Pathogenesis of Bone Erosions in Rheumatoid Arthritis: Not Only Inflammation

Abstract

It is a matter of fact that the inflammatory pathogenesis does not explain all the skeletal manifestations of Rheumatoid Arthritis (RA), and the development of bone involvement is sometimes unconnected from the clinical scores of inflammation. On the basis of recent studies, we would like to make a point of the new available evidence about the metabolic pathogenic component of bone erosions. We assume that in this process an additional role could be played by metabolic factors, such as the parathyroid hormone (PTH), DKK1 (the inhibitor of the Wnt/β catenin pathway) and cortical bone mineral density. The result is a new pathogenic hypothesis for bone erosion in RA, which supplements the inflammatory one: the reduction of osteoblasts activity and the increase of the osteoclasts one, involved in the pathogenesis of bone erosions and osteoporosis, are not only the consequence of the action of inflammatory cytokines, but also of increased levels of DKK1 and PTH. On the other hand, osteoporosis, in particular at the cortical sites, facilitates the appearance of erosions.