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Promising bone-related therapeutic targets for rheumatoid arthritis Choi Y; Arron JR; Townsend MJNat Rev Rheumatol 2009[Oct]; 5 (10): 543-8Rheumatoid arthritis (RA) is a chronic, debilitating autoimmune disease that results in inflammation and structural destruction of the joints. A hallmark of RA pathogenesis is an imbalance of the osteoblast-osteoclast axis driven by inflammatory processes, resulting in elevated bone resorption by osteoclasts. Current therapies used to treat this disease have focused on inhibition of synovitis, but such treatments do not adequately repair damaged bone. A key pathway of osteoclast formation involves the receptor activator of nuclear factor kappaB ligand (RANKL) pathway acting on myeloid progenitor cells. The Wnt pathway has been shown to be important for the differentiation of osteoblasts from mesenchymal lineage precursors, and endogenous Wnt inhibitors, such as Dickkopf1 and sclerostin, might have important roles in osteoclast dysregulation in RA. Inhibition of the RANKL pathway, or blockade of Dickkopf1 and sclerostin, might serve to restore the osteoblast-osteoclast balance and repair bone erosion in RA joints. Such treatments, in combination with anti-inflammatory therapies, could stabilize and repair damaged joints and have the potential to be valuable additions to the armory of RA treatments.|*Drug Delivery Systems[MESH]|Adaptor Proteins, Signal Transducing[MESH]|Arthritis, Rheumatoid/*drug therapy/metabolism/pathology[MESH]|Bone Morphogenetic Proteins/antagonists & inhibitors/metabolism[MESH]|Bone Resorption/drug therapy/metabolism/pathology[MESH]|Genetic Markers[MESH]|Humans[MESH]|Intercellular Signaling Peptides and Proteins/metabolism[MESH]|Joints/drug effects/pathology[MESH]|Osteoblasts/*drug effects/metabolism/pathology[MESH]|Osteoclasts/*drug effects/metabolism/pathology[MESH]|RANK Ligand/metabolism[MESH]|Wnt Proteins/antagonists & inhibitors/metabolism[MESH] |
