Mode & mechanism of low intensity pulsed ultrasound (LIPUS) in fracture repair (original) (raw)
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Highlights
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A mode and mechanism on how LIPUS enhances fracture repair is proposed. - •
LIPUS drives the production of bone specific proteins to enhance bone healing. - •
Integrins, on the surface of cells detect the pressure wave caused by LIPUS. - •
The key gene which is upregulated after LIPUS exposure is COX2. - •
COX2 is critical for LIPUS enhanced production of bone specific proteins.
Abstract
It has been 30
years since the first level one clinical trial demonstrated low intensity pulsed ultrasound (LIPUS) could accelerate fracture repair. Since 1994 numerous investigations have been performed on the effect of LIPUS. The majority of these studies have used the same signal parameters comprised of an intensity of 30
mW/cm2 SATA, an ultrasound carrier frequency of 1.5
MHz, pulsed at 1
kHz with an exposure time of 20
minutes per day. These studies show that a biological response is stimulated in the cell which produces bioactive molecules. The production of these molecules, linked with observations demonstrating the enhanced effects on mineralization by LIPUS, might be considered the general manner, or mode, of how LIPUS stimulates fractures to heal.
We propose a mechanism for how the LIPUS signal can enhance fracture repair by combining the findings of numerous studies. The LIPUS signal is transmitted through tissue to the bone, where cells translate this mechanical signal to a biochemical response via integrin mechano-receptors. The cells enhance the production of cyclo-oxygenese 2 (COX-2) which in turn stimulates molecules to enhance fracture repair. The aim of this review is to present the state of the art data related to LIPUS effects and mechanism.
Keywords
Fracture
LIPUS
Ultrasound
Mechanism
Bone morphogenic protein
Cyclo-oxygenase 2
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© 2016 The Authors. Published by Elsevier B.V.