Knee stabilization in patients with medial compartment knee osteoarthritis

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 [3–6]. 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 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 [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] 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.