This study, indicating significant correlations between body composition and periodontal disease (with WHR being the most significant, followed by BMI, FFM, and S), showed similarities to those observed in other obesity-related health problems. This strengthened arguments that periodontal disease and certain obesity-related systemic illnesses are related, with abnormal fat metabolism possibly being an important factor.

Gingival concentrations of IL-11 and IL-17 are different in diseased gingiva adjacent to 3, 4 to 5, and > or = 6 mm pockets, suggesting that their concentrations change as a consequence of the progression of gingivitis to periodontitis and that both cytokines could have a significant role in this progression. These data may be useful for the design of procedures for prevention of periodontal disease.

VEGF may be a factor in initiation and progression of gingivitis to periodontitis, possibly by promoting expansion of the vascular network coincident to progression of the inflammation.

High-resolution electron energy loss spectroscopy (HREELS) and X-ray photoelectron spectroscopy (XPS) have been used to investigate the adsorption of ferrocene on Ag(100) at 150 K. The HREELS data show that ferrocene adopts an orientation with the molecular axis perpendicular to the Ag(100) surface plane for low exposures. Additionally, no rehybridization is observed at the low temperature employed. Upon multilayer growth, however, the molecular axis becomes canted with respect to the surface normal. XPS for monolayer ferrocene gives Fe 2p binding energies of 707.9 and 720.8 eV for the 2p3/2 and 2p1/2 transitions, respectively, and C 1s binding energy of 284.9 eV. Monolayer surface coverage represents a molecular footprint of about one ferrocene per nine Ag surface atoms. Multilayer ferrocene grows in a layer-by-layer fashion and shows HREELS and XPS

Human leptin is present within healthy and marginally inflamed gingiva and decreases in concentration as the adjacent probing depth increases. When leptin concentrations decreased (> or =3 mm sulcus), VEGF concentrations increased, suggesting that leptin could be released from gingiva coincident to vascular expansion. Thus, gingiva, in addition to adipose tissue, could be a source of circulating leptin in patients with periodontal disease. This possibility requires further investigation.

Our results suggested the possibility that the IL-23/IL-17 immune response was present within chronically inflamed gingiva. This is a host response that had not been reported previously in periodontal disease and may be an important factor in the chronic nature of the disease.

Periodontal inflammation may not successfully resolve because of accumulation of IL-6 and IL-18, and decreased concentrations of IL-12, within diseased gingiva. Because of the highly significant correlation between IL-18 concentration and gingival sulcular depth, IL-18 may be a useful target for either preventive or palliative therapy for periodontitis.

The results of the study suggest that changes in alveolar bone density and levels of bone resorptive cytokines in saliva may be secondary to changes in menopausal status. These changes may predispose loss of alveolar bone with resultant loss of teeth.