BACKGROUND: The purpose of this study was to assess concentrations of angiopoietin (Ang)-1 at various stages of gingival inflammation. Ang-1 is an anti-inflammatory mediator present in various inflammatory diseases. However, its presence during the pathogenesis of gingival inflammation has not been established in vivo. METHODS: Gingiva was obtained from 110 human donors before extraction of the adjacent teeth. The tissue was grouped based on adjacent probing depth and bleeding on probing (BOP). Gingiva adjacent to a <or=3-mm sulcus without BOP was classified as "normal" (N); gingiva adjacent to a 3-mm sulcus with BOP was classified as "diseased, slight" (DS); gingiva adjacent to a 4- to 6-mm sulcus featuring BOP was classified as "diseased, moderate" (DM); and gingiva adjacent to >6-mm sulci was classified as "diseased, severe" (DSev). Tissues were solublized, and concentrations of interleukin (IL)-1beta and -6, tumor necrosis factor (TNF)-alpha, endothelin (ET)-1, Ang-1, vascular cell adhesion molecule (VCAM)-1, and vascular endothelial growth factor (VEGF) were assessed by enzyme-linked immunosorbent assay. Data were compared by factorial analysis of variance, the post hoc Tukey test, and the Pearson correlation test. Groups were defined as significantly different when P <0.05. RESULTS: Gingival concentrations of IL-1beta and -6, TNF-alpha, VEGF, and ET-1 were significantly greater, and VCAM-1 and Ang-1 were significantly lower, in DSev and DM than in N and DS tissues (P <0.05). In addition, gingival concentrations of IL-6, VEGF, and ET-1 were significantly greater, and VCAM-1 and Ang-1 were significantly lower, in DSev than in DM tissues (P <0.05). There were significant positive correlations among sulcular depth, IL-1beta and -6, TNF-alpha, VEGF, and ET-1 and negative correlations among VCAM-1, Ang-1, sulcular depth, and the other biomarkers (P <0.001). CONCLUSIONS: Depleted tissue concentrations of Ang-1 may allow gingival inflammation to become more severe because VEGF and ET-1 secretion become less inhibited. Thus, the tissues become edematous and more likely to develop BOP.
BACKGROUND: The purpose of this study was to assess concentrations of angiopoietin (Ang)-1 at various stages of gingival inflammation. Ang-1 is an anti-inflammatory mediator present in various inflammatory diseases. However, its presence during the pathogenesis of gingival inflammation has not been established in vivo. METHODS:Gingiva was obtained from 110 human donors before extraction of the adjacent teeth. The tissue was grouped based on adjacent probing depth and bleeding on probing (BOP). Gingiva adjacent to a <or=3-mm sulcus without BOP was classified as "normal" (N); gingiva adjacent to a 3-mm sulcus with BOP was classified as "diseased, slight" (DS); gingiva adjacent to a 4- to 6-mm sulcus featuring BOP was classified as "diseased, moderate" (DM); and gingiva adjacent to >6-mm sulci was classified as "diseased, severe" (DSev). Tissues were solublized, and concentrations of interleukin (IL)-1beta and -6, tumor necrosis factor (TNF)-alpha, endothelin (ET)-1, Ang-1, vascular cell adhesion molecule (VCAM)-1, and vascular endothelial growth factor (VEGF) were assessed by enzyme-linked immunosorbent assay. Data were compared by factorial analysis of variance, the post hoc Tukey test, and the Pearson correlation test. Groups were defined as significantly different when P <0.05. RESULTS: Gingival concentrations of IL-1beta and -6, TNF-alpha, VEGF, and ET-1 were significantly greater, and VCAM-1 and Ang-1 were significantly lower, in DSev and DM than in N and DS tissues (P <0.05). In addition, gingival concentrations of IL-6, VEGF, and ET-1 were significantly greater, and VCAM-1 and Ang-1 were significantly lower, in DSev than in DM tissues (P <0.05). There were significant positive correlations among sulcular depth, IL-1beta and -6, TNF-alpha, VEGF, and ET-1 and negative correlations among VCAM-1, Ang-1, sulcular depth, and the other biomarkers (P <0.001). CONCLUSIONS: Depleted tissue concentrations of Ang-1 may allow gingival inflammation to become more severe because VEGF and ET-1 secretion become less inhibited. Thus, the tissues become edematous and more likely to develop BOP.