Knee osteoarthritis (OA) involves the progressive destruction of articular cartilage and can cause substantial disability among middle-age 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, compressive loads on the medial tibiofemoral joints are increased in the presence of varus knee alignment and may be manifested as elevated knee adduction moments during walking, both of which have become hallmarks of the disease (3–6).
Our recent study demonstrated that patients with medial knee OA co-contract the quadriceps and gastrocnemius muscles on the medial side of the knee joint to a greater extent than that in age-matched control subjects, during the early stance phase of walking (6). Larger magnitudes of medial co-contraction in the presence of higher knee adduction moments seems counterintuitive, since this process would appear to further increase the compressive load on the painful medial articular surface. We assert, however, that the higher co-contraction of the medial muscle is a direct response to the frontal plane laxity that appears on only the medial side of the knee joint. In fact, patients with isolated medial knee OA and genu varum were shown to have significantly greater laxity of the medial joint, as demonstrated on stress radiographs and depicted in Figure 1, compared with an uninjured control group, whereas no such difference was observed on the lateral side of the knee joint (6).
Figure 1. Measurement of laxity in the medial knee joint. Medial laxity is the difference (in mm) between the medial opening measured on a radiograph undertaken during valgus stress load (left) and the medial opening measured on a radiograph undertaken during varus stress load (right). Lateral laxity is measured in a similar manner in the lateral compartment of the knee.
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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 used interchangeably; however, laxity is measured statically and may not have any relation to how the knee functions under dynamic conditions. In the present study, we use the operational definition of joint instability suggested by Irrgang et al, in which joint instability is 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 proportion of patients with OA report perceiving sensations of joint instability which diminish physical function. Insight into the manner in which patients attempt to control laxity to minimize instability is vital to understanding disease progression and would facilitate the design of treatment programs to improve outcomes in patients with medial knee OA.
Evidence suggests that frontal plane stability may be enhanced by reflexive responses elicited in muscles surrounding the knee by stimulating periarticular medial and lateral joint structures (11–13). 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) activated the medial collateral ligament with electrical stimulation of uninjured human knees, thus demonstrating that afferent information from the ligament produces a reflexive response in the medial knee muscles. Buchanan et al (12) determined that a similar reflexive response from muscles on the medial side of the joint (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 the perception of instability during routine activities of daily living, individuals with medial knee OA appear to use greater co-contraction of the medial muscles 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 in 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 the strategy that 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 co-contraction of the medial muscle. We also hypothesized that the greater magnitude of muscle co-contraction would be related to joint laxity and instability.
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- PATIENTS AND METHODS
This study provides insight into the stabilization strategy used by individuals with medial knee OA and genu varum that could hasten joint destruction. These observations have important implications for the prospect of rehabilitation. As we hypothesized, subjects with knee OA responded to a mechanical 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. Subjects with OA 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 propagate a cycle of cartilage deterioration.
Before the plate translated, the individuals with medial knee OA who reported having greater knee stability during daily activities maintained higher medial muscle co-contraction, which 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 (29, 30) extremities, 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 the 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 (31–34). Higher muscle stiffness may increase the responsiveness of muscles, a speculation that 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 the preload imposed on the medial joint structures as a result of the thigh-stabilization system. Tension of the stabilization straps caused the subjects' knees to be 2–3° more valgus than the knee position during typical standing; however, the change in position with the straps was equal in both groups, and therefore its influence should have been equivalent in both groups. Further research is needed to measure muscle stiffness to confirm its relationship to muscle responsiveness, but greater preactivation of the medial quadriceps and hamstring muscles could be an effective adaptation for minimizing instability through increased muscle stiffness (35–37).
Our data demonstrate that people with knee OA and genu varum use higher medial co-contraction when under conditions of potentially destabilizing perturbation. Patients with knee OA also use greater magnitudes of muscle co-contraction than do uninjured subjects during functional activities (6, 15, 38), presumably to minimize instability. The purpose of our co-contraction equation was to determine how muscles that are antagonists 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 in 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 an equal, but high, magnitude of 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 as a measure of co-contraction, 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 2 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 hamstrings 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. It may therefore 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 and a sensation of knee instability and demonstrated altered muscle-activation patterns that are consistent with the results reported by others. Shultz et al (41) demonstrated that uninjured subjects with more anterior-posterior knee laxity used greater muscle preactivation, 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, the results of the study by Schultz et al 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 reported having 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, but it appears that these subjects with OA were either incapable of unloading the joint quickly or also used axial loading to help stabilize the joint when it was 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), in which agility and neuromuscular training were added to the rehabilitation regimen of a patient who had knee OA and reported having knee instability. They found that after treatment, the patient experienced no more episodes of instability, had higher knee function, and reported having less knee pain during daily activities. Although the mechanisms behind the improved outcome following neuromuscular training in this patient with OA are 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 those cases in which muscles cannot be retrained in such a manner, other investigators 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 (48–51), 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 the findings of Slemenda et al (51), who found that even relatively small increases in quadriceps femoris strength, particularly in women, was predictive of a 20–30% decrease in the odds of 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, and to understand the long-term effect of altered muscle activity on the progression of OA. Nevertheless, the results of this study suggest that the relationship between muscle function and knee OA is highly complex. Therefore, knowledge of the strategies that improve knee stability and function is important for the development of treatment approaches that could improve outcomes in individuals with medial knee OA.