Teriparatide (human PTH1–34) compensates for impaired fracture healing in COX-2 deficient mice

Kiminori Yukata, Chao Xie, Tian Fang Li, Matthew L. Brown, Tsukasa Kanchiku, Xinping Zhang, Hani A. Awad, Edward M. Schwarz, Christopher A. Beck, Jennifer H. Jonason, Regis J. O'Keefe

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


Genetic ablation of cyclooxygenase-2 (COX-2) in mice is known to impair fracture healing. To determine if teriparatide (human PTH1–34) can promote healing of Cox-2-deficient fractures, we performed detailed in vivo analyses using a murine stabilized tibia fracture model. Periosteal progenitor cell proliferation as well as bony callus formation was markedly reduced in Cox-2−/− mice at day 10 post-fracture. Remarkably, intermittent PTH1–34 administration increased proliferation of periosteal progenitor cells, restored callus formation on day 7, and enhanced bone formation on days 10, 14 and 21 in Cox-2-deficient mice. PTH1–34 also increased biomechanical torsional properties at days 10 or 14 in all genotypes, consistent with enhanced bony callus formation by radiologic examinations. To determine the effects of intermittent PTH1–34 for callus remodeling, TRAP staining was performed. Intermittent PTH1–34 treatment increased the number of TRAP positive cells per total callus area on day 21 in Cox-2−/− fractures. Taken together, the present findings indicate that intermittent PTH1–34 treatment could compensate for COX-2 deficiency and improve impaired fracture healing in Cox-2-deficient mice.

Original languageEnglish
Pages (from-to)150-159
Number of pages10
StatePublished - May 2018


  • Cyclooxygenase-2 (COX-2)
  • Fracture healing
  • Parathyroid hormone (PTH)
  • Periosteum
  • Prostaglandin


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