Oral diseases such as periodontitis and gingivitis are inflammatory processes induced by bacterial biofilms. The bacterial factor lipopolysaccharide (LPS) is an important virulence factor of gram-negative bacteria, and plays an essential role in triggering periodontal inflammation. LPS activates macrophages and causes an inflammatory response including synthesis and release of cytokines – an important strategy utilized by the host to resist periodontal bacteria.

Dental composites modulate cytokine signaling in cellsDue to incomplete curing and degradation of dental composites, cells in the oral cavity may be exposed to monomers and filler particles. A recent study at NIOM investigated the effect of two typical composite filler particles and a methacrylate monomer on the macrophage immune response to LPS. Release of the pro-inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) from RAW 264.7 macrophages was measured as well as the cellular viability.

Exposure to nanosilica, quartz or triethyleneglycol dimethacrylate (TEGDMA) followed by exposure to LPS resulted in lower IL-1β release compared to LPS treatment alone. After combined exposure, TEGDMA and filler particles resulted in an additive reduction of the cytokine release. The cellular viability and TNF-α release were not significantly affected by any exposures.

Clinical significance
An attenuated cytokine release may have implications for the macrophage immune response and result in impaired bacterial clearance. This study also emphasizes the need to consider the effects of combined exposure to degradation products in risk assessment of dental composites.

The full study is described in the following
TEGDMA and filler particles from dental composites additively attenuate LPS-induced cytokine release from the macrophage cell line RAW 264.7.
Mathisen GH, Ansteinsson V, Samuelsen JT, Becher R, Dahl JE, Bølling AK.
Clin Oral Investig. 2014 Mar 11.

NIOM Newsletter May 2014