Share this article on:

00005768-199712000-0000300005768_1997_29_1561_vergis_translations_12article< 79_0_6_6 >Medicine & Science in Sports & Exercise©1997The American College of Sports MedicineVolume 29(12)December 1997pp 1561-1566Sagittal plane translations of the knee in anterior cruciate deficient subjects and controls[Clinical Sciences: Clinically Relevant]VERGIS, ANIL; HINDRIKS, MISHA; GILLQUIST, JANDepartment of Sports Medicine, Faculty of Health Sciences, Linköping University, SWEDENSubmitted for publication November 1995.Accepted for publication December 1996.ABSTRACTSagittal plane translations of the knee in anterior cruciate deficient subjects and controls. Med. Sci. Sports Exerc., Vol. 29, No. 12, pp. 1561-1566, 1997. Static anterior-posterior (AP) laxity is one of the commonly used criteria in selecting patients for cruciate ligament reconstructions, but in reality dynamic AP laxity plays a more important role. The aim of thisin vivo study was to compare the sagittal translation of the knee during active and passive motion, signifying dynamic AP laxity, with static AP laxity in healthy subjects (controls) and patients with anterior cruciate ligament deficiency. The sagittal plane knee translations were recorded and compared in both knees of nine healthy subjects (Controls) and seven patients with confirmed unilateral ACL deficiency during dynamic and static situations with an electrogoniometer system. In all groups during the ascents the tibia moved anteriorly in relation to the femur, whereas during the decents it moved posteriorly. The static anterior-posterior translation was significantly smaller in the control knee than in both healthy and injured knees of the ACL deficient group (P < 0.05). The injured knee showed the same laxity (92%) as the uninjured knee during dynamic activities, but it was 46% of static laxity. Also in the injured knees, the dynamic active laxity was larger during descents than ascents (P < 0.05). The results indicate that there is also a change in mechanics of the noninjured knee following injury to the contralateral knee and that this population of patients with ACL deficiency had good control over their abnormal anterior-posterior laxity.Static anterior-posterior (AP) laxity is one of the commonly used criteria in selecting patients for cruciate ligament reconstructions, but in reality dynamic AP laxity plays a more important role. In vivo sagittal laxity testing with different measuring devices, which represents static AP laxity, has been reported by several authors(1,5,6,8,14-16), but sagittal plane translation during passive motion, signifying dynamic AP laxity, has mostly been reported in vitro (4). Although there are several reports of sagittal plane translations in the active motion with different test designs(9,11-13), including a single step up-step down stair walking design reported by Vergis and Gillquist(20), we did not find any reports comparing static laxity with dynamic laxity in the literature. The aim of this in vivo study was to compare the sagittal translation of the knee during active and passive motion, signifying dynamic AP laxity, with static AP laxity in healthy subjects (controls) and patients with anterior cruciate ligament deficiency.MATERIALS AND METHODSProtocol and subjects Sixteen subjects took part in the study. Both knees of nine healthy subjects (control group: six male, three female) without any previous history of knee joint trauma and seven patients (anterior cruciate ligament group: five male, two female) with unilateral ACL deficiency, which had been confirmed by arthroscopy, were investigated. Measurements were recorded during anterior-posterior laxity testing, passive flexion-extension, and single step ascents and descents. The age of the subjects ranged from 16 to 34 yr (median: 24 yr). The weight of the subjects ranged from 53 to 90 kg (median: 70 kg). The height of the subjects ranged from 165 to 192 cm (median: 176 cm). There was no difference between the controls and the ACL-deficient subjects with regard to age, weight, and height.Equipment and procedure. The equipment has been described(9,11,12,20). A computerized goniometer linkage system measuring three tibial rotations and sagittal translation(CA-4000, OS Inc., Hayward CA) was fixed to the knee by broad elastic bands. The system is composed of three parts, the femoral and tibial frames and a rotation module. Three goniometers in the rotation module measured the relative rotation between the femur and tibia. The postentiometer for sagittal motion mounted in the tibial frame registered the difference in position between a spring loaded patellar pad and the fixation point on the tibial tuberosity during one flexion and extension cycle. The linear accuracy of the sagittal parallelogram linkage was 0.1 mm and the angular accuracy for the potentiometers was 0.125 °.The potentiometer which registered the knee flexion extension was aligned with the center of the lateral femoral epicondyle. The system was zeroed with the test person lying relaxed with the knee fully extended. During the testing, the alignment of the potentiometers was checked repeatedly in the zeroing screen of the computer. The protocol was repeated with fresh zeroing if the values were different from the original. Data were sampled from the four potentiometers by a computer at a rate of 100 Hz.Laxity testing. The subject sat with the lower legs supported by a leg holder (OS, Inc.). The medial joint line of both knees was aligned at the level of the hinge between the positioning seat and the leg holder. In this position both limbs were strapped to the device just above the patella without constraining it and above the ankle. The test was done at 20 ° of knee flexion according to the flexion potentiometer. When the subject relaxed, a perpendicular force of up to 135 N was applied three times at the level of the tibial tuberosity with a force handle equipped with a load sensor anteriorly and posteriorly.Passive motion. The passive motion was performed both while the subject was sitting and standing. For recording the posterior limit of passive motion, the subject was seated. The instrumented limb was supported at the foot in full knee extension by the examiner, and when the subject relaxed the examiner flexed the knee to 90 ° and then extended it. For recording the anterior limit of passive motion, the subject stood on the noninstrumented limb at the edge of a step (height, 15 cm; width, 45 cm; and length, 60 cm) with the limb hanging relaxed. The subject kept his/her balance by holding on to a vertical post. The instrumented limb was supported at the foot, and the knee was passively flexed and extended by the examiner. When the subject stood with a flexed knee, the weight of the limb created an anterior passive motion limit, whereas when the subject sat on a couch with an extended knee, it created a posterior passive limit (Figs. 1a and b). Each subject had six trials on each limb with three repetitions of each motion.Figure 1-Showing the forces acting on the knee while recording the a) anterior and b) posterior limits of passive motion. Fant: anterior translatory force; Fpost: posterior translatory force;M, mass of the leg; g, acceleration because of gravity; d, moment arm of massM; L, length of the leg; l, distance between heel and center of mass of leg; and224: is the flexion angle of the knee.Active motion. The stair was a single step as described above. The subject stood with both legs 20 cm in front of the step. For recording of the motion pattern during ascent (concentric quadriceps activity), the instrumented limb was lifted and planted on the step, the body was elevated, and the noninstrumented limb followed. Thus the ascent cycle consisted of one unloaded flexion followed by a loaded extension. In the descent (eccentric quadriceps activity), the noninstrumented limb was lifted and planted on the ground, the body lowered, and the instrumented limb followed. The descent cycle consisted of one loaded flexion followed by an unloaded extension. Each subject had six trials on each limb with three repetitions of each activity.Data reduction. A customized software program based on a commercially available software (MICROSOFT FOXPRO version 2.6) was used for data reduction.Calculations. The data were evaluated with the STATISTICA program(StatSoft Inc., Tulsa, OK) using the sagittal plane knee translation (mm), the change in flexion angle (degrees), and the change in force (Newton) for calculations.Laxity testing. From the anterior and posterior force displacement curves, the total static anterior-posterior translation (SAPT) was calculated (Fig. 2). For this, on the anterior force-displacement curve, the inflexction point (the point of most obvious increase in stiffness) was determined by a line fitting program. This program fitted two line segments into the force displacement curve, as inFigure 3. A sum of squares error function was calculated between the line segments and the actual data. The same process was repeated for all the data points within the relevant area, and the position corresponding to the minimum of the error function was chosen as the“Inflection point,” i.e., where the two lines L1 and L2 intersect. At this point the values of position (Ia) and force were noted, and at a similar force the value of position was also noted in the posterior force-displacement curve (Ip). The difference between values of position (Ia - Ip) was defined as the SAPT. The SAPT for a subject was calculated as the mean of the three trials because the difference between trials was not significant.Figure 2-Total static anterior posterior laxity in a typical force displacement curve. L1, L2, lines of the line fitting program; Ia, Ip, values of tibial position relative to femur at the anterior and posterior inflection points (the points of most obvious increase in stiffness); A, total static anterior laxity; P, total static posterior laxity; SAPT, total static anterior posterior laxity calculated as the difference between the values of position at the anterior and posterior inflection points. The positive and negative forces signify the anterior and posterior forces applied on the tibia, respectively.Figure 3-Curves showing mean and SD anterior and posterior limits of passive motion in control and ACL deficient subjects. ACLNI, ACL-I, noninjured and injured knees of ACL deficient group; AL, anterior limit of passive motion; PL, posterior limit of passive motion; A, anterior; P, posterior; MPT, maximal passive translation calculated as the difference between the values of position in the loops of the anterior and posterior motion limit curves at 45°.Passive motion. The total passive translation (TPT) was calculated as the difference between the values of position in the loops of the anterior and posterior motion limit curve for every 5 °. At 45 ° of knee flexion, the anterior and posterior translatory forces were of the same magnitude and the TPT at this angle was defined as the maximal passive translation (MPT) (Fig. 3). MPT for a subject was calculated as the mean of the three trials because there were no significant differences among trials. This was expressed as a percentage of SAPT and used for statistical evaluation.Active motion. From the loop formed by the flexion extension curves during the ascent and descent cycles, the active translation was calculated as the difference between the arms of the loops(Figs. 4a and b). The values of position in the flexion curve were always subtracted from those of the extension curve for corresponding flexion angles, and the maximal absolute difference was defined as the maximal active translation (MAT). Anterior translation was positive and posterior translation negative. The MAT for a subject in a situation was calculated as the mean of the three trials in that situation because there were no significant differences among trials. The knee flexion angle (KFA) at which MAT occurred and the maximum flexion angle (MFA) were also recorded and calculated in a similar manner. The MAT was expressed as a percentage of SAPT and MPT and used for statistical evaluations.Figure 4-a) Curves showing mean and SD of ascent cycle in control and ACL deficient subjects: ACL-NI, ACL-I, noninjured and injured knees of ACL deficient group; A, anterior; p, posterior; UF, unloaded flexion; LE, loaded extension; MAT, maximal translation during ascent cycle and the arrow heads signify the direction of translation. b) Curves showing mean and SD of descent cycle in control and ACL deficient subjects; ACL-NI, ACL-I, noninjured and injured knees of ACL deficient group; A, anterior; P, posterior; LF, loaded flexion; UE, unloaded extension; MAT, maximal translation during descent cycle and the arrow heads signify the direction of translation.Reproducibility. The inter-trial variation of the maximal translation in the static, passive, and active situation was calculated, and the variability among trials was expressed as the mean difference and 95% confidence interval.Statistics. The effect of the independent variables such as injury status, test situation, knee flexion angle, and applied laxity forces on the dependent variable sagittal plane knee translation was analyzed by ANOVA and post hoc Scheffe's tests. The variation in the sagittal plane knee translation between the trials was analyzed by repeated measures ANOVA. We used Student's t-tests for paired samples to compare the means of right versus left and injured versus noninjured knees. Student'st- tests for unpaired samples were used to compare the means of control versus injured and noninjured knees. In all instances, a statistical limit of P < 0.05 was selected.RESULTSAn overview is given in Tables 1 and 2.TABLE 1. Mean ± SD for static and dynamic laxity.TABLE 2. Mean ± SD for knee flexion angle for maximal translation and maximal flexion angle of the knee.Reproducibility. In SAPT testing the mean difference between the trials was 0.5 mm ± 0.6 and the 95% confidence interval was ± 0.1 mm. In the active motion the mean difference between trials was 0.8 mm± 0.7 mm, and in the passive motion it was 0.5 mm ± 0.4 mm. The 95% confidence interval was ± 0.2 mm in both situations.Laxity measurements. In the control knees the force at the inflection point ranged from 55 to 102 N (mean: 84 N) and the SAPT ranged from 3 to 11 mm (mean: 7 mm). In the noninjured knees of ACL deficient patients, the force ranged from 55 to 100 N (mean: 77 N) and the SAPT ranged from 7 to 12 mm (mean: 9 mm), but in the injured knees the force ranged from 65 to 105 N(mean: 89 N) and the SAPT ranged from 9 to 17 mm (mean: 13 mm). The SAPT was significantly smaller in the control knees than in both healthy and injured knees of the ACL deficient group (P < 0.05), but the mean force at the inflection point was similar in all groups (P > 0.05).Passive motion. The MPT was similar in the control and the noninjured knees of ACL deficient patients (P > 0.05), and it ranged from 1 mm to 6 mm (mean: 2 mm). The MPT in the injured knee of the ACL deficient group ranged from 3 to 8 mm (mean: 6 mm), and it was significantly larger than the MPT of the control group (P < 0.05), but it was similar to the MPT of the noninjured knees (P > 0.05). In all groups the MPT was approximately 40 ± 18% of the SAPT measurement.Active motion. In all groups during the ascent cycle, the tibia moved anteriorly (positive translation), but during the descent cycle it moved posteriorly (negative translation) (Figs. 4a and b). There were no differences between the right and left knees in the control group(P > 0.05), but the MAT differed significantly among individuals with a range of 3 to 11 mm (mean: 6 mm) (P < 0.05). In the ACL deficient group also, the MAT differed significantly among individuals within a similar range as the control group (P < 0.05).In the control group the MAT for ascents and descents were similar and occurred at similar KFA (MAT: 6 ± 2 mm; KFA: 39 ± 11 °)(P > 0.05). The MAT for ascents and descents were the same as the SAPT and three times larger than the MPT (range: 1-6 times; median: 3 times). This pattern was similar in the noninjured knees of the ACL deficient group(P > 0.05), the same as the SAPT, and four times larger than the MPT (range: 1-20 times; median: 2 times).However, in the injured knees of the ACL deficient group, the MAT was significantly smaller during ascent than descent (P < 0.05), but KFA at which MAT occurred was significantly larger during ascent than descent(P < 0.05). Also during ascent, a larger concavity was noted in the loaded extension curve of the injured knees as compared with that of the control knees (Fig. 4a). During descent the MAT was 51± 7% of the SAPT, but during ascent it was 42 ± 7% of the SAPT. This was significantly smaller than the control and noninjured knees of the ACL deficient group (P < 0.05). The MAT in the injured knees of the ACL deficient group when expressed as a percentage of the noninjured knees was similar during ascent (83 ± 38%) and descent (101 ± 43%)(P > 0.05). In all groups, significantly smaller MFA was seen during ascent than descent (P < 0.05).DISCUSSIONAlthough the principle of the AP laxity measurement is simple, significant difficulties arise in the execution of the test with instrumented devices. As the relative displacements between tibia and femur are measured, the soft tissue mantles over the bones complicate adequate fixation of external devices to femur and tibia. Slippage of the devices may contribute to measurement errors, but the added effect from the soft tissue is constant in the individual subject. However, the small mean difference among trials in this study may indicate that this error was minimal.Since we are measuring the AP translation of tibia relative to patella and not femur, the AP motion of patella relative to femur may have contributed to the measurement error. However, Edixhoven et al. (8) have shown by roentgen stereo photogrammetric studies that the error is extremely small, ≈ 1-3% of the measured AP displacement (8).The reproducibility of the static AP laxity and dynamic active AP laxity was good as reported earlier(11-13,20). In an in vitro cadaver model, Blankevoort et al. (4) reported the motion of tibia relative to femur to be variable within the envelope of passive motion but reproducible along the envelope. Although the passive motionin vivo could depend on a number of factors, muscle activation being one, we achieved good reproducibility of dynamic passive AP laxity at 45 ° in our study by instructing the subjects to relax, as the weight of the limb ensured that the tibial motion relative to femur was along the passive limit.However, within both control and ACL deficient groups, the inter-individual variation in MAT was large as reported earlier(13,20). The size and direction of AP translation of tibia was similar to that described earlier (20).Smaller SAPT in control knees than in both healthy and injured knees of the ACL deficient group could reflect changes in the mechanics of the noninjured knee following injury to the contralateral knee as reported by Andriacchi et al. (2) or it could be that subjects with such a pattern are predisposed to an injury to ACL. The above reasoning could also be applied to the finding of similar MPT in injured and noninjured knees. However, the finding of significantly smaller MPT in the control knees than in the injured knees of the ACL deficient group was as expected.The significantly smaller MAT (42% of SAPT) during ascents in the injured knees compared with controls and noninjured knees reflects that these patients have good control of their abnormal AP laxity. Similar behavior has been reported in ACL deficient patients previously(7,10,17), and it may result from good muscular corrdination or articular geometry. The phenomenon of quadriceps avoidance described by Andriacchi and Birac (3) may also be responsible for the smaller MAT.The larger MAT during descents than ascents in injured knees does not seem surprising. The translation is in a posterior direction during descents, and these patients pull the tibia posteriorly in the phase of unloaded extension, probably by hamstrings activity.The results of this study show that this population of patients with ACL deficiency have good control over their abnormal AP laxity while performing functional activities. This is probably a result of hamstring muscle activity(18), but since simultaneous recording of EMG was not done, it is not possible to objectively verify this assumption. However, increased hamstring activity has been demonstrated in a group of patients with ACL ruptures when anterior displacement of tibia was provoked by active extension of knee against resistance (19).This study was passed by the human ethical committee of Linköping University vide permit 94 068. It was supported by grants from the Swedish National Center for Research in Sports, Swedish Society of Medicine, and Lion's Research Fund.The authors appreciate the effort of Tuomas Räsänen, Research Engineer, Department of Sports Medicine, Faculty of Health Sciences, Linköping University, Sweden, in designing the software program, for line fitting, used in this study.Present address for Misha Hindriks: Bassin 146 E, 62 11 AL Maastricht, The Netherlands.Address for correspondence: Dr. Anil Vergis, Department of Sports Medicine, University Hospital, 581 85 Linköping, Sweden. E-mail:anil.vergis@ort.Liu.se.REFERENCES1. Andersson, C. and J. Gillquist. Instrumented testing for evaluation of sagittal knee laxity. Clin. Orthop. 256:178-184, 1990. [CrossRef] [Full Text] [Medline Link] [Context Link]2. Andriacchi, T. P., G. B. J. Andersson, R. W. Fermier, D. Stern, and J. O. Galante. A study of lower limb mechanics during stair climbing. J. Bone Joint Surg. 62A:749-757, 1980. [Context Link]3. Andriacchi, T. P. and D. Birac. Functional testing in anterior cruciate ligament-deficient knee. Clin. Orthop. 288:40-47, 1993. [CrossRef] [Full Text] [Medline Link] [Context Link]4. Blankevoort, L., R. Huiskes, and A. de Lange. The envelope of passive knee joint motion. J. Biomech. 2:705-720, 1988. [Context Link]5. Daniel, D. M. and M. L. Stone. KT-1000 anterior-posterior displacement measurements. In: Knee Ligaments: Structure Function Injury and Repair. D. M. Daniel, W. Akeson, and O'Conner (Ed.). New York: Raven, 1990, pp. 427-447. [Context Link]6. Fridén, T., K. Sommerlath, N. Egund, J. Gillquist, L. Ryd, and A. Lindstrand. Instability after anterior cruciate ligament rupture: measurements of sagittal laxity compared in 11 cases. Acta Orthop. Scand. 63:593-598, 1992. [Medline Link] [Context Link]7. Fridén, T., N. Egund, and A. Lindstrand. Comparison of symptomatic versus non symptomatic patients with chronic anterior cruciate ligament deficiency. Am. J. Sports Med. 21:389-393, 1993. [Context Link]8. Edixhoven, P., R. de Graaf, J. G. van Rens, and T. J. Sloof. Accuracy and reproducibility of instrumented knee-drawer tests.J. Orthop. Res. 5:378-387, 1987. [CrossRef] [Medline Link] [Context Link]9. Goertzen, D., M. Lysholm, K. Messner, and J. Gillquist. Sagittal translation of the tibia during stair walking in normal volunteers: reproducibility of an electrogoniometric method. Isokinet. Exerc. Sci. 5:19-23, 1995. [Context Link]10. Jonsson, H. and J. Karrholm. Three-dimensional knee joint movements during a step-up: evaluation after anterior cruciate ligament rupture. J. Orthop. Res 12:769-779, 1993. [Context Link]11. Lysholm, M., D. Goertzen, and K. Messner. Reproducibility of sagittal plane knee translation during isokinetic exercises. Isokinet. Exerc. Sci. 4:16-21, 1994. [Context Link]12. Lysholm, M. and K. Messner. Sagittal plane translation of the tibia in anterior cruciate ligament deficient knees during commonly used rehabilitation exercises. Scand J. Med. Sci. Sports 5:49-56, 1995. [CrossRef] [Medline Link] [Context Link]13. Marans, H. J., R. W. Jackson, N. D. Glossop, and C. Young. Anterior cruciate ligament insufficiency: a dynamic three-dimensional motion analysis. Am. J. Sports Med. 17:325-332, 1989. [CrossRef] [Medline Link] [Context Link]14. Markolf, K. L., A. Kochan, and H. C. Amstutz. Measurement of knee stiffness and laxity in patients with documented absence of the anterior cruciate ligament. J. Bone Joint Surg. 66A:242-253, 1984. [Context Link]15. Neuschwander, D. C., D. D. Drez, R. M. Paine, and J. C. Young. Comparison of anterior laxity measurements in anterior cruciate deficient knees with two instrumented testing devices. Orthop. 13:299-302, 1990. [Context Link]16. Noyes, F. R., E. S. Grood, and W. J. Suntay. Three-dimensional motion analysis of clinical stress tests for anterior knee subluxations. Acta Orthop. Scand. 60:308-318, 1989. [Medline Link] [Context Link]17. Noyes, F. R., P. A. Mooar, D. S. Matthews, and D. L. Butler. The symptomatic anterior cruciate deficient knee. Part I: the long term functional disability in athletically active individuals. J. Bone Joint Surg. 65A:154-162, 1983. [Context Link]18. Noyes, F. R., O. D. Schipplein, T. P. Andriacchi, S. R. Saddemi, and R. Weise R. The anterior cruciate deficient knee with varus alignment: an analysis of gait adaptations and dynamic joint loadings.Am. J. Sports Med. 20:707-716, 1992. [CrossRef] [Medline Link] [Context Link]19. Solomonov, M., R. Baratta, B. H. Zhou, et al. The synergistic action of ACL and thigh muscles in maintaining joint stability.Am. J. Sports Med. 15:207-213, 1987. [Context Link]20. Vergis, A. and J. Gillquist. Sagittal plane translation of the knee during stair walking in healthy volunteers measured by an electrogoniometer chain. Scand. J. Med. Sci. Sports 5:353-357, 1995. [CrossRef] [Medline Link] [Context Link]KNEE KINEMATICS; HUMAN; STEP ASCENT; STEP DESCENT; ELECTROGONIOMETER SYSTEMovid.com:/bib/ovftdb/00005768-199712000-0000300003086_1990_256_178_andersson_instrumented_|00005768-199712000-00003#xpointer(id(R1-3))|11065213||ovftdb|00003086-199007000-00026SL00003086199025617811065213P51[CrossRef]10.1097%2F00003086-199007000-00026ovid.com:/bib/ovftdb/00005768-199712000-0000300003086_1990_256_178_andersson_instrumented_|00005768-199712000-00003#xpointer(id(R1-3))|11065404||ovftdb|00003086-199007000-00026SL00003086199025617811065404P51[Full Text]00003086-199007000-00026ovid.com:/bib/ovftdb/00005768-199712000-0000300003086_1990_256_178_andersson_instrumented_|00005768-199712000-00003#xpointer(id(R1-3))|11065405||ovftdb|00003086-199007000-00026SL00003086199025617811065405P51[Medline Link]2364607ovid.com:/bib/ovftdb/00005768-199712000-0000300003086_1993_288_40_andriacchi_functional_|00005768-199712000-00003#xpointer(id(R3-3))|11065213||ovftdb|00003086-199303000-00006SL0000308619932884011065213P53[CrossRef]10.1097%2F00003086-199303000-00006ovid.com:/bib/ovftdb/00005768-199712000-0000300003086_1993_288_40_andriacchi_functional_|00005768-199712000-00003#xpointer(id(R3-3))|11065404||ovftdb|00003086-199303000-00006SL0000308619932884011065404P53[Full Text]00003086-199303000-00006ovid.com:/bib/ovftdb/00005768-199712000-0000300003086_1993_288_40_andriacchi_functional_|00005768-199712000-00003#xpointer(id(R3-3))|11065405||ovftdb|00003086-199303000-00006SL0000308619932884011065405P53[Medline Link]8458153ovid.com:/bib/ovftdb/00005768-199712000-0000300000150_1992_63_593_friden_measurements_|00005768-199712000-00003#xpointer(id(R6-3))|11065405||ovftdb|SL0000015019926359311065405P56[Medline Link]1471502ovid.com:/bib/ovftdb/00005768-199712000-0000300005156_1987_5_378_edixhoven_reproducibility_|00005768-199712000-00003#xpointer(id(R8-3))|11065213||ovftdb|SL000051561987537811065213P58[CrossRef]10.1002%2Fjor.1100050310ovid.com:/bib/ovftdb/00005768-199712000-0000300005156_1987_5_378_edixhoven_reproducibility_|00005768-199712000-00003#xpointer(id(R8-3))|11065405||ovftdb|SL000051561987537811065405P58[Medline Link]3625361ovid.com:/bib/ovftdb/00005768-199712000-0000300013584_1995_5_49_lysholm_rehabilitation_|00005768-199712000-00003#xpointer(id(R12-3))|11065213||ovftdb|SL00013584199554911065213P62[CrossRef]10.1111%2Fj.1600-0838.1995.tb00011.xovid.com:/bib/ovftdb/00005768-199712000-0000300013584_1995_5_49_lysholm_rehabilitation_|00005768-199712000-00003#xpointer(id(R12-3))|11065405||ovftdb|SL00013584199554911065405P62[Medline Link]7882129ovid.com:/bib/ovftdb/00005768-199712000-0000300000475_1989_17_325_marans_insufficiency_|00005768-199712000-00003#xpointer(id(R13-3))|11065213||ovftdb|SL0000047519891732511065213P63[CrossRef]10.1177%2F036354658901700303ovid.com:/bib/ovftdb/00005768-199712000-0000300000475_1989_17_325_marans_insufficiency_|00005768-199712000-00003#xpointer(id(R13-3))|11065405||ovftdb|SL0000047519891732511065405P63[Medline Link]2729481ovid.com:/bib/ovftdb/00005768-199712000-0000300000150_1989_60_308_noyes_subluxations_|00005768-199712000-00003#xpointer(id(R16-3))|11065405||ovftdb|SL0000015019896030811065405P66[Medline Link]2750506ovid.com:/bib/ovftdb/00005768-199712000-0000300000475_1992_20_707_noyes_adaptations_|00005768-199712000-00003#xpointer(id(R18-3))|11065213||ovftdb|SL0000047519922070711065213P68[CrossRef]10.1177%2F036354659202000612ovid.com:/bib/ovftdb/00005768-199712000-0000300000475_1992_20_707_noyes_adaptations_|00005768-199712000-00003#xpointer(id(R18-3))|11065405||ovftdb|SL0000047519922070711065405P68[Medline Link]1456365ovid.com:/bib/ovftdb/00005768-199712000-0000300013584_1995_5_353_vergis_electrogoniometer_|00005768-199712000-00003#xpointer(id(R20-3))|11065213||ovftdb|SL000135841995535311065213P70[CrossRef]10.1111%2Fj.1600-0838.1995.tb00058.xovid.com:/bib/ovftdb/00005768-199712000-0000300013584_1995_5_353_vergis_electrogoniometer_|00005768-199712000-00003#xpointer(id(R20-3))|11065405||ovftdb|SL000135841995535311065405P70[Medline Link]8775720Sagittal plane translations of the knee in anterior cruciate deficient subjects and controlsVERGIS, ANIL; HINDRIKS, MISHA; GILLQUIST, JANClinical Sciences: Clinically Relevant1229