The severity and outcome of chronic arthritis is determined by the balance between destructive and homeostatic or anabolic molecular signaling pathways. Increasing evidence suggests a role for embryonic signaling pathways, essential for development and growth, in the maintenance of tissue homeostasis and in the induction of repair. Untimely or inappropriate activation of such pathways may also have a role in the progression of some diseases. Bone morphogenetic proteins (BMPs), originally identified as protein factors that induce a cascade of endochondral bone formation, have critical functions in cell proliferation, differentiation, adhesion and death. We have previously identified different BMPs in patients with chronic arthritis . In this study, we evaluate the effect of shifting the balance in BMP signaling by reducing endogenous levels of noggin, a BMP antagonist, in a mouse model of systemic auto-immune arthritis (collagen-induced arthritis [CIA]), a model of cartilage destruction (methylated BSA [mBSA]-induced monoarthritis) and a model of ankylosing enthesitis and spondyloarthritis (spontaneous arthritis in male DBA/1 mice).