Joint homeostasis is maintained by loading, synovial lubrication, and a plethora of resident and migrating immune cells, cytokines, and signaling molecules. If this balance is disrupted by either local or systemic factors, the body responds with articular inflammation. Persisting inflammation, like in the case of rheumatoid arthritis and osteoarthritis, causes progressive joint destruction which often results in debilitating pain and reduced quality of life. This thesis outlines cellular and molecular pathways relevant in inflammatory and degenerative joint pathologies that contribute to disease progression, and which may be exploitable in the development of future therapeutics.
