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Georg Schett, MD; Stefan Kiechl, MD

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The primary aim of our study was to test whether low-grade systemic inflammation as estimated by hs-CRP level is linked to the risk of nontraumatic fractures.¹ The hypothesis that inflammation interferes with bone metabolism and affects fracture risk is intriguing from a pathophysiologic and therapeutic viewpoint. Our and other recent epidemiological data^1-2 support this view and intend to stimulate further research efforts in the field.

We, however, fully agree with Cheng that development and validation of a risk score considering well-established predictors of nontraumatic fractures and novel laboratory markers such as soluble receptor activator of nuclear factor B ligand (RANKL)³ and CRP level¹ is the next logical step. This work is currently in progress, and preliminary data indicate that addition of RANKL and CRP level to a base model including age, sex, and menopausal status results in a significant gain in area . . . [Full Text of this Article]

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