Osteoimmunologie: Wie die Entzündung den Knochenstoffwechsel beeinflusst

 

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Zusammenfassung

Der Knochenumbau zeichnet sich durch ein ausgeglichenes Verhältnis zwischen Knochenresorption und Knochenaufbau aus. Auf zellulärer Ebene sind die Osteoblasten für den Knochenaufbau und die Osteoklasten für den Knochenabbau verantwortlich. Über ein fein abgestimmtes Zusammenspiel von molekularen Mechanismen, Zytokinen, Hormonen und Wachstumsfaktoren wird dabei die Knochenhomöostase gewährleistet. Das RANK/RANKL/OPG-System ist aktiv an der Reifung von Osteoklasten mit konsekutiv erhöhtem Knochenabbau beteiligt. Störungen der Knochenhomöostase können bei erhöhtem Abbau mit entzündlich-destruktiven Manifestationen und/oder einer Osteoporose einhergehen, hingegen bei erhöhtem Anbau eine Osteopetrose induzieren. Die vorliegende Übersichtsarbeit fokussiert auf die bekannten molekularen Mechanismen und pathophysiologischen Stoffwechselwege dieser Remodellingprozesse, insbesondere unter dem Einfluss von Entzündungsmediatoren, und stellt auch die Verbindung von Forschung zur Klinik dar.

Abstract

Bone remodelling is characterized by a balance between bone resorption and bone formation. The osteoblasts are responsible for bone synthesis and the osteoclasts for bone resorption. A finely adjusted interaction between molecular mechanisms leads, via cytokines, hormones and growth factors, to a homeostasis of the bone metabolism. Here, the RANK/RANKL/OPG-system is actively involved in the differentiation and function of osteoclasts and seems to play a central role in most pathophysiological mechanisms. An increased osteoclast activity results in inflammatory destructive manifestations and/or osteoporosis whereas an increased osteoblast activity can result in osteopetrosis. The present overview describes the known pathophysiological relevant metabolic pathways in this remodelling process especially the effect of inflammation on bone metabolism, and presents the links from bench to bedside.

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