The identification in 1998 of the main antigenic substrate recognized by autoantibodies was a dramatic turning point in our understanding of rheumatoid arthritis (RA) biology. Now, two decades later, antibodies to citrullinated proteins are viewed no longer as mere biomarkers for RA, but also as major pathophysiological factors involved in the development of bone loss and joint pain. These pathogenic effects are ascribable to abnormal autoantibody glycosylation via a pathway involving the Th17T cells. In the future, abnormal autoantibody glycosylation may serve as a disease activity biomarker and suggest novel treatment strategies.