Background Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are systemic, immune-mediated diseases. RA's main targets are the peripheral joints while AS has the axial skeleton and enthesis as the principal affected areas. RA is characterized by bone erosions and impaired repair whilst AS is typified by bone overgrowth. The causes for these differences are not yet understood; however we hypothesize that AS patients' monocytes receive reduced osteoclastogenic stimuli and/or have abnormal capacity to respond to them.
Objectives The aim of this study was to characterize AS patients' bone remodeling and pro osteoclastogenesis inflammatory environment and monocyte phenotypes as compared to RA patients and healthy controls.
Methods Untreated AS or RA 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 characterization. Serum was collected for cytokine and bone remodeling factors quantification. This study was approved by the hospital's ethics committee.
Results We found that RANKL T and B lymphocyte expression was significantly higher in AS and RA patients when compared to healthy donors (p=0.0445 and 0.0016, respectively). Frequency of both classical (CD14brightCD16negative) and non-classical (CD14dimCD16positive) was increased in AS and RA patients when compared to healthy donors (p<0.0001 and p=0.0227, respectively). However, in the classical subpopulation RANK expression was lower in AS patients as compared to RA patients and healthy controls (p=0.0073). In accordance, CTX-I and P1NP serum level were also lower in AS patients than in healthy controls (p=0.0100 and p=0.0195, respectively).
Conclusions 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.
Disclosure of Interest None declared