The knee adduction moment during gait has been noted for its potential role in the pathogenesis of knee osteoarthritis (1,3,14,29). Larger-than-normal external knee adduction moments have been associated with the incidence (3), severity (30), and rate of progression of tibiofemoral osteoarthritis (20). The mechanism for cartilage degeneration is believed to involve loading factors that alter the mechanical environment of the cartilage. The knee adduction moment influences the mediolateral distribution of load across the tibial plateau, such that larger adduction moments concentrate more load on the medial tibiofemoral compartment. It is theorized that larger-than-normal adduction moments alter the mechanical state of the medial tibiofemoral cartilage, leading to osteoarthritic changes (1). Although little prospective data exist to support the relationship between knee adduction moments and the development of knee joint osteoarthritis, we have recently found larger-than-normal knee adduction moments during walking in arthroscopic partial meniscectomy (APM) patients at 11 wk postsurgery (40), a population at increased risk of early-onset knee osteoarthritis (7).
Muscles play an important role in controlling joint moments via their action as actuators and brakes. The quadriceps contribute to the support of moments in the frontal plane while walking, particularly during early stance (32). It has been shown that coactivation of the quadriceps and hamstring muscle groups support up to 85% of static adduction loads at the knee (17). Lower limb muscles also play a role in the frontal plane acceleration of the center of mass, via mediolateral ground reaction forces, which affect knee adduction moments (21,22). Quadriceps strength deficits have been reported for many knee pathologies, including osteoarthritis (33), ACL-injured (37), and meniscectomy patients up to 4 yr postsurgery (9-11,18), which may contribute to poor stabilization of frontal plane loading of the knee during gait. Herzog and Longino (12) provided pilot data that suggested that as little as 4 wk of experimentally induced knee extensor muscle weakness can yield initial signs of joint degeneration in the knees of rabbits.
The quadriceps muscles also control sagittal plane loading of the knee joint during gait (8,16). Lewek et al. (16) reported a reduced external knee flexion moment for weak ACL reconstruction patients (<80% of uninvolved knee extension strength) compared with those with normal knee strength (>90%). Similarly, Rudolph et al. (28) found external knee flexion moments to be positively correlated with quadriceps strength in unstable ACL-deficient patients (r = 0.765, P = 0.030). These findings were in association with reduced range of knee motion and suggested to interfere with the normal ability of the knee to absorb shock during weight acceptance (21) and may have also affected upper body motion. Currently, there is no evidence for sagittal plane motion and moments as a mechanism for the development of knee osteoarthritis; moreover, these gait changes may exist because of knee pathology and weakness, which may be present in the APM population.
The purpose of this study was to investigate the relationship between muscular strength about the knee and knee joint motion and moments during gait in patients who had undergone APM. It was hypothesized that APM patients would have reduced knee extensor strength compared with a healthy, age-matched control group. It was also hypothesized that patients with strength deficits would walk with reduced knee flexion motion, reduced external knee flexion moments, and increased external knee adduction moments compared with those with normal strength levels.
The APM group comprised 102 patients (87 males), aged 17-51 yr, who had surgery, on average, 11 wk (SD, 4.3) prior to testing (resection of the injured region of the meniscus only). The control group comprised 42 adults (25 males) aged 24 to 56 yr. All subjects were screened and excluded if they had radiographic evidence of knee osteoarthritis, with surgery reports also used to screen APM subjects. All subjects were further screened for previous or current back, hip, knee, or ankle joint disease, pain, or injury (including previous meniscus tear); any form of arthritis; diabetes; cardiac, circulatory, or neurological conditions; multiple sclerosis; stroke; lower limb fractures; bone or joint conditions; and any other disease or injury that may affect gait patterns or predispose to knee osteoarthritis. The study was approved by the Human Research Ethics Committee at the University of Western Australia, and informed written consent was obtained from all subjects before their participation in the study.
Forty-five percent of the APM group had surgery on the left knee, whereas 55% had a right knee meniscectomy. Most APM subjects had sustained an injury to the posterior horn of the meniscus, with only three subjects having surgery performed for an anterior horn injury. Medial meniscectomy was performed in 79% of the patient group; lateral meniscectomy was performed on 17%, whereas 4% had both menisci surgically treated. Results were similar for subjects with medial versus lateral meniscectomy, and data were, therefore, pooled.
All subjects had physical activity levels, knee strength, gait patterns, and static knee alignment assessed, as well as completed a Knee Osteoarthritis Outcome Survey (KOOS) (27). Physical activity levels were measured using an Actigraph physical activity monitor (Computer Science and Applications Inc., Fort Walton Beach, FL). The monitor was worn by each subject for 7 d, carried on an adjustable belt that was secured firmly over the iliac crest. Subjects wore the monitor for 7 d, and the average daily hours of physical activity was determined. Subjects were tested for isometric and isokinetic concentric knee strength using a Biodex dynamometer (Biodex Medical, Shirley, NY). Strength testing was performed on the APM subject's affected limb, whereas a limb was randomly selected for control subjects, resulting in 43% left and 57% right knees analyzed. Isometric knee flexion and extension strength was tested at 75° and 45° of knee flexion, respectively. Concentric knee flexion and extension strength was measured through a range of 0° to 90° of knee flexion at 180° s−1. Warm-up exercises were performed before strength testing, and subjects were given adequate rest between trials to minimize fatigue. Subjects were verbally encouraged during the test, and each was repeated at least twice to ensure a maximum effort was achieved.
Three-dimensional gait analysis was conducted at subjects' freely chosen walking speed. A custom seven-segment "cluster" model was used to estimate hip, knee, and ankle kinematic and kinetic data (6), using data collected from a 50-Hz VICON motion analysis system (Oxford Metrics, Oxford, UK) and two AMTI force plates (AMTI, Watertown, MI) operating at 2000 Hz. Gait data were analyzed as we have previously described (35,36,40). Gait velocity (m·s−1) was measured from the pelvis center motion averaged over the 3-s data collection period. Stride length (m) and step width (m) were measured between right and left calcaneal markers in the sagittal and frontal planes, respectively. The kinematic parameters analyzed were knee angle at heel strike, peak knee flexion during weight acceptance, peak knee extension during late stance, and knee range of motion (ROM). Knee ROM was calculated as the excursion of the knee angle from heel strike to peak knee flexion in the weight acceptance phase of stance. The peak loading rate was determined as the peak gradient of the vertical ground reaction force following heel strike. The joint kinetic parameters analyzed were peak knee flexion moment during early stance, peak knee extension moment during late stance, peak knee adduction moment during early stance, minimum knee adduction moment during midstance, peak knee adduction moment during late stance, and average knee adduction moment over stance. Knee moments were expressed as external moments applied to the joint.
Within a week of the gait analyses, standard radiographic x-rays of a full lower limb with knee in 0° flexion and in weight-bearing position (Marquet view) were taken at the Perth Radiological Clinic. A specialized x-ray calibration rig was used, which allowed subjects to assume a standing posture (24). The knee alignment variable used in this study was the hip-knee-ankle angle. The angle was measured between mechanical axes of the femur and tibia, with the femur (tibia) axis defined as a line running through center points of the hip (knee) and knee (ankle) joints. Knee pain and function were measured using the KOOS. The KOOS is a superset of the Western Ontario and McMaster Universities Osteoarthritis Survey, which has previously been validated for the assessment of knee pain and function during daily activities (27).
Strength data were normalized by removing the slope of the relationship between the moment and body weight (BW) from the moment data for the purpose of categorizing APM subjects into subgroups of either "weak" or "normal" knee extension strength. APM subjects with normalized isometric knee strength of more than one SD below the mean of the control group were classified as weak, with all others classified as normal. The isometric tests of strength were a less discriminating measure of knee strength than were isokinetic tests, with APM patients performing relatively better on isometric measures. In fact, Stam et al. (38) has previously demonstrated that isokinetic testing is more sensitive for small strength differences than isometric testing in meniscectomy patients. We categorized patients based on their isometric knee extension strength, confident that this was a more moderate measure to differentiate between groups. The weak subgroup demonstrated significantly poorer performances in all strength tests compared with APM normal and controls, indicating that our criterion was appropriate to categorize them as weak.
Between-group differences in age, height, and weight variables were examined using t-tests. Strength and gait moment data were statistically tested using ANCOVA, with BW and age entered as covariates. Scheffe post hoc tests were used to determine the significance of interactions. The level of significance was set at P = 0.05.
There was no between-group differences in subject height; yet, the APM patients were, on average, heavier than controls, and the APM normal strength subgroup were also heavier than controls. One method to control for this difference while examining kinetic data is to divide the moment variable by BW, although this has associated problems. If one assumes the moment term (M) has a linear relationship with BW, this can be written as M = mBW + c, where m and c are the constants of the linear function. When divided by BW, the equation becomes M/BW = m + c/W, resulting in the normalized moment, M/BW, having a residual correlation of c/W, with M/BW becoming smaller as BW increases (23). The relationships between BW and each of the moment parameters from the control and APM groups were analyzed using GraphPad Prism (Windows version 5.01, GraphPad Software, San Diego, CA) and showed similar regression slopes between groups (P > 0.429); however, the y-intercepts were nonzero (P < 0.002). Therefore, we chose to control for the confounding influence of BW through its inclusion as a covariate in the statistical analyses, because this accounts for the residual relationship between BW and joint moments.
Twenty-seven percent of the APM subjects were classified as weak. The APM weak subgroup was significantly older than controls (P = 0.025) (Table 1). The APM normal, APM weak, and control groups were similar in height (P > 0.10). The APM weak were significantly heavier than control (P = 0.034), whereas the APM normal were not (P = 0.052). Again, we statistically adjusted for age and BW by using these variables as covariates in the statistical analyses.
Control and APM groups recorded similar levels of physical activity (P = 0.422). APM subjects categorized as weak had significantly reduced levels of physical activity compared with those categorized with normal strength (P = 0.019) (Table 1). APM normal and APM weak had similar self-reported knee function (P = 0.540) and pain (P = 0.407). No significant between-group or between-subgroup differences existed in hip-knee-ankle angle (P > 0.30).
While controlling for BW and age, the concentric knee extension strength of the APM group was less than the control group (P < 0.001) (Table 1). Concentric knee flexion strength of the APM group was also significantly reduced compared with controls (P = 0.033). Isometric knee extension and flexion strength were similar between APM and control groups (P = 0.196 and P = 0.664, respectively). Covariates age and BW were significantly associated with strength (P < 0.01).
Walking speed, stride length, and step width were similar between APM normal, APM weak, and control (P > 0.127) (Table 2). Sagittal plane knee kinematics were also similar between groups (P > 0.201). While controlling for BW and age, there were no significant differences in peak loading rate (P > 0.639), peak knee flexion moment (P > 0.400), and peak knee extension moment (P > 0.240) among control, normal, and weak APM (Table 2, Fig. 1).
While controlling for BW and age, APM weak subjects walked with larger average knee adduction moments over stance compared with APM normal (P = 0.011) and control (P = 0.033) (Fig. 2). Furthermore, the first peak of the knee adduction moment was greater for APM weak compared with APM normal (P = 0.032) and control (P = 0.005). APM weak also showed a trend for a larger adduction moment midstance trough compared with APM normal (P = 0.050). The peak knee adduction moment during late stance was significantly greater for APM weak compared with APM normal (P = 0.020) and control (P = 0.028). APM normal subjects had significantly greater adduction moment peak in early stance and late stance compared with control (P = 0.005). The covariate age was not significantly associated with any joint moments, whereas BW was significantly associated with all joint moments (P < 0.001), except the peak knee extension moments.
The knee adduction moment during the stance phase of gait has been implicated as a mechanical factor contributing to the development of knee osteoarthritis (1,3,14,29). We have recently shown larger-than-normal knee adduction moments in patients who have undergone APM (40), a population at increased risk of early onset of knee osteoarthritis (7). This study aimed to examine associations between muscular strength about the knee and the motion and moments acting at the knee during gait in an APM population.
The APM group produced reduced concentric knee extension strength compared with controls (Table 1), supporting the first hypothesis. These results are consistent with previous research that found knee extensor strength deficits in a group of 10 post-APM patients compared with a group of matched healthy subjects, preoperatively and at 3 and 8 wk postoperatively (9). In fact, quadriceps weakness has been shown to persist at 12 wk (18), 6 months (11), and 4 yr post-APM (10). Furthermore, concentric knee extensor strength deficits of approximately 20% have been shown to persist, even after 8 wk of knee strength training in postmeniscectomy patients (38).
Although tests of strength were only conducted at the knee joint, APM are likely to have a general lower limb weakness. The APM weak group was also weaker in concentric knee flexion, indicating a general muscle weakness about the knee, perhaps due to reduced levels of physical activity found in this group, compared with the APM normal and controls (Table 1). Persistent muscle weakness following meniscectomy may contribute to gait abnormalities, compromise joint stability, and have detrimental effects on the maintenance of healthy cartilage by altering the mechanical environment of the tissue. In rabbits, quadriceps weakness that was experimentally induced for 4 wk resulted in functional deficits and evidence of knee joint degeneration (12), suggesting that muscle weakness may act as an independent causative factor for knee osteoarthritis. Patients who have had an APM rapidly develop knee osteoarthritis within 5 yr in some reports (7), and the muscle weakness following APM may similarly initiate cartilage degeneration and alter the mechanical environment of the knee joint. Slemenda et al. (34) showed that females who developed incident knee osteoarthritis after 31 months had 18% lower knee extensor strength than female controls at baseline (P = 0.053).
Sagittal plane kinematics and kinetics were similar between APM normal, APM weak, and control groups (Table 2, Fig. 1), which was inconsistent with our hypothesis that APM subgroup with reduced knee extension strength would exhibit a reduced range of knee flexion and smaller knee flexion moments. These findings suggest that quadriceps and hamstrings weakness seen in the weak APM group had no substantial effect on sagittal plane motion and loading. Contrasting results have been reported for populations with ACL injury (8,16,28) and those with knee arthritis (5,39). The absence of a similar association in our meniscectomy population may be due to different age group, pathology, and/or the relatively good joint function, low pain, and other symptoms, as seen in KOOS scores (Table 1). For example, greater knee adduction moments have previously been reported in individuals with predominantly moderate knee osteoarthritis compared with controls despite no significant differences in sagittal plane moments (3).
The results of this study supported our hypothesis that larger frontal plane knee moments exist in meniscectomy patients with knee extensor weakness. Compared with control and APM patients with normal knee extensor strength, the weak APM patients had larger knee adduction moments over stance (Fig. 2). These results indicate that weak APM patients, in particular, walk with increased force on the medial compartment of the tibiofemoral joint (29), a common site for osteoarthritis in this population (15). Animal studies have shown site-specific initiation of degenerative changes to articular cartilage (42) in response to short-term high loading, whereas in humans, dynamic load on the medial compartment can predict radiographic progression of osteoarthritis (20). Andriacchi et al. (1,2) suggest that initiation of osteoarthritis is associated with a shift in ambulatory loads to regions that are unable to adequately adapt, leading to cartilage damage and establishing an environment for progression of osteoarthritis. In view of this evidence, we suggest that weak APM patients, in particular, are at increased risk of developing knee osteoarthritis, a hypothesis that requires investigation via prospective studies.
Evidence exists to implicate muscle weakness in the onset and progression of knee osteoarthritis. Reduced quadriceps strength is associated with both radiographic and symptomatic osteoarthritis of the knee (4,12,13,33). Slemenda et al. (33) found that women who developed incident knee osteoarthritis over a period of approximately 2.5 yr were 18% weaker in knee extensor strength at baseline than those who did not develop osteoarthritis. It has also been speculated that quadriceps weakness contributes to the development of knee osteoarthritis via reduced shock absorption during impulse loading at heel strike while walking (19,26,31), but we found no evidence for that in the weak APM patients who showed normal peak loading rates. Knee adduction moments across the stance phase of gait is associated with presence, severity, and progression of knee osteoarthritis (3,20,30), likely due to increased loads on the medial tibiofemoral joint, and knee muscle weakness may be associated with this feature of gait.
This study has shown that the weak APM patients, with weak knee extensors and flexors, have larger knee adduction moments than those with normal strength and controls, a feature of gait that is predictive of knee osteoarthritis (20). However, normal knee flexion and extension motion and moments in the gait of the weak APM suggest that the knee muscles were effective in this plane, albeit operating at a greater capacity, compared with APM with normal strength and controls. One premise for examining associations between knee extensors and knee adduction moments was based on work by Shelburne et al. (32), which showed quadriceps supported much of the knee adduction moment while walking. However, other lower limb muscles have the potential to influence knee adduction moments (17,32). Knee flexor weakness in the weak APM may affect both knee and hip function. As discussed above, the knee muscle weaknesses observed may be indicative of a general lower limb weakness that may affect upper body motion. The position of the knee relative to the ground reaction force vector will determine the moment arm about this joint, so that motion of the center of mass in the mediolateral plane can alter the knee adduction moment. Control of the center of mass position is likely to play a large role in the size of the knee adduction moment. Indeed, larger hip abductor moments (indicative of hip adductor muscle forces) are associated with reduced knee adduction moments (21,22). However, it is not clear what the link is between knee muscle weakness and large knee adduction moments, and future research should examine other lower limb weaknesses in relation to upper body posture and control.
We have reported strength deficits and gait patterns in APM patients, on average, 11 wk postsurgery. With longer recovery time, patients may improve knee strength and regain normal gait patterns, eliminating the increased risk of knee osteoarthritis that has been speculated here. At 6 months post-APM, an isokinetic knee extensor strength deficit of 18% has been observed in the operated leg compared with the nonoperated leg (11) with a 9% deficit seen at 4 yr (10). If rabbit knees show cartilage defects after only 4 wk of quadriceps weakness (12), this period of quadriceps weakness in APM patients may be adequate for the associated loading characteristics to alter the mechanical properties of the articular cartilage to a point that is susceptible to damage from additional load (1,2). Longitudinal studies are required to examine the relationship between knee strength and gait patterns over time in an APM population and their influence on the development of knee osteoarthritis. The potential role of muscular weakness and large knee adduction moments in the mechanism of the initial meniscal injury should also be examined because this cross-sectional study does not refute the possibility that the differences observed in strength and gait patterns in APM patients existed before the meniscal injury.
The menisci provide improved articulation for the medial and lateral tibiofemoral joints. Removal of part of the meniscus alters this physical environment, and there is no evidence that partial meniscectomy affects lower limb alignment. This study did not examine differences related to the amount or area of the excised meniscus, which should be considered in future work. However, we found no differences in frontal leg alignment between normal and weak APM subgroups, as measured by the angle between mechanical axes of the femur and tibia.
Following an APM, individuals experience larger-than-normal knee adduction moments during gait (40), which are particularly great in patients with reduced knee extension strength. As the knee adduction moment tends to load the medial articular surface of the tibiofemoral joint and is implicated in the progression of knee joint degeneration, APM patients with quadriceps weakness may be at particular risk of developing knee osteoarthritis (20,25,41). Retaining muscle strength following meniscectomy should be a priority in a patient's recovery from surgery. Further indicating the importance of restoring strength is the report of quadriceps weakness at 4 yr post-APM, which significantly affects knee function, pain, and quality of life (10). We suggest, therefore, that post-APM patients would likely benefit from an intervention aimed at increasing lower limb strength to improve knee loading patterns, pain, and function.
Conflict of Interest: There are no conflicts of interest or professional relationships with companies or manufacturers who will benefit from the results of the present study. The results of the present study do not constitute endorsement of the product by the authors or ACSM. We thank Mr. Alec Buttfield, Ms. Catherine Hill, Ms. Donna Ferguson, Mr. Rob King, Mr. Chris Winby, and Mr. Shane Ilich for assistance with data collection and processing. We also thank the following surgeons for their support in recruiting patients: Mr. Keith Holt, Mr. Greg Witherow, Mr. Greg Janes, Mr. Peter Annear, Mr. Hari Goonatillake, Mr. Dermot Collopy, Mr. David Colvin, and Mr. Peter Campbell. We also acknowledge Dr. Stephen Davis and Ms. Simone Mattfield for assistance in the radiology clinic. We acknowledge the financial support of the NHMRC (to DGL and GWS) and Western Australian Medical Research Infrastructure Fund (to DGL).
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Keywords:©2008The American College of Sports Medicine
QUADRICEPS; WEAKNESS; GAIT; OSTEOARTHRITIS