Intranuclear Delivery of Nuclear Factor-Kappa B p65 in a Rat Model of Tooth Replantation

Int J Mol Sci. 2021 Feb 17;22(4):1987. doi: 10.3390/ijms22041987.

Abstract

After avulsion and replantation, teeth are at risk of bone and root resorption. The present study aimed to demonstrate that the intra-nuclear transducible form of transcription modulation domain of p65 (nt-p65-TMD) can suppress osteoclast differentiation in vitro, and reduce bone resorption in a rat model of tooth replantation. Cell viability and nitric oxide release were evaluated in RAW264.7 cells using CCK-8 assay and Griess reaction kit. Osteoclast differentiation was evaluated using quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and tartrate-resistant acid phosphatase (TRAP) staining. Thirty-two maxillary rat molars were extracted and stored in saline (n = 10) or 10 µM nt-p65-TMD solution (n = 22) before replantation. After 4 weeks, specimens were scored according to the inflammatory pattern using micro-computed tomography (CT) imaging and histological analyses. nt-p65-TMD treatment resulted in significant reduction of nitric oxide release and osteoclast differentiation as studied using PCR and TRAP staining. Further, micro-CT analysis revealed a significant decrease in bone resorption in the nt-p65-TMD treatment group (p < 0.05). Histological analysis of nt-p65-TMD treatment group showed that not only bone and root resorption, but also inflammation of the periodontal ligament and epithelial insertion was significantly reduced. These findings suggest that nt-p65-TMD has the unique capabilities of regulating bone remodeling after tooth replantation.

Keywords: intra-nucleus delivery; nuclear factor kappa B; osteoclast; tooth replantation.

MeSH terms

  • Animals
  • Cell Differentiation
  • Cell Nucleus / metabolism*
  • Cell Survival
  • Mice
  • Models, Animal
  • Molar / diagnostic imaging
  • Nitric Oxide / metabolism
  • Osteoclasts / metabolism
  • RAW 264.7 Cells
  • Rats
  • Tooth Replantation*
  • Transcription Factor RelA / metabolism*
  • Transduction, Genetic
  • X-Ray Microtomography

Substances

  • Transcription Factor RelA
  • Nitric Oxide