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Prolonged Endochondral Bone Healing in Senescence is Shortened by Low-Intensity Pulsed Ultrasound in a Manner Dependent on COX-2

Authors
Journal
Ultrasound in Medicine & Biology
0301-5629
Publisher
Elsevier
Publication Date
Volume
36
Issue
7
Identifiers
DOI: 10.1016/j.ultrasmedbio.2010.04.011
Keywords
  • Cyclooxygenase-2 (Cox-2)
  • Prostaglandin E2(Pge2)
  • Fracture Healing
  • Low-Intensity Pulsed Ultrasound (Lipus)
Disciplines
  • Chemistry
  • Medicine

Abstract

Abstract To test whether mechanical loading produces faster healing in aged mice, fractured femurs of aged 1-year-old mice were subjected to low-intensity pulsed ultrasound (LIPUS), a treatment that is routinely used to help heal fractures in humans. Cyclooxygenase-2 knockout mice (COX-2 −/−), which lack an immediate early mediator of mechanical stimulation, were also studied by histochemistry, microcomputed tomography and quantitative polymerase chain reaction to determine the role of COX-2. The healing in the aged COX-2 −/− mice is slow during the endochondral bone remodeling (>30 d), a period generally prolonged in senescence. For aged wild-type mice, LIPUS halved the endochondral phase to about 10 d, whereas that was not the case for aged COX-2 −/− mice, which showed no apparent shortening of the prolonged endochondral-phase healing time. Injecting prostaglandin E 2 receptor agonists, however, rescued the COX-2 −/− callus from insensitivity to LIPUS. In conclusion, COX-2 is a limiting factor in the delayed endochondral bone healing and is induced by LIPUS, which normalizes healing rate to the wild-type level. (E-mail: [email protected])

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