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<p>In rheumatoid arthritis (RA), local and systemic inflammation and immobility lead to both generalized and local bone loss and an increased risk of fractures. Osteo-immunology, the shared mechanisms and crosstalk between immunology and bone has revealed insight in the pathogenesis: the upregulated inflammatory cytokines (TNFa, IL-1 and IL6) and, apart from that, anticitrullinated proteins antibodies (ACPA) stimulate the osteoclastogenesis with upregulated RANKL leading to increased bone resorption, while recent data also show an inhibited bone formation. Initially with the TNF blocker infliximab, and later with bDMARDS other biologics and even with combination of conventional DMARDs, generalized bone loss and erosions could be arrested. In the research agenda, lack of long-term data, fracture data and data on bone quality with HRpQCT was discussed, as well as exciting new data on erosion repair in studies with tocilizumab and baractinib. To summarize, the enormous developments both in the basic field of osteoimmunology combined with the introduction of powerful anti-inflammatory drugs in RA strongly prevents the local and generalized bone loss in RA.</p>

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Osteoimmunology: Can We Prevent Bone Loss in Rheumatoid Arthritis with Modern Antirheumatic Drugs?

  • 期刊论文

  • 发表日期：

    2026年4月11日

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  • Hennie G. Raterman,
  • Giovanni Adami,
  • Patricia Clark,
  • Glenn Haugeberg,
  • Jorge Morales Torres,
  • Luis Vidal Neira,
  • Leith Zakraoui,
  • Cristiano Zerbini,
  • Osvaldo D. Messina,
  • Willem F. Lems

摘要

In rheumatoid arthritis (RA), local and systemic inflammation and immobility lead to both generalized and local bone loss and an increased risk of fractures. Osteo-immunology, the shared mechanisms and crosstalk between immunology and bone has revealed insight in the pathogenesis: the upregulated inflammatory cytokines (TNFa, IL-1 and IL6) and, apart from that, anticitrullinated proteins antibodies (ACPA) stimulate the osteoclastogenesis with upregulated RANKL leading to increased bone resorption, while recent data also show an inhibited bone formation. Initially with the TNF blocker infliximab, and later with bDMARDS other biologics and even with combination of conventional DMARDs, generalized bone loss and erosions could be arrested. In the research agenda, lack of long-term data, fracture data and data on bone quality with HRpQCT was discussed, as well as exciting new data on erosion repair in studies with tocilizumab and baractinib. To summarize, the enormous developments both in the basic field of osteoimmunology combined with the introduction of powerful anti-inflammatory drugs in RA strongly prevents the local and generalized bone loss in RA.