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DOI: 10.1055/s-0034-1368247
Osteoporose – inflammatorische Effekte auf den Knochenstoffwechsel und das Frakturrisiko
Osteoporosis – Inflammatory Effects on Bone Metabolism and Fracture RiskPublikationsverlauf
Publikationsdatum:
23. April 2014 (online)
Zusammenfassung
Sowohl experimentelle als auch epidemiologische Studien haben gezeigt, dass proinflammatorische Zytokine, insbesondere Interleukin-1, Interleukin-6 und Tumornekrosefaktor-α, wichtige Regulatoren im Knochenmetabolismus darstellen. Zudem wird vermutet, dass proinflammatorischen Zytokinen auch in der Pathogenese des altersassoziierten und östrogenmangelinduzierten Knochenmasseverlusts eine bedeutende Rolle zugeschrieben werden kann. Obwohl eine Beschleunigung des Knochenabbaus bei Patienten mit chronisch-entzündlichen Systemerkrankungen bereits belegt werden konnte, ist die endgültige Bedeutung proinflammatorischer Zytokine in der Ätiologie der Osteoporose noch unklar. Einige Studien lassen zwar einen Zusammenhang zwischen erhöhten Konzentrationen proinflammatorischer Zytokine und einer Verminderung der Knochendichte sowie einem gesteigerten Frakturrisiko vermuten, in Summe ist die Evidenzlage jedoch eher rar und erlaubt keine eindeutigen Rückschlüsse auf die Effekte einzelner Zytokine im Knochenstoffwechsel. Um exakter definieren zu können, welche Parameter einer systemischen Inflammation in welchem Stadium der Pathogenese einer Osteoporose zum Tragen kommen, werden weitere Studien vonnöten sein. Besonders auch vor dem Hintergrund der Entwicklung eines geeigneten diagnostischen Markers für den Kliniker, mit dem sich das Osteoporoserisiko und damit auch das Frakturrisiko besser vorhersagen lässt. Dies würde im Krankheitsverlauf frühzeitige Interventionen zum Erhalt eines mikroarchitektonisch gesunden und stabilen Knochens, bspw. durch den Einsatz einer Anti-Zytokin-Therapie, erleichtern.
Abstract
There is a large body of evidence that proinflammatory cytokines, particularly interleukin-1, interleukin-6, and tumour necrosis factor-α, play an important role in bone metabolism. Moreover, it is suspected that proinflammatory cytokines are also important in the pathogenesis of age- and estrogen deficiency-related bone loss. Although an accelerated decrease in bone mass is observed in patients with chronic inflammatory disorders, the definite meaning of proinflammatory cytokines in the aetiology of osteoporosis is still unclear. Some studies suggest a relationship between increased concentrations of proinflammatory cytokines and a decrease in bone mineral density, as well as an increased risk of fracture. In sum, the evidence is rather scarce and does not permit any clear conclusions about the effects of single cytokines in bone metabolism. To be able to define more exactly at which stage of the pathogenesis of osteoporosis parameters of a systemic inflammation take effect, further studies will be necessary, particularly for developing suitable diagnostic markers for clinicians. These diagnostic markers may be able to identify patients at risk for osteoporosis and therefore predict fracture risks. Thus, early interventions to preserve bone health, for example, by anti-cytokine therapy, could be more effective and efficient.
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