Leptin within healthy and diseased human gingiva

Background: Plasma leptin concentrations are reported to be elevated in pat ients with inflammatory diseases. There is no consensus concerning the biol ogical mechanism for this phenomenon. To date, tissue leptin concentrations have not been assessed within normal or inflamed gingiva. The purpose of t his study was to assess concentrations of human leptin within healthy and d iseased gingiva to define its possible role in periodontal disease progress ion. Methods: Healthy (non-hemorrhagic gingiva adjacent to a less than or equal to3 mm gingival sulcus) and inflamed gingiva (hemorrhagic gingiva adjacent to a less than or equal to3 mm periodontal pocket) were studied. Leptin, va scular endothelial growth factor (VEGF; to assess potential vascular expans ion), and interleukin-6 (IL-6; to assess periodontal disease activity and s everity) concentrations were assessed within solubilized gingival biopsies by enzyme-linked immunosorbent assay. Data were grouped by sulcular depth a nd compared by factorial analysis of variance, regression analysis, and Sch effe comparisons. Results: Leptin concentrations were highest within gingiva adjacent to a le ss than or equal to3 mm sulcus and progressively declined within gingiva ad jacent to a less than or equal to3 mm sulcus. VEGF concentrations were high est within gingiva adjacent to 4 to 6 mm pockets and nearly equivalent in h ealthy (less than or equal to3 mm sulcus) and severely diseased gingiva (>6 mm sulcus). IL-6 was positively correlated and leptin negatively correlate d with adjacent probing depth; IL-6 concentration was significantly higher and leptin significantly lower in gingiva adjacent to >6 mm pockets compare d to sites adjacent to <6 mm pockets (P <0.001). Conclusions: Human leptin is present within healthy and marginally inflamed gingiva and decreases in concentration as the adjacent probing depth incre ases. When leptin concentrations decreased (greater than or equal to3 mm su lcus), VEGF concentrations increased, suggesting that leptin could be relea sed from gingiva coincident to vascular expansion. Thus, gingiva, in additi on to adipose tissue, could be a source of circulating leptin in patients w ith periodontal disease. This possibility requires further investigation.