RT Journal Article
SR Electronic
T1 Bone loss before the clinical onset of rheumatoid arthritis in subjects with anticitrullinated protein antibodies
JF Annals of the Rheumatic Diseases
JO Ann Rheum Dis
FD BMJ Publishing Group Ltd and European League Against Rheumatism
SP 854
OP 860
DO 10.1136/annrheumdis-2012-202958
VO 73
IS 5
A1 Arnd Kleyer
A1 Stephanie Finzel
A1 Jürgen Rech
A1 Bernhard Manger
A1 Manuel Krieter
A1 Francesca Faustini
A1 Elisabeth Araujo
A1 Axel J Hueber
A1 Ulrike Harre
A1 Klaus Engelke
A1 Georg Schett
YR 2014
UL http://ard.bmj.com/content/73/5/854.abstract
AB Objective Anticitrullinated protein antibodies (ACPA) are a major risk factor for bone loss in rheumatoid arthritis (RA). We have recently shown that ACPA directly induce bone loss by stimulating osteoclast differentiation. As ACPA precede the clinical onset of RA by years, we hypothesised that ACPA positive healthy individuals may already show skeletal changes. Methods We performed a comparative micro-CT analysis of the bone microstructure in the metacarpophalangeal joints of ACPA positive and ACPA negative healthy individuals without clinical signs of arthritis. Results ACPA positive (n=15) and negative (n=15) healthy individuals were not different in age (48.2±4.1 vs 51.4±3.8 years, p=0.57) or gender (eight women and two men in both groups). Bone mineral density was significantly reduced in ACPA positive individuals (mean±SEM 280±11 mg/cm3) compared with controls (327±6). 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) compared with controls (0.32±0.03 mm). Areas of cortical porosity were significantly (p=0.0005) more widespread in ACPA positive (mean±SEM 7.4±1.4%) than in ACPA negative individuals (1.0±0.3%). Discussion Structural bone damage starts before the clinical onset of arthritis in subjects with ACPA. These findings revise the concept that bone damage is an exclusive consequence of synovitis in patients with RA.