Article Text
Abstract
Objectives Bone loss is a well-established consequence of rheumatoid arthritis (RA). To date, bone disease in RA is exclusively characterised by bone density measurements, while the functional properties of bone in RA are undefined. This study aimed to define the impact of RA on the functional properties of bone, such as failure load and stiffness.
Methods Micro-finite element analysis (µFEA) was carried out to measure failure load and stiffness of bone based on high-resolution peripheral quantitative CT data from the distal radius of anti-citrullinated protein antibody (ACPA)-positive RA (RA+), ACPA-negative RA (RA−) and healthy controls (HC). In addition, total, trabecular and cortical bone densities as well as microstructural parameters of bone were recorded. Correlations and multivariate models were used to determine the role of demographic, disease-specific and structural data of bone strength as well as its relation to prevalent fractures.
Results 276 individuals were analysed. Failure load and stiffness (both P<0.001) of bone were decreased in RA+, but not RA−, compared with HC. Lower bone strength affected both female and male patients with RA+, was related to longer disease duration and significantly (stiffness P=0.020; failure load P=0.012) associated with the occurrence of osteoporotic fractures. Impaired bone strength was correlated with altered bone density and microstructural parameters, which were all decreased in RA+. Multivariate models showed that ACPA status (P=0.007) and sex (P<0.001) were independently associated with reduced biomechanical properties of bone in RA.
Conclusion In summary, µFEA showed that bone strength is significantly decreased in RA+ and associated with fractures.
- rheumatoid arthritis
- bone strength
- fracture
- micro-finite element analysis
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Footnotes
Handling editor Josef S Smolen
Contributors FS, DS, AK, AJH and JR collected the data. AK, GS, DS, FS, KE and A-ML analysed and interpreted the data. FS, DS, AK and GS prepared and revised the manuscript. AK, DS and GS designed the study.
Funding This study was supported by the Deutsche Forschungsgemeinschaft (SPP1468-IMMUNOBONE; CRC1181;CRC1181-A01), the Bundesministerium für Bildung und Forschung (BMBF; project METARTHROS), the Marie Curie project OSTEOIMMUNE, the TEAM project of the European Union and the IMI-funded project RTCure.
Competing interests None declared.
Patient consent Obtained.
Ethics approval The study was conducted upon approval of the local ethics committee of the University Clinic of Erlangen and with the authorisation of the National Radiation Safety Agency (Bundesamt für Strahlenschutz).
Provenance and peer review Not commissioned; externally peer reviewed.