Document Detail


High pressure may inhibit periprosthetic osteogenesis.
MedLine Citation:
PMID:  19921349     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Mechanical effects have been demonstrated to activate periprosthetic osteoclasts and hence to promote bone resorption. However, the periprosthetic mechanical effect on osteoblast function is not clearly understood. The purpose of this study was to explore whether the high pressure on bone caused by a prosthesis affects periprosthetic osteoblast function. We applied static pressure of various magnitudes to SV40-transfected human fetal osteoblast cells, then assayed bioactivities compared to cells cultured without pressure (control). The results showed that osteoblast proliferation, differentiation, apoptosis, necrosis, and mineralization were all sensitive to static pressure, and the effects were magnitude dependent. Low-level static pressure (20 kPa) enhanced osteogenesis. Under 50-100 kPa static pressure, proliferation was inhibited and apoptosis was enhanced, but the cellular phenotype could be maintained. High pressure (250-500 kPa) totally inhibited the bioactivity of the osteoblasts and induced necrosis. Mineralization nodules decreased significantly under 100 kPa pressure, while no nodules could be found under 250 and 500 kPa pressure. RUNX2, COL-1, and BGP mRNA expression was significantly downregulated under 250 and 500 kPa. SOX9 expression was significantly upregulated at 100 kPa but significantly downregulated at 250 and 500 kPa. RANKL/OPG expression was increased under pressure, and the differences were significant at 100 and 500 kPa. These results suggest that periprosthetic high pressure may inhibit osteogenesis and promote osteoclastogenesis. Countermeasures should be developed to improve periprosthetic osteogenesis.
Authors:
Kongzu Hu; Chengtao Wang; Xianlong Zhang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-11-17
Journal Detail:
Title:  Journal of bone and mineral metabolism     Volume:  28     ISSN:  1435-5604     ISO Abbreviation:  J. Bone Miner. Metab.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-05-10     Completed Date:  2010-08-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9436705     Medline TA:  J Bone Miner Metab     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  289-98     Citation Subset:  IM    
Affiliation:
Department of Orthopaedics, Shanghai 6th Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, People's Republic of China.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / physiology
Biological Markers / metabolism
Bone Remodeling / physiology
Bone Resorption / metabolism*
Calcification, Physiologic / physiology
Cell Differentiation / physiology
Cell Line, Transformed
Cell Proliferation
Gene Expression Regulation / physiology
Humans
Necrosis / pathology
Osteoblasts / metabolism,  pathology
Osteoclasts / metabolism,  pathology
Osteogenesis / physiology*
Periprosthetic Fractures / prevention & control
Pressure / adverse effects*
RNA, Messenger / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Time Factors
Chemical
Reg. No./Substance:
0/Biological Markers; 0/RNA, Messenger

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