Bone Loss Before Clinical Onset of Rheumatoid Arthritis o Subjects with Anti-Citrullinated Protein Antibodies

Stephanie Finzel¹, Veronika Lang², Arnd Kleyer¹, Juergen Rech³, Bernhard Manger¹, Elizabeth Araujo¹, Axel J. Hueber⁴, Ulrike Harre⁵ and Georg Schett¹, ¹Dept of Medicine 3, Rheumatology and Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany, ²Dept. of Medicine, Rheumatology and Clinical Immunology, University of Erlangen-Nuremberg, Germany, ³Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany, ⁴Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany, ⁵Institute for Clinical Immunology, Institute for Clinical Immunology, University of Erlangen-Nuremberg, Erlangen, Germany

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: anti-CCP antibodies, anti-citrullinated protein/peptide antibodies (ACPA), Bone density, computed tomography (CT) and rheumatoid arthritis (RA)

Session Information

Title: Imaging of Rheumatic Diseases: Magnetic Resonance Imaging, Computed Tomography and X-ray

Session Type: Abstract Submissions (ACR)

Background/Purpose: Anti-citrullinated protein antibodies (ACPA) are a major risk factor for rapid disease progression in rheumatoid arthritis (RA). We have recently shown that ACPA directly induce bone loss by stimulating osteoclast differentiation (Harre et al, J Clin Invest 2012;122:1791). As ACPA precede the clinical onset of RA we hypothesized that ACPA positive healthy individuals may shows skeletal changes.

Methods: performed a comparative micro computed tomography analysis of the bone microstructure in the metacarpophalangeal joints (MCPJ) of ACPA positive and -negative healthy individuals without signs of arthritis.

Results:

ACPA positive (N= 10) and -negative (N= 10) healthy individuals were not different in age (48.2 ± 4.1 vs. 51.4 ± 3.8 years, p = 0.57) and gender (each 8 females and 2 males). Bone minaral density was significantly reduced in ACPA-positive individuals (mean ± SEM: 280 ± 11 mg/ccm) as compared to controls (327 ± 6 mg/ccm). Bone loss was based on cortical bone changes with significant (p = 0.044) reduction in cortical thickness in the ACPA-positive group (mean ± SEM: 0.22 ± 0.03 mm) as compared to controls (0.32 ± 0.03 mm).

Conclusion:

Structural bone damage starts before the clinical onset of arthritis in subjects with ACPA. These findings revise the concept of bone damage as an exclusive consequence of synovitis in ACPA positive individuals.

Disclosure:

S. Finzel,
None;

V. Lang,
None;

A. Kleyer,
None;

J. Rech,
None;

B. Manger,
None;

E. Araujo,
None;

A. J. Hueber,
None;

U. Harre,
None;

G. Schett,
None.

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