By 2030, it is estimated that 67 million people will have osteoarthritis (OA) in the US and the majority of them will have OA in the knee that begins in middle age. Patients endure pain for many years before they have a total knee replacement. The number of years that knee OA patients endure pain takes a toll on their knee function and quality of life but it also impacts how the nervous system processes pain signals. Central sensitization of pain is a heightened response to painful stimuli that is a protective mechanism designed to allow the body to heal. Under normal circumstances, central sensitization subsides when tissue healing is complete. However, sometimes central sensitization persists and pain is exaggerated or no longer originates from a peripheral source. This abnormal sensory processing can lead to misdiagnosis and poor outcomes to treatments because the source of the pain is in the central nervous system not in peripheral tissues. Central sensitization of pain has been demonstrated in people with knee OA and it is exacerbated by another anomalous pain mechanism: reduced conditioned pain modulation (CPM). CPM involves the application of a painful conditioning stimulus that elicits a reduction in the perception of pain. The presence of central sensitization and reduced conditioned pain modulation can make knee OA much harder to treat, however clinicians are now augmenting traditional physical therapy interventions with treatments like cognitive behavioral therapy and mind-body treatments that can influence how the central nervous system processes the pain signals. Unfortunately, those interventions do not influence the movement patterns used by people that can hasten joint degeneration including reduced knee motion and higher muscle co-contraction combined with buckling. These movements produce greater loads and higher shear forces in the knee that are particularly detrimental to articular cartilage. Recently physical therapy interventions have been developed to address the abnormal movement and muscle activation patterns but none have been shown to be any more effective than traditional aerobic or strengthening exercises. This may be due to deficits in the ability to learn new motor programs to stabilize the knee which is highly plausible considering that motor output and motor learning rely on accurate sensory feedback that we know is impaired in people with knee OA. This study will investigate the presence of central sensitization and reduced CPM and their influence on motor adaptation and learning in this population. The results will provide valuable insight into motor control that can be used to furthe develop treatments that will improve knee function while slowing progress of the disease.