RANK, RANKL and OPG in inflammatory arthritis and periprosthetic osteolysis

C. T. Ritchlin, Edward M. Schwarz, R. J. O'Keefe, R. J. Looney

Research output: Contribution to journalReview articlepeer-review

46 Scopus citations

Abstract

Elucidation of the receptor activator of nuclear factor kappa B (RANK), its ligand (RANKL) and osteoprotegerin (OPG) as the final effectors of bone resorption has transformed our understanding of metabolic bone diseases and revealed novel therapeutic targets. Activation of the RANK-RANKL signaling pathway is directly responsible for dramatic focal erosions that are observed in inflammatory arthritis and aseptic loosening of orthopaedic implants. While these conditions share many features common to all metabolic bone disorders (e.g., osteoclastic resorption), they exhibit several unique properties, which are highlighted in this review. Most important is the relative inability of bisphosphonate therapy to inhibit osteolysis in joint inflammation and periprosthetic joint loosening and the unexpected effectiveness of anti-cytokine therapy in both rheumatoid and psoriatic arthritis. Herein, we provide a review of the role of RANK, RANKL and OPG in erosive arthritis and periprosthetic osteolysis and discuss the potential of anti-RANKL therapy for these conditions.

Original languageEnglish
Pages (from-to)276-284
Number of pages9
JournalJournal of Musculoskeletal Neuronal Interactions
Volume4
Issue number3
StatePublished - Sep 2004

Keywords

  • Aseptic loosening
  • Osteoclast precursors (OCP)
  • Psoriatic arthritis(PsA)
  • Rheumatoid arthritis (RA)
  • Tumor necrosis factor-alpha (TNFα)

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