Bone damage in rheumatoid arthritis: mechanistic insights and approaches to prevention

Rheum Dis Clin North Am. 2010 May;36(2):385-404. doi: 10.1016/j.rdc.2010.03.003.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Arthritis, Rheumatoid / immunology
  • Arthritis, Rheumatoid / pathology*
  • Bone Resorption / immunology
  • Bone Resorption / pathology*
  • Bone Resorption / prevention & control*
  • Bone and Bones / immunology
  • Bone and Bones / pathology*
  • Humans
  • Osteoblasts / immunology
  • Osteoblasts / pathology
  • Osteoclasts / immunology
  • Osteoclasts / pathology