Relationship between gingival angiopoietin-1 concentrations and depth of the adjacent gingival sulcus.
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.
Lester
S Reid
SR
Department of Periodontics and Preventive Sciences, School of Dentistry, University of Mississippi, Jackson, MS, USA.
Bain
Jennifer L
JL
Serio
Francis G
FG
Harrelson
Bradley D
BD
Johnson
Roger B
RB
D000328:Adult; D000368:Aged; D042683:Angiopoietin-1 / Q000032:analysis*; D019332:Endothelin-1 / Q000032:analysis; D005260:Female; D005881:Gingiva / Q000737:chemistry* / Q000473:pathology; D005884:Gingival Hemorrhage / Q000145:classification / Q000378:metabolism; D005891:Gingivitis / Q000145:classification / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D053583:Interleukin-1beta / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D008297:Male; D008875:Middle Aged; D010514:Periodontal Pocket / Q000145:classification / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis; D055815:Young Adult
C467630:ANGPT1 protein, human; D042683:Angiopoietin-1; D019332:Endothelin-1; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A