Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are systemic, immune-mediated diseases. In RA the main target are the peripheral joints while in AS the axial skeleton and enthesis are affected. RA is characterised by bone repair impairment and AS by exaggerated repair, leading to joint ankylosis. The cause for these differences is not yet understood, however we hypothesize that monocytes from AS patients exhibit reduced responses to osteoclastogenic and/or migratory stimulus.
The aim of this work was to characterise bone remodelling regulators and the inflammatory signals that promote osteoclastogenesis and the circulating monocyte subpopulations to understand their response to inflammation and osteoclastogenic signals in untreated AS patients and compare them to RA patients and healthy controls.
Untreated RA or AS patients with active disease and age and gender-matched healthy donors were recruited for this study. Blood was collected for flow cytometry measurements of RANKL expression and monocyte subpopulation characterisation. Serum was collected for cytokine and bone turnover marker quantification.
We found that RANKL lymphocyte expression is higher in AS and RA patients when compared to healthy donors. When analyzing the monocyte sub-populations we found that both in the classical and the intermediate subpopulations, RANK expression was decreased in AS patients as compared to RA patients and healthy controls. In accordance, CTX-I serum level was also lower in AS patients than in healthy controls.
In conclusion, and despite comparable osteoclastogenic stimuli in AS and RA patients, RANK expression is reduced in AS circulating monocytes which may contribute to the bone forming phenotype observed in AS patients.
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