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Cyclo-oxygenase 2 function is essential for bone fracture healing.

Ann Marie Simon1, Michaele Beth Manigrasso, J Patrick O'Connor

  • 1Department of Orthopaedics, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark 07103, USA.

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research
|June 11, 2002
PubMed
Summary

Cyclo-oxygenase 2 (COX-2) is essential for fracture healing, not fetal bone development. Inhibiting COX-2 with NSAIDs or gene mutation prevents bone repair, highlighting its critical role in endochondral ossification.

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Area of Science:

  • Biomedical Science
  • Orthopedics
  • Inflammation Research

Background:

  • Fracture healing shares similarities with fetal bone development but includes an inflammatory phase.
  • Cyclo-oxygenase 2 (COX-2) produces prostaglandins at inflammation sites.

Purpose of the Study:

  • To investigate the necessity of COX-2 activity in the fracture healing process.
  • To differentiate the role of COX-2 in fracture healing versus fetal bone development.

Main Methods:

  • Rats were treated with COX-2-selective NSAIDs (celecoxib, rofecoxib).
  • Fracture healing was assessed using radiographic, histological, and mechanical testing.
  • Fracture healing was also examined in mice with a COX-2 gene mutation.

Main Results:

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  • COX-2 inhibition via NSAIDs led to complete fracture healing failure in rats.
  • Mice lacking the COX-2 gene also exhibited failed fracture healing.
  • Histological analysis indicated COX-2 is crucial for endochondral ossification during healing.

Conclusions:

  • COX-2 activity is indispensable for successful fracture healing.
  • The role of COX-2 in fracture healing is distinct from its role in fetal bone development, where it is not essential.
  • COX-2 selective NSAIDs impede fracture healing by inhibiting COX-2 activity.