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Arthritis Rheum. Author manuscript; available in PMC 2006 September 1.
Published in final edited form as:
PMCID: PMC1343471
Knee stabilization in patients with medial compartment knee osteoarthritis
Michael D. Lewek, PhD, PT, Doctor of Philosophy student, Dan K. Ramsey, PhD, Research Scientist, Lynn Snyder-Mackler, ScD, PT, Professor, and Katherine S. Rudolph, PhD, PT, Assistant Professor
Michael D. Lewek, Department of Physical Therapy and Biomechanics and Movement Science Program, University of Delaware, Newark, DE 19716 when this work was completed.
Corresponding Author: Katherine S. Rudolph, Address: 301 McKinly Lab, University of Delaware, Newark, DE 19716, Phone: (302) 831-4235, Fax: (302) 831-4234, Email: krudolph/at/

Individuals with medial knee osteoarthritis (MKOA) experience knee laxity and instability. Muscle stabilization strategies may influence the long term integrity of the joint. In this study we determined how individuals with medial knee OA respond to a rapid valgus knee movement to investigate the relationship between muscle stabilization strategies and knee instability.

Twenty one subjects with MKOA and genu varum, and 19 control subjects were tested. Subjects stood with the test limb on a moveable platform that translated laterally to rapidly stress the knee’s medial periarticular structures and create a potentially destabilizing feeling at the knee joint. Knee motion and muscle responses were recorded. Subjects rated their knee instability with a self-report questionnaire about knee instability during daily activities.

Prior to plate movement the OA subjects demonstrated more medial muscle co-contraction (p=0.014). Following plate movement the OA subjects shifted less weight off the test limb (p = 0.013) and had more medial co-contraction (p=0.037). Those without instability had higher VMMH co-contraction than those who reported more instability (p=0.038). Knee stability correlated positively with VMMH co-contraction prior to plate movement (r = 0.459; p = 0.042).

This study demonstrates that individuals with MKOA attempt to stabilize the knee with greater medial muscle co-contraction in response to laxity that appears on only the medial side of the joint. This strategy presumably contributes to higher joint compression and could exacerbate joint destruction and needs to be altered to slow or stop the progression of the OA disease process.

Knee osteoarthritis (OA) involves the progressive destruction of articular cartilage and can cause substantial disability among middle aged and older adults [1, 2]. Many factors contribute to the development of knee OA including heredity, biochemical changes in articular cartilage, and biomechanical compressive loads that lead to joint damage. In people with medial knee OA, medial tibiofemoral compressive loads are increased in the presence of varus knee alignment and may be seen as higher knee adduction moments during walking, both of which have become hallmarks of the disease [36]. Our recent work demonstrates that patients with medial knee OA co-contract the quadriceps and gastrocnemius muscles on the medial side of the knee joint more than age matched controls during the early stance phase of walking [6]. Larger magnitudes of medial co-contraction in the presence of a higher knee adduction moment seems counterintuitive since it would appear to further increase the compressive load on the painful medial articular surface. We assert, however, that the higher medial muscle co-contraction is a direct response to frontal plane laxity that appears on only the medial side of the joint. In fact, patients with isolated medial knee OA and genu varum had significantly greater medial joint laxity on stress films (Figure 1) compared to an uninjured control group, while no such difference was observed on the lateral side [6].
Figure 1Figure 1
Measurement of medial joint laxity.

The presence of greater frontal plane laxity in individuals with knee OA has been well established [7, 8]. The terms joint laxity and instability are often uses interchangeably, however laxity is measured statically and may not relate to how the knee functions under dynamic conditions. We use the operational definition of Irrgang et al. who define joint instability as the patient’s perception of the extent to which “shifting, buckling and giving way” in the knee interferes with daily activities [9]. Recently, Fitzgerald et al. [10] reported that a significant portion of patients with OA report sensations of perceived joint instability that diminishes physical function. Insight into the manner in which patients attempt to control laxity to minimize instability is vital to understanding disease progression and in the design of treatment programs to improve outcomes in patients with medial knee OA.

Evidence suggests frontal plane stability may be enhanced by reflexive responses elicited in muscles surrounding the knee by stimulating periarticular medial and lateral joint structures [1113]. Palmer [13] found that mechanical stimulation of the deep portion of the medial collateral ligament results in activation of the semimembranosis, sartorius, and vastus medialis of the cat hindlimb. Kim et al. [11] stimulated the medial collateral ligament with electrical stimulation in uninjured human knees and demonstrated that afferent information from the ligament produced a reflexive response in the medial knee muscles. Buchanan et al. [12] determined that a similar reflexive response from muscles with medial moment arms (vastus medialis, semitendinosis, gracilis, and sartorius) was elicited by a rapid valgus movement of the knee. The presence of excessive medial joint laxity in individuals with medial compartment knee OA may delay or inhibit neuromuscular responses because greater joint excursions are required to activate high threshold mechanoreceptors [14]. Thus, when an unexpected perturbation occurs, the unprepared neuromuscular system may be incapable of appropriately activating the correct muscles to stabilize the joint. To counteract this, and avoid feelings of instability during routine activities of daily living, individuals with medial knee OA appear to use greater medial muscle co-contraction to help stabilize the knee [6]. This observation of altered muscle activity patterns was made during level walking [6, 15], a relatively low level task. When individuals with medial knee OA are faced with higher level tasks that may challenge knee stability, such as changing direction, the knee can be subjected to substantial valgus loads [16]. Such activities may challenge the lax medial joint structures to a greater extent. Because muscle activity patterns are seen to be altered even during a simple walking task [6, 15], the use of a potentially destabilizing valgus movement, which challenges the lax medial compartment may provide greater insight into the muscle activation patterns used by patients with medial knee OA.

Higher muscle co-contraction can lead to high joint compressive forces [17] that could hasten the progression of OA. As joint destruction progresses, instability may increase, requiring higher muscle co-contraction. In this scenario, the very strategy that was adopted to stabilize the joint could be that which initiates a downward spiral of joint destruction. Without a thorough understanding of muscle stabilization in the knee with medial compartment OA we cannot develop appropriate training programs to help improve joint stability, lessen disease progression and improve patient function. In this study we set out to determine the manner in which individuals with medial compartment knee OA and excessive medial joint laxity respond to a potentially destabilizing event at the knee during standing. We hypothesized that the individuals with medial knee OA would stabilize the knee with greater medial muscle co-contraction. We also hypothesized that the greater magnitude of muscle co-contraction would be related to joint laxity and instability.


Forty subjects participated in this study. Twenty-one patients (7 females, 14 males ranging in age from 39 to 64 years old, mean = 49.3, SD = 7.0; and a BMI of 30.0±4.3) with symptomatic, medial knee osteoarthritis and genu varum (OA group) were referred by an orthopedic surgeon. Skeletal alignment was assessed from a weight-bearing radiograph [18], and were referred for our study if the weight bearing line was less than 35%. The OA group had an average weight-bearing line of 19.1 ± 12.0%. The diagnosis of OA was made from the clinical history, a physical examination, and radiographic changes observed from a standing postero-anterior radiograph with knees flexed to 30° [19]. Joint space width was measured at the narrowest location of both the medial and lateral compartments using calipers to the nearest 0.1mm. All subjects in the OA group showed joint space narrowing in the medial compartment (medial compartment: 2.0±1.4mm; lateral compartment: 6.4 ± 1.4mm). A group of nineteen control subjects of similar age and gender to the OA group (7 females, 12 males ranging in age from 38 to 62 years old, mean = 49.3, SD = 5.8; and a BMI of 28.3 ± 4.9) with neutral knee alignment was also tested. The control group had a weight bearing line of 44.3 ± 8.1% and had 4.9 ± 1.0mm of joint space in the medial compartment and 6.0±1.6mm in the lateral compartment. Subjects were not included if they were pregnant, had a history of ligament deficiency, neurological impairment, impaired balance or history of unexplained falls, rheumatoid arthritis, total knee replacement in either knee, any other orthopedic problems in the hips, ankles or spine, or a body mass index (BMI) ≥ 40.0. The test limb comprised the involved limb for the OA subjects and a randomly chosen limb for the control subjects. All subjects were informed of the purpose of the study and signed informed consent forms approved by the Human Subjects Review Board prior to testing.

Measurement of Joint Laxity
Measurements of frontal plane joint laxity has been described previously [6]. Briefly, frontal plane laxity was measured from stress radiographs taken with subjects lying supine with the knee supported and flexed 20°. A TELOS stress device (Austin & Associates, Fallston, MD) was used to reliably apply a 15daN (33lbs) force to generate varus and valgus forces [20]. Joint space was measured during both varus and valgus stresses and medial and lateral joint laxity was calculated as shown in Figure 1 [21]. Intraclass correlation coefficients (ICC) (3, 1) of repeated measurements on eight healthy subjects revealed reliability of 0.95 for lateral and 0.97 for medial laxity measurements using these methods.

Assessment of Knee Joint Function and Instability
All subjects rated their knee function using the Knee Outcome Survey-Activities of Daily Living Scale (KOS-ADLS) [9]. Instability was assessed from a six point scale from the following question: “To what degree does giving way, buckling or shifting of the knee affect your level of daily activity?” taken from the KOS-ADLS. The reliability of this particular question for assessing knee instability in individuals with knee OA has been reported as an ICC of 0.72, indicated that it is adequate for the determination of the presence of knee instability [10].

Muscle Activity and Motion Capture
Subjects stood with the feet shoulder width apart, and the test limb on a movable platform. A positioning actuator (NSK Ltd, Tokyo, Japan) translated the platform 5.8cm laterally in 195msec, at a peak velocity of 40 cm/sec. The subject’s contralateral foot was positioned on a 6-component force platform (Bertec Corp, Worthington, OH), to monitor weight bearing. The involved limb’s distal thigh was restrained from translating laterally with cuffs and cables that were bolted firmly to the wall (Figure 2). To ensure that the motion was isolated to the knee, an additional strap was secured around the pelvis to restrict motion. The subject stood comfortably with equal weight bearing on each limb. Five 3-second trials were collected in which the plate was triggered to move at a random interval within the three seconds. Subjects were unaware of when the plate would be triggered to move.
Figure 2Figure 2
Set-up for valgus perturbation.

Motion of markers placed on the thigh and shank were collected at 120Hz using a six camera passive motion analysis system (VICON 512, Oxford Metrics, UK). Electromyographic (EMG) data were recorded simultaneously from the test limb at 1920Hz with a 16-channel system (Motion Lab Systems, Baton Rouge, LA). Surface electrodes recorded EMG from the vastus lateralis (VL), biceps femoris long head (LH), semitendinosis (MH), the medial and lateral heads of the gastrocnemius (MG and LG respectively), and the distal portion of the vastus medialis (VM) [22]. Fine wire electrodes were inserted 2 cm apart into the sartorius and gracilis muscle along the longitudinal length of the muscle. Electrode placement was confirmed through muscle testing [23]. Signals were collected with the muscles at rest and from maximum voluntary isometric contractions (MVIC).

Data Management and Processing
Marker trajectory and force plate data were filtered with a 4th order, low pass Butterworth filter, with cutoff frequencies of 6Hz and 40Hz, respectively. Vertical ground reaction force was normalized to body weight. Knee joint angles were calculated with Euler angles (Move3D, NIH Biomechanics Laboratory, Bethesda, MD). Variables included the magnitude of limb loading, the time to unload the test limb, sagittal and frontal plane knee angles, frontal plane knee excursion and the time (in msec) to reach peak valgus during plate movement (see Figure 3).
Figure 3Figure 3
Representative trial to monitor the reflexive response.

EMG data were filtered with a 350Hz low pass Butterworth filter, full wave rectified and filtered again with a phase corrected 8th order, 20Hz-low pass Butterworth filter to generate a linear envelope (Labview 6i, National Instruments, Austin, TX). The linear envelopes were normalized to the maximum signal obtained during the MVIC trials.

The reflex muscle responses were evaluated over two intervals. The baseline interval comprised the 100msec period prior to the onset of plate movement. The “long loop” interval was a fixed window from 40–175msec after the onset of plate movement [11]. This time frame was chosen to constitute the muscle response that occurs following the monosynaptic stretch reflex, but prior to what would be elicited volitionally. It is thought that this response is mediated subconsciously, with afferent commands being sent to the cerebellum and brain stem [24]. The magnitude of the muscle activity of individual muscles was evaluated by integrating the individual linear envelopes over the long loop reflex interval. Muscle co-contraction was also calculated across the baseline and long loop intervals. Co-contraction is defined as the simultaneous activation of antagonistic muscles and was calculated according to Equation 1 [25]:

equation M1
Equation 1

This method, developed in our laboratory, incorporates the relative activation of antagonistic muscles with their magnitudes to evaluate the level of co-contraction that is likely to lead to joint compression. Co-contraction was calculated for the vastus lateralis-lateral hamstrings (VLLH), vastus medialis-medial hamstrings (VMMH), vastus lateralis-lateral gastrocnemius (VLLG), and vastus medialis-medial gastrocnemius (VMMG) muscle groups.

Data Analysis
Joint laxity, joint kinematics, and weight bearing timing and loads, were compared between groups using independent samples t-tests (SPSS 11.0, Chicago, IL). Group differences in the percentage of trials with an observed muscle response were compared using independent t-tests after undergoing an arc sine transformation [26]. Multivariate analysis of variance (MANOVA) was used to determine group differences in muscle integrals and co-contraction indices. The factors included: side (medial/lateral); group (OA/control); muscle (VMMG, VMMH, VLLG, VLLH or VM, VL, MH, LH, MG, LG). Two-way ANOVAs (side by muscle) were used to determine differences in co-contraction and integrated EMG values. T-tests with Bonferroni correction were used for post-hoc testing. Spearman rank correlation coefficients were used to assess the relationship between instability and joint laxity and muscle co-contraction. Measures of joint laxity and muscle co-contraction were converted to ordinal data for the purposes of the Spearman rank correlation analysis only. Significance was established when p ≤ 0.05.


The OA group had 5.0 ± 1.7mm of medial joint laxity that was significantly greater than the control group whose laxity measured 3.3 ± 0.9 (p = 0.001). No difference in lateral joint laxity was measured: the OA group had 3.4 ± 1.7mm, and the control group had 4.1 ± 1.5mm of lateral laxity (p = 0.19). No subject in the control group (n = 19) complained of instability, while 17 of 21 subjects (81%) in the OA group reported that they experienced knee instability. Of the 17 OA subjects who reported instability, 14 subjects complained that instability affected the ability to perform activities of daily living. Eight subjects with knee OA reported that instability affected the ability to perform daily activities slightly; three stated that instability affected them moderately; and two subjects reported that instability affected them severely. One subject reported that instability prevented all daily activities. No significant relationship was observed between medial joint laxity and self reported knee instability in the OA group (r = −0.098, p = 0.690).

Prior to Translation
The series of straps used to stabilize the femur were pulled firmly and in doing so, the knees were positioned in more valgus than the subjects had when standing without the stabilization system. Compared to the standing posture before the application of the straps, the straps put stress on the knee to produce a similar change in frontal plane position in both groups; the OA group was in an average of 2.7±2.3° more valgus, while the control group was in an average of 3.3±2.3° more valgus (p=0.410). Prior to plate movement, no difference was observed in the knee flexion angle between the groups (OA: 4.1° ± 5.4 and control group: 3.6° ± 6.6; p = 0.783) and the OA group had less valgus (0.6° ± 4.9) than the control group (6.0° ± 5.4; p = 0.002). The OA group had greater co-contraction of the VMMG muscles (4.9 ± 5.7) than the control group (1.4 ± 1.6; p = 0.014) before plate translation. The 7 OA subjects who reported no instability or instability that did not affect their daily activities had significantly larger VMMH co-contraction levels prior to plate translation than the 14 OA subjects who reported instability (stable OA: 3.80 ± 3.08, unstable OA 1.67 ± 1.18; p=0.038). In the OA subjects, higher VMMH co-contraction correlated positively with greater knee stability (r = 0.459; p = 0.042) during the baseline interval.

During Translation
As the plate translated laterally, the knee of the test limb moved more into valgus (Figure 3). No group difference in valgus excursion was observed between the OA (2.5° ± 1.0) and control (2.7 ± 0.7) groups (p = 0.699), although the OA group had significantly lower valgus angles (3.2° ± 4.8) than the control group (8.7° ± 5.4) at the end of the movement (p = 0.002). All subjects reached peak knee valgus before the end of plate movement and the time to reach the peak valgus position was no different between groups, (OA group: 173 ± 17msec and control group: 173 ± 16msec; p = 0.911). During plate translation, all subjects unloaded the test limb by transferring weight to the contralateral limb. The OA group shifted 17.9±4.9%BW off of the test limb, which was less than the 22.0±5.0%BW that the control group shifted off of the test limb (p=0.013). The OA group also appeared to take a longer time to shift the weight off the test limb (199 ± 44msec) compared to the control group (181 ± 13msec; p = 0.094) but the difference was not statistically significant at the p<0.05 level.

Not every muscle responded to the valgus perturbation during every trial but muscle activation was different between the groups. The OA group showed a significantly higher percentage of trials of medial hamstring (OA: 97% ± 7.3; Controls 79% ±29.4; p = 0.021) and sartorius (OA: 72.2% ± 34.1; Control: 41.2% ± 35.0; p = 0.015) activation than the control group.

When comparing the EMG integrals of the individual medial and lateral muscles, the OA subjects used more medial than lateral muscle activity (side by muscle interaction p=0.010) and post-hoc testing revealed that both the hamstrings (p=0.001) and gastrocnemius (p=0.011) muscles were more active on the medial side. The control subjects had higher medial muscle activity only in the hamstring muscles (p=0.020) (Figure 4).

Figure 4Figure 4
Integrated muscle activity during long loop interval.

The level of muscle co-contraction between the medial and lateral muscles during the long loop interval showed a significant side by group interaction (p=0.039) (Figure 5). Post-hoc testing revealed that the control group showed no difference in the level of co-contraction on the medial and lateral sides (p=0.106) of the joint, whereas the OA group showed higher VMMH than VLLH co-contraction (p=0.037) although there was no significant difference between the VMMG and the VLLG (p=0.079).

Figure 5Figure 5
Co-contraction indices during the “long-loop” interval for the OA and control groups.


This study provides insight into the stabilization strategy used by individuals with medial knee OA and genu varum that could hasten joint destruction and has important implications for rehabilitation. As we hypothesized, subjects with knee OA responded to a perturbation that was designed to stress medial periarticular structures and create a potentially destabilizing sensation, with greater co-contraction on the medial side of the joint. They also showed greater axial loading that could result in greater medial joint compression. The OA subjects in this study had more laxity on the medial side of the joint and the majority reported knee instability that interfered with daily activities. Our data, therefore, suggest that the manner in which individuals with medial knee OA attempt to cope with the threat of knee instability might contribute to further joint destruction and progress a cycle of cartilage deterioration.

Before the plate translated, the individuals with medial knee OA who had greater knee stability during daily activities maintained higher medial muscle co-contraction that might represent a strategy to augment joint stability by increasing reflex mediated joint stiffness. Others have demonstrated that in both the upper [27, 28] and lower extremities [29, 30], higher background muscle activity yields increased reflexive joint stiffness, potentially providing greater joint stability. Greater background muscle activity, as seen on the medial side of the joint in the OA group could increase the reflexive joint stiffness through increased muscle stiffness. Muscle stiffness is controlled in part by the γ-motoneuron system which is influenced by afferent information from muscles, ligament mechanoreceptor and joint afferents from other structures including the joint capsule and skin. This afferent input has a strong effect on the γ-motoneuron system that provides continuous preparatory adjustments to muscle stiffness [3134]. Higher muscle stiffness may increase the responsiveness of muscles, a speculation which is supported by our data indicating significantly greater frequencies of responses in the medial hamstrings and sartorius muscles in the OA group. One factor that could have influenced the responses to the perturbation is pre-load on the medial joint structures resulting from the thigh stabilization system. Tension of the stabilization straps caused the subjects to be in 2–3o more valgus than the knee position during typical standing, however the change in position with the straps was equal in both groups so it’s influence should have been equivalent in both groups. Further research is needed to measure muscle stiffness to confirm its relationship with muscle responsiveness but greater pre-activation of the medial quadriceps and hamstring muscles could be an effective adaptation for minimizing instability through increased muscle stiffness [3537].

During the potentially destabilizing perturbation, our data demonstrate that people with knee OA and genu varum use higher medial co-contraction. Patients with knee OA also use greater magnitudes of muscle co-contraction than uninjured subjects during functional activities [6, 15, 38], presumably to minimize instability. The purpose of our co-contraction equation is to determine how antagonist pairs might contribute to joint compression. The level of muscle activation that contributes to joint compression occurs when the relative activation of the muscles is equal and relatively high amplitude. It should be noted that there are many other methods of assessing co-contraction, including an assessment of the timing of concurrent activity [39] or ratios of peak muscle activity [38]. When ratios are used, muscles that are active at equal but small magnitudes will appear to have the same level of co-contraction as muscles with equal and high magnitude EMG activities. In addition if the peak magnitudes are found at relatively different points in the experimental cycle they would not be said to co-contract according to our operational definition of co-contraction that requires the simultaneous activation of 2 muscles. When timing alone is used, the co-contraction value of a condition when one muscle might have very low magnitude EMG that is active concurrently with a muscle with high magnitude EMG will be equivalent to a condition when 2 muscles are simultaneously active at very high or very low magnitudes. By combining the relative activation of two muscles (ratio) and multiplying it by the sum of the magnitudes our method characterizes the co-contraction that could result in higher joint compression. Although the concurrent activation of quadriceps and hamstring muscles is capable of resisting frontal plane forces [40], large magnitudes of medial co-contraction, as evident in the OA group may result in greater damaging compressive loads in the knee. Instead it may be more beneficial to retrain muscles to be activated selectively, rather than simultaneously to minimize joint compression, and perhaps increase joint stability.

The presence of medial laxity and knee instability may play an important role in the adaptation of muscle activity patterns in people with medial knee OA. Our subjects with knee OA had both increased medial joint laxity, as well as complaints of instability and demonstrated altered muscle activation patterns that are consistent with the results of others. Shultz et al. [41] demonstrated that uninjured subjects with more anterior-posterior knee laxity used greater muscle pre-activation, greater reflex activation, and delayed responses in the muscles that were antagonistic to the imposed perturbation. Although the direction of laxity measurements and testing was performed in a different plane from the testing in our study, her results underscore the fact that neuromuscular control of the knee can be influenced by joint laxity.

Unlike other studies of muscle activation in response to varus/valgus perturbations [12, 42] our testing paradigm included axial loading of the knee joint through weight bearing. The subjects with knee OA maintained more load on the limb during the perturbation, which was unexpected. None of the subjects complained of discomfort during the test, however, they reported experiencing pain and instability during daily activities. We would have expected the subjects to unload the limb more quickly to avoid potential discomfort or instability, however it appears that the subjects with OA are either incapable of unloading the joint quickly or they also use axial loading to help stabilize the joint when it is perturbed. If this strategy is one that individuals with OA adopt during functional activities, the increased and prolonged joint loading, coupled with varus alignment, high adduction moments and higher medial co-contraction would be particularly detrimental. Rehabilitation may be more effective if it addresses the role of joint loading along with improved neuromuscular responses to help the OA subjects to improve dynamic knee stability.

This speculation is underscored by a recent case report by Fitzgerald et al. [43] who described the addition of agility and neuromuscular training to the rehabilitation of a patient who had knee osteoarthritis and had complaints of knee instability. They found that after treatment, the patient experienced no more episodes of instability, had higher knee function and less knee pain during daily activities. Although the mechanisms behind the improved outcome following neuromuscular training in this patient with OA is not known, studies on neuromuscular training in other patient populations [44, 45] demonstrate the possibility that such training can improve knee stability and promote more selective recruitment of muscles that may preserve joint integrity. In the case that muscles can not be retrained in such a manner, others have advocated the use of orthoses such as ‘unloading braces’ [46] and heel wedges [47] to minimize medial joint loading which may reduce pain and allow higher function in some patients.

Muscle strength has long been an important part of the management of people with knee OA [4851] but Sharma et al [52] recently reported that strong quadriceps muscles are associated with a greater likelihood of progression of knee OA in patients with knee malalignment or excessive frontal plane laxity. This is in contrast to Slemenda et al. [51] who found that even relatively small increases in quadriceps femoris strength, particularly in women, predicted a 20–30% decrease in the odds for having OA, suggesting that quadriceps strength is an integral component for preventing knee OA. The lack of consensus on the role of the quadriceps muscles may be due to the emphasis on muscle strength rather than the manner in which patients activate the muscles surrounding the knee. Knee instability has only recently been identified as an important aspect of the disease process [6, 10]. Our work suggests that when treating patients with knee OA, knee instability is a problem that if left untreated, might lead to the development of a neuromuscular joint stabilization strategy that could hasten progression of the disease. Continued research is needed to identify whether increased co-contraction leads to higher muscle stiffness or more joint loading as well as the long term effect of altered muscle activity on the progression of OA. However, the results of this study suggest that the relationship between muscle function and OA is highly complex and understanding the strategies that improve knee stability and function is important in developing treatments that improve outcomes in individuals with medial knee OA.


The authors wish to thank William Newcomb, MD for his valuable assistance with subject recruitment, Laura C. Schmitt, MPT for her assistance with data collections, and Laurie Andrews, RTR for assistance with the stress radiographs.

Funding provided by the National Institute of Health (1P20RR016458, 2T32HD007490), Foundation for Physical Therapy (PODS II), American College of Sports Medicine (Doctoral Student Research Grant), EBI Medical, LP
All author affiliations

Michael D. Lewek, Department of Physical Therapy and Biomechanics and Movement Science Program, University of Delaware, Newark, DE 19716 when this work was completed.

Dan K. Ramsey, Department of Physical Therapy and Biomechanics and Movement Science Program, University of Delaware, Newark, DE 19716.

Lynn Snyder-Mackler, Department of Physical Therapy and Biomechanics and Movement Science Program, University of Delaware, Newark, DE 19716.

Katherine S. Rudolph, Department of Physical Therapy and Biomechanics and Movement Science Program, University of Delaware, Newark, DE 19716.

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