pain with stair climbing does not necessarily mean the patient has patellofemoral OA. Similar results were also found for whether anterior knee pain was predictive of patellofemoral OA, suggesting that the accuracy of asking patients about pain location may not be the best discriminator of actual joint Joint-level impairment OA is often considered as a loss of cartilage thickness within the joint; however, recent evidence has revealed that changes in and around the joint actually are part of the disease process. Advanced imaging techniques, such as magnetic resonance imaging (MRI), and new biochemical analyses have revealed that there are changes to many of the soft tissues, fluids, and bony structures in individuals with knee OA. Cartilage deterioration Cartilage loss remains the hallmark characteristic of knee OA progression. The presence and amount of cartilage loss is typically assessed using X-rays, which are relatively low-cost and quick to complete compared with more advanced imaging techniques. Recently, sophisticated MRI acquisition and analysis techniques have revealed that other morphological changes occur within cartilage during the OA process that are distinct from the deterioration seen on X-rays. Specifically, scientists have determined that cartilage in very early or “pre-OA” conditions undergoes a loss of proteoglycan content (Baum et al., 2013). This decreases the cartilage’s ability to hold water, which can reduce its ability to withstand compressive and shear forces and make it more likely to degrade from mechanical stress. Developing new methods to identify patients early in the disease process when cartilaginous changes may not appear on normal radiographs is a high-priority research area. If patients can be identified and treated before actual loss of cartilage tissue occurs, it may be possible to prevent the disability, pain, and functional deficits associated with end-stage disease. Change in muscle function It is often assumed that that changes in muscle function or progressive weakness happens as a result of decreased physical activity in the presence of knee pain and OA. Results from several large studies have shown that when there is a decrease in functional ability in individuals with knee OA there is also a decrease in muscle strength (Ruhdorfer, Wirth, & Eckstein, 2016). However, there is also evidence from large meta-analyses to suggest that muscle weakness may actually precede future OA (Øiestad, Juhl, Eitzen, & Thorlund, 2015). This means that individuals who are weaker are at a greater risk of developing OA in the future. Strengthening should be considered an important component of any preventive rehabilitation strategy for individuals at risk for OA. In the clinic setting and in research studies, muscle strength is often defined as the peak force from a maximal voluntary isometric contraction. While this is a reliable way to measure strength, individuals with knee OA may have muscle dysfunction beyond isometric weakness. Individuals with knee OA have greater activation deficits than individuals without knee OA (Lewek, Rudolph, & Snyder-Mackler, 2004). Activation deficits are defined as the difference between force output from the quadriceps when maximally stimulated using electrical stimulation and force output when the patient kicks as hard as they can without any augmentation from electrical stimulation, as in a maximal voluntary isometric contraction (Figure 3). When the patient is asked to kick as hard as possible, there is a rapid increase in the force output that plateaus for several seconds. However, when the burst of electrical stimulation is provided midway through the trial, there is a large increase in the force output, suggesting that the capability of the muscle exceeded what the patient was able to do on their own. The ratio of maximal force with and without electrical stimulation is defined as the activation ratio. In the example shown in Figure 3, the individual had an activation ratio of 75%, or an activation deficit of 25%. This is an important measure as greater activation deficits indicate a lack of full motor unit excitability and can
cartilage loss (Stefanik et al., 2014). Physical therapists evaluating patients with knee pain should rely on clinical presentation, but may consider obtaining X-rays if patellofemoral knee OA is suspected.
impair functional ability in persons with OA (Fitzgerald, Piva, Irrgang, Bouzubar, & Starz, 2004). Interventions that reduce activation deficits have the potential to improve not only strength, but also functional performance. Figure 3: Quadriceps Strength Testing With and Without Activation Deficit
Note. From Western Schools, 2018. In addition to lower peak force developed by the quadriceps, patients with knee OA also may have lower rates of force development. This means that they may not be able to generate muscle force and muscle power quickly, which is related to diminished gait function in patients with OA (Winters & Rudolph, 2014). The rate at which a person can generate muscle force is important for dynamic abilities, particularly when responding to unanticipated perturbations. Reduced rate of force development may make a person more susceptible to falls if they cannot generate muscle contraction quickly enough to overcome an unexpected loss of balance. When evaluating and treating muscle function in patients with knee OA, factors other than peak muscle strength should be addressed. Although researchers have identified several types of muscle dysfunction, it is not entirely clear what the underlying mechanisms of poor muscle function are in patients with OA. Some of the weakness may be attributed to disuse atrophy as the patient modifies his or her levels of activity. Artificially induced swelling and pain in the knee joint also have been shown to immediately reduce muscle force production in healthy patients, suggesting that afferent signals can attenuate muscle output. Other studies have shown that individuals with knee OA have greater intramuscular fat, which can reduce the physiological cross-sectional area (Kumar et al., 2014). Regardless of the underlying mechanism, increasing quadriceps strength, improving rate of force development, and decreasing muscle activation deficits are common targets in rehabilitation of Osteoarthritis should be considered a disease of the bone, as well as a disease of the cartilage and soft tissue. Emerging evidence has shown that subchondral bone marrow lesions are associated with knee OA (Teichtahl et al., 2017), which can lead to a rapid loss of cartilage and OA progression (Edwards et al., 2016). Bone marrow lesions are diagnosed using MRI, but our understanding of how and why these lesions lead to more pain and faster OA progression is not well understood. This is an emerging area of research in the field of OA that supports the theory that factors other than cartilage loss play a role in this disease. patients with knee OA. Subchondral edema
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Book Code: PTNC1023
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