Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic joint inflammation, articular bone erosion and consequently joint destruction that can lead to complete loss of function. RA is not simply a disease of the joints but can affect many other organs and cause, for instance, systemic osteoporosis, a loss of bone mass. Nowadays there are many therapeutics available that can significantly reduce the impact of RA. However, bone destruction and osteoporosis still remains an issue for rheumatologists. Therefore, an efficient long-term therapeutic approach to target bone erosion still need to be established.
Final goal of this project was to establish a therapeutic approach to target bone remodeling in arthritis, thus not only blocking bone erosion caused by osteoclasts, but also inducing new bone formation by osteoblasts, in order to restore bone mass.
While looking for unknown pathways involved in RA bone metabolism, some clinical evidences, together with few experimental studies and our previous results led us to hypothesize an involvement of the neurotransmitter dopamine in bone erosion in RA. Dopamine (DA) is a neurotransmitter (a chemical messenger) of the central nervous system controlling movement, emotion, cognition, and neuroendocrine interactions. Recent evidence supports a key role of dopamine in the modulation of immune response.
Our hypothesis was that dopamine is involved in bone metabolism in RA. Main goal of this project was therefore to characterize the influence of the dopaminergic pathway on bone metabolism in RA and to identify its potential as therapeutic target towards a bone protective agent.
