Posttraumatic knee osteoarthritis (OA) occurs frequently after anterior cruciate ligament reconstruction (ACLR), with radiographic OA observed in more than 50% of people within 10–20 yr after their ACLR (20). Knee OA after ACLR is a disease frequently faced by younger adults (27) and has the potential to age the knee by 30 yr (21). Symptoms such as impaired knee confidence, fear of reinjury, premature cessation of physical activity, and reduced quality of life are typically reported in young adults (15,24). Nonsurgical treatment strategies are required to reduce the burden associated with posttraumatic knee OA. Therefore, it is important to identify gait characteristics that can be targeted with interventions in these individuals.
In nontraumatic knee OA, the medial compartment is affected in 56%–68% of people, whereas lateral compartment affects only 9%–11% of people (11,22). As a result, research efforts to date have focused predominantly on the medial knee compartment. A high external knee adduction moment (KAM) during walking is a predictor of nontraumatic medial knee OA progression (3,32) and hence has been investigated in a number of conservative intervention studies (16,33). After ACLR, abnormal gait patterns frequently may persist (13), and the resulting joint motion and loading may play a role in the initiation and progression of posttraumatic knee OA (7).
The evidence for higher KAM in people after ACLR is not conclusive (6,26,37). Butler et al. (6) found that approximately 5 yr after ACLR, individuals walked with 21% larger peak KAM compared with healthy controls. Recent studies have failed to confirm this finding, noting no KAM differences (37) or lower KAM in individuals after ACLR (26). The prominent differences in KAM between studies may be partly due to differences associated with sex, graft type, and/or time since surgery. However, lack of evidence of higher KAM in ACLR may also support the finding that lateral knee OA is more common after ACLR, as lateral knee OA has been observed in more than 50% of individuals with posttraumatic knee OA 10–15 yr after ACLR (1,4). Consequently, the KAM in nontraumatic knee OA may not be the most significant predictor of initiation and/or progression of posttraumatic OA.
Biomechanical changes in knee behavior may be related to abnormal gait features at adjacent joints, such as the hip and ankle (23,39). In nontraumatic knee OA populations, lateral knee OA has been associated with greater hip adduction joint angles and lower hip adduction moments (39). Although these gait adaptations may ultimately be exhibited to reduce pain during walking, they may increase knee joint loads, which could lead to faster progression of OA (23).
Although posttraumatic lateral knee OA is common after ACLR, little is known about gait characteristics associated with this condition. The aims of this study were to compare, between people with predominant lateral knee OA after ACLR and healthy controls, (i) knee kinematics and net joint moments and (ii) trunk, pelvis, hip, and ankle kinematics and joint moments. It was hypothesized that lateral knee OA after ACLR would be associated with lower knee flexion, adduction, and internal rotation angles as well as lower knee flexion, adduction, and external rotation moments.
MATERIALS AND METHODS
Study design and participants
A cross-sectional study design was used, comparing gait biomechanics between people with lateral knee OA after ACLR and healthy controls. Volunteers who had undergone a primary ACLR (hamstring tendon or patellar tendon graft) in the past 5–20 yr were recruited from the community via advertisements and referrals from orthopedic surgeons and health and medical practitioners. An a priori power assessment based on previously published differences in peak KAM between nontraumatic lateral knee OA and healthy controls revealed that at least 14 individuals per group were needed to provide a minimum of 80% power to detect differences in KAM (5).
Volunteers were included if they were age ≥16 yr at the time of ACLR and had symptomatic OA (10) according to the Knee Injury and Osteoarthritis Outcome Score criteria and radiographic OA (≥1 grade osteophyte) in the lateral tibiofemoral (TFJ) or patellofemoral (PFJ) compartment (2); radiographs were graded from semiflexed posteroanterior weight-bearing radiographs with the feet externally rotated by 10°. Healthy controls were included if they were age 18–40 yr, were participating in physical activity for at least 30 min·d−1 for 5 d·wk−1, and had no lower limb injury in the past year or previous surgery. The exclusion criteria for all participants were the following: (i) previous lower limb arthroplasty, (ii) previous hip or knee fractures, (iii) concomitant pain from the hips, ankles, feet, or lumbar spine, (iv) neurological or medical conditions, (v) contraindications for x-ray (e.g., pregnancy), and (vi) inability to understand written and spoken English. An additional exclusion criterion for the lateral OA group was medial > lateral TFJ osteophyte severity. All participants provided a written informed consent before data collection. Ethics approval for the study was obtained from the University of Melbourne Human Research Ethics Committee (HREC, 1238328.2).
Demographic data including age, sex, body mass, height, and body mass index (BMI) were recorded. TFJ and PFJ disease severity was graded by a trained observer (K.M.C.) (intrarater reliability, κ = 0.75–0.84). The radiographs in PA views were used to assess frontal plane knee alignment by a single investigator (H.F.H.) (intraclass correlation coefficient, 0.89), as described previously (18).
Participants walked overground at their self-selected speed while kinematics data were acquired at a sample rate of 120 Hz by tracking marker trajectories placed on each subject using a nine-camera motion analysis system (VICON Motion Systems, Oxford, United Kingdom). Ground reaction force data were simultaneously acquired using three force plates (Advanced Mechanical Technology, Watertown, Massachusetts) at a sample rate of 1080 Hz. The hip joint center was defined according to Harrington et al. (14), whereas the orientation of the knee flexion–extension axis was determined using a dynamic optimization procedure (30). The anatomic reference frames for the pelvis and lower extremity segments were defined as described previously (29). All kinematic data were filtered with a low-pass Butterworth filter with a cutoff of 6 Hz, whereas ground force data were filtered with a low-pass filter with a cutoff of 30 Hz. Trunk, hip, knee, and ankle joint kinematics and moments were calculated during the stance phase of gait (29). All subject gait data were averaged across three individual trials, and moment data were normalized to body mass.
Patient-reported outcome measures
Knee confidence and pain were assessed in people with lateral knee OA after ACLR (8). Participants were asked question 3 from the Knee Injury and Osteoarthritis Outcome Score quality of life subscale: “How much are you troubled by lack of confidence in your knees?” This question is provided with a five-point Likert scale, with the following possible responses: (i) not at all, (ii) mildly, (iii) moderately, (iv) severely, and (v) extremely. A score of 0 indicates no trouble with lack of confidence, whereas a score of 4 indicates lack of confidence. Kinesiophobia was also assessed in people with lateral knee OA after ACLR using the Tampa Scale of Kinesiophobia (36). The Tampa scale quantifies fear of movement and reinjury due to movement and physical activity. It consists of statements on subjective experience of injury and physical activity on a scale from 0 to 68, where a higher score indicates greater fear of reinjury due to movement. Upon completion of the gait trials, lateral knee OA participants were asked to rate their average level of knee pain during the walking task on a 100-mm visual analog scale. The scale was anchored by “no pain” (score of 0) and “worst imaginable pain” (score of 100).
Shapiro–Wilk analyses were used to assess data homogeneity and normality. Between-group differences in participant characteristics were assessed using independent t-tests for time-dependent variables, and chi-square tests for categorical variables. Between-group differences in joint angles and net joint moments were assessed at the point of the first peak because, in most cases, this corresponds to the point of contralateral toe-off and the time of peak hip and knee moments (25). Because no participant characteristics (age, sex, BMI, radiographic disease severity, or frontal plane knee alignment) were correlated with the peak joint angles and net joint moments, no covariates were included in the analyses. Relations among joint kinematics, joint moments, and patient-reported outcome measures were evaluated with the Pearson correlation coefficient (r). All data were analyzed using SPSS (SPSS, Chicago, IL), with α set at 0.05.
Nineteen people with lateral knee OA after ACLR and 25 healthy controls were included in this study. Participants in the lateral knee OA group (age, 37 ± 7 yr; height, 1.72 ± 0.06 m; body mass, 80 ± 10 kg; BMI, 27 ± 3 kg·m−2; 13 hamstring-tendon graft; six patellar-tendon grafts) were approximately 6 yr older (mean difference, 6 yr; 95% confidence interval (CI), 2–10) and weighed 11 kg more (11 kg, 4.5–17.5) than healthy control group (age, 31 ± 6 yr; height, 1.73 ± 0.10 m; body mass, 69 ± 11 kg; BMI, 23 ± 2 kg·m−2). The percentages of men in the lateral OA group and healthy controls were 79% and 56%, respectively. Individuals in the lateral OA group had undergone ACLR 12 ± 4 yr ago and had valgus malalignment measured on x-ray (187° ± 3°). The average values of walking speed of the lateral knee OA group and healthy control group were 1.46 ± 0.13 m·s−1 and 1.53 ± 0.17 m·s−1, respectively. There was no significant difference in walking speed between groups (P = 0.144).
There were significant differences in peak knee joint angles between those with lateral knee OA after ACLR and the healthy controls (Fig. 1A–F). Peak knee flexion angle was significantly greater in people with lateral knee OA after ACLR compared with that in controls (mean difference, 3.51°; 95% CI, 0.89–6.14; P = 0.010) (Fig. 1A). Peak knee internal rotation angle was significantly lower in the lateral knee OA group compared with that in the controls (mean difference, −3.30°; 95% CI, −6.16 to −0.50; P = 0.022) (Fig. 1C; Table 1). Peak KAM was lower in the lateral knee OA group (mean difference, −0.12 N·m·kg−1; 95% CI, −0.24 to 0.00; P = 0.058) (Fig. 1E), as was the external rotation moment (mean difference, −0.01 N·m·kg−1; 95% CI, −0.02 to 0.00; P = 0.055) (Fig. 1F); however, these differences were not significant.
There were no significant differences in peak trunk kinematics between the lateral knee OA group and controls (Fig. 2A–C). Peak anterior pelvic tilt angle was significantly greater in people with lateral knee OA compared with that in the healthy controls (mean difference, 3.12°; 95% CI, 0.38–5.86; P = 0.027) (Fig. 2D). Relative to healthy controls, those with lateral knee OA after ACLR had significantly greater peak hip flexion angle (mean difference, 5.09°; 95% CI, 1.85–8.32; P = 0.003) (Fig. 3A). There were no significant differences in hip joint moments between the two groups (Fig. 3D–F). At the ankle joint, there were no significant differences in kinematics (Table 1; Fig. 4); however, those with lateral knee OA after ACLR had significantly greater peak ankle dorsiflexion moment compared with healthy controls (mean difference, 0.11 N·m·kg−1; 95% CI, 0.02–0.21; P = 0.023) (Fig. 4D). A trend of lower peak ankle external rotation moment was observed in the lateral knee OA group (mean difference, −0.01 N·m·kg−1; 95% CI, −0.02 to 0.00; P = 0.055) (Fig. 4E); however, this was not significant.
A small number of significant correlations between patient-reported outcome and biomechanical variables were observed in people with lateral knee OA after ACLR. Those with worse knee confidence (r = 0.654, P = 0.002) and worse kinesiophobia (r = 0.518, P = 0.023) had greater peak trunk flexion. People with worse knee pain had greater knee flexion angles (r = 0.535, P = 0.018).
People with predominant lateral knee OA after ACLR had greater peak knee flexion and greater knee external rotation angles than healthy controls during walking. In addition, lateral knee OA participants had greater peak pelvic anterior tilt and hip flexion angles compared with controls. There were no significant differences observed in net joint moments, except for a significantly greater peak ankle dorsiflexion moment in those with lateral knee OA after ACLR. In the lateral knee OA group, we also observed that worse knee confidence and kinesiophobia correlated with greater peak trunk flexion angles and greater knee pain correlated with greater peak knee flexion angles.
People with lateral knee OA after ACLR walked with greater peak flexion angles, including greater peak knee and hip flexion and greater anterior pelvic tilt. Although no previous studies have reported gait biomechanics in people with OA after ACLR, increased anterior pelvic tilt and greater peak hip flexion angles have been reported in people with nontraumatic PFJ OA (12). The increased anterior pelvic tilt and hip flexion angle found in the current study may serve to reduce the external knee flexion moment and knee joint reaction force. This could also explain the absence of a heightened knee flexion moment in the presence of increased knee flexion angles. The observed walking pattern of prominent joint flexion has been described in people with acute experimental knee effusion (35) and may represent a protective adaptation after the original knee trauma. In an experimental study, increased flexion of the knee was associated with greater hamstring coactivation, theorized to enhance knee joint stability (34). It is plausible that people with lateral knee OA after ACLR also walk with joint flexion pattern in an attempt to stabilize the knee joint.
We observed significantly lower peak knee internal rotation angles in people with lateral knee OA after ACLR compared with those in healthy controls. Abnormal tibial rotation has been previously reported in cohorts with ACL injury and who have undergone ACLR (7,13,28,38). This finding is also consistent with our previous study that showed that people with valgus alignment and PFJ OA after ACLR had more external rotation (or less internal rotation) than those who had not developed OA after ACLR (9). In contrast, no differences in transverse plane motion were observed in those with nontraumatic lateral knee OA subjects (39). This may suggest that alterations in transverse plane kinematics due to knee trauma and ACLR result in knee pathology different from that seen in nontraumatic knee OA subjects. Abnormal transverse plane tibial rotation after ACLR shifts contact areas of the cartilage, which may increase load on infrequently loaded regions of the cartilage, resulting in accelerated cartilage degradation (7).
In the current study, we observed a nonsignificant trend toward lower KAM in those with lateral knee OA after ACLR. In nontraumatic knee OA populations, lower KAM has been associated with lateral knee OA (5,39). Whereas Butler et al. (5) and Weidow et al. (39) reported larger differences in KAM between nontraumatic lateral knee OA and healthy controls (41% and 63% lower, respectively), these studies were conducted in elderly people and they may have had greater valgus malalignment than the younger adults included in our study. In the present study, we may have been underpowered to detect between-group differences in peak KAM. However, it is notable that all participants with predominant lateral posttraumatic OA exhibited KAM, albeit lower than that in the healthy control group. KAM has been used as a surrogate for the load distribution between the medial and lateral knee compartments (31). As such, the trend toward lower KAM observed in the lateral posttraumatic knee OA participants is likely to reflect a larger proportion of the TFJ load at the lateral knee compartment than that in healthy controls. Considering that the medial TFJ has greater capacity to withstand joint loads (7), it may be that greater lateral joint load distribution in this subgroup may initiate or progress to lateral compartment disease.
The results of this study highlight that gait characteristics associated with posttraumatic lateral knee OA are different from those reported in nontraumatic lateral knee OA. People with lateral knee OA after ACLR walk with increased peak hip and knee flexion angles and reduced peak knee internal rotation angles, whereas these biomechanical features were not observed in people with nontraumatic lateral knee OA during walking (39). Because of the cross-sectional nature of the present study, it is unknown whether altered gait mechanics were evident before injury in this patient population. However, it is also likely that ACL injury and reconstruction may alter the mechanics of initiation and progression of OA. It could be speculated that neuromuscular differences observed after ACLR such as muscle weakness, altered activation patterns (17), and different joint kinematics may be consequences of the initial injury and/or the surgical reconstruction related to the position and/or tensioning of the ACL graft (28). Therefore, understanding the biomechanical and neuromuscular adaptations to ACLR and any changes in these over time after ACLR may shed more light on mechanisms responsible for development of premature knee OA after ACLR.
Worse knee pain correlated with increased peak knee flexion angle in people with lateral knee OA after ACLR. This finding suggests that lateral knee OA subjects may walk with increased knee flexion despite increased pain as a consequence of muscle weakness rather than as a compensatory mechanism. In the present study, forward lean of the trunk, which has been observed in total knee arthroplasty subjects as a compensatory mechanism for quadriceps weakness (19), was associated with worse knee confidence and kinesiophobia in lateral knee OA after ACLR. To date, no studies have evaluated the relation between knee confidence and kinesiophobia with gait biomechanics, although worse knee confidence has been associated with poorer physical function (15). This study indicates that greater trunk flexion may be a compensatory strategy used by those with more psychological impairments. Because of the cross-sectional nature of our research design, it is not possible to determine the temporal relation between psychological and biomechanical impairments. However, it seems that impairments such as lack of knee confidence and kinesiophobia should be considered in the treatment of people with lateral knee OA after ACLR (15).
This study has important clinical implications. Currently, posttraumatic knee OA after ACLR is managed with interventions designed for nontraumatic knee OA. The findings of the current study suggest that effective management of knee OA after ACLR requires a multidisciplinary approach that ought to address compartment-specific biomechanical, psychological, and functional deficits because these deficits are distinct from those with nontraumatic knee OA subjects. Interventions including gait retraining, knee bracing, foot orthoses, taping, strengthening exercises, pain management, psychological interventions, and therapeutic exercise programs may be used to address impairments in this patient population. A comprehensive multidisciplinary approach, if implemented at an early stage after ACLR, may assist in slowing the development of posttraumatic knee OA.
There are a number of limitations of this study that should be acknowledged. Firstly, people in the lateral knee OA group were older and weighed more than the healthy controls. However, age and body mass did not correlate with any of our biomechanical variables of interest. Secondly, although we did not obtain knee radiographs for healthy controls, it was confirmed that healthy controls were asymptomatic, with no self-reported lower limb pathology. Given the cost and unnecessary radiation exposure, radiographs could not be justified in this situation. Thirdly, we determined our sample size on the basis of previous nontraumatic lateral knee OA cohorts before commencement of our study. On the basis of previously published KAM, 14 people per group were required (5). However, our findings suggest that biomechanical data pertaining to those with nontraumatic lateral knee OA differ from lateral knee OA after ACLR. Thus, we may have been underpowered power to detect meaningful differences in kinematics and moments in this specific population. Indeed, a post hoc sample size calculations indicate that a total sample size of 100 (i.e., 50 people per group) would have been required to detect a statistically significant between-group difference in KAM for the magnitude observed in our study. Fourthly, by not comparing our posttraumatic lateral knee OA data with those of nontraumatic lateral knee OA population, we cannot make any firm conclusions about differences between these two populations. However, our choice of control group allowed us to document the differences in gait variables compared with those in a group of individuals, who were similar in age and who did not have ACLR. Finally, because of the relatively small sample size, we were unable to investigate the influence of sex differences and graft type on lower limb biomechanics in this patient population.
This study found that people with lateral knee OA after ACLR exhibited higher knee flexion, lower knee internal rotation angles, and higher pelvic anterior tilt and hip flexion angles. Increased sagittal plane knee and trunk joint flexion angles were moderately related to worse knee pain, confidence, and kinesiophobia. Therefore, to effectively manage posttraumatic lateral knee OA after ACLR, targeted treatments such as gait retraining, knee bracing, taping, and strengthening exercises should be investigated to mitigate abnormal gait characteristics seen at the hip, pelvis, knee, and ankle, along with consideration of psychological factors. Compartment-specific interventions designed specifically for posttraumatic knee OA may aid in slowing disease progression and thus mitigate the burden of this problematic disease.
H. F. H. is supported by a National Health and Medical Research Council (Australia) Postgraduate Scholarship (#813021), and N. J. C. is supported by a National Health and Medical Research Council (Australia) Research Training (Postdoctoral) Fellowship (#628918). DJO Global provided funding for the radiographs.
The authors’ contributions are as follows: conception and design, H. F. H., N. J. C., D. C. A., S. M. C., and K. M. C.; data acquisition, H. F. H., N. J. C., and D. C. A.; data analysis and interpretation, H. F. H., N. J. C., D. C. A., S. M. C., and K. M. C.; and drafting the article, H. F. H., N. J. C., D. C. A., S. M. C., and K. M. C. All authors approved the final version to be submitted for publication.
The authors have no conflict of interest to disclose. The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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