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Effect of Tumor Necrosis Factor Inhibitor Therapy on Osteoclasts Precursors in Rheumatoid Arthritis.

Abstract Objective. Tumor necrosis factor (TNF) increases circulating osteoclast (OC) precursors numbers by promoting their proliferation and differentiation. The aim of this study was to assess the effect of TNF inhibitors (TNFi) on the differentiation and activity of OC in rheumatoid arthritis (RA) patients. Methods. Seventeen RA patients treated with TNFi were analyzed at baseline and after a minimum follow-up period of 6 months. Blood samples were collected to assess receptor activator of nuclear factor kappa-B ligand (RANKL) surface expression on circulating leukocytes and frequency and phenotype of monocyte subpopulations. Quantification of serum levels of bone turnover markers, in vitro OC differentiation assays, and qRT-PCR for OC specific genes was performed. Results. After TNFi therapy, patients had reduced RANKL surface expression in B-lymphocytes and the frequency of circulating classical CD14(bright)CD16(-) monocytes was decreased. Serum levels of sRANKL, sRANKL/OPG ratio, and CTX-I were reduced in RA patients after TNFi treatment. Moreover, after exposure to TNFi, osteoclast differentiation and activity were decreased, as well as the expression of TRAF6 and cathepsin K. Conclusion. We propose that TNFi arrests bone loss and erosion, through two pathways: direct reduction of osteoclast precursor numbers and inhibition of intracellular signaling pathways acting through TRAF6.
PMID
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Authors

Mayor MeshTerms

Arthritis, Rheumatoid

Monocyte-Macrophage Precursor Cells

Osteoclasts

Keywords
Journal Title biomed research international
Publication Year Start




PMID- 28286757
OWN - NLM
STAT- MEDLINE
DA  - 20170313
DCOM- 20170317
LR  - 20170317
IS  - 2314-6141 (Electronic)
VI  - 2017
DP  - 2017
TI  - Effect of Tumor Necrosis Factor Inhibitor Therapy on Osteoclasts Precursors in
      Rheumatoid Arthritis.
PG  - 2690402
LID - 10.1155/2017/2690402 [doi]
AB  - Objective. Tumor necrosis factor (TNF) increases circulating osteoclast (OC)
      precursors numbers by promoting their proliferation and differentiation. The aim 
      of this study was to assess the effect of TNF inhibitors (TNFi) on the
      differentiation and activity of OC in rheumatoid arthritis (RA) patients.
      Methods. Seventeen RA patients treated with TNFi were analyzed at baseline and
      after a minimum follow-up period of 6 months. Blood samples were collected to
      assess receptor activator of nuclear factor kappa-B ligand (RANKL) surface
      expression on circulating leukocytes and frequency and phenotype of monocyte
      subpopulations. Quantification of serum levels of bone turnover markers, in vitro
      OC differentiation assays, and qRT-PCR for OC specific genes was performed.
      Results. After TNFi therapy, patients had reduced RANKL surface expression in
      B-lymphocytes and the frequency of circulating classical CD14brightCD16-
      monocytes was decreased. Serum levels of sRANKL, sRANKL/OPG ratio, and CTX-I were
      reduced in RA patients after TNFi treatment. Moreover, after exposure to TNFi,
      osteoclast differentiation and activity were decreased, as well as the expression
      of TRAF6 and cathepsin K. Conclusion. We propose that TNFi arrests bone loss and 
      erosion, through two pathways: direct reduction of osteoclast precursor numbers
      and inhibition of intracellular signaling pathways acting through TRAF6.
FAU - Perpetuo, Ines P
AU  - Perpetuo IP
AUID- ORCID: 0000-0001-7671-2539
AD  - Rheumatology Research Unit, Instituto de Medicina Molecular, Faculdade de
      Medicina, Universidade de Lisboa, Lisboa, Portugal.
FAU - Caetano-Lopes, Joana
AU  - Caetano-Lopes J
AUID- ORCID: 0000-0003-0310-4641
AD  - Rheumatology Research Unit, Instituto de Medicina Molecular, Faculdade de
      Medicina, Universidade de Lisboa, Lisboa, Portugal.
FAU - Rodrigues, Ana Maria
AU  - Rodrigues AM
AD  - Rheumatology Research Unit, Instituto de Medicina Molecular, Faculdade de
      Medicina, Universidade de Lisboa, Lisboa, Portugal.
FAU - Campanilho-Marques, Raquel
AU  - Campanilho-Marques R
AD  - Rheumatology Research Unit, Instituto de Medicina Molecular, Faculdade de
      Medicina, Universidade de Lisboa, Lisboa, Portugal; Rheumatology Department,
      Hospital de Santa Maria, Centro Hospitalar Lisboa Norte, EPE, Lisbon Academic
      Medical Centre, Lisboa, Portugal.
FAU - Ponte, Cristina
AU  - Ponte C
AD  - Rheumatology Research Unit, Instituto de Medicina Molecular, Faculdade de
      Medicina, Universidade de Lisboa, Lisboa, Portugal; Rheumatology Department,
      Hospital de Santa Maria, Centro Hospitalar Lisboa Norte, EPE, Lisbon Academic
      Medical Centre, Lisboa, Portugal.
FAU - Canhao, Helena
AU  - Canhao H
AD  - EpiDoC Unit, CEDOC, NOVA Medical School, Universidade Nova de Lisboa, Lisboa,
      Portugal.
FAU - Ainola, Mari
AU  - Ainola M
AD  - Musculoskeletal Diseases and Inflammation Research Group, Biomedicum Helsinki 1, 
      Faculty of Medicine, Institute of Clinical Medicine, University of Helsinki,
      Helsinki, Finland.
FAU - Fonseca, Joao E
AU  - Fonseca JE
AUID- ORCID: 0000-0003-1432-3671
AD  - Rheumatology Research Unit, Instituto de Medicina Molecular, Faculdade de
      Medicina, Universidade de Lisboa, Lisboa, Portugal; Rheumatology Department,
      Hospital de Santa Maria, Centro Hospitalar Lisboa Norte, EPE, Lisbon Academic
      Medical Centre, Lisboa, Portugal.
LA  - eng
PT  - Journal Article
DEP - 20170213
PL  - United States
TA  - Biomed Res Int
JT  - BioMed research international
JID - 101600173
RN  - 0 (RANK Ligand)
RN  - 0 (TNF Receptor-Associated Factor 6)
RN  - 0 (TNF protein, human)
RN  - 0 (TNFSF11 protein, human)
RN  - 0 (Tifab protein, human)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.22.38 (CTSK protein, human)
RN  - EC 3.4.22.38 (Cathepsin K)
SB  - IM
MH  - Adult
MH  - *Arthritis, Rheumatoid/drug therapy/metabolism/pathology
MH  - Cathepsin K/biosynthesis
MH  - Female
MH  - Follow-Up Studies
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - *Monocyte-Macrophage Precursor Cells/metabolism/pathology
MH  - Monocytes/metabolism/pathology
MH  - *Osteoclasts/metabolism/pathology
MH  - RANK Ligand/biosynthesis
MH  - TNF Receptor-Associated Factor 6/biosynthesis
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
PMC - PMC5327780
COI - The authors declare no competing interests regarding the publication of this
      paper.
EDAT- 2017/03/14 06:00
MHDA- 2017/03/18 06:00
CRDT- 2017/03/14 06:00
PHST- 2016/10/01 [received]
PHST- 2017/01/04 [accepted]
AID - 10.1155/2017/2690402 [doi]
PST - ppublish
SO  - Biomed Res Int. 2017;2017:2690402. doi: 10.1155/2017/2690402. Epub 2017 Feb 13.

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