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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 RMD+Open
2017 ; 3
(1
): e000365
Nephropedia Template TP
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English Wikipedia
Methotrexate and low-dose prednisolone downregulate osteoclast function by
decreasing receptor activator of nuclear factor-?? expression in monocytes from
patients with early rheumatoid arthritis
#MMPMID28955481
Perpétuo IP
; Caetano-Lopes J
; Rodrigues AM
; Campanilho-Marques R
; Ponte C
; Canhão H
; Ainola M
; Fonseca JE
RMD Open
2017[]; 3
(1
): e000365
PMID28955481
show ga
OBJECTIVE: Rheumatoid arthritis (RA) is a systemic, immune-mediated inflammatory
disease that ultimately leads to bone erosions and joint destruction.
Methotrexate (MTX) slows bone damage but the mechanism by which it acts is still
unknown. In this study, we aimed to assess the effect of MTX and low-dose
prednisolone (PDN) on circulating osteoclast (OC) precursors and OC
differentiation in patients with RA. METHODS: Patients with RA before and at
least 6 months after MTX therapy were analysed and compared with healthy donors.
A blood sample was collected in order to assess receptor activator of NF-??
(RANK) ligand surface expression on circulating leucocytes and frequency and
phenotype of monocyte subpopulations. Quantification of serum levels of bone
turnover markers and cytokines and OC differentiation assays were performed.
RESULTS: Classical activation markers of monocytes and RANK increased in patients
with RA at baseline, compared with control healthy donors, and after MTX and
low-dose PDN (MTX+PDN) exposure they decreased to control levels. Although the
number of OC was not different between groups, the percentage of resorbed area
and the resorbed area per pit reduced after treatment. Serum soluble receptor
activator of nuclear factor-kappa (RANKL) levels increased at baseline compared
with healthy donors and normalised after therapy. CONCLUSION: Our results suggest
that MTX+PDN play an important role in downregulating OC function, which we
believe occurs through the decrease in RANK surface expression in monocytes.