≥70% |
| Side-to-side difference on passive anterior pull < 5 mm | 38% | 32% | No statistically significant between-group difference in the distribution of laxity |
| Side-to-side difference on passive anterior pull 5–7 mm | 41% | 41% | Same as above |
| Side-to-side difference on passive anterior pull > 7 mm | 21% | 26% | 21% of potential copers had obvious passive laxity > 7 mm |
The data of Hurd et al. settle a clinical point. After the acute swelling and pain have settled, dynamic performance in controlled hopping and in daily activity does not match, millimeter for millimeter, the passive anterior laxity. A difference in coordinated muscle control, or in movement strategy, is a possible reason, although this screen did not measure neuromuscular control directly. Millimeters on an arthrometer cannot by themselves establish the functional level at that time, and they are not a sufficient basis, alone, for the direction of treatment. The finding that 42% passed a short-term screen cannot be used to deny the passive mechanical action of the ACL, or to treat a "potential coper" as a patient already shown to return, without surgery and over the long term, safely to sport that demands sudden stops and changes of direction. The "10-year prospective trial" in the title of that study is the period over which patients were enrolled, not 10 years of follow-up for each of the 345. Repairable meniscal tears and injuries of more than one ligament were excluded, and the hops were tested in a functional brace. Even so, 58% of these athletes failed the early screen after the swelling had settled and strength had reached 70%. Active adjustment can operate only in tasks for which the muscles have time to respond. In a sudden collision, an unanticipated change of direction, or a landing close to full extension while the posterior shear component of the hamstrings is limited [6], a knee without the ACL as its primary passive restraint still faces instability and the risk of secondary injury to the meniscus and the cartilage.
Mechanical reading of the bedside anterior examination, and separate appraisal of clinical outcomes
On manual clinical examination, the Lachman test at 20°–30° of flexion and the anterior drawer test at 90° reflect passive restraint under different mechanical conditions. In cadaveric tests under passive anterior load, in situ force in the whole ACL is higher near 20°–30° [3], the increase in anterior translation after cutting is larger [4,5], the posterior block of the medial meniscal posterior horn against the femoral condyle is weaker than it is in deep flexion [5], and the posterior shear component of the hamstrings near extension is smaller than it is at 90° [6]. At the 90° anterior-drawer position the ACL still carries the main passive anterior resistance [1,3]. The hamstring tendons, though, lie nearly parallel to the tibial plateau, so a patient who tenses even slightly opposes the examiner's anterior pull directly. An intact body and posterior horn of the medial meniscus, and the lateral structures, also join the block more readily once displacement is larger [4,5].
Three conditions govern the reading of these two signs:
- Check the starting reference position of the tibia. Before a 90° anterior drawer, sight across the height of the tibial tuberosities on the two sides and palpate the step at the anterior tibiofemoral margin, so that the false picture from posterior sag after PCL rupture, described above, is excluded [1].
- Keep the comparison with the other knee, and register both the displacement and the stiffness of the endpoint. Physiologic anterior laxity ranges widely among normal individuals [2]. The uninjured knee is the reference, and the added anterior translation is felt together with the change in the slope of resistance [1].
- Do not equate an increase in passive anterior laxity, taken alone, with a complete ACL rupture. Anterior translation also increases with physiologic high laxity that is symmetric on the two sides, and with a partial tear in which the remaining intact fibers can still supply the main anterior resistance [1,2]. When protective muscle contraction from acute pain, or a joint effusion, limits the force the maneuver can apply, a complete rupture may show only a small difference in displacement under a low-force pull [1].
The pattern of displacement and force in cadaveric tests at 20°–30° of flexion does not, by itself, imply that in the awake patient the Lachman test is more sensitive than the 90° anterior drawer in every clinical population. The systematic review and bivariate random-effects meta-analysis of Sokal et al. in 2022 included 24 studies of manual examination, performed awake and without anesthesia, for the diagnosis of partial or complete ACL tears. Studies of knees with other ligament injuries were excluded. Non-blocking meniscal tears were allowed. Seventeen studies used arthroscopy or open exploration as the reference standard, and seven used MRI. Twelve entered the bivariate summary [9]. The bivariate summary in original Table 4 gives a Lachman sensitivity of 81% (95% confidence interval 73%–87%) and a specificity of 85% (73%–92%), and an anterior-drawer sensitivity of 83% (77%–88%) and a specificity of 85% (64%–95%). In the pooled population the point estimates of the two tests lie close to each other. Earlier expectations of the sensitivity of the Lachman test in the awake patient were too high [9].
The cadaveric pattern and the pooled clinical accuracy answer different questions. A cadaver specimen has neither the pain of an awake patient nor active neuromuscular defense, and the clamps remove the error of holding the limb in the hands. In the awake outpatient examination, a large thigh or an examiner with small hands can make it difficult to maintain a stable hold on the distal femur during the Lachman test. Studies have mixed acute and chronic cases, and subsequent laxity of secondary restraints in the chronic phase can make a positive 90° anterior drawer more likely. Partial tears have been mixed in as well. Differences of this kind in the conditions of examination may narrow the gap between the two tests in a pooled population. Sokal et al. did not themselves test these particular reasons. Of the 24 studies in that review, only 2 were free of risk of bias on QUADAS-2, and the review is not a paired comparison, inside one homogeneous acute cohort, of which test is the better. The result cannot be turned around into the claim that the anterior drawer is better than the Lachman, and it is no reason to drop the Lachman test in the acute phase [9]. In clinic the two tests should be used together, and the mechanics should be used to read where they agree and where they differ. A markedly lax Lachman test with only a mild increase on the 90° anterior drawer fits an isolated ACL rupture with tense hamstrings, or with intact restraint from the medial meniscus. If anterior translation is large at both angles, or if the slip in deep flexion at 60°–90° is equally prominent, the search should follow the clues already set out: the posterior horn or body of the medial meniscus, or the lateral and anterolateral auxiliary structures [4,5].
Outcomes of treatment and of follow-up have to be weighed separately as well. One loose sentence, "anterior stability has been restored," would run three different things together:
- Improvement in the passive anterior restraint (fewer millimeters of anterior translation on examination or on the arthrometer, and a better resisting endpoint) reflects stronger static restraint under a unidirectional pull at low and moderate load. The sign itself cannot tell the contribution of graft remodeling from that of scar. As the model of Seon et al. shows for knees that also had a subtotal medial meniscectomy, single-bundle reconstruction can leave residual laxity even after it has lowered anterior translation by a large amount [5]. A knee that is statically tight has not, on that account, recovered dynamic control.
- Current performance on one controlled task (no obvious abnormal anterior translation on a slow step-up [7], for example, or passing a single-leg hop and symptom screen while wearing a brace [8]) shows only that the patient can complete the movement under the load and the protection of that task. It does not establish that the passive mechanical restraint has been restored. It also does not mean that the knee will stay stable, without a brace, in high-intensity competitive sport.
- Absence of repeated instability after return to sudden stops and changes of direction depends on the primary passive restraint, on secondary structures such as the menisci and the capsule, and on neuromuscular control across the joint, maintaining joint congruence under high load and shear in more than one direction. Passive laxity, current performance on controlled tasks, and dynamic stability after return to sport have to be reported separately in the record and in the appraisal of outcome. That separate report is what shows the real state of recovery after ACL injury and after treatment.
References
- [1]
Butler DL, Noyes FR, Grood ES. Ligamentous restraints to anterior-posterior drawer in the human knee. A biomechanical study. J Bone Joint Surg Am. 1980;62(2):259–270. PMID: 7358757. DOI: https://doi.org/10.2106/00004623-198062020-00013
- [2]
Amis AA, Dawkins GP. Functional anatomy of the anterior cruciate ligament. Fibre bundle actions related to ligament replacements and injuries. J Bone Joint Surg Br. 1991;73(2):260–267. PMID: 2005151. DOI: https://doi.org/10.1302/0301-620X.73B2.2005151
- [3]
Sakane M, Fox RJ, Woo SL, Livesay GA, Li G, Fu FH. In situ forces in the anterior cruciate ligament and its bundles in response to anterior tibial loads. J Orthop Res. 1997;15(2):285–293. PMID: 9167633. DOI: https://doi.org/10.1002/jor.1100150219
- [4]
Willinger L, Athwal KK, Holthof S, Imhoff AB, Williams A, Amis AA. Role of the Anterior Cruciate Ligament, Anterolateral Complex, and Lateral Meniscus Posterior Root in Anterolateral Rotatory Knee Instability: A Biomechanical Study. Am J Sports Med. 2023;51(5):1136–1145. PMID: 36917838. DOI: https://doi.org/10.1177/03635465231161071
- [5]
Seon JK, Gadikota HR, Kozanek M, Oh LS, Gill TJ, Li G. The effect of anterior cruciate ligament reconstruction on kinematics of the knee with combined anterior cruciate ligament injury and subtotal medial meniscectomy: an in vitro robotic investigation. Arthroscopy. 2009;25(2):123–130. PMID: 19171270. DOI: https://doi.org/10.1016/j.arthro.2008.09.020
- [6]
Li G, Rudy TW, Sakane M, Kanamori A, Ma CB, Woo SL. The importance of quadriceps and hamstring muscle loading on knee kinematics and in-situ forces in the ACL. J Biomech. 1999;32(4):395–400. PMID: 10213029. DOI: https://doi.org/10.1016/S0021-9290(98)00181-X
- [7]
Hosseini A, Li JS, Gill TJ 4th, Li G. Meniscus Injuries Alter the Kinematics of Knees With Anterior Cruciate Ligament Deficiency. Orthop J Sports Med. 2014;2(8):2325967114547346. PMID: 26535357. DOI: https://doi.org/10.1177/2325967114547346
- [8]
Hurd WJ, Axe MJ, Snyder-Mackler L. A 10-Year Prospective Trial of a Patient Management Algorithm and Screening Examination for Highly Active Individuals with ACL Injury. Part II: Determinants of Dynamic Knee Stability. Am J Sports Med. 2008;36(1):48–56. PMID: 17932399. DOI: https://doi.org/10.1177/0363546507308191
- [9]
Sokal PA, Norris R, Maddox TW, Oldershaw RA. The diagnostic accuracy of clinical tests for anterior cruciate ligament tears are comparable but the Lachman test has been previously overestimated: a systematic review and meta-analysis. Knee Surg Sports Traumatol Arthrosc. 2022;30(10):3287–3303. PMID: 35150292. DOI: https://doi.org/10.1007/s00167-022-06898-4