Bone damage in rheumatoid arthritis: mechanistic insights and approaches to prevention.
In rheumatoid arthritis (RA), cells within the inflamed synovium and pannus elaborate a variety of cytokines, including tumor necrosis factor (TNF) alpha, interleukin (IL)-1, IL-6, and IL-17, that contribute to inflammation, and may directly affect bone. The receptor activator of NF-kappaB (RANK) ligand/RANK/osteoprotegerin pathway plays a critical role in regulating osteoclastogenesis in articular bone erosions in RA. Proinflammatory cytokines can modulate this pathway, and may also affect the ability of the osteoblast to repair bone at sites of articular erosion. In this review, the authors discuss the current understanding of pathogenic mechanisms of bone erosion in RA and examine current therapeutic approaches to prevent this damage.
Division of Rheumatology, Department of Medicine, University of Massachusetts Medical School, UMass Memorial Medical Center, Lazare Research Building, Suite 223, 364 Plantation Street, Worcester, MA 01605, USA.
Sougata
S
Karmakar
Jonathan
J
Kay
Ellen M
EM
Gravallese
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000473:pathology*; D001862:Bone Resorption / Q000276:immunology / Q000473:pathology* / Q000517:prevention & control*; D001842:Bone and Bones / Q000276:immunology / Q000473:pathology*; D006801:Humans; D010006:Osteoblasts / Q000276:immunology / Q000473:pathology; D010010:Osteoclasts / Q000276:immunology / Q000473:pathology