Osteoarthritis (OA) is a complex disease affecting articular cartilage and joint tissues. Macrophages in OA synovium contribute to the inflamed joint environment by releasing inflammatory mediators promoting cartilage loss. What remains unknown is how macrophages interact with synovial mesenchymal progenitor cells (sMPCs) in the joint. sMPCs are able to differentiate into cartilage but for unknown reasons, sMPC chondrogenic capacity is lost in OA. This thesis elucidates the relationship between macrophages and sMPC using synovial explants obtained from OA and normal patients. I found that altered macrophage activity (through cytokine stimulation and/or macrophage depletion) differentially regulates the chondrogenic capacity of sMPCs in a patient-specific manner. Also, the secretory profile of the explant is different between normal and OA patients in response to treatment. Taken together, there is heterogeneity within the responses of the OA patients, highlighting the need for personalized approaches to repair the cartilage within the OA joint.