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.

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.