Modulation of Osteoblast Differentiation in Rat Calvarial Cells: Investigations into Effects of Mechanical Load and Interleukin-1β
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Authors
Brigman, Brian E.
Issue Date
2000-07
Volume
Issue
Type
Dissertation
Language
en_US
Keywords
Alternative Title
Abstract
The relationship between mechanical loading and adaptive changes in bony architecture was noted more than one hundred years ago, however, the mechanism of this process is still not understood. Effects of mechanical loading of bones in vivo include bone formation, though it is unclear if this represents upregulation of existing osteoblasts or increased differentiation of osteoblasts. In vitro effects of mechanical loading of osteoblast-like cells include increased proliferation, changes in collagen production and increased prostaglandin formation. No in vitro study has reported increased bone formation nor has been able to determine if mechanical load induces differentiation of osteoprogenitor cells.
This study used an in vitro mechanical loading model of rat calvarial osteoblasts to determine if loading affected differentiation of osteoprogenitor cells. Measurements of prostaglandin and nitric oxide, two possible mediators of the effects of mechanical load in vivo were also made.
This study was unable to correlate mechanical loading in vitro with increased differentiation of osteoprogenitors. Measurements of prostaglandin and nitric oxide were also inconclusive using this model. Possible reasons for the inability to detect these potential effects are discussed.
Description
Citation
Publisher
Creighton University
License
Copyright is retained by the Author. A non-exclusive distribution right is granted to Creighton University and to ProQuest following the publishing model selected above.
Copyright is retained by the Author. A non-exclusive distribution right is granted to Creighton University and to ProQuest following the publishing model selected above.
Copyright is retained by the Author. A non-exclusive distribution right is granted to Creighton University and to ProQuest following the publishing model selected above.