Entzündung und Knochenabbau

P. Pietschmann; U. Föger-Samwald; I. Ellinger; K. Kerschan-Schindl

doi:10.1055/s-0037-1622015

Osteologie, Table of Contents

Osteologie 2014; 23(03): 173-178
DOI: 10.1055/s-0037-1622015

Osteoimmunologie

Schattauer GmbH

Entzündung und Knochenabbau

Rheumatoide ArthritisInflammation and new bone resorptionRheumatoid arthritis

P. Pietschmann

¹Institut für Pathophysiologie und Allergieforschung, Zentrum für Pathophysiologie, Infektiologie und Immunologie, Medizinische Universität Wien, Österreich

,

U. Föger-Samwald

¹Institut für Pathophysiologie und Allergieforschung, Zentrum für Pathophysiologie, Infektiologie und Immunologie, Medizinische Universität Wien, Österreich

,

I. Ellinger

¹Institut für Pathophysiologie und Allergieforschung, Zentrum für Pathophysiologie, Infektiologie und Immunologie, Medizinische Universität Wien, Österreich

,

K. Kerschan-Schindl

²Universitätsklinik für Physikalische Medizin und Rehabilitation, Medizinische Universität Wien, Österreich

› Author Affiliations

Abstract

Zusammenfassung

Die rheumatoide Arthritis zählt zu den häufigsten Autoimmunerkrankungen und ist der Prototyp einer osteoimmunen Erkrankung. Zu den Knochenmanifestationen der Erkrankungen gehören Erosionen und die systemische Osteoporose. In Tiermodellen und klinischen Studien wurde gezeigt, dass bei der rheumatoiden Arthritis die Knochendestruktion im Wesentlichen durch eine exzessive Osteoklastenaktivität zustande kommt. Proinflammatorische Zytokine spielen bei der Zerstörung von entzündeten Gelenken eine wichtige Rolle; bei der rheumatoiden Arthritis steigern RANKL, Tumornekrosefaktor-, Interleukin-1, Interleukin-6 und Interleukin-17 die Generation und Aktivierung von Osteoklasten und propagieren so die Knochendestruktion. Neueste Ergebnisse sprechen dafür, dass Antikörper gegen citrullinierte Peptide direkt die Knochenresorption aktivieren könnten. Im Gegensatz zur Knochenresorption ist die Knochenformation im Bereich der Erosionen meist supprimiert. Dies wird durch Antagonisten des Wnt-Signaltransduktionsweges (z. B. Dickkopf-1) mediiert. Die Osteoimmunologie zeigt somit neue therapeutische Ansatzpunkte für zukünftige Behandlungsstrategien der rheumatoiden Arthritis auf.

Summary

Rheumatoid arthritis is among the most frequent autoimmune diseases and is a prototype of an osteoimmune disease. Bone manifestations of the disease include erosions and systemic osteoporosis. Animal models and clinical studies consistently demonstrate that bone destruction in rheumatoid arthritis is predominantly due to excessive osteoclast activity. Proinflammatory cytokines play an important role in the destruction of inflamed joints; in rheumatoid arthritis RANKL, tumour necrosis factor-, interleukin-1, interleukin-6 and interleukin-17 increase osteoclast generation and activation and thus mediate bone destruction. Recent data suggest that antibodies against citrullinated peptides directly induce bone resorption. In contrast to bone resorption, bone formation at the sites of erosions typically is suppressed; this is mediated by antagonists of the wnt pathway, e. g. an upregulation of dickkopf-1. Targeting osteoimmune pathways thus appears to be a promising future treatment strategy for rheumatoid arthritis.

Schlüsselwörter

Rheumatoide Arthritis - osteoimmune Erkrankung - Zytokine - RANK-RANKL - Tumornekrosefaktor- - Interleukine - Wnt-Signaltransduktionsweg

Keywords

Rheumatoid arthritis - osteoimmune disease - cytokines - RANK-RANKL - tumour necrosis factor- - interleukins - wnt pathway

Full Text

References

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