Low-intensity pulsed ultrasound inhibits lipopolysaccharide-induced IL-6 and RANKL expression in osteoblasts

J Oral Sci. 2017;59(2):303-309. doi: 10.2334/josnusd.16-0624.

Abstract

Periodontal disease is caused by inflammation induced by Porphyromonas gingivalis (P.g.) lipopolysaccharide (LPS) and involves expression of proinflammatory cytokines such as interleukin (IL)-1, IL-6, tumor necrosis factor-α, and receptor activator of nuclear factor kappa B ligand (RANKL), which are implicated in bone resorption. Low-intensity pulsed ultrasound (LIPUS) is commonly used in the treatment of bone fracture. However, the mechanisms by which LIPUS inhibits LPS-induced inflammatory cytokines are poorly understood. Therefore, we investigated the effects of LIPUS on LPS-induced expression of the proinflammatory cytokines IL-6 and RANKL. MC3T3-E1 cells were incubated in the presence or absence of P.g. LPS and then stimulated with LIPUS for 30 min/day for a maximum of 14 days. LPS increased mRNA and protein expressions of IL-6 and RANKL on day 14. In addition, mRNA expression of COX-2 LPS was higher after 3 and 7 days of LIPUS treatment. PGE2 was induced by LPS after 7 and 14 days of culture. LIPUS suppressed all stimulatory effects of LPS. These results suggest that LIPUS inhibits LPS-induced expression of inflammation cytokines by suppressing PGE2 production and might thus have potential applications in the treatment of periodontitis.

Keywords: LIPUS; LPS; PGE2; proinflammatory cytokine.

MeSH terms

  • 3T3 Cells
  • Animals
  • Enzyme-Linked Immunosorbent Assay
  • Interleukin-6 / metabolism*
  • Lipopolysaccharides / pharmacology*
  • Mice
  • Osteoblasts / drug effects*
  • Osteoblasts / metabolism
  • RANK Ligand / metabolism*
  • Real-Time Polymerase Chain Reaction
  • Ultrasonics*

Substances

  • Interleukin-6
  • Lipopolysaccharides
  • RANK Ligand