Angiopoeitin-1 and the Progression of Gingival Inflammation

Objective: To assess the concentrations of angiopoetin (AP)-1 at various stages of gingival inflammation. AP-1 is an anti-inflammatory mediator present in various inflammatory diseases. However, its role in the pathogenesis of gingival inflammation has not been established in vivo.

Methods: Gingiva was obtained from 110 human donors prior to extraction of the adjacent teeth. The tissue was grouped based on adjacent pocket depth and bleeding on probing (BOP). Gingiva adjacent to a £ 3 mm sulcus without BOP was classified as ²normal″; (N); gingiva adjacent to a 3 mm sulcus with BOP was classified as ²diseased, slight″; (DS). Gingiva adjacent to a 4-6 mm sulcus featuring BOP was classified as ²diseased, moderate″ (DM) and gingiva adjacent to > 6 mm sulci was classified as ²diseased, severe″(DSev). Tissues were solublized and IL-6, endothelin (ET)-1, AP-1, vascular cell adhesion molecule (VCAM)-1 and vascular endothelial growth factor (VEGF) concentrations were assessed by ELISA. Data were compared by factorial analysis of variance, post-hoc Tukey test, and Pearson′s correlation test. Groups were defined as significantly different when p<0.05.

Results: Gingival concentrations of VCAM-1, IL-6, VEGF, and ET-1 was significantly greater, and AP-1 was significantly lower, in DSev and DM than in N and DS tissues (p<0.05). In addition, gingival concentrations of VCAM-1, IL-6, VEGF, and ET-1 were significantly greater, and AP-1 was significantly lower, in DSev than in DM tissues (p<0.05). There were significant positive correlations between sulcular depth, VCAM-1, IL-6, VEGF and ET-1 and negative correlations between AP-1, sulcular depth, and the other biomarkers (p<0.05).

Conclusion: Reduced tissue concentrations of AP-1 may act as a progression factor for gingival inflammation because VEGF and ET-1 expression becomes less inhibited. Thus, the tissues become edematous and more likely to develop BOP.