There is significant and growing evidence for the contribution of joint mechanical factors (joint loading, movement) to knee OA disease initiation and progression. Animal models have led to hypotheses regarding the importance of dose and time pattern of joint loading to the progression of knee OA, and these models are beginning to be corroborated in longitudinal studies of knee OA progression in humans. There appears to be a complex interaction between joint mechanics and biochemical changes within the joint's soft tissues, and response at the subchondral bone level that stimulate the disease cascade in an individual. Risk factors such as obesity, female sex, joint malalignment (static or dynamic), can contribute to the cascade by reducing the tolerance of joint tissue or by applying forces on joint tissues that are not accustomed or conditioned to the loading.
Studies of the biomechanics of human motion, typically of walking, have provided us with important information on how the human knee mechanical environment behaves in the absence or presence of knee OA. Most human biomechanics research to date has been cross-sectional in nature: 1) characterizing the multitude of joint movement, joint force, and at times joint neuromuscular control differences in knee OA as compared to healthy individuals, as well as 2) differences in movement and force patterns with increasing severity of knee OA and after arthroplasty surgery. This body of work has taught us that individuals with knee OA typically walk increasingly slower, with less joint range of motion, and with atypical patterns of joint loading and muscle activation which are usually higher and more sustained (lack of unloading). We have also discovered that while TKA surgery restores some aspects of joint function, patterns of movement, loading and neuromuscular control during walking often remain irregular for many individuals after surgery.
It is difficult to determine causation from cross-sectional observation alone, and so more recent research efforts are focusing on longitudinal models, which follow individuals over time to understand the predictive nature of risk factors. Some research has associated excessive frontal plane torque (i.e. knee adduction moment) during gait with radiographic progression of medial compartment knee OA. However, there has been little comprehensive investigation into the three-dimensional mechanical joint environment and knee OA development and progression. Here in Halifax, we are in the final stages of a long-term longitudinal knee OA study that is providing evidence for the role of a number of specific knee kinematic, kinetic and neuromuscular patterns in knee OA progression. This information is allowing us to examine specific hypotheses on knee OA initiation and progression that will provide the knowledge necessary to move forward in developing efficacious early prevention and treatment strategies for knee OA to delay the need for arthroplasty surgery. This is also providing patient-specific information on joint level mechanics that is helping to explain the variability in outcome of TKA surgery, which has utility in efforts to develop a more tailored patient-specific surgical strategy for optimizing outcome.
How we use and load our joints during daily activity is an important aspect in understanding the OA process. Yet the problem is clearly multifactorial and the solution multidisciplinary. To address the burden of knee OA in Canada, we need to be working together among disciplines to better understand the link between risk factors and joint integrity so that we can offer earlier, more effective and more patient-specific approaches to knee OA treatment and management.