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Dtsch Med Wochenschr 2013; 138(37): 1845-1849
DOI: 10.1055/s-0033-1349486
Übersicht | Review article
Rheumatologie, Osteologie
© Georg Thieme Verlag KG Stuttgart · New York

Osteoimmunologie: Wie die Entzündung den Knochenstoffwechsel beeinflusst

Osteoimmunology: How inflammation influences bone metabolism
U. Lange
1   Professur für Internistische Rheumatologie, Osteologie, Physikalische Medizin der Universität Gießen; Kerckhoff-Klinik, Abteilung Rheumatologie, klinische Immunologie, Osteologie, Physikalische Medizin; Bad Nauheim
,
J. Teichmann
2   Klinikum Lüdenscheid, Klinik für Allgemeine Innere Medizin, Gastroenterologie und Endokrinologie, Lüdenscheid
,
G. Schett
3   Medizinische Klinik 3 – Immunologie und Rheumatologie, Universität Erlangen
,
E. Neumann
4   Lehrstuhl Innere Medizin/SP Rheumatologie der Universität Gießen; Kerckhoff-Klinik, Abteilung Rheumatologie, klinische Immunologie, Osteologie, Physikalische Medizin, Bad Nauheim
,
U. Müller-Ladner
4   Lehrstuhl Innere Medizin/SP Rheumatologie der Universität Gießen; Kerckhoff-Klinik, Abteilung Rheumatologie, klinische Immunologie, Osteologie, Physikalische Medizin, Bad Nauheim
› Author Affiliations
Further Information

Publication History

16 May 2013

31 July 2013

Publication Date:
04 September 2013 (online)

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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.

Schlüsselwörter

Knochenstoffwechsel - Remodelling - Osteoporose - RANK/RANKL/OPG

Keywords

bone metabolism - remodelling - osteoporosis - RANK/RANKL/OPG
 

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