Chronic joint diseases have a major impact on society as patients suffer from pain and disability. The spectrum of arthritic disorders is wide including autoimmune and autoinflammatory diseases such as rheumatoid arthritis, ankylosing spondylitis and related spondyloarthritides but also the more prevalent osteoarthritic diseases. The latter appear to be mainly the consequence of injury, strain and aging in a predisposing genetic background. The therapeutic options for chronic inflammatory and immune joint diseases have greatly increased over the last decade by the use of targeted anti-cytokine or anti-immune cell drugs. However, such a shift towards successful treatment has not been achieved for osteoarthritis. In addition, control of inflammation does not equal cure of the disease as relapse occurs as soon as the treatment is interrupted, and only limited tissue repair has been observed. Bone morphogenetic proteins are potent regulators of cell proliferation, differentiation and apoptosis and they have come into the spotlight in arthritis research. Here, we summarize the recent data on the role of bone morphogenetic proteins in joint protection and repair and but also their potential disease promoting or controlling roles. These data are presented in the context of a systems biology view of joint diseases based on their histomorphological phenotype rather than on existing clinical classifications.