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Georg Schett, MD; Stefan Kiechl, MD; Siegfried Weger, MD; Angelo Pederiva, MD; Agnes Mayr, MD; Manuele Petrangeli, MD; Friedrich Oberhollenzer, MD; Rolando Lorenzini, MD; Kurt Redlich, MD; Roland Axmann, MD; Jochen Zwerina, MD; Johann Willeit, MD

Arch Intern Med. 2006;166:2495-2501.

Background  Chronic inflammatory diseases are associated with bone loss and an enhanced fracture risk. It is unknown, however, whether low-grade inflammation in healthy individuals, as estimated by the high-sensitivity C-reactive protein (hs-CRP) level, interferes with bone metabolism and affects the risk of nontraumatic fractures.

Methods  Lifetime bone fractures were carefully recorded in the cohort of the population-based Bruneck Study (n = 919) along with information on the date of occurrence and associated circumstances. The serum level of hs-CRP was measured from blood samples collected during the 1990 baseline examination and the 1995, 2000, and 2005 follow-up examinations. In addition, lifestyle and demographic characteristics, bone ultrasonographic data at the heel, and variables of bone metabolism were assessed.

Results  Between September 1, 1990, and August 31, 2005, 69 subjects experienced nontraumatic hip or vertebral fractures. The incidence of nontraumatic fractures was 1.3, 3.8, and 13.9 per 1000 person-years in the tertile groups for hs-CRP. In multivariate pooled logistic regression analysis, the adjusted relative risk (95% confidence interval) of nontraumatic fracture in the highest vs lowest tertile group for hs-CRP was 9.4 (3.6-24.8) (P<.001). The exclusion of subjects with cardiovascular disease, dementia, malignancies, and chronic inflammatory disease had little effect on the results obtained. The hs-CRP level was unrelated to ultrasonographic measures of bone density, but showed an inverse relation to laboratory markers of bone turnover, like -crosslaps and osteocalcin concentration (P<.001).

Conclusions  The hs-CRP level is a significant and independent risk predictor of nontraumatic fracture. This finding is consistent with the hypothesis of a tight interplay between low-grade inflammation and bone turnover.

Author Affiliations: Department of Internal Medicine III and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany (Drs Schett, Axmann, and Willeit); Division of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna (Drs Schett, Redlich, and Zwerina), and Department of Neurology, Medical University Innsbruck, Innsbruck (Drs Kiechl and Willeit), Austria; and Departments of Internal Medicine (Drs Weger, Pederiva, and Oberhollenzer), Laboratory Medicine (Drs Mayr and Petrangeli), and Radiology (Dr Lorenzini), Bruneck Hospital, Bruneck, Italy.

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