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Nonsteroidal anti-inflammatory drug effects on osteoblastic cell cycle, cytotoxicity, and cell death

Je-Ken Chang1, Gwo-Jaw Wang, Shiu-Ting Tsai

  • 1Department of Orthopaedics, School of Medicine, Orthopaedic Research Center, Kaohsiung Medical University Chug-Ho Memorial Hospital, Kaohsiung, Taiwan.

Connective Tissue Research
|March 21, 2006
PubMed

Insights

Nonsteroidal anti-inflammatory drugs (NSAIDs) arrest osteoblast cell cycle and induce cell death, potentially hindering bone formation. Piroxicam demonstrated the least impact on osteoblast function among the tested NSAIDs.

Area of Science:

  • Biomedical Sciences
  • Pharmacology
  • Cell Biology

Background:

  • Nonsteroidal anti-inflammatory drugs (NSAIDs) are known to impede bone repair and remodeling in vivo.
  • Previous in vitro research indicated that specific NSAIDs, indomethacin and ketorolac, inhibit osteoblast proliferation.

Purpose of the Study:

  • To investigate the effects of four NSAIDs on osteoblast cell cycle kinetics, cytotoxicity, and cell death patterns.
  • To determine if the mechanisms of NSAID-induced osteoblast dysfunction are prostaglandin-dependent.

Main Methods:

  • Primary osteoblast cultures were established from rat fetal calvaria.
  • Osteoblasts were treated with four different NSAIDs.
  • Cell cycle progression, cytotoxicity, and cell death (apoptosis and necrosis) were analyzed.

Main Results:

  • NSAIDs significantly arrested the osteoblast cell cycle at the G(0)/G(1) phase.
  • NSAIDs induced significant cytotoxicity and cell death in osteoblasts, with apoptosis being more prevalent than necrosis.
  • Piroxicam exhibited the least inhibitory effect on osteoblast function compared to other NSAIDs tested.
  • The cytotoxic and apoptotic effects appeared independent of prostaglandin synthesis.

Conclusions:

  • NSAID-induced cell cycle arrest and apoptosis in osteoblasts represent a key mechanism contributing to their negative impact on bone formation.
  • These findings provide insights into the cellular mechanisms underlying NSAID-associated bone healing complications.

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