A research team at the University of Massachusetts Medical School in Worcester has made important findings regarding bone erosion and formation that may lead to better treatment options for people impacted by rheumatoid arthritis (RA).
Ellen Gravallese, MD, rheumatology division chief and professor of medicine and cell biology at the University of Massachusetts, received a two-year disease-targeted research grant from the ACR Research and Education Foundation in 2008 to study how osteoclasts and osteoblasts affect bone erosion and healing in RA.
Her lab had previously published studies identifying osteoclasts as cell types involved in bone erosion in patients with RA. In addition, her team had identified receptor activator of NF-κB ligand in synovial tissue as an important factor driving osteoclast differentiation in arthritis. With the clinical use of disease-modifying and biologic agents, rheumatologists observed that the osteoclast-mediated erosive process could be retarded or even arrested. However, there was little evidence of new bone formation. “There was no further erosion, but it’s rare to see bone repair,” says Dr. Gravallese. “In normal bone remodeling, osteoblasts would fill in bone that had been lost or removed.”