Individuals who sustain an intra-articular knee injury are at a high risk of developing posttraumatic knee osteoarthritis (PTOA) 10-20 years later. Compensatory activation patterns of knee muscles in response to the trauma may persist past the acute injury phase and result in abnormal mechanical loading and subsequent osteoarthritis of the knee. This dissertation aimed to use surface electromyography (sEMG) to explore abnormal leg muscle activation patterns and their possible involvement in PTOA development in individuals who suffered a previous knee injury 3-12 years ago. The first part of this thesis presents methodological investigations related to two sEMG-based assessments of knee muscle activation strategies. It was shown that 1) sEMG amplitude-based co-contraction indices during gait exhibit poor between-day reliability and 2) the magnitude of intermuscular coherence strongly depends on the configuration and alignment of the sEMG electrodes. Building on the methodological findings, the second part of this thesis investigated the association between a previous knee injury and leg muscle activation during walking and squatting while considering the influence of sex. Sex-specific abnormalities in quadricep and hamstring muscle activation patterns were present for the affected leg in individuals more than three years after a previous knee injury. Altered quadricep and hamstring muscle activation may result in abnormal movement and loading of the knee joint and thus be linked to mechanical risk factors for PTOA development. This dissertation could not provide evidence, however, that altered thigh muscle activation was associated with more self-reported knee pain or symptoms indicative of PTOA development. From a methodological perspective, the poor reliability of current sEMG-based markers for abnormal muscle activation may lower the sensitivity to detect associations with risk factors for PTOA. From a conceptual perspective, the development of PTOA is not solely based on joint mechanics but depends on the interplay between mechanical, biological, and structural abnormalities of the joint following a knee injury. Therefore, the pathway to PTOA is likely unique to each individual such that a consistent association between abnormal muscle activation following a knee injury and PTOA risk may not exist.