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Gait analysis using external skin markers provides scope for the study of kinematic and kinetic parameters shown on different total knee arthroplasties (TKA). Thus an appropriate methodology is of great importance for the collection and correlation of valid data. Calibration of equipment is of great importance before measurements, to assure accuracy. Force plates should be calibrated to 1080 Hz and optoelectronic cameras should use 120 Hz frequency, because of the nature of gait activity. Davis model which accurately defines the position of the markers is widely accepted and cited, for the gait analysis of TKA's. To ensure the reproducibility of the measurement, a static trial at the anatomical position must be captured. Following, all acquisitions of dynamic data must be checked for consistency in walking speed, and abnormal gait style because of fatigue or distraction. To establish the repeatability of the measurement, this procedure must be repeated at a pre-defined number of 3-5 gait cycles. Anthropometric measurements should be combined with three-dimensional marker data from the static trial to provide positions of the joint's center and define anatomical axes of total knee arthroplasty. Kinetic data should be normalized to bodyweight (BW) and percentage of BW and height depending on the study. External moments should also be calculated by using inverse dynamics and amplitude-normalized to body mass (Nm/kg). Gait analysis using external skin markers provides scope for the study of biomechanical parameters shown on different TKAs. Thus a standard gait analysis methodology when measuring TKA biomechanical parameters is necessary for the collection and correlation of accurate, adequate, valid and reproducible data. Further research should be done to clarify if the development of a specific kinematic model is appropriate for a more accurate definition of total knee implant joint center in measurements concerning 3D gait analysis.

Purpose The purpose of this study is to examine the association between the development of articular cartilage pathology and knee rotation after single-bundle anterior cruciate ligament (ACL) reconstruction. Methods Seventeen patients that underwent single-bundle ACL reconstruction and did not have any cartilage lesions at the time of surgery based on the Outerbridge classiication or meniscal injury that required meniscectomy > 20% were examined by MRI and in the biomechanics laboratory at a 6-year minimum follow-up. Cartilage lesions that occurred after reconstruction were graded on MRI according to a modiied Noyes scale. For cartilage evaluation, the lateral and medial femoral condyles were divided into 9 segments each (lateral, central, and medial third and each third was divided into anterior, central, and posterior segment). Tibial rotation during a pivoting task was measured with optoelectronic motion analysis system and side-to-side diferences of tibial rotation between the reconstructed and contralateral intact knees were calculated. The association between the total modiied Noyes scale score (outcome variable) and side-to-side diferences of tibial rotation after controlling for meniscectomy and meniscal repair was investigated with hierarchical regression models. Results Side-to-side diference of tibial rotation was associated with total modiied Noyes scale score (p = 0.015, β = 0.667, adjusted R 2 = 42.1%). All patients developed new cartilage lesions in MRI located mainly at the central region of the lateral femoral condyle and less frequently in the central and anterior regions of the medial femoral condyle. Conclusion Abnormally increased tibial rotation that persists after ACL-R is signiicantly associated with the development of new articular cartilage lesions at mean 8.4 years after reconstruction which were located mainly at the central region of the LFC and secondarily in the central and anterior regions of the MFC (more supericial lesions). These indings suggest that there is emerging evidence that abnormal rotational kinematics is a potential risk factor for the pathogenesis and onset of posttraumatic articular cartilage degeneration after ACLR. Level of evidence IV.

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