PMID- 22034083
OWN - NLM
STAT- MEDLINE
DCOM- 20120914
LR  - 20220409
IS  - 1529-0131 (Electronic)
IS  - 0004-3591 (Linking)
VI  - 64
IP  - 4
DP  - 2012 Apr
TI  - Regulation of subchondral bone osteoblast metabolism by cyclic compression.
PG  - 1193-203
LID - 10.1002/art.33445 [doi]
AB  - OBJECTIVE: Recent data have shown that abnormal subchondral bone remodeling plays 
      an important role in osteoarthritis (OA) onset and progression, and it was 
      suggested that abnormal mechanical pressure applied to the articulation was 
      responsible for these metabolic changes. This study was undertaken to evaluate 
      the effects of cyclic compression on osteoblasts from OA subchondral bone. 
      METHODS: Osteoblasts were isolated from sclerotic and nonsclerotic areas of human 
      OA subchondral bone. After 28 days, the osteoblasts were surrounded by an 
      abundant extracellular matrix and formed a resistant membrane, which was 
      submitted to cyclic compression (1 MPa at 1 Hz) for 4 hours. Gene expression was 
      evaluated by reverse transcription-polymerase chain reaction. Protein production 
      in culture supernatants was quantified by enzyme-linked immunosorbent assay or 
      visualized by immunohistochemistry. RESULTS: Compression increased the expression 
      of genes coding for interleukin-6 (IL-6), cyclooxygenase 2, RANKL, fibroblast 
      growth factor 2, IL-8, matrix metalloproteinase 3 (MMP-3), MMP-9, and MMP-13 but 
      reduced the expression of osteoprotegerin in osteoblasts in both sclerotic and 
      nonsclerotic areas. Colalpha1(I) and MMP-2 were not significantly affected by 
      mechanical stimuli. Nonsclerotic osteoblasts were significantly more sensitive to 
      compression than sclerotic ones, but after compression, differences in messenger 
      RNA levels between nonsclerotic and sclerotic osteoblasts were largely reduced or 
      even abolished. Under basal conditions, sclerotic osteoblasts expressed similar 
      levels of alpha5, alphav, beta1, and beta3 integrins and CD44 as nonsclerotic osteoblasts but 
      30% less connexin 43, an important mechanoreceptor. CONCLUSION: Genes involved in 
      subchondral bone sclerosis are mechanosensitive. After compression, nonsclerotic 
      and sclerotic osteoblasts expressed a similar phenotype, suggesting that 
      compression could be responsible for the phenotype changes in OA subchondral 
      osteoblasts.
CI  - Copyright (c) 2012 by the American College of Rheumatology.
FAU - Sanchez, Christelle
AU  - Sanchez C
AD  - University of Liege, Liege, Belgium.
FAU - Pesesse, Laurence
AU  - Pesesse L
FAU - Gabay, Odile
AU  - Gabay O
FAU - Delcour, Jean-Pierre
AU  - Delcour JP
FAU - Msika, Philippe
AU  - Msika P
FAU - Baudouin, Caroline
AU  - Baudouin C
FAU - Henrotin, Yves E
AU  - Henrotin YE
LA  - eng
GR  - Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20111027
PL  - United States
TA  - Arthritis Rheum
JT  - Arthritis and rheumatism
JID - 0370605
RN  - 0 (Interleukins)
RN  - 0 (Osteoprotegerin)
RN  - 0 (RANK Ligand)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 1.14.99.1 (PTGS2 protein, human)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
SB  - IM
MH  - Aged
MH  - Bone Remodeling/*physiology
MH  - Bone and Bones/*metabolism
MH  - Cyclooxygenase 2/genetics/metabolism
MH  - Fibroblast Growth Factor 2/genetics/metabolism
MH  - Humans
MH  - Interleukins/genetics/metabolism
MH  - Matrix Metalloproteinases/genetics/metabolism
MH  - Osteoarthritis, Knee/genetics/*metabolism
MH  - Osteoblasts/cytology/*metabolism
MH  - Osteoprotegerin/genetics/metabolism
MH  - RANK Ligand/genetics/metabolism
MH  - Stress, Physiological/*physiology
EDAT- 2011/10/29 06:00
MHDA- 2012/09/15 06:00
CRDT- 2011/10/29 06:00
PHST- 2011/10/29 06:00 [entrez]
PHST- 2011/10/29 06:00 [pubmed]
PHST- 2012/09/15 06:00 [medline]
AID - 10.1002/art.33445 [doi]
PST - ppublish
SO  - Arthritis Rheum. 2012 Apr;64(4):1193-203. doi: 10.1002/art.33445. Epub 2011 Oct 
      27.