Aktuelle Rheumatologie 2012; 37(04): 254-259
DOI: 10.1055/s-0032-1314794
Übersichtsarbeit
© Georg Thieme Verlag KG Stuttgart · New York

Molekulare Mechanismen der Osteoporose bei entzündlich-rheumatischen Erkrankungen

Molecular Mechanisms of Osteoporosis in Inflammatory Rheumatic Diseases
E. Neumann
1   Internal Medicine and Rheumatology, University of Gießen, Bad Nauheim
› Author Affiliations
Further Information

Publication History

Publication Date:
09 July 2012 (online)

Zusammenfassung

Der Knochenumbau beim gesunden Menschen findet durch ein ausgeglichenes Verhältnis von Knochenresorption zu Knochenaufbau statt. Auf zellulärem Niveau wird dieser Prozess über die Osteoklasten- und Osteoblastenaktivität reguliert. Die Osteoporose ist durch eine reduzierte Knochendichte charakterisiert. Auf zellulärer Ebene verschiebt sich bei Verlust der Knochendichte das Gleichgewicht auf die Seite der Aktivierung von Osteoklasten. Das Immunsystem ist in der Lage, über die Beeinflussung des RANK/RANKL/OPG-Systems den Knochenumbau zu beeinflussen. Hierbei tragen Entzündung und insbesondere chronische Entzündungsprozesse zur Verschiebung des Umbaugleichgewichts in Richtung Knochenabbau bei. Eine Entzündung kann die Reifung und Funktion von Osteoklasten und Osteoblasten direkt oder indirekt modifizieren. Auf molekularer Ebene werden durch pro-entzündliche Zytokine das RANK/RANKL/OPG sowie weitere Stoffwechselwege beeinflusst, die an der Entstehung der Osteoporose beteiligt sind.

Abstract

Bone remodelling in healthy persons is characterised by balanced bone resorption and bone formation. On the cellular level, bone remodelling is regulated by a balanced osteoclast and osteoblast activity. Osteoporosis is characterised by bone loss. On a cellular level, the balance is shifted towards the side of osteoclast activation and activity. The immune system is able to influence bone remodelling via the RANK/RANKL/OPG system. Inflammatory processes directly and indirectly modify the differentiation and function of osteoclasts and play a central role in most of the pathophysiological pathways active in osteoporosis. Inflammation and, especially, chronic inflammatory pathways contribute to the shift of the bone remodelling balance in the direction of bone resorpion, leading to osteoporosis.

 
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