Endotoxin affinity for orthodontic brackets.

Abstract

Endotoxin, cell envelope lipopolysaccharide produced by gram-negative bacteria can activate an immune response through a variety of pathways. In addition, it can stimulate bone resorption and reduce the periodontal tissue's healing capacity. Previous studies have documented the affinity of lipopolysaccharide for restorative materials. This study evaluated the affinity of lipopolysaccharide for commercially available orthodontic brackets. Stainless steel, ceramic, plastic, and "gold" brackets were exposed to 10 EU/mm2radiolabeled Porphyromonas gingivalis or Escherichia coli lipolpoysaccharide in water and incubated for 24 hours at 37 degrees C. Brackets were then transferred to fresh lipopolysaccharide-free water and incubated for 24 hours at 37 degrees C to evaluate elution. This elution transfer was continued up to 96 hours total incubation. Lipopolysaccharide adherence and elution levels were calculated after treatment, and elution solutions were evaluated through liquid scintillation spectrometry. Mean initial lipopolysaccharide adherence ranged from 2.42 +/- 0.26 EU/mm2(E. coli, plastic) to 6.75 +/- 0.34 EU/mm2 (P. gingivalis, stainless steel). P. gingivalis lipopolysaccharide adherence was significantly greater than E. coli lipopolysaccharide adherence for all bracket types. Moreover, for each lipopolysaccharide type, stainless steel brackets exhibited significantly greater lipopolysaccharide adherence. Regarding elution, only the P. gingivalis lipopolysaccharide-exposed ceramic and plastic brackets at 24 hours and the stainless steel and ceramic brackets at 48 hours eluted measurable lipopolysaccharide. Results from this study demonstrate that P. gingivalis and E. coli LPS exhibit a high affinity for orthodontic brackets. In vivo, this affinity could affect the concentration of LPS in the gingival sulcus, thereby contributing to inflammation in tissues adjacent to the brackets.